Biology and Medicine

Advances in the investigation of the physical universe we live in.
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Typhoon
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Re: Biology and Medicine

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May the gods preserve and defend me from self-righteous altruists; I can defend myself from my enemies and my friends.
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BBC | World's first lab-grown burger is eaten in London
Scientists took cells from a cow and, at an institute in the Netherlands, turned them into strips of muscle that they combined to make a patty.

Researchers say the technology could be a sustainable way of meeting what they say is a growing demand for meat.
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Synchronized virtual reality heartbeat triggers out-of-body experiences
New research demonstrates that triggering an out-of-body experience (OBE) could be as simple as getting a person to watch a video of themselves with their heartbeat projected onto it. According to the study, it's easy to trick the mind into thinking it belongs to an external body and manipulate a person's self-consciousness by externalizing the body's internal rhythms. The findings could lead to new treatments for people with perceptual disorders such as anorexia and could also help dieters too.
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Heracleum Persicum
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.


WxMSrfjSotI



.

Rob Reeser was a typical family man. He coached his daughter's basketball team, golfed with his son, and enjoyed spending time at home with his family.

But all that changed when Reeser was diagnosed with severe Parkinson’s disease.

"I tried every medication possible," says Reeser, who was 30 when he was diagnosed. None of the drugs controlled his shaking; soon, he could no longer play sports, feed himself, or continue his work as a municipal clerk.

Then he came to Ohio State’s Wexner Medical Center and met Dr. Ali Rezai, who is on the forefront of an innovative technology called deep brain stimulation, or DBS. Using a small implant in the brain, DBS functions like a pacemaker: tiny electrodes regulate electrical signals.

[url=Rob Reeser was a typical family man. He coached his daughter's basketball team, golfed with his son, and enjoyed spending time at home with his family.

But all that changed when Reeser was diagnosed with severe Parkinson’s disease.

"I tried every medication possible," says Reeser, who was 30 when he was diagnosed. None of the drugs controlled his shaking; soon, he could no longer play sports, feed himself, or continue his work as a municipal clerk.

Then he came to Ohio State’s Wexner Medical Center and met Dr. Ali Rezai, who is on the forefront of an innovative technology called deep brain stimulation, or DBS. Using a small implant in the brain, DBS functions like a pacemaker: tiny electrodes regulate electrical signals.

As soon as Rezai and his team turned on the DBS device, Reeser’s tremors stopped.

"I feel like I’ve got my life back,” he says.

- As soon as Rezai and his team turned on the DBS device, Reeser’s tremors stopped.

"I feel like I’ve got my life back,” he says.


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Azrael
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cultivate a white rose
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Biochemistry and Genetics of Red Hair

Image
An Uyghur girl in Kashgar, China's Xinjiang region, with red hair

The pigment pheomelanin gives red hair its distinctive color. Red hair has far more of the pigment pheomelanin than it has of the dark pigment eumelanin.

The genetics of red hair, discovered in 1997, appear to be associated with the melanocortin-1 receptor (MC1R), which is found on chromosome 16. Red hair is associated with fair skin color because of low concentrations of eumelanin throughout the body of those with red hair. This lower melanin-concentration confers the advantage that a sufficient concentration of important Vitamin D can be produced under low light conditions. However, when UV-radiation is strong (as in regions close to the equator) the lower concentration of melanin leads to several medical disadvantages, such as a higher risk of skin cancer.

The MC1R recessive variant gene that gives people red hair and non-tanning skin is also associated with freckles, though it is not uncommon to see a redhead without freckles. Eighty percent of redheads have an MC1R gene variant,[3] and the prevalence of these alleles is highest in Scotland and Ireland. The alleles that code for red hair occur close to the alleles that affect skin color, so it seems that the phenotypic expression for lighter skin and red hair are interrelated.

Red hair can originate from several changes on the MC1R-gene. If one of these changes is present on both chromosomes then the respective individual is likely to have red hair. This type of inheritance is described as an autosomal recessive mode of inheritance. Even if both parents do not have red hair themselves, both can be carriers for the gene and have a redheaded child.

Genetics

The alleles Arg151Cys, Arg160Trp, Asp294His, and Arg142His on MC1R are shown to be recessives for the red hair phenotype.[26] The gene HCL2 (also called RHC or RHA) on chromosome 4 may also be related to red hair.[27][28]

In species other than primates, red hair has different genetic origins and mechanisms.

Evolution

Origins

Red hair is the rarest natural hair color in humans. The non-tanning skin associated with red hair may have been advantageous in far-northern climates where sunlight is scarce. Studies by Bodmer and Cavalli-Sforza (1976) hypothesized that lighter skin pigmentation prevents rickets in colder climates by encouraging higher levels of Vitamin D production and also allows the individual to retain heat better than someone with darker skin.[29] In 2000, Harding et al. concluded that red hair was not the result of positive selection and instead proposed that it occurs because of a lack of negative selection. In Africa, for example, red hair is selected against because high levels of sun would be harmful to untanned skin. However, in Northern Europe this does not happen, so redheads come about through genetic drift.[26]

Estimates on the original occurrence of the currently active gene for red hair vary from 20,000 to 100,000 years ago.[30][31]

Source Wikipedia
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Heracleum Persicum
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Re: Biology and Medicine

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.



Middle-Aged Men, Too, Can Blame Estrogen for That Waistline


.

It is the scourge of many a middle-aged man: he starts getting a pot belly, using lighter weights at the gym and somehow just doesn’t have the sexual desire of his younger years.
..

Estrogen, the female sex hormone, turns out to play a much bigger role in men’s bodies than previously thought, and falling levels contribute to their expanding waistlines just as they do in women’s.

The discovery of the role of estrogen in men is “a major advance,” said Dr. Peter J. Snyder, a professor of medicine at the University of Pennsylvania, who is leading a big new research project on hormone therapy for men 65 and over. Until recently, testosterone deficiency was considered nearly the sole reason that men undergo the familiar physical complaints of midlife.

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Ancient Viruses That Function in Early Human Development May Play Role in Cancer

July 31, 2013 — The St. Laurent Institute, a non-profit medical research institute focused on the systems biology of disease, today announced in a study published in the July edition of Genome Biology, that genetic matter, previously ignored by the scientific community, may play an important role in cancer. The study, "VlincRNAs controlled by retroviral elements are a hallmark of pluripotency and cancer" found that novel non-coding parts of the human genome known as vlincRNAs (very long intergenic, non-coding RNAs) triggered by ancient viruses, participate in the biology of stem cells, and in the development of cancer. Importantly, the group of researchers from U.S., Europe and Russia found that the elimination of these vlincRNAs caused the death of cancer cells.

"Understanding this previously ignored part of the human genome, its role in human development, and how it may be taken over by disease, opens a new frontier in science with important implications for medical advances," said Philipp Kapranov, Ph.D., lead researcher at the St. Laurent Institute. "Future research into the role and function of vlincRNAs holds promise for both highly targeted diagnostic tests and more precise cancer treatments.

Up to 98 percent of human genomic matter is known as "junk" or "dark matter" non-coding DNA, and had for years attracted little interest among scientists who doubted its role in human health and disease. Recent research has begun to identify that part of that non-coding DNA is used by the cell to make RNA such as vlincRNA, highly tissue-specific RNA chains of unusually large lengths, many of which are only found in embryonic or cancerous cells. VlincRNAs found in these two types of cells tend to be expressed based upon genetic signals from ancient viruses that invaded our ancestors' genome millions of years ago and were gradually "domesticated" over evolutionary time. The number of vlincRNAs expressed by these domesticated viral sequences correlates with both embryonic development and malignant cancers.

"St. Laurent Institute has adapted true single-molecule sequencing technology to global transcriptome analysis, providing state-of-the-art technology for the measurement of the output of the human genome," said Georges St. Laurent III, Scientific Director of the St. Laurent Institute. "Based upon this technology, we now have a greater understanding of transcriptome regulation, with potential to lead to therapeutic targets and better disease diagnostics."

About the study

The observational study published in Genome Biology utilized publicly available and unpublished data sets to find 2,147 vlincRNAs that cover 10 percent of the human genome, suggesting that their production is a common, yet undiscovered, feature of human DNA. The vlincRNAs were shown to be present in cancerous cells as well as stem cells and normal human tissues. Certain types of vlincRNAs, especially those triggered by the signals from domesticated ancient viruses, are seen at specific stages of normal development.

Researchers found that some of these vlincRNAs are co-opted by cancer-associated transcriptional programs. Importantly, removal of these RNAs causes the death of cancer cells providing a clear direction for the development of therapeutics and better diagnostics for cancer patients. VlincRNAs may contribute to the regulation of gene expression in the nucleus of the cell. Future study of vlincRNAs may illuminate the biological principles that link together stem cells and cancer.

http://www.sciencedaily.com/releases/20 ... 093915.htm
The complexity of the human biology is mind staggering. Once we come to understand it fully - and we will - we may have a very long living, disease free humanity, with capabilities beyond our imagination.
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Re: Biology and Medicine

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May the gods preserve and defend me from self-righteous altruists; I can defend myself from my enemies and my friends.
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Alzheimer's breakthrough hailed as 'turning point'

The discovery of the first chemical to prevent the death of brain tissue in a neurodegenerative disease has been hailed as the "turning point" in the fight against Alzheimer's disease.

More work is needed to develop a drug that could be taken by patients.

But scientists say a resulting medicine could treat Alzheimer's, Parkinson's, Huntington's and other diseases.

In tests on mice, the Medical Research Council showed all brain cell death from prion disease could be prevented.

Prof Roger Morris, from King's College London, said: "This finding, I suspect, will be judged by history as a turning point in the search for medicines to control and prevent Alzheimer's disease."

He told the BBC a cure for Alzheimer's was not imminent but: "I'm very excited, it's the first proof in any living animal that you can delay neurodegeneration.

"The world won't change tomorrow, but this is a landmark study."

Cells starve

The research team at the Medical Research Council Toxicology Unit, based at the University of Leicester, focused on the natural defence mechanisms built into brain cells.

When a virus hijacks a brain cell it leads to a build-up of viral proteins. Cells respond by shutting down nearly all protein production in order to halt the virus's spread.

However, many neurodegenerative diseases involve the production of faulty or "misfolded" proteins. These activate the same defences, but with more severe consequences.

The misfolded proteins linger and the brain cells shut down protein production for so long that they eventually starve themselves to death.

This process, repeated in neurons throughout the brain, can destroy movement or memory or even kill, depending on the disease.

This process is thought to take place in many forms of neurodegeneration, so safely disrupting it could treat a wide range of diseases.

The researchers used a compound which prevented those defence mechanisms kicking in and in turn halted neurodegeneration.

The study, published in Science Translational Medicine, showed mice with prion disease developed severe memory and movement problems. They died within 12 weeks.

However, those given the compound showed no sign of brain tissue wasting away.

Lead researcher Prof Giovanna Mallucci told the BBC news website: "They were absolutely fine, it was extraordinary.

"What's really exciting is a compound has completely prevented neurodegeneration and that's a first.

"This isn't the compound you would use in people, but it means we can do it and it's a start."

She said the compound offered a "new pathway that may well give protective drugs" and the next step was for drug companies to develop a medicine for use in humans.

'Very dramatic'

Prof Mallucci's lab is also testing the compound on other forms of neurodegeneration in mice but the results have not yet been published.

Side effects are an issue. The compound also acted on the pancreas, meaning the mice developed a mild form of diabetes and lost weight.

Any human drug would need to act only on the brain. However, this gives scientists and drug companies a starting point.

David Allsop, professor of neuroscience at Lancaster University described the results as "very dramatic and highly encouraging" but cautioned that more research was needed to see how the findings would apply to diseases such as Alzheimer's and Parkinson's.

Dr Eric Karran, the director of research at the charity Alzheimer's Research UK, said: "Targeting a mechanism relevant to a number of neurodegenerative diseases could yield a single drug with wide-reaching benefits, but this compound is still at an early stage.

"It will be important for these findings to be repeated and tested in models of other neurodegenerative diseases, including Alzheimer's disease."

http://www.bbc.co.uk/news/health-24462699
I hope it will be ready on time for people of my age.
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Blood Vessel Cells Can Repair, Regenerate Organs

Oct. 8, 2013 — Damaged or diseased organs may someday be healed with an injection of blood vessel cells, eliminating the need for donated organs and transplants, according to scientists at Weill Cornell Medical College.

In studies appearing in recent issues of Stem Cell Journal and Developmental Cell, the researchers show that endothelial cells -- the cells that make up the structure of blood vessels -- are powerful biological machines that drive regeneration in organ tissues by releasing beneficial, organ-specific molecules.

They discovered this by decoding the entirety of active genes in endothelial cells, revealing hundreds of known genes that had never been associated with these cells. The researchers also found that organs dictate the structure and function of their own blood vessels, including the repair molecules they secrete.

Together, the studies show that endothelial cells and the organs they are transplanted into work together to repair damage and restore function, says the study's lead investigator, Shahin Rafii, M.D., a professor of genetic medicine and co-director of the medical college's Ansary Stem Cell Institute and Tri-SCI Stem Center. When an organ is injured, its blood vessels may not be able to repair the damage on their own because they may themselves be harmed or inflamed, says Dr. Rafii, who is also an investigator at the Howard Hughes Medical Institute.

"Our work suggests that that an infusion of engineered endothelial cells could engraft into injured tissue and acquire the capacity to repair the organ," he says. "These studies -- along with the first molecular atlas of organ-specific blood vessel cells reported in the Developmental Cell paper-- will open up a whole new chapter in translational vascular medicine and will have major therapeutic application.

"Scientists had thought blood vessels in each organ are the same, that they exist to deliver oxygen and nutrients. But they are very different," and each organ is endowed with blood vessels with unique shape and function and delegated with the difficult task of complying with the metabolic demands of that organ, Dr. Rafii adds.

Creating an endothelial cell genetic 'atlas'

In the Developmental Cell study, the research team examined nine different tissues at homeostasis -- a steady, healthy state -- as well as liver and bone marrow recovering from a traumatic injury.

The scientists developed technology that helped them obtain "a pure population of endothelial cells in a very rapid time frame," says the study's lead author, Dr. Daniel Nolan, a senior scientist in Dr. Rafii's laboratory during this study who became an employee of Angiocrine Bioscience after it was completed. AB is housed at Weill Cornell Medical College and founded on various technologies based on Dr. Rafii's work.

From these cells, they were able to take a snapshot of all the genes that are being expressed in the various populations of endothelial cells known as vascular beds.

They found that endothelial cells possess tissue-specific genes that code for unique growth factors, adhesion molecules, and factors regulating metabolism. "We knew that these gene products were critical to the health of a particular tissue, but before our study it was not appreciated that these factors originate in the endothelial cells," Dr. Nolan says.

"We also found that the healing, or regeneration of tissue, in the liver and in the bone marrow were unexpectedly different -- including the repair molecules, known as angiocrine growth factors, that were expressed by the endothelial cells," says Dr. Olivier Elemento, who performed the complex computational calculations for the studies.

Blood vessels differ among various organs because the endothelial cells have to constantly adapt to the metabolic, biomechanical, inflammatory and immunological needs of that particular organ, says Dr. Michael Ginsberg, a senior postdoctoral associate in Dr. Rafii's laboratory during this study. Ginsberg also became an employee of Angiocrine Bioscience after the study ended. "And we have now found how endothelial cells have learned to behave differently in each organ and adjust to the needs of those organs," he says.

These findings raise the question as to how endothelial cells have the capacity to adapt to the biological demands of each organ. Is it possible to design "immature" endothelial cells that could allow scientists to identify the means by which the microenvironmental cues educate them to become more specialized endothelial cells?

"Versatile endothelial cells" for organ therapy

To address this issue, the scientists postulated that endothelial cells derived from embryonic stem cells could behave as resilient endothelial cells, being able to be taught how to act like an organ-specific blood vessel. Indeed, in the Stem Cell Journal study, the team generated endothelial cells from mouse embryonic stem cells that were functional, transplantable and responsive to microenvironmental signals.

These embryonic-derived endothelial cells "are versatile, so they can be transplanted into different tissues, become educated by the tissue, and acquire the characteristics of the native endothelial cells," says the study's senior author, Dr. Sina Rabbany, an adjunct associate professor of genetic medicine and bioengineering in medicine at Weill Cornell Medical College.

Dr. Rabbany says researchers can propagate these cells in large numbers in the laboratory. "We now know what it takes to keep these cells healthy, stable and viable for transplantation," he says.

In fact, in the Developmental Cell study, the researchers transplanted these generic endothelial cells generated by Dr. Rabbany's team into the liver of a mouse and found that it became indistinguishable from native endothelial cells. This also occurred when cells were grafted into kidneys. "These naive endothelial cells acquire the phenotype -- the molecular profile and signature -- of the native pre-existing endothelial cells due to the unique microenvironment in the organ," Dr. Ginsberg says.

"These transplanted endothelial cells are being educated by the unique biophysical mincroenvironment organ in which they are placed. They morph into endothelial cells that belong in the organ, and that can repair it," he adds. "If you have a heart injury and you need to reform some of your cardiomyocytes, the endothelial cells that are around the heart secrete factors that are specific for helping a heart repair itself," Dr. Rabbany says.

However, to translate these studies to the clinical setting the scientists have to generate endothelial cells that have similar immune constitution -"immunocompatible" with the recipient patient. "Endothelial cells could be derived from human embryonic pluripotent stem cells as well as by somatic cell nuclear transfer (SCNT)," says Dr. Zev Rosenwaks, director and physician-in-chief of the Ronald O. Perelman and Claudia Cohen Center for Reproductive Medicine and director of the Stem Cell Derivation Laboratory of Weill Cornell Medical College and a co-author on the studies. "In the SCNT approach, the nucleus of a somatic cell is introduced into the human egg resulting in the generation of embryonic stem cells that would generate endothelial cells that are a genetic match of the patient," says Dr. Daylon James, assistant professor of reproductive biology at Weill Cornell, who was instrumental in designing protocols to generate endothelial cells from human embryonic stem cells.

"Alternatively, to overcome the bioethical issues associated with human embryos or eggs and potential predisposition of the embryonic stem cells to produce cancer cells, one can take cells discarded after a diagnostic prenatal amniocentesis and turn them into endothelial cells capable of repairing and regenerating blood vessels. Freezing and stockpiling such cells will allow transplantation of these cells to a genetically diverse population of patients," adds Dr. Rosenwaks, referring to work published last October in the journal Cell. Ginsberg is an inventor on this technology, which Angiocrine has licensed.

Additional preclinical investigation is required before study of endothelial cell transplantation in humans is possible, but the therapeutic potential of endothelial cell transplantation is endless, Dr. Rafii says. "They could also be used as Trojan horses to block tumor growth, they could be altered to carry toxic chemicals. They could become biological cruise missiles, directed to do many things inside diseased organs," he says. "Our work has just begun."

http://www.sciencedaily.com/releases/20 ... 152218.htm
I live in a permanent state of wonder...
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Re: Biology and Medicine

Post by noddy »

some medical doom dooom doooooooooooooooooom.

http://www.pbs.org/wgbh/pages/frontline ... cs-period/
The more you use an antibiotic, the more you expose a bacteria to an antibiotic, the greater the likelihood that resistance to that antibiotic is going to develop. So the more antibiotics we put into people, we put into the environment, we put into livestock, the more opportunities we create for these bacteria to become resistant. …We also know that we’ve greatly overused antibiotics and in overusing these antibiotics, we have set ourselves up for the scenario that we find ourselves in now, where we’re running out of antibiotics.

We are quickly running out of therapies to treat some of these infections that previously had been eminently treatable. There are bacteria that we encounter, particularly in health-care settings, that are resistant to nearly all — or, in some cases, all — the antibiotics that we have available to us, and we are thus entering an era that people have talked about for a long time.

For a long time, there have been newspaper stories and covers of magazines that talked about “The end of antibiotics, question mark?” Well, now I would say you can change the title to “The end of antibiotics, period.”
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May the gods preserve and defend me from self-righteous altruists; I can defend myself from my enemies and my friends.
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http://www.fastcoexist.com/3022050/futu ... ur-doctors


A friend of mine works in IT at this hospital. They are building up a supercomputer that will crunch analytics taken directly from the hospital's instruments. They are also putting together a massive database of DNA in order to start looking for particular patterns.
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Voracious Worm Evolves to Eat Biotech Corn Engineered to Kill It

One of agricultural biotechnology’s great success stories may become a cautionary tale of how short-sighted mismanagement can squander the benefits of genetic modification.

After years of predicting it would happen — and after years of having their suggestions largely ignored by companies, farmers and regulators — scientists have documented the rapid evolution of corn rootworms that are resistant to Bt corn.

Until Bt corn was genetically altered to be poisonous to the pests, rootworms used to cause billions of dollars in damage to U.S. crops. Named for the pesticidal toxin-producing Bacillus thuringiensis gene it contains, Bt corn now accounts for three-quarters of the U.S. corn crop. The vulnerability of this corn could be disastrous for farmers and the environment.

“Unless management practices change, it’s only going to get worse,” said Aaron Gassmann, an Iowa State University entomologist and co-author of a March 17 Proceedings of the National Academy of Sciences study describing rootworm resistance. “There needs to be a fundamental change in how the technology is used.”

First planted in 1996, Bt corn quickly became hugely popular among U.S. farmers. Within a few years, populations of rootworms and corn borers, another common corn pest, had plummeted across the midwest. Yields rose and farmers reduced their use of conventional insecticides that cause more ecological damage than the Bt toxin.

By the turn of the millennium, however, scientists who study the evolution of insecticide resistance were warning of imminent problems. Any rootworm that could survive Bt exposures would have a wide-open field in which to reproduce; unless the crop was carefully managed, resistance would quickly emerge.

Key to effective management, said the scientists, were refuges set aside and planted with non-Bt corn. Within these fields, rootworms would remain susceptible to the Bt toxin. By mating with any Bt-resistant worms that chanced to evolve in neighboring fields, they’d prevent resistance from building up in the gene pool.

But the scientists’ own recommendations — an advisory panel convened in 2002 by the EPA suggested that a full 50 percent of each corn farmer’s fields be devoted to these non-Bt refuges — were resisted by seed companies and eventually the EPA itself, which set voluntary refuge guidelines at between 5 and 20 percent. Many farmers didn’t even follow those recommendations.

Fast forward to 2009, when Gassmann responded to reports of extensive rootworm damage in Bt cornfields in northeast Iowa. Populations there had become resistant to one of the three Bt corn varieties. (Each variety produces a different type of Bt toxin.) He described that resistance in a 2011 study; around the same time, reports of rootworm-damaged Bt corn came in from parts of Illinois, Minnesota, Nebraska and South Dakota. These didn’t represent a single outbreak, but rather the emergence, again and again, of resistance.

In the new paper, Gassmann describes further incidents of Bt resistance in other parts of Iowa. He also found rootworms resistant to a second variety of Bt corn. Moreover, being resistant to one variety heightened the chances of resistance to another. That means corn engineered to produce multiple Bt toxins — so-called stacked varieties — won’t do much to slow the evolution of rootworm resistance, as was originally hoped.

Farmers likely won’t stop using Bt corn, as it’s still effective against other pests — but as rootworms become more resistant, said Gassmann, farmers will turn to insecticides, thus increasing their costs and losing the ecological benefits originally gained by using Bt corn. As entomologists concerned by rootworm resistance wrote to the EPA in 2012, “When insecticides overlay transgenic technology, the economic and environmental advantages of rootworm-­protected corn quickly disappear.”

Entomologist Bruce Tabashnik of the University of Arizona called Bt resistance “an increasingly serious problem,” and said that refuge sizes need to be increased dramatically and immediately. He and other scientists have pushed the EPA to double current refuge requirements, but so far without success.

“Biotech companies have successfully lobbied EPA for major reductions in refuge requirements,” said Tabashnik.

Entomologist Elson Shields of Cornell University agrees. “Resistance was caused because the farmers did not plant the required refuges and the companies did not enforce the planting of refuges,” said Shields, who has written that “a widespread increase in trait failure may be just around the corner.”

In addition to increasing refuge sizes, farmers also need to vary the crops planted on their fields, rather than planting corn season after season, said Gassmann. Breaks in the corn cycle naturally disrupt rootworm populations, but the approach fell from favor as the high price of corn made continuous planting appealing. “Continuous corn is the perfect habitat for rootworm,” said Gassmann.

Shields also lamented the difficulty he and other academic scientists long experienced when trying to study Bt corn. Until 2010, after organized objections by entomologists at major agricultural universities forced seed companies to allow outside researchers to study Bt corn, the crop was largely off-limits. Had that not been the case, said Shields, resistance could have been detected even earlier, and perhaps stalled before it threatened to become such a problem.

“Once we had legal access, resistance was documented in a year,” Shields said. “We were seeing failures earlier but were not allowed to test for resistance.”

There’s a lesson to be learned for future crop traits, Shields said. Rootworm resistance was expected from the outset, but the Bt seed industry, seeking to maximize short-term profits, ignored outside scientists. The next pest-fighting trait “will fall under the same pressure,” said Shields, “and the insect will win. Always bet on the insect if there is not a smart deployment of the trait.”
“There are a lot of killers. We’ve got a lot of killers. What, do you think our country’s so innocent? Take a look at what we’ve done, too.” - Donald J. Trump, President of the USA
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YMix wrote:
Voracious Worm Evolves to Eat Biotech Corn Engineered to Kill It

One of agricultural biotechnology’s great success stories may become a cautionary tale of how short-sighted mismanagement can squander the benefits of genetic modification.

After years of predicting it would happen — and after years of having their suggestions largely ignored by companies, farmers and regulators — scientists have documented the rapid evolution of corn rootworms that are resistant to Bt corn.

Until Bt corn was genetically altered to be poisonous to the pests, rootworms used to cause billions of dollars in damage to U.S. crops. Named for the pesticidal toxin-producing Bacillus thuringiensis gene it contains, Bt corn now accounts for three-quarters of the U.S. corn crop. The vulnerability of this corn could be disastrous for farmers and the environment.

“Unless management practices change, it’s only going to get worse,” said Aaron Gassmann, an Iowa State University entomologist and co-author of a March 17 Proceedings of the National Academy of Sciences study describing rootworm resistance. “There needs to be a fundamental change in how the technology is used.”

First planted in 1996, Bt corn quickly became hugely popular among U.S. farmers. Within a few years, populations of rootworms and corn borers, another common corn pest, had plummeted across the midwest. Yields rose and farmers reduced their use of conventional insecticides that cause more ecological damage than the Bt toxin.

By the turn of the millennium, however, scientists who study the evolution of insecticide resistance were warning of imminent problems. Any rootworm that could survive Bt exposures would have a wide-open field in which to reproduce; unless the crop was carefully managed, resistance would quickly emerge.

Key to effective management, said the scientists, were refuges set aside and planted with non-Bt corn. Within these fields, rootworms would remain susceptible to the Bt toxin. By mating with any Bt-resistant worms that chanced to evolve in neighboring fields, they’d prevent resistance from building up in the gene pool.

But the scientists’ own recommendations — an advisory panel convened in 2002 by the EPA suggested that a full 50 percent of each corn farmer’s fields be devoted to these non-Bt refuges — were resisted by seed companies and eventually the EPA itself, which set voluntary refuge guidelines at between 5 and 20 percent. Many farmers didn’t even follow those recommendations.

Fast forward to 2009, when Gassmann responded to reports of extensive rootworm damage in Bt cornfields in northeast Iowa. Populations there had become resistant to one of the three Bt corn varieties. (Each variety produces a different type of Bt toxin.) He described that resistance in a 2011 study; around the same time, reports of rootworm-damaged Bt corn came in from parts of Illinois, Minnesota, Nebraska and South Dakota. These didn’t represent a single outbreak, but rather the emergence, again and again, of resistance.

In the new paper, Gassmann describes further incidents of Bt resistance in other parts of Iowa. He also found rootworms resistant to a second variety of Bt corn. Moreover, being resistant to one variety heightened the chances of resistance to another. That means corn engineered to produce multiple Bt toxins — so-called stacked varieties — won’t do much to slow the evolution of rootworm resistance, as was originally hoped.

Farmers likely won’t stop using Bt corn, as it’s still effective against other pests — but as rootworms become more resistant, said Gassmann, farmers will turn to insecticides, thus increasing their costs and losing the ecological benefits originally gained by using Bt corn. As entomologists concerned by rootworm resistance wrote to the EPA in 2012, “When insecticides overlay transgenic technology, the economic and environmental advantages of rootworm-­protected corn quickly disappear.”

Entomologist Bruce Tabashnik of the University of Arizona called Bt resistance “an increasingly serious problem,” and said that refuge sizes need to be increased dramatically and immediately. He and other scientists have pushed the EPA to double current refuge requirements, but so far without success.

“Biotech companies have successfully lobbied EPA for major reductions in refuge requirements,” said Tabashnik.

Entomologist Elson Shields of Cornell University agrees. “Resistance was caused because the farmers did not plant the required refuges and the companies did not enforce the planting of refuges,” said Shields, who has written that “a widespread increase in trait failure may be just around the corner.”

In addition to increasing refuge sizes, farmers also need to vary the crops planted on their fields, rather than planting corn season after season, said Gassmann. Breaks in the corn cycle naturally disrupt rootworm populations, but the approach fell from favor as the high price of corn made continuous planting appealing. “Continuous corn is the perfect habitat for rootworm,” said Gassmann.

Shields also lamented the difficulty he and other academic scientists long experienced when trying to study Bt corn. Until 2010, after organized objections by entomologists at major agricultural universities forced seed companies to allow outside researchers to study Bt corn, the crop was largely off-limits. Had that not been the case, said Shields, resistance could have been detected even earlier, and perhaps stalled before it threatened to become such a problem.

“Once we had legal access, resistance was documented in a year,” Shields said. “We were seeing failures earlier but were not allowed to test for resistance.”

There’s a lesson to be learned for future crop traits, Shields said. Rootworm resistance was expected from the outset, but the Bt seed industry, seeking to maximize short-term profits, ignored outside scientists. The next pest-fighting trait “will fall under the same pressure,” said Shields, “and the insect will win. Always bet on the insect if there is not a smart deployment of the trait.”
Interesting. I wonder what effect alternating the corn varieties year by year would have?
"I fancied myself as some kind of god....It is a sort of disease when you consider yourself some kind of god, the creator of everything, but I feel comfortable about it now since I began to live it out.” -- George Soros
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Re: Biology and Medicine

Post by Nonc Hilaire »

Doc wrote:
YMix wrote:
Voracious Worm Evolves to Eat Biotech Corn Engineered to Kill It

One of agricultural biotechnology’s great success stories may become a cautionary tale of how short-sighted mismanagement can squander the benefits of genetic modification.

After years of predicting it would happen — and after years of having their suggestions largely ignored by companies, farmers and regulators — scientists have documented the rapid evolution of corn rootworms that are resistant to Bt corn.

Until Bt corn was genetically altered to be poisonous to the pests, rootworms used to cause billions of dollars in damage to U.S. crops. Named for the pesticidal toxin-producing Bacillus thuringiensis gene it contains, Bt corn now accounts for three-quarters of the U.S. corn crop. The vulnerability of this corn could be disastrous for farmers and the environment.

“Unless management practices change, it’s only going to get worse,” said Aaron Gassmann, an Iowa State University entomologist and co-author of a March 17 Proceedings of the National Academy of Sciences study describing rootworm resistance. “There needs to be a fundamental change in how the technology is used.”

First planted in 1996, Bt corn quickly became hugely popular among U.S. farmers. Within a few years, populations of rootworms and corn borers, another common corn pest, had plummeted across the midwest. Yields rose and farmers reduced their use of conventional insecticides that cause more ecological damage than the Bt toxin.

By the turn of the millennium, however, scientists who study the evolution of insecticide resistance were warning of imminent problems. Any rootworm that could survive Bt exposures would have a wide-open field in which to reproduce; unless the crop was carefully managed, resistance would quickly emerge.

Key to effective management, said the scientists, were refuges set aside and planted with non-Bt corn. Within these fields, rootworms would remain susceptible to the Bt toxin. By mating with any Bt-resistant worms that chanced to evolve in neighboring fields, they’d prevent resistance from building up in the gene pool.

But the scientists’ own recommendations — an advisory panel convened in 2002 by the EPA suggested that a full 50 percent of each corn farmer’s fields be devoted to these non-Bt refuges — were resisted by seed companies and eventually the EPA itself, which set voluntary refuge guidelines at between 5 and 20 percent. Many farmers didn’t even follow those recommendations.

Fast forward to 2009, when Gassmann responded to reports of extensive rootworm damage in Bt cornfields in northeast Iowa. Populations there had become resistant to one of the three Bt corn varieties. (Each variety produces a different type of Bt toxin.) He described that resistance in a 2011 study; around the same time, reports of rootworm-damaged Bt corn came in from parts of Illinois, Minnesota, Nebraska and South Dakota. These didn’t represent a single outbreak, but rather the emergence, again and again, of resistance.

In the new paper, Gassmann describes further incidents of Bt resistance in other parts of Iowa. He also found rootworms resistant to a second variety of Bt corn. Moreover, being resistant to one variety heightened the chances of resistance to another. That means corn engineered to produce multiple Bt toxins — so-called stacked varieties — won’t do much to slow the evolution of rootworm resistance, as was originally hoped.

Farmers likely won’t stop using Bt corn, as it’s still effective against other pests — but as rootworms become more resistant, said Gassmann, farmers will turn to insecticides, thus increasing their costs and losing the ecological benefits originally gained by using Bt corn. As entomologists concerned by rootworm resistance wrote to the EPA in 2012, “When insecticides overlay transgenic technology, the economic and environmental advantages of rootworm-­protected corn quickly disappear.”

Entomologist Bruce Tabashnik of the University of Arizona called Bt resistance “an increasingly serious problem,” and said that refuge sizes need to be increased dramatically and immediately. He and other scientists have pushed the EPA to double current refuge requirements, but so far without success.

“Biotech companies have successfully lobbied EPA for major reductions in refuge requirements,” said Tabashnik.

Entomologist Elson Shields of Cornell University agrees. “Resistance was caused because the farmers did not plant the required refuges and the companies did not enforce the planting of refuges,” said Shields, who has written that “a widespread increase in trait failure may be just around the corner.”

In addition to increasing refuge sizes, farmers also need to vary the crops planted on their fields, rather than planting corn season after season, said Gassmann. Breaks in the corn cycle naturally disrupt rootworm populations, but the approach fell from favor as the high price of corn made continuous planting appealing. “Continuous corn is the perfect habitat for rootworm,” said Gassmann.

Shields also lamented the difficulty he and other academic scientists long experienced when trying to study Bt corn. Until 2010, after organized objections by entomologists at major agricultural universities forced seed companies to allow outside researchers to study Bt corn, the crop was largely off-limits. Had that not been the case, said Shields, resistance could have been detected even earlier, and perhaps stalled before it threatened to become such a problem.

“Once we had legal access, resistance was documented in a year,” Shields said. “We were seeing failures earlier but were not allowed to test for resistance.”

There’s a lesson to be learned for future crop traits, Shields said. Rootworm resistance was expected from the outset, but the Bt seed industry, seeking to maximize short-term profits, ignored outside scientists. The next pest-fighting trait “will fall under the same pressure,” said Shields, “and the insect will win. Always bet on the insect if there is not a smart deployment of the trait.”
Interesting. I wonder what effect alternating the corn varieties year by year would have?
From what I have read, none. The recommendations were to plant 1/4 fields in non-resistant crops to lure off the predators but greed led to overplanting the resistant varieties.
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Typhoon
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Re: Biology and Medicine

Post by Typhoon »

Forget the tin foil, it's parasites that run the show . . .

CfqO1U6lfDs
May the gods preserve and defend me from self-righteous altruists; I can defend myself from my enemies and my friends.
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Re: Biology and Medicine

Post by Endovelico »

Finding turns neuroanatomy on its head: Researchers present new view of myelin
April 18, 2014 -Harvard University

Myelin, the electrical insulating material long known to be essential for the fast transmission of impulses along the axons of nerve cells, is not as ubiquitous as thought, according to a new work lead by Professor Paola Arlotta of the Harvard Stem Cell Institute (HSCI) and the University's Department of Stem Cell and Regenerative Biology, in collaboration with Professor Jeff Lichtman, of Harvard's Department of Molecular and Cellular Biology.

"Myelin is a relatively recent invention during evolution," says Arlotta. "It's thought that myelin allowed the brain to communicate really fast to the far reaches of the body, and that it has endowed the brain with the capacity to compute higher level functions." In fact, loss of myelin is a feature of a number of devastating diseases, including multiple sclerosis and schizophrenia.

But the new research shows that despite myelin essential roles in the brain, "some of the most evolved, most complex neurons of the nervous system have less myelin than older, more ancestral ones" Arlotta, co-director of the HSCI neuroscience program, says.

What this means, Arlotta says, is that the higher in the cerebral cortex one looks -- the closer to the top of the brain, which is its most evolved region -- the less myelin one finds. Not only that, but "neurons in this part of the brain display a brand new way of positioning myelin along their axons that has not been previously seen. They have 'intermittent myelin' with long axon tracts that lack myelin interspersed among myelin-rich segments.

Arlotta continues: "contrary to the common assumptions that neurons use a universal profile of myelin distribution on their axons, the work indicate that different neurons choose to myelinate their axons differently. In classic neurobiology textbooks myelin is represented on axons as a sequence of myelinated segments separated by very short nodes that lack myelin. This distribution of myelin was tacitly assumed to be always the same, on every neuron, from the beginning to the end of the axon. This new work finds this not to be the case."

The results of the research by Arlotta and post doctoral fellow Giulio Srubek Tomassy, the first author on the report, are published in the latest edition of Science, the journal of the American Association for the Advancement of Science.

The paper is accompanied by a "Perspective" by R. Douglas Fields, of the Eunice Kennedy Shriver National Institute of Child Health and Human Development, at the National Institutes of Health, who says that Arlotta and Tomassy's findings raise important questions about the purpose of myelin, "are likely to spark new concepts about how information is transmitted and integrated in the brain."

Arlotta and Tomassy collaborated closely on the new work with postdoctoral fellow Daniel Berger of the Lichtman group, which generated one of the two massive electron microscopy data bases that made the work possible.

"The fact that it is the most evolved neurons, the ones that have expanded dramatically in humans, suggests that what we're seeing might be the "future." As neuronal diversity increases and the brain needs to process more and more complex information, neurons change the way they use myelin to "achieve" more," says Arlotta.

It is possible, said Tomassy, that these profiles of myelination "may be giving neurons an opportunity to branch out and 'talk' to neighboring neurons." For example, because axons cannot make synaptic contacts when they are myelinated, a possibility is that these long myelin gaps may be needed to increase neuronal communication and synchronize responses across different neurons. Perhaps, he and Arlotta postulate, the intermittent myelin is intended to fine-tune the electrical impulses traveling along the axons, in order to allow the emergence of highly complex neuronal behaviors.

http://www.sciencedaily.com/releases/20 ... 161429.htm
I have always found it intuitive that evolution is still going on, as far as our species is concerned. I'm sure things will become very interesting as time goes by.
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Re: Biology and Medicine

Post by Heracleum Persicum »

.

vzJFzNr5YL4
Tarantula hawk wasps are species of spider wasps that seize tarantulas as food for their little ones (larvae!)
They prefer female tarantulas, because male tarantulas are typically emaciated from ignoring food while they search for females. They seek females in their burrows, capturing, stinging and paralyzing the spider, dragging the prey back to their own burrow, or to a specially prepared nest with a covered entrance, where a single egg is laid upon the spider's body. When the larvae hatch it begins sucking the juices from the paralyzed, but still living spider. As it grows, the larvae plunges deeper into the spiders body, feeding voraciously while avoiding vital organs to keep the host fresh. Eventually, an adult Tarantula Hawk wasp emerges from the nest and the life cycle begins once again.
Tarantula wasps rarely sting people as they are very docile however, if provoked they may sting. Their sting is among the most painful in the insect world
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Endovelico
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Chickenosaurus

Post by Endovelico »

Fun...

0QVXdEOiCw8
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Parodite
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Re: Biology and Medicine

Post by Parodite »

Israeli discovery could reverse Alzheimer’s damage

Research by a Tel Aviv University team may point the way to protecting cells from the damage wrought by Alzheimer’s disease, and even reverse damage that the disease caused before treatment. The method involves a protein similar to one which protects the brain from damage, but which is lacking in Alzheimer’s patients.
[...]
Deep down I'm very superficial
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Endovelico
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Re: Biology and Medicine

Post by Endovelico »

Functional nerve cells from skin cells
May 21, 2014 - University of Cambridge


A new method of generating mature nerve cells from skin cells could greatly enhance understanding of neurodegenerative diseases, and could accelerate the development of new drugs and stem cell-based regenerative medicine.

The nerve cells generated by this new method show the same functional characteristics as the mature cells found in the body, making them much better models for the study of age-related diseases such as Parkinson's and Alzheimer's, and for the testing of new drugs.

Eventually, the technique could also be used to generate mature nerve cells for transplantation into patients with a range of neurodegenerative diseases.

By studying how nerves form in developing tadpoles, researchers from the University of Cambridge were able to identify ways to speed up the cellular processes by which human nerve cells mature. The findings are reported in the May 27th edition of the journal Development.

Stem cells are our master cells, which can develop into almost any cell type within the body. Within a stem cell, there are mechanisms that tell it when to divide, and when to stop dividing and transform into another cell type, a process known as cell differentiation. Several years ago, researchers determined that a group of proteins known as transcription factors, which are found in many tissues throughout the body, regulate both mechanisms.

More recently, it was found that by adding these proteins to skin cells, they can be reprogrammed to form other cell types, including nerve cells. These cells are known as induced neurons, or iN cells. However, this method generates a low number of cells, and those that are produced are not fully functional, which is a requirement in order to be useful models of disease: for example, cortical neurons for stroke, or motor neurons for motor neuron disease.

In addition, for age-related diseases such as Parkinson's and Alzheimer's, both of which affect millions worldwide, mature nerve cells which show the same characteristics as those found in the body are crucial in order to enhance understanding of the disease and ultimately determine the best way to treat it.

"When you reprogramme cells, you're essentially converting them from one form to another but often the cells you end up with look like they come from embryos rather than looking and acting like more mature adult cells," said Dr Anna Philpott of the Department of Oncology, who led the research. "In order to increase our understanding of diseases like Alzheimer's, we need to be able to work with cells that look and behave like those you would see in older individuals who have developed the disease, so producing more 'adult' cells after reprogramming is really important."

By manipulating the signals which transcription factors send to the cells, Dr Philpott and her collaborators were able to promote cell differentiation and maturation, even in the presence of conflicting signals that were directing the cell to continue dividing.

When cells are dividing, transcription factors are modified by the addition of phosphate molecules, a process known as phosphorylation, but this can limit how well cells can convert to mature nerves. However, by engineering proteins which cannot be modified by phosphate and adding them to human cells, the researchers found they could produce nerve cells that were significantly more mature, and therefore more useful as models for disease such as Alzheimer's.

Additionally, very similar protein control mechanisms are at work to mature important cells in other tissues such as pancreatic islets, the cell type that fails to function effectively in type 2 diabetes. As well as making more mature nerves, Dr Philpott's lab is now using similar methods to improve the function of insulin-producing pancreas cells for future therapeutic applications.

"We've found that not only do you have to think about how you start the process of cell differentiation in stem cells, but you also have to think about what you need to do to make differentiation complete -- we can learn a lot from how cells in developing embryos manage this," said Dr Philpott.

http://www.sciencedaily.com/releases/20 ... 133708.htm
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Re: Biology and Medicine

Post by Apollonius »

Antibiotic-resistant bacteria disarmed with fungus compound - Kelly Crowe, CBC News, 25 June 2014
http://www.cbc.ca/news/health/antibioti ... -1.2686293


Researchers at McMaster University in Hamilton have discovered a way to disarm one of the most frightening weapons bacteria have developed to resist antibiotic drugs.

And they discovered this potentially lifesaving compound in an unlikely place: a soil sample from a national park in Nova Scotia.

The discovery is featured today on the cover of the prestigious journal Nature.

"Our finding offers the first hope that we might be able to get around this resistance mechanism," said Prof. Gerry Wright, who led the research.

The discovery targets antibiotic-resistant "superbugs," which produce an enzyme called NDM-1 (New Delhi metallo-beta-lactamase), allowing them to fight off almost every antibiotic in the medicine cabinet, including carbepenems — an important class of drugs that doctors keep in reserve as a last resort against multi-resistant bacteria.

The emergence of NDM-1 in pathogens such as E. coli has turned formerly treatable infections into potentially deadly diseases. The only weapons left on the shelf are highly toxic with extreme side-effects, and doctors predict the bugs will soon develop resistance even to those drugs.

"It’s an antibiotic resistance enzyme that we didn’t really know about until about five years ago. It has spread around the world and multiple organisms have acquired it, and so it’s become a pretty significant public health threat in a very short period of time," Wright said.

"NDM-1 is the pinnacle of antibiotic resistance," said Dr. John Conly, director of the Centre for Antimicrobial Resistance at the University of Calgary. NDM-1 has spread to every continent except Antarctica, and there have been NDM-1 outbreaks in Canada, including in B.C.’s Fraser Valley.

With so much concern in the medical community, Wright went looking for something that could tackle NDM-1. What he found was sitting in a refrigerator in his laboratory. That’s where he keeps his collection of soil bacteria, harvested from random samples of Canadian dirt that he has asked students and friends to collect as they travel around the country.

Those bacteria produce hundreds of chemical compounds, which they use to defend themselves against other bacteria — chemicals that might ultimately become the basis of future drugs for humans.

"We screened that collection for molecules that would reverse this resistance, that would block this NDM-1 protein," Wright said, "and lo and behold, we found one." ...
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