Disease Controlling

Mấy tháng trước có người bạn tag mình vào một post đang thảo luận sôi nổi về việc ứng dụng Trí Tuệ Nhân Tạo và Máy Học để xem có loại thuốc nào có thể sử dụng để hạn chế sự tấn công của virus corona. Mình có trao đổi với team Scientists của <a href="https://genetica.asia/" rel="noopener noreferrer" target="_blank">Genetica</a>. Sau mấy tiếng thảo luận, bọn mình rút ra kết luận là không practical, vì quy trình của việc thử nghiệm thuốc sẽ mất rất nhiều thời gian, feedback loop cho machine learning sẽ&nbsp;rất dài và không hiệu quả.Nhưng nhờ buổi thảo luận đó, các bạn Scientists lại gợi ý là. Sao máy không học dữ liệu của các đại dịch toàn cầu trong quá khứ. Các đại dịch như SARS-CoV đã tràn qua cả Việt Nam, hay đại dịch MERS-CoV (đại dịch Hô hấp cấp Trung Đông) đã làm điên đảo thế giới một thời. Các đại dịch này đều liên quan đến các chủng của virus corona.Các bạn nói và bắt tay vào làm luôn. Sau mỗi đại dịch, các nhà khoa học đã công bố dữ liệu nghiên cứu về khả năng nhiễm virus của con người. Nghiên cứu đã chỉ ra rằng có những người mang các gen làm cho họ dễ nhiễm virus hơn những người khác rất nhiều. Không chỉ dừng lại ở đó, các nghiên cứu cũng chỉ ra rằng với một số người mang các gen “xấu", khi bị nhiễm SARS-CoV, thời gian chữa trị sẽ kéo dài và hậu quả của SARS-CoV để lại nhiều hơn hẳn những người khác.Mình rất tự hào về đội ngũ Scientists của Genetic	a. Ngay trong mùa dịch, các bạn đã ra lò sản phẩm <a href="https://genetica.asia/products/g-immunity" rel="noopener noreferrer" target="_blank">G-Immunity</a> với các thông tin cụ thể về nguy cơ nhiễm virus của mỗi con người thông qua thông số gen của họ. Hệ thống máy học của Genetica đã học từ hơn 250 các công trình nghiên cứu quốc tế, tự động lọc ra hơn 30 gen và hơn 80 các đột biến có tác động lớn nhất đến nguy cơ nhiễm virus qua đường hô hấp.Mỗi lần một đại dịch toàn cầu qua đi, nó không chỉ để lại những tổn hại về kinh tế hay sức khoẻ, mà nó cũng mang lại những thông tin hữu ích để chúng ta khai thác, giúp phòng vệ cho loài người trong các đại dịch trong tương lai. Hy vọng những thông tin gene mà hệ thống của Genetica “học" từ đại dịch SARS-CoV, MERS-CoV, H1N1, H5N1, ... sẽ giúp đánh giá nguy cơ nhiễm virus của mỗi người, và qua đó có thể cá nhân hoá việc phòng tránh virus cho thật hiệu quả.(Bài đăng trên trang cá nhân của anhTuấn Cao - CEO Genetica®)&nbsp;Để biết thêm chi tiết. Mời các bạn download Genetica Mobile App để tìm hiểu thêm:<ul><li>iOS: <a href="https://apps.apple.com/us/app/genetica/id1475880490" rel="noopener noreferrer" target="_blank">https://apps.apple.com/us/app/genetica/id1475880490</a></li><li>Android: <a href="https://play.google.com/store/apps/details?id=com.genetica.id" rel="noopener noreferrer" target="_blank">https://play.google.com/store/apps/details?id=com.genetica.id</a></li></ul>

Sau mỗi đại dịch, các nhà khoa học đã công bố dữ liệu nghiên cứu về khả năng nhiễm virus của con người. Nghiên cứu đã chỉ ra rằng có những người mang các gen làm cho họ dễ nhiễm virus hơn những người khác rất nhiều.

Học được gì từ những đại dịch toàn cầu trong quá khứ?

Professor Philippe Froguel and his fellow reasearchers discovered a new obesity gene that plays an essential role in the maturation of several key hormones that control food intake. Therefore, the mutation of this gene increase the risk of excessive weight and severe obesity.PCSK 1 is the name of this newly-found obesity gene that regulates several key hormones that control food intake. It produces an enzyme called proconvertase 1 which activates several hormones and circulating peptides (e.g., insulin, glucagon, melanocortin) controlling appetite. One version of this gene increases the risk of becoming severely obese and have contributed to weight gain in general populations. In addition, this gene version also causes insulin abnomalities hightening the tendency to be hypoglycemic after meals.This discovery shows that apparently minor abnormalities in a key enzyme for the maturation of several hormones involved in controlling appetite (insulin, GLP1, melanocortin) are enough to significantly increase the risk of severe obesity and to lead to excessive weight in the general population.To put this into context, after the early 2008 discovery that frequent variants in the melanocortin 4 receptor play a role in obesity (also published in Nature Genetics), the French-British team demonstrated that severe obesity and common weight gain have a common genetic base principally linked to defects in the complex hormone system (including some hormones produced by the intestine) and in specific receptors in certain areas of the brain that regulate food intake and satiation. At a time when the ratio of obesity (body-mass index greater than 40 kg/m2) has doubled in the past decade, these results highlight the importance of early dietary control to prevent and reduce obesity.Reference: https://www.sciencedaily.com/releases/2008/07/080714153802.ht

PCSK 1 is the name of this newly-found obesity gene that regulates several key hormones that control food intake.

Gene Produces Hormones That Lead To Obesity

Geneticists reported that nearly half of US populations with European ancestry carry a variant in FTO gene relating to gain weight, which puts them at risk of obesity. Some scientists also found that this FTO variant is associated with a loss of brain tissue - putting more than one third of US population at risk of a wealth of diseases like Alzheimer's. Individuals with the "bad" FTO gene version had an average of 8% less tissue in the frontal lobes, the "command center" of the brain, and 12% less in the occipital lobes, areas in the back of the brain responsible for vision and perception. As a result, if you have the bad FTO gene, your weight affects your brain adversely in terms of loss tissue. In the contrast, if you don't carry this FTO version, higher body weight doesn't translate into brain deficits. But the news is not necessarily negative because carriers of the risk gene can do physically exercises and eat a balanced diet to resist both obesity and brain decline.Full article here: https://www.sciencedaily.com/releases/2010/04/100419162308.htm

Geneticists reported that nearly half of US populations with European ancestry carry a variant in FTO gene relating to gain weight, which puts them at risk of obesity.

Obesity gene, carried by more than a third of the US population, leads to brain tissue loss

Obesity is a disease that occurs when a person’s body accumulates and stores excessive amounts of body fat. It was once thought that only the modernization environment has impact on the rocket rates of obesity. However, recent studies suggest that genetics contribute to 40-70% of obesity with the discovery of more than 50 genes that are strongly associated with obesity. While changes in the environment have significantly increased obesity rates over the last 20 years, the presence or absence of genetic factors protect us from or predispose us to obesity.&nbsp;There was three genes with clear functions being found to be associated with obesity, namely: Leptin, POMC and MC4R gene.&nbsp;Nonetheless, the most common gene which predispose for people to gain excess weight still remains as unclear function. It is the fat mass and obesity-associated gene (FTO), which is found in up to 43% of the population. In the presence of readily accessible food, those with the fat mass and obesity-associated gene may have challenges limiting their caloric intake.&nbsp;It is practical to test for the FTO gene and other genes and by knowing this can help you understand your risk for obesity and obesity-related conditions like diabetes and heart disease.If you have genes that predispose you to obesity, are you predestined to develop obesity? No! While these genes can increase appetite and reduce metabolism, following a consistent treatment plan that incorporates effective nutritional, physical activity, and behavioral approaches can help prevent and treat obesity. If weight continues to be a struggle, consider seeing an obesity medicine specialist to help develop a comprehensive medical obesity treatment plan.Reference: https://obesitymedicine.org/obesity-and-genetics/

It is practical to test for the FTO gene and other genes and by knowing this can help you understand your risk for obesity and obesity-related conditions like diabetes and heart disease.

Defining Obesity’s Interplay among Environment, Behavior, and Genetics

Stroke is the second most common cause of both death and disability-adjusted life-years worldwide, but its molecular mechanisms remain poorly understood. Recently, an international research consortium has identified 22 new genetic risk factors for stroke, make it now to be in total 32 independent genomic regions associated with stroke.The results of the largest genetic study on stroke thus far were now published online in the journal Nature Genetics. The study was based on DNA samples of 520,000 European, North- and South American, Asian, African, and Australian participants of whom 67,000 had a stroke. These were derived from 29 large studies.Stroke can originate from alterations in various parts of the vasculature including large arteries, small arteries, the heart, and the venous system and the researchers found genetic risk factors implicated in each of these mechanisms. They showed that some genetic risk factors contribute to specific mechanisms and others to stroke susceptibility at large. They further found shared genetic influences between stroke caused by vessel occlusion (the most common cause of stroke) and stroke caused by rupture of a blood vessel (the most catastrophic cause of stroke), often thought to have opposite mechanisms.When the researchers took a closer look on the genomic areas pinpointed in the study, they noticed that several of them overlap with genomic areas known to be implicated in related vascular conditions such as atrial fibrillation, coronary artery disease, venous thrombosis, or vascular risk factors, especially elevated blood pressure, and less so hyperlipidemia.By adding data on gene expression, protein expression, and other characteristics in multiple cell types and tissues compiled by their co-investigators the researchers obtained first insights into the specific genes, molecular pathways, and cell and tissue types through which the new genetic risk factors cause stroke.The researchers further found that the genes they identified are enriched in drug targets for antithrombotic therapy, used to re-open occluded blood vessels in patients with acute stroke or to prevent vascular events including stroke. “These findings illustrate the potential of genetics for drug discovery,” says Martin Dichgans.Full article: https://www.en.uni-muenchen.de/news/press-services/press-releases/2018/dichgans_megastroke.html&nbsp;

Stroke can originate from alterations in various parts of the vasculature including large arteries, small arteries, the heart, and the venous system and the researchers found genetic risk factors implicated in each of these mechanisms.

32 risks of leading to a stroke

Most researchers conclude that ADHD is primarily a neurological or brain-based disorder. It is either present at birth, or it develops early on in childhood. Although our everyday surroundings can affect the severity of symptoms, these environmental factors do not seem to be the primary cause of the disorder.In fact, researcher was conducted and results indicate that the estimated heritability of ADHD (i.e., the proportion of a trait that can be attributed to genetics) ranges from 75 to 91%. This does not mean a parent of an ADHD child must have ADHD. It does mean that the gene for ADHD exists in the family line of one of the biological parents. The specific gene has not yet been identified.Twin studies support a genetic basis for ADHD. Concordance rates (the occurrence of similar traits) are higher among identical twins (58-82%) than fraternal twins (31%-38%). (Martin, Scourfield, &amp; McGuffin, 2002). Interestingly, when one twin has ADHD, but the other does not, the 'normal' twin is still more likely to have problems with impulse control. Although genetics play a key role in ADHD, the specific genes have not yet been identified.For now, what we know about ADHD is just at protein levels as it is a result of reduced brain functioning (particularly frontal lobe) and decreased levels of dopamine. Dopamine is a naturally occurring chemical in the brain that creates sensations of arousal and pleasure. In other words, children with ADHD have cognitive 'sluggishness,' or a slower thinking process than their peers. Hence, stimulants raise brain activity to a level more comparable to their peers. Stimulants also increase their ability to screen out irrelevant stimuli, control impulsive behavior, and to focus on the designated task.Therefore, parents cannot 'prevent' ADHD since it's genetic. However, there are many things caregivers and families can do to enable the success of their ADHD children.That said, there are ways to help children to do their best. Since complications of pregnancy have been linked to ADHD, good prenatal care is a great way to start looking after your child's health. Eat healthy, avoid alcohol and drugs, and see your doctor regularly to make sure you are doing everything within your power to give your baby a healthy start in life.Full article here: https://www.gulfbend.org/poc/view_doc.php?type=doc&amp;id=13868&amp;cn=3

Although our everyday surroundings can affect the severity of symptoms, these environmental factors do not seem to be the primary cause of the disorder.

Causes of ADHD - Genetics

Tuberous sclerosis is also called tuberous sclerosis complex, is an uncommon genetic disorder that causes noncancerous (benign) tumors — unexpected overgrowths of normal tissue — to develop in many parts of the body, most commonly in the brain, eyes, kidneys, heart, lungs, and skin, although any part of the body can be affected.Signs and symptoms vary widely, depending on where the growths develop and how severely a person is affected. Some common symptoms including skin abnormalities, seizures, cognitive disabilities, behavioral problems, kidney problems, heart issues, lung problems, eye abnormalities, etc.<h2>Tuberous sclerosis can be the result of either:&nbsp;</h2>- A random cell division error. About two-thirds of people who have tuberous sclerosis have a new mutation in either the TSC1 or TSC2 gene — the genes associated with tuberous sclerosis — and do not have a family history of tuberous sclerosis.&nbsp;- Inheritance. About one-third of people who have tuberous sclerosis inherit an altered TSC1 or TSC2 gene from a parent who has the disorder.&nbsp;If you have tuberous sclerosis, you have up to a 50 percent chance of passing the condition to your biological children. The severity of the condition may vary. A parent with tuberous sclerosis may have a child who has a milder or more severe form of the disorder.&nbsp;It also means that if a child is diagnosed with tuberous sclerosis without a family history of the condition, both parents may consider screening for tuberous sclerosis as well.&nbsp;Furthermore, people with tuberous sclerosis may consider genetic counseling before their reproductive years to understand their risk of passing on the condition and their reproductive options.Read more: https://www.mayoclinic.org/diseases-conditions/tuberous-sclerosis/symptoms-causes/syc-20365969

Signs and symptoms vary widely, depending on where the growths develop and how severely a person is affected. Some common symptoms including skin abnormalities, seizures, cognitive disabilities, behavioral problems, kidney problems, heart issues, lung problems, eye abnormalities, etc.

What is Tuberous Sclerosis? Causes and signs

Tuberous sclerosis

Researchers have known that genes contribute to autism since the 1970s, when a team found that identical twins often share the condition. Since then, scientists have been racking up potential genetic culprits in autism, a process that DNA-decoding technologies have accelerated in the past decade.As this work has progressed, scientists have unearthed a variety of types of genetic changes that can underlie autism. The more scientists dig into DNA, the more intricate its contribution to autism seems to be.<h2>How do researchers know genes contribute to autism?</h2>Since the first autism twin study in 1977, several teams have compared autism rates in twins and shown that autism is highly heritable. When one identical twin has autism, there is about an 80 percent chance that the other twin has it too. The corresponding rate for fraternal twins is around 40 percent.However, genetics clearly does not account for all autism risk. Environmental factors also contribute to the condition — although researchers disagree on the relative contributions of genes and environment. Some environmental risk factors for autism, such as exposure to a maternal immune response in the womb or complications during birth, may work with genetic factors to produce autism or intensify its features.<h2>Is there such a thing as an autism gene?</h2>Not really. There are several conditions associated with autism that stem from mutations in a single gene, including fragile X and Rett syndromes. But less than 1 percent of non-syndromic cases of autism stem from mutations in any single gene. So far, at least, there is no such thing as an ‘autism gene’ — meaning that no gene is consistently mutated in every person with autism. There also does not seem to be any gene that causes autism every time it is mutated."Still, the list of genes implicated in autism is growing. Researchers have tallied 65 genes they consider strongly linked to autism, and more than 200 others that have weaker ties. Many of these genes are important for communication between neurons or control the expression of other genes.<h2>How do these genes contribute to autism?</h2>Changes, or mutations, in the DNA of these genes can lead to autism. Some mutations affect a single DNA base pair, or ‘letter.’ In fact, everyone has thousands of these genetic variants. A variant that is found in 1 percent or more of the population is considered ‘common’ and is called a single nucleotide polymorphism, or SNP.Common variants typically have subtle effects and may work together to contribute to autism. ‘Rare’ variants, which are found in less than 1 percent of people, tend to have stronger effects. Many of the mutations linked to autism so far have been rare. It is significantly more difficult to find common variants for autism risk, although some studies are underway.Other changes, known as copy number variations (CNVs), show up as deletions or duplications of long stretches of DNA and often include many genes.But mutations that contribute to autism are probably not all in genes, which make up less than 2 percent of the genome. Researchers are trying to wade into the remaining 98 percent of the genome to look for irregularities associated with autism. So far, these regions are poorly understood.<h2>Are all mutations equally harmful?</h2>No. At the molecular level, the effects of mutations may differ, even among SNPs. Mutations can be either harmful or benign, depending on how much they alter the corresponding protein’s function. A missense mutation, for example, swaps one amino acid in the protein for another. If the substitution doesn’t significantly change the protein, it is likely to be benign. A nonsense mutation, on the other hand, inserts a ‘stop’ sign within a gene, causing protein production to halt prematurely. The resulting protein is too short and functions poorly, if at all.<h2>How do people acquire mutations?</h2>Most mutations are inherited from parents, and they can be common or rare. Mutations can also arise spontaneously in an egg or sperm, and so are found only in the child and not in her parents. Researchers can find these rare ‘de novo’ mutations by comparing the DNA sequences of people who have autism with those of their unaffected family members. Spontaneous mutations that arise after conception are usually ‘mosaic,’ meaning they affect only some of the cells in the body.&nbsp;<h2>Can genetics explain why boys are more likely than girls to have autism?</h2>Perhaps. Girls with autism seem to have more mutations than do boys with the condition. And boys with autism sometimes inherit their mutations from unaffected mothers. Together, these results suggest that girls may be somehow resistant to mutations that contribute to autism and need a bigger genetic hit to have the condition.<h2>Is there a way to test for mutations before a child is born?</h2>Clinicians routinely screen the chromosomes of a developing baby to identify large chromosomal abnormalities, including CNVs. There are prenatal genetic tests for some syndromes associated with autism, such as fragile X syndrome. But even if a developing baby has these rare mutations, there is no way to know for sure whether he will later be diagnosed with autism.Reference: https://www.spectrumnews.org/news/autism-genetics-explained/

As this work has progressed, scientists have unearthed a variety of types of genetic changes that can underlie autism. The more scientists dig into DNA, the more intricate its contribution to autism seems to be.

Autism genetics, explained

Autism - or more precisely the autism spectrum disorders (ASDs) - represent a broad group of developmental disorders characterized by impaired social interactions, problems with verbal and nonverbal communication, and repetitive behaviors or severely limited activities and interests.It has become the most commonly diagnosed childhood developmental disorder. According to the Centers for Disease Control Prevention in 2007, autism spectrum disorders now affect 1 in every 150 children in the United States. Statistics from the U.S. Department of Education and other government agencies indicate that autism diagnoses are increasing at the rate of 10 to 17 percent per year. Autism can affect any individual and is not based on ethnic, racial or social background. And, it is four times more common in boys than in girls.Scientists are not certain what causes autism, but it's likely that both genetics and environment play a role. The causes of autism may be divided into 'idiopathic', (of unknown cause) which is the majority of cases, and 'secondary,' in which a chromosome abnormality, single-gene disorder or environmental agent can be identified. Approximately 15 percent of individuals with autism can be diagnosed with secondary autism; the remaining 85 percent have idiopathic autism.Researchers have identified a number of genes associated with autism. Studies of people with autism have found irregularities in several regions of the brain. Other studies suggest that people with autism have abnormal levels of serotonin or other neurotransmitters in the brain. These abnormalities indicate that autism usually results from the disruption of normal brain development early in fetal development caused by defects in genes that control brain growth and that regulate how neurons communicate with each other. These are preliminary findings and require further study.The risk that a brother or sister of an individual who has idiopathic autism will also develop autism is around 4 percent, plus an additional 4 to 6 percent risk for a milder condition that includes language, social or behavioral symptoms. Brothers have a higher risk (about 7 percent) of developing autism, plus the additional 7 percent risk of milder autism spectrum symptoms, over sisters whose risk is only about 1 to 2 percent.When the cause of autism is a chromosome abnormality or a single-gene alteration, the risk that other brothers and sisters will also have autism depends on the specific genetic cause."Reference: https://www.genome.gov/Genetic-Disorders/Autism&nbsp;

Autism - or more precisely the autism spectrum disorders (ASDs) - represent a broad group of developmental disorders characterized by impaired social interactions, problems with verbal and nonverbal communication, and repetitive behaviors or severely limited activities and interests.

Disease Controlling

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