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Genetics

Genetics + Family Environment Impact Childhood Obesity – PsychCentral.com

A new international study finds that around 35-40 percent of a childs BMI (Body Mass Index) how fat or thin they are is inherited from their parents.

Investigators say that for the most obese children, the proportion rises to 55-60 percent, thus more than half of their tendency towards obesity is determined by genetics and family environment.

University of Sussex researchers used data on the heights and weights of 100,000 children and their parents across the world, including the U.K., U.S., China, Indonesia, Spain, and Mexico.

Investigators found that the intergenerational transmission of BMI is approximately constant at around 0.2 per parent; i.e., each childs BMI is, on average, 20 percent due to the mother and 20 percent due to the father.

The pattern of results, said lead author Professor Peter Dolton of the University of Sussex, is remarkably consistent across all countries, irrespective of their stage of economic development, degree of industrialization, or type of economy.

Professor Dolton says, Our evidence comes from trawling data from across the world with very diverse patterns of nutrition and obesity, from one of the most obese populations USA to two of the least obese countries in the world, China and Indonesia.

This gives an important and rare insight into how obesity is transmitted across generations in both developed and developing countries.We found that the process of intergenerational transmission is the same across all the different countries.

The findings are published in the journal Economics and Human Biology.

Interestingly, the effect of parents BMI on their childrens BMI depends on what the BMI of the child is. Researchers discovered that consistently, across all populations studied, the parental effect was lowest for the thinnest children and highest for the most obese children.

For the thinnest child their BMI is 10 percent due to their mother and 10 percent due to their father. For the fattest child this transmission is closer to 30 percent due to each parent.

Said Dolton, This shows that the children of obese parents are much more likely to be obese themselves when they grow up the parental effect is more than double for the most obese children what it is for the thinnest children.

These findings have far-reaching consequences for the health of the worlds children. They should make us rethink the extent to which obesity is the result of family factors, and our genetic inheritance, rather than decisions made by us as individuals.

Source: University of Sussex

APA Reference Nauert PhD, R. (2017). Genetics + Family Environment Impact Childhood Obesity. Psych Central. Retrieved on February 22, 2017, from https://psychcentral.com/news/2017/02/21/genetics-family-environment-impact-childhood-obesity/116702.html

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Genetics + Family Environment Impact Childhood Obesity - PsychCentral.com

Genetics

Soon, Medication Will be Custom Tailored to Your Specific Genetics – Futurism

Personalized medicine, which involves tailoring health care to each persons unique genetic makeup, has the potential to transform how we diagnose, prevent and treat disease. After all, no two people are alike. Mapping a persons unique susceptibility to disease and targeting the right treatment has deservedly been welcomed as a new power to heal.

The human genome, a complete set of human DNA, was identified and mapped a decade ago. But genomic science remains in its infancy. According to Francis Collins, the director of the National Institutes of Health, It is fair to say that the Human Genome Project has not yet directly affected the health care of most individuals.

Its not that there havent been tremendous breakthroughs. Its just that the gap between science and its ability to benefit most patients remains wide. This is mainly because we dont yet fully understand the complex pathways involved in common chronic diseases.

I am part of a research team that has taken on the ambitious goal of narrowing this gap. New technologies are allowing us to probe DNA, RNA, proteins and gut bacteria in a way that will change our understanding of health and disease. Our hope is to discover novel biological markers that can be used to diagnose and treat common chronic conditions, including Alzheimers disease, heart disease, diabetes and cancer.

But when it comes to preventing the leading causes of death which include chronic diseases, genomics and precision medicine may not do as much as we hope.

Chronic diseases are only partially heritable. This means that the genes you inherit from your parents arent entirely responsible for your risk of getting most chronic diseases.

The estimated heritability of heart disease is about 50 percent. Its 64 percent for Type 2 diabetes mellitus, and 58 percent for Alzheimers disease. Our environment and lifestyle choice are also major factors; they can change or influence how the information coded in our genes is translated.

Chronic diseases are also complex. Rather than being controlled by a few genes that are easy to find, they are weakly influenced by hundreds if not thousands of genes, the majority of which still elude scientists. Unlocking the infinite combinations in which these genes interact with each other and with the environment is a daunting task that will take decades, if ever, to achieve.

While unraveling the genomic complexity of chronic disease is important, it shouldnt detract from existing simple solutions. Many of our deadliest chronic diseases are preventable. For instance, among U.S. adults, more than 90 percent of Type 2 diabetes, 80 percent of coronary arterial disease, 70 percent of stroke and 70 percent of colon cancer are potentially avoidable.

Smoking, weight gain, lack of exercise, poor diet and alcohol consumption are all risk factors for these conditions. Based on their profound impact on gene expression, or how instructions within a gene are manifested, addressing these factors will likely remain fundamental in preventing these illnesses.

A major premise behind personalized medicine is that empowering patients and doctors with more knowledge will lead to better decision-making. With some major advances, this has indeed been the case. For instance, variants in genes that control an enzyme that metabolizes drugs can identify individuals who metabolize some drugs too rapidly (not giving them a chance to work), or too slowly (leading to toxicity). This can lead to changes in medication dosing.

When applied to prevention, however, identifying our susceptibility at an earlier stage has not aided in avoiding chronic diseases. Research challenges the assumption that we will use genetic markers to change our behavior. More knowledge may nudge intent, but that doesnt translate to motivating changes to our lifestyle.

A recent review found that even when people knew their personal genetic risk of disease, they were no more likely to quit smoking, change their diet or exercise. Expectations that communicating DNA-based risk estimates changes behavior is not supported by existing evidence, the authors conclude.

Increased knowledge may even have the unintended consequence of shifting the focus to personal responsibility while detracting from our joint responsibility for improving public health. Reducing the prevalence of chronic diseases will require changing the political, social and economic environment within which we make choices as well as individual effort.

Perhaps the most awaited hope of the genomic era is that we will be able to develop targeted treatments based on detailed molecular profiling. The implication is that we will be able to subdivide disease into new classifications. Rather than viewing Type 2 diabetes as one disease, for example, we may discover many unique subtypes of diabetes.

This already is happening with some cancers. Patients with melanoma, leukemia or metastatic lung, breast or brain cancers can, in some cases, be offered a molecular diagnosis to tailor their treatment and improve their chance of survival.

We have been able to make progress in cancer therapy and drug safety and efficacy because specific gene mutations control a persons response to these treatments. But for complex, chronic diseases, relatively few personalized targeted treatments exist.

Customizing treatments based on our uniqueness will be a breakthrough, but it also poses a challenge: Without the ability to test targeted treatments on large populations, it will make it infinitely harder to discover and predict their response.

The very reason we group people with the same signs and symptoms into diagnoses is to help predict the average response to treatment. There may be a time when we have one-person trials that custom tailor treatment. However, the anticipation is that the timeline to getting to such trials will be long, the failure rate high and the cost exorbitant.

Research that takes genetic risk of diabetes into account has found greater benefit in targeting prevention efforts to all people with obesity rather than targeting efforts based on genetic risk.

We also have to consider decades of research on chronic diseases that suggest there are inherent limitations to preventing the global prevalence of these diseases with genomic solutions. For most of us, personalized medicine will likely complement rather than replace one-size-fits-all medicine.

Where does that leave us? Despite the inherent limitations to the ability of genomic medicine to transform health care, medicine in the future should unquestionably aspire to be personal. Genomics and molecular biosciences will need to be used holistically in the context of a persons health, beliefs and attitudes to fulfill their power to greatly enhance medicine.

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Soon, Medication Will be Custom Tailored to Your Specific Genetics - Futurism

Genetics

Jurors In Toxic Tort Litigation Take Genetics Seriously – Law360 (subscription)

Kirk Hartley Can jurors grasp the role of genetics in personal injury claims alleged to arise from exposure to specific chemicals? Can judges grasp the issues well enough to really help expert witnesses present the issues clearly, and to help jurors understand?

Not long ago, we saw the first asbestos trial making explicit reference to a plaintiff with BAP1 mutations and the alleged role of those mutations in the causation story. The point of this article is to provide some more specific information from...

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Jurors In Toxic Tort Litigation Take Genetics Seriously - Law360 (subscription)

Embryology

How to make a ‘three-parent’ baby – Science News for Students (blog)

A baby born in April 2016 may have opened the door to a new world of reproductive medicine. This boy became one of the first intentional three-parent babies. The vast majority of this boys DNA came from his mother and his father. A small bit of extra DNA came from an unrelated woman. This child got some of his genetic inheritance from each of these adults.

Because of that bonus DNA from the unrelated woman, some people say babies like this boy have three parents.

Scientists didnt go to all of the effort to mix the DNA from these three people as an experiment. In fact, they did it to overcome a problem in the boys mother. That woman had a problem with her mitochondria (MY-toh-KON-dree-uh). These are important little structures or organelles present in her cells.

Many cells, including those that make up humans, contain special components that function like little organs. That gives rise to their name, organelles, which actually means little organs. Organelles perform special tasks for their parent cells. And one of the more notable of these organelles is the mitochondrion. Its main job is to help power its cell. To do this, the mitochondria harvest energy contained in the bonds linking atoms in the cells fuel (such as glucose). Mitochondria then use that energy to create another molecule, known as ATP (for adenosine triphosphate). That ATP actually serves as the energy source for cells.

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Mitochondria, one of several types of organelles found within the cytoplasm of a cell, contain a small amount of DNA. A mutation in that DNA can cause disease.

ttsz/iStockphoto

But some of the mitochondria in the boys mother have a mutation. That genetic alteration causes Leigh syndrome, a fatal disorder. Most of her mitochondria work properly. That's whythe mom does not have the killer disease. But she can pass on DNA from the faulty mitochondria to her children. And this can put them at risk of Leigh syndrome. Two of her children had already died from the disease. She also had suffered four miscarriages.

It was in hopes of giving this couple a healthy baby that doctors worked to find healthy mitochondria to substitute for her unhealthy ones. Normally, a woman passes on her mitochondria to her offspringthrough her egg (dads sperm dont contribute any). These organelles also contain a small amount of DNA just 37 genes. (Most of the roughly 20,000 protein-producing genes needed to make a human are stored in a compartment called the nucleus.) Mutations in some mitochondrial genes most often pose a risk to organs that need lots of energy, such as the brain and muscles. There is no cure or effective treatment for many of these mitochondrial diseases.

The technique used to create the baby boy is new and controversial. His birth, though, caps nearly three decades of work to to produce healthy human eggs by manipulatingthe organelle. The new baby appears to have been saved from a deadly genetic disease. Still, there are ethical and safety concerns about his three-parent heritage.

And a three-parent baby girl born in January raises even more concerns in part, just because she is a girl.

Researchers first began swapping mitochondria between egg cells to treat infertility problems almost 20 years ago. Jacques Cohen was one of those researchers.

Hes a scientist who studies human embryos. In the late 1990s, he and colleagues at Saint Barnabas Medical Center in Livingston, N.J., were looking for a way to help women who were unable to have children by in vitro fertilization. Also known as IVF, this process involves taking egg cells from a woman and sperm cells from a man, then incubating them in a dish. Some of those eggs and sperm will combine to form embryos the first stages of creating a new individual.

With in vitro fertilization, or IVF, an embryo that developed in a laboratory dish is transferred into a womans womb where it may develop into a baby.

herbap/iStockphoto

Doctors then transfer some of those embryos into the womans womb. With luck, one or more will develop into a baby. But some couples embryos never developed normally. No one knows why. Cohens group thought a dose of cytoplasm the jellylike guts of a cell from a donor egg might give the implanted embryos a better shot at success.

Cytoplasm is the most complicated fluid in the universe, says Cohen. It contains mitochondria, other organelles, proteins and other molecules that do the work of the cell. The mother's egg normally supplies all the goodies an embryo needs to live for the first few steps of development. But Cohen thought that some of his patients eggs might need extra help.

So he extracted 10 to 15 percent of the cytoplasm from an egg donated by another woman. He injected this along with a single sperm cell into a recipient egg. From 1996 to 2001, he performed the procedure 37 times. And this technique proved quite successful. It produced 17 babies for 13 couples!

Cohen later tested eight of the children born this way. Two carried some mitochondria that had come from the donor. That was in addition to some that came from the childs actual mother. Some of the other six children may have had donor mitochondria at levels too low for his tests to see back then, Cohen now says. But the finding made him curious.

So Cohen and his colleagues tracked down 13 of the 17 children. All were now teenagers. In surveys, their parents said that the kids seemed basically healthy. Cohen doesnt know whether mitochondria or other parts of the cytoplasm played a role in producing the children. His group stopped performing the technique in 2001 (because of regulatory issues).

Other scientists have also tried to replace faulty mitochondria more intentionally. The first such attempt in 1983. And it involved mice.

Pronuclei are the central, DNA-containing parts of fertilized eggs. One comes from the egg and another comes from dads sperm. At this early stage in development, the two have not yet fused into a single nucleus. (Nuclei is the plural form of nucleus.)

In a technique known as pronuclear transfer, researchers fertilized the mother mouses egg and a donor egg at the same time. The pronuclei were removed from the donor's fertilized egg and discarded. Those from the mothers fertilized egg were sucked out and then injected into the empty donor egg.

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Pronuclear transfer was the first technique that scientists tried in their attempts to keep diseases due to faulty mitochondria from being passed from a mother to her child.

T. Tibbitts; Third scientific review of the safety and efficacy of methods to avoid mitochondrial disease through assisted conception, Human Fertilisation and Embryology Authority, June 2014

Talk of applying thistechnique in humans promptly raised a few concerns.

Some people claimed that it is not ethical. They argued that it manipulates maybe even destroys two embryos.

Thats one issue. Scientists have a more technical one. They note that mitochondria tend to glom onto the nuclei. So unacceptably high numbers of mitochondria from the mothers egg including disease-carrying ones may still find their way into the donor egg, notes Shoukhrat Mitalipov. He is a mitochondrial biologist at Oregon Health & Science University in Portland.

Last June, scientists reported they had refined pronuclear transfer to reduce the number of disease-carrying mitochondria that could enter embryos. Fewer than 2 percent of the mitochondria from the mothers egg made it into the donors egg. But an earlier study suggested that even a half that amount might be dangerous. Thats because mutant mitochondria may copy themselves. Eventually, they might take over the cell and cripple its energy production.

Fertility clinics in the United Kingdom are allowed to use pronuclear transfer to make human babies where there was a high risk of mitochondrial diseases. In fact, none has done so. yet New York fertility doctor John Zhang is involved in the new baby boys case. He tried the pronuclear-transfer technique with colleagues at Sun-Yat Sen University of Medical Science in Guangzhou, China. That was more than 10 years ago. Five embryos that were made this way were implanted into a 30-year-old woman. Three grew into fetuses. None, however, survived to birth. Zhang published these results last year in Reproductive Biomedicine Online.

In January 2017, doctors in Ukraine announced that a baby girl was born from this method. Her parents had tried IVF. But, like Cohens patients, the couples fertilized eggs never grew into an embryo that could be implanted. Instead of adding cytoplasm from a donor egg as Cohen had, fertility doctor Valery Zukin at the Nadiya Clinic in Kiev instead used pronuclear transfer. And they report success a baby girl.

Labs in Ukraine and Germany confirmed that most of the babys DNA is from her mother and father. Only her mitochondrial DNA comes from an egg donor. Zukin used the same technique again. Another couple is now expecting a baby boy next month.

Some people are concerned that these babies might have health problems later. Some people also may see this as an ethical problem. Why? The technique was not used to prevent mitochondrial diseases, but instead as a type of fertility treatment.

Marcy Darnovsky is one of the critics. She is executive director of the Center for Genetics and Society in Berkeley, Calif. Doctors such as Zukin are selling unproven and possibly dangerous services to customers, she charges. This is the ugly face of commercial and status incentives driving unscientific human experimentation, she said in statement about the baby girls birth.

Doctors used a different technique spindle transfer to produce the baby boy born last April. The bodys genes reside in the DNA found in the bodys 46 different chromosomes. When a cell divides to create egg or sperm cells, it splits those 46 chromosomes into two equal sets of 23. To get portioned out properly, those chromosomes attach themselves to protein fibers. Those fibers are known asspindles. The new transplant technique gets its name from those fibers.

The technique starts with two unfertilized egg cells. One comes from the mother and the other from a donor. In both cells, a membrane surrounding the nucleus has broken down. The spindle in each has not, however, completed a separation of the chromosomes.

Researchers removethe spindle and its attached chromosomes from the donor egg and discardthem. Then they dothe same to the mothers egg except that they keep her spindle and chromosomes. These they injectinto the donors nearly empty egg. Then the researchers add the dads sperm cell into this egg to fertilize it.

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The three-parent baby boy born last year was created using a this technique, called spindle transfer.

T. Tibbitts; Third scientific review of the safety and efficacy of methods to avoid mitochondrial disease through assisted conception, Human Fertilisation and Embryology Authority, June 2014

Mitalipov in Portland pioneered spindle transfer. In 2009 he showed that he could produce healthy baby monkeys with it. Those experiments showed that fewer of the moms mitochondria made it into the donor egg than with pronuclear transfer. Typically, the carryover amounted to 1 percent or less.

But Mitalipov would like to do even better. This 1 percent is haunting us, he says.

Spindle transfer has another possible downside: Chromosomes may fall off the spindle. That could result in an embryo with too few chromosomes or too many if some are left in the egg from the donor. Both cases usually result in abnormal development. Of the five embryos on which Zhang performed spindle transfer, only one developed normally. That was the baby boy born last April.

Tests reportedly found that he has 1 percent of his moms mitochondrial DNA. At 3 months old, he appeared healthy. What his health will look like, long-term, however, is unknown. Besides the risk of even trace levels of mitochondria ballooning, another study suggests that the childs health, over time, might be affected by mismatches between the parents nuclear DNA (which is not from mitochondria) and the donors mitochondrial DNA.

Some researchers take issue with the moniker three-parent baby. Cohen, for one, says the term is wrong. Mitochondrial DNA does not contribute to a persons traits. So, he argues, the person who donates mitochondrial DNA is hardly a "parent."

Andrew R. La Barbera agrees. He is chief scientific officer of the American Society for Reproductive Medicine. A persons essence as a human being comes from their nuclear genetic material, he says, not their mitochondrial genetic material." So children conceived using mitochondrial transfer have just two parents, he maintains.

But there are bigger controversies here than what makes a parent. Opponents of these techniques worry that none has been fully tested.

Darnovsky says, We wish the baby and family well, and hope the baby stays healthy. But until these techniques are shown to be safe, she says, I have a lot of concerns about this child and about future efforts to use these techniques.

Zhang also drew fire for going to Mexico to perform the procedure. In America, researchers are banned from doing things that could alter human DNA in a way that can be passed from generation to generation. Spindle and pronuclear transfer both do this. The worry is that genetic changes of future generations wont stop with preventing diseases. Policy makers wanted to outlaw efforts to make genetically enhanced designer babies.

However, a panel of experts said in February 2016 that it is ethical to make three-parent baby boys. But not girls. Why? Fathers almost never pass mitochondria on to their babies. So baby boys born through such techniques should never pass along the donors mitochondria.

A baby girl, though? That would be a very different story.

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How to make a 'three-parent' baby - Science News for Students (blog)

Cell Biology

Molecular biology: Fingerprinting cell identities – Science Daily

Every cell has its own individual molecular fingerprint, which is informative for its functions and regulatory states. Researchers from Ludwig-Maximilians-Universitaet (LMU) in Munich have now carried out a comprehensive comparison of methodologies that quantify RNAs of single cells.

The cell is the fundamental unit of all living organisms. Hence, in order to understand essential biological processes and the perturbations that give rise to disease, one must first dissect the functions of cells and the mechanisms that regulate them. Modern high-throughput protein and nucleic-acid sequencing techniques have become an indispensable component of this endeavor. In particular, single-cell RNA sequencing (scRNA-seq) permits one to determine the levels of RNA molecules -- the gene copies -- that are expressed in a given cell, and several versions of the methodology have been described in recent years. The spectrum of genes expressed in a given cell amounts to a molecular fingerprint, which yields a detailed picture of its current functional state. "For this reason, the technology has become an extraordinarily valuable tool, not only for basic research but also for the development of new approaches to treat diseases," says LMU biologist Wolfgang Enard. Enard and his team have now undertaken the first comprehensive comparative analysis of the various RNA sequencing techniques, with regard to their sensitivity, precision and cost efficiency. Their results appear in the leading journal Molecular Cell.

The purpose of scRNA-seq is to identify the relative amounts of the messenger RNA (mRNA) molecules present in the cells of interest. mRNAs are the blueprints that specify the structures of all the proteins made in the cell, and represent "transcribed" copies of the corresponding genetic information encoded in specific segments of the genomic DNA in the cell nucleus. In the cytoplasm surrounding the nucleus, the nucleotide sequences of mRNAs are "translated" into the amino-acid sequences of proteins by molecular machines called ribosomes. Thus a complete catalog of the mRNAs in a cell provides a comprehensive view of the proteins that it produces, and tells one what subset of the thousands of genes in the genome are active and how their activity is regulated. Furthermore, aberrant patterns of gene activity point to disturbances in gene expression and cell function, and reveal the presence of specific pathologies. The scRNA-seq procedure itself can be carried out using commercially available kits, but many researchers prefer to assemble the components required for their preferred formulations themselves.

In order to ascertain which of the methods currently in use is most effective and economical, Enard and his colleagues applied six different methods to mouse embryonal stem cells and compared the spectra of mRNAs detected by each of them. They then used this data to compute how much it costs for each method to reliably detect differently expressed genes between two cell types. "This comparison revealed that some of the commercial kits are ten times more expensive than the corresponding home-made versions," Enard says. However, the researchers point out that the choice of the optimal method largely depends on the conditions and demands of the individual experiment. "It does make a difference whether one wants to analyze the activity of hundreds of genes in thousands of individual cells, or thousands of genes in hundreds of cells," Enard says. "We were able to demonstrate which method is best for a given purpose, and we also obtained data that will be useful for the further development of the technology."

The new findings are of particular interest in the field of genomics. For example, scRNA-seq is a fundamental prerequisite for the success of the effort to assemble a Human Cell Atlas -- one of the most ambitious international projects in genomics since the initial sequencing of the human genome. It aims to provide no less than a complete inventory of all the cell types and subtypes in the human body at all stages of development from embryo to adult on the basis of their patterns of gene activity. It is estimated that the total number of cells in the human body is on the order of 3.5 1013. Scientists expect that such an atlas would revolutionize our knowledge of human biology and our understanding of disease processes.

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Molecular biology: Fingerprinting cell identities - Science Daily

Anatomy

9 ‘Grey’s Anatomy’ Actors Who Were Close to Being Series Regulars – Wetpaint

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9 'Grey's Anatomy' Actors Who Were Close to Being Series Regulars - Wetpaint

Anatomy

Grey’s Anatomy Round Table: Is Bailey Cut Out For Being Chief? – TV Fanatic

OnGrey's Anatomy Season 13 Episode 13the friction between members of the hospital got infinitely worse, and sides were being taken amongst the attendings. The other attendings, Maggie in particular, made April's first day as interim Chief of Surgery, difficult.

Eliza begin the second phase of her teaching program, which allowed Ben and Stephanie to perform solo surgeries with no aid. Ben's surgery was successful but Stephanie's went badly.

Join TV Fanatics Tiffany, Amanda, and Jasmine as they discuss whether it was fair that the others ostracizedApril, whether a truce is on the horizon amongst the fractured group of friends, and much more.

Do you think it was fair that the other doctors ostracized April for taking Meredith's position?

Tiffany: I know it may seem childish but yes. I didn't buy April's argument that she was just doing her job. I think she saw an opportunity to have a higher position, even if it belonged to someone else, and took it.

I understand it, a lot of people who do it but don't pretend like you did it for some other, nobler reason. Especially considering how strongly she felt about Webber's cause right before that.

Amanda: I think it was really unfair for the doctors to turn their backs. Was April really supposed to say no? The patients would suffer. Someone needs to help out and take charge without Meredith there.

I also find it really annoying that Meredith seems to do no wrong in the eyes of her friends, but April is constantly criticized or made fun of. The girl went into a war zone and helped people. That's a lot more than a lot of these other doctors have done. Give the woman some credit. She's a great doctor.

Jasmine: I'll fall somewhere in the middle with this. It was childish, but I completely understand it and I probably would have been the same way. It didn't spill over into them not being able to do their jobs.

I don't think April was being opportunistic. I do think that April is a chronic do-gooder, obsessively so, and that has been an issue for her ever since Derek brought her back after her mistake.

I feel like in April's mind she had to take it. She knew what it was like to lose her job before, and she didn't want a repeat of that again. She was offered the position after Meredith was suspended, so I get feeling like she had no choice.

Plus, if she didn't take it, and no one else would touch it, then somebody knew would potentially be brought in, and that is the root of the problem as it is. I don't like April's choice, and I would have shut her out too, but I get why she did it. And I agree with Amanda about Meredith. It's irritated me for all thirteen seasons.

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Did finding out that Eliza never lost a child before this one make you sympathize with her more? Or does it make you question her methods even further?

Tiffany: Nope, still hate her. It was definitely her fault they lost the little boy. Stephanie is a great resident and I initially thought she'd be fine but why in the world would you risk a kid's life on a first-time solo surgery?

I think they got a little too caught up in their excitement and it became more about the surgery than the patient. This seems to happen a lot with Minnick. She's so focused on her methods and the residents that she doesn't consider anyone or anything else.

Amanda: I don't feel one way or the other about Eliza, but it does seem unrealistic that she would make it this far in her career without seeing a child die. If her reaction was any indication, she's a lot more fragile than she's been letting on.

Jasmine: Words cannot describe how little I care about Eliza. I'm just done with her. I find her character incredibly irritating for so many reasons. One of which, what Tiffany mentioned above. I can't deal with this woman's total disregard for patients.

She makes Yang look like Mother Theresa. I find her attitude and approach abhorrent, and the fact that she never lost a kid before, and has limited experience in things outside of her field, tells me she's not a good fit here.

Quotables from Week Ending February 17, 2017

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Is Bailey cut out for being Chief or do you think it would be better if someone else took over?

Tiffany: I think Bailey will ultimately be a great chief, but right now she's not acting like Bailey, she's impersonating Catherine and Catherine would not make a good chief. She's pushy, arrogant, stubborn, and thinks she knows what's best for everyone.

It was her whispering in Bailey's ear that caused all these problems to begin with. Bailey could have upgraded the teaching program and brought in Minnick without blindsiding Webber and pushing him out altogether. Now it's gone so far I think she's just too proud to stop it. At this point, I only see things getting worse.

Amanda: I think Bailey is a wonderful Chief. She has made some missteps along the way, but she's ultimately trying to do what she thinks is best for the hospital. Sometimes being the boss means you won't be popular with your employees when you make difficult decisions.

Jasmine: I think Bailey worked her whole life to get to this point. Hell, Richard trained and mentored her to get to this point. She's his legacy. I think she's great when she handles things on her own.

But the Bailey of late, she's not walking her own path and she's being too easily influenced by too many outside forces. I love Bailey. She's a force of nature, but I'm not seeing much of that Bailey right now.

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Do you think we're closer to a truce being called between the doctors involved in this Bailey and Eliza versus Richard and Meredith debacle?

Tiffany: I don't think so. If anything it looks like sides are forming -- Bailey, Minnick, Catherine and April against everyone else.

Amanda: I don't see an end in sight right now. Everyone is still fuming and both sides are drawing firmer lines in the sand.

Jasmine: Initially, I was thinking we may have been closer to a truce, what with Eliza breaking down and Bailey and Webber getting to share some of their feelings with each other, but now I'm thinking it's going to be a while.

It looks like more lines are being drawn in the sand, and with Alex coming back...who knows what's going to happen next? They may be more divided than ever.

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Are there other storylines or plots that you miss? Or are you enjoying the Webber and Minnick one?

Tiffany: I'm not necessarily enjoying the Webber/Minnick storyline but I'm definitely invested (#TeamWebber). I'm ready for Alex to come back to the hospital and wondering when we'll finally see Owen's mysterious sister.

Amanda: I want to get to Alex's transition back to working at the hospital. I have hated this Webber/Minnick storyline from day one. Everyone is acting like a child and it needs to stop!

Jasmine: I, too, am invested enough in this arc to not be too bothered by it. I like the fact that it does involve multiple characters. I just want some resolution on a few things, like the Omelia situation.

I also feel like they teased this potential story arc about Owen's sister, and we haven't seen anything else. And there are a few characters that are so underused or misused right now. It wouldn't kill them to show some other things too.

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What was your favorite and/or least favorite part of the episode?

Tiffany: I think my least favorite part was seeing April and Catherine celebrate over dinner. One of the best doctors is suspended, there is nothing but conflict within the hospital staff, and they just lost a child but yeah, celebrate.

I'm all about strong females but the two of them, along with Bailey and Minnick, have created an unhappy, cantankerous, atmosphere and the way they're forcing their new found power down everyone's throats bothers me.

Amanda: I liked seeing April stand up for herself against Jackson. She was right when she said no one takes her seriously. Someone needed to help out, and she had every right to step in and work with the patients.

Jasmine: My least favorite part was almost the entire situation with the kid. Stephanie reminds me of Yang sometimes, which I like, but I seriously disliked the way she got dragged into Eliza's cavalier attitude towards patients.

I can't quite put my finger on what makes it so different than what the original characters (especially Christina) used to do or say, but it is. Somehow it's...too far and unbecoming.

My favorite scene was Webber comforting Stephanie. Fantastic scene.

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Who was the MVP?

Tiffany: Webber. He was resistant at first but when he joined Warren in the OR it really seemed like he was ready to assist him. Then after Bailey butted in, and screamed at him, he still stepped up for Stephanie when Minnick flaked on her.

Amanda: Arizona was great at playing both sides of the feud at the hospital. She's obviously on Webber's side, but she was still able to lend an ear to Minnick and give her some advice.

Jasmine: Ben. He kicked ass on his first solo surgery and it made me so proud. He also called Bailey and Webber out on behaving like children and ruining his moment, and I loved that. Go Ben!

Do you agree with our Round Table? Hit the comments below!

You can watch Grey's Anatomy online right here via TV Fanatic!

Grey's Anatomy Photo Preview of "Back Where You Belong"

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Jasmine Blu is a staff writer for TV Fanatic. Follow her on Twitter.

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Grey's Anatomy Round Table: Is Bailey Cut Out For Being Chief? - TV Fanatic

Human Behavior

A desert university’s deep connection to the jungle – UNM Newsroom

Nearly two decades ago, researchers at The University of New Mexico took interest in a project that took them to the lush jungles of southwestern Uganda. Not far from the borders of the Congo, these desert-dwelling Anthropologists established relationships with the local residents of the tree topsforming a bond that has catapulted UNM to international status as a leader in in the comparison of human and primate physiology.

UNM Professors Melissa Emery Thompson and Martin Muller were graduate students when they became involved with the Kibale Chimpanzee Project. Established in 1987, the project is a long-term field study of the behavior, ecology and physiology of a community of approximately 55 wild chimpanzees. Emery Thompson and Muller have received funding for this work from the National Science Foundation, National Institutes of Health, the Leakey Foundation and the Wenner-Gren Foundation for Anthropological Research.

There are only a half-dozen research sites that have been in existence as long as this one at UNM, says Muller. Its exciting to be out in the wild watching these animals behave. We now have 30 years of datasome of the chimps who weve studied have been around that entire time. We knew them as little kids and now as older adults. We can see and understand the whole life span of these animals which greatly benefits our research.

The participation of UNM Anthropologists in the Kibale Project led to the development of the Hominoid Reproductive Ecology Laboratory at UNM. The lab is an extension of the field lab in Uganda but also focuses more broadly on developing minimally invasive research on the interactions between physiology and behavior.

The researchers are able to collect urine and feces from the chimpanzees and use them to study stress, reproductive function, energetic condition and health.

We have validated and created new ways to use this material, says Emery Thompson. For instance, we have developed markers for quantifying the energetic condition of the animals, including the amount of muscle mass that they have.

A little-known fact about the University is that it stores the greatest amount of these types of samples in the world. The over 30,000 urine samples represent decades of devotion to studying the human-like primates.

Chimpanzees spend a lot of their time in trees, so we are able to collect the samples when they fall down, says Emery Thompson. Chimpanzees also build nests in the trees at night and, just like humans, urinate when they wake up in the morning. Our field staff wakes up very early in the morning to hike out to the nests before the chimpanzees wake up to collect this urine on plastic bags held underneath the trees.

"We have one of the most interdisciplinary labs of its kind, as we collaborate with psychologists, biologists, clinicians and even economists." ProfessorMelissa Emery Thompson

Muller, who is the current Co-director of the Kibale Project has a particular interest in what comparisons between chimpanzee and human behavior and physiology can tell us about human evolution.

We have a National Science Foundation grant right now to look at infant and juvenile development. Were looking at how maternal health might affect juvenile health, growth and behavior, said Muller. Were also looking to see if, for example, testosterone levels predict how males will compete when they grow up.

The researchers also have a grant from the National Institute of Aging to look at the other side of lifehow various factors and experiences influence aging. The average chimp lives to the age of 15 to 20, but if they live that long, their mortality rate decreases, giving them the potential to live well into their 50s. The oldest chimp studied as part of the Project died at 63.

The importance of the research methods these UNM professors specialize in has increased exponentially with recent laws classifying chimps as endangered animals both in the wild and captivity.

Since 2015, it is illegal for individuals or groups to take chimpanzees captive. Invasive research on chimpanzees has also been severely restricted. The Endangered Species Act has helped hundreds of chimps in U.S. laboratories and road side zoos. Most have been sent to sanctuaries where they have proper space and an environment to live in social groups, critical for emotional health.

As chimpanzee research continues to thrive at UNM, Emery Thompson and Muller are very excited about the new expanded assay facilitythe Comparative HuMan and Primate Physiology (CHmPP) Laboratory, to be included in the scheduled Physics, Astronomy, and Interdisciplinary Sciences (PAIS) building.

In the next two years we will be expanding our CHmPP Labexpanding the technologies we use in our own research and creating more opportunities to work with other disciplines, said Emery Thompson. For example, our project collaborates with the Center for Stable Isotopes on studies of chimpanzee nutrition and weaning, so getting everyone under one roof will benefit our research immensely.

Emery Thompson added, We have one of the most interdisciplinary labs of its kind, as we collaborate with psychologists, biologists, clinicians and even economists. For behavioral scientists of all kinds, its important to be able to test subjects without causing stress or interfering with natural behavior.

The CHmPP Lab will be located in the planned Physics & Astronomy and Interdisciplinary Science (PAIS) center on UNMs main campus. The PAIS building will be home to a variety of interdisciplinary science centers that are at the forefront of their various fieldsdoing groundbreaking research that will provide one-of-a-kind opportunities for students and professors.

Our laboratory attracts very high-quality graduate students, says Emery Thompson. They are excited about the opportunity to work with the Kibale Chimpanzee Projects rich dataset and to learn valuable laboratory skills that complement their field research.

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A desert university's deep connection to the jungle - UNM Newsroom

Genetics

Genetics, family set-up play a big role in your tendency to put on weight – Hindustan Times

As per a new study, up to 40% of your body-mass index (BMI) may have been inherited from your parents. The report adds that nearly half of a kids tendency towards obesity is determined by genetics and family environment.

Your obesity worries you? Do you feel guilty every time you have a candy? This research should help you deal with it. A recent study says that up to 40% of your body-mass index may have been inherited from your parents. It adds that more than half of a kids tendency towards obesity is determined by genetics and family environment.

For the most obese children, the proportion rises to 55-60%, researchers said.

The study, led by the University of Sussex in the UK, used data on the heights and weights of 100,000 children and their parents spanning six countries worldwide: the UK, US, China, Indonesia, Spain and Mexico.

The researchers found that the intergenerational transmission of body-mass index (BMI) is almost constant at around 0.2 per parent -- that is each childs BMI on average is around 20% due to the mother and 20% due to the father.

The pattern of results is remarkably consistent across all countries, irrespective of their stage of economic development, degree of industrialisation, or type of economy, said Peter Dolton, Professor at the University of Sussex in the UK.

Our evidence comes from trawling data from across the world with very diverse patterns of nutrition and obesity -- from one of the most obese populations -- the US -- to two of the least obese countries in the world -- China and Indonesia.

This gives an important and rare insight into how obesity is transmitted across generations in both developed and developing countries, said Dolton.

We found that the process of intergenerational transmission is the same across all the different countries, he said.

Up to 40% of your body-mass index (BMI) comes from your parents. (Shutterstock)

The study also shows how the effect of parents BMI on their childrens BMI depends on what the BMI of the child is. Consistently, across all populations studied, they found the parental effect to be lowest for the thinnest children and highest for the most obese children.

For the thinnest child their BMI is 10% due to their mother and 10% due to their father. For the fattest child this transmission is closer to 30% due to each parent.

This shows that the children of obese parents are much more likely to be obese themselves when they grow up - the parental effect is more than double for the most obese children what it is for the thinnest children, said Dolton.

The findings were published in the journal Economics and Human Biology.

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Genetics, family set-up play a big role in your tendency to put on weight - Hindustan Times

Genetics

Video: Understand the difference between genetics and genomics in 1 minute – Genetic Literacy Project

We hear the terms genetics and genomics being used in countless scientific studies as well as more mainstream news reports. But despite the two words sounding similar, genetics and genomics refer to two very different things. Do you know the difference between these two terms? What separates genetics from genomics and vice versa? Here is how you can find out in one minute.

The GLP aggregated and excerpted this blog/article to reflect the diversity of news, opinion, and analysis. Watch the original video:What is the Difference Between Genetics and Genomics?

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Video: Understand the difference between genetics and genomics in 1 minute - Genetic Literacy Project