StemCell Therapy

Genes are by no means a crystal ball, but they can be used to forecast susceptibility to a variety of conditions, from cancers and heart disease to chronic inflammatory conditions. As such, they can help healthcare professionals and patients make better care decisions.

Generally speaking, whenpeople today think about genetic predispositions, theythink about their parents and family trees.However, those inherited genetic variationsbequeathed by ourparents and grandparents are only a portion ofacomplete genetic picture and often not the most revealing one.Thegenetic variationsmost commonly linked to disease are actually?not?the ones from your parents; rather, they areacquiredas one ages.

Mom and Dad Cant Take All the Heat forAll Health ChallengesUnlike inheritedgenetic predispositions,accumulatedgenetic changes(otherwise known as somatic)are the result ofenvironmental influences, such as smoking, chemicals or ultra-violet radiation. They can also stem from common errorscells make as they duplicate themselves over time.The expansion of these detrimental variations cause damage to DNA within blood cells,aphenomenon known as clonal hematopoiesis (CH), whichincreases susceptibility to many diseases, including many types of cancer.

Germline variations in genes still indicate potential vulnerabilities, with one in five healthy adults estimated to carry an inherited marker. However, these genetic abnormalities represent a static metric. Once individuals are tested for inherited variations, they will never need to do so again. Whats more, many of the predispositions that surfaced through this testing can be addressed through lifestyle and medical interventions. It boils down to being aware of them.

Somatic changes, on the other hand, can happen at any stage of life. While many of these changes have no clinical ramifications, some of them can exacerbate predispositions inherited from our parents because the disease is often the result of multiple genetic variations banding together, inherited or acquired.

The chances of an acquired variation accumulating and accelerating within the body increase significantly as we age, generally after the age of 40 and growing each decade. This could drastically change a patients health profile, casting inherited vulnerabilities into a new light without any warning or symptoms.

Understanding Accumulated VariationsA growing body of research links somatic changes to an increased likelihood of blood cancers and cardiovascular disease, both heart disease and stroke. The same research reveals that these accumulated genetic variations contribute to infection and severe inflammatory reactions, some of which are associated with severe cases of Covid-19.

A study conducted byJAMA Cardiologyexplores theconnectionbetween accumulated genetic change anda pro-inflammatory immune response that resembles the exaggerated cytokine release syndrome (CRS)experienced by patients with severeCovid-19.Notably,the researchfoundthat patients who experienced the most extreme inflammatory response carried variationsTET2 and DMNT3A, both of which accumulate in genes over time.

Another research report published inCancersanalyzingpatients hospitalized with severe Covid-19disease found a much higher frequency of clonal hematopoiesis (CH) of indeterminate potential (sometimes called clonal hematopoiesis of indeterminate potential or CHIP) ),an age-associated condition in cells,in all age groups.

Additionally,accumulatedDNA damage to the JAK2 gene has been found in alargeproportion of cancer-free patients with venous thrombosis, a known complicationof Covid-19.While preliminary,the findingsdemonstratecompellingcorrelations betweensomaticgenetic change andCovid-19 severity that could be used to identify patients prone to complications early, intervene soonerand inform treatment strategies.

It is believed thatproviders can applythese correlations to other areas of care toassess an individuals susceptibilityto a wide range of diseases, and ultimately improve and extend quality of life.

Improving Care Decisions with Somatic insightsAugmenting currenthealth assessmentsand care strategies with accumulated geneticdatacan open new pathways for disease detection, response and prevention.The scientificand medicalcommunitieshaveonly scratched the surface ofwhat we can learn from these insights. Even so,understanding somatic damage showsgreatpromise for helping individualsstay ahead of their health concerns and respond in a more informed way.

Photo: Andy, Getty Images

See the article here:
Accumulated genetic variations: What they are and why they matter to a complete health picture - MedCity News

Getting to the guts of local evolution

The microbiota of mammals is a product of coevolution. However, humans exhibit a range of adaptive peculiarities that can be quite geographically specific. The human microbiota also displays a variety of community compositions and a range of overlapping and redundant metabolic characteristics that can alter host physiology. For example, lactase persistence is a genetic characteristic of European populations, but in populations lacking the lactase gene, milk sugar digestion is endowed by the microbiota instead. Suzuki and Ley review the evidence for the role that the microbiota plays in local adaptation to new and changing human circumstances.

Science, this issue p. eaaz6827

When human populations expanded across the globe, they adapted genetically to local environments in response to novel selection pressures. Drivers of selection include exposure to new diets, climates, or pathogens. Humans harbor microbiotas that also respond to changes in local conditions and changes in their hosts. As a result, microbiotas may alter the adaptive landscape of the host through modification of the environment. Examples include changes to a foods nutritional value, the hosts tolerance to cold or low amounts of oxygen, or susceptibility to invading pathogens. By buffering or altering drivers of selection, the microbiota may change host phenotypes without coevolution between host and microbiota. Functions of the microbiota that are beneficial to the host may arise randomly or be acquired from the environment. These beneficial functions can be selected without the host exerting genetic control over them. Hosts may evolve the means to maintain beneficial microbes or to pass them to offspring, which will affect the heritability and transmission modes of these microbes. Examples in humans include the digestion of lactose via lactase activity (encoded by the LCT gene region) in adults and the digestion of starch by salivary amylase (encoded by the AMY1 gene)both are adaptations resulting from shifts in diet. The allelic variation of these genes also predicts compositional and functional variation of the gut microbiota. Such feedback between host alleles and microbiota function has the potential to influence variation in the same adaptive trait in the host. How the microbiota modifies host genetic adaptation remains to be fully explored.

In this paper, we review examples of human adaptations to new environments that indicate an interplay between host genes and the microbiota, and we examine in detail the LCTBifidobacterium and the AMY1Ruminococcus interactions. In these examples, the adaptive host allele and adaptive microbial functions are linked. We propose host mechanisms that can replace or recruit beneficial microbiota functions during local adaptation. Finally, we search for additional examples where microbiotas are implicated in human genetic adaptations, in which the genetic basis of adaptation is well described. These range from dietary adaptations, where host and microbial enzymes can metabolize the same dietary components (e.g., fatty acid and alcohol metabolism), through climate-related adaptations, where host and microbes can induce the same physiological pathway (e.g., cold-induced thermogenesis, skin pigmentation, and blood pressure regulation), to adaptations where hosts and microbes defend against the same local pathogens (e.g., resistance to malaria, cholera, and others). These examples suggest that microbiota has the potential to affect host evolution by modifying the adaptive landscape without requiring coevolution.

Well-studied examples of local adaptation across diverse host species can be revisited to elucidate previously unappreciated roles for the microbiota in host-adaptive evolution. In the context of human adaptation, knowledge of microbial functions and host genemicrobe associations is heavily biased toward observations made in Western populations, as these have been the most intensively studied to date. Testing many of the interactions proposed in this Review between host genes under selection and the microbiota will require a wider geographic scope of populations in their local contexts. Because genes under strong selection in humans are often involved in metabolic and other disorders and can vary between populations, future investigations of host genemicrobe interactions that relate to human adaptation may contribute to a deeper understanding of microbiota-related diseases in specific populations. Investigating host genemicrobe interactions in a wider variety of human populations will also help researchers go beyond collections of anecdotes to form the basis of a theory that takes microbial contributions to host adaptation into account in a formal framework. A better understanding of reciprocal interactions between the host genome and microbiota in the context of adaptive evolution will add another dimension to our understanding of human evolution as we moved with our microbes through time and space.

When human populations adapt genetically to new environments, their microbiotas may also participate in the process. Microbes can evolve faster than their host, which allows them to respond quickly to environmental change. They also filter the hosts environment, thereby altering selective pressures on the host. Illustrated here are examples of interactions between adaptive host alleles and adaptive microbiota functions where the microbiota likely modified the adaptive landscape in response to changes in diet (e.g., changes in levels of starch and milk consumption), exposure to local pathogens (e.g., malaria parasites and Plasmodium spp.), and changes in local climate (e.g., cold stress and hypoxia). In this paper, we discuss the resulting relationships between host-adaptive alleles and microbiota functions.

As human populations spread across the world, they adapted genetically to local conditions. So too did the resident microorganism communities that everyone carries with them. However, the collective influence of the diverse and dynamic community of resident microbes on host evolution is poorly understood. The taxonomic composition of the microbiota varies among individuals and displays a range of sometimes redundant functions that modify the physicochemical environment of the host and may alter selection pressures. Here we review known human traits and genes for which the microbiota may have contributed or responded to changes in host diet, climate, or pathogen exposure. Integrating hostmicrobiota interactions in human adaptation could offer new approaches to improve our understanding of human health and evolution.

Continue reading here:
The role of the microbiota in human genetic adaptation - Science

When applying genetics to the study of COVID-19, scientists are learning a lot. Our DNA codes for proteins, some of which are required for SARS-CoV-2 to interact with and infect a host cell, others that are implicated in the downstream effects of viral infection, such as inflammatory responses. But how do scientists choose which genes to study?A new study by Dr Thomas Stoeger, a postdoc at North Western University, suggests there is a historical bias involved; scientists are studying human genes that have already been heavily investigated, independent of COVID-19.

In this installment of Teach Me in 10, Stoeger expands on the key points of this study and the implications of bias in scientific research.

Full research publication: Meta-Research: COVID-19 research risks ignoring important host genes due to pre-established research patterns.

For more Teach Me in 10 videos, check out our hub page.

Are you a Facebook user? Like the Teach Me in 10 Facebook page to engage and network with the video audience.

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Teach Me in 10 Why COVID-19 Genetics Research May Be Biased With Dr Thomas Stoeger - Technology Networks

Scientists at Boyce Thompson Institute have produced a high-quality chromosome-scale genome sequence for the currant tomato Solanum pimpinellifolium, the wild progenitor of the modern cultivated tomato Solanum lycopersicum.

Solanum pimpinellifolium in Botanisk tidsskrift, 1872.

Tomato is the worlds leading vegetable crop with a total production of 182 million tons and a worth over US $60 billion in 2018.

Solanum pimpinellifolium carrying red, small, and round fruits is the wild progenitor of the cultivated tomato.

It was domesticated in South America to give rise to Solanum lycopersicum var. cerasiforme, which was later improved into the big-fruited tomato Solanum lycopersicum var. lycopersicum in Mesoamerica.

Although other groups had previously sequenced Solanum pimpinellifolium, the new reference genome is more complete and accurate, thanks in part to cutting-edge sequencing technologies that are able to read very long pieces of DNA, said co-lead author Dr. Zhangjun Fei, a researcher at Boyce Thompson Institute and Robert W. Holley Center for Agriculture and Health at the U.S. Department of Agricultures Agricultural Research Service.

Older sequencing technologies that read short pieces of DNA can identify mutations at the single-base level, said co-lead author Dr. Shan Wu, a postdoctoral scientist at Boyce Thompson Institute.

But they arent good at finding structural variants, like insertions, deletions, inversions or duplications of large chunks of DNA.

Many known traits of the tomato are caused by structural variants, so that is why we focused on them, Dr. Fei said.

Structural variants also are understudied because they are more difficult to identify.

The scientists compared their reference genome of Solanum pimpinellifolium to that of the cultivated tomato, called Heinz 1706, and found more than 92,000 structural genetic variants.

They then combed the tomato pan-genome, a database with the genomes of more than 725 cultivated and closely related wild tomatoes, and discovered structural variants related to many important traits.

For example, the modern cultivated tomato has some genomic deletions that reduce their levels of lycopene, a red pigment with nutritional value, and an insertion that reduces their sucrose content.

Identification of the additional genetic diversity captured in the Solanum pimpinellifolium genome provides breeders with opportunities to bring some of these important features back to store-bought tomatoes, said co-author Dr. Jim Giovannoni, a researcher at Boyce Thompson Institute and Robert W. Holley Center for Agriculture and Health at the U.S. Department of Agricultures Agricultural Research Service.

The authors found many other structural variants that could be of interest to plant breeders, including variants in numerous disease-resistance genes and in genes involved in fruit size, ripening, hormonal regulation, metabolism, and the development of flowers, seeds and leaves.

They also found structural variants associated with regulating the expression of genes involved in the biosynthesis of lipids in fruit skin, which could help improve the fruits post-harvest performance.

So much genetic diversity was lost during tomato domestication, Dr. Fei said.

These data could help bring some of that diversity back and result in tomatoes that taste better, are more nutritious and more resilient.

The results appear in the journal Nature Communications.

_____

X. Wang et al. 2020. Genome of Solanum pimpinellifolium provides insights into structural variants during tomato breeding. Nat Commun 11, 5817; doi: 10.1038/s41467-020-19682-0

This article is based on a press-release provided by Boyce Thompson Institute.

Continued here:
Researchers Sequence Genome of Tomato's Wild Ancestor | Genetics - Sci-News.com

Researchers based at the Neuroscience Institute at the University of Sheffield in the UK have identified a new genetic risk factor for Motor Neurone Disease (MND) in so-called 'junk DNA'.

The newly discovered genetic changes are present in up to 1% of MND patients.

The research, published in the journal Cell Reports, focused on genetic mutations in non-coding DNA, often known as junk DNA because it does not directly encode protein sequences. Non-coding DNA makes up more than 99% of the human genome, but currently is relatively unexplored.This research also includes new methods for studying mutations in non-coding DNA which could be applied to other diseases.

The authors of the study reported that they determined an existing neuroprotective drug developed at the University of California San Diego (UCSD) called SynCav1 could help MND patients carrying the newly discovered genetic mutation.

An experimental gene therapy for the treatment of neurological disorders such as MND and Alzheimers disease, SynCav1 has been licensed to CavoGene LifeSciences.

MND or Amyotrophic Lateral Sclerosis (ALS), as it is also known, affects motor neurons in the brain and spinal cord that form the connection between the nervous system and muscles to enable movement of the body. The progressive disease affects a patient's ability to walk, talk, use their arms and hands, eat and breathe.

Around 5,000 people in the UK and 30,000 people in the US are currently living with MND, with numbers expected to rise.

High-income countries currently have the highest rates of motor neuron diseases worldwide, and the burden is increasing with the ageing population, shows an analysis of the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016.

Dr Jonathan Cooper-Knock, lead author of the study and NIHR clinical lecturer in Neurology at the Neuroscience Institute at the University of Sheffield, said: "Until now scientists have never systematically examined non-coding or junk DNA in relation to the development of MND.

"Not only have we identified a mutation in junk DNA which puts people at risk of developing a certain form of the MND, but we have also found that by targeting the mutated gene with the established neuroprotective drug called SynCav1, it might be possible to halt or potentially prevent the disease progressing in those patients.

"This is a significant breakthrough in terms of genetic risk factors driving personalized medicine for MND patients."

Link:
An experimental gene therapy may be effective for MND patients with a newly discovered genetic mutation - BioPharma-Reporter.com

New genetic differences have been discovered to play a vital role in regulating blood pressure, according to research part funded by us and published in Nature Genetics.

Researchers based at the University of Cambridge and round the world studied the genetic make-up of 1.3 million people with diverse ancestries. They found 106 new regions of DNA and 87 new rare genetic variations associated with blood pressure.

The rare genetic variants had an eight times greater effect on blood pressure compared to more common variants. Thirty-two of the rare variants were located within newly identified sections of DNA linked to blood pressure, and 55 were located within genes already known to be associated with its regulation.

The importance of the work is illustrated by the finding that six of the genes identified in this study, four of which contain rare variants, are already drug targets for heart and circulatory conditions. This suggests that the other genes identified may also be good targets for developing new drugs.

The researchers therefore hope that these findings will lead to new ways to prevent and treat high blood pressure.

Professor Sir Nilesh Samani, our Medical Director, said:

This major study has revealed new underlying genetic factors which add to the blueprint of what dictates our blood pressure.

High blood pressure is a major risk factor for heart and circulatory diseases. These new discoveries should shed light on potential new ways to prevent and treat high blood pressure and ensure its in a healthy range, ultimately to reduce deadly heart attacks and strokes.

Read more about high blood pressure

Read more:
Rare genetic differences play vital role in blood pressure - British Heart Foundation

A new report added by Research Dive offers insights and puts forth the impact of COVID-19 catastrophe on the global human genetics market. According to the report, the human genetics market is estimated to grow at a significant rate and generate robust revenue share by 2027 during the forecast period from 2020 to 2027.

The report provides brief summary and an in-depth information of the market by collecting data from industry experts and different sources prevalent in the market. The statistics presented in the report are extensive, reliable, and the outcome of an exhaustive analytical research. The report offers qualitative and quantitative trend analysis for the period of 2020-2027 to assist stakeholders to understand the overall market scenario. Comprehensive analysis of the key segments validates the types of products used in the industry and their applications.

MARKET SEGMENTATION

On the basis of type, the global human genetics market is segmented into:

Product Type Segmentation Prenatal Genetics Cytogenetics Molecular Genetics & Symptom Genetics

For More Detail Insights, Download Sample Copy of the Report at: https://www.researchdive.com/request-toc-and-sample/2137

On the basis of application, the global human genetics market is segmented into:

Cytogenetics Molecular Genetics Prenatal Genetics Symptom Genetics Research Center Industry Segmentation Forensic Laboratories Hospital

On the basis of region, the global human genetics market is segmented into:

North America U.S. Canada Mexico

Europe Germany UK France Spain Italy Rest of Europe

Asia-Pacific Japan China India Australia South Korea Rest of Asia-Pacific

LAMEA Brazil Argentina Saudi Arabia South Africa UAE Rest of LAMEA

Connect with Our Analyst to Contextualize Our Insights for Your Business: https://www.researchdive.com/connect-to-analyst/2137

KEY COMPANIES COVERED

The research report summarizes and outlines several aspects of the key players operating in the global human genetics market such as company snapshot, business performance, product portfolio, recent developments & strategies, SWOT analysis, and many more. The key players listed are:

LGC Forensics Agilent Technologies QIAGEN N.V. Bode Technology Illumina Thermo Fisher Scientific Inc. Promega Corporation Orchid Cellmark Inc. NextOmics GE Healthcare Takara Bio Inc. Oxford Nanopore Pacific Biosciences

RECENT DEVELOPMENTS

The key players of the market are adopting several strategies to obtain a leading position in the global industry. For instance, in August 2020, Ancestry launched AncestryHealth, a product that features next-generation sequencing with an ability to screen the genes associated with blood disorders, breast cancer, colon cancer, and heart disease.

Contact Us:

Mr. Abhishek PaliwalResearch Dive30 Wall St. 8th Floor, New YorkNY 10005 (P)+ 91 (788) 802-9103 (India)+1 (917) 444-1262 (US) TollFree : +1 -888-961-4454Email:support@researchdive.comLinkedIn:https://www.linkedin.com/company/research-diveTwitter:https://twitter.com/ResearchDiveFacebook:https://www.facebook.com/Research-DiveBlog:https://www.researchdive.com/blogFollow us on:https://covid-19-market-insights.blogspot.com

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Insights on Human Genetics Market 2020 to 2027: COVID-19 Impact Analysis, Drivers, Opportunity Analysis, Restraints, and Forecast - The Courier

MELBOURNE, Australia, Dec. 02, 2020 (GLOBE NEWSWIRE) -- Molecular diagnostics company Genetic Technologies Ltd (ASX: GTG; NASDAQ: GENE, the Company), announced today that they have entered into a three-year partnership agreement with mental health company, Taliaz, for the distribution rights of their PREDICTIX products in Australia, New Zealand and the USA (Agreement).

Key Highlights

The Agreement will support GTG to expand its product offering and establish the mental health vertical by harnessing PREDICTIX, Taliazs pioneering decision-support and management platform to optimize patient treatment for mental health disorders. Starting in the field of depression, this genomic-based, Artificial Intelligence (AI) driven antidepressant selection technology, marks GTGs first foray into pharmacogenomics1.

George Muchnicki, GTGs Interim CEO stated: We are incredibly pleased to have partnered with Taliaz to bring their predictive and personalized mental health product to Australia and New Zealand. GTG are at the forefront of providing personalized and predictive products to empower patients to make informed decisions about their health. This distribution agreement is our first external product partnership and our first product within the mental health vertical. Mental health has remained at the forefront of media discussions and government initiatives within Australia, New Zealand and globally due to the ongoing social and economic impact and given the impact from the current global pandemic. We look forward to working closely with the Taliaz team to deliver their product into these markets at this critical time.

The execution of the Agreement is reliant on product regulatory clearance by the Therapeutic Goods Administration (TGA) in Australia and Food and Drug Administration (FDA) in the USA. Once cleared, GTG has committed to providing a minimum distribution of 8,000 tests over the initial three-year term with an associated minimum cost to GTG of $200,000 over the term, inclusive of licencing fees and a percentage based fee per test paid to Taliaz. Subject to the regulatory clearance process, GTG anticipates that PREDICTIX will be made available for sale and distribution in Australia and New Zealand in Q3 FY21 on GTGs existing Consumer Initiated Testing (CIT) platform, with end-customer pricing to be determined but anticipated to be in line with existing GTG product pricing.

PREDICTIX, developed by the private Israeli company, Taliaz, addresses the growing burden on society from depression, with 1 in 10 Americans2 and 1 in 8 Australians3 prescribed antidepressants per year. PREDICTIX enables a more accurate and rapid treatment plan for patients suffering from depression, reducingtreatment costs and the overall associated economic burden.

PREDICTIX is an algorithmic-based decision support tool that can improve todays antidepressant prescribing accuracy by 47%4. Combining DNA testing with AI, PREDICTIX empowers doctors to improve the assessment, treatment, and management of mental health disorders.

The PREDICTIX technology uses AI to analyse multiple data streams, including patients genomic, clinical history and demographic background, providing doctors with a personalized patient report. The report ranks the statistical efficacy and potential side effects of various antidepressant medication based on each patients genetic makeup andhealth record. This helps doctors optimize prescribing decisions for patients diagnosed with depressive disorder, where there is currently a long and painful trial and error period. PREDICTIX is CE-registered and commercially available in the UK, France and Israel, with the process underway for TGA approval.

Dekel Taliaz, CEO and Co-founder of Taliaz said, We are excited to partner with Genetic Technologies, world-leaders in the genetic risk assessment space. This new partnership will support rapid commercialization of PREDICTIX to help more depression sufferers in Australia, New Zealand and the USA, while adding a complementary and advanced mental health solution to GTGs growing suite of DNA tests.

The Agreement strengthens GTGs mission in creating a suite of tests to enable a holistic and predictive health assessment for patients, which can be adjusted to address the individual patient risks and needs. Establishing the first product within the mental health and pharmacogenetic space continues GTGs progress towards being able to offer a highly comprehensive suite of polygenic risk assessment tests via GTGs CIT platform and additional sales and marketing avenues as these are progressed.

This announcement was approved by the Board of Directors of Genetic Technologies Limited.

About Genetic Technologies Limited

Genetic Technologies Limited (ASX: GTG; Nasdaq: GENE) is a diversified molecular diagnostics company. GTG offers cancer predictive testing and assessment tools to help physicians proactively manage patient health. The Companys lead products GeneType for Breast Cancer for non-hereditary breast cancer and GeneType for Colorectal Cancer are clinically validated risk assessment tests and are first in class. Genetic Technologies is developing a pipeline of risk assessment products.

For more information, please visit http://www.gtglabs.com

About Taliaz

Taliaz is revolutionizing the treatment and management of mental health disorders with PREDICTIX. PREDICTIX is a CE-registered product that provides an advanced decision support software for psychiatrists and general practitioners. Harnessing artificial intelligence, PREDICTIX can enable easy, effective and rapid patient assessment, improved prescribing precision and management for a wide range of mental health conditions. Starting in the field of depression, the PREDICTIX Genetics and PREDICTIX Digital products can improve todays prescribing accuracy by up to 47%4.

For more information, please visit predictix.ai.

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Genetic Technologies Secures US and ANZ Distribution Rights for PREDICTIX - BioSpace

Washington, D.C. November 30, 2020 Today Consumer Federation of America released a new report,Marketing Direct-to-Consumer Genetic Testing: Are Consumers Getting What They Think They Are?It examines the claims direct-to-consumer (DTC) genetic testing companies make for these services, the information they provide to consumers about them, the variance of results from one company to another, the up-selling that occurs, and the companies terms of service and privacy policies. With the holidays coming up and DTC genetic testing companies promoting their services as the perfect gift, we wanted to help educate consumers about the benefits, limitations, and risks of these tests, said report author, Susan Grant, CFAs Director of Consumer Protection and Privacy. Nick Roper, Administrative and Advocacy Associate at CFA, assisted her with the research.

Conducted with a grant from the Rose Foundation, the study focused on six companies: 23andMe, Ancestry, FamilyTreeDNA, HomeDNA, LivingDNA, and MyHeritage. In order to compare the results, CFAs Grant took the basic ancestry tests from each company. We found that theres much about these tests consumers may not realize, said Grant. They need to be better informed and better protected.

What the CFA Study Found

Consumers might be surprised to know that most DTC genetic tests are not reviewed by the government before theyre marketed to confirm the claims made for them, their accuracy, or their validity, said Grant. There is a lot of helpful information on DTC genetic testing companies websites about genetics and how their services work, but were concerned that not many consumers will delve into it and assume theyll get more detailed and conclusive results than they actually will.

Recommendations

On the basis of the study, CFA made these recommendations:

DTC genetic testing companies should refrain from making specific accuracy claims.

In conjunction with the report, CFA released tips for consumers,9 Questions and Answers about DTC Genetic Testing.The full report ishere. A shorter version of the report is availablehere.

Read the original:
Are Consumers Getting What They Think They Are with Genetic Testing? - YubaNet

Most camels and their cousins, alpacas and llamas, have a reputation for being somewhat irritable and belligerent; thats backed up with occasional bouts of spitting, biting and cantankerous behaviour. They have been domesticated for a few thousand years, but they still seem to have a lofty sense of dignity despite humans trying to break their spirit. The noble camel has endured being a beast of burden and even a racing animal. But becoming a dairy animal is a work in progress as patient folks who handle them have found out since they were first tamed. Humans have milked or tried to milk camels for thousands of years; the milk is particularly nutritious and a protein source in many middle east and African societies to this day. The fact that massive camel dairy operations have sprung up would indicate that camel milk is still popular within the middle easts urbanized community and has a growing interest in other parts of the world. Camel dairy operations have started up in the USA and Australia to supply new markets, but they are modest in size. The biggest hurdle is trying to turn the camel into an efficient dairy animal with ever-increasing regular milk production assisted by mechanical handling. Thats a description of the typical bovine dairy animal of today.From a dairy perspective, the camel cow is genetically 200 years behind the average bovine dairy cow. The camel is nowhere near as docile, cooperative, nor as remotely productive as a modern dairy cow. Thats the result of longtime intensive selection as none of the other milked species started out as happy, productive dairy animals. However, modern Western-style camel dairy operations are making progress through a genetic selection process, camel training and unique camel milking and handling equipment. Some of the large middle east camel dairy operations employ highly skilled professionals that guide production increases.Interestingly, a small tribal group in Northern Kenya who are highly dependent on camel milk has, through selection, created a higher milk yielding strain of camel, so it can be done. The one fast-track system to a better milking camel cow is through mass selection. In the middle east and Australia, they have access to literally hundreds of thousands of local camel cows, both wild and captive. That enables them through a process of elimination to find the one cow in a hundred that might make a good docile camel dairy cow for a commercial dairy operation. However, selection would seem to be the easy part; its the milking part where it gets more complicated. Unlike other milking species like goats, sheep and bovines, the camel does not easily let down its milk; it needs significant stimulation and then only produces at intervals. In traditional settings, the presence of a camel cows calf provides the stimulation, and a person then hand milks the cow. Considering the camels cranky nature, that alone would seem to be a dangerous and haphazard process, never mind the food safety and sanitation concerns. Clearly, that wont work in a commercial dairy operation where thousands of camels have to be milked twice a day. Hence the big sophisticated operators in the middle east have developed protocols and equipment that eliminates most calf stimulation. Still, they must be using some sort of method to keep milk production up on a regular and consistent basis. All of that would seem to be transferable to a potentially large operation in Alberta, but a reliable source of camels would be needed. The other part is the huge capital investment, one of the largest middle east dairies started with an investment of $20 million and now has over 500 employees. Granted, this large operator controls camel milk from production to processing to worldwide marketing. It must be profitable as these large operations continue to expand in the middle east. A substantial commercial camel dairy operation in North America would have some advantages. Firstly, there is seemingly a large local market to absorb camel milk. Secondly is camel feed. The big outfits in the middle east import large quantities of costly alfalfa hay and other feedstuffs from Australia and North America to provide consistent quality feed to produce a steady supply of milk. Mammals, in general, produce surplus milk only through excess fat and protein consumption. But feed and markets arent enough of an advantage its finding enough of those darned cranky camel cows to milk. More next time. Will Verboven is an ag opinion writer and ag policy advisor.

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Cranky camels make difficult dairy cows part two but technology and genetics are making some headway - Brooks Bulletin

The unique male [white] giraffe now stands aloneafter a female and her calf were killed by poachers in March.

[A] GPS tracking device, secured to one of the animals horns, will give hourly updates of his location, said the Ishaqbini Hirola Community Conservancy in a press release on [November 17].

Rangers will be able to monitor the giraffes movements in the conservancy located in Garissa County, eastern Kenya.

The giraffes grazing range has been blessed with good rains in the recent past and the abundant vegetation bodes well for the future of the white male, said Ahmed Noor, manager of the Ishaqbini Hirola Community Conservancy.

Noor thanked the Kenya Wildlife Service, Save Giraffes Now and the Northern Rangelands Trust (NRT) for their help in safeguarding wildlife species.

Our mission is to work with communities, enable them [to] be resilient, secure their livelihoods as well as protect the unique wildlife like the only known white giraffe, said Antony Wandera, senior wildlife monitoring officer at the NRT.

The male giraffe has a rare genetic trait called leucism, which results in the partial loss of pigmentation in an animal and makes it easy to spot for poachers on the arid savannah.

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Last surviving white giraffe, a genetic anomaly, fitted with GPS tracker to deter poachers - Genetic Literacy Project

1. Background

a. This Scholarship has been established to provide financial assistance to a PhD student who is undertaking research in law and genetics.

b. This Scholarship is funded by an Australian Research Council (ARC) research project.

a. The Scholarship is offered subject to the applicant having an unconditional offer of admission or being currently enrolled to study full-time in a PhD within the University of Sydney Law School.

b. Applicants must be willing to conduct research in law and genetics.

c. Applicants must hold an Honours degree (first class or second upper) or equivalent in Law.

d. Applicants must have previous research experience in Law.

a. The successful applicant will be awarded the Scholarship on the basis of:

I. academic merit,

II. area of study and/or research proposal,

III. curriculum vitae,

IV. a personal statement which demonstrates their interest in law and genetics

V. and previous research achievements, and

VI. previous research experience.

b. The successful applicant will be awarded the Scholarship on the nomination of the Sydney Law School Associate Dean (Research Education) and the relevant research supervisor(s), or their nominated delegate(s).

a. The Scholarship will provide a stipend allowance of $26,300 per annum for up to three years, subject to satisfactory academic performance.

b. The recipient may apply for an extension of the stipend allowance for up to six months.

c. Periods of study already undertaken towards the degree prior to the commencement of the Scholarship will be deducted from the maximum duration of the Scholarship excluding the potential extension period.

d. The Scholarship is for commencement in the relevant research period in which it is offered and cannot be deferred or transferred to another area of research without prior approval.

e. No other amount is payable.

f. The Scholarship and any potential extension period will be offered subject to ARC approval and the availability of funding.

a. Progression is subject to passing the annual progress review.

a. The Scholarship recipient receives up to 20 working days recreation leave each year of the Scholarship and this may be accrued. However, the student will forfeit any unused leave remaining when the Scholarship is terminated or complete. Recreation leave does not attract a leave loading and the supervisor's agreement must be obtained before leave is taken.

b. The Scholarship recipient may take up to 10 working days sick leave each year of the Scholarship and this may be accrued over the tenure of the Scholarship. Students with family responsibilities, caring for sick children or relatives, or experiencing domestic violence, may convert up to five days of their annual sick leave entitlement to carers leave on presentation of medical certificate(s). Students taking sick leave must inform their supervisor as soon as practicable.

a. The Scholarship recipient may not normally conduct research overseas within the first six months of award.

b. The Scholarship holder may conduct up to 12 months of their research outside Australia. Approval must be sought from the student's supervisor and the Sydney Law School Associate Dean (Research Education) via application to the Higher Degree by Research Administration Centre (HDRAC), and will only be granted if the research is essential for completion of the degree. All periods of overseas research are cumulative and will be counted towards a student's candidature. Students must remain enrolled full-time at the University and receive approval to count time away.

a. The Scholarship recipient cannot suspend their award within their first six months of study, unless a legislative provision applies.

b. The Scholarship recipient may apply for up to 12 months suspension of the Scholarship for any reason during the tenure of the Scholarship. Periods of Scholarship suspension are cumulative and failure to resume study after suspension will result in the award being terminated. Approval must be sought from the student's supervisor and the Sydney Law School Associate Dean (Research Education) via application to the Higher Degree by Research Administration Centre (HDRAC). Periods of study towards the degree during suspension of the Scholarship will be deducted from the maximum tenure of the Scholarship.

a. The Scholarship recipient must notify HDRAC, and their supervisor promptly of any planned changes to their enrolment including but not limited to: attendance pattern, suspension, leave of absence, withdrawal, course transfer, and candidature upgrade or downgrade. If the award holder does not provide notice of the changes identified above, the University may require repayment of any overpaid stipend.

a. The Scholarship will be terminated:

I. on resignation or withdrawal of the recipient from their research degree,

II. upon submission of the thesis or at the end of the award,

III. if the recipient ceases to be a full-time student and prior approval has not been obtained to hold the Scholarship on a part-time basis,

IV. upon the recipient having completed the maximum candidature for their degree as per the University of Sydney (Higher Degree by Research) Rule 2011 Policy,

V. if the recipient receives an alternative primary stipend scholarship. In such circumstances this Scholarship will be terminated in favour of the alternative stipend scholarship where it is of higher value,

VI. if the recipient does not resume study at the end of a period of approved leave, or

VII. If the recipient ceases to meet the eligibility requirements specified for this Scholarship, (other than during a period in which the Scholarship has been suspended or during a period of approved leave).

b. The Scholarship may also be terminated by the University before this time if, in the opinion of the University:

I. the course of study is not being carried out with competence and diligence or in accordance with the terms of this offer,

II. the student fails to maintain satisfactory progress, or

III. the student has committed misconduct or other inappropriate conduct.

c. The Scholarship will be suspended throughout the duration of any enquiry/appeal process.

d. Once the Scholarship has been terminated, it will not be reinstated unless due to University error.

a. Where during the Scholarship a student engages in misconduct, or other inappropriate conduct (either during the Scholarship or in connection with the students application and eligibility for the Scholarship), which in the opinion of the University warrants recovery of funds provided, the University may require the student to repay payments made in connection with the Scholarship. Examples of such conduct include and without limitation; academic dishonesty, research misconduct within the meaning of the Research Code of Conduct (for example, plagiarism in proposing, carrying out or reporting the results of research, or failure to declare or manage a serious conflict of interests), breach of the Code of Conduct for Students and misrepresentation in the application materials or other documentation associated with the Scholarship.

b. The University may require such repayment at any time during or after the Scholarship period. In addition, by accepting this Scholarship, the student consents to all aspects of any investigation into misconduct in connection with this Scholarship being disclosed by the University to the funding body and/or any relevant professional body.

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Postgraduate Research Scholarship in Law and Genetics - News - The University of Sydney

Rare Disease Genetic Testing Market analysis report gives clear idea about the market potential for each geographical region based on the growth rate, macroeconomic parameters, consumer buying patterns, possible future trends, and market demand and supply scenarios. Competitive analysis is the major feature of any market research report, and hence Rare Disease Genetic Testing Market report covers many points including strategic profiling of key players in the market, analyse core competencies of key players, and draw a competitive landscape for the Rare Disease Genetic Testing industry. Different components which are in charge of market development, has been analyzed clearly in this report.

A reliable Rare Disease Genetic Testing Market report conducts the market overview with respect to general market conditions, market improvement, market scenarios, development, cost and profit of the specified market regions, position and comparative pricing between major players. The report involves the market drivers and limitations which are obtained from SWOT analysis. By working with a number of steps of collecting and analysing market data, this finest Rare Disease Genetic Testing Market research report is framed with the expert team. The large scale Rare Disease Genetic Testing Market report comprises of various segments linked to Rare Disease Genetic Testing industry and market with comprehensive research and analysis.

Rare disease genetic testing market is expected to gain market growth in the forecast period of 2020 to 2027. Data Bridge Market Research analyses the market to account to grow at a CAGR of 8.30% in the above-mentioned forecast period. The increase in the facilities for patients affected by rare diseases has been directly impacting the growth of rare disease genetic testing market.

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GlobalRare Disease Genetic TestingMarket Scope and Market Size

Rare disease genetic testing market is segmented on the basis of disease type, technology, specialty and end use. The growth amongst these segments will help you analyze meager growth segments in the industries, and provide the users with valuable market overview and market insights to help them in making strategic decisions for identification of core market applications.

Rare Disease Genetic Testing Market Country Level Analysis:

The countries covered in the Rare Disease Genetic Testing Market report are U.S., Canada, Mexico in North America, Germany, Poland, Ireland, Italy, U.K., France, Spain, Netherland, Belgium, Switzerland, Turkey, Russia, Rest of Europe in Europe, Japan, China, India, South Korea, New Zealand, Vietnam, Australia, Singapore, Malaysia, Thailand, Indonesia, Philippines, Rest of Asia-Pacific (APAC) in Asia-Pacific (APAC), Brazil, Argentina, Chile, Rest of South America as a part of South America, U.A.E, Saudi Arabia, Egypt, Kuwait, South Africa, Rest of Middle East and Africa (MEA) as a part of Middle East and Africa (MEA).

Check Table of Contents of This Report @ https://www.databridgemarketresearch.com/toc/?dbmr=global-rare-disease-genetic-testing-market

Leading Rare Disease Genetic Testing manufacturers/companies operating at both regional and global levels:

Quest Diagnostics, Inc., Centogene N.V., Eurofins Scientific, Strand Life Sciences, Ambry Genetics, PerkinElmer, Inc., Macrogen, Inc., Baylor Genetics, Color, Health Network Laboratories, L.P., Preventiongenetics, Progenity, Inc., Invitae Corporation, 3billion, Inc., Arup Laboratories, Coopersurgical, Inc., Fulgent Genetics, Myriad Genetics, Inc., Laboratory Corporation Of America Holdings and Opko Health, Inc., among other domestic and global players.

Key points of the report

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Table Of Contents: Rare Disease Genetic Testing MarketPart 01: Executive Summary

Part 02: Scope Of The Report

Part 03: Research Methodology

Part 04: Market Landscape

Part 05: Pipeline Analysis

Part 06: Market Sizing

Part 07: Five Forces Analysis

Part 08: Market Segmentation

Part 09: Customer Landscape

Part 10: Regional Landscape

Part 11: Decision Framework

Part 12: Drivers And Challenges

Part 13: Market Trends

Part 14: Vendor Landscape

Part 15: Vendor Analysis

Part 16: Appendix

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Rare Disease Genetic Testing Market To Account To Grow At A CAGR Of 8.30% In The Forecast Period Of 2020 To 2027 | Top Companies- Quest Diagnostics,...

The information below has been supplied by dairy marketers and other industry organizations. It has not been edited, verified or endorsed by Hoards Dairyman.

New Generation Genetics is excited to welcome Lauren Hendel as U.S. Sales and Progeny Specialist effective December 1, 2020.

Lauren brings diverse experience and knowledge of the dairy genetics industry. This includes experience in marketing, daughter progeny identification and photography, customer service, and A.I. bull care, collection, and semen processing.Most recently, she worked as a Genetic Consultant in southern Wisconsin.In this role she helped customers reach their genetic goals through sire selection and mating.

Laurens passion for Brown Swiss began at a young age. Growing up, she was actively involved on her familys 400-cow dairy, near Caledonia, MN. Hendel Farms has been home to registered Brown Swiss since 1922.

Lauren has an ideal skill set for this position and will be a very valuable asset to NGG going forward, stated CEO Dan Gilbert.We are confident Breeders in the Midwest and West will benefit and appreciate working with her.

Lauren is a graduate of the University of Minnesota Twin Cities with a Bachelor of Animal Science and minor in Agricultural and Food Business Management. While there she was active in the Gopher Dairy Club, and a member of the dairy judging and dairy challenge teams.

Lauren will be working out of the home office in Fort Atkinson, WI and will be covering semen sales in the Midwest & Western regions of the USA. Lauren will also coordinate progeny photography, assist with NGG's social media platform, press releases, advertising, web site maintenanceand other office responsibilities.

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New Generation Genetics is excited to welcome Lauren Hendel as US Sales and Progeny Specialist effective December 1, 2020. - Hoard's Dairyman

Researchers inserted genes into mouse eye cells to protect and restore the optic nerve (red fibers in microscope image of healthy mouse retina, above).

By Kelly ServickDec. 2, 2020 , 5:30 PM

Do old and damaged cells remember what it was like to be young? Thats the suggestion of new study, in which scientists reprogrammed neurons in mouse eyes to make them more resistant to damage and able to regrow after injurylike the cells of younger mice. The study suggests that hallmarks of aging, and possibly the keys to reversing it, lie in the epigenome, the proteins and other compounds that decorate DNA and influence what genes are turned on or off.

The idea that aging cells hold a memory of their young epigenome is very provocative, says Maximina Yun, a regenerative biologist at the Dresden University of Technology who was not involved in the work. The new study supports that [idea], but by no means proves it, she adds. If researchers can replicate these results in other animals and explain their mechanism, she says, the work could lead to treatments in humans for age-related disease in the eye and beyond.

Epigenetic factors influence our metabolism, our susceptibility to various diseases, and even the way emotional trauma is passed through generations. Molecular biologist David Sinclair of Harvard Medical School, who has long been on the hunt for antiaging strategies, has also looked for signs of aging in the epigenome.

The big question was, is there a reset button? he says. Would cells know how to become younger and healthier?

In the new study, Sinclair and his collaborators aimed to rejuvenate cells by inserting genes that encode reprogramming factors,which regulate gene expressionthe reading of DNA to make proteins. The team chose three of the four factors scientists have used for more than 10 years to turn adult cells into induced pluripotent stem cells, which resemble the cells of an early embryo. (Exposing animals to all four factors can cause tumors.)

The team focused specifically on neurons at the back of the eye called retinal ganglion cells. These cells relay information from light-sensitive photoreceptors to the brain using long tendrillike structures called axons, which make up the optic nerve. Theres a stark divide between youth and age in these cells: An embryonic or newborn mouse can regenerate the optic nerve if it gets severed, but that ability vanishes with time.

To test whether their treatment could bring back some of that resilience, Sinclair and colleagues crushed the optic nerves of mice using forceps and injected a harmless virus into the eye carrying the genes for the three reprogramming factors. The injection prevented some damaged retinal ganglion cells from dying and even prompted some to grow new axons reaching back to the brain, the team reports today in Nature.

When the researchers looked at methylation patternsthe DNA location of chemical tags called methyl groups that regulate gene expressionthey found that changes caused by the injury resembled those in aging mouse cells. In certain parts of the genome, the treatment reversed those changes. The researchers also found that the benefits of the introduced genes depended on cells ability to alter their methylation patterns: Mice lacking certain enzymes necessary to remove methyl groups from DNA saw no benefit to the treatment.

Thats really something special, says Leonard Levin, a visual neuroscientist at McGill University. The experiments suggest how the famous and well-studied reprogramming factors restore cells. But big questions remain, he says: How do these factors cause methyl groups to be added or removed? How does that process help retinal ganglion cells?

Sinclairs team also tested the approach in mice with a condition meant to mimic glaucoma, a leading cause of age-related blindness in humans. In glaucoma, the optic nerve gets damaged, often by a buildup of pressure in the eye. Sinclair and his colleagues injected tiny beads into the animals eyes that prevented normal drainage and increased pressure, which damaged retinal ganglion cells.

Four weeks later, the animals visual acuity had declined by about 25%, as measured by a vision test in which mice move their heads to track the movement of vertical bars displayed on computer monitors. But after the genetic treatment, the animals gained back roughly half of their lost acuitythe first demonstration of restored vision in mice after this glaucomalike injury.

Still, the improvement in acuity was small, Levin notes. And, he says, the treated mice were in a relatively early stage of damage, not the state of near or total blindness that people experience when glaucoma goes untreated for years. So its too early to say whether this approach could benefit people who have lost much of their vision. Levin adds that there are already very good treatments for early-stage glaucoma to prevent vision loss with medicated eye drops or surgery to lower eye pressure.

In a final set of experiments, Sinclair and colleagues injected the reprogramming-factor genes into the eyes of 1-year-old healthy mice, roughly the mouse equivalent of middle-age. By this stage, the animals had visual acuity scores about 15% lower than their 5-month-old counterparts. Four weeks after treatment, older mice had similar acuity scores to younger ones. In their cells, the researchers saw patterns of DNA methylation and gene expression resembling those of younger animals.

In the three sets of experiments, Sinclair says, the cells seemed to respond to the reprogramming factors by fine-tuning their gene expression to match a youthful state. He sees that behavior as a hint that cells keep a record of their epigenetic past, even though its not clear how that record is stored. A company Sinclair cofounded, Life Biosciences, is developing treatments for diseases associated with aging, including glaucoma, and he says hes now planning to test the safety of this gene therapy approach in larger animals.

Yun says that as a strategy for reversing aging or treating disease, resetting the epigenome is a very difficult one. Reprogramming cells to an earlier state carries a risk of prompting uncontrolled growth and cancer.Future studies should test how the three factors affect other types of cells and tissues and confirm that reprogrammed cells maintain their youthful state long-term, she says. There are a lot of roads to be traveled.

Originally posted here:
Researchers restore lost sight in mice, offering clues to reversing aging - Science Magazine

Aging has implications for a wide range of diseases. Researchers have been looking for ways to halt the aging process for millennia, but such methods remain elusive. Scientists at Harvard Medical School have now offered a glimmer of hope that the aging clock in the eye could be reversedat least in animals.

By reprogramming the expression of three genes, the Harvard team successfully triggered mature nerve cells in mice eyes to adopt a youthful state. The method reversed glaucoma in the mice and reversed age-related vision loss in elderly mice, according to results published in Nature.

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If further studies prove out the concept, they could pave the way for therapies that employ the same approach to repair damagein other organs and possibly treat age-related diseases in humans, the team said.

The researchers focused on the Yamanaka factors, which are four transcription factorsOct4, Sox2, Klf4 and c-Myc. In a Nobel Prize-winning discovery, Shinya Yamanaka found that the factors can change the epigenomehow genes are turned on or offand can thereby transform mature cellsback to a stem cell-like state. It has been hypothesized that changes to the epigenome drive cell aging, especially a process called DNA methylation, by which methyl groups are tagged onto DNA.

Past researches have tried to use the four Yamanaka factorsto turn back the age clock in living animals, but doing so caused cells to adopt unwanted new identities and induced tumor growth.

RELATED:Restoring eyesight with genetically engineered stem cells

To test whether the approach works in living animals, the scientists used adeno-associated virus to deliver the three genes into the retina of mice with optic nerve injuries. The treatment led to a two-fold increase in the number of retinal ganglion cells, which are neurons responsible for receiving and transmitting visual information. Further analysis showed that the injury accelerated DNA methylation age, while the gene cocktail counteracted that effect.

Next the scientists tested whether the gene therapy could also work in disease settings. In a mouse model of induced glaucomawhich is a leading cause of age-related blindness in peoplethe treatment increased nerve cell electrical activity and the animals visual acuity.

But can the therapy also restore vision loss caused by natural aging? In elderly, 12-month-old mice, the gene therapy also restored ganglion cells electrical activity as well as visual acuity, the team reported.

By comparing cells from the treated micewith retinal ganglion cells from young, 5-month-old mice, the researchers found that mRNA levels of 464 genes were altered during aging, and the gene therapy reversed 90% of those changes. The scientists also noticed reversed patterns of DNA methylation, which suggests that DNA methylation is not just the marker but rather the driver behind aging.

What this tells us is the clock doesn't just represent timeit is time. If you wind the hands of the clock back, time also goes backward, the studys senior author, David Sinclair, explained in a statement.

The study marks the first time that glaucoma-induced vision loss was reversednot just slowedin living animals, according to the team.

RELATED:Reprogrammed skin cells restore sight in mouse models of retinal disease

Other researchers are also studying regenerative approaches to treating eye diseases. A research group at the Centre for Genomic Regulation in Barcelona just showed that by modifying mesenchymal stem cells to express chemokine receptors Ccr5 and Cxcr6, retinal tissue could be saved from degeneration.

The idea of reversing age-related decline in humans by epigenetic reprogramming with a gene therapy is exciting, Sinclair said. The Harvard researchers intend to do more animal work that could allow them to start clinical trials in people with glaucoma in about two years.

Our study demonstrates that it's possible to safely reverse the age of complex tissues such as the retina and restore its youthful biological function, Sinclair said. If affirmed through further studies, these findings could be transformative for the care of age-related vision diseases like glaucoma and to the fields of biology and medical therapeutics for disease at large.

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Reversing vision loss by turning back the aging clock - FierceBiotech

The study of 1,000 Canadians requiring vision correction, conducted by research firm Leger, showed that 34 per cent of Canadians requiring vision correction say their eyes feel more tired during the pandemic than they did before, which is a possible sign of digital eyestrain, a condition caused by spending too much time in front of screens. A study found the effects of long-term computer use on the eyes suggest that digital eyestrain is a form of evaporative dry eye. As a result, tears evaporate on the surface of the eye and can cause them to feel dry, tired or irritated. Despite this:

"While it's tempting to turn to streaming services and e-books for entertainment after long days of working and learning on screens, I'm seeing patients in my clinic who are suffering from sore, tired eyes as a result, which could be a sign of dry eye caused by digital eyestrain," says Dr. Shawn Moore, optometrist at Orillia Optometry. "Conditions like dry eye can also present as blurry vision, so if you're experiencing changes in your eyesight, patients still need to prioritize seeing an optometrist at this time to re-assess their vision care needs. Your eye doctor might recommend using an eye drop with lipids, like SYSTANE COMPLETE, or switching to a daily disposable contact lens featuring water gradient technology, like DAILIES TOTAL1."

In addition to dry eye and worsening vision, the survey showed that Canadians are frustrated with the inconvenience and nuisance of foggy glasses caused by wearing a mask and glasses together while running errands. Three-quarters of Canadians who wear glasses say their glasses fog up when wearing masks; 35 per cent say they adjust their glasses more when wearing them with masks; and more than half of Canadians (51 per cent) requiring vision correction wear contact lenses when going outside.

Experiencing changes with your vision during COVID-19? The following steps could help:

For more information, talk to your eye care professional to learn more about DAILIES TOTAL1 or SYSTANE COMPLETE.

Study Methodology An online survey of 1,000 Canadians who wear corrective eye wear was completed between September 22 and September 27, 2020, using Leger's online panel. For comparative purposes, a probability sample of 1000 respondents would have a margin of error of 3.1%, 19 times out of 20.

About Alcon Alcon helps people see brilliantly. As the global leader in eye care with a heritage spanning more than seven decades, Alcon offers the broadest portfolio of products to enhance sight and improve people's lives. Alcon's Surgical and Vision Care products touch the lives of more than 260 million people in over 140 countries each year living with conditions like cataracts, glaucoma, retinal diseases and refractive errors. More than 20,000 Alcon associates are enhancing the quality of life through innovative products, partnerships with eye care professionals and programs that advance access to quality eye care. For more information, visit http://www.alcon.ca.

2020 Alcon Inc. 11/20 CA-DT1-2000097

SOURCE Alcon Canada

For further information: Viktoria Kiely, Cohn & Wolfe, [emailprotected], 647.259.3273

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Many Canadians believe COVID lifestyle changes are affecting their eyes - Canada NewsWire

Since my early 20s, Ive been making spectacles of myself in a manner of speaking. During my boyhood years, my right eye had occasional encounters with things like tennis balls and a toy pistol, so my distance vision needed correction. Ive worn eyeglasses ever since. However, being nearsighted, I dont need them for things up close.

My wife is different. Thanks to recent cataract surgery, she now has near-perfect farsighted vision. Its seeing things up close that poses problems. Combined, we can boast 20:20 vision both far and near, even though lots of things havent looked all that good in 2020.

If you were to choose, which would you prefer? Flawless farsighted vision, or excellent close-up vision? In terms of physical eyesight, a good argument could be made for either. It depends on what youre wanting to do.

But spiritually speaking, Im convinced being farsighted has to be the preferred choice. The Bible affirms this over and over. Its at the heart of the Christian faith being willing to trust in things we can only see from afar, despite disheartening circumstances that might surround us.

The Scriptures abound with numerous examples of what we might call spiritual farsightedness. Jesus, speaking to the doubting disciple Thomas after he insisted on seeing visible proof of His resurrection, said, Because you have seen Me, you have believed; blessed are those who have not seen and yet have believed (John 20:29).

After suffering a series of personal losses, including his children, and wracked by painful sores over his entire body, Job declared, I know that my Redeemer lives, and that in the end he will stand upon the earth. I myself will see him with my own eyes I, and not another. How my heart yearns within me! (Job 19:26-27).

Here are some other passages that underscore this emphasis on the value of spiritual far-sight:

So we fix our eyes not on what is seen, but on what is unseen, since what is seen is temporary, but what is unseen is eternal (2 Corinthians 4:18).

For we walk by faith, not by sight (2 Corinthians 5:7).

While we wait for the blessed hope the glorious appearing of our great God and Savior, Jesus Christ (Titus 2:13).

Dear friends, now we are children of God, and what we will be has not yet been made known. But we know that when he appears, we shall be like him, for we shall see him as he is (1 John 3:2).

The 11th chapter of the book of Hebrews speaks extensively about the need for spiritual farsightedness, even when the way ahead seems dark or obscured:

Now faith is the substance of things hoped for, the evidence of things not seen (Hebrews 11:1).

By faith Noah, when warned about things not yet seen, in holy fear built an ark to save his family (Hebrews 11:7).

By faith Abraham, when called to go to a place he would later receive as an inheritance, obeyed and went, even though he did not know where he was going (Hebrew 11:8).

All these people were still living by faith when they died. They did not receive the things promised; they only saw them and welcomed them from a distance (Hebrews 11:13).

After citing other glowing examples of unwavering, unconquerable faith, the chapter reaffirms, These were all commended for their faith, yet none of them received what had been promised. God had planned something better for us so that only together with us would they be made perfect (Hebrews 11:39-40).

We find ourselves in the closing days of an unforgettable year many of us wish we could forget. What weve been seeing, up close and personal, often hasnt passed the eye test. This is all the more reason for practicing, as did the biblical patriarchs, a faith that looks not down but ahead toward a not yet seen, but promised future of joy and peace. Anticipating the time when well be experiencing the words of the old hymn, It Is Well With My Soul: when the faith shall be sight.

* * *

Robert J. Tamasy is a veteran journalist, former newspaper editor and magazine editor. Bob has written, co-authored and edited more than 15 books. These include the newly published, Marketplace Ambassadors; Business At Its Best: Timeless Wisdom from Proverbs for Todays Workplace; Tufting Legacies, The Heart of Mentoring, and Pursuing Life With a Shepherds Heart. A weekly business meditation he edits, Monday Manna, is translated into more than 20 languages and sent via email around the world by CBMC International. The address for his blog is http://www.bobtamasy.blogspot.com. His email address is btamasy@comcast.net.

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Bob Tamasy: Overcoming The Obstacle Of Near-Sightedness - The Chattanoogan

JOCKEY Danny Cook is fighting to save his eyesight after suffering horrific facial injuries when he was kicked by a horse.

The Jumps star needed 50 stitches to his face and suffered a broken nose and fractured eye socket following the terrifying incident last month.

2

Cook, 37, was rushed to hospital and treated for head wounds after being kicked at Market Rasen in October.

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Incredibly, he made his racing comeback on November 21 but pulled out of last Sunday's races at Carlisle after falling off Definitly Red at Newcastle on Saturday.

Cook said he chose not to ride because he cannot see properly in one eye - and could be forced to retire if it does not improve.

He told the Yorkshire Post: "I'm going to take time out to get myself sorted.

"If they operate, there's an 80 per cent chance my sight will be even worse so I need to weigh up all the options.

"Hopefully I will know more in the next week. If it doesn't get better I will not return."

Cook - who has total career earnings on the track of just under 3m - is desperate to return to racing and had been looking forward to riding again over the busy Christmas schedule.

But that is now all on hold as he waits to find out if his vision will ever return to normal.

2

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He told the Racing Post: "Ive been having trouble with my eyesight since Ive been back riding. Im going to see the specialist and try to get something sorted.

"This is the time of year when you want to race as much as you can. All the good horses are out.

"It's frustrating being off but it's a necessity because I'm not able to ride to my full capacity with only one eye."

He added: "Mentally I am good to go and I am confident and strong.

"But the vision is very much impaired when I go into a jump - it's not helping.

"I have got to look after myself. If I can't ride at my best, I must get myself sorted.

"Whatever happens I have had a good innings and hopefully it is not the end."

Cook's admission he may be forced to retire comes after fellow jockey Harry Cobden was lucky to avoid serious injury over the weekend.

He fell underneath charging horses at Newbury but was shown walking to the on-course ambulance.

And just last week Flat rider Eoin Walsh was rushed to hospital with a broken back following a fall at Chelmsford.

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Jockey Danny Cook fighting to save eyesight and career after needing 50 stitches to his face when kicked by - The Sun

Doctors point to a rising incidence in retinal vascular occlusions this year; patients also report sudden onset of double vision

Ophthalmologists have been seeing more patients with complaints of eyesight loss this year, and doctors suspect COVID-19 may have a role to play.

Doctors are relying on literature from other countries to confirm their diagnosis and suspicions. The retina is a thin layer of tissue at the back of the inside of the eye which receives light from the lens and sends it as neural signals to the brain through the optic nerve. When blood supply to the eye is hindered, the retina cannot function.

Mohan Rajan of Rajan Eye Care Hospital said he was seeing patients with loss of vision or double vision. Occlusions of the retinal blood vessels, following COVID-19 infection, have been reported. This is akin to a heart attack to a cardiologist and a stroke to a neurologist, he said.

Arteries and veins of the retina are exposed to the same pathological processes, and this affects ocular circulation as well. Patients have also reported a sudden onset of double vision and drooping of eyelids following COVID-19, due to paralysis of the nerves of the eye, he said.

Priya Sivakumar, neuro-ophthalmologist, Aravind Eye Care Hospital, Puducherry, said there had been an increase in the number of patients coming with loss of vision. Since initially testing for COVID-19 was not easily accessible, these patients were treated with steriods.

We could not test the patients for COVID-19 but suspected it as a cause because of the change in trend between last year and the current. Last year, we treated 20 patients in whom both eyes were affected.This year, from March to October, we have seen around 40 patients, she said. In her experience, the patients recovered when treated early.

Rajiv Raman, senior retina consultant, department of vitreo-retina, Sankara Nethralaya, said people recovering from COVID-19 had a tendency to form clots, which were treated using blood thinners. Occlusion (clot) in the blood vessel can occur in arteries and veins. If it occurs in an artery in the eye, the first six hours are the golden hours within which vision can be restored in some cases. In case of a vein occlusion, vision can be improved, to an extent, with treatment, but it might not return to normal, he said.

Dr. Rajiv said the hospital had not analysed its data. But in general, we are seeing more retinal vascular occlusions now. The occlusions could also be due to cardiovascular disease, diabetes or hypertension. Sankara Nethralaya, being a tertiary care centre, has been seeing many vivid recovered patients from across the country now, he added.

There seems to be more incidence of retinal vascular occlusions. There is emerging literature evidence supporting this fact.

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COVID-19 could be reason for increase in patients with eyesight loss, say doctors - The Hindu