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Category Archives: Transhuman News

DNA analysis now helps solve lesser crimes, too

Posted: January 6, 2014 at 8:48 pm

By Scott Daugherty The Virginian-Pilot January 6, 2014

CHESAPEAKE

DNA. For more than two decades, it's helped police solve heinous murders and catch serial rapists.

Specially trained forensic scientists routinely examine evidence, recover biological samples and conduct tests to develop a bad guy's DNA profile - the telltale genetic information contained in our cells. The evidence has become a mainstay of Virginia courtrooms, not to mention TV cop shows.

And in recent years, the science has become so commonplace it's even started popping up in misdemeanor cases. Police and prosecutors hope DNA will bolster their efforts in an unusual drunken driving case pending in General District Court.

"Twenty years ago, DNA was reserved for homicides and maybe some sexual assaults," said Brad Jenkins, biology program manager for the state's Department of Forensic Science. "But not anymore."

Police investigating a felony may submit biological evidence to one of the state's four labs for DNA testing, Jenkins said. His staff members routinely help detectives investigate robberies, assaults and burglaries.

And, when possible, the lab also will screen evidence from a misdemeanor.

"We don't do a lot of misdemeanors, but it does happen on occasion," Jenkins said, explaining that such reviews typically happen only after a member of his staff discusses the case with a prosecutor.

Budget constraints prevent the labs from helping with all misdemeanor investigations.

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Study: ‘Jumping genes’ linked to schizophrenia

Posted: at 8:48 pm

Roaming bits of DNA that can relocate and proliferate throughout the genome, called "jumping genes," may contribute to schizophrenia, a new study suggests. These rogue genetic elements pepper the brain tissue of deceased people with the disorder and multiply in response to stressful events, such as infection during pregnancy, which increase the risk of the disease. The study could help explain how genes and environment work together to produce the complex disorder and may even point to ways of lowering the risk of the disease, researchers say.

Schizophrenia causes hallucinations, delusions and a host of other cognitive problems, and afflicts roughly 1 percent of all people. It runs in families -- a person whose twin sibling has the disorder, for example, has a roughly 50-50 chance of developing it. Scientists have struggled to define which genes are most important to developing the disease, however; each individual gene associated with the disorder confers only modest risk. Environmental factors such as viral infections before birth also have been shown to increase risk of developing schizophrenia, but how and whether these exposures work together with genes to skew brain development and produce the disease is still unclear, says Tadafumi Kato, a neuroscientist at the RIKEN Brain Science Institute in Wako City, Japan, and co-author of the new study.

Over the past several years, a new mechanism for genetic mutation has attracted considerable interest from researchers studying neurological disorders, Kato says. Informally called jumping genes, these bits of DNA can replicate and insert themselves into other regions of the genome, where they either lie silent, doing nothing; start churning out their own genetic products; or alter the activity of their neighboring genes. If that sounds potentially dangerous, it is: Such genes are often the culprits behind tumor-causing mutations and have been implicated in several neurological diseases. However, jumping genes also make up nearly half the current human genome, suggesting that humans owe much of our identity to their audacious leaps.

Recent research by neuroscientist Fred Gage and colleagues at the University of California, San Diego, has shown that one of the most common types of jumping gene in people, called L1, is particularly abundant in human stem cells in the brain that ultimately differentiate into neurons and plays an important role in regulating neuronal development and proliferation. Although Gage and colleagues have found that increased L1 is associated with mental disorders such as Rett syndrome, a form of autism, and a neurological motor disease called Louis-Bar syndrome, "no one had looked very carefully" to see if the gene might also contribute to schizophrenia, he says.

To investigate that question, principal investigator Kazuya Iwamoto, a neuroscientist; Kato; and their team at RIKEN extracted brain tissue of deceased people who had been diagnosed with schizophrenia as well as several other mental disorders, extracted DNA from their neurons, and compared it with that of healthy people. Compared with controls, there was a 1.1-fold increase in L1 in the tissue of people with schizophrenia, as well as slightly less elevated levels in people with other mental disorders such as major depression, the team reported last week in Neuron.

Next, the scientists tested whether environmental factors associated with schizophrenia could trigger a comparable increase in L1. They injected pregnant mice with a chemical that simulates viral infection and found that their offspring did show higher levels of the gene in their brain tissue. An additional study in infant macaque monkeys, which mimicked exposure to a hormone also associated with increased schizophrenia risk, produced similar results. Finally, the group examined human neural stem cells extracted from people with schizophrenia and found that these, too, showed higher levels of L1.

The fact that it is possible to increase the number of copies of L1 in the mouse and macaque brains using established environmental triggers for schizophrenia shows that such genetic mutations in the brain may be preventable if such exposures can be avoided, Kato says. He says he hopes that the "new view" that environmental factors can trigger or deter genetic changes involved in the disease will help remove some of the disorder's stigma.

Combined with previous studies on other disorders, the new study suggests that L1 genes are more active in the brain of patients with neuropsychiatric diseases, Gage says. He cautions, however, that no one yet knows whether they are actually causing the disease. "Now that we have multiple confirmations of this occurring in humans with different diseases, the next step is to determine if possible what role, if any, they play."

One tantalizing possibility is that as these restless bits of DNA drift throughout the genomes of human brain cells, they help create the vibrant cognitive diversity that helps humans as a species respond to changing environmental conditions, and produces extraordinary "outliers," including innovators and geniuses such as Picasso, says UC San Diego neuroscientist Alysson Muotri. The price of such rich diversity may be that mutations contributing to mental disorders such as schizophrenia sometimes emerge. Figuring out what these jumping genes truly do in the human brain is the "next frontier" for understanding complex mental disorders, he says. "This is only the tip of the iceberg."

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Study: 'Jumping genes' linked to schizophrenia

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Discovery spotlights key role of mystery RNA modification in cells

Posted: at 8:47 pm

4 hours ago University of Chicago graduate student Xiao Wang and her colleagues based the results of their Nature paper on RNA modification on analysis of HeLa cells, a line of human cells widely used in laboratory research. Credit: Rob Kozloff/University of Chicago

Researchers had known for several decades that a certain chemical modification exists on messenger ribonucleic acid (mRNA), which is essential to the flow of genetic information. But only recently did experiments at the University of Chicago show that one major function of this modification governs the longevity and decay of RNA, a process critical to the development of healthy cells.

The chemical modification on mRNA in question is called N6-methyladenosine (m6A). A recent study by UChicago scientists reveals how the m6A modification on mRNA could affect the half life of mRNA that in turn regulates cellular protein quantities That discovery could provide fundamental insights into healthy functioning and disorders such as obesity, diabetes, and infertility.

The m6A modification "affects a huge number of messenger RNA in human cells, and yet we did not know its exact function," said Chuan He, professor in chemistry at UChicago and a recently selected investigator of the Howard Hughes Medical Institute. He, Xiao Wang and 11 co-authors from UChicago, University of California, San Diego, and Peking University reported their findings on m6A in the Jan. 2 issue of Nature.

RNA in human cells becomes constantly depleted as it produces proteins, an instability that is essential to biology. "Whenever a cells starts to differentiate, transform into a different type of cell, it needs to express a different set of proteins using a different set of messenger RNA," He said. "It can't be the original set."

The disposal of old RNA allows for the addition of new RNA and the production of different proteins. The Nature study documents that this process is regulated by the insertion or removal of a methyl, a chemical group commonly found in organic compounds.

"Biology is about protein expression regulation: which proteins, how many and at what point," He explained. "If you have the right pattern you get healthy cells. If you get the wrong pattern, you get disease."

It is well known that genetic factors can control protein expression, but the methylation and demethylation of RNA can be epigeneticoperating independent of the sequence of deoxyribonucleic acid (DNA). "This is a very important yet under-explored field," said Wang, the study's lead author and a graduate student in chemistry at UChicago. "It's also a field that is expanding very quickly."

Researchers had long known the presence of the m6A methylation on messenger RNA, but why this occurred remained unknown. He and his associates took a major step in 2011 when they discovered the reverse of the methylation process, demethylation. This discovery involved a so-called "eraser protein" that removed the methyl from RNA, a defect of which leads to obesity. "We basically said, 'Look, if you have certain defect of this function, you get obesity, so there's something going on fundamentally interesting. This methylation appears to play important roles in biological regulation."

He and his associates have now shown that the methylation affects the decay of messenger RNA. "People who are interested in messenger RNA decay or all kinds of cytoplasmic RNA biology now have a new pathway to consider," Wang said.

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Discovery spotlights key role of mystery RNA modification in cells

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‘BILLION-YEAR DISK’ to help FUTURE LIFEFORMS study us

Posted: at 8:47 pm

Quick guide to disaster recovery in the cloud

Boffins have devised a storage medium that could hold data for up to one billion years and claim recent accelerated ageing tests have shown "million-year" survivability.

The study's authors are Jeroen de Vries of the University of Twente MESA and Institute for Nanotechnology, and colleagues Dimitri Schellenberg, Leon Abelmann1, Andreas Manz and Miko Elwenspoek.

Their paper (PDF), in pre-print in ArXiv, is titled "Towards Gigayear Storage Using a Silicon-Nitride/Tungsten Based Medium".

Its abstract states: "If we want to preserve anything about the human race which can outlast the human race itself, we require a data storage medium designed to last for 1 million to 1 billion years."

Well, yes, er ... back to the technology.

The authors, involved with The Human Document Project, write: "To ensure that knowledge about human life is available for many future generations or even future lifeforms we require a form of data storage suitable for storage at extreme timescales."

The storage medium is "tungsten encapsulated by silicon nitride which, according to elevated temperature tests, will last for well over the suggested time."

Current 4TB hard drives can store data for about 10 years before the content starts decaying, the authors say. Tape will last a few decades and archival paper could last 500 years with the right environment.

The study's authors write: "A new type of storage medium is required where the longevity of the data is more important than the storage density," and this WORM-type medium should last for one million to one billion years with stored data being readable using electro-magnetic waves:

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'BILLION-YEAR DISK' to help FUTURE LIFEFORMS study us

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John Mauldin Forecast 2014 – The Human Transformation Revolution

Posted: at 8:47 pm

The End of Growth?

There is a school of thought that sees the first and second industrial revolutions as having been driven by specific innovations that are so unique and so fundamental that they are unlikely to be repeated. Where will we find any future innovation that is likely to have as much impact as the combustion engine or electricity or (pick your favorite)?

This is a widespread school of thought and is nowhere better illustrated than in the work of Dr. Robert Gordon, who is a professor of economics at Northwestern University and a Nobel laureate. I have previously written about his latest work, a papercalled Is US Economic Growth Over?

Before I audaciously suggest that he and other matriculants in his school of thought confuse theproductsof industrial revolutions with theircauses,and thus despair over the prospects for future growth, lets examine a little bit of what he actually says. (You can of course read the original paper, linked above.) To do that we can turn to an article by Benjamin Wallace-Wells that I cited inOutside the Boxlast June. He explains Robert Gordons views better than anyone I am aware of.

[T]he scope of his [Gordon's] bleakness has given him, over the past year, a newfound public profile, Wallace-Wells notes. Gordon offers us two key predictions, both discomfiting. The first pertains to the near future, when, he says, our economy will grow at less than half its average rate over the last century because of a whole raft of structural headwinds.

His second prediction is even more unsettling. He thinks the forces that drove the second industrial revolution (beginning in 1870 and originating largely in the US) were so powerful and so unique that they cannot be equaled in the future.

(A corollary view of Gordons, mentioned only indirectly in Wallace-Wellss article, is that computers and the internet and robotics and nanotech and biotech are no great shakes compared to the electric grid and internal combustion engine, as forces for economic change. Which is where he and I part company.)

Gordon thinks, in short, that we do not understood how lucky we have been, nor do we comprehend how desperately difficult our future is going to be. Quoting from Wallace-Wells:

What if everything weve come to think of as American is predicated on a freak coincidence of economic history? And what if that coincidence has run its course?

Picture this, arranged along a time line.

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John Mauldin Forecast 2014 - The Human Transformation Revolution

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Guttate psoriasis – Wikipedia, the free encyclopedia

Posted: at 8:47 pm

Guttate psoriasis Classification and external resources

Back torso lesions, 30 year old female patient

Guttate psoriasis (also known as "Eruptive psoriasis") is a type of psoriasis that presents as small (0.5-1.5cm in diameter) lesions over the upper trunk and proximal extremities; it is found frequently in young adults.[1]:410[2]:194 Guttate psoriasis is classically triggered by a bacterial infection, usually an upper respiratory tract infection.[3]:726

For some people it starts as a throat infection, or strep throat. After the throat infection has cleared up the person can feel fine for several weeks before noticing the appearance of red spots. They appear small at first, like a dry red spot which is slightly itchy. When scratched or picked the top layer of dry skin is removed, leaving dry, red skin beneath with white, dry areas marking where flakes of dry skin stop and start. In the weeks that follow the spots can grow to as much as an inch in diameter. Some of the larger ones may form a pale area in the centre which is slightly yellow. Treatment is often a mild steroid, such as hydrocortisone, but this is not always effective. Other treatment include exposing the affected area of the skin to sunlight (while avoiding sunburn). The condition often but not always clears up on its own. The guttate psoriasis can occur on any part of the body, particularly the legs, arms, torso, eyelids, back, bottom, bikini-line and neck. Generally the parts of the body most affected are seen on the arms, legs, back and torso. Enthusiastic exfoliation can lead to bleeding so care and moisturisation are important to keep the affected skin healthy.

Link:
Guttate psoriasis - Wikipedia, the free encyclopedia

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Single faulty gene causes major type 2 diabetes symptom in mice

Posted: at 8:47 pm

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New research from the US reported in the journal Diabetes, shows that the loss of just one gene in mice is enough to cause fasting hyperglycemia - a major symptom of type 2 diabetes.

In their paper, researchers from the College of Medicine at the University of Illinois at Chicago (UIC) explain how malfunctions in insulin-producing pancreatic beta cells is a common feature of type 2 diabetes.

Lead author Bellur S. Prabhakar, professor and head of microbiology and immunology at UIC, says they found that when a gene called MADD is not working properly, insulin is not released into the bloodstream. Lack of insulin means the body is unable to regulate blood sugar or glucose - a major feature of diabetes.

About 8% of Americans and more than 360 million people around the world have type 2 diabetes, a disease that in turn can lead to more serious conditions like cardiovascular disease, kidney failure, blindness, and loss of limbs.

In healthy people without diabetes, the beta cells of the pancreas release insulin into the bloodstream to help regulate blood sugar levels which rise after eating.

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No ‘brakes’ — Study finds mechanism for increased activity of oncogene in certain cancers

Posted: at 8:47 pm

PUBLIC RELEASE DATE:

6-Jan-2014

Contact: Anita Srikameswaran 412-578-9193 University of Pittsburgh Schools of the Health Sciences

PITTSBURGH, Jan. 6, 2014 The increased activation of a key oncogene in head and neck cancers could be the result of mutation and dysfunction of regulatory proteins that are supposed to keep the gene, which has the potential to cause cancer, in check, according to a new study led by researchers at the University of Pittsburgh School of Medicine. The findings, published in the early online version of the Proceedings of the National Academy of Sciences, suggest a new target for drugs to treat head and neck tumors, as well as other cancers.

Many research teams have found activation and increased signaling of a protein known as Signal Transducer and Activator of Transcription 3 (STAT3) in different kinds of cancers, and it is associated with poor prognosis, said senior author Jennifer Grandis, M.D., Distinguished Professor of Otolaryngology, Pitt School of Medicine, and director of the Head and Neck Program at the University of Pittsburgh Cancer Institute (UPCI), partner with UPMC CancerCenter. In adult tissues, STAT3 triggers the production of other proteins that promote the growth and survival of cancer cells.

"Until now, the question of why STAT3 could be hyperactivated has gone unanswered," Dr. Grandis said. "Our findings reveal a possible mechanism for this abnormal activity, which could help us develop new cancer drugs."

Noting that gene aberrations in STAT3 itself rarely occurred in head and neck cancers, she and her colleagues looked for mutations in other proteins associated with increased activity of STAT3. To be activated, STAT3 must be phosphorylated, meaning a phosphate group is added to it. Many cancer drugs work by inhibiting enzymes called kinases that encourage this process. The team focused instead on the other side of the biochemical seesaw in which enzymes called phosphatases deactivate proteins by removing phosphates.

To their surprise, they found head and neck tumors with elevated STAT3 were associated with mutations in the PTPR family of phosphatases. When they reproduced the mutations in computational and lab models, they saw that they led to dysfunction of the enzymes.

"Because the phosphatases don't work properly, phosphate groups don't get removed from STAT3 appropriately, and it stays activated," Dr. Grandis explained. "These mutations essentially get rid of the brakes that might otherwise slow or even stop cancer development."

It might be possible one day to screen tumors for mutations in the PTPR group and then treat them with drugs that inhibit STAT3's activity, she added.

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No 'brakes' -- Study finds mechanism for increased activity of oncogene in certain cancers

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Gene Patent Case Fuels U.S. Court Test of Stem Cell Right

Posted: at 8:47 pm

As scientists get closer to using embryonic stem cells in new treatments for blindness, spinal cord injuries and heart disease, a U.S. legal debate could determine who profits from that research.

Consumer Watchdog, a nonprofit advocacy group, wants an appeals court to invalidate a University of Wisconsin-Madisons patentfor stem cells derived from human embryos, saying its too similar to earlier research. The Santa Monica, California, group also says the U.S. Supreme Courts June ruling limiting ownership rights of human genes should apply to stem cells, a potentially lucrative field for medical breakthroughs.

The challenge to Wisconsin Alumni Research Foundation, the universitys licensing arm, is about whether patents help or hinder U.S. stem-cell research, which has been stymied by political debate. The consumer group says it drives up the cost of research by requiring companies and some academics to pay a licensing fee to the university.

What were asking the government to do is say WARF has no right to the patent, said Dan Ravicher, executive director Public Patent Foundation in New York, which is handling the challenge for Consumer Watchdog. Its like the government sent a check to WARF they didnt deserve.

Consumer Watchdog lost a challenge at the U.S. Patent and Trademark Office in January 2013. It wants the Court of Appeals for the Federal Circuit in Washington to review that decision and consider new arguments based on the Supreme Courts finding that genes -- like stem cells -- are a natural material that cant be patented. Beyond the science question, the case has become a flashpoint over how far members of the public can go to invalidate patents on policy grounds.

While the patent expires in April 2015 and the university has other stem-cell-related patents, Consumer Watchdog is continuing a six-year battle to invalidate it because stem-cell research is starting to get some traction into therapeutic uses, Ravicher said.

The promise of embryonic stem cells is to create or repair tissues and organs using material taken from eggs fertilized in the laboratory. The cells created can be replicated indefinitely, and with the right biological cues, may aid in treating damaged heart tissue and spinal cords, or generate therapies for diabetes and cancer. Companies like StemCells Inc. (STEM) and Advanced Cell Technology Inc. are testing therapies to treat macular degeneration, a cause of blindness.

The next paradigm shift in medicine will be advances in cell therapy -- its under way, said Jason Kolbert, senior biotechnology analyst with Maxim Group LLC in New York. He said pharmaceutical makers such as Teva Pharmaceutical Industries Ltd. (TEVA) of Petach Tikva, Israel, and Pfizer (PFE) Inc. of New York are working with stem-cell researchers on new therapies.

Stem-cell science in the U.S. was curbed in 2001 when then-President George W. Bush issued an executive order limiting research to existing cell lines amid controversy over human embryo destruction, even though they were never in a womans uterus. President Barack Obama reversed that order in 2009.

Some scientists have avoided the public debate by using adult cells to find the unlimited potential they have in embryonic cells.

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Gene Patent Case Fuels U.S. Court Test of Stem Cell Right

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Gene Mutation Increases Certain Health Risks For Blacks, Study Finds

Posted: at 8:47 pm

A study that made its way from the Middle East to New York has identified a gene mutation found in those of African descent, shedding some light on why a significant number of black people are predisposed to certain diseases. NY1's Erin Billups filed the following report.

Too much fat or triglycerides in the blood stream leads to heart disease, type 2 diabetes, obesity and stroke are all diseases that are are found at higher rates among people of African ancestry.

Ronald Crystal, chair of Genetic Medicine at Weill Cornell Medical College, says they've found a genetic variation they believe is partially responsible.

"When we looked at the medical literature we found that it had been discovered 20 years ago but was thought to be a very rare mutation," says Dr. Crystal.

It turned out this mutation of a protein gene called Apo-E was relatively common among people native to the Middle Eastern country Qatar.

"Apo-E is a gene that we all have. It codes for a protein that helps us carry fats in our blood," explains Dr. Crystal.

The mutation they discovered in Qatari with African ancestry increases the amount of fat in the blood.

"So we then looked in Africans, and we found that in fact the mutation was pretty common in the Africans as well. Then we transferred the concept to New York. And it turns out it was pretty common in African Americans," says Dr. Crystal.

They looked at the DNA of 2,000 black New Yorkers, the largest study of the three.

"What it means is that four out of 100 New York African Americans have a mutation that will increase the levels of fats, specifically triglycerides in their blood. It's a mild increase, and it's only one little part of the whole puzzle," explains Dr. Crystal.

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Gene Mutation Increases Certain Health Risks For Blacks, Study Finds

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Page 4,160«..10 20..4,1594,1604,161 4,162..4,170 4,180..»

Category Archives: Transhuman News

DNA analysis now helps solve lesser crimes, too

Study: ‘Jumping genes’ linked to schizophrenia

Discovery spotlights key role of mystery RNA modification in cells

‘BILLION-YEAR DISK’ to help FUTURE LIFEFORMS study us

John Mauldin Forecast 2014 – The Human Transformation Revolution

Guttate psoriasis – Wikipedia, the free encyclopedia

Single faulty gene causes major type 2 diabetes symptom in mice

No ‘brakes’ — Study finds mechanism for increased activity of oncogene in certain cancers

Gene Patent Case Fuels U.S. Court Test of Stem Cell Right

Gene Mutation Increases Certain Health Risks For Blacks, Study Finds

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