StemCell Therapy

Personalized medicine relies on tests to help determine an individuals response to certain medications.

Personalized medicine takes into account your unique genetic makeup. Unlike "genetic medicine," which is directed at such inherited diseases as sickle cell anemia, personalized medicine can help your doctor tailor treatment for conditions such as heart disease and deep vein thrombosis. This enables him/her to focus on prevention, detection and early intervention.

Your genetic makeup also affects which medicines work best for youand how you respond to them. Your doctor can prescribe targeted treatment based on both:

We offer two such tests, which represent the forefront of personalized medicine. They can determine your response to two of the most widely prescribed drugs.

Marketed as Coumadin and Jantoven, warfarin thins the blood to help prevent and treat deep vein thrombosis, stroke, heart attack, atrial fibrillation and other diseases of the arteries and veins. The right dosage is crucial. Too low a dose could increase the risk of a life-threatening blood clot. Too high a dose could increase bleeding risk. Plus, your response to a specific dose can vary widely. We offer the AccuType Warfarin test to help your physician determine the appropriate dosage based on your genetic information.

Marketed as Plavix, clopidogrel is another blood thinner. The AccuType CP test identifies if youre unlikely to respond well to the drug and therefore at increased risk for stroke or heart attack. It also identifies if youre likely to be overly sensitive to the drug and therefore at increased risk for bleeding episodes.

Personalized medicine, including these two laboratory tests, can help make possible:

The rest is here:
Health and Wellness : Personalized Medicine

Designer babies, the end of diseases, genetically modified humans that never age. Outrageous things that used to be science fiction are suddenly becoming reality. The only thing we know for sure is that things will change irreversibly.

Support us on Patreon so we can make more videos (and get cool stuff in return): https://www.patreon.com/Kurzgesagt?ty=h

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soundcloud: http://bit.ly/2aRxNZdbandcamp: http://bit.ly/2berrSWhttp://www.epic-mountain.com

Thanks to Volker Henn, James Gurney and (prefers anonymity) for help with this video!

THANKS A LOT TO OUR LOVELY PATRONS FOR SUPPORTING US:

Jeffrey Schneider, Konstantin Kaganovich, Tom Leiser, Archie Castillo, Russell Eishard, Ben Kershaw, Marius Stollen, Henry Bowman, Ben Johns, Bogdan Radu, Sam Toland, Pierre Thalamy, Christopher Morgan, Rocks Arent People, Ross Devereux, Pascal Michaud, Derek DuBreuil, Sofia Quintero, Robert Swiniarski, Merkt Kzlrmak, Michelle Rowley, Andy Dong, Saphir Patel, Harris Rotto, Thomas Huzij, Ryan James Burke, NTRX, Chaz Lewis, Amir Resali, The War on Stupid, John Pestana, Lucien Delbert, iaDRM, Jacob Edwards, Lauritz Klaus, Jason Hunt, Marcus : ), Taylor Lau, Rhett H Eisenberg, Mr.Z, Jeremy Dumet, Fatman13, Kasturi Raghavan, Kousora, Rich Sekmistrz, Mozart Peter, Gaby Germanos, Andreas Hertle, Alena Vlachova, Zdravko aek

SOURCES AND FURTHER READING:

The best book we read about the topic: GMO Sapiens

https://goo.gl/NxFmk8

(affiliate link, we get a cut if buy the book!)

Good Overview by Wired:http://bit.ly/1DuM4zq

timeline of computer development:http://bit.ly/1VtiJ0N

Selective breeding: http://bit.ly/29GaPVS

DNA:http://bit.ly/1rQs8Yk

Radiation research:http://bit.ly/2ad6wT1

inserting DNA snippets into organisms:http://bit.ly/2apyqbj

First genetically modified animal:http://bit.ly/2abkfYO

First GM patent:http://bit.ly/2a5cCox

chemicals produced by GMOs:http://bit.ly/29UvTbhhttp://bit.ly/2abeHwUhttp://bit.ly/2a86sBy

Flavr Savr Tomato:http://bit.ly/29YPVwN

First Human Engineering:http://bit.ly/29ZTfsf

glowing fish:http://bit.ly/29UwuJU

CRISPR:http://go.nature.com/24Nhykm

HIV cut from cells and rats with CRISPR:http://go.nature.com/1RwR1xIhttp://ti.me/1TlADSi

first human CRISPR trials fighting cancer:http://go.nature.com/28PW40r

first human CRISPR trial approved by Chinese for August 2016:http://go.nature.com/29RYNnK

genetic diseases:http://go.nature.com/2a8f7ny

pregnancies with Down Syndrome terminated:http://bit.ly/2acVyvg( 1999 European study)

CRISPR and aging:http://bit.ly/2a3NYAVhttp://bit.ly/SuomTyhttp://go.nature.com/29WpDj1http://ti.me/1R7Vus9

Help us caption & translate this video!

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Genetic Engineering Will Change Everything Forever ...

Stems cell therapy is a cutting-edge technology that is now widely being used in orthopedic and sports medicine. The procedure involves using a patients own stem cells, which have the unique property of being able to develop into many different cell types, to treat injuries and arthritis.

Stem cells can be found in our bone marrow, fat cells and other tissues. These cells are frequently taken from the bone marrow or from a small amount of fat tissue, where a high concentration of stem cells can be extracted. This concentration is known as bone marrow aspirate or lipoaspirate respectively.

The aspirate is then injected into the site of injury so the cells can help repair the injured or degenerative tissue. Stem cell therapy is also commonly used to treat arthritis, meniscal tears and a variety of orthopedic and medical conditions. Patients can experience significant pain relief within one to two months after the procedure.

Although stem cell therapy has been used for decades, it is still considered experimental in orthopedic and sports medicine. Stem cell therapy should not be used as the first step in treating an orthopedic injury.

In addition, the risk of bone marrow aspiration for stem cell therapy includes infection, prolonged bleeding, pain at the aspiration or injection site, bruising and nerve injury.

The best way to determine if you are a candidate for stem cell therapy is to have a thorough evaluation by a physician experienced with stem cell therapies. Stem cell therapy is usually not covered by insurance. However, depending on the type of treatment that is needed, partial reimbursement may be possible.

Dr. Alicia Carter is respected in her field for her experience, personal care, and non-operative approach to orthopedic and sports injuries. As a clinical instructor at Columbia University College of Physicians and Surgeons, she is tasked with staying on the forefront of new technologies that are impacting and improving peoples lives. Dr. Carter has almost a decade of experience in the field of regenerative medicine and she is an active member of the International Society of Regenerative Medicine. Patients prefer her patience, her gentle hand and her anesthetizing techniques, which allow her to perform procedures with minimal or no discomfort. She has successfully treated patients with stem cell therapy and will work with you to determine if its right for you.

Dr. Carter offers complimentary monthly group stem cell therapy information sessions. These sessions do fill quickly so contact our office to reserve your spot today.

Book Now!

Q: Does Dr. Carter perform stem cell treatments for the spine (cervical, thoracic and lumbar) and joints? A: Yes. Dr. Carter treats virtually all orthopedic and sports conditions and can use stem cell treatments for most, including disorders and injuries of the cervical spine.

Q: Where does Dr. Carter get the stem cells from?A: Stem cells can be obtained from the bone marrow/pelvic bone or from a small amount of abdominal fat tissue.

Q: Is stem cell therapy covered by insurance? A: Stem cell therapy is typically not covered by insurances. However, depending on your condition, partial reimbursement may be possible. Reimbursement questions can be answered in more detail after your consult and once we know more about your insurance coverage.

Q: How much does stem cell therapy cost?A: The price can vary depending on the type of condition being treated and whether bone marrow aspirate or fat tissue is utilized to acquire the stem cells.

Q: Do I have to pay for the initial consult? A: It depends on your insurance plan. If you have to pay upfront for initial consult, then it will be deducted from the total cost of the stem cell procedure if you are a candidate. If youre not a candidate, then the consultation feet is nonrefundable however, alternative treatments will be thoroughly discussed. We will gladly submit the consult visit claim to your insurance company on your behalf, which may or may not be reimbursable.

Originally posted here:
Stem Cell Therapy For Orthopedic Injuries and Arthritis ...

Palliative management has consisted of lifestyle changes (diet, exercise, activity restrictions, and others), physical therapy, injections and medication. When severe, surgery has been an option for both joint and spine degenerative disease. Joint replacement, disc replacement and fusion were available to those with severe limitations in function related to the degenerative process.

These surgeries hold both great promise and great risk. Surgery results in irreversible structural change. It is a bridge burner in the respect that surgery forever changes the anatomy. In many cases surgical outcome is good and justifies this change in anatomy. In some, however, the change results in worsening of the original pain and overall worsening of function. Statistics show poorer outcomes with each successive surgery. Unfortunately, it is difficult, if not impossible to predict a successful surgical intervention in any individual patient.

Successful treatment is usually temporary and measured over years since surgical joint prosthetics wear out and require revision and replacement. Spine fusion speeds the degenerative process at adjacent vertebral levels.

Stem cell therapy, available now, is a means to stimulate healing in patients suffering both joint and disc related pain. Although we do not know how long lasting this treatment will be, we do know that the structure of the joint or spine is not changed with regenerative treatment.When patients are properly selected, outcomes are quite good. Best of all, stem cell treatment does not change anatomy and surgical options continue to be open and available if necessary.

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Stem Cell Therapy - Stem Cells Heal Me

Nanomedicine, refers to highly specific medical intervention at the molecular level for curing disease or repairing damaged tissues. Though in its infancy, could we be looking at the future of medicine? Early clinical trials certainly look promising.How Nanomedicine Works

Nanomedicine works by injecting nanoparticles into the body Can be used to: Deliver medicine Find and treat disease Repair damaged cells

One human hair is approximately 80,000 nanometers wideApplications of Nanomedicine

Drug Delivery Using nanotechnology to deliver medicine, diabetic rats kept stable blood sugar levels for 10 days after injection Cancer Diagnosis and Treatment Using microRNA from a patients blood plasma and nanotechnology: Medical professionals can determine if lung cancer is present Begin treatment the same day Using Nano-Therm therapy to overheat brain cancer cells helps to destroy them In clinical trials, those with recurrent glioblastoma survived a median of 13 months More than double the survival rate of those not receiving Nano-Therm therapyNanotechnology is already commonly used in sunscreen and to make tennis balls more bouncy

Flu Testing Todays flu tests are: Time consuming Inaccurate Nanomedicine gold flu testing provides: Instant results Immediate treatment cycle to avoid spreading to others commercial nanotech testing no more than 5 years away Cell Feedback Nanomedicine can be used to test cells response to drugs offering new drug testing methods Provides instant feedback to how cells respond to medicine Can save years and millions of dollars on testing and clinical trials Can improve current medications

In a 1956, Arthur C. Clarke first envisioned the concept of nanotechnology in a short story, The Next TenantsAdvantages of Nanomedicine

Faster diagnosis of many ailments More precise treatments of conditions such as cancer Repair tissue deep within the body Target only diseased organs, lessening the need for drugsSources

https://commonfund.nih.gov/nanomedicine/overview.aspx http://www.understandingnano.com/medicine.html http://pubs.acs.org/doi/abs/10.1021/nn400630x http://www.nature.com/nnano/journal/v6/n10/full/nnano.2011.147.html http://www.dana.org/news/features/detail_bw.aspx?id=35592 http://pubs.rsc.org/en/Content/ArticleLanding/2011/AN/C1AN15303J http://onlinelibrary.wiley.com/doi/10.1002/smll.201001642/abstract http://www.clinam.org/benefits.html

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The Future Of Nano Medicine

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Chlebowski RT, Kuller LH, Prentice RL, Stefanick ML, Manson JE, Gass M. Breast cancer after use of estrogen plus progestin in postmenopausal women. N Engl J Med. 2009 Feb 5. 360(6):573-87. [Medline].

Yao S, McCarthy PL, Dunford LM, Roy DM, Brown K, Paplham P. High prevalence of early-onset osteopenia/osteoporosis after allogeneic stem cell transplantation and improvement after bisphosphonate therapy. Bone Marrow Transplant. 2008 Feb. 41(4):393-8. [Medline].

Salooja N, Szydlo RM, Socie G, Rio B, Chatterjee R, Ljungman P. Pregnancy outcomes after peripheral blood or bone marrow transplantation: a retrospective survey. Lancet. 2001 Jul 28. 358(9278):271-6. [Medline].

Winther JF, Boice JD Jr, Frederiksen K, Bautz A, Mulvihill JJ, Stovall M. Radiotherapy for childhood cancer and risk for congenital malformations in offspring: a population-based cohort study. Clin Genet. 2009 Jan. 75(1):50-6. [Medline]. [Full Text].

Nagarajan R, Robison LL. Pregnancy outcomes in survivors of childhood cancer. J Natl Cancer Inst Monogr. 2005. (34):72-6. [Medline].

Bakker B, Massa GG, Oostdijk W, Van Weel-Sipman MH, Vossen JM, Wit JM. Pubertal development and growth after total-body irradiation and bone marrow transplantation for haematological malignancies. Eur J Pediatr. 2000 Jan-Feb. 159(1-2):31-7. [Medline].

Somali M, Mpatakoias V, Avramides A, Sakellari I, Kaloyannidis P, Smias C. Function of the hypothalamic-pituitary-gonadal axis in long-term survivors of hematopoietic stem cell transplantation for hematological diseases. Gynecol Endocrinol. 2005 Jul. 21(1):18-26. [Medline].

Anserini P, Chiodi S, Spinelli S, Costa M, Conte N, Copello F. Semen analysis following allogeneic bone marrow transplantation. Additional data for evidence-based counselling. Bone Marrow Transplant. 2002 Oct. 30(7):447-51. [Medline].

Sanders JE, Hawley J, Levy W, Gooley T, Buckner CD, Deeg HJ. Pregnancies following high-dose cyclophosphamide with or without high-dose busulfan or total-body irradiation and bone marrow transplantation. Blood. 1996 Apr 1. 87(7):3045-52. [Medline].

Sanders JE, Hoffmeister PA, Woolfrey AE, Carpenter PA, Storer BE, Storb RF. Thyroid function following hematopoietic cell transplantation in children: 30 years'' experience. Blood. 2009 Jan 8. 113(2):306-8. [Medline]. [Full Text].

Cohen A, Rovelli A, Merlo DF, van Lint MT, Lanino E, Bresters D. Risk for secondary thyroid carcinoma after hematopoietic stem-cell transplantation: an EBMT Late Effects Working Party Study. J Clin Oncol. 2007 Jun 10. 25(17):2449-54. [Medline].

Hoffmeister PA, Madtes DK, Storer BE, Sanders JE. Pulmonary function in long-term survivors of pediatric hematopoietic cell transplantation. Pediatr Blood Cancer. 2006 Oct 15. 47(5):594-606. [Medline].

Cerveri I, Zoia MC, Fulgoni P, Corsico A, Casali L, Tinelli C. Late pulmonary sequelae after childhood bone marrow transplantation. Thorax. 1999 Feb. 54(2):131-5. [Medline].

Uderzo C, Pillon M, Corti P, Tridello G, Tana F, Zintl F. Impact of cumulative anthracycline dose, preparative regimen and chronic graft-versus-host disease on pulmonary and cardiac function in children 5 years after allogeneic hematopoietic stem cell transplantation: a prospective evaluation on behalf of the EBMT Pediatric Diseases and Late Effects Working Parties. Bone Marrow Transplant. 2007 Jun. 39(11):667-75. [Medline].

Faraci M, Barra S, Cohen A, Lanino E, Grisolia F, Miano M. Very late nonfatal consequences of fractionated TBI in children undergoing bone marrow transplant. Int J Radiat Oncol Biol Phys. 2005 Dec 1. 63(5):1568-75. [Medline].

Rieger CT, Rieger H, Kolb HJ, Peterson L, Huppmann S, Fiegl M. Infectious complications after allogeneic stem cell transplantation: incidence in matched-related and matched-unrelated transplant settings. Transpl Infect Dis. 2009 Jun. 11(3):220-6. [Medline].

de Medeiros CR, Moreira VA, Pasquini R. Cytomegalovirus as a cause of very late interstitial pneumonia after bone marrow transplantation. Bone Marrow Transplant. 2000. 26:443-444.

Afessa B, Litzow MR, Tefferi A. Bronchiolitis obliterans and other late onset non-infectious pulmonary complications in hematopoietic stem cell transplantation. Bone Marrow Transplant. 2001 Sep. 28(5):425-34. [Medline].

Palmas A, Tefferi A, Myers JL, Scott JP, Swensen SJ, Chen MG. Late-onset noninfectious pulmonary complications after allogeneic bone marrow transplantation. Br J Haematol. 1998 Mar. 100(4):680-7. [Medline].

Patriarca F, Skert C, Bonifazi F, Sperotto A, Fili C, Stanzani M. Effect on survival of the development of late-onset non-infectious pulmonary complications after stem cell transplantation. Haematologica. 2006 Sep. 91(9):1268-72. [Medline].

Faraci M, Bekassy AN, De Fazio V, Tichelli A, Dini G. Non-endocrine late complications in children after allogeneic haematopoietic SCT. Bone Marrow Transplant. 2008. 41 Suppl 2:S49-57.

Cooke KR, Krenger W, Hill G, Martin TR, Kobzik L, Brewer J. Host reactive donor T cells are associated with lung injury after experimental allogeneic bone marrow transplantation. Blood. 1998 Oct 1. 92(7):2571-80. [Medline].

Majeski EI, Paintlia MK, Lopez AD, Harley RA, London SD, London L. Respiratory reovirus 1/L induction of intraluminal fibrosis, a model of bronchiolitis obliterans organizing pneumonia, is dependent on T lymphocytes. Am J Pathol. 2003 Oct. 163(4):1467-79. [Medline]. [Full Text].

Soci G, Salooja N, Cohen A, Rovelli A, Carreras E, Locasciulli A. Nonmalignant late effects after allogeneic stem cell transplantation. Blood. 2003 May 1. 101(9):3373-85. [Medline].

Original post:
Long-Term Effects of Bone Marrow Transplantation: Overview ...

Gene therapy is a technology aimed at correcting or fixing a gene that may be defective. This exciting and potentially transformative area of research is focused on the development of potential treatments for monogenic diseases, or diseases that are caused by a defect in one gene.

The technology involves the introduction of genetic material (DNA or RNA) into the body, often through delivering a corrected copy of a gene to a patients cells to compensate for a defective one, using a viral vector.

The technology involves the introduction of genetic material (DNA or RNA) into the body, often through delivering a corrected copy of a gene to a patients cells to compensate for a defective one, using a viral vector.

Viral vectors can be developed using adeno-associated virus (AAV), a naturally occurring virus which has been adapted for gene therapy use. Its ability to deliver genetic material to a wide range of tissues makes AAV vectors useful for transferring therapeutic genes into target cells. Gene therapy research holds tremendous promise in leading to the possible development of highly-specialized, potentially one-time delivery treatments for patients suffering from rare, monogenic diseases.

Pfizer aims to build an industry-leading gene therapy platform with a strategy focused on establishing a transformational portfolio through in-house capabilities, and enhancing those capabilities through strategic collaborations, as well as potential licensing and M&A activities.

We're working to access the most effective vector designs available to build a robust clinical stage portfolio, and employing a scalable manufacturing approach, proprietary cell lines and sophisticated analytics to support clinical development.

In addition, we're collaborating with some of the foremost experts in this field, through collaborations with Spark Therapeutics, Inc., on a potentially transformative gene therapy treatment for hemophilia B, which received Breakthrough Therapy designation from the US Food and Drug Administration, and 4D Molecular Therapeutics to discover and develop targeted next-generation AAV vectors for cardiac disease.

Gene therapy holds the promise of bringing true disease modification for patients suffering from devastating diseases, a promise were working to seeing become a reality in the years to come.

Excerpt from:
Gene Therapy | Pfizer: One of the world's premier ...

"Type O" redirects here. It is not to be confused with type 0.

A blood type (also called a blood group) is a classification of blood based on the presence and absence of antibodies and also based on the presence or absence of inherited antigenic substances on the surface of red blood cells (RBCs). These antigens may be proteins, carbohydrates, glycoproteins, or glycolipids, depending on the blood group system. Some of these antigens are also present on the surface of other types of cells of various tissues. Several of these red blood cell surface antigens can stem from one allele (or an alternative version of a gene) and collectively form a blood group system.[1] Blood types are inherited and represent contributions from both parents. A total of 36 human blood group systems are now recognized by the International Society of Blood Transfusion (ISBT).[2] The two most important ones are ABO and the Rh blood group systems; they determine someone's blood type (A, B, AB and O, with +, or null denoting RhD status) for suitability in blood transfusion.

A complete blood type would describe a full set of 30 substances on the surface of red blood cells, and an individual's blood type is one of many possible combinations of blood-group antigens.[3] Across the 36 blood groups, over 340 different blood-group antigens have been found.[2] Almost always, an individual has the same blood group for life, but very rarely an individual's blood type changes through addition or suppression of an antigen in infection, malignancy, or autoimmune disease.[4][5][6][7] Another more common cause in blood type change is a bone marrow transplant. Bone-marrow transplants are performed for many leukemias and lymphomas, among other diseases. If a person receives bone marrow from someone who is a different ABO type (e.g., a type A patient receives a type O bone marrow), the patient's blood type will eventually convert to the donor's type.

Some blood types are associated with inheritance of other diseases; for example, the Kell antigen is sometimes associated with McLeod syndrome.[8] Certain blood types may affect susceptibility to infections, an example being the resistance to specific malaria species seen in individuals lacking the Duffy antigen.[9] The Duffy antigen, presumably as a result of natural selection, is less common in ethnic groups from areas with a high incidence of malaria.[10]

The ABO blood group system involves two antigens and two antibodies found in human blood. The two antigens are antigen A and antigen B. The two antibodies are antibody A and antibody B. The antigens are present on the red blood cells and the antibodies in the serum. Regarding the antigen property of the blood all human beings can be classified into 4 groups, those with antigen A (group A), those with antigen B (group B), those with both antigen A and B (group AB) and those with neither antigen (group O). The antibodies present together with the antigens are found as follows:

1. Antigen A with antibody B2. Antigen B with antibody A3. Antigen AB has no antibodies4. Antigen nil (group O) with antibody A and B.

There is an agglutination reaction between similar antigen and antibody (for example, antigen A agglutinates the antibody A and antigen B agglutinates the antibody B). Thus, transfusion can be considered safe as long as the serum of the recipient does not contain antibodies for the blood cell antigens of the donor.

The ABO system is the most important blood-group system in human-blood transfusion. The associated anti-A and anti-B antibodies are usually immunoglobulin M, abbreviated IgM, antibodies. ABO IgM antibodies are produced in the first years of life by sensitization to environmental substances such as food, bacteria, and viruses.[citation needed] The original terminology used by Karl Landsteiner in 1901 for the classification was A/B/C; in later publications "C" became "O".[11] "O" is often called 0 (zero, or null) in other languages.[11][12]

The Rh system (Rh meaning Rhesus) is the second most significant blood-group system in human-blood transfusion with currently 50 antigens. The most significant Rh antigen is the D antigen, because it is the most likely to provoke an immune system response of the five main Rh antigens. It is common for D-negative individuals not to have any anti-D IgG or IgM antibodies, because anti-D antibodies are not usually produced by sensitization against environmental substances. However, D-negative individuals can produce IgG anti-D antibodies following a sensitizing event: possibly a fetomaternal transfusion of blood from a fetus in pregnancy or occasionally a blood transfusion with D positive RBCs.[13] Rh disease can develop in these cases.[14] Rh negative blood types are much less common in Asian populations (0.3%) than they are in European populations (15%).[15] The presence or absence of the Rh(D) antigen is signified by the + or sign, so that, for example, the A group is ABO type A and does not have the Rh (D) antigen.

As with many other genetic traits, the distribution of ABO and Rh blood groups varies significantly between populations.

Thirty-three blood-group systems have been identified by the International Society for Blood Transfusion in addition to the common ABO and Rh systems.[16] Thus, in addition to the ABO antigens and Rh antigens, many other antigens are expressed on the RBC surface membrane. For example, an individual can be AB, D positive, and at the same time M and N positive (MNS system), K positive (Kell system), Lea or Leb negative (Lewis system), and so on, being positive or negative for each blood group system antigen. Many of the blood group systems were named after the patients in whom the corresponding antibodies were initially encountered.

Transfusion medicine is a specialized branch of hematology that is concerned with the study of blood groups, along with the work of a blood bank to provide a transfusion service for blood and other blood products. Across the world, blood products must be prescribed by a medical doctor (licensed physician or surgeon) in a similar way as medicines.

Much of the routine work of a blood bank involves testing blood from both donors and recipients to ensure that every individual recipient is given blood that is compatible and is as safe as possible. If a unit of incompatible blood is transfused between a donor and recipient, a severe acute hemolytic reaction with hemolysis (RBC destruction), renal failure and shock is likely to occur, and death is a possibility. Antibodies can be highly active and can attack RBCs and bind components of the complement system to cause massive hemolysis of the transfused blood.

Patients should ideally receive their own blood or type-specific blood products to minimize the chance of a transfusion reaction. Risks can be further reduced by cross-matching blood, but this may be skipped when blood is required for an emergency. Cross-matching involves mixing a sample of the recipient's serum with a sample of the donor's red blood cells and checking if the mixture agglutinates, or forms clumps. If agglutination is not obvious by direct vision, blood bank technicians usually check for agglutination with a microscope. If agglutination occurs, that particular donor's blood cannot be transfused to that particular recipient. In a blood bank it is vital that all blood specimens are correctly identified, so labelling has been standardized using a barcode system known as ISBT 128.

The blood group may be included on identification tags or on tattoos worn by military personnel, in case they should need an emergency blood transfusion. Frontline German Waffen-SS had blood group tattoos during World War II.

Rare blood types can cause supply problems for blood banks and hospitals. For example, Duffy-negative blood occurs much more frequently in people of African origin,[19] and the rarity of this blood type in the rest of the population can result in a shortage of Duffy-negative blood for these patients. Similarly for RhD negative people, there is a risk associated with travelling to parts of the world where supplies of RhD negative blood are rare, particularly East Asia, where blood services may endeavor to encourage Westerners to donate blood.[20]

Pregnant women may carry a fetus with a blood type which is different from their own. In those cases, the mother can make IgG blood group antibodies. This can happen if some of the fetus' blood cells pass into the mother's blood circulation (e.g. a small fetomaternal hemorrhage at the time of childbirth or obstetric intervention), or sometimes after a therapeutic blood transfusion. This can cause Rh disease or other forms of hemolytic disease of the newborn (HDN) in the current pregnancy and/or subsequent pregnancies. Sometimes this is lethal for the fetus; in these cases it is called hydrops fetalis.[21] If a pregnant woman is known to have anti-D antibodies, the Rh blood type of a fetus can be tested by analysis of fetal DNA in maternal plasma to assess the risk to the fetus of Rh disease.[22] One of the major advances of twentieth century medicine was to prevent this disease by stopping the formation of Anti-D antibodies by D negative mothers with an injectable medication called Rho(D) immune globulin.[23][24] Antibodies associated with some blood groups can cause severe HDN, others can only cause mild HDN and others are not known to cause HDN.[21]

To provide maximum benefit from each blood donation and to extend shelf-life, blood banks fractionate some whole blood into several products. The most common of these products are packed RBCs, plasma, platelets, cryoprecipitate, and fresh frozen plasma (FFP). FFP is quick-frozen to retain the labile clotting factors V and VIII, which are usually administered to patients who have a potentially fatal clotting problem caused by a condition such as advanced liver disease, overdose of anticoagulant, or disseminated intravascular coagulation (DIC).

Units of packed red cells are made by removing as much of the plasma as possible from whole blood units.

Clotting factors synthesized by modern recombinant methods are now in routine clinical use for hemophilia, as the risks of infection transmission that occur with pooled blood products are avoided.

Table note1. Assumes absence of atypical antibodies that would cause an incompatibility between donor and recipient blood, as is usual for blood selected by cross matching.

An Rh D-negative patient who does not have any anti-D antibodies (never being previously sensitized to D-positive RBCs) can receive a transfusion of D-positive blood once, but this would cause sensitization to the D antigen, and a female patient would become at risk for hemolytic disease of the newborn. If a D-negative patient has developed anti-D antibodies, a subsequent exposure to D-positive blood would lead to a potentially dangerous transfusion reaction. Rh D-positive blood should never be given to D-negative women of child bearing age or to patients with D antibodies, so blood banks must conserve Rh-negative blood for these patients. In extreme circumstances, such as for a major bleed when stocks of D-negative blood units are very low at the blood bank, D-positive blood might be given to D-negative females above child-bearing age or to Rh-negative males, providing that they did not have anti-D antibodies, to conserve D-negative blood stock in the blood bank. The converse is not true; Rh D-positive patients do not react to D negative blood.

This same matching is done for other antigens of the Rh system as C, c, E and e and for other blood group systems with a known risk for immunization such as the Kell system in particular for females of child-bearing age or patients with known need for many transfusions.

Blood plasma compatibility is the inverse of red blood cell compatibility.[28] Type AB plasma carries neither anti-A nor anti-B antibodies and can be transfused to individuals of any blood group; but type AB patients can only receive type AB plasma. Type O carries both antibodies, so individuals of blood group O can receive plasma from any blood group, but type O plasma can be used only by type O recipients.

Table note1. Assumes absence of strong atypical antibodies in donor plasma

Rh D antibodies are uncommon, so generally neither D negative nor D positive blood contain anti-D antibodies. If a potential donor is found to have anti-D antibodies or any strong atypical blood group antibody by antibody screening in the blood bank, they would not be accepted as a donor (or in some blood banks the blood would be drawn but the product would need to be appropriately labeled); therefore, donor blood plasma issued by a blood bank can be selected to be free of D antibodies and free of other atypical antibodies, and such donor plasma issued from a blood bank would be suitable for a recipient who may be D positive or D negative, as long as blood plasma and the recipient are ABO compatible.[citation needed]

In transfusions of packed red blood cells, individuals with type O Rh D negative blood are often called universal donors. Those with type AB Rh D positive blood are called universal recipients. However, these terms are only generally true with respect to possible reactions of the recipient's anti-A and anti-B antibodies to transfused red blood cells, and also possible sensitization to Rh D antigens. One exception is individuals with hh antigen system (also known as the Bombay phenotype) who can only receive blood safely from other hh donors, because they form antibodies against the H antigen present on all red blood cells.[29][30]

Blood donors with exceptionally strong anti-A, anti-B or any atypical blood group antibody may be excluded from blood donation. In general, while the plasma fraction of a blood transfusion may carry donor antibodies not found in the recipient, a significant reaction is unlikely because of dilution.

Additionally, red blood cell surface antigens other than A, B and Rh D, might cause adverse reactions and sensitization, if they can bind to the corresponding antibodies to generate an immune response. Transfusions are further complicated because platelets and white blood cells (WBCs) have their own systems of surface antigens, and sensitization to platelet or WBC antigens can occur as a result of transfusion.

For transfusions of plasma, this situation is reversed. Type O plasma, containing both anti-A and anti-B antibodies, can only be given to O recipients. The antibodies will attack the antigens on any other blood type. Conversely, AB plasma can be given to patients of any ABO blood group, because it does not contain any anti-A or anti-B antibodies.

Typically, blood type tests are performed through addition of a blood sample to a solution containing antibodies corresponding to each antigen. The presence of an antigen on the surface of the blood cells is indicated by agglutination. An alternative system for blood type determination involving no antibodies was developed in 2017 at Imperial College London which makes use of paramagnetic molecularly imprinted polymer nanoparticles with affinity for specific blood antigens.[31] In these tests, rather than agglutination, a positive result is indicated by decolorization as red blood cells which bind to the nanoparticles are pulled toward a magnet and removed from solution.

In addition to the current practice of serologic testing of blood types, the progress in molecular diagnostics allows the increasing use of blood group genotyping. In contrast to serologic tests reporting a direct blood type phenotype, genotyping allows the prediction of a phenotype based on the knowledge of the molecular basis of the currently known antigens. This allows a more detailed determination of the blood type and therefore a better match for transfusion, which can be crucial in particular for patients with needs for many transfusions to prevent allo-immunization.[32][33]

Blood types were first discovered by an Austrian Physician Karl Landsteiner working at the Pathological-Anatomical Institute of the University of Vienna (now Medical University of Vienna). In 1900, he found that blood sera from different persons would clump together (agglutinate) when mixed in test tubes, and not only that some human blood also agglutinated with animal blood.[34] He wrote a two-sentence footnote:

The serum of healthy human beings not only agglutinates animal red cells, but also often those of human origin, from other individuals. It remains to be seen whether this appearance is related to inborn differences between individuals or it is the result of some damage of bacterial kind.[35]

This was the first evidence that blood variation exists in humans. The next year, in 1901, he made a definitive observation that blood serum of an individual would agglutinate with only those of certain individuals. Based on this he classified human bloods into three groups, namely group A, group B, and group C. He defined that group A blood agglutinates with group B, but never with its own type. Similarly, group B blood agglutinates with group A. Group C blood is different in that it agglutinates with both A and B.[36] This was the discovery of blood groups for which Landsteiner was awarded the Nobel Prize in Physiology or Medicine in 1930. (C was later renamed to O after the German Ohne, meaning without, or zero, or null.[37]) The group AB was discovered a year later by Landsteiner's students Adriano Sturli, and Alfred von Decastello.[38][39]

In 1927, Landsteiner, with Philip Levine, discovered the MN blood group system,[40] and the P system.[41] Development of the Coombs test in 1945,[42] the advent of transfusion medicine, and the understanding of ABO hemolytic disease of the newborn led to discovery of more blood groups. As of 2018, the International Society of Blood Transfusion (ISBT) recognizes 346 blood group antigens which are assigned to 36 blood groups.[2]

A popular belief in Japan is that a person's ABO blood type is predictive of their personality, character, and compatibility with others. This belief is also widespread in South Korea[43] and Taiwan. The theory reached Japan in a 1927 psychologist's report, and the government of the time commissioned a study aimed at breeding better soldiers.[43] Interest in the theory faded in the 1930s. Ultimately, the discovery of DNA in the following decades indicated that DNA instead had an important role in both heredity generally and personality specifically. Interest in the theory was revived in the 1970s by Masahiko Nomi, a broadcaster with a background in law rather than science.[43] The theory is widely accepted in Japanese and South Korean popular culture.[44]

Originally posted here:
Blood type - Wikipedia

I survived that accident with all my organs intact . I was hospitalized for 19 days at CIMA hospital.I got burnt on my hands and legs, left and right side. The most dangerous was my left side,There was a hole in my instep, where the power exited it was 3 inches wide and 5 inches kind of oblong shape, The bones going to my toes were exposed as well as tendons the depth ouch. Lest say to the bones.I commenced treatment with the hospital , doing Vac and then Honey patch. Finally discharged and resumed treatment with Beachside clinic under Doctor,s guidance. This treatment was done twice weekly and this lasted till December, the healing process was very good , but in a slow progression.On December 4 2017 I met Dr Leslie and he gave me a quick review on what he can do to make this wound close up in 6 weeksI was very impressed with his presentation, I went on his web site and looked up his work also googled.I finally discussed this with a RN from USA who is knowledgeable on STEM CELLS . I was now convinced that Dr Leslies stems cells is the best thing to do, I made an appointment and got the stem cells done on the 14 of Dec 2017 in his clinic in San JoseAt the time of the procedure the wound was huge, but after the stem transplant on my first visit after the stem cells, I have seen very positive signs of rapid healing of my wound, I did two PRP injection Jan 4 and Jan 13 , both PRP did have very positive resultsThe wound is now One inch in diameterMo

December, 2017

See the rest here:
Stem Cell Transplant Reviews, Comments, Testimonials ...

Michael F. Chiang, MD, is Knowles Professor of Ophthalmology & Medical Informatics and Clinical Epidemiology at the Oregon Health & Science University (OHSU) Casey Eye Institute, and is Vice-Chair (Research) in the ophthalmology department. His clinical practice focuses on pediatric ophthalmology and strabismus. He is board-certified in clinical informatics, and is an elected Fellow of the American College of Medical Informatics. His research has been NIH-funded since 2003, and involves applications of telemedicine, clinical information systems, computer-based image analysis, and genotype-phenotype correlation to improve delivery of health care. His group has published over 140 peer-reviewed journal papers. He directs an NIH-funded T32 training program in visual science for graduate students & postdoctoral fellows at OHSU, directs an NIH-funded K12 mentored clinician-scientist program in ophthalmology, and teaches in both the ophthalmology & biomedical informatics departments. Before coming to OHSU in 2010, he spent 9 years at Columbia University, where he was Anne S. Cohen Associate Professor of Ophthalmology & Biomedical Informatics, director of medical student education in ophthalmology, and director of the introductory graduate student course in biomedical informatics.Dr. Chiang received a B.S. in Electrical Engineering & Biology from Stanford University, and an M.D. from Harvard Medical School & the Harvard-MIT Division of Health Sciences and Technology. He received an M.A. in Biomedical Informatics from Columbia University, where he was an NLM fellow in biomedical informatics. He completed residency and pediatric ophthalmology fellowship training at the Johns Hopkins Wilmer Eye Institute. He is past Chair of the American Academy of Ophthalmology (AAO) Medical Information Technology Committee, Chair of the AAO IRIS Registry Data Analytics Committee, member of the AAO IRIS Registry Executive Committee, and member of the AAO Board of Trustees. He is Associate Editor for the Journal of the American Medical Informatics Association (JAMIA), Associate Editor for the Journal of the American Association for Pediatric Ophthalmology & Strabismus, and serves on the Editorial Boards for Ophthalmology, Ophthalmology Retina, Asia-Pacific Journal of Ophthalmology, and EyeNet. He has received Top Doctor awards from Castle Connolly, Best Doctors in America, and Portland Monthly magazine, and has received numerous research and teaching awards.

Excerpt from:
The 3rd Asia Pacific Tele-Ophthalmology Society Symposium

Following hematopoietic cell transplantation (HCT), recipients will be immunocompromised and may also have treatment-related organ and tissue damage. Transplant recipients therefore require careful monitoring in the early post-transplant period to ensure that complications are recognized early, while there are more therapeutic options and while treatments can be more effective.

Better clinical care and management of early post-transplant complications have led to significantly lower rates of transplant-related mortality (TRM) over time. Figure 1 shows that one-year TRM has become significantly lower over time for unrelated donor transplants in adults with leukemia, lymphoma, myeloproliferative neoplasms, and myelodysplastic syndromes (pointwise p-value at all time points <0.001). [1]

Download slide: Transplant-Related Mortality after Adult Bone Marrow or PBSC Transplantation for Malignant Diseases

The most common complications that may occur in the early post-transplant period from transplant infusion to one year post-transplant are listed below. Recognizing marrow transplant complications early is critical to the health of transplant recipients, and a timely collaboration with the transplant center to develop a treatment plan is recommended.

Because it is a complex disease with many manifestations, chronic graft-versus-host disease (GVHD) is discussed separately.

Oral Mucositis

Oral mucositis is inflammation of oral mucosa that typically manifests as erythema or ulcerations. It can result from the cytotoxic effects of chemotherapy- and radiation-based pre-transplant conditioning regimens. [2,3]

Mouth sores associated with acute graft-versus-host disease (GVHD) may also develop 2-4 weeks post-transplant. The severity and the patient's hematologic status govern appropriate oral management. Meticulous oral hygiene and palliation of symptoms are essential.

Acute Graft-Versus-Host Disease (GVHD)

Acute GVHD is a common complication of allogeneic transplantation in which activated donor T cells attack the tissues of the transplant recipient after recognizing host tissues as antigenically foreign. The resulting inflammatory cytokines can cause tissue damage, and the commonly involved organs include the liver, skin, mucosa, and the gastrointestinal tract.

By classical definition, GVHD appearing before day 100 post-transplant is acute GVHD, and GVHD appearing after day 100 is chronic GVHD. However, acute GVHD may still occur later than 100 days post transplant (e.g., during tapering of immunosupressive drugs, or following a donor lymphocyte infusion). Some patients may also develop an overlap syndrome, where features of both acute and chronic GVHD are present. [4,5]

Stem Cell Graft Failure

Graft failure is a rare, but life-threatening complication following allogeneic HCT. The most common cause of graft failure is an immunological rejection of the graft mediated by recipient T cells, natural killer cells, and/or antibodies. Other causes are infection, recurrent disease, or an insufficient number of stem cells in the donated graft. Graft failure occurs in approximately 5% of allogeneic transplants. [6]

The rate of failure can vary by graft source, and is increased in HLA-mismatched grafts, unrelated-donor grafts, T cell-depleted grafts, and umbilical cord blood grafts. Patients allo-sensitized through prior blood transfusions or pregnancy, and those receiving reduced-intensity conditioning are also at a higher risk of experiencing graft failure.

If graft failure occurs, treatment is a second HCT, using cells from the same donor or from a different donor. Patients experiencing graft failure after a cord blood transplant cannot get backup cells from the same cord blood unit. However, it may be possible to use a different cord blood unit or a backup adult donor instead.

Early Infections

All transplant recipients are susceptible to infections and require careful monitoring, which allows for timely administration of antibacterial, antiviral, and/or antifungal agents. [7]

Average times of full immune recovery are:

Common infections in early and later post-transplant time periods are shown below.

> 0-3 Months:

> 3 Months:

Organ Injury/Toxicity

Organ injury and toxicity following transplant can include hepatic veno-occlusive disease (VOD) also known as sinusoidal obstruction syndrome, renal failure, pulmonary toxicity, thrombotic microangiopathy (TMA), and cardiovascular complications.

In the early post-transplant neutropenic period, there is an increased risk of various bacterial, fungal, and viral infections of the lung, and pneumonia develops in 40% to 60% of transplant recipients. [8] The pneumonias that can occur include herpes simplex pneumonitis, cytomegalovirus pneumonitis, and Pneumocystis carinii pneumonia.

Bronchiolitis obliterans syndrome and bronchiolitis obliterans organizing pneumonia can appear later (post day 100) in the transplant recovery period. Bronchiolitis obliterans is closely associated with chronic GVHD and may result from alloimmunologic injury to host bronchiolar epithelial cells. [8,9]

Chronic kidney disease (CKD) is associated with the use of TBI in the transplant conditioning regimen, although many cases are idiopathic. TBI-associated CKD has a typical latency of 3-6 months from irradiation to injury. CKD after transplantation may not be recognized early due to competing clinical priorities such as the treatment of GVHD, and monitoring for infections and disease recurrence. [10]

Sinusoidal obstructive syndrome (SOS) also known as veno-occlusive disease (VOD) of the liver (SOS/VOD) is the result of damage to the hepatic sinusoids, resulting in biliary obstruction. Risk factors include the use of busulfan, TBI, infection, acute GVHD, and pre-existing liver dysfunction due to iron overload or hepatitis. [11]

Transplant-associated TMA is a rare complication after allogeneic transplantation, and can occur after autologous transplantation. Risk factors for TMA include pre-transplant conditioning with busulfan, fludarabine, platinum-based chemotherapy, and total body irradiation (TBI). TMA is also associated with the use of the calcineurin inhibitors, tacrolimus and cyclosporine. Transplant-associated TMA syndromes present as hemolytic uremic syndrome (HUS) or thrombotic thrombocytopenic purpura (TTP). [12]

Cardiovascular complications may manifest as subclinical abnormalities or present as overt congestive heart failure or angina. The cardiac complications include any cardiac dysfunction due to cardiomyopathy, valvular anomaly, or conduction anomaly. [13]

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Early complications of hematopoietic cell transplant

The adaptive immune system, also known as the acquired immune system or, more rarely, as the specific immune system, is a subsystem of the overall immune system that is composed of highly specialized, systemic cells and processes that eliminate pathogens or prevent their growth. The adaptive immune system is one of the two main immunity strategies found in vertebrates (the other being the innate immune system). Adaptive immunity creates immunological memory after an initial response to a specific pathogen, and leads to an enhanced response to subsequent encounters with that pathogen. This process of acquired immunity is the basis of vaccination. Like the innate system, the adaptive system includes both humoral immunity components and cell-mediated immunity components.

Unlike the innate immune system, the adaptive immune system is highly specific to a particular pathogen. Adaptive immunity can also provide long-lasting protection; for example, someone who recovers from measles is now protected against measles for their lifetime. In other cases it does not provide lifetime protection; for example, chickenpox. The adaptive system response destroys invading pathogens and any toxic molecules they produce. Sometimes the adaptive system is unable to distinguish harmful from harmless foreign molecules; the effects of this may be hayfever, asthma or any other allergy. Antigens are any substances that elicit the adaptive immune response. The cells that carry out the adaptive immune response are white blood cells known as lymphocytes. Two main broad classesantibody responses and cell mediated immune responseare also carried by two different lymphocytes (B cells and T cells). In antibody responses, B cells are activated to secrete antibodies, which are proteins also known as immunoglobulins. Antibodies travel through the bloodstream and bind to the foreign antigen causing it to inactivate, which does not allow the antigen to bind to the host.[1]

In acquired immunity, pathogen-specific receptors are "acquired" during the lifetime of the organism (whereas in innate immunity pathogen-specific receptors are already encoded in the germline). The acquired response is called "adaptive" because it prepares the body's immune system for future challenges (though it can actually also be maladaptive when it results in autoimmunity).[n 1]

The system is highly adaptable because of somatic hypermutation (a process of accelerated somatic mutations), and V(D)J recombination (an irreversible genetic recombination of antigen receptor gene segments). This mechanism allows a small number of genes to generate a vast number of different antigen receptors, which are then uniquely expressed on each individual lymphocyte. Since the gene rearrangement leads to an irreversible change in the DNA of each cell, all progeny (offspring) of that cell inherit genes that encode the same receptor specificity, including the memory B cells and memory T cells that are the keys to long-lived specific immunity.

A theoretical framework explaining the workings of the adaptive immune system is provided by immune network theory. This theory, which builds on established concepts of clonal selection, is being applied in the search for an HIV vaccine.

Adaptive immunity is triggered in vertebrates when a pathogen evades the innate immune system and (1) generates a threshold level of antigen and (2) generates "stranger" or "danger" signals activating dendritic cells.[2]

The major functions of the adaptive immune system include:

The cells of the adaptive immune system are T and B lymphocytes; lymphocytes are a subset of leukocyte. B cells and T cells are the major types of lymphocytes. The human body has about 2 trillion lymphocytes, constituting 2040% of white blood cells (WBCs); their total mass is about the same as the brain or liver. The peripheral blood contains 2% of circulating lymphocytes; the rest move within the tissues and lymphatic system.[1]

B cells and T cells are derived from the same multipotent hematopoietic stem cells, and are morphologically indistinguishable from one another until after they are activated. B cells play a large role in the humoral immune response, whereas T cells are intimately involved in cell-mediated immune responses. In all vertebrates except Agnatha, B cells and T cells are produced by stem cells in the bone marrow.[3]

T progenitors migrate from the bone marrow to the thymus where they are called thymocytes and where they develop into T cells. In humans, approximately 12% of the lymphocyte pool recirculates each hour to optimize the opportunities for antigen-specific lymphocytes to find their specific antigen within the secondary lymphoid tissues.[4] In an adult animal, the peripheral lymphoid organs contain a mixture of B and T cells in at least three stages of differentiation:

Adaptive immunity relies on the capacity of immune cells to distinguish between the body's own cells and unwanted invaders. The host's cells express "self" antigens. These antigens are different from those on the surface of bacteria or on the surface of virus-infected host cells ("non-self" or "foreign" antigens). The adaptive immune response is triggered by recognizing foreign antigen in the cellular context of an activated dendritic cell.

With the exception of non-nucleated cells (including erythrocytes), all cells are capable of presenting antigen through the function of major histocompatibility complex (MHC) molecules.[3] Some cells are specially equipped to present antigen, and to prime naive T cells. Dendritic cells, B-cells, and macrophages are equipped with special "co-stimulatory" ligands recognized by co-stimulatory receptors on T cells, and are termed professional antigen-presenting cells (APCs).

Several T cells subgroups can be activated by professional APCs, and each type of T cell is specially equipped to deal with each unique toxin or microbial pathogen. The type of T cell activated, and the type of response generated, depends, in part, on the context in which the APC first encountered the antigen.[2]

Dendritic cells engulf exogenous pathogens, such as bacteria, parasites or toxins in the tissues and then migrate, via chemotactic signals, to the T cell-enriched lymph nodes. During migration, dendritic cells undergo a process of maturation in which they lose most of their ability to engulf other pathogens, and develop an ability to communicate with T-cells. The dendritic cell uses enzymes to chop the pathogen into smaller pieces, called antigens. In the lymph node, the dendritic cell displays these non-self antigens on its surface by coupling them to a receptor called the major histocompatibility complex, or MHC (also known in humans as human leukocyte antigen (HLA)). This MHC: antigen complex is recognized by T-cells passing through the lymph node. Exogenous antigens are usually displayed on MHC class II molecules, which activate CD4+T helper cells.[2]

Endogenous antigens are produced by intracellular bacteria and viruses replicating within a host cell.The host cell uses enzymes to digest virally associated proteins, and displays these pieces on its surface to T-cells by coupling them to MHC. Endogenous antigens are typically displayed on MHC class I molecules, and activate CD8+ cytotoxic T-cells. With the exception of non-nucleated cells (including erythrocytes), MHC class I is expressed by all host cells.[2]

Cytotoxic T cells (also known as TC, killer T cell, or cytotoxic T-lymphocyte (CTL)) are a sub-group of T cells that induce the death of cells that are infected with viruses (and other pathogens), or are otherwise damaged or dysfunctional.[2]

Naive cytotoxic T cells are activated when their T-cell receptor (TCR) strongly interacts with a peptide-bound MHC class I molecule. This affinity depends on the type and orientation of the antigen/MHC complex, and is what keeps the CTL and infected cell bound together.[2] Once activated, the CTL undergoes a process called clonal selection, in which it gains functions and divides rapidly to produce an army of armed effector cells. Activated CTL then travels throughout the body searching for cells that bear that unique MHC Class I + peptide.[citation needed]

When exposed to these infected or dysfunctional somatic cells, effector CTL release perforin and granulysin: cytotoxins that form pores in the target cell's plasma membrane, allowing ions and water to flow into the infected cell, and causing it to burst or lyse. CTL release granzyme, a serine protease that enters cells via pores to induce apoptosis (cell death). To limit extensive tissue damage during an infection, CTL activation is tightly controlled and in general requires a very strong MHC/antigen activation signal, or additional activation signals provided by "helper" T-cells (see below).[2]

On resolution of the infection, most effector cells die and phagocytes clear them awaybut a few of these cells remain as memory cells.[3] On a later encounter with the same antigen, these memory cells quickly differentiate into effector cells, dramatically shortening the time required to mount an effective response.[citation needed]

CD4+ lymphocytes, also called "helper" or "regulatory" T cells, are immune response mediators, and play an important role in establishing and maximizing the capabilities of the adaptive immune response.[2] These cells have no cytotoxic or phagocytic activity; and cannot kill infected cells or clear pathogens, but, in essence "manage" the immune response, by directing other cells to perform these tasks.

Helper T cells express T cell receptors (TCR) that recognize antigen bound to Class II MHC molecules. The activation of a naive helper T-cell causes it to release cytokines, which influences the activity of many cell types, including the APC (Antigen-Presenting Cell) that activated it. Helper T-cells require a much milder activation stimulus than cytotoxic T cells. Helper T cells can provide extra signals that "help" activate cytotoxic cells.[3]

Classically, two types of effector CD4+ T helper cell responses can be induced by a professional APC, designated Th1 and Th2, each designed to eliminate different types of pathogens. The factors that dictate whether an infection triggers a Th1 or Th2 type response are not fully understood, but the response generated does play an important role in the clearance of different pathogens.[2]

The Th1 response is characterized by the production of Interferon-gamma, which activates the bactericidal activities of macrophages, and induces B cells to make opsonizing (coating) and complement-fixing antibodies, and leads to cell-mediated immunity.[2] In general, Th1 responses are more effective against intracellular pathogens (viruses and bacteria that are inside host cells).

The Th2 response is characterized by the release of Interleukin 5, which induces eosinophils in the clearance of parasites.[6] Th2 also produce Interleukin 4, which facilitates B cell isotype switching.[2] In general, Th2 responses are more effective against extracellular bacteria, parasites including helminths and toxins.[2] Like cytotoxic T cells, most of the CD4+ helper cells die on resolution of infection, with a few remaining as CD4+ memory cells.

Increasingly, there is strong evidence from mouse and human-based scientific studies of a broader diversity in CD4+ effector T helper cell subsets. Regulatory T (Treg) cells, have been identified as important negative regulators of adaptive immunity as they limit and suppresses the immune system to control aberrant immune responses to self-antigens; an important mechanism in controlling the development of autoimmune diseases.[3] Follicular helper T (Tfh) cells are another distinct population of effector CD4+ T cells that develop from naive T cells post-antigen activation. Tfh cells are specialized in helping B cell humoral immunity as they are uniquely capable of migrating to follicular B cells in secondary lymphoid organs and provide them positive paracrine signals to enable the generation and recall production of high-quality affinity-matured antibodies. Similar to Tregs, Tfh cells also play a role in immunological tolerance as an abnormal expansion of Tfh cell numbers can lead to unrestricted autoreactive antibody production causing severe systemic autoimmune disorders.[7]

The relevance of CD4+ T helper cells is highlighted during an HIV infection. HIV is able to subvert the immune system by specifically attacking the CD4+ T cells, precisely the cells that could drive the clearance of the virus, but also the cells that drive immunity against all other pathogens encountered during an organism's lifetime.[3]

Gamma delta T cells ( T cells) possess an alternative T cell receptor (TCR) as opposed to CD4+ and CD8+ T cells and share characteristics of helper T cells, cytotoxic T cells and natural killer cells. Like other 'unconventional' T cell subsets bearing invariant TCRs, such as CD1d-restricted natural killer T cells, T cells exhibit characteristics that place them at the border between innate and adaptive immunity. On one hand, T cells may be considered a component of adaptive immunity in that they rearrange TCR genes via V(D)J recombination, which also produces junctional diversity, and develop a memory phenotype. On the other hand, however, the various subsets may also be considered part of the innate immune system where a restricted TCR or NK receptors may be used as a pattern recognition receptor. For example, according to this paradigm, large numbers of V9/V2 T cells respond within hours to common molecules produced by microbes, and highly restricted intraepithelial V1 T cells respond to stressed epithelial cells.

B Cells are the major cells involved in the creation of antibodies that circulate in blood plasma and lymph, known as humoral immunity. Antibodies (also known as immunoglobulin, Ig), are large Y-shaped proteins used by the immune system to identify and neutralize foreign objects. In mammals, there are five types of antibody: IgA, IgD, IgE, IgG, and IgM, differing in biological properties; each has evolved to handle different kinds of antigens. Upon activation, B cells produce antibodies, each of which recognize a unique antigen, and neutralizing specific pathogens.[2]

Antigen and antibody binding would cause five different protective mechanism:

Like the T cell, B cells express a unique B cell receptor (BCR), in this case, a membrane-bound antibody molecule. All the BCR of any one clone of B cells recognizes and binds to only one particular antigen. A critical difference between B cells and T cells is how each cell "sees" an antigen. T cells recognize their cognate antigen in a processed form as a peptide in the context of an MHC molecule,[2] whereas B cells recognize antigens in their native form.[2] Once a B cell encounters its cognate (or specific) antigen (and receives additional signals from a helper T cell (predominately Th2 type)), it further differentiates into an effector cell, known as a plasma cell.[2]

Plasma cells are short-lived cells (23 days) that secrete antibodies. These antibodies bind to antigens, making them easier targets for phagocytes, and trigger the complement cascade.[2] About 10% of plasma cells survive to become long-lived antigen-specific memory B cells.[2] Already primed to produce specific antibodies, these cells can be called upon to respond quickly if the same pathogen re-infects the host, while the host experiences few, if any, symptoms.

Although the classical molecules of the adaptive immune system (e.g., antibodies and T cell receptors) exist only in jawed vertebrates, a distinct lymphocyte-derived molecule has been discovered in primitive jawless vertebrates, such as the lamprey and hagfish. These animals possess a large array of molecules called variable lymphocyte receptors (VLRs for short) that, like the antigen receptors of jawed vertebrates, are produced from only a small number (one or two) of genes. These molecules are believed to bind pathogenic antigens in a similar way to antibodies, and with the same degree of specificity.[8]

When B cells and T cells are activated some become memory B cells and some memory T cells. Throughout the lifetime of an animal these memory cells form a database of effective B and T lymphocytes. Upon interaction with a previously encountered antigen, the appropriate memory cells are selected and activated. In this manner, the second and subsequent exposures to an antigen produce a stronger and faster immune response. This is "adaptive" because the body's immune system prepares itself for future challenges, but is "maladaptive" of course if the receptors are autoimmune. Immunological memory can be in the form of either passive short-term memory or active long-term memory.

Passive memory is usually short-term, lasting between a few days and several months. Newborn infants have had no prior exposure to microbes and are particularly vulnerable to infection. Several layers of passive protection are provided by the mother. In utero, maternal IgG is transported directly across the placenta, so that, at birth, human babies have high levels of antibodies, with the same range of antigen specificities as their mother.[2] Breast milk contains antibodies (mainly IgA) that are transferred to the gut of the infant, protecting against bacterial infections, until the newborn can synthesize its own antibodies.[2]

This is passive immunity because the fetus does not actually make any memory cells or antibodies: It only borrows them. Short-term passive immunity can also be transferred artificially from one individual to another via antibody-rich serum.

In general, active immunity is long-term and can be acquired by infection followed by B cells and T cells activation, or artificially acquired by vaccines, in a process called immunization.

Historically, infectious disease has been the leading cause of death in the human population. Over the last century, two important factors have been developed to combat their spread: sanitation and immunization.[3] Immunization (commonly referred to as vaccination) is the deliberate induction of an immune response, and represents the single most effective manipulation of the immune system that scientists have developed.[3] Immunizations are successful because they utilize the immune system's natural specificity as well as its inducibility.

The principle behind immunization is to introduce an antigen, derived from a disease-causing organism, that stimulates the immune system to develop protective immunity against that organism, but that does not itself cause the pathogenic effects of that organism. An antigen (short for antibody generator), is defined as any substance that binds to a specific antibody and elicits an adaptive immune response.[1]

Most viral vaccines are based on live attenuated viruses, whereas many bacterial vaccines are based on acellular components of microorganisms, including harmless toxin components.[1] Many antigens derived from acellular vaccines do not strongly induce an adaptive response, and most bacterial vaccines require the addition of adjuvants that activate the antigen-presenting cells of the innate immune system to enhance immunogenicity.[3]

Most large molecules, including virtually all proteins and many polysaccharides, can serve as antigens.[2] The parts of an antigen that interact with an antibody molecule or a lymphocyte receptor, are called epitopes, or antigenic determinants. Most antigens contain a variety of epitopes and can stimulate the production of antibodies, specific T cell responses, or both.[2] A very small proportion (less than 0.01%) of the total lymphocytes are able to bind to a particular antigen, which suggests that only a few cells respond to each antigen.[3]

For the adaptive response to "remember" and eliminate a large number of pathogens the immune system must be able to distinguish between many different antigens,[1] and the receptors that recognize antigens must be produced in a huge variety of configurations, in essence one receptor (at least) for each different pathogen that might ever be encountered. Even in the absence of antigen stimulation, a human can produce more than 1 trillion different antibody molecules.[3] Millions of genes would be required to store the genetic information that produces these receptors, but, the entire human genome contains fewer than 25,000 genes.[9]

Myriad receptors are produced through a process known as clonal selection.[1][2] According to the clonal selection theory, at birth, an animal randomly generates a vast diversity of lymphocytes (each bearing a unique antigen receptor) from information encoded in a small family of genes. To generate each unique antigen receptor, these genes have undergone a process called V(D)J recombination, or combinatorial diversification, in which one gene segment recombines with other gene segments to form a single unique gene. This assembly process generates the enormous diversity of receptors and antibodies, before the body ever encounters antigens, and enables the immune system to respond to an almost unlimited diversity of antigens.[2] Throughout an animal's lifetime, lymphocytes that can react against the antigens an animal actually encounters are selected for actiondirected against anything that expresses that antigen.

Note that the innate and adaptive portions of the immune system work together, not in spite of each other. The adaptive arm, B, and T cells couldn't function without the innate system' input. T cells are useless without antigen-presenting cells to activate them, and B cells are crippled without T cell help. On the other hand, the innate system would likely be overrun with pathogens without the specialized action of the adaptive immune response.

The cornerstone of the immune system is the recognition of "self" versus "non-self". Therefore, the mechanisms that protect the human fetus (which is considered "non-self") from attack by the immune system, are particularly interesting. Although no comprehensive explanation has emerged to explain this mysterious, and often repeated, lack of rejection, two classical reasons may explain how the fetus is tolerated. The first is that the fetus occupies a portion of the body protected by a non-immunological barrier, the uterus, which the immune system does not routinely patrol.[2] The second is that the fetus itself may promote local immunosuppression in the mother, perhaps by a process of active nutrient depletion.[2] A more modern explanation for this induction of tolerance is that specific glycoproteins expressed in the uterus during pregnancy suppress the uterine immune response (see eu-FEDS).

During pregnancy in viviparous mammals (all mammals except Monotremes), endogenous retroviruses (ERVs) are activated and produced in high quantities during the implantation of the embryo. They are currently known to possess immunosuppressive properties, suggesting a role in protecting the embryo from its mother's immune system. Also, viral fusion proteins cause the formation of the placental syncytium[10] to limit exchange of migratory cells between the developing embryo and the body of the mother (something an epithelium can't do sufficiently, as certain blood cells specialize to insert themselves between adjacent epithelial cells). The immunodepressive action was the initial normal behavior of the virus, similar to HIV. The fusion proteins were a way to spread the infection to other cells by simply merging them with the infected one (HIV does this too). It is believed that the ancestors of modern viviparous mammals evolved after an infection by this virus, enabling the fetus to survive the immune system of the mother.[11]

The human genome project found several thousand ERVs classified into 24 families.[12]

A theoretical framework explaining the workings of the adaptive immune system is provided by immune network theory, based on interactions between idiotypes (unique molecular features of one clonotype, i.e. the unique set of antigenic determinants of the variable portion of an antibody) and 'anti-idiotypes' (antigen receptors that react with the idiotype as if it were a foreign antigen). This theory, which builds on the existing clonal selection hypothesis and since 1974 has been developed mainly by Niels Jerne and Geoffrey W. Hoffmann, is seen as being relevant to the understanding of the HIV pathogenesis and the search for an HIV vaccine.

One of the most interesting developments in biomedical science during the past few decades has been elucidation of mechanisms mediating innate immunity. One set of innate immune mechanisms is humoral, such as complement activation. Another set comprises pattern recognition receptors such as toll-like receptors, which induce the production of interferons and other cytokines increasing resistance of cells such as monocytes to infections.[13] Cytokines produced during innate immune responses are among the activators of adaptive immune responses.[13] Antibodies exert additive or synergistic effects with mechanisms of innate immunity. Unstable HbS clusters Band-3, a major integral red cell protein;[14] antibodies recognize these clusters and accelerate their removal by phagocytic cells. Clustered Band 3 proteins with attached antibodies activate complement, and complement C3 fragments are opsonins recognized by the CR1 complement receptor on phagocytic cells.[15]

A population study has shown that the protective effect of the sickle-cell trait against falciparum malaria involves the augmentation of adaptive as well as innate immune responses to the malaria parasite, illustrating the expected transition from innate to adaptive immunity.[16]

Repeated malaria infections strengthen adaptive immunity and broaden its effects against parasites expressing different surface antigens. By school age most children have developed efficacious adaptive immunity against malaria. These observations raise questions about mechanisms that favor the survival of most children in Africa while allowing some to develop potentially lethal infections.

In malaria, as in other infections,[13] innate immune responses lead into, and stimulate, adaptive immune responses. The genetic control of innate and adaptive immunity is now a large and flourishing discipline.

Humoral and cell-mediated immune responses limit malaria parasite multiplication, and many cytokines contribute to the pathogenesis of malaria as well as to the resolution of infections.[17]

The adaptive immune system, which has been best-studied in mammals, originated in jawed fish approximately 500 million years ago. Most of the molecules, cells, tissues, and associated mechanisms of this system of defense are found in cartilaginous fishes.[18] Lymphocyte receptors, Ig and TCR, are found in all jawed vertebrates. The most ancient Ig class, IgM, is membrane-bound and then secreted upon stimulation of cartilaginous fish B cells. Another isotype, shark IgW, is related to mammalian IgD. TCRs, both / and /, are found in all animals from gnathostomes to mammals. The organization of gene segments that undergo gene rearrangement differs in cartilaginous fishes, which have a cluster form as compared to the translocon form in bony fish to mammals. Like TCR and Ig, the MHC is found only in jawed vertebrates. Genes involved in antigen processing and presentation, as well as the class I and class II genes, are closely linked within the MHC of almost all studied species.

Lymphoid cells can be identified in some pre-vertebrate deuterostomes (i.e., sea urchins).[19] These bind antigen with pattern recognition receptors (PRRs) of the innate immune system. In jawless fishes, two subsets of lymphocytes use variable lymphocyte receptors (VLRs) for antigen binding.[20] Diversity is generated by a cytosine deaminase-mediated rearrangement of LRR-based DNA segments.[21] There is no evidence for the recombination-activating genes (RAGs) that rearrange Ig and TCR gene segments in jawed vertebrates.

The evolution of the AIS, based on Ig, TCR, and MHC molecules, is thought to have arisen from two major evolutionary events: the transfer of the RAG transposon (possibly of viral origin) and two whole genome duplications.[18] Though the molecules of the AIS are well-conserved, they are also rapidly evolving. Yet, a comparative approach finds that many features are quite uniform across taxa. All the major features of the AIS arose early and quickly. Jawless fishes have a different AIS that relies on gene rearrangement to generate diversity but has little else in common with the jawed vertebrate AIS. The innate immune system, which has an important role in AIS activation, is the most important defense system of invertebrates and plants.

Immunity can be acquired either actively or passively. Immunity is acquired actively when a person is exposed to foreign substances and the immune system responds. Passive immunity is when antibodies are transferred from one host to another. Both actively acquired and passively acquired immunity can be obtained by natural or artificial means.

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Adaptive immune system - Wikipedia

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Track 1:Pharmaceutical Biotechnology and Drug Design

Pharmaceutical Biotechnology is the science that covers all technologies required for producing, manufacturing and registration of biological drugs. Pharmaceutical companies use biotechnology for manufacturing drugs, pharmacogenomics, gene therapy, and genetic testing. Biotech companies make biotechnology products by manipulating and modifying organisms, usually at molecular level. Pharmaceutical Biotechnology is an increasingly important area of science and technology. It contributes in design and delivery of new therapeutic drugs, diagnostic agents for medical tests, and in gene therapy for correcting the medical symptoms of hereditary diseases. The Pharmaceutical Biotechnology is widely spread, ranging from many ethical issues to changes in healthcare practices and a significant contribution to the development of national economy. Euro Biotechnology 2018 will focus on Biopharmaceuticals Discovery, Biopharmaceutical Regulations and Validations, Biologics and Biosimilars and Clinical Research/Clinical trials, Biotechnology Conferences.

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7th World Congress on Mass Spectrometry June 20-22, 2018 Rome, Italy ; 23rd International Pharmaceutical BiotechnologyConferences December 10-11, 2018 Rome, Italy ; 18th World Pharma Congress October 18-20, 2018 Warsaw, Poland ;16th International Conference and Exhibition on Pharmaceutical Formulations July 26-27, 2018 Rome, Italy ; 17th Annual Congress on Pharmaceutics & Drug Delivery Systems September 20-22, 2018 Prague, Czech Republic;16th Annual European Pharma Congress May 20-21, 2019 Zurich, Switzerland ; Pharma Serialisation Summit June 19-21, 2018 Zurich, Switzerland ; European Congress on Pharma August 13-14 , 2018 Paris, France ; Pharma R&D March 04-06, 2019 Paris, France ; 6th Asia Pacific Biotechnology Conferences August 15-16, 2018 Singapore; 22nd World Congress on Biotechnology July 10-11, 2018 Bangkok, Thailand; 18th European Conferences on Biotechnology July 1 - 4, 2018 Geneva, Switzerland,Biotechnology Conferences.

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Spanish Society of Biotechnology, The Pharmaceutical Society of Ireland, Russian Medical Society, Society for Engineering in Agriculture, Society of Microbial Ecology and Disease, Manchester University Pharmaceutical Society, Italian Society of Biochemistry and Molecular Biology, European Society for Precision Engineering and Nanotechnology, Society for Chemical Engineering Biotechnology, Romanian Society of Medical Mycology and Mycotoxicology, New Zealand Plant Protection Society, International Society for Pharmaceutical Engineering, Pharmaceutical Society of Australia,Biotechnology Conferences.

USA:Mexican Society for Biotechnology and Bioengineering, Society for Biological Engineering, National Society of Agriculture, The Protein Society, Pharmaceutical Marketing Society,Biotechnology Conferences.

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Korean Society of Food Science And Technology, Pharmaceutical Society of Singapore, Korean Society of Gene and Cell Therapy, Pharmaceutical Society of Singapore, Indian Society of Nano science And Nanotechnology, Tanta Pharmaceutical Scientific Society (TPSS), Iran Society for Cell Biology, Israel Societies for Experimental Biology, Society for Industrial Microbiology and Biotechnology (SIMB), Malaysian Pharmaceutical Society, Japanese Society for Quantitative Biology, Society for Biotechnology,Biotechnology Conferences.

Track 2 : Microbial Biotechnology

Microbial biotechnology, enabled by genome studies, will lead to breakthroughs such as improved vaccines and better disease-diagnostic tools, improved microbial agents for biological control of plant and animal pests, modifications of plant and animal pathogens for reduced virulence, development of new industrial catalysts and fermentation organisms, and development of new microbial agents for bioremediation of soil and water contaminated by agricultural runoff,Biotechnology Conferences.

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Annual Industrial Biotechnology and Bioprocessing Congress September 17-18, 2018 San Diego, California, USA; 3th International Conference on Microbial Interactions & Microbial Ecology July 19-20, 2018 Rome, Italy; Applied Microbiology October 15-16, 2018 Ottawa, Canada and Microbial Biotechnology October 15-16, 2018 Ottawa, Canada ; 12th World Congress on Biotechnology June 28-29, 2018 Amsterdam, Netherlands and 12th World Congress on Microbiology June 28-29, 2018 Amsterdam, Netherlands ; European Congress on Pharma August 13-14 , 2018 Paris, France ; Pharma R&D March 04-06, 2019 Paris, France ; 6thAsia Pacific Biotechnology ConferencesAugust 15-16, 2018 Singapore; 22ndWorld Congress on BiotechnologyJuly 10-11, 2018Bangkok,Thailand;18thEuropean Conferences on BiotechnologyJuly 1 - 4, 2018 Geneva, Switzerland,Biotechnology Conferences; 5th World Congress on Microbial Biotechnology September 17-18, 2018 Lisbon, Portugal,

Related Societies:

Europe:

Spanish Society of Biotechnology, The Pharmaceutical Society of Ireland, Russian Medical Society, Society for Engineering in Agriculture, Society of Microbial Ecology and Disease, Manchester University Pharmaceutical Society, Italian Society of Biochemistry and Molecular Biology, European Society for Precision Engineering and Nanotechnology, Society for Chemical Engineering Biotechnology, Romanian Society of Medical Mycology and Mycotoxicology, New Zealand Plant Protection Society, International Society for Pharmaceutical Engineering, Pharmaceutical Society of Australia,Biotechnology Conferences.

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Mexican Society for Biotechnology and Bioengineering, Society for Biological Engineering, National Society of Agriculture, The Protein Society, Pharmaceutical Marketing Society,Biotechnology Conferences.

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Korean Society of Food Science And Technology, Pharmaceutical Society of Singapore, Korean Society of Gene and Cell Therapy, Pharmaceutical Society of Singapore, Indian Society of Nano science And Nanotechnology, Tanta Pharmaceutical Scientific Society (TPSS), Iran Society for Cell Biology, Israel Societies for Experimental Biology, Society for Industrial Microbiology and Biotechnology (SIMB), Malaysian Pharmaceutical Society, Japanese Society for Quantitative Biology, Society for Biotechnology,Biotechnology Conferences.

Track 3: Nano Biotechnology

Nano Biotechnology is a discipline in which tools from nanotechnology are developed and applied to study biological phenomena. Nano biotechnology, bio nanotechnology, and Nano biology are terms that refer to the intersection of nanotechnology and biology. Bio nanotechnology and Nano biotechnology serve as blanket terms for various related technologies. The most important objectives that are frequently found in Nano biology involve applying Nano tools to relevant medical/biological problems and refining these applications. Developing new tools, such as peptide Nano sheets, for medical and biological purposes is another primary objective in nanotechnology,Biotechnology Conferences.

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8th International Conference and Expo on Nanosciences Nov 26-28,2018 Barcelona, Spain; 24th World Nano Conference May 07-08, 2018 Rome, Italy; World Congress on Nano medicine September 17-19, 2018 Abu Dhabi, UAE; World Congress on Nanotechnology in Healthcare September 17-19, 2018 Abu Dhabi, UAE; Advanced Nanotechnology October 04-05 2018 Moscow, Russia; 8th International Conference and Expo on Nanotechnology Nov 26-28,2018 Barcelona, Spain ; International Conference On Nanomedicine And Nanobiotechnology September 26-28, 2018 Rome ; Nanotech & Nanobiotechnology July 12-13, 2018 Paris, France ; 4th International Conference On Nanobiotechnology April 9 - 11, 2019 Rome, Italy, 18thEuropean Congress on BiotechnologyJuly 1 - 4, 2018 Geneva, Switzerland,Biotechnology Conferences.

Related Societies:

Europe:

Spanish Society of Biotechnology, The Pharmaceutical Society of Ireland, Russian Medical Society, Society for Engineering in Agriculture, Society of Microbial Ecology and Disease, Manchester University Pharmaceutical Society, Italian Society of Biochemistry and Molecular Biology, European Society for Precision Engineering and Nanotechnology, Society for Chemical Engineering Biotechnology, Romanian Society of Medical Mycology and Mycotoxicology, New Zealand Plant Protection Society, International Society for Pharmaceutical Engineering, Pharmaceutical Society of Australia,Biotechnology Conferences.

USA:

Mexican Society for Biotechnology and Bioengineering, Society for Biological Engineering, National Society of Agriculture, The Protein Society, Pharmaceutical Marketing Society,Biotechnology Conferences.

Asia:

Korean Society of Food Science And Technology, Pharmaceutical Society of Singapore, Korean Society of Gene and Cell Therapy, Pharmaceutical Society of Singapore, Indian Society of Nano science And Nanotechnology, Tanta Pharmaceutical Scientific Society (TPSS), Iran Society for Cell Biology, Israel Societies for Experimental Biology, Society for Industrial Microbiology and Biotechnology (SIMB), Malaysian Pharmaceutical Society, Japanese Society for Quantitative Biology, Society for Biotechnology,Biotechnology Conferences.

Track 4: Stem Cell Biotechnology and Regenerative Medicine

Stem cell biotechnology is a field of biotechnology that develops tools and therapeutics through modification and engineering of stem cells. Stem cell biotechnology is important in regenerative medicine. Regenerative medicine is an Inter disciplinary branch that tends to repair or regenerate damaged cells or tissues to regain or restore their normal function,Biotechnology Conferences.

Related: Stem cell Conferences | Regenerative Medicine Conference | Biotechnology Conference | | Biotechnology Conferences 2018 | Biotechnology Conferences | Biotechnology Conferences 2018 USA | Biotechnology Conferences|Biotechnology Conferences.

12th Annual Conference on Stem Cell and Regenerative Medicine June 04-06, 2018 Prague, Czech Republic ; 10th Annual Conference on Stem Cell and Regenerative Medicine October 08-09, 2018 Zurich, Switzerland ; World Congress and Expo on Cell & Stem Cell Research September 13-15, 2018 Paris, France ; 11th Annual Conference on Stem Cell and Regenerative Medicine October 15-16, 2018 Helsinki, Finland ; International Conference On Cell and Stem Cell Research August 17-18, 2018 Singapore ; Modeling Cell-Cell Interactions Governing Tissue Repair and Disease August 19 - 24, 2018 ; Stem Cell Conference Basel 2018 August 29-31, 2018 Basel, Switzerland; 6th Asia Pacific Biotechnology Conferences August 15-16, 2018 Singapore; 22nd World Congress on Biotechnology July 10-11, 2018 Bangkok, Thailand, 18thEuropean BiotechnologyConferencesJuly 1 - 4, 2018 Geneva, Switzerland,Biotechnology Conferences.

Related Societies:

Europe:

Spanish Society of Biotechnology, The Pharmaceutical Society of Ireland, Russian Medical Society, Society for Engineering in Agriculture, Society of Microbial Ecology and Disease, Manchester University Pharmaceutical Society, Italian Society of Biochemistry and Molecular Biology, European Society for Precision Engineering and Nanotechnology, Society for Chemical Engineering Biotechnology, Romanian Society of Medical Mycology and Mycotoxicology, New Zealand Plant Protection Society, International Society for Pharmaceutical Engineering, Pharmaceutical Society of Australia.,Biotechnology Conferences.

USA:

Mexican Society for Biotechnology and Bioengineering, Society for Biological Engineering, National Society of Agriculture, The Protein Society, Pharmaceutical Marketing Society,Biotechnology Conferences.

Asia:

Korean Society of Food Science And Technology, Pharmaceutical Society of Singapore, Korean Society of Gene and Cell Therapy, Pharmaceutical Society of Singapore, Indian Society of Nano science And Nanotechnology, Tanta Pharmaceutical Scientific Society (TPSS), Iran Society for Cell Biology, Israel Societies for Experimental Biology, Society for Industrial Microbiology and Biotechnology (SIMB), Malaysian Pharmaceutical Society, Japanese Society for Quantitative Biology, Society for Biotechnology,Biotechnology Conferences.

Track 5: Medical Biotechnology

Medical Biotechnology is the use of living cells and cell materials to research and produce pharmaceutical and diagnostic products that help treat and prevent human diseases. leading to the development of several innovative techniques for preventing, diagnosing, and treating diseases,Biotechnology Conferences.

Related: Medical Biotechnology Conferences | Biotechnology Conference | Regenerative conferences | Biotechnology Conferences 2018 | Biotechnology Conferences | Biotechnology Conferences 2018 USA | Biotechnology Conferences|Biotechnology Conferences.

11th International Conference on Tissue Engineering & Regenerative Medicine October 18-20, 2018 Rome, Italy; 12th World Conference on Human Genomics and Genomic MedicineApril 22-23, 2019 Abu Dhabi, UAE; 4th International Conference on Advances in Biotechnology and Bioscience November 15-17, 2018 Frankfurt, Germany ; 11th International Conference on Tissue Engineering & Regenerative Medicine October 18-20, 2018 Rome, Italy ; Medical Biotechnology May 24-25, 2018 Ghent, Belgium ; 6th Asia Pacific Biotechnology Conferences August 15-16, 2018 Singapore; 22nd World Congress on Biotechnology July 10-11, 2018 Bangkok, Thailand,18th European BiotechnologyConferences July 1 - 4, 2018 Geneva, Switzerland,Biotechnology Conferences.

Related Societies:

Europe:

Spanish Society of Biotechnology, The Pharmaceutical Society of Ireland, Russian Medical Society, Society for Engineering in Agriculture, Society of Microbial Ecology and Disease, Manchester University Pharmaceutical Society, Italian Society of Biochemistry and Molecular Biology, European Society for Precision Engineering and Nanotechnology, Society for Chemical Engineering Biotechnology, Romanian Society of Medical Mycology and Mycotoxicology, New Zealand Plant Protection Society, International Society for Pharmaceutical Engineering, Pharmaceutical Society of Australia,Biotechnology Conferences.

USA:

Mexican Society for Biotechnology and Bioengineering, Society for Biological Engineering, National Society of Agriculture, The Protein Society, Pharmaceutical Marketing Society,Biotechnology Conferences.

Asia:

Korean Society of Food Science And Technology, Pharmaceutical Society of Singapore, Korean Society of Gene and Cell Therapy, Pharmaceutical Society of Singapore, Indian Society of Nano science And Nanotechnology, Tanta Pharmaceutical Scientific Society (TPSS), Iran Society for Cell Biology, Israel Societies for Experimental Biology, Society for Industrial Microbiology and Biotechnology (SIMB), Malaysian Pharmaceutical Society, Japanese Society for Quantitative Biology, Society for Biotechnology.

Track 6: Oncolytic Biotechnology

Oncolytic Biotechnology is the study of oncolytic virus, the virus that preferentially infects and kills cancer cells. As the infected cancer cells are destroyed by oncolysis, they release new infectious virus particles or virions to help destroy the remaining tumour. Oncolytic viruses are thought not only to cause direct destruction of the tumour cells, but also to stimulate host anti-tumour immune responses,Biotechnology Conferences.

Related: Cancer Biotechnology Conferences | Biotechnology Conference | Regenerative conferences | Biotechnology Conferences 2018 | Biotechnology Conferences | Biotechnology Conferences 2018 USA | Biotechnology Conferences|Biotechnology Conferences.

11th International Virology and Microbiology July 27-28, 2018 Vancouver, Canada ; 11th World Congress on Virology and Infectious Diseases May 17-18, 2018 Tokyo, Japan ; 2nd International Conference on Cancer Biology, Therapeutics and Drug Discovery & Delivery October 03-04, 2018 Los Angeles, California, USA ; Beatson International Cancer Conference July 01- 04, 2018 Glasgow, Scotland ; 36th World Cancer Conference October 11-13, 2018 Zurich, Switzerland; 6th Asia Pacific Biotechnology Conferences August 15-16, 2018 Singapore; 22nd World Congress on Biotechnology July 10-11, 2018 Bangkok, Thailand, 18thEuropean BiotechnologyConferences July 1 - 4, 2018 Geneva, Switzerland,Biotechnology Conferences.

Related Societies:

Europe:

Spanish Society of Biotechnology, The Pharmaceutical Society of Ireland, Russian Medical Society, Society for Engineering in Agriculture, Society of Microbial Ecology and Disease, Manchester University Pharmaceutical Society, Italian Society of Biochemistry and Molecular Biology, European Society for Precision Engineering and Nanotechnology, Society for Chemical Engineering Biotechnology, Romanian Society of Medical Mycology and Mycotoxicology, New Zealand Plant Protection Society, International Society for Pharmaceutical Engineering, Pharmaceutical Society of Australia,Biotechnology Conferences.

USA:

Mexican Society for Biotechnology and Bioengineering, Society for Biological Engineering, National Society of Agriculture, The Protein Society, Pharmaceutical Marketing Society,Biotechnology Conferences.

Asia:

Korean Society of Food Science And Technology, Pharmaceutical Society of Singapore, Korean Society of Gene and Cell Therapy, Pharmaceutical Society of Singapore, Indian Society of Nano science And Nanotechnology, Tanta Pharmaceutical Scientific Society (TPSS), Iran Society for Cell Biology, Israel Societies for Experimental Biology, Society for Industrial Microbiology and Biotechnology (SIMB), Malaysian Pharmaceutical Society, Japanese Society for Quantitative Biology, Society for Biotechnology,Biotechnology Conferences.

Track 7: Molecular Biotechnology and Genetics

Molecular biotechnology is the use of laboratory techniques to study and modify nucleic acids and proteins for applications in areas such as human and animal health, agriculture, and the environment. Molecular biotechnology results from the convergence of many areas of research, such as molecular biology, microbiology, biochemistry, immunology, genetics, and cell biology. It is an exciting field fueled by the ability to transfer genetic information between organisms with the goal of understanding important biological processes or creating a useful product. The tools of molecular biotechnology can be applied to develop and improve drugs, vaccines, therapies, and diagnostic tests that will improve human and animal health. Molecular biotechnology has applications in plant and animal agriculture, aquaculture, chemical and textile manufacturing, forestry, and food processing.

Related: Molecular Biotechnology Conferences | Biotechnology Conference | Regenerative conferences | Biotechnology Conferences 2018 | Biotechnology Conferences | Biotechnology Conferences 2018 USA | Biotechnology Conferences|Biotechnology Conferences.

Biochemistry & Molecular Biology October 11-12, 2018 Amsterdam, Netherlands ; International Conference on Molecular Biology and Medicine August 27-28, 2018 Dubai, UAE ; World Congress on Advanced Structural and Molecular Biology 2018 August 22-23, 2018 Rome, Italy ; World Congress on Plant Science and Molecular Biology September 12-13, 2018 Singapore ; 6th Annual Congress on Medicine of Molecules September 17-18, 2018 Abu Dhabi, UAE; 10th Annual Conference on Stem Cell October 08-09, 2018 Zurich, Switzerland; 10th Annual Conference on Stem Cell Regenerative Medicine October 08-09, 2018 Zurich, Switzerland; 6th Asia Pacific Biotechnology Conferences August 15-16, 2018 Singapore; 22nd World Congress on Biotechnology July 10-11, 2018 Bangkok, Thailand, 18thEuropean BiotechnologyConferencesJuly 1 - 4, 2018 Geneva, Switzerland,Biotechnology Conferences.

Related Societies:

Europe:

Spanish Society of Biotechnology, The Pharmaceutical Society of Ireland, Russian Medical Society, Society for Engineering in Agriculture, Society of Microbial Ecology and Disease, Manchester University Pharmaceutical Society, Italian Society of Biochemistry and Molecular Biology, European Society for Precision Engineering and Nanotechnology, Society for Chemical Engineering Biotechnology, Romanian Society of Medical Mycology and Mycotoxicology, New Zealand Plant Protection Society, International Society for Pharmaceutical Engineering, Pharmaceutical Society of Australia,Biotechnology Conferences.

USA:

Mexican Society for Biotechnology and Bioengineering, Society for Biological Engineering, National Society of Agriculture, The Protein Society, Pharmaceutical Marketing Society,,Biotechnology Conferences.

Asia:

Korean Society of Food Science And Technology, Pharmaceutical Society of Singapore, Korean Society of Gene and Cell Therapy, Pharmaceutical Society of Singapore, Indian Society of Nano science And Nanotechnology, Tanta Pharmaceutical Scientific Society (TPSS), Iran Society for Cell Biology, Israel Societies for Experimental Biology, Society for Industrial Microbiology and Biotechnology (SIMB), Malaysian Pharmaceutical Society, Japanese Society for Quantitative Biology, Society for Biotechnology,Biotechnology Conferences.

Track 8: Environmental Biotechnology

Environment biotechnology is applied and used to study the natural environment. Environmental biotechnology could also imply that one try to harness biological process for commercial uses and exploitation. It is "the development, use and regulation of biological systems for remediation of contaminated environment and for environment-friendly processes (green manufacturing technologies and sustainable development). Environmental biotechnology can simply be described as the optimal use of nature, in the form of plants, animals, bacteria, fungi and algae, to produce renewable energy, food and nutrients in a synergistic integrated cycle of profit making processes where the waste of each process becomes the feedstock for another process.

Related: Environmental Biotechnology Conferences | Plant Biotechnology Conferences | Agricultural Biotechnology Conferences | Biotechnology Conferences 2018 | Biotechnology Conferences | Biotechnology Conferences 2018 USA | Biotechnology Conferences|Biotechnology Conferences.

36th International Conference on Environmental Chemistry & Water Resource Management September 24-25, 2018 Chicago, Illinois, USA; 20th International Conference on Environmental Biotechnology and Bioremediation January 15 - 16, 2018 Zurich, Switzerland; International Society for Environmental Biotechnology June 25-28, 2018 Chania, Greece; 10th Annual Conference on Stem Cell Regenerative Medicine October 08-09, 2018 Zurich, Switzerland; 6th Annual Congress on Biology, 6th Annual Congress on Medicine of Molecules September 17-18, 2018 Abu Dhabi, UAE; 8th International Conference and Expo on Nanosciences Nov 26-28,2018 Barcelona, Spain; 6th Asia Pacific Biotechnology Conferences August 15-16, 2018 Singapore; 22nd World Congress on Biotechnology July 10-11, 2018 Bangkok, Thailand, 18thEuropean BiotechnologyConferences July 1 - 4, 2018 Geneva, Switzerland,Biotechnology Conferences.

Related Societies:

Europe:

Spanish Society of Biotechnology, The Pharmaceutical Society of Ireland, Russian Medical Society, Society for Engineering in Agriculture, Society of Microbial Ecology and Disease, Manchester University Pharmaceutical Society, Italian Society of Biochemistry and Molecular Biology, European Society for Precision Engineering and Nanotechnology, Society for Chemical Engineering Biotechnology, Romanian Society of Medical Mycology and Mycotoxicology, New Zealand Plant Protection Society, International Society for Pharmaceutical Engineering, Pharmaceutical Society of Australia,Biotechnology Conferences.

USA:

Mexican Society for Biotechnology and Bioengineering, Society for Biological Engineering, National Society of Agriculture, The Protein Society, Pharmaceutical Marketing Society,Biotechnology Conferences.

Asia:

Korean Society of Food Science And Technology, Pharmaceutical Society of Singapore, Korean Society of Gene and Cell Therapy, Pharmaceutical Society of Singapore, Indian Society of Nano science And Nanotechnology, Tanta Pharmaceutical Scientific Society (TPSS), Iran Society for Cell Biology, Israel Societies for Experimental Biology, Society for Industrial Microbiology and Biotechnology (SIMB), Malaysian Pharmaceutical Society, Japanese Society for Quantitative Biology, Society for Biotechnology,Biotechnology Conferences.

Track 9: Plant and Forest Biotechnology

Plant Biotechnology is a set of techniques used to adapt plants for specific needs or opportunities. Situations that combine multiple needs and opportunities are common, it is prominent in the field of medicine interfacing biotechnology and bioinformatics, the molecular characterization of medicinal plants; molecular farming; and result from chemistry, nanotechnology, pharmacology, agriculture, Biomass and biofuels as well. Plant Biotechnology is the technology which is used for getting modern product with high yield and at faster rate. Biotechnology is being used as a tool to grow trees with special characteristics. When used responsibly, society and the environment can benefit from advanced tree breeding technologies.

Related Conferences: Biotechnology Conferences | Plant Biotechnology | Agricultural Biotechnology | Biotechnology Conferences 2018 | Biotechnology Conferences | Biotechnology Conferences 2018 USA | Biotechnology Conferences|Biotechnology Conferences.

World congress on Plant Pathology & Plant Biotechnology September 24- 25, 2018 Dallas, USA; Agriculture & Horticulture April 08-09, 2019 Prague, Czech Republic; 6th Global Summit on Plant Science October 29-30, 2018 Valencia, Spain; International Association For Plant Biotechnology ConferencesAugust 19-24, 2018 Dublin, Ireland ; Plant Metabolic Engineering Jun 15-16, 2019 Lucca (Barga), Italy. 6th Asia Pacific Biotechnology Conferences August 15-16, 2018 Singapore; 22nd World Congress on Biotechnology July 10-11, 2018 Bangkok, Thailand, 18thEuropean Congress on BiotechnologyJuly 1 - 4, 2018 Geneva, Switzerland,Biotechnology Conferences.

Related Societies:

Europe:

Spanish Society of Biotechnology, The Pharmaceutical Society of Ireland, Russian Medical Society, Society for Engineering in Agriculture, Society of Microbial Ecology and Disease, Manchester University Pharmaceutical Society, Italian Society of Biochemistry and Molecular Biology, European Society for Precision Engineering and Nanotechnology, Society for Chemical Engineering Biotechnology, Romanian Society of Medical Mycology and Mycotoxicology, New Zealand Plant Protection Society, International Society for Pharmaceutical Engineering, Pharmaceutical Society of Australia,Biotechnology Conferences.

USA:

Mexican Society for Biotechnology and Bioengineering, Society for Biological Engineering, National Society of Agriculture, The Protein Society, Pharmaceutical Marketing Society,Biotechnology Conferences.

Asia:

Korean Society of Food Science And Technology, Pharmaceutical Society of Singapore, Korean Society of Gene and Cell Therapy, Pharmaceutical Society of Singapore, Indian Society of Nano science And Nanotechnology, Tanta Pharmaceutical Scientific Society (TPSS), Iran Society for Cell Biology, Israel Societies for Experimental Biology, Society for Industrial Microbiology and Biotechnology (SIMB), Malaysian Pharmaceutical Society, Japanese Society for Quantitative Biology, Society for Biotechnology.,Biotechnology Conferences.

Track 10: Food and Feed Biotechnology

See the original post here:
Biotechnology Conferences | Biotechnology Conferences 2018 ...

Past Conference Information

GlobalConference onPlant ScienceandMolecular Biology2017Report:

Magnus Grouptakes a great pride in declaring the GlobalConference on Plant Science and Molecular Biology (GPMB 2017) which was held in Valencia, Spain, during September 11-13, 2017.

Plant Science Conference 2017witnessed an amalgamation of outstanding speakers who enlightened the crowd with their knowledge and confabulated on various new-fangled topics related to the field of Plant Science and Molecular Biology. The extremely well-known conference hosted by Magnus Group was marked with the attendance of young and brilliant researchers, business delegates and talented student communities representing diverse countries around the world.

For GPMB 2017 Final Program:Click Here

The theme of the conference is Accentuate Innovations and Emerging Novel Research in Plant Sciences. The meeting captivated a vicinity of utilitarian discussions on novel subjects like Plant Physiology and Biochemistry, Plant Biotechnology, Plant Pathology: Mechanisms Of Disease, Applications In Plant Sciences And Plant Research, to mention a few. The three days event implanted a firm relation of upcoming strategies in the field of Plant Science and Molecular Biology with the scientific community. The conceptual and pertinent knowledge shared, will correspondingly foster organizational collaborations to nurture scientific accelerations.

For GPMB 2017 Gallery:Click Here

GPMB 2017Organizing Committee

Prof. Ammann Klaus, University of Bern, Switzerland

Prof. Leif Sundheim, Norwegian Institute of Bioeconomy Research, Norway

Prof. Cornelia Butler Flora, Kansas State University, USA

Dr. Monica Ruffini Castiglione, University of Pisa, Italy

Dr. Samir C. Debnath, St. Johns Research and Development Centre, Canada

The Organizing Committee would like to thank the moderatorsDr. Victoria A Piunova, IBM Almaden Research Center, United States, Dr. Selcuk Aslan, Max Planck Institute of Molecular Plant Physiology, Germany and Dr. Susan Yvonne Jaconis, CSIRO Agriculture, Australia for their contributions which ensued in smooth functioning of the conference.

The highlights of the conference were the keynote forum by prominent scientists,Prof. Klaus Ammann, University of Bern, Switzerland; Prof. Cornelia Butler Flora, Kansas State University, USA; Dr. Monica Ruffini Castiglione, University of Pisa, Italy; Prof. Leif Sundheim, Norwegian Institute of Bioeconomy Research, Norway; Dr. Samir C. Debnath, St. Johns Research and Development Centre, Canada; Dr. Goutam Gupta, Los Alamos National Laboratory, USA; Dr. Elena Rakosy-Tican, Babes-Bolyai University, Romania; Dr. Ivica Djalovic, Institute of Field and Vegetable Crops, Serbia; gave their fruitful contributions in the form of very informative presentations and made the conference a top notch one.

Magnus Groupis privileged to thank the Organizing Committee Members, Keynote speakers, Session chairs on transcribing the sessions, in a varied and variegate manner to make this conference a desirable artifact.

Speakers of GPMB 2017

Day 1: Speakers

Antonova Galina Feodosievna, VN Sukachev Institute of Forest Siberian Branch of Russian Academy of Sciences, Russian Federation

Cezary Piotr Sempruch, Siedlce University of Natural Sciences and Humanities, Poland

Ivan Paponov, Norwegian Institute of Bioeconomy Research, Norway

Malgorzata Adamiec, Adam Mickiewicz University, Institute of Experimental Biology, Poland

Michael Handford, Universidad de Chile, Chile

Natalia Repkina, Institute of Biology Karelian Research Centre of the Russian Academy of Sciences, Russia

Elide Formentin, University of Padova, Italy

Magdalena Opalinska, University of Wroclaw, Poland

Moses Kwame Aidoo, Ben-Gurion University of the Negev, Israel

Yuke He, Shanghai Institutes for Biological Sciences, China

Sameera Omar Bafeel, King Abdulaziz University, Science college, Saudi Arabia

Joerg Fettke, University of Potsdam, Germany

Siti Nor Akmar Abdullah, Universiti Putra Malaysia, Malaysia

Alberto Guillen Bas, University of Valencia, Spain

Carmen Quinonero Lopez, University of Copenhagen, Denmark

Laura Fattorini, Sapienza University of Rome, Italy

Meltem Bayraktar, Ahi Evran University, Turkey

Victoria Cristea, Babes-Bolyai University Cluj-Napoca, Romania

Selcuk Aslan, Max Planck Institute of Molecular Plant Physiology, Germany

Sofia Kourmpetli, Cranfield Soil and AgriFoodInstitute, UK

Seanna Hewitt, Washington State University, USA

Javier Terol Alcayde, Centro de Genomica, IVIA , Spain

Susan Yvonne Jaconis, CSIRO Agriculture, Australia

Magdalena Szechynska-Hebda, Institute of Plant Physiology, Polish Academy of Sciences, Australia

Acga Cheng, University of Malaya, Malaysia

Henrik Toft Simonsen, Technical University of Denmark, Denmark

Yeyun Xin, China National Hybrid Rice Research and Development Center, China

Sandhya Mehrotra, Birla Institute of Technology and Science Pilani, India

Gustavo Souza, Federal University of Pernambuco Bioscience Center, Brazil

Rachel Swee-Suak Ko, Academia Sinica, ABRC/BCST, Taiwan, Province of China

Yougasphree Naidoo, School of Life Sciences, South africa

Julian Witjaksono, The Assessment Institute for Agricultural Technology of Souhteast Sulawesi, Indonesia

Day-1 Posters

Lingling Shang, The Faculty of Agriculture and Food Sciences, Laval University, Canada

Nahaa Miqad Alotaibi, Swansea University, United Kingdom

Layla Al Hijab, West of England Universtiy, United Kingdom

Tomasz Goral, Plant Breeding and Acclimatization Institute NRI, Poland

Mikhail Oliveira Leastro, Instituto Biologico de Sao Paulo, Brazil

Michael Handford, Universidad de Chile, Chile

Polzella Antonella, University of Molise, Italy

Wisniewska Halina, Institute of Plant Genetics Polish Academy of Sciences, Poland

Costel Sarbu, Babes-Bolyai University Cluj-Napoca, Romania

Benjamin Dubois, Walloon Agricultural Research Center (CRA-W), Belgium

Sandra Cichorz, Plant Breeding and Acclimatization Institute - NRI, Poland

Elzbieta Kochanska-Czembor, Plant Breeding and Acclimatization Institute, Poland

Woo Taek Kim, Yonsei University, Republic of Korea

Prashanth Tamizhselvan, Masaryk University, CEITEC MU, Czech Republic

Yun Hee Kim, Gyeongsang National University, Republic of Korea

Nada Bezic, University of Split, Croatia

Havrlentova Michaela, Research Institute for Plant Productio, Slovakia

Seok Keun Cho, Yonsei University, Republic of Korea

Prasanna Angel Deva, Ben Gurion University of the Negev, Israel

Kebede Mesfin Haile, Kangwon National University, Korea

Lidia Kowalska, Plant Breeding and Acclimatization Institute, Poland

Motyleva Svetlana Mikhailivna, FSBSI ARHIBAN, Russian Federation

Paulina Drozdz, Forest Research Institute, Poland

Chul Han An, Korea Research Institute of Bioscience and Biotechnology, Republic of Korea

Jurga Jankauskiene, Nature Research Centre, Lithuania

Day 2: Speakers

Victoria A Piunova, IBM Almaden Research Center, United States

Miroslava Cuperlovic-Culf, National Research Council Canada, Canada

Paola Leonetti, IPSP-CNR, Italy

Giulia Chitarrini, Fondazione Edmund Mach, Italy

Antonio Domenech-Carbo, University of Valencia, Spain

Nurshafika Mohd Sakeh, Universiti Putra Malaysia, Malaysia

Adel Saleh Hussein Al-Abed, National Center for Agricultural Research and Extension, Jordan

Manju Sharma, Amity Institute of Biotechnology, India

Sergio Molinari, IPSP-CNR, Italy

Jaroslava Ovesna, Crop Research institute, czech Rpublic

John B. Carrigan, RebelBio SOSV, Ireland

Bardouki Haido, VIORYL S.A., Greece

Natalia Tomas Marques, Universidade do Algarve, Portugal

Azza M. Salama, Cairo University, Egypt

Chang-Yoon JI, University of Science & Technology, Korea

Kgabo Martha Pofu, Agricultural Research Council, South Africa

Siegfried Zerche, Leibniz-Institute of Vegetable- & Ornamental Crops, Germany

Piergiorgio Stevanato, University of Padova, Italy

Seong Wook Yang, Yonsei University, Republic of Korea

Alexander Hahn, Max Planck Institute for Biophysic, Germany

Klaus Harter, University of Tuebingen, Center for Plant Molecular Biology, Germany

Laigeng Li, Institute of Plant Physiology and Ecology, China

Thomas C Mueller, University of Tennessee, United States

The rest is here:
Plant Biology Conferences 2019 | Plant Biotechnology ...

Genetics, study of heredity in general and of genes in particular. Genetics forms one of the central pillars of biology and overlaps with many other areas, such as agriculture, medicine, and biotechnology.

Since the dawn of civilization, humankind has recognized the influence of heredity and applied its principles to the improvement of cultivated crops and domestic animals. A Babylonian tablet more than 6,000 years old, for example, shows pedigrees of horses and indicates possible inherited characteristics. Other old carvings show cross-pollination of date palm trees. Most of the mechanisms of heredity, however, remained a mystery until the 19th century, when genetics as a systematic science began.

Genetics arose out of the identification of genes, the fundamental units responsible for heredity. Genetics may be defined as the study of genes at all levels, including the ways in which they act in the cell and the ways in which they are transmitted from parents to offspring. Modern genetics focuses on the chemical substance that genes are made of, called deoxyribonucleic acid, or DNA, and the ways in which it affects the chemical reactions that constitute the living processes within the cell. Gene action depends on interaction with the environment. Green plants, for example, have genes containing the information necessary to synthesize the photosynthetic pigment chlorophyll that gives them their green colour. Chlorophyll is synthesized in an environment containing light because the gene for chlorophyll is expressed only when it interacts with light. If a plant is placed in a dark environment, chlorophyll synthesis stops because the gene is no longer expressed.

Genetics as a scientific discipline stemmed from the work of Gregor Mendel in the middle of the 19th century. Mendel suspected that traits were inherited as discrete units, and, although he knew nothing of the physical or chemical nature of genes at the time, his units became the basis for the development of the present understanding of heredity. All present research in genetics can be traced back to Mendels discovery of the laws governing the inheritance of traits. The word genetics was introduced in 1905 by English biologist William Bateson, who was one of the discoverers of Mendels work and who became a champion of Mendels principles of inheritance.

Read More on This Topic

heredity

clear in the study of genetics. Both aspects of heredity can be explained by genes, the functional units of heritable material that are found within all living cells. Every member of a species has a set of genes specific to that species. It is this set of genes that provides

Although scientific evidence for patterns of genetic inheritance did not appear until Mendels work, history shows that humankind must have been interested in heredity long before the dawn of civilization. Curiosity must first have been based on human family resemblances, such as similarity in body structure, voice, gait, and gestures. Such notions were instrumental in the establishment of family and royal dynasties. Early nomadic tribes were interested in the qualities of the animals that they herded and domesticated and, undoubtedly, bred selectively. The first human settlements that practiced farming appear to have selected crop plants with favourable qualities. Ancient tomb paintings show racehorse breeding pedigrees containing clear depictions of the inheritance of several distinct physical traits in the horses. Despite this interest, the first recorded speculations on heredity did not exist until the time of the ancient Greeks; some aspects of their ideas are still considered relevant today.

Hippocrates (c. 460c. 375 bce), known as the father of medicine, believed in the inheritance of acquired characteristics, and, to account for this, he devised the hypothesis known as pangenesis. He postulated that all organs of the body of a parent gave off invisible seeds, which were like miniaturized building components and were transmitted during sexual intercourse, reassembling themselves in the mothers womb to form a baby.

Aristotle (384322 bce) emphasized the importance of blood in heredity. He thought that the blood supplied generative material for building all parts of the adult body, and he reasoned that blood was the basis for passing on this generative power to the next generation. In fact, he believed that the males semen was purified blood and that a womans menstrual blood was her equivalent of semen. These male and female contributions united in the womb to produce a baby. The blood contained some type of hereditary essences, but he believed that the baby would develop under the influence of these essences, rather than being built from the essences themselves.

Aristotles ideas about the role of blood in procreation were probably the origin of the still prevalent notion that somehow the blood is involved in heredity. Today people still speak of certain traits as being in the blood and of blood lines and blood ties. The Greek model of inheritance, in which a teeming multitude of substances was invoked, differed from that of the Mendelian model. Mendels idea was that distinct differences between individuals are determined by differences in single yet powerful hereditary factors. These single hereditary factors were identified as genes. Copies of genes are transmitted through sperm and egg and guide the development of the offspring. Genes are also responsible for reproducing the distinct features of both parents that are visible in their children.

In the two millennia between the lives of Aristotle and Mendel, few new ideas were recorded on the nature of heredity. In the 17th and 18th centuries the idea of preformation was introduced. Scientists using the newly developed microscopes imagined that they could see miniature replicas of human beings inside sperm heads. French biologist Jean-Baptiste Lamarck invoked the idea of the inheritance of acquired characters, not as an explanation for heredity but as a model for evolution. He lived at a time when the fixity of species was taken for granted, yet he maintained that this fixity was only found in a constant environment. He enunciated the law of use and disuse, which states that when certain organs become specially developed as a result of some environmental need, then that state of development is hereditary and can be passed on to progeny. He believed that in this way, over many generations, giraffes could arise from deerlike animals that had to keep stretching their necks to reach high leaves on trees.

British naturalist Alfred Russel Wallace originally postulated the theory of evolution by natural selection. However, Charles Darwins observations during his circumnavigation of the globe aboard the HMS Beagle (183136) provided evidence for natural selection and his suggestion that humans and animals shared a common ancestry. Many scientists at the time believed in a hereditary mechanism that was a version of the ancient Greek idea of pangenesis, and Darwins ideas did not appear to fit with the theory of heredity that sprang from the experiments of Mendel.

Before Gregor Mendel, theories for a hereditary mechanism were based largely on logic and speculation, not on experimentation. In his monastery garden, Mendel carried out a large number of cross-pollination experiments between variants of the garden pea, which he obtained as pure-breeding lines. He crossed peas with yellow seeds to those with green seeds and observed that the progeny seeds (the first generation, F1) were all yellow. When the F1 individuals were self-pollinated or crossed among themselves, their progeny (F2) showed a ratio of 3:1 (3/4 yellow and 1/4 green). He deduced that, since the F2 generation contained some green individuals, the determinants of greenness must have been present in the F1 generation, although they were not expressed because yellow is dominant over green. From the precise mathematical 3:1 ratio (of which he found several other examples), he deduced not only the existence of discrete hereditary units (genes) but also that the units were present in pairs in the pea plant and that the pairs separated during gamete formation. Hence, the two original lines of pea plants were proposed to be YY (yellow) and yy (green). The gametes from these were Y and y, thereby producing an F1 generation of Yy that were yellow in colour because of the dominance of Y. In the F1 generation, half the gametes were Y and the other half were y, making the F2 generation produced from random mating 1/4 Yy, 1/2 YY, and 1/4 yy, thus explaining the 3:1 ratio. The forms of the pea colour genes, Y and y, are called alleles.

Mendel also analyzed pure lines that differed in pairs of characters, such as seed colour (yellow versus green) and seed shape (round versus wrinkled). The cross of yellow round seeds with green wrinkled seeds resulted in an F1 generation that were all yellow and round, revealing the dominance of the yellow and round traits. However, the F2 generation produced by self-pollination of F1 plants showed a ratio of 9:3:3:1 (9/16 yellow round, 3/16 yellow wrinkled, 3/16 green round, and 1/16 green wrinkled; note that a 9:3:3:1 ratio is simply two 3:1 ratios combined). From this result and others like it, he deduced the independent assortment of separate gene pairs at gamete formation.

Mendels success can be attributed in part to his classic experimental approach. He chose his experimental organism well and performed many controlled experiments to collect data. From his results, he developed brilliant explanatory hypotheses and went on to test these hypotheses experimentally. Mendels methodology established a prototype for genetics that is still used today for gene discovery and understanding the genetic properties of inheritance.

Mendels genes were only hypothetical entities, factors that could be inferred to exist in order to explain his results. The 20th century saw tremendous strides in the development of the understanding of the nature of genes and how they function. Mendels publications lay unmentioned in the research literature until 1900, when the same conclusions were reached by several other investigators. Then there followed hundreds of papers showing Mendelian inheritance in a wide array of plants and animals, including humans. It seemed that Mendels ideas were of general validity. Many biologists noted that the inheritance of genes closely paralleled the inheritance of chromosomes during nuclear divisions, called meiosis, that occur in the cell divisions just prior to gamete formation.

It seemed that genes were parts of chromosomes. In 1910 this idea was strengthened through the demonstration of parallel inheritance of certain Drosophila (a type of fruit fly) genes on sex-determining chromosomes by American zoologist and geneticist Thomas Hunt Morgan. Morgan and one of his students, Alfred Henry Sturtevant, showed not only that certain genes seemed to be linked on the same chromosome but that the distance between genes on the same chromosome could be calculated by measuring the frequency at which new chromosomal combinations arose (these were proposed to be caused by chromosomal breakage and reunion, also known as crossing over). In 1916 another student of Morgans, Calvin Bridges, used fruit flies with an extra chromosome to prove beyond reasonable doubt that the only way to explain the abnormal inheritance of certain genes was if they were part of the extra chromosome. American geneticist Hermann Joseph Mller showed that new alleles (called mutations) could be produced at high frequencies by treating cells with X-rays, the first demonstration of an environmental mutagenic agent (mutations can also arise spontaneously). In 1931 American botanist Harriet Creighton and American scientist Barbara McClintock demonstrated that new allelic combinations of linked genes were correlated with physically exchanged chromosome parts.

In 1908 British physician Archibald Garrod proposed the important idea that the human disease alkaptonuria, and certain other hereditary diseases, were caused by inborn errors of metabolism, suggesting for the first time that linked genes had molecular action at the cell level. Molecular genetics did not begin in earnest until 1941 when American geneticist George Beadle and American biochemist Edward Tatum showed that the genes they were studying in the fungus Neurospora crassa acted by coding for catalytic proteins called enzymes. Subsequent studies in other organisms extended this idea to show that genes generally code for proteins. Soon afterward, American bacteriologist Oswald Avery, Canadian American geneticist Colin M. MacLeod, and American biologist Maclyn McCarty showed that bacterial genes are made of DNA, a finding that was later extended to all organisms.

A major landmark was attained in 1953 when American geneticist and biophysicist James D. Watson and British biophysicists Francis Crick and Maurice Wilkins devised a double helix model for DNA structure. This model showed that DNA was capable of self-replication by separating its complementary strands and using them as templates for the synthesis of new DNA molecules. Each of the intertwined strands of DNA was proposed to be a chain of chemical groups called nucleotides, of which there were known to be four types. Because proteins are strings of amino acids, it was proposed that a specific nucleotide sequence of DNA could contain a code for an amino acid sequence and hence protein structure. In 1955 American molecular biologist Seymour Benzer, extending earlier studies in Drosophila, showed that the mutant sites within a gene could be mapped in relation to each other. His linear map indicated that the gene itself is a linear structure.

In 1958 the strand-separation method for DNA replication (called the semiconservative method) was demonstrated experimentally for the first time by American molecular biologist Matthew Meselson and American geneticist Franklin W. Stahl. In 1961 Crick and South African biologist Sydney Brenner showed that the genetic code must be read in triplets of nucleotides, called codons. American geneticist Charles Yanofsky showed that the positions of mutant sites within a gene matched perfectly the positions of altered amino acids in the amino acid sequence of the corresponding protein. In 1966 the complete genetic code of all 64 possible triplet coding units (codons), and the specific amino acids they code for, was deduced by American biochemists Marshall Nirenberg and Har Gobind Khorana. Subsequent studies in many organisms showed that the double helical structure of DNA, the mode of its replication, and the genetic code are the same in virtually all organisms, including plants, animals, fungi, bacteria, and viruses. In 1961 French biologist Franois Jacob and French biochemist Jacques Monod established the prototypical model for gene regulation by showing that bacterial genes can be turned on (initiating transcription into RNA and protein synthesis) and off through the binding action of regulatory proteins to a region just upstream of the coding region of the gene.

Technical advances have played an important role in the advance of genetic understanding. In 1970 American microbiologists Daniel Nathans and Hamilton Othanel Smith discovered a specialized class of enzymes (called restriction enzymes) that cut DNA at specific nucleotide target sequences. That discovery allowed American biochemist Paul Berg in 1972 to make the first artificial recombinant DNA molecule by isolating DNA molecules from different sources, cutting them, and joining them together in a test tube. These advances allowed individual genes to be cloned (amplified to a high copy number) by splicing them into self-replicating DNA molecules, such as plasmids (extragenomic circular DNA elements) or viruses, and inserting these into living bacterial cells. From these methodologies arose the field of recombinant DNA technology that presently dominates molecular genetics. In 1977 two different methods were invented for determining the nucleotide sequence of DNA: one by American molecular biologists Allan Maxam and Walter Gilbert and the other by English biochemist Fred Sanger. Such technologies made it possible to examine the structure of genes directly by nucleotide sequencing, resulting in the confirmation of many of the inferences about genes originally made indirectly.

In the 1970s Canadian biochemist Michael Smith revolutionized the art of redesigning genes by devising a method for inducing specifically tailored mutations at defined sites within a gene, creating a technique known as site-directed mutagenesis. In 1983 American biochemist Kary B. Mullis invented the polymerase chain reaction, a method for rapidly detecting and amplifying a specific DNA sequence without cloning it. In the last decade of the 20th century, progress in recombinant DNA technology and in the development of automated sequencing machines led to the elucidation of complete DNA sequences of several viruses, bacteria, plants, and animals. In 2001 the complete sequence of human DNA, approximately three billion nucleotide pairs, was made public.

A time line of important milestones in the history of genetics is provided in the table.

Classical genetics, which remains the foundation for all other areas in genetics, is concerned primarily with the method by which genetic traitsclassified as dominant (always expressed), recessive (subordinate to a dominant trait), intermediate (partially expressed), or polygenic (due to multiple genes)are transmitted in plants and animals. These traits may be sex-linked (resulting from the action of a gene on the sex, or X, chromosome) or autosomal (resulting from the action of a gene on a chromosome other than a sex chromosome). Classical genetics began with Mendels study of inheritance in garden peas and continues with studies of inheritance in many different plants and animals. Today a prime reason for performing classical genetics is for gene discoverythe finding and assembling of a set of genes that affects a biological property of interest.

Cytogenetics, the microscopic study of chromosomes, blends the skills of cytologists, who study the structure and activities of cells, with those of geneticists, who study genes. Cytologists discovered chromosomes and the way in which they duplicate and separate during cell division at about the same time that geneticists began to understand the behaviour of genes at the cellular level. The close correlation between the two disciplines led to their combination.

Plant cytogenetics early became an important subdivision of cytogenetics because, as a general rule, plant chromosomes are larger than those of animals. Animal cytogenetics became important after the development of the so-called squash technique, in which entire cells are pressed flat on a piece of glass and observed through a microscope; the human chromosomes were numbered using this technique.

Today there are multiple ways to attach molecular labels to specific genes and chromosomes, as well as to specific RNAs and proteins, that make these molecules easily discernible from other components of cells, thereby greatly facilitating cytogenetics research.

Microorganisms were generally ignored by the early geneticists because they are small in size and were thought to lack variable traits and the sexual reproduction necessary for a mixing of genes from different organisms. After it was discovered that microorganisms have many different physical and physiological characteristics that are amenable to study, they became objects of great interest to geneticists because of their small size and the fact that they reproduce much more rapidly than larger organisms. Bacteria became important model organisms in genetic analysis, and many discoveries of general interest in genetics arose from their study. Bacterial genetics is the centre of cloning technology.

Viral genetics is another key part of microbial genetics. The genetics of viruses that attack bacteria were the first to be elucidated. Since then, studies and findings of viral genetics have been applied to viruses pathogenic on plants and animals, including humans. Viruses are also used as vectors (agents that carry and introduce modified genetic material into an organism) in DNA technology.

Molecular genetics is the study of the molecular structure of DNA, its cellular activities (including its replication), and its influence in determining the overall makeup of an organism. Molecular genetics relies heavily on genetic engineering (recombinant DNA technology), which can be used to modify organisms by adding foreign DNA, thereby forming transgenic organisms. Since the early 1980s, these techniques have been used extensively in basic biological research and are also fundamental to the biotechnology industry, which is devoted to the manufacture of agricultural and medical products. Transgenesis forms the basis of gene therapy, the attempt to cure genetic disease by addition of normally functioning genes from exogenous sources.

The development of the technology to sequence the DNA of whole genomes on a routine basis has given rise to the discipline of genomics, which dominates genetics research today. Genomics is the study of the structure, function, and evolutionary comparison of whole genomes. Genomics has made it possible to study gene function at a broader level, revealing sets of genes that interact to impinge on some biological property of interest to the researcher. Bioinformatics is the computer-based discipline that deals with the analysis of such large sets of biological information, especially as it applies to genomic information.

The study of genes in populations of animals, plants, and microbes provides information on past migrations, evolutionary relationships and extents of mixing among different varieties and species, and methods of adaptation to the environment. Statistical methods are used to analyze gene distributions and chromosomal variations in populations.

Population genetics is based on the mathematics of the frequencies of alleles and of genetic types in populations. For example, the Hardy-Weinberg formula, p2 + 2pq + q2 = 1, predicts the frequency of individuals with the respective homozygous dominant (AA), heterozygous (Aa), and homozygous recessive (aa) genotypes in a randomly mating population. Selection, mutation, and random changes can be incorporated into such mathematical models to explain and predict the course of evolutionary change at the population level. These methods can be used on alleles of known phenotypic effect, such as the recessive allele for albinism, or on DNA segments of any type of known or unknown function.

Human population geneticists have traced the origins and migration and invasion routes of modern humans, Homo sapiens. DNA comparisons between the present peoples on the planet have pointed to an African origin of Homo sapiens. Tracing specific forms of genes has allowed geneticists to deduce probable migration routes out of Africa to the areas colonized today. Similar studies show to what degree present populations have been mixed by recent patterns of travel.

Another aspect of genetics is the study of the influence of heredity on behaviour. Many aspects of animal behaviour are genetically determined and can therefore be treated as similar to other biological properties. This is the subject material of behaviour genetics, whose goal is to determine which genes control various aspects of behaviour in animals. Human behaviour is difficult to analyze because of the powerful effects of environmental factors, such as culture. Few cases of genetic determination of complex human behaviour are known. Genomics studies provide a useful way to explore the genetic factors involved in complex human traits such as behaviour.

Some geneticists specialize in the hereditary processes of human genetics. Most of the emphasis is on understanding and treating genetic disease and genetically influenced ill health, areas collectively known as medical genetics. One broad area of activity is laboratory research dealing with the mechanisms of human gene function and malfunction and investigating pharmaceutical and other types of treatments. Since there is a high degree of evolutionary conservation between organisms, research on model organismssuch as bacteria, fungi, and fruit flies (Drosophila)which are easier to study, often provides important insights into human gene function.

Many single-gene diseases, caused by mutant alleles of a single gene, have been discovered. Two well-characterized single-gene diseases include phenylketonuria (PKU) and Tay-Sachs disease. Other diseases, such as heart disease, schizophrenia, and depression, are thought to have more complex heredity components that involve a number of different genes. These diseases are the focus of a great deal of research that is being carried out today.

Another broad area of activity is clinical genetics, which centres on advising parents of the likelihood of their children being affected by genetic disease caused by mutant genes and abnormal chromosome structure and number. Such genetic counseling is based on examining individual and family medical records and on diagnostic procedures that can detect unexpressed, abnormal forms of genes. Counseling is carried out by physicians with a particular interest in this area or by specially trained nonphysicians.

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What does it mean to be a genetic counseling student?

At the University of South Carolina it means you become part of the team from day one: an engaged learner in our genetics center.You'll have an experienced faculty who are open door mentors in your preparation for this career.

You'll have access in the classroom and in the clinic to the geneticist and genetic counselor faculty in our clinical rotation network oftwelve genetic centers. The world of genetic counseling will unfold for you in two very busy years, preparing you to take on the dozens of roles open to genetic counselors today.

Rigorous coursework, community service, challenging clinical rotations and a research-based thesis will provide opportunity for tremendous professional growth.

We've been perfecting our curriculum formore than 30 years to connect the knowledge with the skills youll need as a genetic counselor. Our reputation for excellence is known at home and abroad. We carefully review more than 140 applications per year to select thenine students who will graduate from the School of Medicine Genetic Counseling Program. Our alumni are our proudest accomplishment and work in the best genetic centers throughout the country. They build on our foundation to achieve goals in clinical care, education, research and industry beyond what we imagined.

First in the Southeast and tenth in the nation, we are one of 39 accredited programs in the United States. We have graduatedmore than 200 genetic counselors, many of whom are leading the profession today.

Weve received highly acclaimed Commendations for Excellence from the South Carolina Commission of Higher Education. American Board of Genetic Counseling accreditation was achieved in 2000, reaccreditation in 2006 and, most recently, theAccreditation Council for Genetic Counselingreaccreditation was awarded, 2014-2022.

You'll have the chance to form lifelong partnerships with our core and clinical rotation faculty. Build your professional network with geneticists and genetic counselors throughout the Southeast.

One of our program's greatest assets is our alumni. This dedicated group regularly teaches and mentors our students,serves on our advisory board, and raises money for our endowment.You'll enjoy the instant connection when meeting other USC Genetic Counseling graduates. As a student, you'll benefit from the alumni networkand all they have to offer you. Check out our Facebook group.

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Genetic Counseling - School of Medicine | University of ...

Color blindness, also known as color vision deficiency, is the decreased ability to see color or differences in color.[2] Simple tasks such as selecting ripe fruit, choosing clothing, and reading traffic lights can be more challenging.[2] Color blindness may also make some educational activities more difficult.[2] However, problems are generally minor, and most people find that they can adapt.[2] People with total color blindness (achromatopsia) may also have decreased visual acuity and be uncomfortable in bright environments.[2]

The most common cause of color blindness is an inherited problem in the development of one or more of the three sets of color sensing cones in the eye.[2] Males are more likely to be color blind than females, as the genes responsible for the most common forms of color blindness are on the X chromosome.[2] As females have two X chromosomes, a defect in one is typically compensated for by the other, while males only have one X chromosome.[2] Color blindness can also result from physical or chemical damage to the eye, optic nerve or parts of the brain.[2] Diagnosis is typically with the Ishihara color test; however, a number of other testing methods also exist.[2]

There is no cure for color blindness.[2] Diagnosis may allow a person's teacher to change their method of teaching to accommodate the decreased ability to recognize colors.[1] Special lenses may help people with redgreen color blindness when under bright conditions.[2] There are also mobile apps that can help people identify colors.[2]

Redgreen color blindness is the most common form, followed by blueyellow color blindness and total color blindness.[2] Redgreen color blindness affects up to 8% of males and 0.5% of females of Northern European descent.[2] The ability to see color also decreases in old age.[2] Being color blind may make people ineligible for certain jobs in certain countries.[1] This may include being a pilot, train driver and working in the armed forces.[1] The effect of color blindness on artistic ability, however, is controversial.[1] The ability to draw appears to be unchanged, and a number of famous artists are believed to have been color blind.[1]

In almost all cases, color blind people retain blueyellow discrimination, and most color-blind individuals are anomalous trichromats rather than complete dichromats. In practice, this means that they often retain a limited discrimination along the redgreen axis of color space, although their ability to separate colors in this dimension is reduced. Color blindness very rarely refers to complete monochromatism.[3]

Dichromats often confuse red and green items. For example, they may find it difficult to distinguish a Braeburn apple from a Granny Smith or red from green of traffic lights without other cluesfor example, shape or position. Dichromats tend to learn to use texture and shape clues and so may be able to penetrate camouflage that has been designed to deceive individuals with normal color vision.[4]

Colors of traffic lights are confusing to some dichromats as there is insufficient apparent difference between the red/amber traffic lights and sodium street lamps; also, the green can be confused with a grubby white lamp. This is a risk on high-speed undulating roads where angular cues cannot be used. British Rail color lamp signals use more easily identifiable colors: The red is blood red, the amber is yellow and the green is a bluish color. Most British road traffic lights are mounted vertically on a black rectangle with a white border (forming a "sighting board") and so dichromats can more easily look for the position of the light within the rectangletop, middle or bottom. In the eastern provinces of Canada horizontally mounted traffic lights are generally differentiated by shape to facilitate identification for those with color blindness.[citation needed] In the United States, this is not done by shape but by position, as the red light is always on the left if the light is horizontal, or on top if the light is vertical. However, a lone flashing light (e.g. red for stop, yellow for caution) is still problematic.

Color vision deficiencies can be classified as acquired or inherited.

Color blindness is typically an inherited genetic disorder. It is most commonly inherited from mutations on the X chromosome but the mapping of the human genome has shown there are many causative mutationsmutations capable of causing color blindness originate from at least 19 different chromosomes and 56 different genes (as shown online at the Online Mendelian Inheritance in Man (OMIM)). Two of the most common inherited forms of color blindness are protanomaly (and, more rarely, protanopia the two together often known as "protans") and deuteranomaly (or, more rarely, deuteranopia the two together often referred to as "deutans").[12] Both "protans" and "deutans" (of which the deutans are by far the most common) are known as "redgreen color-blind" which is present in about 8 percent of human males and 0.6 percent of females of Northern European ancestry.[13]

Some of the inherited diseases known to cause color blindness are:

Inherited color blindness can be congenital (from birth), or it can commence in childhood or adulthood. Depending on the mutation, it can be stationary, that is, remain the same throughout a person's lifetime, or progressive. As progressive phenotypes involve deterioration of the retina and other parts of the eye, certain forms of color blindness can progress to legal blindness, i.e., an acuity of 6/60 (20/200) or worse, and often leave a person with complete blindness.

Color blindness always pertains to the cone photoreceptors in retinas, as the cones are capable of detecting the color frequencies of light.

About 8 percent of males, and 0.6 percent of females, are red-green color blind in some way or another, whether it is one color, a color combination, or another mutation.[14] The reason males are at a greater risk of inheriting an X linked mutation is that males only have one X chromosome (XY, with the Y chromosome carrying altogether different genes than the X chromosome), and females have two (XX); if a woman inherits a normal X chromosome in addition to the one that carries the mutation, she will not display the mutation. Men do not have a second X chromosome to override the chromosome that carries the mutation. If 8% of variants of a given gene are defective, the probability of a single copy being defective is 8%, but the probability that two copies are both defective is 0.08 0.08 = 0.0064, or just 0.64%.

Other causes of color blindness include brain or retinal damage caused by shaken baby syndrome, accidents and other trauma which produce swelling of the brain in the occipital lobe, and damage to the retina caused by exposure to ultraviolet light (10300nm). Damage often presents itself later on in life.

Color blindness may also present itself in the spectrum of degenerative diseases of the eye, such as age-related macular degeneration, and as part of the retinal damage caused by diabetes. Another factor that may affect color blindness includes a deficiency in Vitamin A.[15]

Some subtle forms of colorblindness may be associated with chronic solvent-induced encephalopathy (CSE), caused by longtime exposure to solvent vapors.[16]

Redgreen color blindness can be caused by ethambutol,[17] a drug used in the treatment of tuberculosis.

Based on clinical appearance, color blindness may be described as total or partial. Total color blindness is much less common than partial color blindness.[18] There are two major types of color blindness: those who have difficulty distinguishing between red and green, and who have difficulty distinguishing between blue and yellow.[19][20]

Immunofluorescent imaging is a way to determine redgreen color coding. Conventional color coding is difficult for individuals with redgreen color blindness (protanopia or deuteranopia) to discriminate. Replacing red with magenta or green with turquoise improves visibility for such individuals.[21]

The different kinds of inherited color blindness result from partial or complete loss of function of one or more of the different cone systems. When one cone system is compromised, dichromacy results. The most frequent forms of human color blindness result from problems with either the middle or long wavelength sensitive cone systems, and involve difficulties in discriminating reds, yellows, and greens from one another. They are collectively referred to as "redgreen color blindness", though the term is an over-simplification and is somewhat misleading. Other forms of color blindness are much more rare. They include problems in discriminating blues from greens and yellows from reds/pinks, and the rarest forms of all, complete color blindness or monochromacy, where one cannot distinguish any color from grey, as in a black-and-white movie or photograph.

Protanopes, deuteranopes, and tritanopes are dichromats; that is, they can match any color they see with some mixture of just two primary colors (whereas normally humans are trichromats and require three primary colors). These individuals normally know they have a color vision problem and it can affect their lives on a daily basis. Two percent of the male population exhibit severe difficulties distinguishing between red, orange, yellow, and green. A certain pair of colors, that seem very different to a normal viewer, appear to be the same color (or different shades of same color) for such a dichromat. The terms protanopia, deuteranopia, and tritanopia come from Greek and literally mean "inability to see (anopia) with the first (prot-), second (deuter-), or third (trit-) [cone]", respectively.

Anomalous trichromacy is the least serious type of color deficiency.[22] People with protanomaly, deuteranomaly, or tritanomaly are trichromats, but the color matches they make differ from the normal. They are called anomalous trichromats. In order to match a given spectral yellow light, protanomalous observers need more red light in a red/green mixture than a normal observer, and deuteranomalous observers need more green. From a practical standpoint though, many protanomalous and deuteranomalous people have very little difficulty carrying out tasks that require normal color vision. Some may not even be aware that their color perception is in any way different from normal.

Protanomaly and deuteranomaly can be diagnosed using an instrument called an anomaloscope, which mixes spectral red and green lights in variable proportions, for comparison with a fixed spectral yellow. If this is done in front of a large audience of males, as the proportion of red is increased from a low value, first a small proportion of the audience will declare a match, while most will see the mixed light as greenish; these are the deuteranomalous observers. Next, as more red is added the majority will say that a match has been achieved. Finally, as yet more red is added, the remaining, protanomalous, observers will declare a match at a point where normal observers will see the mixed light as definitely reddish.[citation needed]

Protanopia, deuteranopia, protanomaly, and deuteranomaly are commonly inherited forms of redgreen color blindness which affect a substantial portion of the human population. Those affected have difficulty with discriminating red and green hues due to the absence or mutation of the red or green retinal photoreceptors.[12][23] It is sex-linked: genetic redgreen color blindness affects males much more often than females, because the genes for the red and green color receptors are located on the X chromosome, of which males have only one and females have two. Females (46, XX) are redgreen color blind only if both their X chromosomes are defective with a similar deficiency, whereas males (46, XY) are color blind if their single X chromosome is defective.[24]

The gene for redgreen color blindness is transmitted from a color blind male to all his daughters who are heterozygote carriers and are usually unaffected. In turn, a carrier woman has a fifty percent chance of passing on a mutated X chromosome region to each of her male offspring. The sons of an affected male will not inherit the trait from him, since they receive his Y chromosome and not his (defective) X chromosome. Should an affected male have children with a carrier or colorblind woman, their daughters may be colorblind by inheriting an affected X chromosome from each parent.[24]

Because one X chromosome is inactivated at random in each cell during a woman's development, deuteranomalous heterozygotes (i.e. female carriers of deuteranomaly) are potentially tetrachromats, because they will have the normal long wave (red) receptors, the normal medium wave (green) receptors, the abnormal medium wave (deuteranomalous) receptors and the normal autosomal short wave (blue) receptors in their retinas.[25][26][27] The same applies to the carriers of protanomaly (who have two types of short wave receptors, normal medium wave receptors, and normal autosomal short wave receptors in their retinas). If, by chance, a woman is heterozygous for both protanomaly and deuteranomaly she could be pentachromatic. This situation could arise if, for instance, she inherited the X chromosome with the abnormal long wave gene (but normal medium wave gene) from her mother who is a carrier of protanomaly, and her other X chromosome from a deuteranomalous father. Such a woman would have a normal and an abnormal long wave receptor, a normal and abnormal medium wave receptor, and a normal autosomal short wave receptor 5 different types of color receptors in all. The degree to which women who are carriers of either protanomaly or deuteranomaly are demonstrably tetrachromatic and require a mixture of four spectral lights to match an arbitrary light is very variable. In many cases it is almost unnoticeable, but in a minority the tetrachromacy is very pronounced.[25][26][27] However, Jameson et al.[28] have shown that with appropriate and sufficiently sensitive equipment all female carriers of red-green color blindness (i.e. heterozygous protanomaly, or heterozygous deuteranomaly) are tetrachromats to a greater or lesser extent.

Since deuteranomaly is by far the most common form of red-green blindness among men of northwestern European descent (with an incidence of 8%), then the carrier frequency (and of potential deuteranomalous tetrachromacy) among the females of that genetic stock is 14.7% (= [92% 8%] 2).[24]

Those with tritanopia and tritanomaly have difficulty discriminating between bluish and greenish hues, as well as yellowish and reddish hues.

Color blindness involving the inactivation of the short-wavelength sensitive cone system (whose absorption spectrum peaks in the bluish-violet) is called tritanopia or, loosely, blueyellow color blindness. The tritanope's neutral point occurs near a yellowish 570nm; green is perceived at shorter wavelengths and red at longer wavelengths.[31] Mutation of the short-wavelength sensitive cones is called tritanomaly. Tritanopia is equally distributed among males and females. Jeremy H. Nathans (with the Howard Hughes Medical Institute) demonstrated that the gene coding for the blue receptor lies on chromosome 7, which is shared equally by males and females. Therefore, it is not sex-linked. This gene does not have any neighbor whose DNA sequence is similar. Blue color blindness is caused by a simple mutation in this gene.

Total color blindness is defined as the inability to see color. Although the term may refer to acquired disorders such as cerebral achromatopsia also known as color agnosia, it typically refers to congenital color vision disorders (i.e. more frequently rod monochromacy and less frequently cone monochromacy).[33][34]

In cerebral achromatopsia, a person cannot perceive colors even though the eyes are capable of distinguishing them. Some sources do not consider these to be true color blindness, because the failure is of perception, not of vision. They are forms of visual agnosia.[34]

Monochromacy is the condition of possessing only a single channel for conveying information about color. Monochromats possess a complete inability to distinguish any colors and perceive only variations in brightness. It occurs in two primary forms:

The typical human retina contains two kinds of light cells: the rod cells (active in low light) and the cone cells (active in normal daylight). Normally, there are three kinds of cone cells, each containing a different pigment, which are activated when the pigments absorb light. The spectral sensitivities of the cones differ; one is most sensitive to short wavelengths, one to medium wavelengths, and the third to medium-to-long wavelengths within the visible spectrum, with their peak sensitivities in the blue, green, and yellow-green regions of the spectrum, respectively. The absorption spectra of the three systems overlap, and combine to cover the visible spectrum. These receptors are known as short (S), medium (M), and long (L) wavelength cones, but are also often referred to as blue, green, and red cones, although this terminology is inaccurate.[36]

The receptors are each responsive to a wide range of wavelengths. For example, the long wavelength "red" receptor has its peak sensitivity in the yellow-green, some way from the red end (longest wavelength) of the visible spectrum. The sensitivity of normal color vision actually depends on the overlap between the absorption ranges of the three systems: different colors are recognized when the different types of cone are stimulated to different degrees. Red light, for example, stimulates the long wavelength cones much more than either of the others, and reducing the wavelength causes the other two cone systems to be increasingly stimulated, causing a gradual change in hue.

Many of the genes involved in color vision are on the X chromosome, making color blindness much more common in males than in females because males only have one X chromosome, while females have two. Because this is an X-linked trait, an estimated 23% of women have a 4th color cone[25] and can be considered tetrachromats. One such woman has been reported to be a true or functional tetrachromat, as she can discriminate colors most other people can't.[26][27]

The Ishihara color test, which consists of a series of pictures of colored spots, is the test most often used to diagnose redgreen color deficiencies.[37] A figure (usually one or more Arabic digits) is embedded in the picture as a number of spots in a slightly different color, and can be seen with normal color vision, but not with a particular color defect. The full set of tests has a variety of figure/background color combinations, and enable diagnosis of which particular visual defect is present. The anomaloscope, described above, is also used in diagnosing anomalous trichromacy.

Position yourself about 75cm from your monitor so that the colour test image you are looking at is at eye level, read the description of the image and see what you can see!! It is not necessary in all cases to use the entire set of images. In a large scale examination the test can be simplified to six tests; test, one of tests 2 or 3, one of tests 4, 5, 6, or 7, one of tests 8 or 9, one of tests 10, 11, 12, or 13 and one of tests 14 or 15.[this quote needs a citation]

Because the Ishihara color test contains only numerals, it may not be useful in diagnosing young children, who have not yet learned to use numbers. In the interest of identifying these problems early on in life, alternative color vision tests were developed using only symbols (square, circle, car).

Besides the Ishihara color test, the US Navy and US Army also allow testing with the Farnsworth Lantern Test. This test allows 30% of color deficient individuals, whose deficiency is not too severe, to pass.

Another test used by clinicians to measure chromatic discrimination is the Farnsworth-Munsell 100 hue test. The patient is asked to arrange a set of colored caps or chips to form a gradual transition of color between two anchor caps.[38]

The HRR color test (developed by Hardy, Rand, and Rittler) is a redgreen color test that, unlike the Ishihara, also has plates for the detection of the tritan defects.[39]

Most clinical tests are designed to be fast, simple, and effective at identifying broad categories of color blindness. In academic studies of color blindness, on the other hand, there is more interest in developing flexible tests to collect thorough datasets, identify copunctal points, and measure just noticeable differences.[40]

There is generally no treatment to cure color deficiencies. The American Optometric Association reports a contact lens on one eye can increase the ability to differentiate between colors, though nothing can make you truly see the deficient color.[41]

Optometrists can supply colored spectacle lenses or a single red-tint contact lens to wear on the non-dominant eye, but although this may improve discrimination of some colors, it can make other colors more difficult to distinguish. A 1981 review of various studies to evaluate the effect of the X-chrom contact lens concluded that, while the lens may allow the wearer to achieve a better score on certain color vision tests, it did not correct color vision in the natural environment.[42] A case history using the X-Chrom lens for a rod monochromat is reported[43] and an X-Chrom manual is online.[44]

Lenses that filter certain wavelengths of light can allow people with a cone anomaly, but not dichromacy, to see better separation of colors, especially those with classic "red/green" color blindness. They work by notching out wavelengths that strongly stimulate both red and green cones in a deuter- or protanomalous person, improving the distinction between the two cones' signals. As of 2013, sunglasses that notch out color wavelengths are available commercially.[45]

Many applications for iPhone and iPad have been developed to help colorblind people to view the colors in a better way. Many applications launch a sort of simulation of colorblind vision to make normal-view people understand how the color-blinds see the world. Others allow a correction of the image grabbed from the camera with a special "daltonizer" algorithm.

The GNOME desktop environment provides colorblind accessibility using the gnome-mag and the libcolorblind software. Using a gnome applet, the user may switch a color filter on and off, choosing from a set of possible color transformations that will displace the colors in order to disambiguate them. The software enables, for instance, a colorblind person to see the numbers in the Ishihara test.

Color blindness affects a large number of individuals, with protanopia and deuteranopia being the most common types.[12] In individuals with Northern European ancestry, as many as 8 percent of men and 0.4 percent of women experience congenital color deficiency.[47]

The number affected varies among groups. Isolated communities with a restricted gene pool sometimes produce high proportions of color blindness, including the less usual types. Examples include rural Finland, Hungary, and some of the Scottish islands.[citation needed] In the United States, about 7 percent of the male populationor about 10.5 million menand 0.4 percent of the female population either cannot distinguish red from green, or see red and green differently from how others do (Howard Hughes Medical Institute, 2006[clarification needed]). More than 95 percent of all variations in human color vision involve the red and green receptors in male eyes. It is very rare for males or females to be "blind" to the blue end of the spectrum.[48]

The first scientific paper on the subject of color blindness, Extraordinary facts relating to the vision of colours, was published by the English chemist John Dalton in 1798[50] after the realization of his own color blindness. Because of Dalton's work, the general condition has been called daltonism, although in English this term is now used only for deuteranopia.

Color codes present particular problems for those with color deficiencies as they are often difficult or impossible for them to perceive.

Good graphic design avoids using color coding or using color contrasts alone to express information;[51] this not only helps color blind people, but also aids understanding by normally sighted people by providing them with multiple reinforcing cues.[citation needed]

Designers need to take into account that color-blindness is highly sensitive to differences in material. For example, a redgreen colorblind person who is incapable of distinguishing colors on a map printed on paper may have no such difficulty when viewing the map on a computer screen or television. In addition, some color blind people find it easier to distinguish problem colors on artificial materials, such as plastic or in acrylic paints, than on natural materials, such as paper or wood. Third, for some color blind people, color can only be distinguished if there is a sufficient "mass" of color: thin lines might appear black, while a thicker line of the same color can be perceived as having color.[citation needed]

Designers should also note that redblue and yellowblue color combinations are generally safe. So instead of the ever-popular "red means bad and green means good" system, using these combinations can lead to a much higher ability to use color coding effectively. This will still cause problems for those with monochromatic color blindness, but it is still something worth considering.[52]

When the need to process visual information as rapidly as possible arises, for example in an emergency situation, the visual system may operate only in shades of gray, with the extra information load in adding color being dropped.[citation needed] This is an important possibility to consider when designing, for example, emergency brake handles or emergency phones.

Color blindness may make it difficult or impossible for a person to engage in certain occupations. Persons with color blindness may be legally or practically barred from occupations in which color perception is an essential part of the job (e.g., mixing paint colors), or in which color perception is important for safety (e.g., operating vehicles in response to color-coded signals). This occupational safety principle originates from the Lagerlunda train crash of 1875 in Sweden. Following the crash, Professor Alarik Frithiof Holmgren, a physiologist, investigated and concluded that the color blindness of the engineer (who had died) had caused the crash. Professor Holmgren then created the first test using different-colored skeins to exclude people from jobs in the transportation industry on the basis of color blindness.[53] However, there is a claim that there is no firm evidence that color deficiency did cause the collision, or that it might have not been the sole cause.[54]

Color vision is important for occupations using telephone or computer networking cabling, as the individual wires inside the cables are color-coded using green, orange, brown, blue and white colors.[55] Electronic wiring, transformers, resistors, and capacitors are color-coded as well, using black, brown, red, orange, yellow, green, blue, violet, gray, white, silver, gold.[56]

Some countries have refused to grant driving licenses to individuals with color blindness. In Romania, there is an ongoing campaign to remove the legal restrictions that prohibit colorblind citizens from getting drivers' licenses.[57]

The usual justification for such restrictions is that drivers of motor vehicles must be able to recognize color-coded signals, such as traffic lights or warning lights.[52]

While many aspects of aviation depend on color coding, only a few of them are critical enough to be interfered with by some milder types of color blindness. Some examples include color-gun signaling of aircraft that have lost radio communication, color-coded glide-path indications on runways, and the like. Some jurisdictions restrict the issuance of pilot credentials to persons who suffer from color blindness for this reason. Restrictions may be partial, allowing color-blind persons to obtain certification but with restrictions, or total, in which case color-blind persons are not permitted to obtain piloting credentials at all.[citation needed]

In the United States, the Federal Aviation Administration requires that pilots be tested for normal color vision as part of their medical clearance in order to obtain the required medical certificate, a prerequisite to obtaining a pilot's certification. If testing reveals color blindness, the applicant may be issued a license with restrictions, such as no night flying and no flying by color signalssuch a restriction effectively prevents a pilot from holding certain flying occupations, such as that of an airline pilot, although commercial pilot certification is still possible, and there are a few flying occupations that do not require night flight and thus are still available to those with restrictions due to color blindness (e.g., agricultural aviation). The government allows several types of tests, including medical standard tests (e.g., the Ishihara, Dvorine, and others) and specialized tests oriented specifically to the needs of aviation. If an applicant fails the standard tests, they will receive a restriction on their medical certificate that states: "Not valid for night flying or by color signal control". They may apply to the FAA to take a specialized test, administered by the FAA. Typically, this test is the "color vision light gun test". For this test an FAA inspector will meet the pilot at an airport with an operating control tower. The color signal light gun will be shone at the pilot from the tower, and they must identify the color. If they pass they may be issued a waiver, which states that the color vision test is no longer required during medical examinations. They will then receive a new medical certificate with the restriction removed. This was once a Statement of Demonstrated Ability (SODA), but the SODA was dropped, and converted to a simple waiver (letter) early in the 2000s.[58]

Research published in 2009 carried out by the City University of London's Applied Vision Research Centre, sponsored by the UK's Civil Aviation Authority and the US Federal Aviation Administration, has established a more accurate assessment of color deficiencies in pilot applicants' redgreen and yellowblue color range which could lead to a 35% reduction in the number of prospective pilots who fail to meet the minimum medical threshold.[59]

Inability to distinguish color does not necessarily preclude the ability to become a celebrated artist. The 20th century expressionist painter Clifton Pugh, three-time winner of Australia's Archibald Prize, on biographical, gene inheritance and other grounds has been identified as a protanope.[60] 19th century French artist Charles Mryon became successful by concentrating on etching rather than painting after he was diagnosed as having a redgreen deficiency.[61]

A Brazilian court ruled that people with color blindness are protected by the Inter-American Convention on the Elimination of All Forms of Discrimination against Person with Disabilities.[62][63][64]

At trial, it was decided that the carriers of color blindness have a right of access to wider knowledge, or the full enjoyment of their human condition.

In the United States, under federal anti-discrimination laws such as the Americans with Disabilities Act, color vision deficiencies have not been found to constitute a disability that triggers protection from workplace discrimination.[65]

A famous traffic light on Tipperary Hill in Syracuse, New York, is upside-down due to the sentiments of its Irish American community,[66] but has been criticized due to the potential hazard it poses for color-blind persons.[67]

Some tentative evidence finds that color blind people are better at penetrating certain color camouflages. Such findings may give an evolutionary reason for the high rate of redgreen color blindness.[4] There is also a study suggesting that people with some types of color blindness can distinguish colors that people with normal color vision are not able to distinguish.[68] In World War II, color blind observers were used to penetrate camouflage.[69]

In September 2009, the journal Nature reported that researchers at the University of Washington and University of Florida were able to give trichromatic vision to squirrel monkeys, which normally have only dichromatic vision, using gene therapy.[70]

In 2003, a cybernetic device called eyeborg was developed to allow the wearer to hear sounds representing different colors.[71] Achromatopsic artist Neil Harbisson was the first to use such a device in early 2004; the eyeborg allowed him to start painting in color by memorizing the sound corresponding to each color. In 2012, at a TED Conference, Harbisson explained how he could now perceive colors outside the ability of human vision.[72]

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Color blindness - Wikipedia

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ORTHOPAEDIC MEDICINE SPECIALTIES FOR PAIN TREATMENTOrthopaedic medicine is a specialty devoted to the evaluation, diagnosis and non-operative treatment for pain caused by musculoskeletal diseases to aid in pain management. Diagnostic modalities include a comprehensive history, a detailed and specific physical examination, radiologic evaluations and local anesthetic blocks for pain treatment. Therapeutic modalities for pain management encompass manipulations, corticosteroid or proliferant injections with and without fluoroscopic guidance, therapeutic exercise and use of pharmaceutical, nutriceutical, herbal and/or homeopathic based pain treatment.

The evolution began in 1741 when Nicholas Andre, at that time a Professor of Medicine at the University of Paris, coined the word orthopaedic. He published a book with the same title. The etymology of orthopaedic is based on two greek roots: orthos and paedia which translate to straight and rearing of children respectively. His illustration of a staff that is used to straighten a growing tree is known world wide.

For more than two centuries orthopaedists were physicians or surgeons concerned with musculoskeletal deformities: scoliosis, infections of bones and joints, poliomyelitis and congenital defects such as Erbs palsy, clubfoot and hip dislocations. Until the 20th century most orthopaedic treatments were manipulations and mechanical support with braces and plaster casts.

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CTI was named the winner of the Vision Award category, which was awarded to the organization for inspiringand deliveringnew thinking to the marketplace and for showcasingNorthern Kentucky as an area of thoughtful, innovative industry leaders.

"We're honored to be recognized by the Northern Kentucky Chamber of Commerce with this award for CTI's continued successes and innovations," according to Timothy J. Schroeder, Founder and CEO.

CTI Clinical Trial and Consulting Services (CTI), a global, privately held, full-service contract research organization announces the acquisition of Eurotrials, a full-service contract research organization, with more than 20 years of experience, and strong local expertise in Europe and Latin America.

CTI is extremely happy to partner with Bexion on the development of this novel therapy in patients who desperately need alternative treatments, stated William Aronstein, PhD, MD, FACP, Vice President, Medical Affairs at CTI. They are an innovative organization with very strong regional ties the drug was initially developed and licensed at a local hospital, early funding has predominantly come from the region, and the management and board have strong local connections.

The expansions in Taiwan and Japan are part of continued efforts to increase capacity for clinical research across Asia, according to Patrick Earley, Vice President, International. We have been working across Asia for a number of years, but felt like a more permanent presence in Taipei and Tokyo would further enhance relationships with local medical centers and biotechnology companies."

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