StemCell Therapy

Allschwil, Switzerland July 6, 2020Idorsia Ltd (SIX: IDIA) today announced positive top-line results of the second pivotal Phase 3 study investigating 10 and 25 mg doses of its dual orexin receptor antagonist, daridorexant, in 924 adult and elderly patients (39.3% 65 years) with insomnia. The study confirms the findings of the first pivotal study, demonstrating efficacy of treatment with daridorexant on objective and subjective sleep parameters and showed positive effects on daytime functioning, with patients reporting no morning sleepiness and no evidence of rebound or withdrawal symptoms upon treatment discontinuation.

On April 20, 2020, the company reported (media release) the results of the first pivotal study with daridorexant where both 25 and 50 mg daridorexant significantly improved both sleep onset and sleep maintenance. Daridorexant 50 mg also significantly improved daytime functioning. All results were sustained over the 3 months of the trial.

In the second study, daridorexant 25 mg significantly improved sleep maintenance as measured objectively in a sleep lab by polysomnography. Daridorexant 25 mg also significantly improved subjective total sleep time as measured daily with a patient diary at home. The results were statistically significant at month 1 and at month 3 for these sleep measures, showing sustained benefit.

Furthermore, the effect of daridorexant 25mg on sleep onset and daytime functioning were numerically consistent with the effects seen in the first study. However, due to the control of the Type 1 error rate for 16 comparisons, these endpoints despite the low p values did not reach statistical significance.

The 10 mg dose of daridorexant showed numerical improvements, across all efficacy measures, of a smaller magnitude than observed on 25 mg, none of which reached statistical significance.

The results of the two large pivotal studies, testing daridorexant at three doses from 10 to 50 mg, now provide a deep understanding of its efficacy and tolerability profile. Furthermore, the similar design of the two Phase 3 studies allows for the twogroups of25 mgandplaceboto be pooledanda pre-planned analysis to be made. This pooled analysis willfurthercharacterize the effect of daridorexant.

Guy Braunstein, MD and Head of Global Clinical Development of Idorsia, commented:

I want to start with a thank you to the study participants, investigators and their support staff, and the Idorsia team for delivering another comprehensive set of robust data. I am delighted to see the replicated effect of 25 mg of daridorexant in this large confirmatory study. The consistency of the treatment effect across both studies is remarkable. I believe the fact that daridorexant improves daytime functioning is a real breakthrough for patients. I am looking forward to the integration of all aspects of the program, including the pooled data, the long-term extension data, the clinical pharmacology program, and all that we can learn from the patient reported outcome instruments. There is a lot of work for us to do as we interact with the health authorities and share the data with the scientific community.

About safety in the studyThe safety profile was consistent with the results of the first study. Treatment-emergent adverse events (TEAEs) during the double-blind study period were reported in 38.2% and 39.3% of the patients treated with 10 and 25 mg daridorexant, respectively (32.7% for placebo). The most frequent TEAEs reported over 3% incidenceand higher on 25 mg of daridorexant than placebo were nasopharyngitis, headache, somnolence and fatigue. The number of patients experiencing serious adverse events was low and balanced across treatment groups (10 mg, 3 patients; 25 mg, 3 patients; placebo, 4 patients). Based on independent blinded adjudication committee assessment, the number of patients reporting excessive daytime sleepiness as AE was low (10 mg, 1 patient; 25 mg, 4 patients; and placebo, 1 patient); 3 patients had AEs of special interest related to sleep paralysis and hallucination. No events denoting cataplexy-like events were reported or adjudicated. There was no next-morning residual effectas assessed every morning by the patients using a visual analog scale; 2 patients reported suicidal ideation (10 mg, 1 patient; 25 mg, 1 patient) with clear alternative causes; no suicide or self-injury were observed. There was no evidence of rebound insomnia, and no withdrawal symptoms upon discontinuation.

EmmanuelMignot,MD and Professor of Psychiatry and Behavioral Sciences at Stanford University, commented:The daridorexant program demonstrates the full potential of orexin receptor antagonism excellent effect and a good safety profile. It is exciting to see this, 20 years after the discovery of the role of orexin in sleep regulation. For me, the improved daytime functioning seen with daridorexant is most impressive. What is important to patients is not only to improve their night sleep but also how they feel during the day. By measuring the benefits of the drug through the day as well as through the night, the program has put patients back at the center of the equation and raised the standard for what we need to see with sleep medications. This ensures the patient need is at the center of prescription decisions when treating insomnia.

Jean-Paul Clozel, MD and Chief Executive Officer of Idorsia, commented:I was stunned by the excellent results of the first study with daridorexant, this time Im struck by the consistency of the efficacy results, including daytime functioning and the safety profile. I am very proud of the great science behind daridorexant and that Idorsia has designed and executed such a comprehensive program, focused on patients, in such a short time. I am convinced that with daridorexant, Idorsia has a unique drug which is going to have a disruptive impact on the insomnia market. The whole company is united in the effort to file the NDA with the US FDA around the end of this year and to prepare for a successful launch. There is certainly a lot of work to be done, but we are already making great progress on all fronts.

Detailed results of the Phase 3 studies will be made available through scientific disclosure at upcoming congresses and in peer-reviewed publications.

About the Phase 3 registration program

The Phase 3 registration program comprises two confirmatory studies of 3-month duration, together with a long-term extension study. Both pivotal studies are complete, having enrolled around 1,850 patients with insomnia at over 160 sites across 18 countries. As insomnia often presents later in life, around 40% of the recruited population was aged 65 years or older. The confirmatory multi-center, double-blind, randomized, placebo-controlled, parallel-group, polysomnography studies investigated three doses of daridorexant (10 mg, 25 mg, and 50 mg) on sleep and daytime functioning parameters, objectively in a sleep lab by polysomnography and subjectively with a daily patient diary at home. The impact of insomnia on patients daytime functioning was measured daily using the sleepiness domain score from the Insomnia Daytime Symptoms and Impacts Questionnaire (IDSIQ) a Patient Reported Outcome (PRO) instrument, validated according to the US Food and Drug Administration (FDA) Guidance for Industry. 806 patients decided to continue treatment in the ongoing 40-week extension study which will measure the effect of all three doses vs. placebo, generating data for long-term treatment of insomnia.

Investor webcastOn April 20, 2020, the company held an investor webcast to discuss the results of the first Phase 3 study with daridorexant. On that occasion, Martine Clozel, MD, Chief Scientific Officer presented a brief overview of the tailored drug discovery efforts that led to the synthesis of daridorexant. This was followed by Guy Braunstein providing an overview of insomnia, the objectives of the Phase 3 program, the methodologies used to measure the effect of daridorexant on patients with insomnia, and the results of the first study. This webcast is available for replay on the corporate website.

The company will hold an investor conference call and webcast to discuss the results of the second Phase 3 study with daridorexant. On the call, Guy Braunstein will present the study results, followed by a Q&A session with Jean-Paul Clozel, Guy Braunstein, and Martine Clozel.

Date: Monday July 6, 2020Time: 14:00 CEST | 13:00 BST | 08:00 EDT

Webcast participants should visit Idorsia's website http://www.idorsia.com 10-15 minutes before the webcast is due to start.

Conference call participants should start calling the number below 10-15 minutes before the conference is due to start.

Dial-in CH: +41 (0)44 580 65 22 / UK: +44 20 3009 2470 / US: +1 (877) 423-0830PIN: 24890393#

Notes to the editor

About insomniaInsomnia is a condition of overactive wake signaling that can have a profound effect on the lives of patients. Insomnia can be defined as difficulty falling asleep and / or staying asleep, occuring at least three times a week for a minimum of three months.

It is estimated that as many as one in ten people suffer from insomnia and its impact is often underestimated. In reality, it can be a distressing condition that can impair quality of life. Sleepless nights can leave people feeling irritable and out of sorts this may affect many aspects of daily life, from studying and employment to social activities and relationships. People who suffer from insomnia may lack the energy or motivation to exercise or to take part in social activities. It can also have a significant economic impact as it increases the risk of accident and injury on the road or in the workplace, and is a leading cause of absenteeism and reduced productivity at work. People with insomnia are more likely to experience feeling down or depressed, lack concentration, and suffer from poor energy levels during the day compared with people who sleep well. In addition, worrying about sleep can cause stress and may lead to negative thought patterns which may in turn make it more difficult to sleep, setting up a vicious circle. Chronic insomnia is associated with cardiovascular and cerebrovascular diseases, and increased mortality.

The goal of treatments for insomnia is to improve sleep quality and quantity, as well as reducing insomnia-related impaired daytime functioning, while avoiding adverse events and next morning residual effect. Current treatment of insomnia includes cognitive behavioral therapy, sleep hygiene recommendations, and pharmacotherapy. The most widely prescribed products on the market that are indicated for insomnia enhance the effects of gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the central nervous system. Such medications are only approved for short-term use and are associated with side effects such as next-morning residual effects, anterograde amnesia, and risk of tolerance and dependence.

About the orexin systemWake and sleep signaling is regulated by intricate neural circuitry in the brain. One key component of this process is the orexin system, which helps promote and consolidate wakefulness. There are two forms of orexin neuropeptides Orexin A and OrexinB. Orexin promotes wakefulness through its receptors OX1R and OX2R. In combination, these neuropeptides and receptors comprise the orexin system. The orexin system stimulates target neurons in the wake system leading to the release of several chemicals (Dopamine, Serotonin, Histamine, Acetylcholine, Norepinephrine) which promote wakefulness. Under normal circumstances, orexin levels rise throughout the day as wakefulness is promoted and then consolidated and fall at night. Overactivity of the orexin system is thought to be an important driver of insomnia.

Idorsias research team has been working on the science of orexin and orexin receptors since they were first described in 1998. The teams initial work led to the conclusion that antagonism of the orexin system was the key to preserving a natural sleep architecture for patients with insomnia. With this as the target the team started to design a dual antagonist with a rapid effect, and a duration of action sufficient for the night but short enough to avoid any negative residual activity the following morning at optimally effective doses.

About dual orexin receptor antagonismDual orexin receptor antagonists or DORAs are an entirely different approach to treating insomnia than previous drug classes, turning down overactive wakefulness by blocking the activity of orexin. DORAs specifically target the orexin system by competitively binding with both receptors and thereby reversibly blocking the activity of orexin. It is hypothesized that blocking orexin receptors reduces the downstream activity of the other wake promoting neurotransmitters that are overactive in insomnia, leading to the clinical efficacy demonstrated by orexin receptor antagonists.

Data supporting daridorexant in insomnia Results of the first Phase 3 study, investigating daridorexant doses 25 and 50mg, were reported in April 2020. The study demonstrated efficacy of treatment with daridorexant on objective and subjective sleep parameters and daytime functoning with no residual effect in the morning, and no evidence of rebound or withdrawal symptoms upon treatment discontinuation.

Daridorexant at both 25 and 50 mg significantly improved sleep onset and sleep maintenance as measured objectively in a sleep lab by polysomnography. Daridorexant also significantly improved subjective total sleep time as measured daily with a patient diary at home. The results were consistently statistically significant at month 1 and at month 3, indicating sustained benefit. Furthermore, treatment with daridorexant improved patients daytime functioning from baseline at month 1 and month 3.

The rate of adverse events was comparable between placebo and daridorexant at both treatment doses. Treatment-emergent adverse events (TEAEs) during the double-blind study period were reported in 37.7% and 37.7% of the patients treated with 25 and 50 mg daridorexant, respectively (34.0% for placebo). The most frequent TEAE reported over 3% incidence and higher than placebo was nasopharyngitis, headache.

Prior to the Phase 3 program, the safety and efficacy of daridorexant in adult and elderly patients with insomnia was evaluated in a comprehensive Phase 2 program, comprising two studies, one of which included zolpidem 10 mg as an active reference. Both studies showed the desired effect on sleep maintenance and onset, with a significant dose-response relationship; treatment was generally well tolerated.

A comprehensive clinical pharmacology program is being conducted totaling approximately 20 studies and including, amongst others, studies assessing abuse liability, drug-drug interactions, next-morning driving, the effect of daridorexant on respiratory function in patients with chronic obstructive pulmonary disease (COPD) or obstructive sleep apnea (OSA), and the pharmacokinetics of daridorexant in patients with liver and renal impairment.

EmmanuelMignot,MD and Professor of Psychiatry and Behavioral Sciences at Stanford University He is a former student of the Ecole Normale Superieure (Ulm, Paris, France) and received his M.D. and Ph.D. from Paris V and VI University in France. He practiced medicine in France for several years before joining Stanford as a faculty member in 1991 and was named Director of the Stanford Center for Narcolepsy in 1993. Dr. Mignot was named the Craig Reynolds Professor of Psychiatry and Behavioral Sciences in 2001. He served as the Director of the Stanford Center of Sleep Sciences and Medicine from 2009 to 2019.

Dr. Mignot is internationally recognized for discovering the cause of narcolepsy. His findings led to the development of new hypnotics that block the hypocretin (orexin) receptor and is likely to have other therapeutic applications as well. His research also demonstrated that narcolepsy is a selective autoimmune disease of the hypocretin system showing the involvement of molecular mimicry in humans with influenza A.

He has received numerous research grants and honors including National Sleep Foundation and National Institute of Health Research Awards, Howard Hughes Medical Institute Investigator and McKnight Neuroscience awards, the Narcolepsy Network professional service award, the Drs. C. and F. Demuth 11th Award for Young Investigators in the Neurosciences, the WC Dement Academic Achievement Award in sleep disorders medicine, the CINP and ACNP awards in neuropharmacology and the Jacobaeus prize.

Dr. Mignot is an elected member of the Association of American Physicians, the Institute of Medicine, and of the National Academy of Sciences (USA). He is the co-author of more than 200 original scientific publications, and he serves on the editorial board of scientific journals in the field of sleep and biology research. Dr. Mignot is an active member of several professional and governmental organizations. He has served as President of the Sleep Research Society, Chair of the National Center on Sleep Disorders Research Advisory board of the National institutes of Health, and Chair of the Board of Scientific Counselors of the National Institute of Mental Health.

Most of Dr. Mignot's current research focuses on the neurobiology, genetics and immunology of narcolepsy, a disorder caused by hypocretin (orexin) cell loss, with indirect interest in the neuroimmunology of other brain disorders. His laboratory uses state of the art human genetics techniques, such as genome wide association, exome or whole genome sequencing in the study of human sleep and sleep disorders, with parallel studies in animal models. His laboratory is also interested in web-based assessments of sleep disorders, computer-based processing of polysomnography (PSG), and outcomes research. Dr. Mignot serves as a consultant to Idorsia.

References

About IdorsiaIdorsia Ltd is reaching out for more - We have more ideas, we see more opportunities and we want to help more patients. In order to achieve this, we will develop Idorsia into one of Europes leading biopharmaceutical companies, with a strong scientific core.

Headquartered in Switzerland - a biotech-hub of Europe - Idorsia is specialized in the discovery and development of small molecules, to transform the horizon of therapeutic options. Idorsia has a broad portfolio of innovative drugs in the pipeline, an experienced team, a fully-functional research center, and a strong balance sheet the ideal constellation to bringing R&D efforts to business success.

Idorsia was listed on the SIX Swiss Exchange (ticker symbol: IDIA) in June 2017 and has over 800 highly qualified specialists dedicated to realizing our ambitious targets.

For further information, please contactAndrew C. WeissSenior Vice President, Head of Investor Relations & Corporate CommunicationsIdorsia Pharmaceuticals Ltd, Hegenheimermattweg 91, CH-4123 Allschwil+41 58 844 10 10www.idorsia.com

The above information contains certain "forward-looking statements", relating to the company's business, which can be identified by the use of forward-looking terminology such as "estimates", "believes", "expects", "may", "are expected to", "will", "will continue", "should", "would be", "seeks", "pending" or "anticipates" or similar expressions, or by discussions of strategy, plans or intentions. Such statements include descriptions of the company's investment and research and development programs and anticipated expenditures in connection therewith, descriptions of new products expected to be introduced by the company and anticipated customer demand for such products and products in the company's existing portfolio. Such statements reflect the current views of the company with respect to future events and are subject to certain risks, uncertainties and assumptions. Many factors could cause the actual results, performance or achievements of the company to be materially different from any future results, performances or achievements that may be expressed or implied by such forward-looking statements. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those described herein as anticipated, believed, estimated or expected.

Read more:
Idorsia announces positive results in the second Phase 3 study of daridorexant - GlobeNewswire

Mutations in either protein CLN6 or CLN8 result in two forms of Batten disease with remarkably similar clinical features. It turns out, as recently shown by the laboratory of Dr. Marco Sardiello, that both proteins work together to equip lysosomes, the waste-disposal hubs of the cell, of the much needed enzymes that process cellular waste.

Batten disease is a family of 13 rare, genetically distinct conditions. Collectively, they are the most prevalent cause of neurodegenerative disease in children, affecting 1 in 12,500 live births in the U.S. One of the Batten disease genes is CLN6. How mutations in this gene lead to the disease has been a mystery, but a study led by researchers at Baylor College of Medicine and published in the Journal of Clinical Investigation reveals how defective CLN6 can result in Batten disease.

People with Batten disease have problems with their cells ability to clear cellular waste, which then accumulates to toxic levels, said first author Dr. Lakshya Bajaj, who was working on this project while a doctorate student in the Sardiello lab at Baylor. Bajaj is currently a post-doctoral associate at Harvard Medical School.

In cells, lysosomes process cellular waste. They are sacs containing enzymes, a type of proteins that break down waste products into its constituent components that the cell can recycle or discard. In Batten disease caused by mutations in CLN6, the lysosomes do not process waste effectively for unknown reasons. This results in waste accumulation. Batten disease is a type of lysosomal storage disorder. Although all types of cells can be affected by defects in lysosomal waste management, brain cells, neurons, are particularly susceptible.

Waste accumulation in neurons perturbs many cellular processes and eventually results in cell death. This leads to the progressive degeneration of motor, physical and intellectual abilities observed in Batten disease patients, Bajaj said.

The connection of CLN6 with Batten disease was a bit of a mystery. This protein is not found in lysosomes, but in the endoplasmic reticulum, a structure inside cells where proteins, including lysosomal enzymes, are made. The endoplasmic reticulum is separate from the lysosomes. So, how do defects in a protein located outside of the lysosomes interfere with lysosomal function?

The Sardiello lab had previously solved a similar mystery involving CLN8, another protein located in the endoplasmic reticulum and whose mutations also cause a type of Batten disease.

We showed that CNL8 assists on the exit of lysosomal enzymes from the endoplasmic reticulum en route to the lysosomes. When CLN8 is defective, the transport of enzymes from their place of synthesis to the final destination is deficient and the lysosomes end up having fewer enzymes to work with, said Sardiello, associate professor of molecular and human genetics at Baylor and corresponding author of this work.

The clinical manifestations of Batten disease caused by CLN8 mutations and those of Batten disease due to defective CLN6 are remarkably similar. This and other evidence led the researchers to suspect that CLN6 and CLN8 might be working together.

Their investigations revealed that CLN6 and CLN8 do interact with each other forming a molecular complex that collects lysosomal enzymes at the endoplasmic reticulum and mediates their trafficking towards the lysosomes.

We propose that CLN8 and CLN6 together herd the enzymes into a hub, a sort of bus stop. Then, CLN8 escorts the enzymes on the bus en route to the lysosomes, while CLN6 remains at the bus stop. CLN8 returns to the bus stop after delivering the enzymes, and they repeat the process, Bajaj said. When CLN6 is defective, the enzymes are not effectively herded into the bus stop and fewer are transported to the lysosomes.

The researchers are interested in finding whether other factors are involved in transporting enzymes to the lysosomes. For instance, whether there are other bus conductors or herders of lysosomal enzymes involved that, if defective, may also contribute to Batten disease.

Other contributors to this work include Jaiprakash Sharma, Alberto di Ronza, Pengcheng Zhang, Aiden Eblimit, Rituraj Pal, Dany Roman, John R. Collette, Clarissa Booth, Kevin T. Chang, Richard N. Sifers, Sung Y. Jung, Jill M. Weimer, Rui Chen and Randy W. Schekman. The authors are affiliated with one or more of the following institutions: Baylor College of Medicine; Texas Childrens Hospital; University of California, Berkeley; Sanford Research, Sioux Falls, South Dakota; and Sanford School of Medicine at the University of South Dakota.

This work was supported by NIH grants NS079618 and GM127492 and grants from the Gwenyth Gray Foundation, Beyond Batten Disease Foundation and NCL-Stiftung. This project was supported in part by IDDRC grant number 1U54 HD083092 from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, the Integrated Microscopy Core and the Proteomics Core at Baylor College of Medicine with funding from NIH (DK56338, and CA125123), CPRIT (RP150578, RP170719), the Dan L Duncan Comprehensive Cancer Center and the John S. Dunn Gulf Coast Consortium for Chemical Genomics.

By Ana Mara Rodrguez, Ph.D.

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Image of the Month: Locating molecular players in Batten disease - Baylor College of Medicine News

Structural biology education commonly employs molecular visualization software, such as PyMol, RasMol, and VMD, to allow students to appreciate structure-function relationships in biomolecules. In on-ground, classroom-based education, these programs are commonly used on University-owned devices with software preinstalled. Remote education typically involves the use of student-owned devices, which complicates the use of such software, owing to the fact that (a) student devices have differing configurations (e.g., Windows vs MacOS) and processing power, and (b) not all student devices are suitable for use with such software. Smartphones are near-ubiquitous devices, with smartphone ownership exceeding personal computer ownership, according to a recent survey. Here, we show the use of a smartphone-based augmented reality app, Augment, in a structural biology classroom exercise, which students installed independently without IT support. Post-lab attitudinal survey results indicate positive student experiences with this app. Based on our experiences, we suggest that smartphone-based molecular visualization software, such as that used in this exercise, is a powerful educational tool that is particularly well-suited for use in remote education. 2020 International Union of Biochemistry and Molecular Biology.

PubMed

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Rapid deployment of smartphone-based augmented reality tools for field and online education in structural biology. - Physician's Weekly

At the School of Health and Rehabilitation Sciences Wellness Pavilion at the Universitys Community Engagement Center in Homewood, members and neighborhood residents will learn to take control of their health.

A campuswide collaboration at the University of Pittsburgh at Johnstown aims to enhance awareness and engagement related to diversity and inclusion, create safe spaces and foster a supportive environment that extends to neighboring communities.

The School of Laws Immigration Law Clinic will establish an asylum clinic to provide forensic evaluations for asylum seekers, train health care providers to perform them and educate medical students about the process of asylum.

These are just a few of the 11 projects named 2020 Pitt Seed Grant recipients, which represent a wide range of research, initiatives, individuals and organizations within the University and the six goals within The Plan for Pitt.

Our call for proposals received a great responseand I congratulate this years grantees. Many of the projects funded this year reflect our continued commitment to social justice and active outreach to communities in need, said Ann E. Cudd, provost and senior vice chancellor. We have committed support to projects that reflect our deep interest in further exploring ways to evaluate teaching effectiveness, as well as to probe innovations in both the advising and remote learning spaces. All of this is important workand I am very excited to support these extremely interesting initiatives.

The Pitt Seed Project Initiative received more than 60 letters of intent and 45 total applications, including 30 from faculty and 15 from staff. Sixty-eight volunteers from various units across Pitt participated in reviewing grant applications. Their recommendations were reviewed and endorsed by Provost Cudd before being presented to and approved by Chancellor Patrick Gallagher.

The 11 proposal summaries and their designated points of contactare:

Brandon Barber, BioE design, innovation and outreach coordinatorSwanson School of Engineering

The purpose of the XProjects Applied Research XPloration (XARX) is to further develop the Pitt XProject programs internal research collaborations and explore new applications of ongoing research, while simultaneously providing students with cocurricular design/engineering experiences that go beyond the classroom. The diverse multidisciplinary teams employ a rigorous process and a proven suite of tools to navigate fast-paced project work, all while gaining practice with project management, prototyping and negotiating stakeholder-client relationships. This innovative approach to design education also creates an environment where students can gain the experience they need to more confidently approach and define complex problems.

April Belback, director for undergraduate advising and mentoringOffice of the Provost

The University ofPittsburghAdvisingCertification andTraining Program (Pitt-ACT)is a large-scale collaboration between the Office of the Provost Undergraduate Studies Academic Innovation Team, the Center for Teaching and Learning and undergraduate academic and advising units across the University. Designed for faculty and staff at Pitt who work with students in an advising and mentoring capacity, the project creates a suite of online onboarding and training materials to help standardize the practice of advising across Pitt.

Kevin Binning, assistant professorDepartment of Psychology in the Kenneth P. Dietrich School of Arts and Sciences

The proposed project will leverage existing institutional datasets to develop, validate and standardize new methods for assessing teaching effectiveness. In particular, the project will quantify the impact that particular instructors have on student outcomes, including subsequent retention, major choice and academic performance. This will be used to help Pitt improve by helping instructors understand the effectiveness of their teaching practices while also providing standardized benchmarks to evaluate the effectiveness of educational interventions.

Josh Cannon, scholar mentorUniversity Honors College

This project seeks to raise the number of National Science Foundation Graduate Research Fellowship Project (NSF GRFP) winners among Pitt's graduate and undergraduate (seniors) populations. The project collaborators will host a series of workshops that provide strategies and guidance on application preparation, as well as bring in faculty and advanced graduate students to provide their own insights and expertise to applicants. Scholars in the appropriate fields will provide draft review services for each application. The seed grant will support this project for the 2020-2021 and 2021-2022 academic years.

Vaughn Cooper, professorDepartment of Microbiology and Molecular Genetics in the School of Medicine

The EvolvingSTEM program addresses the critical need for engaging, equitable learning practices that support student success and promote a well-educated, diverse STEM workforce. Pitt Seed funding will support efforts to provide an after-school program to underserved students from the Pittsburgh Public School system at the Community Engagement Center in Homewoods modern laboratory space. Students will design, conduct and analyze their own bacterial evolution experiment under the guidance of Pitt undergraduate mentors. Student projects will utilize cutting-edge laboratory and computational techniques, including bioinformatic analyses of genomic DNA sequencing data.

Tuangtip Klinbubpa, associate professorDepartment of English at the University of Pittsburgh at Johnstown

This project is a campuswide, collaborative, multidisciplinary, personalized effort that will take place at Pitt-Johnstown and extend to the neighboring communities. The project aimsto enhance awareness and engagement related to diversity and inclusion,sustainably engage Pitt-Johnstown and the neighboring communities in promoting diversity and inclusionand create safe spaces and a supportive environment for all.

Lingfeng Liu, lab instructorDepartment of Chemistry in the Dietrich School of Arts and Sciences

We will bring ECoach, a personalized coaching tool developed at the University of Michigan, to Pitt. ECoach allows professors to personalize feedback to students to support success in large enrollment STEM courses.

Channing Moreland, Wellness Pavilion directorSchool of Health and Rehabilitation Sciences

The School of Health and Rehabilitation Sciences Wellness Pavilion is a student-led space inside The W.E.L.L (Wellness, Education, Living & Learning) at Pitts Community Engagement Center in Homewood. This community-engaged and interdisciplinary space was designed for Homewood and surrounding communities residents to feel heard and empowered to improve, maintain and take control of their health and wellness. To do so, the space provides free evidence-based health and wellness services and programs for residents across the lifespan. Moreover, the pavilion is committed to fostering healthy relationships between students, faculty, staff and community members via interprofessional collaborations and person-centered approaches to care. The Wellness Pavilion intends to maintain and initiate mutually beneficial partnerships within Homewood and surrounding communities to fortify University-specific strategic priorities. Community-based learning will occur at the pavilion, which will advance teaching practices, appeal to diverse applicants seeking admission and/or employment at the University and positively impact the student experience.

Joseph Samosky, assistant professorDepartment of Bioengineering in the Swanson School of Engineering

Classroom to Communityis forstudentswho want to creatively design andinvent solutions for real-worldproblems and needs.Space, resources and mentorship will be provided for students to learn powerfulhuman-centereddesign tools and methods, build bridges with community partners and create diverse teams fromdifferent backgrounds, majors and schools. Together we will co-createan engaging, multidisciplinary experience for students to explore, envision, share and learn from faculty partners and each other as they translate their ideas into something new in the world that benefits others.The projects ultimate goals are to foster a culture of innovation, agency and service; empower students to discover their creative potential; and become agents of positive change.

Sheila Velez Martinez, Jack and Lovell Olender Professor of Refugee, Asylum, and Immigration Lawand director of clinical programsSchool of Law

The Immigration Law Clinic and students and faculty at the School of Medicine are engaged in an effort to establish an asylum clinic that would provide forensic evaluations for asylum seekers. By documenting the physical and psychological sequelae of human rights abuses and submitting a medical-legal affidavit to court, physicians and students can make a difference in whether these individuals are granted asylum or other relief from deportation. The clinic will also train health care providers to perform asylum evaluations and educate medical students about the process of asylum and the role of health care providers in asylum. Shadowing asylum evaluations not only exposes students to the unique points of view of human rights atrocity survivors, but also allows them to observe and practice trauma-informed interviewing and cross-cultural communication.

Anna Wang-Erickson, assistant professor and associate directorInstitute for Infection, Immunity, and Inflammation in Children (i4Kids), Department of Pediatrics in the School of Medicine

Speaking and networking at conferences is crucial to career advancement, and these opportunities often create a need for occasional nonroutine dependent care. This burden disproportionately affects women and people early in their careers. This project aims to create University-wide infrastructure and policies to support the career and professional network development of faculty, staff, postdoctoral fellows and graduate students through occasional nonroutine dependent care support. Additionally, it will evaluate the efficacy and impact of the new infrastructure and policies to improve efforts in building professional networks and promoting work done at Pitt at the international level.

Read more here:
Eleven Faculty and Staff Proposals Receive Pitt Seed Funding - UPJ Athletics

A comprehensiveGlobal Point of Care Molecular Diagnostics Marketanalysis report serves to be an ideal solution for better understanding of the market and high business growth. It has become the requisite of this rapidly changing market place to take up such marker report that makes aware about the market conditions around. This market report comprises of an array of factors that have an influence on the market and industry which are industry insight and critical success factors (CSFs), market segmentation and value chain analysis, industry dynamics, drivers, restraints, key opportunities, technology and application outlook, country-level and regional analysis, competitive landscape, company market share analysis and key company profiles.

Market Analysis:

TheGlobal Point of Care Molecular Diagnostics Marketis estimated to rise from the value of USD 627.6 million in 2017 to an estimated value of USD 1933.2 million by 2025, registering a CAGR of 15.1% during the forecast period of 2018-2025. This growth can be attributed to the rising cases of infectious diseases, and the growing demand for approved Point of Care Molecular Diagnostic tests.

Key Market Competitors:Few of the major competitors currently working on the Point of Care Molecular Diagnostics Market are Agilent Technologies Inc., Abbott, F. Hoffmann-La Roche Ltd., Illumina Inc., Hologic Inc., QIAGEN, Myriad Genetics, Cepheid, Genomic Health, GenePOC Inc., DxNA LLC., Binx Health Inc., Spartan Bioscience Inc., Biocartis, Beckman Coulter Inc., Johnson & Johnson Services Inc., Medtronic, Siemens Healthcare GmbH, Grifols S.A., Abaxis, Bayer AG, bioMrieux SA, Bio-Rad Laboratories Inc., Danaher, OraSure Technologies Inc., BD, Sysmex Corporation, Quidel Corporation, and Meridian Bioscience Inc.

Get Sample Report + All Related Graphs & Charts @https://www.databridgemarketresearch.com/request-a-sample/?dbmr=global-point-of-care-molecular-diagnostics-market

Global Point of Care Molecular Diagnostics Market,By Product (Assays & Kits, Instruments/Analyzers, Services & Software), Application (Respiratory Diseases, Sexually Transmitted Diseases, Hospital-acquired Infection, Oncology, Hepatitis, Others), Technology (Polymerase Chain Reaction, In-Situ Hybridization, Chips and Microarrays, Mass Spectrometry, Sequencing, Isothermal Amplification, Others), End-User (Physician Offices, Hospitals, Research Institutes, Others), Geography (North America, South America, Europe, Asia-Pacific, Middle East & Africa) Industry Trends & Forecast to 2025

Competitive Analysis:

The Global Point of Care Molecular Diagnostics Market is highly fragmented and the major players have used various strategies such as new product launches, expansions, agreements, joint ventures, partnerships, acquisitions, and others to increase their footprints in this market. The report includes market shares of Point of Care Molecular Diagnostics market for global, Europe, North America, Asia Pacific, South America and Middle East & Africa.

Market Definition:Global Point of Care Molecular Diagnostics Market

Point of Care Molecular Diagnostics is diagnostic equipment which is used to determine the cause of infectious disease causing agents. These machines/equipments help determine the accurate cause of these diseases in a timely manner, which is of utmost importance when dealing with these kind of diseases and also to implement the correct course of action.

The advancements and developments in the diagnostics market is attributed to the fact that the healthcare industry is focusing on detection and diagnosis in place of pharmaceuticals and medicines, to prevent the development of the diseases. This trend has directly affected the market growth and is helping the market to grow significantly.

North America had the highest revenue share of around 40% of the market.

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Market Drivers:

Market Restraints:

Segmentation:Global Point of Care Molecular Diagnostics Market

Key Developments in the Market:Global Point of Care Molecular Diagnostics Market

Key Insights in the report:

Market Segmentation:-

To comprehend Global Point of Care Molecular Diagnostics market dynamics in the world mainly, the worldwide Point of Care Molecular Diagnostics market is analyzed across major global regions.

Actual Numbers & In-Depth Analysis, Business opportunities, Market Size Estimation Available in Full Report.

Some of the Major Highlights of TOC covers:

Chapter 1: Methodology & Scope

Definition and forecast parameters

Methodology and forecast parameters

Data Sources

Chapter 2: Executive Summary

Business trends

Regional trends

Product trends

End-use trends

Chapter 3: Industry Insights

Industry segmentation

Industry landscape

Vendor matrix

Technological and innovation landscape

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Point of Care Molecular Diagnostics Market report effectively provides required features of the global market for the population and for the business looking people for mergers & acquisitions, making investments, new vendors or concerned in searching for the appreciated global market research facilities. It offers sample on the size, offer, and development rate of the market. The Point of Care Molecular Diagnostics report provides the complete structure and fundamental overview of the industry market.

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POINT OF CARE MOLECULAR DIAGNOSTICS MARKET EXPECTATION SURGES WITH RISING DEMAND AND CHANGING TRENDS AGILENT TECHNOLOGIES INC., ABBOTT, F. HOFFMANN-LA...

DUBLIN--(BUSINESS WIRE)--The "Array Instruments Market: Global Industry Trends, Share, Size, Growth, Opportunity and Forecast 2020-2025" report has been added to ResearchAndMarkets.com's offering.

The global array instruments market is currently witnessing strong growth. An array instrument is used in laboratories for quantitatively and simultaneously monitoring the expression of multiple genes. It contains numerous small representative tissue samples from hundreds of different cases, which are assembled on a single histologic slide.

The high-throughput approach of the array instrument aids in locating chromosomal expressions and mutations in a genotype, as well as measuring and detecting gene expressions at the messenger RNA (mRNA) or protein level. As a result, it finds applications in molecular and cell biology, genetics, molecular pathology, and for synthesizing and sequencing nucleic acids.

The increasing prevalence of chronic diseases, in confluence with the emerging need for their early detection and diagnosis, represents one of the key factors driving the global array instruments market growth. In addition to this, governments of several countries are investing in the improvement of healthcare facilities, which in turn, is positively influencing the demand for array instruments, especially in emerging economies.

Furthermore, these instruments can be incorporated with a wide range of technologies, owing to which they find applications in different areas of research, such as life sciences and drug discovery. For instance, deoxyribonucleic acid (DNA) microarrays are used for examining changes in gene expression by fluorescent labeling of complementary DNA, whereas tissue microarrays aid in identifying new diagnostic and prognostic markers and targeting cancer in human beings. Other than this, the introduction of advanced technologies, such as microarray-based comparative genomic hybridization (array CGH), is expected to bolster the market growth in the upcoming years. Looking forward, the publisher expects the market to register a CAGR of around 7% during 2020-2025.

Companies Mentioned

Key Questions Answered in this Report:

Key Topics Covered:

1 Preface

2 Scope and Methodology

3 Executive Summary

4 Introduction

4.1 Overview

4.2 Key Industry Trends

5 Global Array Instruments Market

5.1 Market Overview

5.2 Market Performance

5.3 Market Forecast

6 Market Breakup by Application

6.1 Molecular Biology

6.1.1 Market Trends

6.1.2 Market Forecast

6.2 Cell Biology

6.2.1 Market Trends

6.2.2 Market Forecast

6.3 Genetics

6.3.1 Market Trends

6.3.2 Market Forecast

6.4 Molecular Pathology

6.4.1 Market Trends

6.4.2 Market Forecast

6.5 Others

6.5.1 Market Trends

6.5.2 Market Forecast

7 Market Breakup by Technology

7.1 DNA Microarrays

7.1.1 Market Trends

7.1.2 Market Forecast

7.2 Protein Microarrays

7.2.1 Market Trends

7.2.2 Market Forecast

7.3 Cellular Microarrays

7.3.1 Market Trends

7.3.2 Market Forecast

7.4 Tissue Microarrays

7.4.1 Market Trends

7.4.2 Market Forecast

8 Market Breakup by End-User

8.1 Research and Development Laboratories

8.1.1 Market Trends

8.1.2 Market Forecast

8.2 Clinical Diagnostic Labs

8.2.1 Market Trends

8.2.2 Market Forecast

8.3 Agriculture Research Centers

8.3.1 Market Trends

8.3.2 Market Forecast

8.4 Veterinary Laboratories

8.4.1 Market Trends

8.4.2 Market Forecast

8.5 Forensic Centers

8.5.1 Market Trends

8.5.2 Market Forecast

8.6 Others

8.6.1 Market Trends

8.6.2 Market Forecast

9 Market Breakup by Region

9.1 North America

9.2 Asia Pacific

9.3 Europe

9.4 Latin America

9.5 Middle East and Africa

10 SWOT Analysis

11 Value Chain Analysis

12 Porters Five Forces Analysis

13 Price Indicators

14 Competitive Landscape

14.1 Market Structure

14.2 Key Players

14.3 Profiles of Key Players

For more information about this report visit https://www.researchandmarkets.com/r/f83v23

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Outlook on the Array Instruments Global Industry to 2025 - Featuring Affymetrix, Agilent Technologies & Arrayit Among Others -...

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The appearance at the end of 2019 of a new coronavirus and its rapid spread throughout the world until it became a pandemic, has put the scientific community to work with an intensity rarely observed.

Although currently the main international research is focused on the search for the vaccine, the mass immunization as the only way to stop such a contagious virus, another question arises from a characteristic of the virus, or rather how each person responds to the contagion: Why do some die from COVID-19 and others dont get to feel the slightest symptom?

The answer may lie in genetics; thats why Cuba launched a research that takes this factor into account in the response of those who suffered from the disease and those who have already been discharged.

According to the director of the National Center for Medical Genetics, Beatriz Marcheco, the project includes clinical-epidemiological, laboratory, basically hematological, immunological, and DNA studies.

The research began its clinical stage in early June, in the provinces of Pinar del Ro, Cienfuegos and Las Tunas, as well as the municipality of La Lisa, in Havana.

The study seeks to find out the blood group and factor of each individual and to study the subpopulations of lymphocytes that participate in the immune response, using flow cytometry and Elisa assays, explained the specialist in an interview with Granma daily.

Cuba studying genetic factors of patients recovered from COVID-19

After taking the blood sample, these are taken to the laboratories of the National Center for Medical Genetics to submit them to the tests related to the study, in which the Immunoassay Center also participatesthe Immunoglobulin g test is done there to identify if the person has specific antibodies against the SARS-CoV-2 virusand the Center for Molecular Immunology.

The results could help scientists to characterize all the factors related to the incidence of the disease, its lethality and clinical and therapeutic approach in each case.

If, for example, an individual is identified as being more vulnerable to symptoms or severity, strategies to prevent such severity could be applied with early therapeutic interventions, Marcheco added.

By identifying the genetic factors related to clinical severity, we will be taking a significant step at the same time in the objective of developing personalized treatments that respond to individual genetic characteristics, strengthening the implementation of population-based prevention strategies, she explained.

The studies we are conducting also allow us to appreciate how each person is recovering individually from a disease that strongly damages the immune system. Therefore, the research project contains actions that are part of the strategy of our health system in the post-COVID-19 stage of each patient, she said.

The screening also includes the study of a first-degree relative (mother, father, son or daughter, brother or sister) who lives with the positive case and was exposed to the virus, but had no symptoms nor was positive for COVID-19.

The study of these subjects can be very useful in identifying protective factors against the virus and that is also important in terms of prevention, the scientist concluded.

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In what does Cuba's genetic study of patients recovered from COVID-19 consist of? - OnCubaNews

Earlier this year in collaboration with Cambridge University Press, we launched a new open-access scientific journal, aimed at providing an interdisciplinary forum for high quality research on ground-breaking discoveries and predictions in quantitative plant science.

The journal, Quantitative Plant Biology aims to publish papers that enhance our quantitative understanding of how plants function from a physiological and evolutionary perspective.

We asked Editor-in-Chief Dr Olivier Hamant his thoughts on why this new journal is important and how taking a quantitative approach can generate interesting questions and answer them accurately.

Science, is based around finding answers to questions.

First you have to identify what question to ask. Then, when you have a question, you need to develop a strategy around how to answer it.

As scientists, we tend to spend a lot of time on the strategy and less time on finding the right questions to ask.

So, the first question to ask is, what makes a good question?

Often a good question is a simple question. So, what makes a simple question?

A simple question is one that;

Examples of this can be found throughout scientific history, for example when Gregor Mendel asked the simple question; how does heredity work? His attempts to answer this question opened up the new research area; genetics.

Within the broad field of genetics, in my own research we ask the question; how do genes relate to shape? To answer that question, we needed to think outside the discipline, adding mechanics, physics and mathematics. By doing so, we see how genes and proteins are affecting the mechanics of the cells, in turn affecting the shape of the cells and the tissues. In turn, a shape can then affect the gene, through mechanical forces, but also through biochemistry. Altogether, this created a new field of research that some call morphodynamics.

This is what the new journal Quantitative Plant Biology is all about; taking simple questions and trying to address them by formalising an answer. The mathematical formalisation is really important to getting to the bottom of the question and this is what the journal is about.

This is very timely, because we are generating a lot of data at the moment, be it bioimaging, omics, or virtual data we have a lot of data but we need to make sense of it. The quantitative approach is one way to do it.

Finally, you start with a simple question and from that many other questions emerge. By adopting a quantitative approach, we can;

Our brains, as any optical illusion demonstrates, are limited and, as many studies have shown, we are subject to several cognitive biases. This can be problematic as scientists, because we are analysing our data through the lens of our biases.

For example, we are innately conservative and it is easier to stick to what we know than try something new. It is therefore hard to go against established dogma. As Max Planck said; A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die and a new generation grows up that are familiar with it.

Similarly, as humans we struggle with thinking about systems and understanding feedback. For example, take the Cathy Freeway in Houston, Texas, which suffered from heavy traffic jams. Human intuition suggests that if you want to solve the simple question of a traffic jam, you can add another lane to the road and that will alleviate the congestion. However, if you add more lanes, what you actually do is make the road more attractive, meaning more traffic uses them and the jams get worse. This is known as the Braess Paradox. Unable to learn this lesson, planners continued to add lanes to try and relieve the increasing jams and currently the Cathy Freeway has 26 lanes and the jams are as bad as ever.

We can apply the Braess Paradox to food security. A simple solution to food security would be to increase food production. However, there is increasing evidence that if you increase production, you increase the problems associated with distribution and in-turn all you ultimately produce is more food waste.

The quantitative approach provides a way to go around these biases, because it allows us to address the questions in an unbiased way, by trusting the data.

Quantitative approaches also allow us to maximise the output of another revolution; the rise of citizen science, which allows us to dramatically increase our sample sizes and can see huge heterogenous datasets generated from all over the world.

That is why I am really excited to be part of this new Quantitative Plant Biology journal. I really believe it will stimulate effort in the plant community, both to formalise answers to questions and to inspire new questions and new fields of research.

Dr Hamant, is an INRAE Director of research at the RDP institute at ENS de Lyon. A biologist by profession, he tries to understand how plants use forces to control their development, by combining molecular and cellular biology, mechanics and modelling approaches.

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How to know what questions to ask; taking an quantitative approach - The John Innes Centre

DUBLIN--(BUSINESS WIRE)--The "Relapsed or Refractory Mycosis Fungoides (MF) and Szary Syndrome (SS) - Pipeline Insight, 2020" drug pipelines has been added to ResearchAndMarkets.com's offering.

This report outlays comprehensive insights of present clinical development scenario and growth prospects across the Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) market. A detailed picture of the Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) pipeline landscape is provided, which includes the disease overview and Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) treatment guidelines.

The assessment part of the report embraces in-depth Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) commercial assessment and clinical assessment of the Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) pipeline products from the pre-clinical developmental phase to the marketed phase.

In the report, a detailed description of the drug is proffered including mechanism of action of the drug, clinical studies, NDA approvals (if any), and product development activities comprising the technology, Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) collaborations, licensing, mergers and acquisition, funding, designations, and other product-related details.

The report provides insights into:

Scope of the Report

Key Topics Covered

1. Report Introduction

2. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS)

2.1. Overview

2.2. History

2.3. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Symptoms

2.4. Causes

2.5.Pathophysiology

2.6. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Diagnosis

2.6.1. Diagnostic Guidelines

3. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Current Treatment Patterns

3.1. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Treatment Guidelines

4. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) - Analytical Perspective

4.1. In-depth Commercial Assessment

4.1.1. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) companies collaborations, Licensing, Acquisition - Deal Value Trends

4.1.1.1. Assessment Summary

4.1.2. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Collaboration Deals

4.1.2.1. Company-Company Collaborations (Licensing / Partnering) Analysis

4.1.2.2. Company-University Collaborations (Licensing / Partnering) Analysis

4.1.2.3. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Acquisition Analysis

5. Therapeutic Assessment

5.1. Clinical Assessment of Pipeline Drugs

5.1.1. Assessment by Phase of Development

5.1.2. Assessment by Product Type (Mono / Combination)

5.1.2.1. Assessment by Stage and Product Type

5.1.3. Assessment by Route of Administration

5.1.3.1. Assessment by Stage and Route of Administration

5.1.4. Assessment by Molecule Type

5.1.4.1. Assessment by Stage and Molecule Type

5.1.5. Assessment by MOA

5.1.5.1. Assessment by Stage and MOA

5.1.6. Assessment by Target

5.1.6.1. Assessment by Stage and Target

6. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Late Stage Products (Phase-III)

7. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Mid Stage Products (Phase-II)

8. Early Stage Products (Phase-I)

9. Pre-clinical Products and Discovery Stage Products

10. Inactive Products

11. Dormant Products

12. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Discontinued Products

13. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Product Profiles

13.1. Drug Name: Company

13.1.1. Product Description

13.1.1.1. Product Overview

13.1.1.2. Mechanism of action

13.1.2. Research and Development

13.1.2.1. Clinical Studies

13.1.3. Product Development Activities

13.1.3.1. Collaboration

13.1.3.2. Agreements

13.1.3.3. Acquisition

13.1.3.4. Patent Detail

13.1.4. Tabulated Product Summary

13.1.4.1. General Description Table

14. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Key Companies

15. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Key Products

16. Dormant and Discontinued Products

16.1. Dormant Products

16.1.1. Reasons for being dormant

16.2. Discontinued Products

16.2.1. Reasons for the discontinuation

17. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Unmet Needs

18. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Future Perspectives

19. Relapsed or Refractory Mycosis Fungoides (MF) AND Szary Syndrome (SS) Analyst Review

20. Appendix

21. Report Methodology

21.1. Secondary Research

21.2. Expert Panel Validation

Companies Mentioned

For more information about this drug pipelines report visit https://www.researchandmarkets.com/r/nfdd1l

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Relapsed or Refractory Mycosis Fungoides (MF) and Sezary Syndrome (SS) - Global Industry Assessment and Pipeline Insights, 2020 -...

The majority of nutritional advice is general, out of necessity, and some of it does apply to everyonelike eating more vegetables and drinking enough water.

But when it comes to more specific strategieslike how much to eat in order to lose or maintain weight and what you should be eating to achieve thatit can get tricky. New research suggests the issue is complicated because individuals can have different reactions to the amount and type of food compared to others eating the same quantity and meals.

In a small study published in the journal Nature Food, researchers served 19 volunteers four different types of meals comprised of foods ranging from heavy on fruits and vegetables to those typical of a fast food dinner. The people ate these meals over four three-day inpatient periods, which means compliance was closely monitored.

After analyzing urine through molecular profiling technology, researchers found different patterns of chemical composition, suggesting unique responses to the food based on how it was being metabolized. Also, even though everyone ate the same amount of calories, some people excreted more calories through their urine than others, researchers found.

This is because of the way each persons metabolic pathways are activated, a process often called metabolic flexibility, said study coauthor Jeremy Nicholson, Ph.D., professor and pro-vice chancellor of health sciences at Murdoch University in Australia.

Most nutritional advice is general, but we know that one size does not fit all, he told Bicycling. In the future, it will be normal to have individualized diets, but these will be informed by metabolism, not genetics. Thats because through your life, your dynamic phenotype [characteristics that change over time] is influenced not just by genes but also by lifestyle, diet, exercise, gut microbes, medications, and other factors.

In the same way that long-term health risks can be pinpointed through factors like these, it may be possible to tailor healthy eating advice in the same way, using molecular technology to understand an individuals metabolic flexibilityand tweak nutrition plans based on that, Nicholson said.

[Gravel! prepares you with everything you need to know to crush it, including the best gear, how to train, and much more!]

Until the day comes when insights like those become commonplace in a way thats commercially available, it may be helpful to understand that even with healthy foods, you may have a different response than someone else eating the exact same amount and diet.

And, as Nicholson noted, there are metabolic game changers like exercise and gut health that can change how you're reacting to foods, so making healthy changes to those could switch up your metabolic flexibility in the long run.

The bottom line? Its worth noting how you react to different foods, and realizing that everyone is differentwhat works for other people might not work for you. Meeting with a sports dietitian to get a plan thats tailored to you could be a good first step toward eating in a way that benefits your body specifically.

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Why Every Person Reacts Differently to Diets - Bicycling

Internationally, scientists now have on file the genomes of more than 47,000 different samples of the virus that causes COVID-19 up from just one in January. Here's a transmission electron micrograph of SARS-CoV-2 virus particles (orange) isolated from a patient. National Institute of Allergy and Infectious Diseases/National Institutes of Health hide caption

Internationally, scientists now have on file the genomes of more than 47,000 different samples of the virus that causes COVID-19 up from just one in January. Here's a transmission electron micrograph of SARS-CoV-2 virus particles (orange) isolated from a patient.

Scientists are monitoring the virus that causes COVID-19 for genetic changes that could make a vaccine ineffective. But so far, they're not seeing any.

"There's nothing alarming about the way the coronavirus is mutating or the speed at which it's mutating," says Emma Hodcroft, a molecular epidemiologist at the University of Basel in Switzerland. "We don't think this will be a problem [for vaccines] in the short term."

"To date, there have been very few mutations observed," says Peter Thielen, a senior scientist at Johns Hopkins Applied Physics Laboratory. "And any mutations that we do see are likely not having an effect on the function of the virus itself."

That's good news for scientists working to produce an effective vaccine by the end of the year. And it reflects the enormous quantity of genetic information on SARS-CoV-2, the virus that causes COVID-19, that researchers have amassed since the virus appeared in China late last year.

In January, scientists were limited to just one whole genome sequence of the virus. "Today we have over 47,000 coronavirus genomes that have been submitted to international databases," Thielen says.

New genomes are added every day by teams of scientists from around the world. And each time a new one arrives, it gets a close examination, Thielen says.

"What we're looking for in the data is similarity between the virus that first emerged and the genome that had been deposited and any changes that have occurred in the virus," he says. And overall, the viruses circulating today look remarkably similar to the ones first identified in China.

There had been concern about mutations because SARS-CoV-2 is a type of virus capable of quickly changing its genes. But unlike many similar viruses, the coronavirus uses a proofreading system to catch any errors in the genetic code when it begins generating copies of itself.

"The targets for vaccine design today remain the same as we would have designed them in January."

Peter Thielen, Johns Hopkins Applied Physics Laboratory

"So if there's a change, it will actually make a correction at a specific location," Thielen says.

Vaccine developers have been especially concerned about genetic locations that affect something called a spike protein. It's a structure on the surface of the coronavirus that allows it to invade cells.

Spike proteins also give the virus its distinctive appearance and account for its name. Scientists who first viewed a coronavirus through an electron microscope were reminded of the solar corona.

The candidates for a coronavirus vaccine now under development are all designed to teach the immune system to recognize these spike proteins. So far, Thielen says, that's looking like a good strategy.

"The targets for vaccine design today remain the same as we would have designed them in January," he says.

Some other well-known viruses have proved less amenable to the strategy of using the same vaccine from year to year. Influenza, for example, is constantly altering its surface proteins in ways that require annual vaccine updates for each strain that's making the rounds that year.

"Flu just really loves to change these parts," Hodcroft says. "And that's why we can end up with such different flus from season to season."

Measles represents a virus at the other extreme its genome has stayed fairly consistent over the years, at least in the ways that trigger immunity in people after infection. That means children today still get a measles vaccine that was developed in the 1960s, and it provides immunity for a lifetime.

Hodcroft says she thinks SARS-CoV-2 is likely to fall somewhere between the flu and measles when it comes to making a vaccine.

"I think in the short term we'll find something," she says. "The big question is whether this is something we'll be able to vaccinate once and then you never have to get it again, or will it be something you'll have to get every couple of years to keep your immunity up to date."

Scientists are uncertain because the coronavirus is still so new, Hodcroft says.

"We haven't really seen the full diversity of how the virus can mutate," she says. "It gathers mutations over time. We can't speed up time, so we just have to wait and see."

At the moment, though, vaccine developers have more pressing concerns than mutations. First, they'll have to demonstrate that they can produce vaccines that are both safe and effective. Then they'll have to make huge quantities.

"It's not a small feat to manufacture a vaccine for billions of people and then to get it to all of those people," Hodcroft says.

That will take months, she says, in addition to the months required to develop a vaccine in the first place.

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Coronavirus's Genetics Not Changing Much, And That Bodes Well For A Vaccine : Shots - Health News - NPR

Scientists at Sanford Burnham Prebys Medical Discovery Institute and Radboud University Medical Center in the Netherlands have identified mutations in a gene called CNOT1 that affect brain development and impair memory and learning. The study is the first to link neurodevelopmental delays with CNOT1, suggesting that drugs that help restore the genes function may have therapeutic benefit. The research, published in The American Journal of Human Genetics, also revealed that CNOT1 interacts with several known autism spectrum disorder (ASD) genes, opening new research avenues for the condition.Prior to this work, the CNOT1 gene was not on the radar of autism researchers, says Rolf Bodmer, Ph.D., director and professor in the Development, Aging and Regeneration Program at Sanford Burnham Prebys and the studys co-corresponding and co-senior author. This discovery could help us better understand the genetic mechanisms underlying ASD. Our work is also a first step toward exploring drugs that could augment the function of CNOT1 and might be able to help children with neurodevelopmental delays who have these specific mutations.

The cause of developmental disabilities, including ASD, is poorly understood. Research indicates that there may be a genetic component to these conditions, but the precise impact of the genetic variations that have been uncovered to date is unclear. Identifying the underlying cause of developmental disabilities would allow scientists to create diagnostic tests that would provide early diagnoses and potential treatments.

To answer this question, the researchers at Radboud University turned to Bodmer, a world-renowned genetics expert who studies how genes contribute to disease using a fruit fly model. Sreehari Kalvakuri, Ph.D., a postdoctoral researcher in the Bodmer lab, created fruit flies that contained the same CNOT1 variations seen in the patients, including DNA sequences that were misspelled (missense), cut short (truncated) or otherwise altered.

This work identified nine CNOT1 variants that impaired learning and memory, which was measured by several independent approaches including a courtship assay that tested the ability of male fruit flies to remember if their female partners had paired with other males. All of these variants appeared spontaneously (de novo) in the patients, meaning they were not inherited. The scientists also discovered that these CNOT1 mutations interact with known ASD genes revealing a genetic link to ASD that can be further explored.

Fruit flies are a great biological model because we can complete genetic studies very quickly. This work only took a few months instead of the potential decade using a mouse model, says Kalvakuri, the studys co-first author. Additionally, the CNOT1 gene is highly conserved between fruit flies and humans, meaning it does not change much, so we are optimistic these findings can be extrapolated to people.

Next, the scientists plan to identify which molecular components interact with CNOT1, which functions as a scaffold that builds up a larger protein complex. This work might uncover additional potential drug targets for intellectual, learning or memory disorders, including ASD.

The first step toward helping children with neurodevelopmental delays is to determine the cause of the condition, says Bodmer. Our ultimate hope is to find a treatment that could be given as early as possible to help these children stay on track developmentally.

Surprisingly, the findings also have implications for heart disease, the primary focus of Bodmers lab.

A significant fraction of these patients also have cardiac defects, says Bodmer. Conversely, children who are born with heart defects are at a higher risk of developing ASD, too. This study on CNOT1 also provides a previously unknown genetic link between heart function and ASD.

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

Excerpt from:
New Genetic Mutations Linked to ASD - Technology Networks

To some, the idea of taking a summer vacation amid the COVID-19 pandemic is out of the question. With COVID-19 cases reported in all 50 states, the Centers for Disease Control and Prevention recommends people stay home to protect themselves and others from getting sick.

"COVID-19 remains an ongoing pandemic with sustained community transition even if you are traveling to a place with fewer cases," said Dr. Benjamin Singer, assistant professor of medicine (pulmonary and critical care) and biochemistry and molecular genetics at the Northwestern University Feinberg School of Medicine.

To others, a carefully distanced excursion to the woods or a secluded beach is in the works after months of staying close to home.

"There will be lots of people who take trips, come home and everything is fine. But there are going to be other people who take trips and end up sick who wouldnt have otherwise gotten sick if theyd stayed home," said Dr. Emily Landon, associate professor of medicine, infectious diseases expert and epidemiologist at University of Chicago Medicine. "Its really up to you, about what you want to spend your personal risk on."

For those planning a trip away from home this summer, the Tribune asked medical experts what precautions and items to take on every step of a journey by airplane, car or train. What follows are their answers, along with guidance from the CDC, Transportation Security Administration, and other state and federal agencies.

Whatever your plans, dont lose sight of this opportunity to enjoy quality time with those youve been hunkering down with since March. "2020 may not be the summer we thought we would have, but find time to read, explore and find the joy around you and savor what you can," said Dr. Amy Bohnert, associate professor of clinical and developmental psychology at Loyola University Chicago, "That is a gift we can give our kids that will last a lifetime."

BEFORE YOU GO

Q: First off, is travel safe?

CDC: Travel increases your chances of getting and spreading COVID-19. We dont know if one type of travel is safer than others; however, airports, bus stations, train stations and rest stops are all places travelers can be exposed to the virus in the air and on surfaces.

Q: What factors should go into picking a destination?

CDC: The following should be considered when thinking about planning a trip away from home:

Is COVID-19 spreading in your community? Even if you dont have symptoms, you can spread COVID-19 to others while traveling.

Is COVID-19 spreading at your destination? You can get infected while traveling. You can also spread the coronavirus without symptoms to loved ones when you return.

Would you have to quarantine for 14 days after arriving at your destination? Check the state and local requirements.

Q: Are there any groups of people for whom you would not recommend travel for this summer due to the coronavirus pandemic?

Singer: "Higher-risk groups, including older adults and people with chronic health conditions."

Q: Is one form of travel safer or limits exposure to COVID-19 better than others?

Singer: "Staying at home is the safest option, but travel options that allow you to stay socially distant would be considered the safest."

Dr. Erica Hartmann, assistant professor of environmental engineering at Northwestern University: "I personally would opt for modes of transportation that are less densely crowded and allow for lots of ventilation."

TAKING A ROAD TRIP

Q: What is the general guidance?

CDC: Making stops along the way for gas, food or bathroom breaks can put you and your traveling companions in close contact with other people and surfaces. You may have to stop less often, but RV travel typically means staying at RV parks overnight and getting gas and supplies at other public places. These stops may put you and those with you in the RV in close contact with others. One approach for eating is to pick up food at drive-thrus or curbside restaurant service.

Q: Its inevitable Ill need to stop and use the restroom during my trip. Is there any way to prevent germs from following me back to my car?

Hartmann: "Wash your hands. Which really, you should be doing regardless of COVID-19.

"Perhaps not directly related to your question, but remember to practice social distancing in the restroom if there are multiple people in the restroom. And maybe you shouldnt talk while youre in there."

GOING BY AIR?

Q: What is the general guidance?

CDC: Air travel requires spending time in security lines and airport terminals, which can bring you in close contact with other people and frequently touched surfaces. Most viruses and other germs do not spread easily on flights because of how air circulates and is filtered on airplanes. Social distancing, however, is difficult on crowded flights, and you may have to sit near others (within 6 feet), sometimes for hours. This may increase your risk for exposure to the virus that causes COVID-19. Wear a nonmedical, fabric face covering during the flight.

AT THE AIRPORT

Q: A trip to the airport is in my future and Im worried about potential COVID-19 exposure. How can I protect myself in the terminal?

Landon: "My moms 75 years old. Shes been stuck in Florida much longer than usual because of the pandemic, but its time to come home. Shes traveling in a week and a half. Weve had a lot of discussions about what to do. Heres what I would do if I was going to fly right now, and this is what I advised my mom to do, as well.

"When you get in the security line, then try to keep distance from the people around you. Make sure you are wearing your mask, if you can, then manipulate the situation so youre in line with other people wearing their masks. If the person in line in front of you doesnt have a mask on, then let other people go ahead. Security will touch your stuff. Dont freak out about it. Hopefully, they will be wearing masks, too, because thats required and recommended. When you get your stuff back from security what you should do every single time is wash your hands. If you dont have time to stop and wash your hands in the bathroom, then use your hand sanitizer.

"After security, get some space and keep some space between yourself and other people before you have to board your flight. You dont want to be stuck sitting close to other people. Maybe that means finding an empty gate or one that doesnt have a flight going out right now where you can sit at instead. Theres no rule that says you have to sit at your crowded gate before your flight. When its time to line up to board the flight, try to keep some space. Just remember the CDC doesnt count an exposure unless youre within 6 feet of someone for 15 minutes or more. Just wait to get up and only get in line when its your turn. The person standing behind you is going to do what they want to do, and theres not much you can do about it."

ON THE PLANE

Q: I know I will need a face covering. What type would you suggest for the flight?

Landon: "Youll want to bring a really high-quality fabric mask or a medical mask for traveling. You need to make sure your mask is super protective not just preventive. Fabric masks are great for holding in your own respiratory droplets. But if other people arent wearing their masks, then they are not holding in their respiratory droplets. If everyone wears a preventive mask, then, together, everything is safer all around. But if you cant count on other people to do that, then you need to have a really good fabric mask like the World Health Organization recommends. Probably two or three layers with a high thread-count cotton and/or silk inside of it or a filter pocket inside of it. One that fits you well. Thats what I would wear. I find fabric masks to be a lot more comfortable than medical masks.

"I would try not to take off my mask during the flight you may need to in order to have a drink of water on a 4-hour flight. But on a short flight, you could probably get away with drinking before you board and then drinking again when you get off the plane."

Q: What should I do when I arrive at my seat?

Landon: "I would wipe down the armrest and the tray table. If Im in the window seat, then I would wipe that down, too, because thats what people often lean against and put their hands on. Then I would sit in my seat, wash my hands again with hand sanitizer and sit tight. Leave your mask on for the flight.

"Youre really only at risk from the people within a couple of seats of you in any direction. So, two seats behind you, two seats diagonally, two seats in front of you. Thats what youre really worried about.

"If someone is coughing in the back of the plane, then dont freak out. People passing you in the aisle, dont freak out. Theoretically, the window seat is the safest."

Q: I see people sitting near me who have taken off their mask during the flight. What should I do?

Landon: "When we think about how to protect people out in the world from COVID-19, I like to describe it as a layered or stacked approach. We stack up interventions. None is meant to be perfect on its own. You can rely on cleaning your hands, wiping down your seat, keeping your distance from other people these are all ways to reduce your risk when traveling. But some of them arent as easy to do when traveling, like protecting your eyes. So, if other people are coughing or sneezing or have respiratory droplets that are contagious, then that can get in through your eyes. A mask doesnt protect them. And your regular glasses arent great protection either.

If you find yourself stuck on an airplane with someone two rows behind you or one seat behind you coughing or, say, the guy next to you doesnt look all that well you want to be able to add an extra layer of protection.

Dr. Emily Landon, University of Chicago Medicine:

"I strongly recommend bringing one of these plastic face shields that covers your mask. It will help protect your face, your eyes and mask from becoming contaminated. They are really comfortable. The first time you put one on, youre like, This is ridiculous, but you can see your whole face through it. You can wear your mask underneath it. In fact, were recommending them for little kids at school, when schools go back, that they might be a better form of protection than trying to get them to keep their masks on. They are available on Amazon. You could even make one yourself. I would bring one with me. I wouldnt, necessarily, wear it the whole time. I would definitely have it with me so I could add a layer of safety. If I feel like I cant keep my distance from people and other people arent wearing masks, then that would be the time I would want to put on a face shield. The real time to need them is when youre around people who arent wearing masks. I think you need to have something that will help you add a layer of protection if someone else isnt doing their part. That, for me, would be a face shield."

WHAT ABOUT STAYING AT A HOTEL?

Q: What is the general guidance?

CDC: If staying at a hotel, then check the hotels COVID-19 prevention practices before you go. When you are there, limit close contact with others in the lobby or other common areas, take the stairs instead of the elevator and choose contactless options for check-in when possible.

Q: Ive arrived at my destination. Are there any inside surfaces at my lodging I should wipe down as a precaution?

Hartmann: "If youre really set on taking matters into your own hands, focus on high-touch surfaces (keys, doorknobs, light switches, maybe remote controls)."

Q: What should I look for when booking a hotel?

Landon: "The most important thing is to look on the hotels website ahead of time and make sure the hotel has a good written policy about COVID-19. You want to see that they require masks to be worn by staff and guests in the inside common areas all the time. You want to see that they say something about their disinfection plan in rooms. Not just cleaning them in between guests, but they are disinfecting them using an EPA-registered disinfectant and theyve trained their staff in how to do so. You want to see that they have a social distancing plan in place and they have policies for use of their common-use areas like gyms or pools. That means the hotel is taking steps to protect its workers and guests. If the hotel is taking a lot of steps to protect their workers and guests, then its less likely there will be sick people wandering around your hotel, which makes it safer.

"Its important that the hotel has a clear policy, but you want to go a step further. You want to find information on travel websites or talk to someone whos been there recently. I would want to know what is really happening on the ground.

A lot of places have policies. If you call the front desk ahead of time and they have no idea what the hotels policies are, then thats a bad sign.

Q: Is it safe to use a hotels pool?

Landon: "Pools are not inherently bad. Chlorine in pools should kill COVID-19. Thats not a problem, but people dont wear masks when they are in pools. In general, the recommendation in Illinois is that pools are not open for recreation right now, but could be opened for exercise.

"Look for sun loungers to be spaced apart, signs saying the pool is not allowed to be used for recreation, only for exercise, and a limited number of swimmers can be inside at one time. If you scope it out and it appears you can safely do that, then, sure, go ahead and swim some laps."

Q: What about camping?

CDC: Going camping at a time when much of the United States is experiencing community spread of COVID-19 can pose a risk to you if you come in close contact with others or share public facilities (like restrooms or picnic areas) at campsites or along the trails.

Q: What if Im staying with family?

Landon: "Take care of yourself. Be pretty socially distant from people in the week leading up to your trip. If your family is really, really anxious about your visit, then plan to leave a few days early and take a break in a hotel for five days before you stay with family. And get tested, maybe, if everyone is really concerned."

PACKING

Q: What are some precautions to take for any type of travel?

CDC: Consider the following when leaving your home:

- If taking prescription medicine, then bring enough to last you for the entire trip.

- Pack hand sanitizer with at least 60% alcohol.

- Bring a cloth face covering to wear in public places.

- Prepare food and water for your trip. Pack nonperishable food in case restaurants and stores are closed.

- Follow state and local travel restrictions. Check state and local health department information at home, along your route and at your destination.

RETURNING HOME

Q: OK, Ive made it back home after my trip. How can I prevent the entire trips germs from ending up inside my living space?

Hartmann: "Again, wash your hands when you return. Consider disinfecting high-touch objects that you may have had with you or objects that other people outside your trusted circle may have handled, if you intend on using them again very soon."

Landon: "If you come home from a trip, then assume youve been exposed (to the new coronavirus). Get tested five to seven days after your last exposure, stay home for a little extra time. If I was going to travel like that this summer, then I would book another week off afterward so that I wasnt spreading anything that I might have picked up."

OK, THIS IS HARD

Q: My partner wants to travel this summer, but Im unsure about it. Can you suggest some ways we can have a conversation and try to understand each other?

Bohnert: "Partners should strive to appreciate what their partners would and would not feel comfortable doing. It is also important to understand where those concerns come from. Does a partner have a health condition that makes them more vulnerable? Is a partner worried about losing time away from work and reductions in salary if they are exposed? Is your partner worried about the potential of encountering racism? Are they concerned about whether there would be adequate medical care in the place where they are visiting? If one partner is particularly uneasy with one locale, perhaps another that is more familiar, closer to home or involves less time away could provide a more comfortable escape. The more you can understand what specific things make your partner uneasy about traveling, the easier it will be to come up with some options that may be more palatable if one of the partners feels strongly about the need to get away."

Q: After months of sheltering at home, Im now afraid to head out into public and be around other people. What can I do to make a trip away from home seem less stressful?

Bohnert: "To start, I would encourage people to normalize these stressful feelings. After all, we have been told to avoid people and shelter at home to prevent getting sick. So heading out in public runs counter to the advice we have been heeding over the past three months how could we not feel nervous about it?

It would be hard not to feel unsettled by the prospect of being in public after all the precautions we have been asked to take. So dont judge yourself for feeling uncertain.

Dr. Amy Bohnert, Loyola University Chicago:

"Next, try and pinpoint exactly what makes you feel uncomfortable. Is it being in closer contact with others? Fears of dining out? If you can figure out what makes you feel uneasy, you may be able to control some aspects of that situation that will make it feel more manageable. As with most things, when we feel anxious or concerned about a situation, we may seek to avoid it so we dont have to feel anxious. This, of course, reinforces that the situation is something to be feared because when we avoid it, we dont feel worried. So figuring out what you can control wearing a mask (properly), washing/sanitizing your hands and finding less crowded outdoor places where you can better manage how close you have to get to others may make the decision to get out more palatable. All these behaviors will decrease (but not eliminate) the likelihood you get infected if you encounter someone who is contagious."

Q: How can we have a fun, productive summer as a family if we decide to not take a vacation and choose, instead, to stay home?

Bohnert: "For many people, traveling introduces a lovely element of novelty to our lives. We get to see different scenery, eat different foods and have new experiences. With all the novelty we are currently facing and the uncertainty that lies ahead, the risk incurred by traveling may be more than families are ready for during challenging time. But finding little ways to enjoy the spaces and people around you, even while distancing, is important.

"There are many lovely places to explore in the Chicago area during the summertime that provide a nice respite from our homes. Some are closed but may be reopening in the coming weeks. The botanic gardens and forest preserves are lovely, nature-filled spaces. Some of our renowned Chicago university campuses also have splendid grounds in which to stroll. Springfield is a bit farther away but a great place to explore for history buffs, as is Cantigny in the western suburbs."

Consider setting some up some new family rituals bike rides, walks to look for birds, berry picking and picnics can all be nice ways to escape.

Continue reading here:
Should you travel this summer? Heres a guide to vacation amid the coronavirus pandemic. - Peoria Journal Star

In these fractious times, when we are confronting the reality of systemic racism, how can we have an informed discussion about genetics and race?

One way is to calmly state the increasing evidence of meaningful genetic differences between human populations and then engage in honest and robust debate about the social and political implications, if any, of such inter-group divergence.

Back in the real world, meanwhile where open discussion of race and biology is largely taboo (a state of affairs recently exacerbated by DNA pioneer James Watson) a better idea might be to quickly change the subject. So what about the weather, eh?

But battening down the hatches and sitting out the storm isnt really an option. For a start, it would mean blithely ignoring the deluge of data from the recent revolution in molecular biology about our species evolution and of the genetic divergence of separate human populations over time. More importantly, it would also miss the opportunity to genuinely level the playing field for those very peoples most marginalised by an undeniable history of prejudice and neglect.

Note, though, the numerous alternatives for race already employed above: populations, groups, peoples (to which ancestry, descent and the like could also be added). Far from simply being politically correct euphemisms for a tainted term, it is important to distinguish between the word race as it is socially used say, the Black/African American, Native American, White, etc. racial categories used in the US census from the biological sense, used to describe distinct populations within a species.

Because of the historical misuse of the term race, this is an important distinction to make. In 19th century Britain, for example, two groups who would now be simply lumped together as White were regarded as separate biological races namely, and complete with the picturesque descriptors of the time, the careless, squalid, unaspiring Irish and the frugal, foreseeing, self-respecting Scots. (Full disclosure: my own genetic ancestry is of the careless, squalid and uninspiring variety.) A more modern perspective, however, does not deny the existence of genetically distinct indigenous British populations such groupings do indeed exist rather, it avoids describing them in meaningless racial terms. Similarly, the idea of an overarching Black race utterly fails to capture the genetic diversity of African (or African-descended) peoples, irrespective of how we are now able to distinguish genetically related groups within the wider human population of Africa.

Nor is this simply overly-sensitive quibbling over the meaning of a word. Historically, race was often used synonymously with varieties, breeds or sub-species (in the Descent of Man, for instance, Darwin considers at great length what was then still an open question: Arguments in favour of, and opposed to, ranking the so-called races of man as distinct species). But whether we like it or not, words have power, and once-acceptable descriptors of human inter-group variation now carry obvious egregious connotations (such as the slur half-breed).

Indeed, the limitations of language have long been a bane of everyday discussion of human evolution, with phrases and concepts survival of the fittest, say, or struggle for existence inevitably being interpreted in terms of intrinsic worth. Descriptions of sub-species of flora and fauna, for instance, would ruffle few feathers; similar talk of sub-populations of human beings, however, inevitably evokes hierarchical notions of superiority and inferiority. (As a light-heartened analogy, think of the hierarchical distinction between language and dialect then tell the Germans that their language is a dialect of Dutch.)

In sum, then, anyone discussing genetics and race must be conscious of the connotations and impact of words. And this is especially true when engaging in dialogue with those with a standard social science conception of race, one in which human evolved biology is seen as irrelevant to social issues a paradigm, moreover, in which the very idea of human biological difference is treated with the utmost suspicion. Given this latter mindset and the human tendency towards righteous indignation it is hardly surprising that many liberal-minded people react badly when confronted with arguments about human difference that they perceive (rightly or wrongly) as morally offensive. If worthwhile or meaningful discussion of genetics and race is to proceed, therefore, it is beholden on geneticists and their ilk to take this into account not through political timidity but through simple courtesy and common-sense.

Of course, as pointed out above, such is the toxic nature of this topic that open discussion is often avoided, especially by those cowed by the likely reaction of their peers. In this respect, political scientist James Flynn discoverer of the eponymous Flynn effect of rising IQ over time points to the counterproductive nature of intellectual censorship: [T]hose who boycott debate forfeit a chance to persuade. They have put their money on indoctrination and intimidation. A good bet in the short run but over the long course that horse never wins.

The sort of censorious indignation highlighted by Flynn also has another detrimental effect: it opens a space for nationalistic populists and race supremacists to claim they are simply telling it as it is or bravely saying what others are too scared to admit. The losers here, of course, are the very people that the taboos were designed to protect those marginalized minorities likely to face greater prejudice from emboldened bigots.

Moreover, Flynns own work provides a further explicit example of how such taboos can have counterproductive consequences; if Flynn had been unable to research the causes of reported racial differences in IQ he would never have discovered the Flynn effect, the best evidence we have of environmental influences on intelligence (and of how improvements in impoverished environments can lead to dramatic changes in IQ scores over time).

This points not only to the benefits of openly addressing sensitive subjects, but also to a possible way to assuage some of the suspicion that surrounds genetic research into inter-group difference that even if such differences are shown to exist, this does not dictate any particular social or political response. Facts do not determine values.

At the same time, however, facts can certainly inform social policy. Take, for example, the overwhelming evidence of strong genetic influences on academic achievement. Contrary to what many might pessimistically assume, this genetic evidence does not mean that nothing can be done for those currently failing in the education system. As the Flynn effect shows, environmental change does make a difference, despite the high heritability of IQ.

Indeed, the strong genetic determinants of educational attainment are much less straightforward than they appear. For example, some studies that indicate a causal link between genes and learning hinge on the observation that older mothers have offspring who are more likely to succeed in school. As older mothers also have fewer children (with whom they can devote more time and resources), the relevant genetic influence here pertains to fertility rather than academic smarts. Given this, and given a political desire to raise academic attainment amongst specific groups, ameliorative social policy could focus on womens reproductive health and opportunities in marginalised communities.

Be this as it may. The point is that genetic facts including evidence of genetic differences between racial populations carry no necessarily social or political implications. Nevertheless, these same genetic facts may help highlight obstacles to achieving desired social outcomes, and could provide information that assists in overcoming them. In this respect, just as greater awareness of social and environmental barriers can assist in designing policies to reduce inequalities, so too could greater recognition of possible genetic hurdles to improved life outcomes.

In the past in the era of Social Darwinism and eugenics hereditarian political beliefs equated biology with destiny. Unfortunately, much of the present-day antipathy to human genetic research appears premised on a similar erroneous belief: that if human behavior is under the influence of biology/genes then certain social outcomes, such as disparities in wealth or status, are inevitable. Hence the desire to denigrate genetic research that touches on the raw nerve of race for, as many well-intentioned egalitarians may mistakenly believe, if meaningful differences between different peoples really do exist, then the goal of greater equality could prove unattainable.

The biological study of human behavior is notoriously fraught hardly surprising, given that fallible humans are both the subject and the object of scrutiny. Furthermore, given the egregious history of political ideas based on supposed facts of human biology, the results of human behavioral research are often held to a higher standard of proof and most especially with research relating to politically sensitive topics, such as race, gender or sexuality.

Whether always warranted or not, such critical inspection comes with the territory; indeed, one higher standard that human geneticists can impose upon themselves is to understand the motivation of the opposition, however wrong-headed this might appear. Such awareness would not mean avoiding discussion of troublesome topics but it might avoid discussing them in ways more likely to inflame than inform.

A version of this article was originally published by the Genetic Literacy Project on Feb 13, 2019.

Patrick Whittle has a PhD in philosophy and is a freelance writer with a particular interest in the social and political implications of modern biological science. Follow him on his website patrickmichaelwhittle.com or on Twitter @WhittlePM

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Genetics and race: An awkward conversation during volatile times - Genetic Literacy Project

While its undeniable that logging miles has major health benefits, scientists dont exactly understand how it affects your body at the molecular levelbut researchers are attempting to figure that out.

A Stanford University study published in Cell set out to determine what happens in the body just after exercise, and try to get one step closer to explaining exactly what makes exercise so good for your health.

In the study, 36 people aged 40 to 75 completed a peak VO2 testwhich measures maximum oxygen consumption during intense exercise as a marker of aerobic fitnesson a treadmill. Before running, researchers sampled their blood. Then, after about 9 to 10 minutes of running, the participants blood was sampled multiple times: immediately after exercise, and then 15, 30, and 60 minutes after they reached their peaks.

Researchers then completed multi-omic profiling, where they looked at the participants blood to see how exercise affected molecular changes in the cellsincluding how exercise affects immune cells and plasma. Over 17,000 molecules were measured, and 9,815 moleculesmore than halfshowed significant change, Michael Snyder, Ph.D., professor and chair of genetics at the Stanford University School of Medicine, in Stanford, California, told Runners World.

Exercise has a lot of health benefits, but nobody knows how exercise really works, Snyder said. Im not saying our study figured it out, but it gives us a window into whats going on in the body.

Researchers were able to see changes in oxidative stress, which is a harmful chemical process when theres too much of it. They also saw immune system markers and molecular markers of healing and inflammation go up right away as the body began to recover.

These results give a window into different systemic events, such as the potential to look into how oxidative stress affects aging, how exercise affects your immune system, how your body reacts to metabolic stresswhich occurs in exercise as energy depletes, leading to accumulation of lactic acid in musclesand how muscles are engaged during exercise as researchers work to further study the effects exercise has on the body.

I do view it as just trying to work out the choreography of whats going on, Snyder said. Its like a symphony, maybe the violins start off first, then the next instrument and the next come in.

[Smash your goals with a Runners World Training Plan, designed for any speed and any distance.]

This kind of testing can give researchers the ability to see whats happening in peoples bodies, such as seeing how muscle markers and markers for cardiovascular disease are all stimulated and engaged.

While we know that exercise is important for heart health, its not exactly known how it benefits your ticker. This is something researchers hope to use these findings to study more in the future, Snyder said. And, while this test was only done using a treadmill stress test, researchers will look at how molecules in the body are affected by other types of exercise.

Results showed that peoples fitness and health levels were consistent with how much exercise affected the molecules in their bodies. For example, people that were healthy had similar molecular changes before and after exercise; those who were insulin resistant (prediabetic and diabetic) didnt have as large of an immune response, which may be able to show how exercise affects this condition or helps predict the onset of diabetes.

And, through these blood samples, the molecular patterns found anemia that other testing hadnt picked up in one healthy individual, Snyder said.

So what can this tell you about your health? Right now, researchers are still figuring that out. But as the molecules change, they are able to see things like how different systems in your body engage during exercise, how your cardiovascular pathways are affected, and when different types of fat burning may occur. All of these elements give researchers a better look at how exercise engages the entire body.

Were looking at the details of how the symphony is able to play, Snyder said.

In the future, the researchers hope that a version of molecular profiling can be used as a way to measure aerobic fitness and along with typical treadmill testing.

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One Run Can Alter 9,815 Molecules in Your BodyHeres Why Thats Important - runnersworld.com

Genetics is that the study of genes, their functions and their effects. Among the varied sorts of biology like genetic science, developmental genetic science, population genetics and quantitative genetic science, human genetics is that the study that deals with the inheritance happens in folks. It encompasses a range of overlapping fields like classical biology, genetics, genetic science, genetics and plenty of additional.

The Human Genetics Market is expected to exceed at a CAGR of 9.5% in the given forecast period.

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The scope of the report includes a detailed study of Human Genetics Market with the reasons given for variations in the growth of the industry in certain regions.

The report covers detailed competitive outlook including the market share and company profiles of the key participants operating in the global market. Key players profiled in the report include Agilent Technologies, Bode Technology, GE Healthcare, Illumina, LGC Forensics, Orchid Cell mark, Inc., Promega Corporation, QIAGEN N.V., Thermo Fisher Scientific, Inc. Company profile includes assign such as company summary, financial summary, business strategy and planning, SWOT analysis and current developments.

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The Human Genetics Market is Segmented on the lines of Application Type, Methods, Product Type, End-user and Regional Analysis. By Application Type this market is segmented on the basis of Research, Diagnostic, Forensic science and Others. By Methods this market is segmented on the basis of Cytogenetic, Molecular, Presymptomatic and Prenatal.

By Product Type this market is segmented on the basis of Consumables, Devices and Accessories. By End-user this market is segmented on the basis of Hospitals sector, Clinics sector, Research centers sector and Forensic departments sector. By Regional Analysis this market is segmented on the basis of North America, Europe, Asia-Pacific and Rest of the World.

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While the risks for young healthy people are comparatively low, other experts warn about reading too much into the data recorded during lockdown.

Dr Peter Ellis, a lecturer in molecular genetics and reproduction at the School of Biosciences at the University of Kent, notes that Sir Davids data represent only the residual risk not the natural one.

The reason relatively few people have died of Covid is because only a small percentage of the population have had the disease, he says

A more appropriate conclusion in my view would be to rejoice that the lockdown has done its job and thus kept the overall risk of death low.

Also, the fact that younger demographics are comparatively protected does not mean it is necessarily safe for younger people to mix more freely.

This may be true, but it does rely on our ability as a society to cocoon and protect more vulnerable demographics: a feat not achieved by any country so far, warns Dr Ellis.

In any calculation of mortality risks, it can be also misleading to compare infectious and non-infectious causes of death. Car accidents and bombing raids have very different characteristics to viruses and bacteria.

Infectious disease risk is socialised rather than individual, says Dr Ellis. My actions affect others' chances of death as well as my own.

Protect yourself and your family by learning more aboutGlobal Health Security

Read more:
Crunching the numbers: what are the real risks of dying from Covid-19? - Telegraph.co.uk

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Nadia had a cough and it wouldnt go away. She didnt feel like eating. X-rays and ultrasounds, blood work, all turned up nothing. So a decision was made to test Nadia a four-year-old Malayan tiger at the Bronx Zoo in New York for the latest bug going around, the one that had already put much of the world, including her zoo, into lockdown: COVID-19.

On the other side of the globe, a 42-year-old woman in Melbourne had come down with similar symptoms to Nadia the same dry cough, the fatigue. And, when the tests came back from the labs, the sample of the virus found in both human and tiger was near identical too. Within days, another swab with that tell-tale genetic signature would be extracted from a 21-year-old in Taiwan.

How does the same strand of virus end up in a woman in Melbourne, someone in Taiwan, and a tiger in the Bronx?

Unlike historic plagues, COVID-19 is not spreading in a straight line, from house to house or country to country. Instead, versions of the virus each with their own tiny genetic tweaks are jumping from continent to continent via plane (and cruise ship), and crossing back on each other. The story scientists who specialise in reading COVIDs genes see is that of the worlds first truly globalised pandemic.

Since researchers in Wuhan, China, where the outbreak began, first published the genetic code of the virus, hundreds of labs around the world have followed suit. Their efforts to join the dots among patients, under the microscope as well as on the ground, mean this pandemic is being tracked like never before in real time. Already the family tree of COVID-19 is helping us understand where the outbreak came from, how it took hold in different continents and where its going next.

DNA detectives have tracked one distinct strand of coronavirus from Wuhan through Europe, Australia and Taiwan all the way to Nadia the tiger, pictured, at the Bronx Zoo in New York.Credit:Stephen Kiprillis, Kirsten Burghard

There are more viruses in the world than stars in the sky. They are found in almost every corner of the Earth, they fill its oceans. If lined up, side by side, scientists say they would fill our galaxy too. Most of them cant infect us and the few that can we catch mostly from animals in that knife-edge moment of chance when a pathogen long circulating in one species leaps to another.

Ten thousand times smaller than a grain of sand, viruses can drive forward evolution and unleash hell think of them as zombie shells of protein waiting to spring into action.

Theyre half living, half dead, says Professor Seshadri Vasan, from behind several Get Smart-style levels of security at the CSIROs dangerous pathogens lab.

Unlike bacteria, which can thrive wherever it's warm and wet, viruses need a host to survive. They are the pirates of the microscopic world, commandeering the cellular machinery of other organisms to make copies of themselves and spread.

All they need is a way in.

Thats why its Mission Impossible here at the lab, Vasan says.

Some time in late 2019, a coronavirus now known as SARS-CoV-2 found a door into the human genome this tiny ball of protein evolved a spike able to unlock our cells by binding to ACE2 receptors, a type of enzyme found throughout our bodies. In the bustling city of Wuhan, the virus jumped from an animal into a person, most likely through the handling and slaughter of wildlife for the meat, fur and traditional medicine trade. From there, the germ spread like wildfire between humans infecting more than six million people and killing 400,000 within its first six months.

"Trouble wrapped in protein": Inside its spiky outer shell the coronavirus contains a folded-up strand of RNA.Credit:Kirsten Burghard

Beneath the coronaviruss signature spikes, youre looking at an envelope of fat encasing a long strand of RNA. Like our own double-stranded DNA, this holds the viruss instruction manual for making more copies of itself.

Its like a manuscript written in a language made up of only four letters: A, C, G and U, which is more commonly called T, Vasan says. How they are arranged on the page can change how the virus behaves.

SARS-COV-2s manual is long made up of 30,000 letters or nucleotides. By contrast, the influenza strain that caused the worlds last pandemic in 2009, swine flu, was just 13,500 letters long, Vasan says. This is more than twice the size, its a very big virus.

It is also more deadly.

Once a virus is inside a cell, it sets up shop, replicating at speed. Imagine photocopying this viral manuscript, Vasan says but each copy is then used to make the next. Before too long, mistakes smudges or missing letters will start to creep in. These typos are known as mutations. Some of them slow the virus and are dropped from the text over time. Most are silent they dont affect the viruss structure or function and so you can still understand the sentences. But then there are the rarer mistakes, the ones that improve the virus.

Perhaps it's a really bad manuscript, laughs Professor Francois Balloux, who heads up the genetics institute at University College London.

Before it emerged in humans, scientists say two key mutations had already primed SARS-CoV-2 to jump species lines and spread further than the other two dangerous coronaviruses to come before it, SARS-CoV-1 and MERS-CoV. One change allowing the virus to fuse cells together and tunnel its way through the body faster came down to just three letter changes in its RNA code, says Dr Denis Bauer at the CSIRO.

But now that it is circulating in humans, scientists say the coronavirus is mutating at a fairly stable rate about 20 mutations a year, Balloux calculates. Thats a little faster than he expected, although not as fast as less predictable viruses such as influenza, which requires an updated vaccine every season to keep up with all its mutant stains.

Runaway COVID-19 outbreaks in parts of Europe and the Americas have fuelled speculation that more deadly or infectious strains of the virus may be circulating already some early studies have suggested as many as 30 kinds of SARS-CoV-2. But most scientists stress the mutations so far havent changed how the virus behaves.

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Nadias particular virus, for example, when examined under the microscope by Dr Leyi Wang at the University of Illinois, had racked up just six recurrent mutations or protein changes since it travelled out of Wuhan to her zoo in New York.

Critically, Vasan notes, mutations in the RNA code or even observed in how the virus behaves in the petri dish must be matched against clinical outcomes in patients to truly warrant the distinction. Otherwise they might look like theyre having an effect when theyre not, he says. Im not seeing anything sinister in the mutations so far.

At the Bedford lab, which pulls together global genomic data on COVID-19 through the platform Nextstrain, Dr James Hadfield agrees. Most of the time when a virus starts to behave differently its down to its environment not its biology as it encounters different healthcare systems, population vulnerabilities and public health interventions.

Nadia's virus was traced back through Europe to the original outbreak in China.Credit:Stephen Kiprillis, Kirsten Burghard

But mutations do come in handy for tracking the virus. Over time, differences between samples (good, bad and not worth mentioning) build up, leaving tiny molecular clues for scientists to follow each genome is timestamped to when (and where) it was collected.

The small team behind Nexstrain works around the clock to crunch this data when Hadfield signs off in New Zealand, Dr Emma Hodcroft and her colleagues in Switzerland are ready to take over, followed by Dr Trevor Bedfords team in Seattle.

Hodcroft says the very first genomes out of China were just one mutation apart. Six months on, the branches of the tree still arent very long samples of the virus vary by only about 10 recurrent mutations on average and their roots all go back to a common relative: that first genome sequenced in Wuhan. Thats how scientists know the spillover from animals into humans happened recently in China, likely in November 2019.

Now weve moved from the sparks being thrown off by the Chinese epidemic, to individual epidemics starting in certain countries, Hodcroft says.

Local mutations may develop as the virus spreads in a specific community, particularly with much of global travel grounded, but no country has a distinct national strain yet. There is no US strain or Australian strain, Balloux says.

On April 1, a woman was swabbed in Melbourne. Within days, virtually the same genetic signature would be extracted from Nadia in New York.Credit:Stephen Kiprillis, Kirsten Burghard

In Australia, COVID-19 cases are comparatively few but our virus is among the most sequenced in the world. More than 60 per cent of all confirmed Victorian cases have now had their sample sequenced, Dr Sebastian Duchene of the Peter Doherty institute for Infection and Immunity says. And in NSW, genomic detectives have tracked early cases in Australia back to Iran as well as China, based on distinct mutations.

When you compare Australias viral tree with somewhere like the US, you see more genetic diversity, Hadfield says most cases tend to be imported from overseas, giving us not just one initial case or patient zero but hundreds. But where clusters emerge without a clear source, genomic data can help contact tracers crack the case.

Sequencing or tracking the viruss genetic passport has now revolutionised how health authorities fight pandemics, says Professor Benjamin Howden at the Doherty Institute, and will become critically important as countries ease restrictions. In some cases in Victoria, he says, clusters in which people had no known links to each other were uncovered after the lab team traced a connection in the viruss genes.

Usually, when you do contact tracing, everyone in a cluster has the same virus, Duchene says.

This observation is what makes Nadia and her Melbourne strain so strange, on the face of things.

Every dot below is a Victorian case, and every line is a link between that patient and another made by contact tracers. Dots of the same colour share the same genetic virus signature as others. Some clusters, such as the large 75-person outbreak that erupted in March (shown in red down the bottom) were also linked genetically to other clusters although no connections were found on the ground.

Victorian clusters between January 25 and April 29 were linked by genetics as well as contact tracing. Credit:Source: The Doherty Institute

Still, the worlds genomic dataset on COVID-19 is both museum and live recording its not over yet.

Scientists stress they have only part of the picture most virus lineages infecting people will not be sequenced. Even that first sample published in Wuhan did not come from a definitive patient zero but one of the earliest known cases: a 41-year-old worker in the wet market where the virus is suspected to have first broken out or circulated.

We might not ever find the very first because so many people get no symptoms or mild symptoms, Balloux says.

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Vasan warns theres a danger in any outbreak: in the race to find a cure, scientists could pick up the first sample that comes their way and run with it - in the wrong direction. When the Doherty Institute became the first lab outside China to sequence and grow the virus, it was passed like a baton in a relay, straight to Vasan at the CSIRO for mass production as his team test some of the worlds top vaccine candidates.

But in the back of my mind, I wanted to be sure what we were working with was a typical strain, Vasan says.

So, he called in experts in artificial intelligence, including Bauer, to help screen samples for unusual mutations, particularly in areas where changes could cause a real difference to how the virus behaves, such as in its unstable and much-discussed spike. The results were reassuring they found that the first Wuhan strain, now used all around the world as a reference, was a good sample, as were the baseline strains used in Washington, Sydney, Melbourne and elsewhere. Even labs in the UK use our first Victorian strain now, Vasan says.

But they did find some outliers, including a NSW sample which contained a curious deletion. Another, collected in Italy, had mutations in common with both a Sydney virus cluster and one on the other side of the world in Chongqing, China.

Were not sure why, Bauer says. It could have been a recombination, where someone is infected with two lineages of virus at the same time that gave rise to this particular version.

The probability of two different viral lineages evolving the exact same mutations on their own is very low, Bauer says, though Vasan notes not impossible.

Influenza, meanwhile, spits out hybrid strains all the time on a much bigger scale known as reassortment. While coronaviruses can also recombine, they are less likely to produce anything too radically new in one go, Balloux says, because these spiky pathogens come with their own in-built proofreader a kind of molecular quality control.

Bauer likens it to the difference between using a cookie cutter to make Christmas biscuits and letting your toddler loose kneading the dough into the right star shape. Thats probably what allowed it to become larger and more sophisticated than other RNA viruses, she says.

Nadias nasal swabs were tested in two different labs, the University of Illinois and Cornell University, then driven through the night to a government lab for further checks all came back positive.Credit:Stephen Kiprillis, Kirsten Burghard

In Nadia the tiger, one strand of COVID-19 that had stretched all around the world reached the end of the line the big cat is thought to have caught it from a zookeeper without symptoms in March but did not pass it back to another human.

But she was part of a big cat cluster inside the Bronx Zoo. Nadia was tested first in early April because she seemed the sickest but five tigers and three lions would test positive in total. All are now recovering well, says Professor Karen Terio who helped co-ordinate the tests at her zoological pathology lab at the University of Illinois.

Nadia was coughing, which is an odd clinical sign for a tiger, so we had a suspicion, Terio says.

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The labs virologist, Leyi Wang, who had to devise a whole lab test for the felines, admits Nadias positive still came as a shock. The zoo had already been shut for weeks when the tiger got sick [at the end] of March Now were looking at the other cats. The tigers strain was very similar to the human New York virus but the lion samples look a bit different to the tigers. Its not clear yet how they were all infected.

Balloux notes that the fact the virus can infect other species makes it possible two different lineages human and animal could recombine into a hybrid strain down the line. Some think thats how we got COVID-19 to begin with. An old bat coronavirus might have mixed with one in a pangolin [a mammal trafficked in China] or maybe it just jumped to the pangolin or [another mammal] that has ACE2 [receptors] like humans and evolved there.

But he is not worried.

Next to the millions of human COVID-19 cases already confirmed, only a tiny handful of animals, including cats, dogs and ferrets, have tested positive and then only in mild or asymptomatic cases (or at high deliberate doses in the lab). Aside from a cluster of mink in cramped fur farms in the Netherlands, there has been no sign animals can pass the virus back to people. Experts say this suggests transmission between species (notably humans and their pets) is very weak and no cause for alarm.

So how did eight big cats fall sick all at once?

The Bronx Zoo did not answer questions on the circumstances or whether staff members had also tested positive, and Terio says that contact tracing work is ongoing and has not been disclosed to her for privacy reasons. While the cluster does offer new clues about what species are particularly susceptible to SARS-CoV-2, she thinks its probably too much of a leap to say it narrows down the search into the viruss origins.

Evolutionary biologist Professor Edward Holmes points to another cluster, this time of mink falling severely ill in Dutch farms, as the best place to start looking - mink are also widely farmed in China for their fur. Another lead could lie with the highly endangered and heavily trafficked pangolin which has been found via genomics to carry a similar (though not identical) virus. Holmes says the wildlife trade, including fur farming, remains the most likely origin of the pandemic, as happened with SARS and many other outbreaks.

CSIRO scientists are growing both the coronavirus and vaccine candidates in their lab in Geelong, Victoria as part of a global race for a cure.Credit:Stephen Kiprillis, Kirsten Burghard

Fortunately, most scientists say it is unlikely the virus will mutate into something nastier by its very nature a germ wants to spread, not kill.

Over time Vasan expects it will become milder the way past pandemic flu strains have as they adapted to their new host. But, also like pandemic flu, COVID could linger on as a seasonal problem that flares up in the cold winter months at least until it is properly stamped out by vaccination programs.

Back at the CSIROs sprawling lab in Geelong, vast stores of the coronavirus enough for at least two years of vaccine and treatment experimentation sit in high-security freezers at minus 80 degrees. A virus that mutates slowly is unlikely to lose its bite any time soon. But it's also less likely to change to evade a vaccine.

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Im not worried its going to get worse or mutate out of control of a vaccine, Balloux says. Its already [spreading] out of control now. It's already bad."

Finding an effective vaccine or treatment is critical to getting the world back to some degree of normality while so many of us are still susceptible, Vasan says. Scientists developing vaccines arent closing their eyes to the virus genome much of the work is focused on areas of its molecular structure less likely to mutate.

Its like a child in a playground, were keeping an eye on it, Vasan says. That doesnt mean were worried but well keep looking back while [we work], so we know the child is still there.

Of course, for all the attention on COVID-19s genome, he stresses there is still crucial data missing matching, de-identified clinical records that could show the severity, outcome and personal risk factors of each case.

Mother Nature is running a giant experiment all around the world right now. Thats where we need to look to see what the mutations mean.

The problem, Vasan says, is that even very basic patient metadata is maddeningly inconsistent across jurisdictions, both interstate and international and no one is showing much enthusiasm for cleaning it up. Mild and moderate mean different things everywhere.

Of the many thousands of virus samples sequenced and shared worldwide, the CSIRO team managed to find just 300 with meaningful, matching patient information.

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Their resulting analysis was underpowered, Bauer says, but they could already make a preliminary link between changes in clinical outcomes and mutations in the viruss spike protein. Imagine what we could do if we had more.

Only the World Health Organisation could co-ordinate an international approach to streamlining such data into uniform categories, Vasan says, but Australia could still lead the charge with some show and tell.

If we can pull this data together [nationally], we can show the world what it can teach us, he says. What we find out could change the game.

Read more here:
Coronavirus: How COVID-19 is mutating across the world - Sydney Morning Herald

by Stanford Medicine on June 13, 2020 1:30 pm

The Chan Zuckerberg Initiative (CZI) has awarded $1.49 million to research projects involving Stanford Medicine scientists who will investigate emerging ideas about the role of inflammationin disease. The grants will be awarded over a two-year period.

Ami Bhatt is one of the researchers on the Analyzing how inflammation affects the aging brain project that will be receiving funds from the Chan Zuckerberg Initiative. (Courtesy Stanford Medicine)

CZI is a philanthropic organization established byFacebookfounder Mark Zuckerberg and his wife, Priscilla Chan, in 2015.

Following are short descriptions of the projects, their funding amounts and the names of their investigators (lead investigators are listed first):

Analyzing how inflammation affects the aging brain ($525,000): ANNE BRUNET, professor of genetics; AMI BHATT, assistant professor of genetics and of hematology; CHRIS GARCIA, professor of structural biology and of molecular and cellular physiology.

Imaging gut immune cells and microbes to understand health and disease($300,000): LUCY ERIN OBRIEN, assistant professor of molecular and cellular and biology; KC HUANG, professor of bioengineering and of microbiology and immunology.

Studying vascular disease in black and Hispanic patients ($525,000): JOSEPH WU, professor of cardiovascular medicine and director of the Stanford Cardiovascular Institute; ELSIE GYANG ROSS, assistant professor of vascular surgery and of biomedical informatics research; and PHILIP TSAO, professor of cardiovascular medicine.

Understanding how stress and social disparity affect preterm birth ($140,000): Jingjing Li, assistant professor of neurology (UCSF); GARY SHAW, professor of pediatrics; and DAVID K. STEVENSON, professor of pediatrics.

Read this article and more on the Stanford Medicine website.

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Chan Zuckerberg Initiative awards $1.49 million to Stanford researchers | The - Stanford University News

CINCINNATI, June 08, 2020 (GLOBE NEWSWIRE) -- Aerpio Pharmaceuticals, Inc. (Aerpio) (ARPO), a biopharmaceutical company focused on developing compounds that activate Tie2 to treat ocular diseases and diabetic complications, today announced that it is hosting a key opinion leader (KOL) call on a novel mechanism for the treatment of glaucoma on Friday, June 12, 2020 at 11:30am Eastern Time.

The call will feature presentations by Dr. Paul Kaufman M.D. (University of Wisconsin) and Dr. Janey Wiggs, M.D., Ph.D. (Massachusetts Eye and Ear Infirmary and Harvard Medical School), who will discuss the current glaucoma treatment landscape and unmet medical needs, as well as the role of the Tie2 receptor in maintaining intraocular pressure. Drs. Kaufman and Wiggs will be available to answer questions at the conclusion of the event.

Aerpio's management team will also discuss its pipeline candidate, razuprotafib (formerly AKB-9778), for treating patients with glaucoma. Razuprotafib is a small molecule inhibitor that restores Tie2 activation in Schlemms canal and lowers intraocular eye pressure (IOP) via decreasing resistance to outflow from the eye. Razuprotafib has been formulated as a once or twice-daily topical eye drop and is entering a Phase 2 clinical trial in Q3:20, with top line data expected in Q1:21.

Aerpio recently announced positive and statistically significant intraocular eye pressure (IOP) reduction in a Phase 1b trial of 43 glaucoma patients, when razuprotafib was added to prostaglandin treatment. This data set is summarized here.

Paul Kaufman, M.D. is the Ernst H. Brny Emeritus Professor of Ocular Pharmacology and past Chair of the Department of Ophthalmology & Visual Sciences at the University of Wisconsin School of Medicine and Public Health, in Madison, Wisconsin. He is a physician-scientist, specializing in glaucoma and studying the mechanisms of aqueous humor formation and drainage, and the age-related loss of near vision. Dr Kaufman is a past President and past Executive Vice President of the Association for Research in Vision and Ophthalmology (ARVO), past President of the International Society for Eye Research (ISER), and has served on the US National Advisory Eye Council and numerous foundation and corporate scientific advisory boards. He has had continuous research funding from the US National Eye Institute for 40 years and from numerous private foundations, has authored over 375 original scientific articles and 75 book chapters, co-edited several textbooks including the most recent editions of Adlers Physiology of the Eye, and received numerous honors and awards including the Friedenwald Award from ARVO and the Balazs Prize from ISER. He was Editor-in-Chief of Investigative Ophthalmology & Visual Science from 2008 through 2012. Dr. Kaufman also holds an honorary Doctor of Medicine degree from Uppsala University in Sweden, where he was a post-doctoral research fellow.

Janey L. Wiggs, M.D., Ph.D. is a physician-scientist at the Massachusetts Eye and Ear Infirmary and Harvard Medical School. She is currently the Paul Austin Chandler Professor of Ophthalmology and is the Vice Chair for Clinical Research in Ophthalmology at Harvard Medical School. She also directs the CLIA-certified genetic testing laboratory at the Massachusetts Eye and Ear Infirmary and is a co-director of the Ocular Genomics Institute and co-director of the Glaucoma Center of Excellence. Dr. Wiggs received her B.A. and Ph.D. degrees in biochemistry from the University of California at Berkeley and her M.D. degree from Harvard Medical School. She did post-doctoral training in molecular genetics under the direction of Dr. Ted Dryja. Dr. Wiggs completed the ophthalmology residency at the Massachusetts Eye and Ear Infirmary and received fellowship training in glaucoma and also in medical genetics and is certified by the both the American Board of Ophthalmology and the American Board of Medical Genetics. Dr. Wiggs research program is focused on the discovery and characterization of genetic factors that contribute to the blinding eye disease glaucoma and is funded by the National Eye Institute (NEI) as well as other nonprofit foundations. She is investigating the genetic etiologies of both early-onset and adult forms of glaucoma and is the PI of the NEIGHBORHOOD consortium for gene discovery in primary open angle glaucoma and is a founding member of the International Glaucoma Genetics Consortium (IGGC). She has also participated in research programs funded by the US-INDO joint working group (NEI) and the NEI eyeGENE consortium. Dr. Wiggs was the inaugural chair of the Genetics Group for ARVO and is an ARVO gold fellow. She currently serves on the editorial boards of IOVS, JAMA Ophthalmology, Molecular Vision, Journal of Glaucoma, and Annual Reviews in Vision Science. She is a member of the scientific advisory boards for the Glaucoma Research Foundation, Research to Prevent Blindness and the Glaucoma Foundation, and is a past member of the Advisory Council of the National Eye Institute. She has received the Heed Award, the Heed/Knapp Award, the Research to Prevent Blindness Scholar Award, the AAO Honor Award, the Lew Wasserman Merit Award, the Alcon Research Award, the David L. Epstein award from the ARVO Foundation and was a winner of the NEI Audacious Goal competition. She is an elected member of the Glaucoma Research Society, the American Ophthalmological Society, the Academia Ophthalmologica Internationalis and the National Academy of Medicine.

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About RazuprotafibRazuprotafib binds to and inhibits vascular endothelial protein tyrosine phosphatase (VE-PTP), an important negative regulator of Tie2. Decreased Tie2 activity contributes to vascular instability in many diseases including diabetes and more recently has been shown to contribute to the development of increased IOP and glaucoma. Razuprotafib activates the Tie2 receptor irrespective of extracellular levels of its binding ligands, angiopoietin-1 (agonist) or angiopoietin-2 (antagonist) and may be the most efficient pharmacologic approach to maintain normal Tie2 activation. Aerpio is studying a topical ocular formulation of razuprotafib in open angle glaucoma and exploring the utility of subcutaneous razuprotafib for diabetic complications, including diabetic nephropathy.

About Aerpio PharmaceuticalsAerpio Pharmaceuticals, Inc. is a biopharmaceutical company focused on developing compounds that activate Tie2 to treat ocular diseases and diabetic complications. Recently published mouse and human genetic data implicate the Angpt/Tie2 pathway in maintenance of Schlemms canal, a critical component of the conventional outflow tract. The Companys lead compound, razuprotafib (formerly AKB-9778), a first-in-class small molecule inhibitor of vascular endothelial protein tyrosine phosphatase (VE-PTP), is being developed as a potential treatment for open angle glaucoma, and the Company intends to investigate the therapeutic potential of razuprotafib in other indications. The Company is also evaluating development options for ARP-1536, a humanized monoclonal antibody, for its therapeutic potential in the treatment of diabetic vascular complications including nephropathy and diabetic macular edema (DME). The Companys third asset is a bispecific antibody that binds both VEGF and VE-PTP which is designed to inhibit VEGF activation and activate Tie2. This bispecific antibody has the potential to be an improved treatment for wet age-related macular degeneration and DME via intravitreal injection. Finally, the Company has exclusively out-licensed AKB-4924 (now called GB004), a first-in-class small molecule inhibitor of hypoxia-inducible factor-1 (HIF). GB004 is being developed by AKB-4924s exclusive licensor, Gossamer Bio, Inc. (GOSS). For more information, please visit http://www.aerpio.com.

Forward Looking StatementsThis press release contains forward-looking statements. Statements in this press release that are not purely historical are forward-looking statements. Such forward-looking statements include, among other things, the Companys product candidates, including razuprotafib, ARP-1536 and the bispecific antibody asset, the clinical development plan therefor and the therapeutic potential thereof, the Companys plans and expectations with respect to razuprotafib and the development therefor and therapeutic potential thereof in addressing COVID-19 and the intended benefits from the Companys collaboration with Gossamer Bio for GB004, including the continued development of GB004 and the milestone and royalty payments related to the collaboration. Actual results could differ from those projected in any forward-looking statements due to several risk factors. Such factors include, among others, the continued development of GB004 and maintaining and deriving the intended benefits of the Companys collaboration with Gossamer Bio; ability to continue to develop razuprotafib or other product candidates, including in indications related to COVID-19; the inherent uncertainties associated with the drug development process, including uncertainties in regulatory interactions, the design of planned or future clinical trials, commencing clinical trials and enrollment of patients in clinical trials; obtaining any necessary regulatory clearances in order to commence and conduct planned or future clinical trials; the impact of the ongoing COVID-19 pandemic on the Companys business operations, including research and development efforts and the ability of the Company to commence, conduct and complete its planned clinical activities; and competition in the industry in which the Company operates and overall market conditions; and the additional factors set forth in our Annual Report on Form 10-K for the year ended December 31, 2019, as updated by our subsequent Quarterly Reports on Form 10-Q and our other subsequent filings with the SEC.

These forward-looking statements are made as of the date of this press release, and the Company assumes no obligation to update the forward-looking statements, or to update the reasons why actual results could differ from those projected in the forward-looking statements, except as required by law. Investors should consult all the information set forth herein and should also refer to the risk factor disclosure set forth in the reports and other documents the Company files with the SEC available at http://www.sec.gov.

Investors & Media:Gina MarekVP Financegmarek@aerpio.comOrInvestors:Irina KofflerLifeSci Advisorsikoffler@lifesciadvisors.com

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Aerpio Hosting Key Opinion Leader Call on a Novel Mechanism for the Treatment of Glaucoma - Yahoo Finance