How tardigrades protect their DNA to defy death

Article: https://www.sciencenews.org/article/tardigrades-dna-damage-radiation-death

Related Article: https://www.accessscience.com/content/how-tardigrades-protect-their-dna-to-defy-death/SN1910141

Certain species of tardigrades can survive doses of radiation up to 1,000 times that which would kill a human. They owe their ability to do this partly due to their molecular equivalent of cotton candy which allows them to be able to survive outer space. They can survive just about anything including x-rays, cosmic rays, or being doused in hydrogen peroxide.

It is very interesting to see that radiation and chemical exposure result in production of DNA-damaging hydroxyl radicals, molecules composed of oxygen and hydrogen. The cloud it forms similar to cotton candy keeps hydroxyl radicals away from DNA. Although more research is needed, it is interesting to see that researchers don't know yet whether the human proteins also form a similar shield against DNA-damaging chemicals.

I Remember You

Alzheimer’s disease, a disease that is associated with mental decline, causes up to 80% of the dementia cases.  A woman in Columbia that suffers from Alzheimer’s disease for years has yet not developed dementia.  Scientist have come to believe that it is because of a mutation in her genetic code, she is immune to developing dementia.

She developed Alzheimer’s at a very young age due to a Presenilin 1 (PSEN1) gene being mutated.  It is a “E280A mutation, but this isn’t the mutation that caused her immunity to dementia.  The reason for her dementia immunity is because she has 2 mutations called “Christchurch” mutations in he APOE3 genes.  Having 2 of these mutations have helped block the necessary actions for the body to have unnecessary death of brain cells.  If this mutation could be replicated in the lab and applied to individuals suffering from Alzheimer’s, then it may be able to prevent those individuals from developing dementia.  Because the mutation stopped the Alzheimer’s from progressing into dementia, it may not be able to reverse the effects for people already affected by it.  

Original Article: Woman that Doesn't Develop Alzheimer's

Schizophrenia: Genes related to circadian rhythms may be disrupted

New research examines the brains of people with schizophrenia and finds disrupted patterns of expression in genes linked with sleep-wake cycles. Prof. McClung and the team obtained postmortem gene expression data from 150 people, 46 of whom had lived with schizophrenia. The people had been younger than 65 years old when they died, and the researchers had access to the times of death. Specifically, the researchers looked at gene expression in the dorsolateral prefrontal cortex, a brain area involved in cognition and memory. In their present study, Prof. McClung and the team examined the rhythms by which some genes switched on and off in the brains of people with schizophrenia and compared these rhythms with those in the brains of people who did not have the condition. Some of these disruptions affected the functioning of mitochondria. When Seney and McClung compared gene expression in brains from people who died during the day, the control and schizophrenia subjects were not different, but in those who died at night, there were major differences, since genes that had gained a rhythm had hit their low point during the night.

https://www.sciencedaily.com/releases/2019/08/190809085738.htm

https://www.medicalnewstoday.com/articles/326017.php#1

Alzheimer’s Gene Affects Energy Consumption in Mouse Brains

Humans carry three different isoforms of the ApoE gene, which affects Alzheimer’s risk. Liqin Zhao of the University of Kansas and her colleagues previously found that the gene plays a role in brain metabolism when expressed in mice. Zhao’s team engineered female mice to express the human versions of either ApoE2, ApoE3, or ApoE4, and analyzed expression of 43 genes involved in energy metabolism in their cortical tissue. Mice with ApoE2 showed higher levels of proteins needed for glucose uptake and metabolism in their brains relative to animals harboring the most common isoform in humans, ApoE3. Mice with ApoE4 had lower levels of such proteins. The brain tissue’s glucose transport efficiency also varied across the genotypes, and levels of a key glucose-metabolizing enzyme, hexokinase, were reduced in ApoE4 brains. However, ApoE2and ApoE4 brains contained similar levels of proteins involved in using ketone bodies, a secondary source of energy, while ApoE3 brains had lower levels of those proteins. ApoE4 brains’ reduced ability to extract energy from glucose may contribute to Alzheimer’s pathology by reducing synaptic activity and increasing susceptibility to cellular stress. While ApoE4 increases risk of developing Alzheimer’s, ApoE2 lowers it.

https://www.the-scientist.com/the-literature/alzheimers-gene-affects-energy-consumption-in-mouse-brains-64813
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4731873/

Gene Mutations and Migraines

Many people experience headaches, but not as many people experience migraines. Migraines tend to cause intense pain in one side of the head, are often associated with nausea, dizziness, auras, light/noise/smell sensitivity, and they tend to last between 4 and 72 hours. For people who regularly experience migraines, it can be debilitating and make it very difficult to plan things as an attack can happen at any time, sometimes without warning. Some people have specific triggers for migraines and some people don't, but most cases of migraines appear to have a genetic component.

A lot of people who are diagnosed with migraines have at least one immediate family member who also experiences them, suggesting that there is a genetic component to a degree. Although some migraines are solely triggered by lifestyle (such as sudden change in diet or daily routine), researchers have found many different gene mutations that could be responsible for migraines. Unfortunately, because there are many different genes and they don't all affect the same pathways in the brain, there isn't one targeted therapy that could wipe out migraines for everyone.

The most interesting thing about the genetic component of migraines is that there has only been one gene (TRPM8) linked directly to a pain pathway. Considering the fact that migraines are so painful, most people would assume that the related genes would directly affect the pain pathway, but in fact most of the mutations cause changes in neurotransmitter concentrations. Instead of the concentrations causing more nerves to fire, they end up in the bloodstream in the brain, and the increased concentration can actually cause the blood vessels to become inflamed. The inflammation is what causes the intense pain sensation in the brain.

I suffer from migraines myself, so to see so many factors playing a role in migraines it makes it hard to believe that there will ever be a cure. Neurologists typically default to checking for lifestyle changes or imbalances of different chemicals that relate to your diet. But for people like me who can't seem to find a trigger for their migraines, it makes me wonder if my genetics are the sole cause for them. If that is the case, I think it will be very hard to find the right treatments for people like me since it is nearly impossible to sense when a migraine is coming on, and most migraine medications on the market nowadays are only effective if you take them the minute you feel the migraine beginning. More research is desperately needed in this subject because if a common pathway is found somewhere, there may be a common treatment that can be used for everyone that regularly experience migraines. At the very least, more research will allow us to further understand the mechanisms behind migraines and perhaps will clear up many of the gray areas that still remain in this condition.

Links for the articles:

Genetics of migraine in the age of genome-wide association studies:
https://thejournalofheadacheandpain.biomedcentral.com/track/pdf/10.1007/s10194-011-0399-0

Molecular genetics of migraine:
https://link.springer.com/content/pdf/10.1007/s00439-009-0684-z.pdf

When a DNA Test Says You’re a Younger Man, Who Lives 5,000 Miles Away

A patient by the name of Chris Long received a bone marrow transplant four years ago and has discovered that his DNA has been replaced by his donor’s DNA. Even the DNA in his semen had been replaced by the DNA of his donor’s. Now Chris long is referred to as chimera, a person with two sets of DNA. This is very rare and sparks an interest for crime investigators. If Chris Long were a victim or perpetrator investigators would have the DNA of his donor’s instead of his, throwing off the whole case. Even though Chris now has the DNA of his donor’s his brain and personality should remain the same. Where his DNA is going is unimportant to his doctors but not to forensic scientists. A person who is Chimera can commit a crime and mislead crime investigators. 

Links:

https://www.nytimes.com/2019/12/07/us/dna-bone-marrow-transplant-crime-lab.html 

https://www.scientificamerican.com/article/3-human-chimeras-that-already-exist/ 

Herpes' Achilles' Heel

https://www.sciencedaily.com/releases/2019/12/191212104636.htm

Supporting Article:
https://hms.harvard.edu/news/herpes-achilles-heel

The herpes simplex virus (more commonly known as herpes), is a cold sore virus that can enter the body through the mouth, nose, and genitals. The virus stays dormant after initial infection only to be regularly reawakened to cause outbreaks such as cold sores or blisters. Antiviral drugs can prevent repeated outbreaks, but they do not always work. Using human fibroblast cells infected with HSV, Harvard Medical School scientists have successfully used CRISPR-Cas9 gene editing to disrupt not only the actively replicating virus, but also the much harder to reach latent reservoirs. The experiments also show that the DNA of the rapidly replicating virus is more exposed to the Cas9 enzyme — molecular scissors in the CRISPR-Cas9 gene-editing system.

I thought that this article was really interesting because this could be the solution to curing herpes. This article made me hopeful for the future of medicine because people will no longer have to take medication to prevent the virus from spreading.

Choice of Diet

Anorexia nervosa, commonly known as anorexia, is an eating disorder that is associated with food litigation, fear of gaining weight, underweight, and a strong urge to continuously lose weight. On July 15th, 2019, The largest study for Anorexia Nervosa has taken place, examining around 17,000 patients that have been diagnosed with this disorder.  Findings suggest that chemical signals involving both the mentally and physically have confused the mind to behave in this manner, causing the individual to not choose a healthy diet.  Getting these results from one of the largest studies of anorexia yet, the disorder affects up to 2% of women and 0.3% of men. It has been a struggle trying to figure out how to dissect the disorder and treat it all in the same process.  Anorexia shares some of the same character traits as ODC, major depressive disorder and schizophrenia.
Anorexia, like any other mental disorder, should be as big of a priority as our physical and emotional health. That fact that this disorder shares "characteristic single-nucleotide polymorphisms" with other disorders that are affecting a huge percentage of mental health should be highlighted and brought to the attention of our children. Although psychiatrists have struggled to find solutions to 100% treat the people who have been diagnosed, I feel as though sharing what the issue is and helping others gain knowledge of how to treat the Patient in the real world should bring light to the fact that we want to help. I think by acknowledging people with this disorder as if they are the same as anybody else will help a little at least with the mental state.

Original Article: Roots of Anorexia

Birds Songs Show Patterns of Gene Activities

Songbirds species-specific tunes show patterns of gene activity in clusters of neurons called song nuclei. This gene activity is unique to their own species. After looking at the gene expression in the song nuclei of three finch species they identified the genes that are differentially active, and it was discovered 10 percent of the genes in the song nuclei were differentially expressed between the two finch species. These differences could be the reasons the songs of the birds differ. To test these studies they took baby zebra finches, and raised them with adult owl finches to see what songs the birds would sing. The young did learn to mimic the adults songs, but some characteristics resembled the songs sung by their own species. They were never taught these songs, so this suggests that song learning is regulated by genetic differences. With further research this could contribute to understanding how changes in gene regulation could eventually lead to the evolution of species-specific animal behaviors.




Article: https://www.the-scientist.com/image-of-the-day/image-of-the-day--species-specific-songs-66718

Similar Article: https://www.jstor.org/stable/4533896?seq=1#metadata_info_tab_contents

Epigenome Editing to Prevent Neurological Disorders

Genome editing is a controversial subject to say the least. Not only are there various ethical questions to consider when editing an individual's genome, but in many cases the long-term effects of gene editing are unknown. However, few can deny the power of gene editing when it can be used to reverse, and perhaps even eradicate, various diseases. One research team from John's Hopkins is researching how epigenome editing- a way of editing genes without actually altering DNA- can be used to help treat neurological diseases.

The gene this team is targeting is C11orf46. Mutations of this gene lead to the development of WAGR syndrome, which results in intellectual delays and other health problems. The mutations typically culprit to this disease are deletion mutations. So, to study the effect these mutations have on an individual, the researched "silenced" the gene in mice via epigenetic techniques. This means instead of altering the DNA, they altered the chromatin packing the DNA is wrapped in to make this gene harder to access.

By silencing the gene, researchers were able to identify a higher expression of the semaphorin 6A protein. The researchers then used more epigenetic techniques to reduce the expression of this protein, resulting in an increased health in the mice.

This research could lead to incredible advances in finding cures for various neurological diseases. Additionally, the fact that none of the DNA sequences are actually altered would reduce the amount unforeseen long-term effects and make this method more favorable to the general population.

Article: https://www.medicalnewstoday.com/articles/327296.php#4
Related Article (Information on Epigenome Editing): http://gersbach.bme.duke.edu/research/epigenome-editing-and-gene-regulation

Genetic Estimation of Lifespan of Vertebrates

Genetics can now predict the length of the lifespan of vertebrates. This includes species that are long extinct. The team analyzed genomes of species with known lifespans.. From this they identified 42 genes that can be used to predict lifespan. The method screens the 42 genes for CpG sites which are short regions of DNA whose density is related to longevity. These sites regulate gene expression and control aging. However, aging can also be affected by environmental factors.

CpG sites in a genome (green)

DNA methylation can also drive aging to occur by adding methyl groups to the DNA moleculeThis declines the predictability of the CpG sites. These patterns were taken into account in the model. Stil this model most likely overestimates the lifespan of animals in the wild as environmental factors most likely end their lives before their genetics will. When this model was used to predict human lifespan, the results came to 120 years, much higher than the average of 86. Therefore, the human data were excluded from the study.This model is most useful for conservation studies.

I think this could be a useful tool to help scientists involved in conservation efforts or those attempting to help endangered species as it gives them more information about the life of the species they are working with. Obviously, there are some drawbacks as the model is not accurate for all species.

https://www.inverse.com/article/61650-genetic-clock-predicts-lifespan-of-vertebrates

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5485512/

World's Largest Family Tree!

At-home genetic testing kits like AncestryDNA and 23andMe have become increasingly popular.  Geni.com is another heritage mapping company with over 130 million family tree connections worldwide.  Using these profiles, researchers were able to link 13 million people, possibly creating the world’s largest family tree.  How creepy is that?!

article: https://www.smithsonianmag.com/smart-news/worlds-largest-family-tree-stretches-back-five-centuries-180968334/

related article: https://www.sciencemag.org/news/2018/03/thirteen-million-degrees-kevin-bacon-world-s-largest-family-tree-shines-light-life-span

How Height Happens:

Height is all about the length of our bones. Many factors contribute to the height such as hormones and nutrition. Among the factors, there is also genetics. Harvard University researchers conducted functional tests and identified hundreds of genetic "switches" that influence height and demonstrated how one switch alters the function of a gene involved in the difference of height. The study involved 250,000 people and resulted in the finding of about 700 genetic regions associated with height. As each genetic region could contain tens of thousands of DNA variants, all linked together, the researchers narrowed the focus to the variants associated with cartilage growth plates of bones. This narrowed to 60,000 genetic variant switches in the DNA that caused nearby genes to turn on or off in the femurs of developing mice. Of those 60,000, 900 genetic variants were filtered that were involved in bone and cartilage development, and 83 new genetic variations in the human height.

I think studying height is meaningful to understand how many genes work together to influence height and more traits (epistasis). Studies of such can provide a better insight into the evolutionary dynamics of complex genetic systems. I think studying genetic variation will contribute much to personalized medicine in the future because much will be known about how genes function in the body. More studies on identifying similar genetic variations that may influence the risk of developing common diseases such as schizophrenia, cancer, diabetes, and cardiovascular disease are in progress.


Article Publication: December 5, 2017, by Harvard University

Article Link: https://www.sciencedaily.com/releases/2017/12/171205115936.htm
Related Article: https://www.medicalnewstoday.com/articles/315620.php#1

New targeted therapy for anxiety and depression

It has been understood for a while now that genetics plays a huge part in patients with depression and anxiety. Most people are predisposed to the conditions because of the genetics passed down from their parents: if your dad suffers from depression and/or anxiety, you would be more likely to also struggle with the conditions at some point in your life. Current studies aren't denying the fact that genetics play a role, but suggesting that other epigenetic factors are necessary to see the effects of these conditions in people who are predisposed.

The above graphic was pulled from the second article, The CRF system, stress, depression and anxiety—insights from human genetic studies. The graphic outlines one of the most significant pathways that are affected in people with anxiety, depression, and various other mental illnesses. The main focus of this pathway is the corticotropin releasing factor (CRF), which regulates the hypothalamic-pituitary-adrenal axis (HPA axis). The adrenal glands in the body control stress response, most commonly the fight or flight response. Since CRF plays such a key role in the activation or inhibition of the HPA axis, researchers are beginning to look into targeted therapy that can regulate CRF. If CRF is regulated, the HPA axis would be regulated - meaning anxiety and depression responses would be able to be controlled and mitigated.

Since genetics predisposes people to anxiety and depression, and social interactions can shape or alter the DNA, some people may have an enhanced risk of developing these illnesses. For example, someone who has been traumatized by sexual assault and who is genetically predisposed to depression and anxiety will be extremely likely to develop and experience depression and anxiety. On the contrary, someone who is not genetically predisposed but was not lovingly nurtured by their parent growing up still may be likely to develop and experience anxiety and depression because their experience may alter their DNA and how it is expressed which may affect neural links in the brain.

I think the possibility of targeted drug therapies for depression and anxiety are something of the near future. If the HPA axis is the main player in many of the mental illnesses, it may be possible to stop the onset of symptoms in at-risk patients before they even begin, allowing people to live a normal life. If the HPA axis and CRF is a big factor in other mental illnesses like schizophrenia, a drug that targets CRF may be the key to finding a cure for these ailments and since it would be targeted therapy, there is the possibility of little to no side effects. I definitely think this topic deserves more research since there is the possibility of giving patients a whole new life, no matter what their age, so they can have an overall better quality of life.

Article links:

The New Genetics of Mental Illness:
https://www.jstor.org/stable/pdf/24939890.pdf?refreqid=excelsior%3Ad7cc5f97bcf0a23f85a7a8d216164514

The CRF system, stress, depression and anxiety - insights from human genetic studies:
http://web.a.ebscohost.com.ezproxy.stockton.edu/ehost/pdfviewer/pdfviewer?vid=1&sid=41351801-df51-406c-b812-7b8b58e6b823%40sessionmgr4006

Artificial Cells Are Now Able to Mimic Natural Cell Movement

Synthetic cells are used in laboratory settings but don't have all the characteristics of living cells, limiting research. Cell motility was hard to research due to surface enzyme activity, but a new method was discovered that allowed the synthetic cell to actively move. They investigated how ATPase can propel the protocells. ATPase is an enzyme that converts ATP into ADP. In this experiment, the protocells had artificial membranes composed of phosphatidylcholine and the ATPase enzymes were incorporated directly into the membrane. This discovery allows for the first step to be made for other researchers to make artificial cells with enzymatic activity. Research showed that movement for the cells was low for low amounts of ATP but movement also dropped for too much ATP, which was surprising. The researchers concluded that a high ATP concentration would bind to the ATPase and suppress ATP activity and lowering motility. This research allows for new opportunities to understand more about the mechanisms of movements for cells. This will have a huge role on new medical research.

I feel like we always think that science as come so far and that there isn't much else to discover, but this just shows how much we still don't understand. Just trying to replicate a living cell is so complicated and we're finally one step closer to making them act more like natural cells. It's amazing how new discoveries like this are able to open up even more doors. Hopefully this research will help with new medical breakthroughs in the future.

Link: https://www.sciencedaily.com/releases/2019/12/191205155318.htm

Related Link: https://news.psu.edu/story/600705/2019/12/05/research/artificial-cells-act-more-real-thing

Fox Domestication

While a little old the research paper on the domestication of foxes is still quite important. The research project has been breeding foxes based on whether or not they have traits that can be seen as friendly in an attempt to domesticate foxes. The main goal was to see how an animal could be properly domesticated and if there were particular genes related to domestication in animals. After breeding many generations of foxes they managed to get generations that can be seen as domesticated, but that can be a bit subjective I guess. The foxes are kinda comfortable around people and will walk up to them briefly, but they are nowhere near dogs in terms of emotional attachment. Really the foxes are like very emotionally distant cats rather than a dog. And since they are domesticated, there are research groups in many countries trying to further the project by sequencing genomes in an attempt to see if genes have any bearing on it. Last update the project gave showed around 30 potential genes they were looking into and it seemed promising so far.

I have been following this project for a while so I do think it is extremely interesting and important in many ways.The applications of this research only bring up mental images of people just domesticating random animals, but it is quite a bit more important that than. Finding a genetic link to behaviors could really open up a lot of doors into potential uses in therapy. Potential cures to disorders could be found and the fact that this is being brought up shows where science is going in the near future.

Article: https://www.nature.com/articles/s41559-018-0611-6#article-info

DNA Profile is Private? A Florida Judge Just Said Otherwise

Genetic profiles have always been private for everyone but a judge in Florida is about to change that. A detective from Florida requested a warrant to go into and see GEDmatch database that has nearly one million users. This is the first time a judge has arepoved a warrant like this and doing so can bring complications on genetic privacy. The judge allowing this warrant is giving other agencies ideas to request for search warrants on other DNA sites. This means no one’s genetic profile will be safe and their information could be used by anyone.

Links

https://www.nytimes.com/2019/11/05/business/dna-database-search-warrant.html 

https://www.google.com/amp/s/futurism.com/cops-warrant-entire-dna-websites/amp 

Scientists Pinpoint a Gene that is Linked to Left-Handedness

Scientists have officially found four spots in our DNA that are associated in determine whether we write with our right and left hand. Of the four gene regions, three of them deal with proteins involved in brain development and structure. This was deduced from a study of genetics analysis across 400,00 people in the United Kingdom. Of these 400,000, 38,000 of these people were left handed. This study also found that these people that were left handed communicated between the language regions of their right and left brain more efficiently than those in the study that are right handed. This means that they have some sort of "advantage" in verbal tasks. Also, various studies of twins show that genes account for 25% of the variation in left or right handedness. Another study found that the link between left handedness and their respective genetic regions also deal with Parkinson's disease and and schizophrenia. Left handed individuals have a slightly reduced risk of Parkinson's disease, but also have a slightly increase risk for schizophrenia. I think this is a remarkable discovery and is a surprise to me, considering that I believed right or left handedness was simply based upon which hand your parents helped to teach you to write with, or whichever had you took and immediate preference to.

Original Article: https://www.usnews.com/news/health-news/articles/2019-09-05/scientists-id-genes-tied-to-left-handedness
Supporting Article: https://geneticliteracyproject.org/2016/08/29/left-handedness-genes-and-a-matter-of-chance/

Prion Disease

Prion diseases are complicated and often fatal illnesses. This specific prion disease is known as kuru, or the cannibalism disorder. Although extremely rare, it is devastating, and resistance may be attainable. People with a mutation on codon 129 of the prion protein seem to be less susceptible to prion diseases if they have one or two copies. When tested on mice, it was found that a different codon, codon 127, made mice completely resistant when it was mutated. The research shows the reason behind this is because the mutation on codon 127 prevents the prion protein from becoming misshapen, which is what causes the disease.
Researchers are currently working on determining the structure of the mutated protein, and trying to use it as a defence in other diseases. I hope it is successful.



original link: https://www.nature.com/news/genetic-mutation-blocks-prion-disease-1.17725
related link: https://www.nature.com/articles/gim201032

Ebola Rendered Useless when Genetically Modified

The Ebola virus is notorious for being one of the most deadly viruses in the modern world. Akin to many other epidemic-causing pathogens, the Ebola virus has resulted in the deaths in over 11,000 individuals, primarily in West Africa. However, cases of this deadly virus have been documented all over the world, including 66 cases in America and over 3,000 cases in Europe.

Researchers at the Center for Microbial Pathogenesis at Georgia State University performed a study in an attempt to incapacitate Ebola in response to the growing threat of the disease. The team genetically altered a sample of Ebola, specifically changing the VP35 protein. This protein allows Ebola to fight off any early immune responses the host organism may enact. This mutated virus was not only safe for the team to work with, but is also completely ineffective. Additionally, when monkeys who had first been exposed to the mutated version of the virus were later exposed to the wild-type virus, they exhibited immunity to it.

This study is fascinating because it introduces a potential "vaccine" for the Ebola virus. With further animal and human testing, this discovery could be huge. Applications of this mutated virus would be life-changing in areas heavily affected by Ebola, and could hopefully lead to eradication of the disease as a whole.

Article: https://www.usnews.com/news/health-news/articles/2019-09-18/tiny-genetic-tweak-may-stop-ebola-virus-in-its-tracks
Related Website (Paper on the function of VP35): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3061251/

GEDmatch acquisition calls privacy into question

Privacy of genomic data is coming into question as the company GEDmatch was used to identify a suspect in the Golden State Killer case. Crime scene evidence was matched to data uploaded to the site which continues to be used for identification in criminal cases.The terms and conditions of the site were changed to allow law enforcement to actively utilize the site as a resource. Now, with an acquisition to Verogen ( a DNA sequencing company), the site will be more useful to law enforcement. 

    Many genealogists have left the program citing changes that make the data into a product rather than a service. Though the new system requires an opt-in, it can be overridden by a warrant received by law enforcement. The new terms may also be hard to understand and unintentionally trick people. This has caused the amount of data to shrink enormously. 

    I think that law enforcement should be able to utilize sites such as this to match suspect DNA. If you put your DNA information online for everyone to see, it should be able to be used by professionals. This way more criminals could be caught leading to a safer environment. 

https://www.theverge.com/2019/12/10/21005443/golden-state-killer-genetic-database-identity-company-acquisition-crime-scene-dna-data

https://www.npr.org/sections/thetwo-way/2018/04/26/606060349/after-arrest-of-suspected-golden-state-killer-details-of-his-life-emerge

Cardiac Arrest May Be Predicted in Genes

Research shows that cardiac arrest may be able to be predicted by looking at genes. Cardiac arrest is a no symptom, no warning death. One second your fine the next second your dead. Using a gene test it could be predicted people who are at risk. Researchers identified fourteen gene variants that appear to be linked to cardiac arrest. People who carry these genes are three times more likely to die of cardiac arrest. Sudden cardiac arrest is responsible for 325,000 deaths a year, so this finding could be very crucial for helping people with these gene variants. Four major reasons usually result to cardiac arrest including a weakened heart muscle, a heart attack, an abnormal heart rhythm, or dilation or tear in the main artery leading out of the heart, and these diseases tend to run in families. There are genetic variants that cause each of these diseases like the ones they just discovered for cardiac arrest. Comparing the gene variants found in the subjects with the four major diseases, and using control subjects they were able to find fifteen subjects with gene variants who died of sudden cardiac death. All fifteen people carried at least one of the gene variants found, and were not controls in the experiment. Hopefully with this new found gene variants they are able to screen people for if they are at risk, and do necessary treatments to lower their risk.


Article: https://www.usnews.com/news/health-news/articles/2019-11-18/gene-test-might-someday-gauge-your-cardiac-arrest-risk


Related Article: https://consumer.healthday.com/cardiovascular-health-information-20/heart-attack-news-357/gene-test-might-someday-gauge-your-cardiac-arrest-risk-752232.html

Daily Alcohol Consumption Linked to Increased Risk of Cancer

In Japan, scientists studied 63,232 patients and their alcohol use. They screened the patients for other health risks before the study. The study found that patients that drinking 6 ounces of wine, 17 ounces of beer, or 2 ounces of whiskey a day for 10 years can increase risk for cancer by 5 percent. After 40 years of these drinking habits, cancer risk is increased by 54 percent. However, the authors of the study point out that Japanese have a genetic variation which causes them to metabolize alcohol slower, so it may have more of an impact on them.

According to the Centers for Disease Control and Prevention, alcohol has this effect on humans because when we drink alcohol, it breaks down into acetaldehyde. Acetaldehyde is known to damage DNA and prevent the damage from being repaired. When the DNA is damaged, it may cause cells to enter a growth cycle which can lead to tumors.

https://www.cdc.gov/cancer/alcohol/index.htm

nytimes.com/2019/12/09/well/live/alcohol-drinking-cancer.html

We Evolved from Neanderthals

A study has shown that Developmental cells are the cause for the Domestication and Change in Facial Structure between the once Neanderthals and today's "normal" facial structured Humans, as well as some Humans who have rare genetic disorders from prenatal and postnatal growth. It’s all tied around this one gene that goes by the name of BAZ1B. A scientist has concluded that the lack of this "boss-like" cell to be the main reason for the "Williams-Beuren syndrome". The Neural crest cells show up upon the elemental stage of birth as they migrate into different placements throughout the body.  Rising tissues, altering bone and cartilage placements, pigment cells, and other actions take place when these neural crest cells present there presents.

People who have Williams-Beuren syndrome are known to be more talkative, outgoing and not aggressive in any manner. But on the flip side, there is a disorder that includes that extra BAZ1B crest cell that results in the person having difficulty speaking and tend to come off more aggressive than the norm. They also have a different facial structure, more narrow opposed to the Williams-Beuren syndrome. This disorder is formally known as 7q11.23 Duplication syndrome.  All in all, evolution has allowed us to change in appearance, giving rise to less harsh facial features. Imagine how different human beings would look in the next hundred years compared to how we appear today!

Original link: Gene Tied to Facial Development

Identifying Unintended Gene Changes

CRISPR is a developing technique used for genetic modification. Using this technique, scientists will be able to edit DNA, hopefully resulting in the ability to fix genetic disorders, better treat cancer, and modify other organisms to produce otherwise limited chemicals.
 
This technique shows promise, but like any other developing process, it is not without its hiccups. CRISPR can result in unintended gene changes. Typically, these edits come in the form of deletion. Previously, these deletions were difficult to locate. A recent innovation has shortened time required to identify these mistakes significantly. I hope that this improvement to CRISPR efficiency and safety allows to be used to treat more people.

Links:
https://www.labroots.com/trending/genetics-and-genomics/16314/tool-rapidly-detects-unintended-gene-changes-crispr
https://www.nature.com/articles/d41586-018-05736-3

Microbe Might Provide Key to a Longer Healthier Life for Humans

The organism Caenorhabditis elegans has a simple structure but has genetic similarities to humans. This organism is able to change it's cuticle, a skin-like barrier, in response to infection. The nervous system changes the structure of the cuticle. Originally it was believed that the cuticle and human skin work in similar ways, they are just a barrier to infection, there was no response. This discovery may be able to help human health. The researchers used gene splicing and CRISPR gene editing to show that a G-protein-coupled receptor tied to a gene called NPR-8 regulates collagens. Collagens are proteins that are a key part to the structural component of the cuticle. When the NPR-8 was removed, the organism survived longer when exposed to pathogens. Without the receptor, the cuticle was also smooth instead of wrinkled like the wild type. Pathogens try to destroy the cuticle in order to infect the organism and the results showed that the nervous system was able to change its structure based on an immune response. Collagen loss can cause a lot of issues in humans, so studying this natural regulation of collagen may be beneficial to human health.

It would be very beneficial to people if some type of treatment can be made to help collagen regulation, based on the research done on this organism. Humans have an extracellular matrix on all of their organs that have collagen in them. If there is too much or too little collagen, then problems can arise. It would be very cool to see how this organisms natural process of regulating collagen may help people in the future.

Link: https://www.sciencedaily.com/releases/2019/11/191120144950.htm

Related Article: https://advances.sciencemag.org/content/5/11/eaaw4717

E. Coli, an autotrophic bacterium?

A common practice in today’s world is synthesizing bacteria to produce compounds for medicine, energy, and more. One of the most common examples is synthetic Escherichia Coli that has been modified to produce insulin. This method has proven to be highly effective, however there can still be improvements. One such improvement involves the fact that E. Coli is a heterotrophic bacterium, that is, they must eat sugars in order to survive. This can become costly to maintain. One solution to this, is using autotrophic bacteria. Which survive off water and carbon dioxide, through photosynthesis. However, these bacteria have proven difficult to engineer.

So, Ron Milo, a synthetic biologist at the Weizmann Institute of Science in Rehovot, Israel, thought of a fascinating solution. We already have E. Coli that produce desired compounds. So why not make E. Coli an autotrophic bacterium? This is exactly what So, Ron Milo and his team have sought out to do. Instead of making E. Coli a true autotroph, enabling it to undergo photosynthesis. The team inserted a gene into E. Coli’s genome which enables it to eat formate, a simple carbon-containing compound. Which is then converted into ATP, providing energy for the E. Coli. This alone did not provide the desired results. Several other genes which encoded for metabolism enzymes were knocked out to prevent normal energy production.

Again, this was not all that had to be done. Through a starvation process over many generations, formate was increasingly introduced. While sugars were slowly reduced, until the bacteria could solely survive off formate. By combining selective breeding and genetic engineering, So, Ron Milo and colleagues created an E. Coli strain which survives off a carbon containing compound. Eliminating the need to “feed” the bacteria sugars. As far as genetic engineering goes, I find this very interesting. This research has opened many doors to future possibilities for bacterium engineering. Possibly making resource production cheaper. We all like cheaper fuels and medicine!

Link to Article: https://www.sciencemag.org/news/2019/11/microbe-no-longer-needs-eat-food-grow-thanks-bit-genetic-engineering

Related Article: https://www.the-scientist.com/news-opinion/lab-evolved-e--coli-makes-energy-solely-from-carbon-dioxide-66788

Using Gene Therapy to Treat Sickle Cell

As one of the most prevalent genetic disorders, a great number of researchers have been focusing on finding a treatment for sickle cell anemia. Many believe they have found a possible treatment to the disorder and gene therapy is seen as the best way to treat it. The disease works as cells with a specific mutation in the gene that produces B-globin causes protein to form wrong. Gene therapy hopes to add a functioning version of the gene to an afflicted persons bone marrow by using a virus. So far the idea has been formulated but the treatment is far from complete.

While this research is promising and has great potential it seems like its at least a few years away. The rest of the article gave a lot more important info as it explained how it is hard to research the disease as many people who have it live in Sub Saharan Africa where there are fewer research centers. The advances and difficulties in gene therapy were listed quite well and made me much more interested in how research in this field is physically done.

Article:https://www.nature.com/articles/d41586-019-03698-8

Bone Marrow Transplants Replacing DNA?

Chris Long (who was the main case study) had a bone marrow transplant. Although the transplant had done its job, it went further. The DNA from the donor was no longer only affecting Long's blood. Traces of DNA not originally belonging to Long was found in mouth swabs as well as semen samples. It was found that both DNA were in his body. Other cases of this have been noted, and it has played a role in a few criminal instances, as the DNA found at a crime scene showed that there were more than one person who committed the crime, or that it was a completely different person. However, many of these cases all involved a bone marrow transplant, which showed more than one DNA profile.

I think that this is pretty odd as the donors DNA literally spread, and in more than one case so this isn't just a random, once in a lifetime situation. I figured the bone marrow transplant would most definitely effect a patients blood, but not spread throughout his body so that he would have more than one strand of DNA. I'm curious to see how this pans out in the future, and if they will run tests on whether this effects the children's DNA and if it would match the original patients DNA.



https://www.nytimes.com/2019/12/07/us/dna-bone-marrow-transplant-crime-lab.html?searchResultPosition=7

https://medicalxpress.com/news/2018-01-bone-marrow-transplant-dna.html

think before you drink...milk

Penn State researchers traced more than 99% of these dairy cows back to one bull, born in the 1960s.  This genetic homogeneity increases the risk of inherited disorders.  Researchers bred a small batch of new cows using the preserved semen of deceased bulls and compared them to modern-bred dairy cows with the hopes to address any traits that have been lost due to prolonged inbreeding.

article: https://www.scientificamerican.com/article/from-two-bulls-nine-million-dairy-cows/

related article: https://www.sciencedirect.com/science/article/pii/S0022030215000727

Genetically Modified Fungus Kills Parasites

Metarhizium phinghaense is a green fungus that has the ability to kill insects when they come in contact with it.  This fungus is now undergoing studies to see if it can be used to kill insecticide-resistant mosquitoes that carry the Malaria pathogen and prevent the spread of disease.
Researchers have genetically modified the Metarhizium phinghaense fungus to carry a toxin responsible for killing off the mosquitoes, including those carrying Malaria pathogen, called the spider bite toxin.  It is a hybrid toxin that enters the blood of mosquitoes, called hemolymph.  This toxin not only kills the mosquito and stops the transfer of Malaria, but it kills the pathogen themselves so it can't be picked up within the environment.

Brkina Faso, West Africa

In Burkina Faso, a country in West Africa, a study was done to assay the effectiveness of the Metarhizium phinghaense hybrid fungus.  I was performed here because in 2017, 219 million cases of malaria were reported and 92% of those cases originated in Africa, and 93% of the deaths originated in Africa as well.  To perform the study they secured the area with mosquito nets preventing new mosquitos to enter or case study mosquitos to exit.  In their findings that introduced the hybrid fungus to the mosquitos, the fungus killed off 2 generations of mosquitos.
This genetic modification could be the start of bringing down Malaria cases more than 50% percent if everyone would plant them outside of there homes, villages, etc.  The mortality rate would significantly decrease as well.  Although this discovery has great benefits, what would be the consequence to genetically modifying the Metarhizium phinghaense fungus?

Original Article: Science News