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Visual perception – Wikipedia

Sunday, November 27th, 2016

Visual perception is the ability to interpret the surrounding environment by processing information that is contained in visible light. The resulting perception is also known as eyesight, sight, or vision (adjectival form: visual, optical, or ocular). The various physiological components involved in vision are referred to collectively as the visual system, and are the focus of much research in Linguistics, psychology, cognitive science, neuroscience, and molecular biology, collectively referred to as vision science.

The visual system in animals allows individuals to assimilate information from their surroundings. The act of seeing starts when the cornea and then the lens of the eye focuses an image of its surroundings onto a light-sensitive membrane in the back of the eye, called the retina. The retina is actually part of the brain that is isolated to serve as a transducer for the conversion of patterns of light into neuronal signals. The lens of the eye focuses light on the photoreceptive cells of the retina, also known as the rods and cones, which detect the photons of light and respond by producing neural impulses. These signals are processed in a hierarchical fashion by different parts of the brain, from the retina upstream to central ganglia in the brain.

Note that up until now much of the above paragraph could apply to octopi, mollusks, worms, insects and things more primitive; anything with a more concentrated nervous system and better eyes than say a jellyfish. However, the following applies to mammals generally and birds (in modified form): The retina in these more complex animals sends fibers (the optic nerve) to the lateral geniculate nucleus, to the primary and secondary visual cortex of the brain. Signals from the retina can also travel directly from the retina to the superior colliculus.

The perception of objects and the totality of the visual scene is accomplished by the visual association cortex. The visual association cortex combines all sensory information perceived by the striate cortex which contains thousands of modules that are part of modular neural networks. The neurons in the striate cortex send axons to the extrastriate cortex, a region in the visual association cortex that surrounds the striate cortex.[1]

The major problem in visual perception is that what people see is not simply a translation of retinal stimuli (i.e., the image on the retina). Thus people interested in perception have long struggled to explain what visual processing does to create what is actually seen.

There were two major ancient Greek schools, providing a primitive explanation of how vision is carried out in the body.

The first was the "emission theory" which maintained that vision occurs when rays emanate from the eyes and are intercepted by visual objects. If an object was seen directly it was by 'means of rays' coming out of the eyes and again falling on the object. A refracted image was, however, seen by 'means of rays' as well, which came out of the eyes, traversed through the air, and after refraction, fell on the visible object which was sighted as the result of the movement of the rays from the eye. This theory was championed by scholars like Euclid and Ptolemy and their followers.

The second school advocated the so-called 'intro-mission' approach which sees vision as coming from something entering the eyes representative of the object. With its main propagators Aristotle, Galen and their followers, this theory seems to have some contact with modern theories of what vision really is, but it remained only a speculation lacking any experimental foundation. (In eighteenth-century England, Isaac Newton, John Locke, and others, carried the intromission/intromittist theory forward by insisting that vision involved a process in which rayscomposed of actual corporeal matteremanated from seen objects and entered the seer's mind/sensorium through the eye's aperture.)[2]

Both schools of thought relied upon the principle that "like is only known by like", and thus upon the notion that the eye was composed of some "internal fire" which interacted with the "external fire" of visible light and made vision possible. Plato makes this assertion in his dialogue Timaeus, as does Aristotle, in his De Sensu.[3]

Alhazen (965c. 1040) carried out many investigations and experiments on visual perception, extended the work of Ptolemy on binocular vision, and commented on the anatomical works of Galen.[4][5]

Leonardo da Vinci (14521519) is believed to be the first to recognize the special optical qualities of the eye. He wrote "The function of the human eye ... was described by a large number of authors in a certain way. But I found it to be completely different." His main experimental finding was that there is only a distinct and clear vision at the line of sightthe optical line that ends at the fovea. Although he did not use these words literally he actually is the father of the modern distinction between foveal and peripheral vision.[citation needed]

Hermann von Helmholtz is often credited with the first study of visual perception in modern times. Helmholtz examined the human eye and concluded that it was, optically, rather poor. The poor-quality information gathered via the eye seemed to him to make vision impossible. He therefore concluded that vision could only be the result of some form of unconscious inferences: a matter of making assumptions and conclusions from incomplete data, based on previous experiences.[citation needed]

Inference requires prior experience of the world.

Examples of well-known assumptions, based on visual experience, are:

The study of visual illusions (cases when the inference process goes wrong) has yielded much insight into what sort of assumptions the visual system makes.

Another type of the unconscious inference hypothesis (based on probabilities) has recently been revived in so-called Bayesian studies of visual perception.[7] Proponents of this approach consider that the visual system performs some form of Bayesian inference to derive a perception from sensory data. Models based on this idea have been used to describe various visual perceptual functions, such as the perception of motion, the perception of depth, and figure-ground perception.[8][9] The "wholly empirical theory of perception" is a related and newer approach that rationalizes visual perception without explicitly invoking Bayesian formalisms.

Gestalt psychologists working primarily in the 1930s and 1940s raised many of the research questions that are studied by vision scientists today.

The Gestalt Laws of Organization have guided the study of how people perceive visual components as organized patterns or wholes, instead of many different parts. "Gestalt" is a German word that partially translates to "configuration or pattern" along with "whole or emergent structure". According to this theory, there are eight main factors that determine how the visual system automatically groups elements into patterns: Proximity, Similarity, Closure, Symmetry, Common Fate (i.e. common motion), Continuity as well as Good Gestalt (pattern that is regular, simple, and orderly) and Past Experience.

During the 1960s, technical development permitted the continuous registration of eye movement during reading[10] in picture viewing[11] and later in visual problem solving[12] and when headset-cameras became available, also during driving.[13]

The picture to the left shows what may happen during the first two seconds of visual inspection. While the background is out of focus, representing the peripheral vision, the first eye movement goes to the boots of the man (just because they are very near the starting fixation and have a reasonable contrast).

The following fixations jump from face to face. They might even permit comparisons between faces.

It may be concluded that the icon face is a very attractive search icon within the peripheral field of vision. The foveal vision adds detailed information to the peripheral first impression.

It can also be noted that there are three different types of eye movements: vergence movements, saccadic movements and pursuit movements. Vergence movements involve the cooperation of both eyes to allow for an image to fall on the same area of both retinas. This results in a single focused image. Saccadic movements is the type of eye movement that makes jumps from one position to another position and is used to rapidly scan a particular scene/image. Lastly, pursuit movement is smooth eye movement and is used to follow objects in motion.[14]

There is considerable evidence that face and object recognition are accomplished by distinct systems. For example, prosopagnosic patients show deficits in face, but not object processing, while object agnosic patients (most notably, patient C.K.) show deficits in object processing with spared face processing.[15] Behaviorally, it has been shown that faces, but not objects, are subject to inversion effects, leading to the claim that faces are "special".[15][16] Further, face and object processing recruit distinct neural systems.[17] Notably, some have argued that the apparent specialization of the human brain for face processing does not reflect true domain specificity, but rather a more general process of expert-level discrimination within a given class of stimulus,[18] though this latter claim is the subject of substantial debate.

The major problem with the Gestalt laws (and the Gestalt school generally) is that they are descriptive not explanatory. For example, one cannot explain how humans see continuous contours by simply stating that the brain "prefers good continuity". Computational models of vision have had more success in explaining visual phenomena and have largely superseded Gestalt theory. More recently, the computational models of visual perception have been developed for Virtual Reality systemsthese are closer to real-life situation as they account for motion and activities which are prevalent in the real world.[citation needed] Regarding Gestalt influence on the study of visual perception, Bruce, Green & Georgeson conclude:

In the 1970s, David Marr developed a multi-level theory of vision, which analyzed the process of vision at different levels of abstraction. In order to focus on the understanding of specific problems in vision, he identified three levels of analysis: the computational, algorithmic and implementational levels. Many vision scientists, including Tomaso Poggio, have embraced these levels of analysis and employed them to further characterize vision from a computational perspective.[citation needed]

The computational level addresses, at a high level of abstraction, the problems that the visual system must overcome. The algorithmic level attempts to identify the strategy that may be used to solve these problems. Finally, the implementational level attempts to explain how solutions to these problems are realized in neural circuitry.

Marr suggested that it is possible to investigate vision at any of these levels independently. Marr described vision as proceeding from a two-dimensional visual array (on the retina) to a three-dimensional description of the world as output. His stages of vision include:

Transduction is the process through which energy from environmental stimuli is converted to neural activity for the brain to understand and process. The back of the eye contains three different cell layers: photoreceptor layer, bipolar cell layer and ganglion cell layer. The photoreceptor layer is at the very back and contains rod photoreceptors and cone photoreceptors. Cones are responsible for color perception. There are three different cones: red, green and blue. Rods, are responsible for the perception of objects in low light.[21] Photoreceptors contain within them a special chemical called a photopigment, which are embedded in the membrane of the lamellae; a single human rod contains approximately 10 million of them. The photopigment molecules consist of two parts: an opsin (a protein) and retinal (a lipid).[22] There are 3 specific photopigments (each with their own color) that respond to specific wavelengths of light. When the appropriate wavelength of light hits the photoreceptor, its photopigment splits into two, which sends a message to the bipolar cell layer, which in turn sends a message to the ganglion cells, which then send the information through the optic nerve to the brain. If the appropriate photopigment is not in the proper photoreceptor (for example, a green photopigment inside a red cone), a condition called color vision deficiency will occur.[23]

Transduction involves chemical messages sent from the photoreceptors to the bipolar cells to the ganglion cells. Several photoreceptors may send their information to one ganglion cell. There are two types of ganglion cells: red/green and yellow/blue. These neuron cells consistently fireeven when not stimulated. The brain interprets different colors (and with a lot of information, an image) when the rate of firing of these neurons alters. Red light stimulates the red cone, which in turn stimulates the red/green ganglion cell. Likewise, green light stimulates the green cone, which stimulates the red/green ganglion cell and blue light stimulates the blue cone which stimulates the yellow/blue ganglion cell. The rate of firing of the ganglion cells is increased when it is signaled by one cone and decreased (inhibited) when it is signaled by the other cone. The first color in the name if the ganglion cell is the color that excites it and the second is the color that inhibits it. i.e.: A red cone would excite the red/green ganglion cell and the green cone would inhibit the red/green ganglion cell. This is an opponent process. If the rate of firing of a red/green ganglion cell is increased, the brain would know that the light was red, if the rate was decreased, the brain would know that the color of the light was green.[23]

Theories and observations of visual perception have been the main source of inspiration for computer vision (also called machine vision, or computational vision). Special hardware structures and software algorithms provide machines with the capability to interpret the images coming from a camera or a sensor. Artificial Visual Perception has long been used in the industry and is now entering the domains of automotive and robotics.[24][25]

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All About Vision – Humanitarian Eye Care Organizations

Sunday, November 27th, 2016

The organizations listed below help to bring eye care to underserved regions and/or segments of the population with vision challenges. These entities recognize the educational value of AllAboutVision by linking to the appropriate pages of the website.

Your help is needed. Please consider supporting their work with your generous donations.

The Low Vision Center is committed to providing comprehensive non-medical resource services to individuals in the Metropolitan Washington DC area and beyond who are experiencing vision loss. Founded in 1979, this 501(c)3 not-for-profit organization maintains an extensive information and referral network, and introduces clients to adaptive products and strategies designed to help them maintain their independence. The Center offers informational materials and workshops for those living with and serving persons with visual impairment. Learnmore >

SEE International is a leading sight-restoring nonprofit humanitarian organization. SEE works to create a world where everyone has access to high-quality vision care, regardless of their ability to pay. Each year, SEE organizes 175+ sight-restoring programs, and runs a free vision care program in its hometown of Santa Barbara, CA. These programs provide free vision screenings and surgery to people who do not have access to affordable eye care. SEE also trains medical professionals to provide comprehensive eye care worldwide. Since 1974, SEE has screened more than 3.68 million individuals and restored the sight of nearly half a million people. Learnmore >

The World Blind Union (WBU) is the global organization representing the estimated 285 million people worldwide who are blind or partially sighted. Members are organizations of and for the blind in 180 countries, as well as international organizations working in the field of vision impairment. Learnmore >

The Iris Network's mission is to help people who are visually impaired or blind attain independence and community integration. Its services are based on respect for each individual's right to self-direction through informed choices. The Iris Network believes that the education and integration of all individuals will result in a stronger society. Learnmore >

The Ocular Immunology and Uveitis Foundation's mission is to find cures for ocular inflammatory diseases, to correct the worldwide deficit of properly trained ocular immunologists, and to provide education and emotional support for those patients afflicted with ocular inflammatory disease. Learnmore >

Founded in 2006, the Jack McGovern Coats Disease Foundation seeks to increase awareness about Coats Disease, fund research and cultivate a community for support. Learnmore >

The Macular Degeneration Foundation is dedicated to those who have and will develop macular degeneration. We offer this growing community the latest information, news, hope and encouragement. In addition, the Foundation gives financial support to researchers investigating treatments and others helping those coping with the challenges of living with the loss of their central vision. Learnmore >

Blindskills is a unique self-help organization through which people who are blind or visually impaired offer support to each other as they seek to overcome this serious sensory challenge and live their own lives without unnecessary dependence on others. Learnmore >

The OPC (Organisation pour la Prvention de la Ccit - Organization for the Prevention of Blindness) is an international organization for ocular public health. It fights to preserve the sight of as many people as possible in the most deprived populations in French-speaking developing countries. Learnmore >

The North Carolina Association for Parents of Children with Visual Impairments (NC-APVI) is an affiliate of NAPVI, the National Association for Parents of Children with Visual Impairments. We provide leadership, support, and training to assist NC families in helping children reach their full potential. Learnmore >

Glaucoma Research Foundation (GRF) is a national nonprofit founded in 1978 in San Francisco to encourage innovative research toward better treatments for people with glaucoma. GRF has funded more than $50 million of grants and projects and provides education and support for people with glaucoma. Their mission is to prevent vision loss from glaucoma by investing in innovative research, education, and support with the ultimate goal of finding a cure. Learnmore >

Blink Around the World is a global campaign launched by TFOS to promote the importance of eye-health and the need for more innovative research. Dry eye treatment is only one example of a global unmet need in ophthalmology. TFOS' global collaboration among scientists, clinicians and industry professionals facilitates the action needed to help the world see better. Learnmore >

Macular Degeneration Association is a non-profit health organization dedicated to finding a cure for macular degeneration through research, awareness programs and materials which provide information about risk factors, preventative measures, treatments and coping strategies. Age-related macular degeneration is an increasingly prevalent degenerative eye disease, affecting millions of aging seniors. Learnmore >

The mission of The Glaucoma Foundation (TGF) is to develop a cure for glaucoma through innovative research and collaboration. The Foundation encourages and supports basic and applied research in glaucoma and to further efforts to identify and develop novel approaches to preserve visual function and reverse blindness caused by glaucoma. Learnmore >

Essilor Vision Foundation is a 501(c)(3) public charity, founded in 2007 by Essilor of America, with the mission to eliminate poor vision and its lifelong consequences. Learnmore >

Founded in 1986, the National Keratoconus Foundation (NKCF) is a non-profit organization that is part of The Discovery Eye Foundation. The mission of the NKCF is to increase awareness of keratoconus while supporting research on the cause and treatment. Learnmore >

The Usher Syndrome Coalition's mission is to raise awareness about Usher syndrome as the leading cause of deaf-blindness, advance research, and to provide information and support to individuals and families affected by Usher syndrome. Learnmore >

Vision Aware provides free, practical, hands-on information to enhance quality of life and independence for adults with vision loss, their families and friends, caregivers, and related professionals. Learnmore >

Established in 1990, The Vision of Children Foundation is dedicated to the eradication of hereditary childhood blindness and vision disorders. The foundation serves as an informational resource, provides a family support network, sponsors research programs and offers a computer monitor program for visually impaired students. Learnmore >

The mission of the Delta Gamma Center for Children with Visual Impairments is to help children who are blind or visually impaired reach their full potential through family-centered and specialized services and support. Learnmore >

Established in 1971, Volunteer Optometric Services to Humanity (VOSH) provides vision care services to those below poverty level and without access to eye care. VOSH programs supply eyeglasses, treat eye disease and refer or perform vision surgery to more than 100,000 people around the world each year. Learnmore >

The Choroideremia Research Foundation raises funds in support of scientific research leading to a treatment or cure of choroideremia, a hereditary retinal-degenerative disease that causes blindness, educates people affected by the disease and informs the public. Learnmore >

RestoringVision provides new reading and sunglasses at low cost to groups going to developing countries. Since 2003, we have supplied more than 1.7 million glasses to more than 600 different groups. Both reading and sunglasses are easy to dispense and make a dramatic difference in people's lives. Learnmore >

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Costa Rica Adult Life, adult tourism, Escorts …

Friday, November 25th, 2016

COSTA RICA ADULT LIFE and TOURISM - PROSTITUTION, GAY, NIGHTLIFE Besides the family-style movie, theaters, etc etc, Costa Rica has "adult" themed entertainment and offers an array day and nightlife for all tastes.

Many of the "adult places" cater, not only to men, women, and gay/lesbian, but to couples that enjoy a bit of the wildside such as swingers and bi-sexuality. Even the strip clubs men and women offer lap dances.

It is estimated that between 15 and 25% of all visitors to Costa Rica have all or part of their vacation and travel plans is the prostitution and gambling that the country has to offer. In other words, Costa Rica is known world-wide for its adult tourism.

TicoTimes.com Editor Note: If your sexual tastes extends to the underaged, be WARNED, the government will extend your vacation another 35 years at the famous, gray-bar hotel with NO help from any embassy. Tico Times also takes no responsibily of what is listed below and should be used as a guide ONLY - Users use at their own risk.

*NEW* Map of San Jose Gringo Gulch and Zona Roja - Adult Entertainment ADULT RESOURCES SAN JOSE STRIP CLUBS NUDIST CAMPS Del Rey Hotel - Halloween Services to Date and/or Marry Costa Rica Women Costa Rica Gay and Lesbian Nightlife Gay and Lesbian Travel, Hotels, and Resorts in Costa Rica Map of San Josa, Costa Rica Adult Nightlife Strip and Night Club Reviews and Locations in San Jose Best Information Source for Gays

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Media reports about autologous haematopoietic stem cell …

Friday, November 25th, 2016

There are many stories in the media about autologous haematopoietic stem cell transplant, also known as bone marrow transplant, AHSCT or HSCT, as a treatment for MS.

In particular, we are aware that the 60 Minutes program this weekend will provide a report about a patients AHSCT treatment experience in Russia. MS Research Australia was available to interview for this story, however, 60 Minutes declined our involvement.

Media reports often describe AHSCT as being a miracle cure for MS and include personal stories of how it has given people a new lease of life. While the results of this treatment have been life-changing for some people, it is important to recognise that this is unlikely to be a treatment that is appropriate for everyone.

The media reports rarely discuss the full details of the treatment, which is very intensive and carries significant risks. The reports also do not provide a full picture regarding other people who may have received the treatment but had a less positive response. To understand how this treatment option may sit within the range of other treatments available, it is important to look at the results for a broader group of people who have been followed up for longer periods of time. MS Research Australia understands that people with MS will wish to explore all potential avenues of treatment. Every persons situation and experience of MS is unique. However, we do encourage all decisions about any MS treatments especially anyone considering travelling overseas for any form of treatment, to always consult with their Australian health care providers, including their neurologist. Health care providers take into consideration the potential benefits, risks and side effects for an individuals particular circumstances. If considering treatment overseas they can ensure that the individual is fully informed about the range of treatment options available in Australia, the nature of the treatment overseas and the providers of that treatment, what can and cant be expected from the treatment, what other health conditions they may have that may impact on the treatment and management of their MS, and what medical care they may need prior to or during travel, or on their return. It is also important to note that not all countries share the same regulatory standards that apply within Australia. The National Health and Medical Research Council have also produced a guide on overseas treatment considerations.

AHSCT has been used in the treatment of blood cancers for several decades, but its use for severe autoimmune disorders has developed relatively more recently. As the safety and efficacy has not yet been tested in sufficiently large randomised controlled trials specifically for MS and in comparison to currently available MS therapies. Therefore globally it is considered experimental for the treatment of MS.

AHSCT is primarily an immune-suppressing chemotherapy treatment combined with reinfusion of blood stem cells to help re-build the immune system. It aims to regenerate a new immune system that is less likely to attack the brain and spinal cord. Further details on the steps involved in this treatment can be found here.

Generally, the outcomes have shown that people who are younger and who still have active inflammatory disease (new lesions on MRI scans and/or relapses) may achieve better outcomes for reducing or halting disease activity. Studies also suggest that AHSCT does not halt or reverse more long-standing disability, or progressive forms of the disease, and it is therefore unlikely that AHSCT would be recommended as a treatment for patients with secondary progressive or primary progressive MS.

Currently, this treatment is provided in Australia through two observational clinical trials, at St Vincents Hospital, Sydney and Austin Health, Melbourne and by a small number of other centres on a case by case basis. These centres have strict eligibility requirements that have been set by the hospital ethics committees and may only apply to limited numbers of patients with MS who have failed to respond to other standard MS treatments. It is for this reason patients need to be referred to these centres by a neurologist, who can provide a detailed clinical history and MRI findings.

AHSCT is playing a role in the range of treatments available to treat MS in Australia, however, for this to become a standard therapy in Australian hospitals for people with MS, further rigorous evidence for the effectiveness, safety and most appropriate use of AHSCT is still required. While some clinical trials of AHSCT for MS are ongoing, there is also consensus amongst MS organisations globally, as well as researchers and clinicians who are involved in the use of this treatment for MS, that a large scale, gold-standard clinical trial is required.

MS Research Australia together with MS Australia have been actively advocating, and will continue to advocate, to the federal government for accessibility to all suitable treatment options for people with MS in Australia. We have also been encouraging dialogue between hospitals, state health departments, haematologists and neurologists to ensure that AHSCT treatment can be provided in Australia for those who need it.

As research continues to determine the safety and long-term effectiveness of AHSCT and for whom the treatment is most likely to be appropriate and effective, MS Research Australia will continue to actively review all AHSCT studies as they become available and report on them via the MS Research Australia website and other communication channels. We have provided a full overview of what is involved in the AHSCT treatment, and a review of research to date, on our website.

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RUSSIAN STEM-CELL THERAPY – healingtherapies.info

Thursday, November 24th, 2016

We are a part of a global community in which the devastation of spinal cord injury (SCI) bows to no flag, and solutions will not be any countrys exclusive domain. Integrating the diverse pieces of the puzzle necessary to develop real-world solutions requires that we open-mindedly work in cooperation and not in competition. With such cooperation, restored function after SCI will be a coalescing reality and not just a never-ending, elusive pie-in-the-sky dream.

In this spirit of bridge-building, I recently traveled to Moscow, Russia where I became the first American scientist to check-out an innovative stem-cell program for SCI developed by the NeuroVita Clinic under the direction of Dr. Andrey Bryukhovetskiy. His work is especially important because few scientists have accumulated as much hands-on experience as he has in treating human SCI with stem cells, an approach many experts believe will play a key therapeutic role in the future.

The Scientist

Im always amazed how good often emerges from the tragic. For example, the Paralyzed Veterans of America (PVA), whose programs have benefited so many with SCI over the years, was born out of World War IIs violence. Bryukhovetskiys promising stem-cell therapies also grew out of a desire to help paralyzed veterans, in this case, those who sustained injury in Russias Afghan and Chechnya military conflicts.

He is a veteran, specifically a 45-year-old retired Colonel who once directed the Russian Navys neurology department. Because of his long-standing empathy for paralyzed veterans, Bryukhovetskiy expressed a desire to collaborate with US veteran organizations, such as PVA, to accelerate the development of real-world SCI therapies.

Bryukhovetskiy is a charismatic leader passionately committed to his mission and patients. His work in humans is built upon a strong foundation of research using a variety of SCI animal models. Because much of his research has been published in Russian, it is not well appreciated in the worlds English-emphasizing scientific community. As seems to be the case for so many innovators regardless of country, he has often struggled to carry out his pioneering research because the vision behind it runs counter to more entrenched perceptions of what is possible after SCI.

Reflecting Hippocrates ancient wisdom that natural forces within us are the true healers of disease, Bryukhovetskiy told me that stem cells are the medicine within us.

In 2002, Bryukhovetskiy established NeuroVita, a state-of-the-art, private clinic that treats a variety of neurological disorders. The clinic occupies several floors in a wing of the massive N.N. Blokhin Russian Cancer Research Hospital Complex five miles southeast of downtown Moscow. Staff includes numerous physicians and rehabilitation specialists, and has access to the expertise of nearby hospital scientists. Although to date patients have been treated under an official scientific research protocol, soon after my visit, the Russian Health Ministry authorized the use of Bryukhovetsiys stem-cell technology for general clinical practice.

Travel

My trip to Moscow went through ten time zones, taking several days for my luggage to catch up. Because of jet lag and Moscows white nights near the summer solstice, it was difficult to sleep at night but nodding off in the day was common. During my visit, I stayed in clinic-affiliated lodging. Although few understood English, and the Russian Cyrillic alphabet makes understanding even more challenging, I was able to get around with relative ease, e.g., take the subway to the Kremlin and Red Square, go to the market, etc.

As a reflection of our emerging global community, television showed, for example, American sitcoms and Arnold Schwarzenegger movies dubbed in Russian, as well as rock videos featuring Britney Spears, unfortunately still in English. Although I was unable to talk to waiters, American rap music was often loudly played in the background. Fortunately, Bryukhovetskiys assistant Maria Zhukova, a former English teacher, provided excellent translational assistance.

Transplanted Cell Types

Stem cells are progenitor cells that have the potential to differentiate into a variety of cells that theoretically can treat various neurological disorders. Bryukhovetskiy has used both embryonic/fetal and adult stem cells.

Although embryonic/fetal stem cells have the greatest potential to mature into a variety of cell types, they are controversial, and it is difficult to direct their differentiation pathway.

Adult stem cells are found in many tissues, including bone marrow, which produces, for example, hematopoietic stem cells that give rise to blood cells, and nervous tissue, whose stem cells can evolve into neurons and neuronal support cells (i.e., glia). Although adult stem cells usually differentiate into the specialized cells associated with the originating tissue, when certain micro-environmental cues are provided, they can mature into cells associated with other tissue. For example, under appropriate circumstances, bone-marrow-derived stem cells have the potential to become nerve cells.

Certain drugs stimulate the bone-marrow to produce more stem cells, which then spillover into the blood, where they can be collected.

When the patient is the source of the cells (i.e., autologous), there is no immunological rejection when they are re-introduced. In contrast, embryonic/fetal cells represent different genetic material (i.e., allogeneic) and have rejection potential, although to some degree their undifferentiated nature helps minimize this risk.

Bryukhovetsiy no longer uses embryonic/fetal stem cells due to the ethical controversy surrounding their use, their rejection potential, and, most importantly, his belief that autologous, adult stem cells are more effective.

In some patients, Bryukhovetskiy has transplanted autologous olfactory ensheathing cells (OECs) using procedures developed by Englands Dr. Geoffrey Raisman. Although not technically stem cells, OECs have considerable regeneration potential and have been the focus of much attention in the SCI research community. When OECs are transplanted into the injured spinal cord, scientists theorize that these cells promote axonal regeneration by producing insulating myelin sheaths around both growing and damaged axons, secreting growth factors, and generating structural and matrix macromolecules that lay the tracks for axonal elongation.

Assessment Procedures

Improvement was evaluated using a variety of assessment procedures, including the commonly used ASIA (American Spinal Injury Association) impairment scale in which grade A and E represents the most and least severe injury, respectively. Although this scale is frequently used, experts emphasize it is often insensitive to small but significant functional improvements. Bryukhovetsiy has noted this insensitivity in his research; i.e. some of his patients with very real life-enhancing improvements did not improve their ASIA grade. Other measurements included FIM (Functional Independence Measure), which assesses dysfunction in daily-living activities; various electrophysiological tests designed to assess neuronal conduction; magnetic resonance imaging (MRI); and urodynamic testing for bladder function.

Transplantation Procedures

Embryonic/Fetal Cells: In 1996, the Russian Health Ministry authorized Bryukhovetskiy to carry out limited clinical trials in SCI. In these early trials, stem cells, neurons, and glia obtained from a various tissues, including 12-week-old human fetuses, were transplanted into the spinal cord/fluid of 17 patients with SCI. Their ages ranged from 16-52 (average 30) years, and the time interval between injury and transplantation ranged from 1-20 (average 5) years. Six, ten, and one had cervical, thoracic, and lumbar injuries respectively. In addition to cell transplantation, all had a variety of other procedures performed depending upon their unique injuries.

Before treatment, 14 subjects were ASIA grade A and three were grade B. After transplantation (0.5 - 3-year follow-up period), four were grade A, five grade B, and seven grade C. Fifteen had some sensory improvement, seven had motor improvement, and 12 had improved bladder function.

SpheroGel & Autologous Cells: Bryukhovetskiys team has implanted SpheroGel (a biodegradable polymer matrix) with embedded cells in six patients who required reconstructive surgeries. In three, hematopoietic stem cells were embedded, and, in the three others, olfactory cells. At follow-up (3-8 months), two grade-A patients had improved to grade C, and one had advanced to grade B. In one patient (grade B initially), there was no improvement.

Intrathecal Stem-Cell Transfusion: The intrathecal transfusion of autologous hematopoietic stem cells is the procedure most currently used. In this relatively straight-forward procedure involving no surgery, the patients stem cells are collected without anesthesia and stored with viability until they are transfused back into the patient.

To stimulate hematopoietic stem-cell production and, in turn, cell accumulation in the blood, patients typically received eight subcutaneous injections over four days of granulocytic colony-stimulating factor, a drug also called Neupogen or Filgrastim. On day five, the patient is hooked up to a blood separator. Over 3-4 hours, blood is drawn from a vein; processed by the separator, which isolates the stems cells; and returned through another vein.

The collected stem cells are concentrated by centrifugation and slowly frozen in liquid nitrogen (-170o centigrade) in the presence of dimethyl sulfoxide (DMSO), a cryopreservative that allows cells to be frozen with minimal damage. Care is taken to check for infections so that they will not be later introduced behind the protective blood-brain barrier during transfusion.

At the time of transfusion, the stem-cell suspension is thawed and about 5.3-million cells injected intrathecally into the subarachnoid space (i.e., into the spinal fluid) through a L3-L4 lumbar puncture using a local anesthetic. The procedure, which I observed, is quick and straightforward. The patient can repeat the transfusion in two months. Bryukhovetskiy believes multiple transfusions enhance functional recovery.

In contrast to hematopoietic stem cells, positive results have been limited with the intrathecal transfusion of olfactory cells, previously isolated and cultured from the patients nasal tissue.

Although Bryukhovetskiys team has collected stem cells from about 120 patients, for a variety of reasons, including the presence of latent infections, only about 60 have had cells reintroduced. Of these 60, 18 have had the recommended multiple transfusions. In turn, 61% of the 18 showed some functional recovery, in some cases dramatic.

Because most patients transfusions were relatively recent, it is too early to assess long-term benefit. Early improvements are unlikely caused by comparatively slow neuronal regeneration processes and are probably triggered by altering the injury sites environment through the secretion of growth factors and other molecules.

For more scientifically inclined readers, Bryukhovetskiy hypothesizes that the stem-cells regenerative effects are mediated through an important growth factor called ciliary neurotrophic factor (CNTF) and its interaction with a key transmembrane receptor called gp130. This interaction, in turn, influences cell differentiation.

Physical Rehabilitation

Like others who are developing function-restoring therapies, Bryukhovetskiy strongly believes that improvement after treatment depends upon the patients commitment to aggressive physical rehabilitation designed to maximize restored function. Basically, if muscles have been disconnected from brain control for many years, its going to take some real work to build up nascent connections. As such, his clinic emphasizes diverse rehabilitation modalities, ranging from aggressive exercises to passive massage and acupuncture therapy.

Patients

I had the opportunity to interact with a number of NeuroVita patients. Because their treatments have been relatively recent, accrued improvements have been generally modest.

Vladimir, a 40-year old Russian living in Spain, sustained a thoracic T6 complete injury from a 2001 car accident, and started a series of stem-cell transfusions late last year. He believes that these recent transfusions, combined with extensive physical therapy, has resulted in additional leg movement, including the ability to walk in a swimming pool.

An articulate 19-year-old Russian living in Bulgaria, Dmitri sustained a cervical C5-6 injury in a 2000 skiing accident. He has had three transfusions since the beginning of 2005 and has noted new sensation and sweating. He had some slight headaches soon after the transfusions.

From Dagestan, Baziat, 21, sustained a T9-11 injury when she was 19. After four transfusions, she has regained additional leg and hip function.

Alexey, 32, traveled in from the distant Kamchatka Peninsula on Russias far eastern Pacific side, much closer to Alaska than Moscow. He shared with me the challenges of living with a severe physical disability in a remote, almost frontier-like area of Russia. Sustaining a T-8 gunshot injury 11 years ago, he received his first transfusion last year and was scheduled to receive his third during my visit. He has acquired more bladder and bowel function and has increased leg strength and tension.

Olga, 17, sustained a T8-9 injury seven years ago from an accident. Last year, cell-containing SpheroGel was implanted in the 4-cm gap in her spinal cord. Since then, she also has had six intrathecal transfusions. Olga indicated some increased lower-back strength and improved inner sensation.

A year after injury, another Olga had the 5-cm gap at her T12-injury site filled with SpheroGel embedded with regenerative cells. About a year after surgery, she suddenly started gaining some dramatic improvement, which she demonstrated to me in NeuroVitas rehabilitation facility.

These are just the patients that I met. For those interested in further patient feedback, the clinic has developed a DVD with English subtitles that includes interviews with other NeuroVita patients.

Conclusion

Although by itself probably not an end-all SCI panacea, this Russian stem-cell therapy is an exceedingly important piece of the puzzle that brings us ever closer to our overall goal of restored function after injury. Hopefully, American scientists can open-mindedly establish collaborations with Bryukhovetskiy so that Americans with SCI can more readily benefit.

Although Bryukhovetskiys work is of paramount importance, when discussing hot scientific topics like stem-cell therapy, it is easy to lose track of the fact that it is the patient who ultimately counts, not the science. In sciences cold objective eye, the patient becomes a research subject characterized by an impairment-scale, etc, and whose subjective opinions are often left in the dust of our quest for scientific purity.

I was grateful for the opportunity to interact with NeuroVitas patients, appreciating their willingness to share with me not only their pain and frustration, but their hope, optimism, and belief in the future. As a somewhat jaded disability-research veteran, their spirit fueled mine.

In this clinic and others throughout the world I have visited, the face of SCI seems so similar. Often with the support of devoted parents, youthful patients with great resolve, motivation, and old-soul wisdom that belies their youth pursue their dreams of recovery unencumbered with the limited expectations of the past.

In spite of unique injuries, there seems to be a collective soul of SCI in these patients that transcends culture and country. Although the efforts of innovative scientists, such as Bryukhovetskiy, are invaluable, the patients are the true pioneers. They each send forth a ripple of hope that is converging into a powerful current which will inevitably wash away SCIs imprisoning walls.

Contact Information: NeuroVita Clinic, Kashirskoye Avenue 23A, Moscow, Russia; info@neurovita.ru or http://www.NeuroVita.ru.

Adapted from article appearing in September 2005 Paraplegia News (For subscriptions, call 602-224-0500) or go to http://www.pn-magazine.com).

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Stem Cell Treatment for Cerebral Palsy

Thursday, November 24th, 2016

At Beike, our treatment not only focuses on treating the patient current symtoms but also prevents future complications. As cerebral palsy patients mature, the primary symptoms will inevitably lead to futher physical issues that could possibly be avoided.

Possible Improvements after Stem Cell Treatment:

Now lets talk about the stem cells we use in our treatment protocol for Cerebral Palsy.

What are Stem Cells? Stem cells are undifferentiated cells that have the ability to help perform a variety of regenerative functions such as differentiate and replace a wide range of cells in patients body, regulate the immune system and stimulate patients own stem cells. Adult Stem Cells (ACSs) are naturally present in every human being and their task is to regenerate dead and damaged cells during the bodys whole life span. They regenerate cells that are naturally dying (apoptosis) as well as cells injured by other reasons (disease, traumatic injuries etc.). These stem cells have limited differentiation and proliferation potentials, thus they are not likely to create any tumor or cancer. At Beike Biotech, we are only using Umbilical Cord Blood Stem Cells (UCBSC) and Umbilical Cord Mesenchymal Stem Cells (UCMSC) in our treatment protocols, which are 2 types of Adult Stem Cells widely documented and considered as safe by the international scientific community.

How do our Stem Cells help treat Cerebral Palsy? Stem Cells help Cerebral Palsy patients by rebuilding and regenerating the cells that were lost at birth due to a lack of oxygen. These cells will NEVER be naturally regenerated by the body which means the damage that has been done, will NEVER improve.

Is Stem Cell Treatment for Cerebral Palsy Safe? YES Since the companys founding in 2005, more than 20,500 patients (as of January 2016) have been treated with Beikes stem cell technology with no serious adverse outcomes or reactions that have been related to the stem cell transplants. Our medical department doctors review in-depth medical information provided by patients and it is only after this review that patients may be accepted for treatment. All medical procedures present possibility for complications.

As you already know by seeking treatment for Cerebral Palsy, the traditional process of treating Cerebral Palsy is almost as complex as the condition itself. Cerebral Palsy is caused by a lack of oxygen to the brain during birth, being born premature, serious head injuries or infections such as Meningitis. Cerebral Palsy treatment and the everyday life complications are emotionally, physiologically, physically, financially and spiritually draining. The average lifetime cost of treating a child with Cerebral Palsy is $921,000USD, that cost does not include out-of-pocket expenses, visits to the emergency room, lost wages or physosocial effects. Unfortunately, there is no known cure for Cerebral Palsy, conventional treatments options for parents are:

When considering treatment for Cerebral Palsy we focus on all factors that truly determine the level of care the patient needs, also, what a successful outcome would be. It is also important to note that each case of Cerebral Palsy is unique, with unique medical needs for each patient. An example of being able to determine a successful outcome would be as follows; there is no known cure for Cerebral Palsy, so to have the expectation of curing the disease is unrealistic. However, we break down Cerebral Palsy into primary and secondary conditions we are able to identify a realistic treatment outcome, with measurable medical outcomes. An example of a typical primary condition is when a patient has facial muscle control and coordination problems. The facial issues would be considered a primary condition with the secondary conditions being:

Common symptoms caused by Cerebral Palsy

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Blindness Wikipdia

Thursday, November 24th, 2016

Un article de Wikipdia, l'encyclopdie libre.

Blindness, ou L'Aveuglement[1] au Qubec, est un film de science-fiction japono-canado-brsilien ralis par Fernando Meirelles, sorti en 2008.

Il s'agit de l'adaptation du roman Ensaio sobre a Cegueira (1995) de l'crivain portugais Jos Saramago, rcompens par le prix Nobel de littrature en 1998[2]. Le film est prsent en comptition officielle au festival de Cannes 2008[3].

Tout commence quand un homme perd subitement la vue alors quil est au volant de sa voiture, attendant que le feu passe au vert. Trs vite, chacune des personnes quil rencontre: le bon samaritain qui le raccompagne chez lui, son mdecin, les autres patients dans la salle d'attente sont frapps de ccit blanche. Seule la femme du mdecin est mystrieusement pargne. Alors que la contagion stend une vitesse fulgurante, la panique gagne la ville. Les victimes de lpidmie sont de plus en plus nombreuses et les autorits les placent en quarantaine dans un hpital dsaffect. La femme du mdecin, dcide rester auprs de son mari, fait croire qu'elle a galement perdu la vue. lhpital, elle tente dorganiser un semblant de vie quotidienne civilise. Lorsque le confinement dgnre en explosion de violence, elle prend la tte de la rvolte et guide une famille improvise travers la ville dvaste.

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Mesenchymal stem cell – Wikipedia

Wednesday, November 23rd, 2016

Mesenchymal stem cells, or MSCs, are multipotent stromal cells that can differentiate into a variety of cell types,[1] including: osteoblasts (bone cells),[2]chondrocytes (cartilage cells),[3]myocytes (muscle cells)[4] and adipocytes (fat cells). This phenomenon has been documented in specific cells and tissues in living animals and their counterparts growing in tissue culture.

While the terms mesenchymal stem cell and marrow stromal cell have been used interchangeably, neither term is sufficiently descriptive:

In 1924, Russian-born morphologist Alexander A. Maximow used extensive histological findings to identify a singular type of precursor cell within mesenchyme that develops into different types of blood cells.[9]

Scientists Ernest A. McCulloch and James E. Till first revealed the clonal nature of marrow cells in the 1960s.[10][11] An ex vivo assay for examining the clonogenic potential of multipotent marrow cells was later reported in the 1970s by Friedenstein and colleagues.[12][13] In this assay system, stromal cells were referred to as colony-forming unit-fibroblasts (CFU-f).

The first clinical trials of MSCs were completed in 1995 when a group of 15 patients were injected with cultured MSCs to test the safety of the treatment. Since then, over 200 clinical trials have been started. However, most are still in the safety stage of testing.[7]

Subsequent experimentation revealed the plasticity of marrow cells and how their fate could be determined by environmental cues. Culturing marrow stromal cells in the presence of osteogenic stimuli such as ascorbic acid, inorganic phosphate and dexamethasone could promote their differentiation into osteoblasts. In contrast, the addition of transforming growth factor-beta (TGF-b) could induce chondrogenic markers.[citation needed]

The youngest, most primitive MSCs can be obtained from umbilical cord tissue, namely Wharton's jelly and the umbilical cord blood. However MSCs are found in much higher concentration in the Whartons jelly compared to cord blood, which is a rich source of hematopoietic stem cells. The umbilical cord is easily obtained after a birth. It is normally thrown away and poses no risk for collection. The cord MSCs have more primitive properties than other adult MSCs obtained later in life, which might make them a useful source of MSCs for clinical applications.

A rich source for mesenchymal stem cells is the developing tooth bud of the mandibular third molar. While considered multipotent, they may prove to be pluripotent. They eventually form enamel, dentin, blood vessels, dental pulp and nervous tissues, a minimum of 24 other different unique end organs. Because of ease in collection at 810 years of age before calcification and minimal-to-no-morbidity, they probably constitute a major source for research and multiple therapies. These stem cells have been shown capable of producing hepatocytes.

Additionally, amniotic fluid has been shown to be a rich source of stem cells. As many as 1 in 100 cells collected during amniocentesis has been shown to be a pluripotent mesenchymal stem cell.[14]

Adipose tissue is one of the richest sources of MSCs. There are more than 500 times more stem cells in 1 gram of fat than in 1 gram of aspirated bone marrow.[citation needed] Adipose stem cells are actively being researched in clinical trials for treatment of a variety of diseases.

The presence of MSCs in peripheral blood has been controversial. A few groups have successfully isolated MSCs from human peripheral blood and been able to expand them in culture.[15] Australian company Cynata claims the ability to mass-produce MSCs from induced pluripotent stem cells obtained from blood cells.[16][17]

Mesenchymal stem cells are characterized morphologically by a small cell body with a few cell processes that are long and thin. The cell body contains a large, round nucleus with a prominent nucleolus, which is surrounded by finely dispersed chromatin particles, giving the nucleus a clear appearance. The remainder of the cell body contains a small amount of Golgi apparatus, rough endoplasmic reticulum, mitochondria and polyribosomes. The cells, which are long and thin, are widely dispersed and the adjacent extracellular matrix is populated by a few reticular fibrils but is devoid of the other types of collagen fibrils.[18][19]

The International Society for Cellular Therapy (ISCT) has proposed a set of standards to define MSCs. A cell can be classified as an MSC if it shows plastic adherent properties under normal culture conditions and has a fibroblast-like morphology. In fact, some argue that MSCs and fibroblasts are functionally identical.[20] Furthermore, MSCs can undergo osteogenic, adipogenic and chondrogenic differentiation ex-vivo. The cultured MSCs also express on their surface CD73, CD90 and CD105, while lacking the expression of CD11b, CD14, CD19, CD34, CD45, CD79a and HLA-DR surface markers.[21]

MSCs have a great capacity for self-renewal while maintaining their multipotency. Beyond that, there is little that can be definitively said. The standard test to confirm multipotency is differentiation of the cells into osteoblasts, adipocytes and chondrocytes as well as myocytes and neurons. MSCs have been seen to even differentiate into neuron-like cells,[22] but there is lingering doubt whether the MSC-derived neurons are functional.[23] The degree to which the culture will differentiate varies among individuals and how differentiation is induced, e.g., chemical vs. mechanical;[24] and it is not clear whether this variation is due to a different amount of "true" progenitor cells in the culture or variable differentiation capacities of individuals' progenitors. The capacity of cells to proliferate and differentiate is known to decrease with the age of the donor, as well as the time in culture. Likewise, whether this is due to a decrease in the number of MSCs or a change to the existing MSCs is not known.[citation needed]

Numerous studies have demonstrated that human MSCs avoid allorecognition, interfere with dendritic cell and T-cell function and generate a local immunosuppressive microenvironment by secreting cytokines.[25] It has also been shown that the immunomodulatory function of human MSC is enhanced when the cells are exposed to an inflammatory environment characterised by the presence of elevated local interferon-gamma levels.[26] Other studies contradict some of these findings, reflecting both the highly heterogeneous nature of MSC isolates and the considerable differences between isolates generated by the many different methods under development.[27]

The majority of modern culture techniques still take a colony-forming unit-fibroblasts (CFU-F) approach, where raw unpurified bone marrow or ficoll-purified bone marrow Mononuclear cell are plated directly into cell culture plates or flasks. Mesenchymal stem cells, but not red blood cells or haematopoetic progenitors, are adherent to tissue culture plastic within 24 to 48 hours. However, at least one publication has identified a population of non-adherent MSCs that are not obtained by the direct-plating technique.[28]

Other flow cytometry-based methods allow the sorting of bone marrow cells for specific surface markers, such as STRO-1.[29] STRO-1+ cells are generally more homogenous and have higher rates of adherence and higher rates of proliferation, but the exact differences between STRO-1+ cells and MSCs are not clear.[30]

Methods of immunodepletion using such techniques as MACS have also been used in the negative selection of MSCs.[31]

The supplementation of basal media with fetal bovine serum or human platelet lysate is common in MSC culture. Prior to the use of platelet lysates for MSC culture, the pathogen inactivation process is recommended to prevent pathogen transmission.[32]

Mesenchymal stem cells in the body can be activated and mobilized if needed. However, the efficiency is low. For instance, damage to muscles heals very slowly but further study into mechanisms of MSC action may provide avenues for increasing their capacity for tissue repair.[33][34]

A statistical-based analysis of MSC therapy for osteo-diseases (e.g., osteoarthritis) noted that most studies are still underway.[35] Wakitani published a small case series of nine defects in five knees involving surgical transplantation of MSCs with coverage of the treated chondral defects.[36]

At least 218 clinical trials investigating the efficacy of mesenchymal stem cells in treating diseases have been initiated - many of which study autoimmune diseases.[37] Promising results have been shown in conditions such as graft versus host disease, Crohn's disease, multiple sclerosis, systemic lupus erythematosus and systemic sclerosis.[38] While their anti-inflammatory/immunomodulatory effects appear to greatly ameliorate autoimmune disease severity, the durability of these effects are unclear.

However, it is becoming more accepted that diseases involving peripheral tissues, such as inflammatory bowel disease, may be better treated with methods that increase the local concentration of cells.[39]

Many of the early clinical successes using intravenous transplantation came in systemic diseases such as graft versus host disease and sepsis. Direct injection or placement of cells into a site in need of repair may be the preferred method of treatment, as vascular delivery suffers from a "pulmonary first pass effect" where intravenous injected cells are sequestered in the lungs.[40] Clinical case reports in orthopedic applications have been published, though the number of patients treated is small and these methods still lack demonstrated effectiveness.

Scientists have reported that MSCs when transfused immediately a few hours post thawing may show reduced function or show decreased efficacy in treating diseases as compared to those MSCs which are in log phase of cell growth, so cryopreserved MSCs should be brought back into log phase of cell growth in in vitro culture before these are administered for clinical trials or experimental therapies, re-culturing of MSCs will help in recovering from the shock the cells get during freezing and thawing. Various clinical trials on MSCs have failed which used cryopreserved product immediately post thaw as compared to those clinical trials which used fresh MSCs.[41]

Mesenchymal stem cells have been shown to contribute to cancer progression in a number of different cancers, particularly the hematological malignancies because they contact the transformed blood cells in the bone marrow.[42]

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Cell Stem Cell – ScienceDirect.com

Wednesday, November 23rd, 2016

Volume 19, Issue 5 - selected pp. 559-672 (3 November 2016)

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stem cell therapy could help cats with kidney disease …

Wednesday, November 23rd, 2016

Most cat lovers have been touched by kidney disease at least once in their life. I lost my beloved Freddie at age 15 to this silent killer. A new procedure using adult stem cells to facilitate kidney transplantation in cats is being pioneered by the University of Georgia College of Veterinary Medicine.

The treatment of kidney failure in cats has traditionally been limited to changing diet, fluid therapy and a variety of medications and nutritional supplements. In the best cases, we can extend the life of affected cats by a handful of years if diagnosed early.

About 17,000 humans undergo kidney transplantation each year in the US and many enjoy a normal life expectancy after receiving their new kidney. In comparison, only a few cats undergo kidney transplant each year at only three transplant programs based at veterinary teaching hospitals. The low number of feline kidney transplants is primarily due to high cost, organ rejection and complications and ethical dilemmas involving the donor cat.

Cost and ethics aside, many cats are deemed poor transplant candidates. By the time kidney transplant is considered, the cat is often too ill or has developed too many complications. Organ rejection is a primary concern for many of these debilitated patients.

Researchers at the University of Georgia are pioneering the use of adult or mesenchymal stem cells (MSCs) to lower the risk of organ rejection in cats, especially those at higher risk for organ rejection. This procedure is being used for the first time in feline patients after a 2012 study of humans patients. The study found those receiving adult stem cells in conjunction with kidney transplantation had lower risk of organ rejection, fewer post-operative infections and better kidney function one year later.

It looks like adult stem cells help cats in the same ways. To date, two cats have undergone the procedure and are doing incredibly well. Adult stem cells in the UGA cases were obtained from fat tissues and then grown in a lab for about ten days before surgery. According to the researchers, stem cells used without kidney transplantation hasnt shown much success so far in treating chronic renal disease. Other cat candidates are currently being considered for this groundbreaking procedure.

Of course, this procedure is still quite expensive. From an ethical perspective, families of a cat that receive a donated kidney are required to adopt the donor cat, pledge to care for the donor cat for life and commit to treating both the recipient and donor cats.

Most recipient cats will require lifelong medications and injections, often twice a day, to prevent organ rejection. Stem cell therapy doesnt eliminate anti-rejection medication. Stem-cell treatments have been used with some success in treating certain musculo-skeletal conditions, but long-term studies are lacking.

Kidney disease is one of the most common causes of death in cats. I welcome any advances in battling this devastating condition. I understand that kidney transplantation may not be appropriate or possible for the majority of my patients. I appreciate these high-tech advances because I know they represent future breakthroughs that will benefit my typical patients.

If your cat is drinking more water, urinating more frequently, or inexplicably losing weight, have her checked by your vet immediately. Early diagnosis is still our best hope for extending the longevity and quality of life for cats enduring kidney failure.

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Arguments Against Stem Cell Research

Wednesday, November 23rd, 2016

I strongly oppose human cloning, as do most Americans. We recoil at the idea of growing human beings for spare body parts, or creating life for our convenience.President George W. Bush, August 2001

In July 2006, (former) President George W. Bush vetoed a bill to ensure the continuation and expansion of human embryonic stem (hES) cell research in the USA; including the proposition to allow discarded embryos created for IVF to be utilized as sources for new hES cell lines.

This opposition to hES cell research had long been one of his most noted principles throughout his period in office, with the President viewing such research as a means of utilising life for convenience (see above); and serves to emphasise the level of importance now attached to the stem cell research debate.

Having examined the arguments put forth by those in favour of stem cell research (link to arguments in favour of STR), what are the arguments stated by its opponents?

Many opponents of hES cell research state this issue to be the basis of their belief that such use of embryos should not be allowed under any circumstances. To them, the issue of potentiality creates the following problem with regards to hES:

As such, even if the benefits (such as life saving treatments and improved understanding of debilitating illnesses) put forward by supporters of the technology do eventually come in to fruition, these hypothetical ends cannot justify the means; or as George Bush stated when explaining his vetoing of the aforementioned hES bill:

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Medical Costs in Costa Rica vs. U.S.

Wednesday, November 23rd, 2016

Cost of Medical Treatment in Costa Rica can be a 70% saving from that of the U.S.

With the cost of medical on the rise, medical tourists from the United States, Canada and Europe should definitely compare the cost of medical treatment in Costa Rica to what it would cost at home. You can reach Costa Rica from just about everywhere in the U.S. and Canada in 12 hours or less; from Europe in well under a day. Costa Rica has eminently qualified doctors, excellent hospitals, attractive recovery centers, affordable costs, and provides an opportunity for a memorable vacation. Places like Costa Rican Medical Tours offer package deals for both vacation and treatment.

Here are just a couple of reason why Costa Rica is becoming a desire place to have medical treatment.

Costa Rica also boasts some of the best doctors in the world. To see some of the top ones, visit, Costa Rica Doctors

More on Costa Rica medical tourism, visit, Diabetes Cure in Costa Rica, Stem Cell Care Treatment, Wellness and Health Care and Wellness and Rehab

Calypso Cruises

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Nine Things to Know About Stem Cell Treatments

Wednesday, November 23rd, 2016

Stem cells have tremendous promise to help us understand and treat a range of diseases, injuries and other health-related conditions. Their potential is evident in the use of blood stem cells to treat diseases of the blood, a therapy that has saved the lives of thousands of children with leukemia; and can be seen in the use of stem cells for tissue grafts to treat diseases or injury to the bone, skin and surface of the eye. Important clinical trials involving stem cells are underway for many other conditions and researchers continue to explore new avenues using stem cells in medicine.

There is still a lot to learn about stem cells, however, and their current applications as treatments are sometimes exaggerated by the media and other parties who do not fully understand the science and current limitations, and also by clinics looking to capitalize on the hype by selling treatments to chronically ill or seriously injured patients. The information on this page is intended to help you understand both the potential and the limitations of stem cells at this point in time, and to help you spot some of the misinformation that is widely circulated by clinics offering unproven treatments.

It is important to discuss these Nine Things to Know and any research or information you gather with your primary care physician and other trusted members of your healthcare team in deciding what is right for you.

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normande genetics: sustainable genetics that breed quality

Wednesday, November 23rd, 2016

Experience Normande genetics

Another breeding season is here, along with a new opportunity to experience Normande genetics. Please take a look at our Fall 2016proofsand, if it's your first time, take a leap of faith! Whether you graze or not, crossing with Normande offers many benefits. Check our the various pages of our website for more details about the breed's many strong qualities. See more information on ourcatalog pageon how to choose our bulls. As usual, graziers are advised to focus on bulls with low stature indexes for medium size cows if they cross with Holsteins. Low stature is less important if you cross with Jerseys. Finally, do not forget to follow us on Facebook and Twitter for quicker and more frequent news updates.

Normande Genetics was created in 1997 to bring the top dairy genetics of the Normande breed to the American dairyland. Because the U.S. dairy industry had long since cut its grass roots in favor of intensive, high-energy, grain-based systems, we believed that genetics here were no longer well suited to grass-based operations. That insight has been confirmed consistently in interactions with American dairy farmers, whose herds are suffering loss of functionality in fertility and longevity, owing to over-selection for productivity, and secondarily, dairyness.

Originally focused on grazing daires, we quickly realize that the need for different genetics applies to all dairies, and includes conventional ones. Intensive operations are increasingly faced with fertility and health issues, and many of these issues can be attributed to frail genetics or inbreeding.

While the U.S. dairy sire selection process has started to move towards improving functional traits, it will take time to see results in the field. In addition, in-breeding and a narrowing gene pool for most dairy breeds worldwide add to the problem, so there is no easy and short-term answer to the weakening of health traits.

Thats why crossbreeding makes sense. After all, dairy farmers want to lower their cost of operation while increasing their revenue, which means profits and margins replace production as the main benchmarks of success. In turn, genetic traits that contribute to the bottom line become essential, while selecting for milk production becomes relatively less important. For more information about why crossbreeding is a useful tool, you can download this article:

download "Why Crossbreeding?" Article (PDF)

The Normandes traits serve the objectives of both grass-based and conventional operations in two ways: bringing strength and functionality while adding value whenever possible. The Normande has outstanding attributes as a purebred or in a cross-breeding program. The breed has shown successful examples with all U.S. dairy breeds and is often included in three-way crossbreeding programs. The University of Minnesotas new experimental organic herd includes such a cross.

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Aging of wine – Wikipedia

Wednesday, November 23rd, 2016

The aging of wine is potentially able to improve the quality of wine. This distinguishes wine from most other consumable goods. While wine is perishable and capable of deteriorating, complex chemical reactions involving a wine's sugars, acids and phenolic compounds (such as tannins) can alter the aroma, color, mouthfeel and taste of the wine in a way that may be more pleasing to the taster. The ability of a wine to age is influenced by many factors including grape variety, vintage, viticultural practices, wine region and winemaking style. The condition that the wine is kept in after bottling can also influence how well a wine ages and may require significant time and financial investment.[1][2] The quality of an aged wine varies significantly bottle-by-bottle, depending on the conditions under which it was stored, and the condition of the bottle and cork, and thus it is said that rather than good old vintages, there are good old bottles. There is a significant mystique around the aging of wine, as its chemistry was not understood for a long time, and old wines are often sold for extraordinary prices. However, the vast majority of wine is not aged, and even wine that is aged is rarely aged for long; it is estimated that 90% of wine is meant to be consumed within a year of production, and 99% of wine within 5 years.[3]

The Ancient Greeks and Romans were aware of the potential of aged wines. In Greece, early examples of dried "straw wines" were noted for their ability to age due to their high sugar contents. These wines were stored in sealed earthenware amphorae and kept for many years. In Rome, the most sought after winesFalernian and Surrentinewere prized for their ability to age for decades. In the Book of Luke, it is noted that "old wine" was valued over "new wine" (Luke 5:39). The Greek physician Galen wrote that the "taste" of aged wine was desirable and that this could be accomplished by heating or smoking the wine, though, in Galen's opinion, these artificially aged wines were not as healthy to consume as naturally aged wines.[4]

Following the Fall of the Roman Empire, appreciation for aged wine was virtually non-existent. Most of the wines produced in northern Europe were light bodied, pale in color and with low alcohol. These wines did not have much aging potential and barely lasted a few months before they rapidly deteriorated into vinegar. The older a wine got the cheaper its price became as merchants eagerly sought to rid themselves of aging wine. By the 16th century, sweeter and more alcoholic wines (like Malmsey and Sack) were being made in the Mediterranean and gaining attention for their aging ability. Similarly, Riesling from Germany with its combination of acidity and sugar were also demonstrating their ability to age. In the 17th century, two innovations occurred that radically changed the wine industry's view on aging. One was the development of the cork and bottle which allowed producers to package and store wine in a virtually air-tight environment. The second was the growing popularity of fortifying wines such as Port, Madeira and Sherries. The added alcohol was found to act as a preservative, allowing wines to survive long sea voyages to England, The Americas and the East Indies. The English, in particular, were growing in their appreciation of aged wines like Port and Claret from Bordeaux. Demand for matured wines had a pronounced effect on the wine trade. For producers, the cost and space of storing barrels or bottles of wine was prohibitive so a merchant class evolved with warehouses and the finances to facilitate aging wines for a longer period of time. In regions like Bordeaux, Oporto and Burgundy, this situation dramatically increased the balance of power towards the merchant classes.[4]

There is a widespread misconception that wine always improves with age,[3] or that wine improves with extended aging, or that aging potential is an indicator of good wine. Some authorities state that more wine is consumed too old than too young.[5] Aging changes wine, but does not categorically improve it or worsen it. Fruitness deteriorates rapidly, decreasing markedly after only 6 months in the bottle.[5] Due to the cost of storage, it is not economical to age cheap wines, but many varieties of wine do not benefit from aging, regardless of the quality. Experts vary on precise numbers, but typically state that only 510% of wine improves after 1 year, and only 1% improves after 510 years.[3][5]

In general, wines with a low pH (such as Pinot Noir and Sangiovese) have a greater capability of aging. With red wines, a high level of flavor compounds, such as phenolics (most notably tannins), will increase the likelihood that a wine will be able to age. Wines with high levels of phenols include Cabernet Sauvignon, Nebbiolo and Syrah.[4] The white wines with the longest aging potential tend to be those with a high amount of extract and acidity. The acidity in white wines, acting as a preservative, has a role similar to that of tannins in red wines. The process of making white wines, which includes little to no skin contact, means that white wines have a significantly lower amount of phenolic compounds, though barrel fermentation and oak aging can impart some phenols. Similarly, the minimal skin contact with ros wine limits their aging potential.[1][2][5]

After aging at the winery most wood-aged Ports, Sherries, Vins doux naturels, Vins de liqueur, basic level Ice wines and sparkling wines are bottled when the producer feels that they are ready to be consumed. These wines are ready to drink upon release and will not benefit much from aging. Vintage Ports and other bottled-aged Ports & Sherries will benefit from some additional aging.[4]

Champagne and other sparkling wines are infrequently aged, and frequently have no vintage year (no vintage, NV), but vintage champagne may be aged.[4] Aged champagne has traditionally been a peculiarly British affectation, and thus has been referred to as le got anglais "the English taste",[6] though this term also refers to a level of champagne sweetness. In principle champagne has aging potential, due to the acidity, and aged champagne has increased in popularity in the United States since the 1996 vintage.[7] A few French winemakers have advocated aging champagne, most notably Ren Collard (19212009).[8] In 2009, a 184-year-old bottle of Perrier-Jout was opened and tasted, still drinkable, with notes of "truffles and caramel", according to the experts.[9]

A guideline provided by Master of Wine Jancis Robinson[5]

A guideline provided by Master of Wine Jancis Robinson. Note that vintage, wine region and winemaking style can influence a wine's aging potential so Robinson's suggestion of years are very rough estimates of the most common examples of these wines.[5]

The ratio of sugars, acids and phenolics to water is a key determination of how well a wine can age. The less water in the grapes prior to harvest, the more likely the resulting wine will have some aging potential. Grape variety, climate, vintage and viticultural practice come into play here. Grape varieties with thicker skins, from a dry growing season where little irrigation was used and yields were kept low will have less water and a higher ratio of sugar, acids and phenolics. The process of making Eisweins, where water is removed from the grape during pressing as frozen ice crystals, has a similar effect of decreasing the amount of water and increasing aging potential.[2][5]

In winemaking, the duration of maceration or skin contact will influence how much phenolic compounds are leached from skins into the wine. Pigmented tannins, anthocyanins, colloids, tannin-polysaccharides and tannin-proteins not only influence a wine's resulting color but also act as preservatives. During fermentation adjustment to a wine's acid levels can be made with wines with lower pH having more aging potential. Exposure to oak either during fermentation or after (during barrel aging) will introduce more phenolic compounds to the wines. Prior to bottling, excessive fining or filtering of the wine could strip the wine of some phenolic solids and may lessen a wine's ability to age.[1][4]

The storage condition of the bottled wine will influence a wine's aging. Vibrations and heat fluctuations can hasten a wine's deterioration and cause adverse effect on the wines. In general, a wine has a greater potential to develop complexity and more aromatic bouquet if it is allowed to age slowly in a relatively cool environment. The lower the temperature, the more slowly a wine develops.[4] On average, the rate of chemical reactions in wine double with each 18F (8C) increase in temperature. Wine expert Karen MacNeil, recommends keeping wine intended for aging in a cool area with a constant temperature around 55F (13C). Wine can be stored at temperatures as high as 69F (20C) without long term negative effect. Professor Cornelius Ough of the University of California, Davis believes that wine could be exposed to temperatures as high as 120F (49C) for a few hours and not be damaged. However, most experts believe that extreme temperature fluctuations (such as repeated transferring a wine from a warm room to a cool refrigerator) would be detrimental to the wine. The ultra-violet rays of direct sunlight should also be avoided because of the free radicals that can develop in the wine and result in premature oxidation.[2][12]

Wines packaged in large format bottles, such as magnums and 3 liter Jeroboams, seem to age more slowly than wines packaged in regular 750 ml bottles or half bottles. This may be because of the greater proportion of oxygen exposed to the wine during the bottle process. The advent of alternative wine closures to cork, such as screw caps and synthetic corks have opened up recent discussions on the aging potential of wines sealed with these alternative closures. Currently there are no conclusive results and the topic is the subject of ongoing research.[1][4]

One of the short-term aging needs of wine is a period where the wine is considered "sick" due to the trauma and volatility of the bottling experience. During bottling the wine is exposed to some oxygen which causes a domino effect of chemical reactions with various components of the wine. The time it takes for the wine to settle down and have the oxygen fully dissolve and integrate with the wine is considered its period of "bottle shock". During this time the wine could taste drastically different from how it did prior to bottling or how it will taste after the wine has settled. While many modern bottling lines try to treat the wine as gently as possible and utilize inert gases to minimize the amount of oxygen exposure, all wine goes through some period of bottle shock. The length of this period will vary with each individual wine.[2][5]

The transfer of off-flavours in the cork used to bottle a wine during prolonged aging can be detrimental to the quality of the bottle. The formation of cork taint is a complex process which may result from a wide range of factors ranging from the growing conditions of the cork oak, the processing of the cork into stoppers, or the molds growing on the cork itself.[1][2]

During the course of aging, a wine may slip into a "dumb phase" where its aromas and flavors are very muted. In Bordeaux this phase is called the age ingrat or "difficult age" and is likened to a teenager going through adolescence. The cause or length of time that this "dumb phase" will last is not yet fully understood and seems to vary from bottle to bottle.[12]

As red wine ages, the harsh tannins of its youth gradually give way to a softer mouthfeel. An inky dark color will eventually lose its depth of color and begin to appear orange at the edges, and then later eventually turning brown. These changes occur due to the complex chemical reactions of the phenolic compounds of the wine. In processes that begin during fermentation and continue after bottling, these compounds bind together and aggregate. Eventually these particles reach a certain size where they are too large to stay suspended in the solution and precipitate out. The presence of visible sediment in a bottle will usually indicate a mature wine. The resulting wine, with this loss of tannins and pigment, will have a paler color and taste softer, less astringent. The sediment, while harmless, can have an unpleasant taste and is often separated from the wine by decanting.[5]

During the aging process, the perception of a wine's acidity may change even though the total measurable amount of acidity is more or less constant throughout a wine's life. This is due to the esterification of the acids, combining with alcohols in complex array to form esters. In addition to making a wine taste less acidic, these esters introduce a range of possible aromas. Eventually the wine may age to a point where other components of the wine (such as a tannins and fruit) are less noticeable themselves, which will then bring back a heightened perception of wine acidity. Other chemical processes that occur during aging include the hydrolysis of flavor precursors which detach themselves from glucose molecules and introduce new flavor notes in the older wine and aldehydes become oxidized. The interaction of certain phenolics develop what is known as tertiary aromas which are different from the primary aromas that are derived from the grape and during fermentation.[2][4]

As a wine starts to mature, its bouquet will become more developed and multi-layered. While a taster may be able to pick out a few fruit notes in a young wine, a more complex wine will have several distinct fruit, floral, earthy, mineral and oak derived notes. The lingering finish of a wine will lengthen. Eventually the wine will reach a point of maturity, when it is said to be at its "peak". This is the point when the wine has the maximum amount of complexity, most pleasing mouthfeel and softening of tannins and has not yet started to decay. When this point will occur is not yet predictable and can vary from bottle to bottle. If a wine is aged for too long, it will start to descend into decrepitude where the fruit tastes hollow and weak while the wine's acidity becomes dominant.[4]

The natural esterification that takes place in wines and other alcoholic beverages during the aging process is an example of acid-catalysed esterification. Over time, the acidity of the acetic acid and tannins in an aging wine will catalytically protonate other organic acids (including acetic acid itself), encouraging ethanol to react as a nucleophile. As a result, ethyl acetate the ester of ethanol and acetic acidis the most abundant ester in wines. Other combinations of organic alcohols (such as phenol-containing compounds) and organic acids lead to a variety of different esters in wines, contributing to their different flavours, smells and tastes. Of course, when compared to sulfuric acid conditions, the acid conditions in a wine are mild, so yield is low (often in tenths or hundredths of a percentage point by volume) and take years for ester to accumulate.[1]

Coates Law of Maturity is a principle used in wine tasting relating to the aging ability of wine. Developed by the British Master of Wine, Clive Coates, the principle states that a wine will remain at its peak (or optimal) drinking quality for a duration of time that is equal to the time of maturation required to reach its optimal quality. During the evolution (aging) of a wine certain flavors, aromas and textures appear and fade. Rather than developing and fading in unison, these traits each operate on a unique evolutionary path and time line. The principle allows for the subjectivity of individual tastes because it follows the logic that positive traits that appeal to one particular wine taster will continue to persist along the principle's guideline while for another taster these traits might not be positive and therefore not applicable to the guideline. Wine expert Tom Stevenson has noted that there is logic in Coates' principle and that he has yet to encounter an anomaly or wine that debunks it.[13]

An example of the principle in practice would be a wine that someone acquires when it is 9 years of age, but finds it dull. A year later the drinker finds this wine very pleasing in texture, aroma and mouthfeel. Under the Coates Law of Maturity the wine will continue to be drunk at an optimal maturation for that drinker until it has reached 20 years of age at which time those positive traits that the drinker perceives will start to fade.[13]

There is a long history of using artificial means to try to accelerate the natural aging process. In Ancient Rome a smoke chamber known as a fumarium was used to enhance the flavor of wine through artificial aging. Amphorae were placed in the chamber, which was built on top of a heated hearth, in order to impart a smoky flavor in the wine that also seemed to sharpen the acidity. The wine would sometimes come out of the fumarium with a paler color just like aged wine.[14] Modern winemaking techniques like micro-oxygenation can have the side effect of artificially aging the wine. In the production of Madeira and rancio wines, the wines are deliberately exposed to excessive temperatures to accelerate the maturation of the wine. Other techniques used to artificially age wine (with inconclusive results on their effectiveness) include shaking the wine, exposing it to radiation, magnetism or ultra-sonic waves.[4] More recently, experiments with artificial aging through high-voltage electricity have produced results above the remaining techniques, as assessed by a panel of wine tasters.[15] Other artificial wine-aging gadgets include the "Clef du Vin", which is a metallic object that is dipped into wine and purportedly ages the wine one year for every second of dipping. The product has received mixed reviews from wine commentators.[16]

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Genetic Counseling Program Overview – School of Medicine

Wednesday, November 23rd, 2016

Introduction and Program Goals

The Genetic Counseling Training Program, leading to a Master of Science degree in Genetic Counselings, is a two-year academic program comprised of didactic course work, laboratory exposure, research experience and extensive clinical training. The program, directed by Anne L. Matthews, R.N, Ph.D., is an integral component of the teaching and research programs in the Department of Genetics and Genome Sciences (G&GS) at CWRU under the leadership of Dr. Anthony Wynshaw-Boris, MD. Ph.D., chairman of G&GS and the program's medical director, Shawn McCandless M.D., Associate Professor of G&GS and Pediatrics and Director of the Center for Human Genetics, University Hospitals Cleveland Medical Center. The Program is accredited by the Accreditation Counseling of Genetic Counseling (ACGC) and graduates of the program are eligible to apply for Active Candidate Status and sit for the American Board of Genetic Counseling certification examination.

The overall objective of the Genetic Counseling Program is to prepare students with the appropriate knowledge and experiences to function as genetic counselors in a wide range of settings and roles. With unprecedented advances in our understanding of the genetic and molecular control of gene expression and development, and in our ability to apply this knowledge clinically, the Program strives to train students who can interface between patients, clinicians and molecular and human geneticists. Students gain insightful and multifaceted skills that will enable them to be effective genetic counselors, aware of the many new technical advances and often-difficult ethical, legal and social issues that have surfaced in the light of the Human Genome Project. Graduates of the Program will be prepared to work in a variety of settings including both adult and pediatric genetics clinics, specialty clinics such as cancer genetics and metabolic clinics, and prenatal diagnosis clinics, as well as in areas of research or commercial genetics laboratories relevant to genetic counseling and human genetics.

A unique aspect of the Genetic Counseling Training Program that it is housed within Case Western Reserve's Department of Genetics and Genome Sciences that is internationally known for both its clinical expertise and cutting edge research in molecular genetics, model organisms and human genetics. Thus, the Department of G&GS at CWRU provides an interface between human and medical genetics with basic genetics and provides an exciting atmosphere in which to learn and develop professionally. The direct access to both clinical resources and advanced technologies in human and model organisms affords students with an unparalleled environment for achievement. The Graduate Program in Genetics in the Department of Genetics and Genome Sciences provides an interactive and collaborative environment for both pre (genetic counseling and PhD students)- and post-doctoral trainees to come together in a collegial atmosphere. By fostering interactions between pre- and post-doctoral trainees in genetic counseling, medical genetics, and basic research at an early stage of their careers, it is anticipated that graduates will be well-rounded professionals with an understanding of the importance of both clinical and basic research endeavors. Moreover, such resources as the Department of Biomedical Ethics, the Center for Genetic Research, Ethics and Law, the Mandel School of Applied Social Sciences, and the Law-Medicine Center provide for an enriched learning experience for students.

The curriculum consists of 40 semester hours: 22 semester hours of didactic course work and 7 semester hours of research. Additionally, there are three 10-week clinical rotations, one 3-week laboratory rotation and one 6-week summer rotation required of all students, which provide an additional 11 credit hours. Courses include material covering basic genetics concepts, embryology, medical genetics, biochemical genetics, molecular genetics, cytogenetics, genomics, cancer genetics, population genetics, genetic counseling principles, human development, psychosocial issues, interviewing techniques, and ethical and professional issues in genetic counseling.

Clinical rotations include one intensive three-week laboratory rotation in diagnostic cytogenetics and clinical molecular genetics as well as the Maternal Serum Screening program. There are three 10-week clinical rotations during year 2 during which students obtain clinical experience in General Genetics (children and adults) including Specialty Clinics such as Marfan Clinic, Prader-Willi Clinic and Craniofacial Clinic; Prenatal Diagnosis Clinic, and Cancer Genetics Clinic. These rotations take place at The Center for Human Genetics at University Hospitals Cleveland Medical Center, the Genomic Medicine Institute at the Cleveland Clinic and MetroHealth Medical Center. Additionally, there is one off-site rotation - a six-week clinical rotation which is held at Akron Children's Hospital in Akron Ohio during the summer. Moreover, students rotate through the Cleveland-based institutions for weekly observational experiences starting early in year 1 of the program.

Students are also required to attend and participate in a number of other activities such as weekly Clinical Patient Conferences, Genetics Grand Rounds, Departmental Seminars and Journal Club. Students also participate with the doctoral graduate students in the Department of Genetics and Genome Sciences' annual retreat and present their research projects during the poster sessions. In addition, counseling students present their research during the program's Research Showcase. Students also have an opportunity to give educational talks to local schools, participate in DNA Day at local high schools and other groups when available.

Tuition for the 2016-2017 academic year is $1,774.00 per semester hour. Currently, other fees include student health insurance ($986 per semester) and a student activity fee of $14.00 per semester.

The Department of Genetics is unable to provide financial aid or research/teaching assistantships to students; however, it does award some scholarship funding in the form of a monthly stipend to genetic counseling students. The amount of the stipend is determined yearly and will be shared with applicants at the time of their interviews. In addition, the costs of the on-line embryology course as well as the CWRU Technology fee of $426.00 per year are covered by the Department. Moreover, students receive funds to cover the costs associated with their research projects and second year students receive funds to travel to the National Society of Genetic Counselors' annual education conference held in the fall.

Financial aid is available to graduate students. The university has extensive information regarding financial aid and scholarship opportunities to assist students in funding their education. For additional information or assistance, please contact the Office of University Financial Aid at http://case.edu/stage/admissions/financialaid.html or (216) 368-4530.

Clarice Young at (216) 368-3431 or email: clarice.young@case.edu

OR

The Program Director:

Please Note: The Direct Application link will take you to the School for Graduate Studies webpage. Go to Prospective Students - Admissions Information - Graduate Program Applications. You will see a link on the right hand side of the page entitled Application Log In to begin your application.

The application includes:

Fulfillment of the requirements for admission to the School of Graduate Studies at Case Western Reserve University must be met as well as those required by the Genetic Counseling Training Program. An applicant having graduated with excellent academic credentials (minimum undergraduate grade point average of 3.0 on a 4.0 scale) from a fully accredited university or college. Complete credentials must be on file with the School of Graduate Studies

The average GPA for matriculating students is 3.5 and GRE mean scores are approximately, 60-70th percentiles and above. However, we take a holistic view of the applicant's complete file in determining admission, which means we look at everything the applicant has submitted. A high GPA or GRE score will not automatically lead to admission; neither will low scores automatically lead to a denial. *While the CWRU application form asks for your GRE scores, please include the percentile score as well.

The Personal Statement is extremely important and applicants need to pay specific attention to how they present themselves in their Personal Statement. Aspects to remember include: Is the applicant's Personal Statement grammatically sound, and does it give us a clear picture as to who the applicant is? Applicants' should emphasize those experiences which have directly assisted them in becoming aware of and knowledgeable about the genetic counseling profession. Genetic counselors are highly motivated and hardworking individuals. Thus, the admissions committee looks for applicants who demonstrate initiative, self-direction, excellent communication skills and who have "gone the extra mile" to show their passion for becoming a genetic counselor.

Letters of recommendation should be written by individuals who can provide an accurate picture of your academic capabilities, your communication skills (both written and spoken) and your potential to successfully complete graduate education. At least two referees should be faculty from your past institutions. Other excellent referee sources include genetic counselors you have shadowed or supervisors of internships or advocacy experiences which you have had. Recommendation letters from friends or family members are discouraged. Please note, while CWRU provides an on-line recommendation form for referees to complete, your referee should also provide a personal letter to accompany the form.

While the number of applications received by the Program varies from year to year, in general we receive approximately 60+ applications each year. At this time, the Program is able to accept 6 students per year.

January 1st of each year is the application deadline. It is important that all required materials such as GRE scores (including their percentiles), transcripts from all institutions in which you have completed coursework and letters of reference be submitted by the application deadline if you wish to have your application reviewed by the Admissions Committee. If you will be taking a prerequisite course or courses in the upcoming semester that will not be reflected on your current transcripts, please let us know in your personal statement which course or courses you will be taking to meet the pre-requisites. Also, please submit a current CV or resume along with your personal statement. The Program only admits one class per year -- in fall semester. Because of the intensive nature of the Program, all students must be full time, we are unable to accommodate part-time students.

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Association for Integrative Medicine

Wednesday, November 23rd, 2016

Dear Holistic, Alternative and Integrated Health Practitioners,

Peter Redmond D.C.

and all persons interested in Integrative Medicine, We cordially invite you to join our Association for Integrative Medicine.

We believe that the combined knowledge of old and new healing modalities is ultimately superior to a single-model approach to health and wellness.

It is our philosophy that diverse modalities such as Massage, Counseling, Reiki, Yoga, Shiatsu, Biofeedback, Chiropractic, Hypnosis, Homeopathy, Naturopathy, Cranio-Sacral Therapy, the Arts Therapies, Western Medicine and many others can work in conjunction with each other as part of a unified team rather than in competition. This integrated approach ultimately will lead to safer, faster and more effective healthcare.

If you would like to be considered for a position on our Board of directors or advisory Board, please send a written statement as to how you are qualified for the position, why you would make an effective Board member, how you bring diversity or representation of the general public to the Board, and why you are interested in the post, your vision for AIM and how you would be able to assist in achieving it.

For any additional information, questions or comments, please dont hesitate to write or call us.

Sincerely Yours,

Peter Redmond, D.C. and Eric Miller, Ph.D.

Executive Director Eric Miller

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Innate immune system – Wikipedia

Wednesday, November 23rd, 2016

The innate immune system, also known as the non-specific immune system or in-born immunity system,[1] is an important subsystem of the overall immune system that comprises the cells and mechanisms that defend the host from infection by other organisms. The cells of the innate system recognize and respond to pathogens in a generic way, but, unlike the adaptive immune system, the system does not confer long-lasting or protective immunity to the host.[2] Innate immune systems provide immediate defense against infection, and are found in all classes of plant and animal life.

The innate immune system is an evolutionarily older defense strategy, and is the dominant immune system found in plants, fungi, insects, and primitive multicellular organisms.[3]

The major functions of the vertebrate innate immune system include:

Anatomical barriers include physical, chemical and biological barriers. The epithelial surfaces form a physical barrier that is impermeable to most infectious agents, acting as the first line of defense against invading organisms.[4]Desquamation (shedding) of skin epithelium also helps remove bacteria and other infectious agents that have adhered to the epithelial surfaces. Lack of blood vessels and inability of the epidermis to retain moisture, presence of sebaceous glands in the dermis provides an environment unsuitable for the survival of microbes.[4] In the gastrointestinal and respiratory tract, movement due to peristalsis or cilia, respectively, helps remove infectious agents.[4] Also, mucus traps infectious agents.[4] The gut flora can prevent the colonization of pathogenic bacteria by secreting toxic substances or by competing with pathogenic bacteria for nutrients or attachment to cell surfaces.[4] The flushing action of tears and saliva helps prevent infection of the eyes and mouth.[4]

Inflammation is one of the first responses of the immune system to infection or irritation. Inflammation is stimulated by chemical factors released by injured cells and serves to establish a physical barrier against the spread of infection, and to promote healing of any damaged tissue following the clearance of pathogens.[5]

The process of acute inflammation is initiated by cells already present in all tissues, mainly resident macrophages, dendritic cells, histiocytes, Kupffer cells, and mastocytes. These cells present receptors contained on the surface or within the cell, named pattern recognition receptors (PRRs), which recognize molecules that are broadly shared by pathogens but distinguishable from host molecules, collectively referred to as pathogen-associated molecular patterns (PAMPs). At the onset of an infection, burn, or other injuries, these cells undergo activation (one of their PRRs recognizes a PAMP) and release inflammatory mediators responsible for the clinical signs of inflammation.

Chemical factors produced during inflammation (histamine, bradykinin, serotonin, leukotrienes, and prostaglandins) sensitize pain receptors, cause local vasodilation of the blood vessels, and attract phagocytes, especially neutrophils.[5] Neutrophils then trigger other parts of the immune system by releasing factors that summon additional leukocytes and lymphocytes. Cytokines produced by macrophages and other cells of the innate immune system mediate the inflammatory response. These cytokines include TNF, HMGB1, and IL-1.[6]

The inflammatory response is characterized by the following symptoms:

The complement system is a biochemical cascade of the immune system that helps, or complements, the ability of antibodies to clear pathogens or mark them for destruction by other cells. The cascade is composed of many plasma proteins, synthesized in the liver, primarily by hepatocytes. The proteins work together to:

Elements of the complement cascade can be found in many non-mammalian species including plants, birds, fish, and some species of invertebrates.[7]

All white blood cells (WBCs) are known as leukocytes. Leukocytes differ from other cells of the body in that they are not tightly associated with a particular organ or tissue; thus, their function is similar to that of independent, single-cell organisms. Leukocytes are able to move freely and interact with and capture cellular debris, foreign particles, and invading microorganisms. Unlike many other cells in the body, most innate immune leukocytes cannot divide or reproduce on their own, but are the products of multipotent hematopoietic stem cells present in the bone marrow.[2]

The innate leukocytes include: Natural killer cells, mast cells, eosinophils, basophils; and the phagocytic cells include macrophages, neutrophils, and dendritic cells, and function within the immune system by identifying and eliminating pathogens that might cause infection.[3]

Mast cells are a type of innate immune cell that reside in connective tissue and in the mucous membranes. They are intimately associated with wound healing and defense against pathogens, but are also often associated with allergy and anaphylaxis.[5] When activated, mast cells rapidly release characteristic granules, rich in histamine and heparin, along with various hormonal mediators and chemokines, or chemotactic cytokines into the environment. Histamine dilates blood vessels, causing the characteristic signs of inflammation, and recruits neutrophils and macrophages.[5]

The word 'phagocyte' literally means 'eating cell'. These are immune cells that engulf, or 'phagocytose', pathogens or particles. To engulf a particle or pathogen, a phagocyte extends portions of its plasma membrane, wrapping the membrane around the particle until it is enveloped (i.e., the particle is now inside the cell). Once inside the cell, the invading pathogen is contained inside an endosome, which merges with a lysosome.[3] The lysosome contains enzymes and acids that kill and digest the particle or organism. In general, phagocytes patrol the body searching for pathogens, but are also able to react to a group of highly specialized molecular signals produced by other cells, called cytokines. The phagocytic cells of the immune system include macrophages, neutrophils, and dendritic cells.

Phagocytosis of the hosts own cells is common as part of regular tissue development and maintenance. When host cells die, either by programmed cell death (also called apoptosis) or by cell injury due to a bacterial or viral infection, phagocytic cells are responsible for their removal from the affected site.[2] By helping to remove dead cells preceding growth and development of new healthy cells, phagocytosis is an important part of the healing process following tissue injury.

Macrophages, from the Greek, meaning "large eaters," are large phagocytic leukocytes, which are able to move outside of the vascular system by migrating across the walls of capillary vessels and entering the areas between cells in pursuit of invading pathogens. In tissues, organ-specific macrophages are differentiated from phagocytic cells present in the blood called monocytes. Macrophages are the most efficient phagocytes and can phagocytose substantial numbers of bacteria or other cells or microbes.[3] The binding of bacterial molecules to receptors on the surface of a macrophage triggers it to engulf and destroy the bacteria through the generation of a respiratory burst, causing the release of reactive oxygen species. Pathogens also stimulate the macrophage to produce chemokines, which summon other cells to the site of infection.[3]

Neutrophils, along with two other cell types (eosinophils and basophils; see below), are known as granulocytes due to the presence of granules in their cytoplasm, or as polymorphonuclear cells (PMNs) due to their distinctive lobed nuclei. Neutrophil granules contain a variety of toxic substances that kill or inhibit growth of bacteria and fungi. Similar to macrophages, neutrophils attack pathogens by activating a respiratory burst. The main products of the neutrophil respiratory burst are strong oxidizing agents including hydrogen peroxide, free oxygen radicals and hypochlorite. Neutrophils are the most abundant type of phagocyte, normally representing 50-60% of the total circulating leukocytes, and are usually the first cells to arrive at the site of an infection.[5] The bone marrow of a normal healthy adult produces more than 100 billion neutrophils per day, and more than 10 times that many per day during acute inflammation.[5]

Dendritic cells (DCs) are phagocytic cells present in tissues that are in contact with the external environment, mainly the skin (where they are often called Langerhans cells), and the inner mucosal lining of the nose, lungs, stomach, and intestines.[2] They are named for their resemblance to neuronal dendrites, but dendritic cells are not connected to the nervous system. Dendritic cells are very important in the process of antigen presentation, and serve as a link between the innate and adaptive immune systems.

Basophils and eosinophils are cells related to the neutrophil (see above). When activated by a pathogen encounter, histamine-releasing basophils are important in the defense against parasites and play a role in allergic reactions, such as asthma.[3] Upon activation, eosinophils secrete a range of highly toxic proteins and free radicals that are highly effective in killing parasites, but may also damage tissue during an allergic reaction. Activation and release of toxins by eosinophils are, therefore, tightly regulated to prevent any inappropriate tissue destruction.[5]

Natural killer cells (NK cells) are a component of the innate immune system that does not directly attack invading microbes. Rather, NK cells destroy compromised host cells, such as tumor cells or virus-infected cells, recognizing such cells by a condition known as "missing self." This term describes cells with abnormally low levels of a cell-surface marker called MHC I (major histocompatibility complex) - a situation that can arise in viral infections of host cells.[8] They were named "natural killer" because of the initial notion that they do not require activation in order to kill cells that are "missing self." For many years, it was unclear how NK cell recognize tumor cells and infected cells. It is now known that the MHC makeup on the surface of those cells is altered and the NK cells become activated through recognition of "missing self". Normal body cells are not recognized and attacked by NK cells because they express intact self MHC antigens. Those MHC antigens are recognized by killer cell immunoglobulin receptors (KIR) that, in essence, put the brakes on NK cells. The NK-92 cell line does not express KIR and is developed for tumor therapy.[9][10][11][12]

Like other 'unconventional' T cell subsets bearing invariant T cell receptors (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 to produce junctional diversity and develop a memory phenotype. 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 will respond to stressed epithelial cells.

The coagulation system overlaps with the immune system. Some products of the coagulation system can contribute to the non-specific defenses by their ability to increase vascular permeability and act as chemotactic agents for phagocytic cells. In addition, some of the products of the coagulation system are directly antimicrobial. For example, beta-lysine, a protein produced by platelets during coagulation, can cause lysis of many Gram-positive bacteria by acting as a cationic detergent.[4] Many acute-phase proteins of inflammation are involved in the coagulation system.

Also increased levels of lactoferrin and transferrin inhibit bacterial growth by binding iron, an essential nutrient for bacteria.[4]

The innate immune response to infectious and sterile injury is modulated by neural circuits that control cytokine production period. The inflammatory reflex is a prototypical neural circuit that controls cytokine production in spleen.[13] Action potentials transmitted via the vagus nerve to spleen mediate the release of acetylcholine, the neurotransmitter that inhibits cytokine release by interacting with alpha7 nicotinic acetylcholine receptors (CHRNA7) expressed on cytokine-producing cells.[14] The motor arc of the inflammatory reflex is termed the cholinergic anti-inflammatory pathway.

The parts of the innate immune system have different specificity for different pathogens.

Cells of the innate immune system, in effect, prevent free growth of bacteria within the body; however, many pathogens have evolved mechanisms allowing them to evade the innate immune system.[17][18]

Evasion strategies that circumvent the innate immune system include intracellular replication, such as in Mycobacterium tuberculosis, or a protective capsule that prevents lysis by complement and by phagocytes, as in salmonella.[19]Bacteroides species are normally mutualistic bacteria, making up a substantial portion of the mammalian gastrointestinal flora.[20] Some species (B. fragilis, for example) are opportunistic pathogens, causing infections of the peritoneal cavity. These species evade the immune system through inhibition of phagocytosis by affecting the receptors that phagocytes use to engulf bacteria or by mimicking host cells so that the immune system does not recognize them as foreign. Staphylococcus aureus inhibits the ability of the phagocyte to respond to chemokine signals. Other organisms such as M. tuberculosis, Streptococcus pyogenes, and Bacillus anthracis utilize mechanisms that directly kill the phagocyte.

Bacteria and fungi may also form complex biofilms, providing protection from the cells and proteins of the immune system; recent studies indicate that such biofilms are present in many successful infections, including the chronic Pseudomonas aeruginosa and Burkholderia cenocepacia infections characteristic of cystic fibrosis.[21]

Type I interferons (IFN), secreted mainly by dendritic cells,[22] play the central role in antiviral host defense and creation of an effective antiviral state in a cell.[23] Viral components are recognized by different receptors: Toll-like receptors are located in the endosomal membrane and recognize double-stranded RNA (dsRNA), MDA5 and RIG-I receptors are located in the cytoplasm and recognize long dsRNA and phosphate-containing dsRNA respectively.[24] The viral recognition by MDA5 and RIG-I receptors in the cytoplasm induces a conformational change between the caspase-recruitment domain (CARD) and the CARD-containing adaptor MAVS. In parallel, the viral recognition by toll-like receptors in the endocytic compartments induces the activation of the adaptor protein TRIF. These two pathways converge in the recruitment and activation of the IKK/TBK-1 complex, inducing phosphorylation and homo- and hetero-dimerization of transcription factors IRF3 and IRF7. These molecules are translocated in the nucleus, where they induce IFN production with the presence of C-Jun (a particular transcription factor) and activating transcription factor 2. IFN then binds to the IFN receptors, inducing expression of hundreds of interferon-stimulated genes. This leads to production of proteins with antiviral properties, such as protein kinase R, which inhibits viral protein synthesis, or the 2,5-oligoadenylate synthetase family, which degrades viral RNA. These molecules establish an antiviral state in the cell.[23]

Some viruses are able to evade this immune system by producing molecules that interfere with the IFN production pathway. For example, the Influenza A virus produces NS1 protein, which can bind to single-stranded and double-stranded RNA, thus inhibiting type I IFN production. Influenza A virus also blocks protein kinase R activation and the establishment of the antiviral state.[25] The dengue virus also inhibits type I IFN production by blocking IRF-3 phosophorylation using NS2B3 protease complex.[26]

Bacteria (and perhaps other prokaryotic organisms), utilize a unique defense mechanism, called the restriction modification system to protect themselves from pathogens, such as bacteriophages. In this system, bacteria produce enzymes, called restriction endonucleases, that attack and destroy specific regions of the viral DNA of invading bacteriophages. Methylation of the host's own DNA marks it as "self" and prevents it from being attacked by endonucleases.[27] Restriction endonucleases and the restriction modification system exist exclusively in prokaryotes.

Invertebrates do not possess lymphocytes or an antibody-based humoral immune system, and it is likely that a multicomponent, adaptive immune system arose with the first vertebrates.[28] Nevertheless, invertebrates possess mechanisms that appear to be precursors of these aspects of vertebrate immunity. Pattern recognition receptors are proteins used by nearly all organisms to identify molecules associated with microbial pathogens. Toll-like receptors are a major class of pattern recognition receptor, that exists in all coelomates (animals with a body-cavity), including humans.[29] The complement system, as discussed above, is a biochemical cascade of the immune system that helps clear pathogens from an organism, and exists in most forms of life. Some invertebrates, including various insects, crabs, and worms utilize a modified form of the complement response known as the prophenoloxidase (proPO) system.[28]

Antimicrobial peptides are an evolutionarily conserved component of the innate immune response found among all classes of life and represent the main form of invertebrate systemic immunity. Several species of insect produce antimicrobial peptides known as defensins and cecropins.

In invertebrates, pattern recognition proteins (PRPs) trigger proteolytic cascades that degrade proteins and control many of the mechanisms of the innate immune system of invertebratesincluding hemolymph coagulation and melanization. Proteolytic cascades are important components of the invertebrate immune system because they are turned on more rapidly than other innate immune reactions because they do not rely on gene changes. Proteolytic cascades have been found to function the same in both vertebrate and invertebrates, even though different proteins are used throughout the cascades.[30]

In the hemolymph, which makes up the fluid in the circulatory system of arthropods, a gel-like fluid surrounds pathogen invaders, similar to the way blood does in other animals. There are various different proteins and mechanisms that are involved in invertebrate clotting. In crustaceans, transglutaminase from blood cells and mobile plasma proteins make up the clotting system, where the transglutaminase polymerizes 210 kDa subunits of a plasma-clotting protein. On the other hand, in the horseshoe crab species clotting system, components of proteolytic cascades are stored as inactive forms in granules of hemocytes, which are released when foreign molecules, like lipopolysaccharides enter.[30]

Members of every class of pathogen that infect humans also infect plants. Although the exact pathogenic species vary with the infected species, bacteria, fungi, viruses, nematodes, and insects can all cause plant disease. As with animals, plants attacked by insects or other pathogens use a set of complex metabolic responses that lead to the formation of defensive chemical compounds that fight infection or make the plant less attractive to insects and other herbivores.[31] (see: plant defense against herbivory).

Like invertebrates, plants neither generate antibody or T-cell responses nor possess mobile cells that detect and attack pathogens. In addition, in case of infection, parts of some plants are treated as disposable and replaceable, in ways that very few animals are able to do. Walling off or discarding a part of a plant helps stop spread of an infection.[31]

Most plant immune responses involve systemic chemical signals sent throughout a plant. Plants use pattern-recognition receptors to recognize conserved microbial signatures. This recognition triggers an immune response. The first plant receptors of conserved microbial signatures were identified in rice (XA21, 1995)[32][33] and in Arabidopsis (FLS2, 2000).[34] Plants also carry immune receptors that recognize highly variable pathogen effectors. These include the NBS-LRR class of proteins. When a part of a plant becomes infected with a microbial or viral pathogen, in case of an incompatible interaction triggered by specific elicitors, the plant produces a localized hypersensitive response (HR), in which cells at the site of infection undergo rapid programmed cell death to prevent the spread of the disease to other parts of the plant. HR has some similarities to animal pyroptosis, such as a requirement of caspase-1-like proteolytic activity of VPE, a cysteine protease that regulates cell disassembly during cell death.[35]

"Resistance" (R) proteins, encoded by R genes, are widely present in plants and detect pathogens. These proteins contain domains similar to the NOD Like Receptors and Toll-like receptors utilized in animal innate immunity. Systemic acquired resistance (SAR) is a type of defensive response that renders the entire plant resistant to a broad spectrum of infectious agents.[36] SAR involves the production of chemical messengers, such as salicylic acid or jasmonic acid. Some of these travel through the plant and signal other cells to produce defensive compounds to protect uninfected parts, e.g., leaves.[37] Salicylic acid itself, although indispensable for expression of SAR, is not the translocated signal responsible for the systemic response. Recent evidence indicates a role for jasmonates in transmission of the signal to distal portions of the plant. RNA silencing mechanisms are also important in the plant systemic response, as they can block virus replication.[38] The jasmonic acid response, is stimulated in leaves damaged by insects, and involves the production of methyl jasmonate.[31]

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Fibromyalgia and Your Eye Sight – Fibromyalgia-Symptoms.org

Wednesday, November 23rd, 2016

Vision problems can often accompany FMS. Fibromyalgia leads to changes in eyesight because it impacts the nervous system, which is the centre of sensitivity in the body.

When a person develops FMS, usually harmless objects can produce pain and sensitivity.

However symptoms are not homogenous and they can range from mild to severe.

FMS sufferers can for example develop sensitivity to stimuli such as fluorescent lights or to the light produced by a television set.

Contact lenses can cause pain and irritation, while wearing glasses can trigger mysofacial trigger points (TrPs) in the face and the neck. Pain can also be experienced in the ears, teeth and nose.

FMS can also lead to the production of a thick secretion, which subsequently impacts vision.

Night driving can be dangerous for those with FMS, as they often have trouble seeing the lights of oncoming cars.

Seasonal Affective Disorder (SAD) is another complication associated with Fibromyalgia. People with SAD need light to ward off depression, which is another common symptom of FMS.

Sicca syndrome, which leads to irritation dryness in the eyes as well as the mouth and nose, also affects vision and can make the wearing of contacts uncomfortable.

Other symptoms of FMS-related vision problems include postural dizziness, blurred or double vision, and vertigo. FMS can also result in impaired eye-hand coordination.

Beta-carotene (an anti-oxidant and precursor to vitamin A) can be very helpful in treating light sensitivity produced by FMS.

Eye exercises are also be helpful in determining whether your vision problems are a result of FMS. Put one hand on your head above your forehead; then attempt to look at your hand. Pain indicates that your TrPs are especially sensitive. Then, continuing to look up at your hand, look out from the upper corner of each eye separately.

Medications are also usually prescribed to treat eyesight complications; guaifenesin (which liquefies mucus) is a uricosuric drug th

at helps the treatment of FMS because it helps expel uric acid from the body.

For information on Chronic Mysofacial Pain Syndrome, click on the following link: Chronic Mysofacial Pain Syndrome.

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Sight $avers Family Eye Care – Optometry In Richmond, KY …

Wednesday, November 23rd, 2016

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Welcome to Sight $avers Family Eye Care in Richmond. Dr. Richard Steinhauser and the Sight $avers Family Eye Care team strive to provide the finest in optometry services. We invite you to browse our website to learn more about our optometry services, and invite you to join our patient family by scheduling an eye exam appointment at our Richmond office.

Sight $avers Family Eye Care is a full service eye and vision care provider and will take both eye emergencies as well as scheduled appointments. Patients throughout the Richmond area come to Sight $avers Family Eye Care because they know they will receive the personal attention and professional care that is our foundation. Dr. Steinhauser and our team are dedicated to keeping our patients comfortable and well-informed at all times. At Sight $avers Family Eye Care, we will explain every exam and procedure and answer all of our patient's questions. Additionally, at Sight $avers Family Eye Care, we offer vision financing options and will work with vision insurance providers to ensure good eye health and vision care for all of our patients.

Our one-on-one approach to optometry makes Dr. Steinhauser and the Sight $avers Family Eye Care staff the eye and vision care providers of choice in the Richmond area. Our Richmond optometrist offers the following services: complete eye exams, contact lenses, glasses, glaucoma testing, and pre- and post-operative care. For a complete list of services, visit our services page or call our Richmond office at 859-623-3911.

At Sight $avers Family Eye Care, we are dedicated to providing high-quality optometry services in a comfortable environment. Call us at 859-623-3911 or schedule an appointment today online.

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