Category Archives: Human Genetics

Human life could soon be replicated in a laboratory after scientists at the University of Cambridge successfully created artificial mouse embryos.

Scientists developed a mouse embryo structure using stem cells grown in the lab. The cells grew into primitive embryos that had identical internal structures to those that emerge during normal development in the womb.

The purpose of the research is to gain deeper insight into an embryos development just prior to implantation.

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It marks a significant step forward, as previous attempts to grow embryo-like structures using only embryonic stem cells have only had limited success.

Im looking at it as a miracle of nature as well as trying to understand the process. Its incredibly beautiful that we can begin to understand those forces that give rise to self-organization during the earliest stage of development, Professor Zernicka-Goetz told the Guardian.

The researchers used a combination of genetically modified mouse cells, known as master cells, and a 3D scaffold, known as an extracellular matrix, on which the cells could grow. The resulting embryo looks almost identical to a natural mouse embryo.

If carried out on human embryos, the experiment could reveal the cause behind miscarriages and infertility, as it shows how genetic activity varies the way mammals grow right after conception.

The breakthrough, made by a team led by Magdalena Zernicka-Goetz, who last year discovered the way to keep embryos alive in the laboratory for up to 14 days, means that more embryos could be reproduced for research without sperm or egg donations, potentially also removing ethical issues surrounding embryo replication.

Both the embryonic and extraembryonic cells start to talk to each other and become organized into a structure that looks like and behaves like an embryo, said Zernicka-Goetz.

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One in six pregnancies end in miscarriage, though there is still no explicit answer to how this happens.

If we can translate the knowledge into humans it will be incredibly powerful for understanding our own development at a stage when many human lives are lost, the professor said, according to the Times.

However researchers said although the artificial embryo closely resembles a natural one, it is unlikely to develop further into a healthy mouse fetus. This would require a yolk sac, which provides nourishment for the embryo and where blood vessels develop.

Experiments are currently carried out on leftover human embryos from In Vitro Fertilization (IVF), but these are often insufficient and can only be held for a maximum of 14 days under legal frameworks.

The outcome of the experiment has also been criticized by some concerned that it may pave the way for genetically modified (GM) humans.

What concerns me about the possibility of artificial embryos is that this may become a route to creating GM or even cloned babies, the director of Human Genetics Alert, Dr, David King, told the Telegraph.

Until there is an enforceable global ban on those possibilities this kind of research risks doing the scientific groundwork for entrepreneurs who will use the technologies in countries with no regulations.

The findings were published in the journal Science on Thursday.

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Human cloning a step closer after UK scientists create artificial embryos - RT

The recent return of the which bathroom? issueregarding transgender individuals use of public restrooms has made me think about how Ive handled sex and gender in my human genetics textbook.Over the editions, the two topics have diverged. And thats at the crux of misunderstanding.

SEX AND GENDER THROUGH THE EDITIONS

When I wrote the first edition in 1993, coverage of the X and Y chromosomes that make us female or male (sex determination) was squished into a chapter on genetic linkage. I didnt mention gender identity at all.

By the second edition, Matters of Sex was its own chapter, starting with a table called Sexual Identity. The last entry was gender identity, defined as Strong feelings of being male or female, from childhood.

In early 1998, while writing the third edition, I read John Colapintos unforgettable article in Rolling Stone (summarized by Colapintohere) about David Reimer (1965-2004). After Davids penis was removed following a botched circumcision, hisparents were pressured into raising him as a girl, and the infant underwent the first sex reassignment surgery performed on an anatomically normal individual. Its a complex tale. The physician regarded David (then named Brenda) as part of a science experiment of sorts by comparing her to his identical twin Brian.

Brenda/David, however, always knew he was a he, preferring boys games and attire, even peeing standing up without knowing why. When a psychiatrist finally told him of his beginnings at age 14, David sought surgery to return to his male origin.

With Davids help, Colapinto published As Nature Made Him: The Boy Who Was Raised As A Girl in 2000. About that time, I wrote an article, Reevaluating Sex Reassignment, for The Scientist, concluding from interviewing experts that Both clinical trials and case reports powerfully argue for nature over nurture in establishing gender identity. On the surface, that statement could mean that a baby with a penis becomes a man and a baby with a vagina becomes a woman, no matter what. But it also argues for the power of knowing ones gender, whether one has the corresponding anatomy or not.

David Reimers sad story entered my textbook with the third edition. The next leap in my coverage of gender happened after I met Jennifer Finney Boylan, who was born James.

My daughter Heather and I met Jennifer at a bookstore in 2003, just before publication of Jennifers book Shes Not There: A Life in Two Genders. Today shes an outspoken transgender author who predicted in a New York Times op-ed just after the election that the new president would throw out President Obamas protectionof the right of transgender students to use school bathrooms matching their gender identity. Sadly she was right, even though just last April candidate Trump said that people should use the bathroom they feel is appropriate.

At the bookstore all those years ago, Jennifer stayed afterwards to talk with Heather, who was at the time contemplating her future career as a social worker. Jennifers bravery and kindness impressed both of us. No one would go through what she did for something trivial, for just a feeling.

So my next textbook edition included this paragraph:

Transgender is a poorly understood condition related to sexual identity. A transgendered individual has the phenotype and sex chromosomes of one gender, but identifies extremely strongly with the opposite gender. It is a much more profound condition than transvestitism, which refers to a male who prefers womens clothing. The genetic or physical basis of transgender is not known. Some affected individuals have surgery to better match their physical selves with the gender that they feel certain they are.

It was a start. I should have replaced feel with are. To my astonishment, when drafts of that edition were reviewed, instructors asked that the paragraph be removed, because transgender had nothing to do with genetics.

I refused. We cant say a characteristic isnt genetic just because we dont yet have any evidence. But in the next few editions, I fielded the same request, and again ignored it. Writing a textbook brings an authority beyond a mere article or blog post, and I wanted people wondering about transgender taking a course in human genetics to at least find a definition in their textbook.

Meanwhile, I started to wonder if certain genotypes in some way contribute to the overwhelming sense that gender doesnt match genes, chromosomes, or gonads.

HERES WHAT WE KNOW: BIO 101

Sex is set, or determined, when an X chromosome from an egg finds itself in a nucleus with an X or a Y from a sperm. XX=female: XY=male.

For six weeks, the embryo unfurls two sets of indifferent gonads, with two sets of plumbing. At week 6, a gene on the Y called SRY, for sex determining region of the Y, turns on and the fledgling female parts shrivel away. Without SRY, and under guidance of other genes, the male structures vanish instead. So anatomically we all start out with a bit of both.

Mess with the genes and chromosomes behind our sexuality, and mismatches arise. A mutation in a gene called Wnt4, for example, disables the switch to femaleness, and an XX embryo drowns in testosterone. Vagina, cervix, and uterus never develop. In fact, SRY was discoveredin people who looked female but were XYs missing SRY, and people who looked male but were XXs with an SRY gene plunked onto one of the Xs. Another type of female with XY chromosomes has androgen insensitivity syndrome, lacking receptors on cells that bind testosterone, cutting of the hormonal signals necessary for maleness. Several historical figures supposedly had this condition.

Most fascinating is 5-alpha reductase deficiency, in which life begins as a girl, based on appearance. The enzyme to convert testosterone into the form needed to sculpt a penis isnt there, and so external male structures dont develop early on, although interior structures are male. At puberty, the adrenal glands release testosterone, as they normally do, and then the voice deepens, facial hair grows, muscles become leaner, and instead of developing breasts and menstruating, the clitoris swells into a penis and sperm are produced.

In the Dominican Republic, where 5-alpha reductase deficiency is more common due to relatives marrying relatives awhile back, these special adolescents are given their own gender name guevedoces, for penis at age 12 and are fully accepted as whatever they want to be. Most become fertile males. Discovery of the fact that guevedoces have small prostates led to development of the drug finasteride, which inhibits 5-alpha reductase and is used to treat enlarged prostate. The Pulitzer-prize-winning novelMiddlesex, by Jeffrey Eugenides, tells the story of a young man with the condition. Its one of my all-time favorite books.

So the X and Y chromosomes determine sex, unless a single-gene mutation intervenes and then they dont. Could gene variants, perhaps specific sets of them, somehow set the stage for the gestation of a transgender individual? For the upcoming twelfth edition of my textbook, I took a look.

SCANT EVIDENCE FOR TRANSGENDER GENES

A genome-wide association study (GWAS) might be the way to go to identify genes that have variants that affect gender identity. Scan the genomes of a few hundred or thousand transgender individuals and a similar number of controls, perhaps their cisgender siblings, for a few million SNPs (single nucleotide polymorphisms; places in the genome where a DNA base varies in a population). Identify gene variants shared only among the trans. Then look in those genome regions for genes whose functions make sense this might be more objective than rounding up the usual suspects, such as hormone receptors and enzymes needed to synthesize steroids.

Heres what I found:

Thats it.Or at least all I could find. Although clinicaltrials.gov lists 58 studies under transgender, nothing much comes up in the way of genetics. The closest was the exploration of the neovagina study to investigate ways to entice a vaginal microbiometo flourish in a surgically created organ.

A genomewide SNP screen, or even genome sequencing, might one day identify a genetic signature for transgender. Should we even go there? I dont think so. What good could it do? People who are transgender already know it its certain others who have a problem with it. And imagine new parents of a girl told she will identify as a boy, or vice versa. What would they do? Id say just wait and see. Let it be.

Im not a psychologist and clearly out of my depth when matters get beyond genes and chromosomes. Comments welcome! (Are any other nerds glad to hear cis and transoutside of the context of rotation around a double carbon bond or the orientation of allele pairs?)

The rest is here:
Is Transgender Genetic? - PLoS Blogs (blog)

Mendels laws, like any laws in science, are wonderful because they make predictions possible. A woman and man both carry a recessive mutation in the same gene, and each of their children has a 25% chance of inheriting both mutations and the associated health condition. Bio 101.

In contrast to our bizarre new world of alternate facts, multiple interpretations, and both are true scenarios, science is both logical and rational. If an observation seems to counter dogma, then we investigate and get to the truth. Thats what happened for Millie and Hannah, whose stories illustrate two ways that genetic disease can seem to veer from the predictions of Mendels first law: that genes segregate, one copy from each parent into sperm and ova, and reunite at fertilization. (Ill get to embryo engineering at the end.)

Millies situation is increasingly common exome or genome sequencing of a child-parent trio reveals a new (de novo), dominant mutation in the child, causing a disease that is genetic but not inherited.

Hannahs situation is much rarer: inheriting a double dose of a mutation from one parent and no copies of the gene from the other.

Millie McWilliams was born on September 2, 2005. At first she seemed healthy, lifting her head and rolling over when most babies do. But around 6 months, her head became shaky, like an infants. Then she stopped saying dada, recalled her mother Angela.

By Millies first birthday, her head shaking had become a strange, constant swaying. She couldnt crawl nor sit, had bouts of irritability and vomiting, and bit her hands and fingers.

In genetic diseases, odd habits and certain facial features can be clues, but none of the many tests, scans, and biopsies that Millie underwent lead to a diagnosis. Nor were her parents carriers of any known conditions that might explain her symptoms. Still, it was possible that Millie had an atypical presentation of a recessive condition so rare that it isnt included in test panels.

Millie McWilliams

By age 6 Millie couldnt speak, was intellectually disabled, and was confined to a wheelchair, able to crawl only a few feet. Today she requires intensive home-based therapies. But Millie can communicate. She likes to look at what she wants, with an intense stare, said Angela. She loves country music and Beyonc, and every once in awhile something funny will happen and shell break into a big smile.

Millies pediatrician, Dr. Sarah Soden, suggested that trio genome sequencing, just beginning to be done at Childrens Mercy Kansas City(where the child already received care) as part of a long-term project, might help to assemble the clinical puzzle pieces to explain the worsening symptoms. So the little girl and her parents, Angela and Earl, had their genomes sequenced in December 2011. Analyzing the data took months, but Dr. Sodens team finally found a candidate mutation in the child but not her parents. However the gene, ASXL3, hadnt been linked to a childhood disease. Yet.

Its typically a matter of time for gene annotation to catch up to sequencing efforts and clinical clues. In February of 2013, a report in Genome Medicinedescribed four children with mutations in ASXL3 who had symptoms like Millies. Even her facial structures arched eyebrows, flared nostrils, and a high forehead matched those of the other children, as well as the hand-biting. They all haveBainbridge-Ropers syndrome.

One copy of Millies ASXL3 gene is missing two DNA bases, creating an inappropriate stop codon and shortening the encoded proteins. From this new glitch somehow arose the strange symptoms. Because neither Earl nor Angela has the mutation, it must have originated in either a sperm or an egg that went on to become Millie.

Since the paper about Bainbridge-Ropers syndrome was published three years ago, a few dozen individuals have been diagnosed and families have formed a support group and a Facebookpage. Thats huge. Even if a disease has no treatment, as is the case for Bainbridge-Ropers, families find comfort in reaching the end of the diagnostic odyssey and locating others. Said Angela, It was a relief to finally put a name on it and figure out what was actually going on with her, and then to understand that other families have this too. Ive been able to read about her diagnosis and what other kids are going through.

Hannah Sames will be celebrating her 13th birthday next month, and is showing what may be early signs of strength in her muscles after receiving gene therapyinto her spinal cord last summer to treat giant axonal neuropathy (GAN).

When I first met Hannahs mom Lori in 2010, she told me that Hannah had inherited the exact same deletion mutation in the gigaxonin gene from her and her husband Matt. At that time, only a few dozen children were known to have the condition, and that number hasnt risen much. Because of the diseases rarity, I politely asked ifLori and Matt could be cousins but not know it. Shared ancestry seemed a more likely explanation for two identicalextremely rare gene variants occurring in the same child than the parents having the same length deletion just by chance. But no, Matt and Lori arent related.

The answer came just a few months ago: Hannah inherited both of her gigaxonin deletion mutations from Lori, and none from Matt. This is a very rare phenomenon called uniparental disomy (UPD), meaning two bodies from one parent. Like Millie, UPD seemingly defies Mendels law of segregation, with a pair of chromosomes (or their parts) coming solely from one parent, rather than one from each parent.

Lori and Hannah Sames (Dr. Wendy Josephs)

UPD happens during meiosis, the cell division that sculpts egg and sperm. And it requires two exceedingly rare events: Two of Loris chromosome 16s ended up in an egg in which Matts chromosome 16 was lost. Hannah essentially inherited her moms mutation twice, without the protection of her fathers normal chromosome 16. This is especially likely with this particular chromosome because an extra copy of #16 trisomy 16 is the most common extra-chromosome condition associated with miscarriage.

Neither Millies Bainbridge-Ropers syndrome nor Hannahs GAN actually counters Mendels law. Although Millie didnt inherit her mutation, if she were able to have children, she would pass it on with a probability of 1 in 2 to each child, just like the law predicts for dominant inheritance. Likewise, a child of Hannah would inherit one copy of the mutation that causes GAN when present in a double dose, just like the law predicts for recessive inheritance.

As I was writing this post, the National Academy of Sciencesreleased its long-awaited tome on whats being called, among other things, embryonic engineering. Rather than banning editing of the human germline forever, the report foresees certain situations in which gene or genome editing, using CRISPR-Cas9 or some other variation on the theme, might be deployed to prevent disease.

WhileI think its great that the rare scenarios in which genome editing might be useful are finally being spelled out, instead of flaming fears of genetic enhancement spawning designer babies, my thinking aboutMillie and Hannah made me wonder why we would ever need to edit a genome to prevent disease in the first place. To quote the eminent mathematician from Jurassic Park, Ian Malcolm, Yeah, yeah, but your scientists were so preoccupied with whether or not they could that they didnt stop to think if they should.

Preventing illness in a future child of course isnt the same as designing theme park dinosaurs, but like Jurassic Parks technology, I cant imagine why genome editing at very early developmental stages is necessary.Even for an exceedingly rare family situation in which passing on an inherited disease is unavoidable, according to Mendels laws, there are alternatives, although they do not yield a biological child: replace, select, or adopt:

An assisted reproductive technology can replace the sperm (intrauterine insemination) or egg (egg donation or surrogate using her own eggs) of the mutation carrier.

Instead of replacing errant genes early in prenatal development, or even before, I think we should focus on helping the Millies and Hannahs who are no longer fertilized ova or early embryos, but are kids. Thats already starting for Hannah, thanks to the gene therapy technology that has been gestating since 1990. Millies turn hasnt come yet.

So yes, lets set rules for editing the human germline but also consider whether this type of intervention will ever make sense in our overcrowded world.

This article originally appeared on the PLOS DNA Scienceblog under the title Defying Mendelian Genetics and Embryo Engineeringand has been republished with permission from the author.

Ricki Lewis is a long-time science writer with a PhD in genetics. She writes the DNA Science blog at PLOS and contributes regularly to Rare Disease Report and Medscape Medical News. Ricki is the author of the textbook Human Genetics: Concepts and Applications (McGraw-Hill, 12th edition out late summer); The Forever Fix: Gene Therapy and the Boy Who Saved It (St. Martins Press, 2013) and the just-published second edition of Human Genetics: The Basics (Routledge Press, 2017).She teaches Genethics online for the Alden March Bioethics Institute at Albany Medical College and is a genetic counselor at CareNet Medical Group in Schenectady, NY. You can find her at her website or on Twitter at @rickilewis

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Weird world of DNA: What's the best way to help patients with genetic diseases that are not inherited? - Genetic Literacy Project

The Science and Ethics of Editing Human Embryos Chicago Tonight | WTTW The idea of using this technology to edit human embryos to remove genetic mutations so that embryo can be free of disease is a positive thing, he said. The concern and problem is that if you now do research in that setting and you perfect the ...

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The Science and Ethics of Editing Human Embryos - Chicago Tonight | WTTW

Two researchers from a UCLA clinical site explained the genetic approach to diagnosing rare diseases to about 50 UCLA students and faculty members Monday.

In honor of Rare Disease Day, Stanley Nelson and Christina Palmer, principal investigators of a UCLA clinical site, discussed how UCLA participates in the Undiagnosed Diseases Network. UCLA is one of seven clinical sites in the UDN, a network of researchers who study rare diseases and introduce further research possibilities based on a team science approach.

Team science is a collaborative research approach that is based on the overall contribution of the network, which includes clinicians, scientists, genetic counselors and other experts, Palmer said. For example, clinical sites such as UCLA provide patient evaluations while other sites act as laboratory cores that provide DNA sequencing.

Under the UDN, UCLA has worked with 63 patients with rare diseases. The network approach allows patients and physicians to seek out other individuals within the network who may be working with the same disease, Nelson said.

Lab investigations can also address a broad spectrum of rare diseases and increase the speed of testing for disease-specific concerns, Nelson said.

Palmer said patients must go through a comprehensive application process to be evaluated by the UDN. Each patient has to demonstrate that their rare disease has gone through extensive prior evaluation and submit other medical information.

Palmer added some diseases the UCLA researchers study include neurological diseases.

Nelson said the UDN uses genome sequencing in their research, which is done at UCLA prior to clinical evaluation. Sequencing patients DNA before evaluating them can present ethical limitations.

This can overwhelm patients with variants that might not be clinically relevant, Palmer said. There exists a potential for unnecessary tests and possible risks with related procedures, (and) patients wait longer for clinical visit.

Researchers gather phenotypes physical characteristics of participants from medical records, not in-person evaluations, Nelson said. Unlike other disorder researchers, who group patients with similar characteristics, UCLA researchers do not intentionally gather patients with similar phenotypes.

Palmer said clinical evaluations start after genome sequencing. Evaluations take one to five days and may include consultations with specialists and other medical tests.

As a clinical site, UCLA does not focus on treatment or symptom management of rare diseases, Nelson said. Although UCLA researchers aim to diagnose patients, doing so is difficult and not necessarily included in the patient follow-up.

About 70 percent of the patients UCLA is working with are children. Researchers have diagnosed five of 35 completed cases.

Siena Salgado, a third-year human biology and society student who attended the talk, said she had previously studied the sociological impacts of the UDNs structure. She said she was interested in the possible ethical implications of the UDNs genetic-based approach.

Michael Gorin, an ophthalmology and human genetics professor who attended the event, said he thinks the UDN becomes a compensatory process that catches up to other countries with health care systems that already have vested interests in genetic diseases.

The psychological benefit for patients to know why they have a disease is powerful, Gorin said. To be able to tell someone we know what genetic variance is causing this disease, even if we cant treat it removes guilt, uncertainty (and) gives people hope.

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UCLA researchers describe methods for diagnosing diseases using genetics - Daily Bruin

The genetic material of an organism encodes the instructions that guide its development. These codes are not written in stone; they can change or mutate any time during the life of the organism. Single changes in the code can occur spontaneously, as a mutation, causing developmental problems.

Others, as an international team of researchers has discovered, are too numerous to be explained by random mutation processes present in the general population. When such multiple genetic changes occur before or early after conception, they may inform scientists about fundamental knowledge underlying many diseases. The study appears in Cell.

"As a part of the clinical evaluation of young patients with a variety of developmental issues, we performed clinical genomic studies and analyzed the genetic material of more than 60,000 individuals. Most of the samples were analyzed at Baylor Genetics laboratories," said lead author Pengfei Liu, assistant professor of molecular and human genetics Baylor College of Medicine and assistant laboratory director of Baylor Genetics. "Of these samples, five had extreme numbers of genetic changes that could not be explained by random events alone."

The researchers looked at a type of genetic change called copy number variants, which refers to the number of copies of genes in human DNA. Normally we each have two copies of each gene located on a pair of homologous chromosomes.

"Copy number variants in human DNA can be compared to repeated or missing paragraphs or pages of text in a book," said senior author James R. Lupski, Cullen Professor of Molecular and Human Genetics at Baylor. "For instance, if one or two pages are duplicated in a book it could be explained by random mistakes. On the other hand, if 10 different pages are duplicated, you have to suspect that it did not happen by chance. We want to understand the basic mechanism underlying these multiple new copy number variant mutations in the human genome."

The researchers call this phenomenon multiple de novo copy number variants. As the name indicates, the copy number variants are many and new (de novo). The latter means that the patients carrying the genetic changes did not inherit them from their parents because neither the mother nor the father carries the changes.

In this rare phenomenon, the copy number variants are predominantly gains duplications and triplications rather than losses of genetic material, and are present in all the cells of the child. The last piece of evidence together with the fact that the parents do not carry the alterations suggest that the extra copies of genes may have occurred either in the sperm or the egg, the parent's germ cells, and before or very early after fertilization.

"This burst of genetic changes happens only during the early stages of embryonic development and then it stops," Liu said. "Interestingly, despite having a large number of mutations, the young patients present with relatively mild neurological problems."

The researchers are analyzing more patient samples looking for additional cases of multiple copy number variants to continue their investigation of what may trigger this rare phenomenon.

"We hope that as more researchers around the world learn about this and confirm it, the number of cases will increase," Liu said. "This will improve our understanding of the underlying mechanism and of why and how pathogenic copy number variants arise not only in developmental disorders but in cancers."

This discovery was made possible in great measure thanks to the breadth of genetic testing performed and genomic data available at Baylor Genetics laboratory.

"The diagnostics lab Baylor Genetics is one of the pioneers in this new era of clinical genomics-supported medical practice and disease gene discovery research," Lupski said. "They are developing the clinical genomics necessary to foster and support the Precision Medicine Initiative of the National Institutes of Health, and generating the genomics data that further drives human genome research."

Using state-of-the art technologies and highly-trained personnel, Baylor Genetics analyzes hundreds of samples daily for genetic evaluation of patients with conditions suspected to have underlying genetic factors potentially contributing to their disease. Having this wealth of information and insight into the genetic mechanisms of disease offers now the possibility of advancing medicine and basic research in ways that were not available before.

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Striking Number of Genetic Changes Can Occur Early in Human Development - Laboratory Equipment

CAMBRIDGE, MA - Elsevier, a world-leading provider of scientific, technical and medical information products and services, today announced the publication of an updated edition of its valuable reference, Genetics and Evolution of Infectious Diseases, edited by Michel Tibayrenc. This book is aimed at controlling and preventing neglected and emerging worldwide diseases that are a major cause of global morbidity, disability and mortality. Using an integrated approach, the book discusses the constantly evolving field of infectious diseases and their continued impact on the health of populations, especially in resource-limited areas of the world. At the same time, Elsevier announced five additional immunology, virology and microbiology books.

Genetics and Evolution of Infectious Diseases, Second Edition looks at the worldwide human immunodeficiency virus (HIV) pandemic, increasing antimicrobial resistance, and the emergence of many new bacterial, fungal, parasitic and viral pathogens. With contributions from leading authorities, the book includes developments in the field of infectious disease since it was last published in 2010. It demonstrates how the economic, social and political burden of infectious diseases is most evident in developing countries which must confront the dual burden of death and disability due to infectious and chronic illnesses.

Learn more about infectious disease genomics in this sample chapter.

Michel Tibayrenc, M.D., Ph.D., has worked on the evolution of infectious diseases for more than 35 years. He is a director of research emeritus at the French Institut de Recherche pour le Dveloppement (IRD) Montpellier, France, and the founder and principal organizer of the international congresses MEEGID (molecular epidemiology and evolutionary genetics of infectious diseases). The author of more than 200 international papers, Dr, Tibayrenc has been the head of the unit of research "genetics and evolution of infectious diseases" at the IRD research center for 20 years. With his collaborator, Jenny Telleria, he is the founder and scientific adviser of the Bolivian Society of Human Genetics. Dr. Tibayrenc has won the prize of the Belgian Society of Tropical Medicine (1985), and the medal of the Instituto Oswaldo Cruz, Rio de Janeiro (2000), for his work on Chagas disease. A fellow of the American Association for the Advancement of Science, he is the founder and editor-in-chief of the Elsevier journal, "Infection, Genetics and Evolution."

The six new immunology, virology and microbiology titles are:

In order to meet content needs in immunology, virology and microbiology, Elsevier uses proprietary tools to identify the gaps in coverage of the topics. Editorial teams strategically fill those gaps with content written by key influencers in the field, giving students, faculty and researchers the content they need to answer challenging questions and improve outcomes. These new books, which will educate the next generation of immunologists and virologists, and provide critical foundational content for information professionals, are key examples of how Elsevier is enabling science to drive innovation.

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'Genetics and Evolution of Infectious Diseases' Announces Updates - Broadway World

The following is from an interview transcript

Last year, we had a series of mergers in the agribusiness GMO-corporations worldwide. This has created an alarming concentration of corporate power in the hands of basically three corporate groups.

The first one is Bayer AG of Germany, which made a friendly takeover of Monsanto. The reason for this was that Monsanto became identified in the public mind as pure evil and everything bad about GMOs, which was accurate. This became a burden on the whole GMO project. So, Bayer stepped in, which has a friendly image of an aspirin, harmless, nice company, but in fact is the company that invented heroin in the 1880s and made gas for the ovens of Auschwitz during WWII. Its one of the dirtiest agribusiness companies in the world with a series of homicides and pesticides that killed off bee colonies and many other things that are essential to life and to nature.

Flickr.com/Miran Rijavec (public domain)

ChemChina China State Chemical giant for some reason took over Swiss Syngenta, which makes weed-killers.

Then, Dow Chemicals and DuPont merged their GMO businesses together.

So, we have three gigantic corporate groups worldwide controlling the genetically-modified part of the human food chain. As dangerous as the GMO crops are and the more they sell, it is becoming more and more obvious that they are the chemicals that by contract must be applied to those GMO seeds by the corporations. They demand that if you buy roundup ready soybeans or corn, you must use Monsanto (now Bayer) roundup.

Therefore, this is giving more corporate power to the GMO industry than ever before and thats an alarming trend. They are putting pressure on the bureaucracy in Brussels. One example: there was a massive public campaign against the renewal of the license of the European Commission for Glyphosate. Glyphosate is the most widely used weed-killer in the world. Glyphosate is the main ingredient in Monsantos roundup. The other ingredients are Monsantos corporate secret, but the combination of them is one of the most deadly weed-killers.

The World Health Organizations body responsible for assessing genetic dangers made a ruling the last year that Glyphosate was a probable cancer-causing agent.

The license came up for automatic renewal last year a 15-year license. The EU commission for health was prepared to automatically renew it for 15 years. The European Food Safety Authority (EFSA), which is responsible allegedly for the health and safety of European citizens, recommended approval based on a German study by the German Food Safety Agency that was simply lifted 100% from studies given by the private corporation Monsanto! So, the whole chain was corrupt from the beginning and all the information was rigged. In reality tests have shown that in minuscule concentrations, lower than in recommended levels in Europe and in the US, Glyphosate causes kidney disease, liver disease, and other illnesses that are potentially fatal.

Now, Glyphosate has shown up in urine tests, in urban drinking water, in gardens, in ground water and so forth. And that gets into the system of childbearing women, for example, with embryo. Its all in this!

The EU commission, despite a million petitions this is a record setting and despite recommendations from leading scientists around the world to not renew the license, made a compromise under huge industry pressure and renewed it for 18 months. Why did they renew it for that time? Because at the end of 18 months, they were told by Bayer and Monsanto that the takeover of those two giant corporations will be completed and Bayer is going to replace Glyphosate with another, likely more deadly toxin, but not so well-known as Glyphosate. So, they simply bought time. And that is just one example.

This agenda of GMO is not about the health and safety; its not about increasing crop yields thats a lie that has been proven in repeated tests in North America and all around the world. Crop yields for farmers, using GMO plants, may increase slightly for the first 1-2 harvest years, but ultimately decline after 3-4 years. And not only that! Weve been promised by Monsanto and other GMO giants that the use of chemicals will be less, because of these wonderful traits that GMO plants resist. In fact, the weeds become resistant and you have super weeds, which are 5-6 feet in a height and choke out everything. Its a catastrophe. So, farmers end up using added weed killers to kill the super weeds. This whole mad playing around with the genetic makeup of nature is a disaster from the beginning.

The real agenda of GMO, which I have documented in great detail in my book Seeds of Destruction, comes from the Rockefeller Foundation. It comes out of the 1920s-1930s Eugenics movement. The Rockefeller Foundation during the 1930s, right up to the outbreak of World War II when it became politically embracing too, financed the Nazi Eugenics experiments of Kaiser Wilhelm Institute in Berlin and in Munich. Why did they do this? Their goal was the elimination of what they called undesirable eaters. That is called population reduction.

After the war, the head of the American Eugenic Society, who was a good friend of John D. Rockefeller, at the annual conference of the American Eugenic Society said: From today, the new name of eugenics is genetics. Moreover, if you keep that in mind genetic engineering, the Human Genome Project and so forth they all are scientific frauds. Russian scientists have proven that the entire Genome Project utterly disregarded 98% of the scientifically valuable data in favor of 2% that was completely nonsense and a waste of billions of dollars.

Therefore, they have been obsessed with the idea of how to reduce human population in a way that would not be so obvious as simply going out and carrying out mass-sterilization.

Actually, they have done that in Central America together with the World Health Organization by giving certain vaccines that they cooked-up to have abortive effects. Therefore, the women of child-bearing age in Central America were given these vaccines against tetanus. The organization of the Catholic Church became suspicious because the shots were given only to women, not to men. And they found that there was buried in the vaccine an abortive effect that made it impossible for women to conceive and bear children. This is all covert population reduction.

These are the Western patriarchs who believe they are the gods, sitting on the throne with great dignity, controlling mankind. I think they are a bunch of fools, but they have this agenda of genetic manipulation. Its against nature, its chemically unstable. And I have to congratulate the Russian Federation that they had the courage and the moral concern for their own population to ban GMO cultivation across Russia. That was a step forward for mankind. I would hope that Russia will use its influence to get China to do the similar thing, because their agriculture is in dire need of some healthy Russian input. But this step by Russia to make a GMO-free agriculture is a great step for mankind.

Excerpt from:
Genetics Are the New Eugenics: How GMO's Reduce the Human Population - Center for Research on Globalization

Clues to relationship between schizophrenia and rheumatoid arthritis Science Daily ... if individual genetic variants may exist that could have opposing effects on the risk of schizophrenia and rheumatoid arthritis," said co-senior author Vishwajit Nimgaonkar M.D., Ph.D., professor of psychiatry at Pitt's School of Medicine and human ...

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Clues to relationship between schizophrenia and rheumatoid arthritis - Science Daily

Gene Craft: Art in the Biogenetic Ageopened this week at Birmingham Open Media (BOM) in the UK. Aiming to explore thesocial, economic and emotional implications of the most recent breakthroughs in genetics, the exhibition features two living art piecescreated with human DNAby bioartists Laurie Ramsell and Gina Czarnecki.

After theHuman Fertilisation and Embryology Authority (HFEA) approvedthe technology to create three-parent babies in the UK last December, many have started to question the broader implications of genetic technologies. The Gene Craft exhibition elaborates on this concept by presenting living artwork that makes visitors imagine a future of bioengineered beings built and controlled by humans.

The first piece is by British artist Laurie Ramsell,who explores the genetic relationship between humans and model organisms. One of them is the zebrafish, which is routinely used in research to understand basic molecular processes that can then be extrapolated to human biology.

Laurie Ramsells Homdanio Birminghamensis

Homdanio Birminghamensisis a sculpture taking the shape of a zebrafish embryo made from bacterial cellulose and the artists own DNA. The piecewas created in collaboration with professor and bioartist Simon Park. As part of the 100,000 Genomes Project, it is intended to raise public awareness about research into the human genome being pioneered at the University of Birmingham.

The second piece featured in the Gene Craft exhibition is Gina Czarneckis Heirloom, a living portrait of the artists daughters. Skin cells from the girls are cultured and grown onto glass casts of their faces, creating paper-thin portraits with their own DNA.

Gina Czarneckis Heirloom

Heirloom invites visitors to imagine a future where our own cells are grown on demand for medical applications. But, at the same time, it intends to highlight the ethical implicationsof these procedures regarding the ownership of our own biological materials.

Gene Craft: Art in the Biogenetic Age will be open until May 13 in Birmingham. During that time, the BOM gallery will host a series of talks and workshops to bring together artists and scientists and discuss the issues raised by the bioart pieces exhibited.

Images via BOM and Gina Czarnecki

Excerpt from:
Art Made with Human DNA Explores the Future of Genetics in Birmingham - Labiotech.eu (blog)