Biosingularity

Archive for December 2005

The p53 tumor suppressor plays a critical role in cancer formation, and many anticancer strategies aim to activate p53 in order to curb tumor formation. Mdm2 is a key inhibitor of p53 and therefore an attractive target to modulate p53 activity in cells. However, conflicting evidence exists regarding whether or not p53-mediated tumor suppression comes at the cost of accelerated aging.

In the January 1 issue of Genes & Development, Dr. Mary Ellen Perry and colleagues validate the p53 inhibitor, Mdm2, as a promising target for cancer therapies.

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The activity of connections among brain cells significantly affects levels of the toxic protein beta-amyloid (Aß) that is a major cause of Alzheimer’s disease (AD), researchers have found. Aß is produced by the cleavage of amyloid precursor protein (APP) within brain cells.

Findings suggest that the kind of mental activity people practice or drugs they might take for depression or anxiety could affect their AD risk or the disease progression.
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Researchers using a customized atomic force microscope (AFM) have discovered new evidence for how the fibrous scaffolding within our cells, which is made of the protein actin, responds to obstacles in its environment.

The discovery demonstrates a technique for tracking a cell’s growth history, and if it proves valid outside of the laboratory, researchers may one day look for actin-growth clues while tracking the pathways of spreading cancers, immune cells, and other free-moving cells that crawl throughout the body.
AFM.jpg
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Like boxers wearied by a 15-round bout, the immune system’s CD8 T cells eventually become “exhausted” in their battle against persistent viral infection, and less effective in fighting the disease.

In a study to be published Dec. 28 on the journal Nature’s website, researchers at Dana-Farber Cancer Institute and Emory University have traced the problem to a gene that turns off the infection-fighting drive of CD8 T cells in mice. The discovery raises the possibility that CD8 cell exhaustion can be reversed in human patients, reinvigorating the immune system’s defenses against chronic viral infections ranging from hepatitis to HIV, the virus that causes AIDS.

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The world’s deadliest malaria parasite, Plasmodium falciparum, sneaks past the human immune system with the help of a wardrobe of invisibility cloaks. If a person’s immune cells learn to recognize one of the parasite’s many camouflage proteins, the surviving invaders can swap disguises and slip away again to cause more damage. Malaria kills an estimated 2.7 million people annually worldwide, 75 percent of them children in Africa.

Howard Hughes Medical Institute (HHMI) international research scholars in Australia have determined how P. falciparum can turn on one cloaking gene and keep dozens of others silent until each is needed in turn. Their findings, published in the December 28, 2005, issue of Nature, reveal the mechanism of action of the genetic machinery thought to be the key to the parasite’s survival.

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Howard Hughes Medical Institute researchers have discovered a molecular link between a high-fat, Western-style diet, and the onset of type 2 diabetes. In studies in mice, the scientists showed that a high-fat diet disrupts insulin production, resulting in the classic signs of type 2 diabetes.

In an article published in the December 29, 2005, issue of the journal Cell, the researchers report that knocking out a single gene encoding the enzyme GnT-4a glycosyltransferase (GnT-4a ) disrupts insulin production. Importantly, the scientists showed that a high-fat diet suppresses the activity of GnT-4a and leads to type 2 diabetes due to failure of the pancreatic beta cells.

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An international consortium of researchers led by the University of Manchester has cracked the gene code behind a key family of fungi, which includes both the leading cause of death in leukaemia and bone marrow transplant patients and an essential ingredient of soy sauce.

The ‘genome sequences’ or genetic maps for the fungi Aspergillus fumigatus, Aspergillus nidulans and Aspergillus oryzae are published on 22 December in Nature magazine. Despite being from the same fungal family, they have been found to be as genetically different as fish and man.

Aspergillus.jpg

Cleistothecium – sexual spore container, false coloured from Aspergillus nidulans. (Courtesy of Professor Rheinhard Fischer, Institut für Angewandte Biowissenschaften Abt. für Angewandte Mikrobiologie der Universität Karlsruh, with whom copyright remains)

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A UC Riverside-led research team has found that as some populations of an organism evolve a longer lifespan, they do so by increasing only that segment of the lifespan that contributes to “fitness” – the relative ability of an individual to contribute offspring to the next generation. Study results appear Dec. 27 in the online edition of the Public Library of Science – Biology.

The study supports the controversial hypothesis that natural selection – the process in nature by which only organisms best adapted to their environment tend to survive and pass on their genetic characters in increasing numbers to succeeding generations – introduces changes in only a specific segment of an organism’s lifespan.

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In a study to be published in the January 2006 issue of Nature Biotechnology, researchers led by a team of scientists at Memorial Sloan-Kettering Cancer Center have devised a novel strategy that uses stem cell-based gene therapy and RNA interference to genetically reverse sickle cell disease (SCD) in human cells. This research is the first to demonstrate a way to genetically correct this debilitating blood disease using RNA interference technology.
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Despite the prevailing belief that adult brain cells don’t grow, a researcher at MIT’s Picower Institute for Learning and Memory reports in the Dec. 27 issue of Public Library of Science (PLoS) Biology that structural remodeling of neurons does in fact occur in mature brains.

This finding means that it may one day be possible to grow new cells to replace ones damaged by disease or spinal cord injury, such as the one that paralyzed the late actor Christopher Reeve.

Brain.jpg

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A nice article in New York Times by Gina Kolata discussing the recent advances in understanding cancer genes and potential cures.

Read the story here

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Researchers recently discovered that the sea lamprey, a modern representative of ancient jawless vertebrates, fights invading pathogens by generating up to 100 trillion unique receptors. These receptors, referred to as VLRs, are proteins and function like antibodies and T-cell receptors, sentinels of the immune system in all jawed vertebrates, including humans.

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Genes that control the timing of organ formation during development also control timing of aging and death, and provide evidence of a biological timing mechanism for aging, Yale researchers report in the journal Science.

“Although there is a large variation in lifespan from species to species, there are genetic aspects to the processes of development and aging,” said Frank Slack, associate professor of Molecular, Cellular and Developmental Biology and senior author of the paper. “We used the simple, but genetically well-studied, C. elegans worm and found genes that are directly involved in determination of lifespan. Humans have genes that are nearly identical.”

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Using tiny semiconductor crystals, biological probes and a laser, Johns Hopkins University engineers have developed a new method of finding specific sequences of DNA by making them light up beneath a microscope. The researchers, who say the technique will have important uses in medical research, demonstrated its potential in their lab by detecting a sample of DNA containing a mutation linked to ovarian cancer.

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You might expect that a stronger cage is always better. But the power of a new chemical cage announced this week lies in its weakness: It’s about 100 times more efficient at releasing its prisoner than its widely used counterparts. The flimsy molecular pen may help map the brain’s chemical circuitry and decipher the signals that control the beating heart.

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Need a skin graft? A new trachea? A heart patch? Turn on your printer, and let it spit one out. A group of researchers hope printers’ whirs and buzzes will soon be saving lives.
Researchers at three universities have developed bio-ink and bio-paper that could make so-called organ printing a reality. So far, they’ve made tubes similar to human blood vessels and sheets of heart muscle cells, printed in three dimensions on a special printer.

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The Johns Hopkins scientists who first created “mighty mice” have developed, with pharmaceutical company Wyeth and the biotechnology firm MetaMorphix, an agent that’s more effective at increasing muscle mass in mice than a related potential treatment for muscular dystrophy now in clinical trials.

The new agent is a version of a cellular docking point for the muscle-limiting protein myostatin. In mice, just two weekly injections of the new agent triggered a 60 percent increase in muscle size, the researchers report in the Proceedings of the National Academy of Sciences, published online Dec. 5 and available publicly through the journal’s website.
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A team of scientists from the Gladstone Institute of Cardiovascular Disease (GICD) has identified a key factor in heart development that could help advance gene therapy for treating cardiac disorders.

The findings could help cardiac stem cell researchers one day develop strategies for gene and cell- mediated cardiac therapies.

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The ubiquitous and usually harmless E. coli bacterium, which has one-seventh the number of genes as a human, has more than 1,000 of them involved in metabolism and metabolic regulation. Activation of random combinations of these genes would theoretically be capable of generating a huge variety of internal states; however, researchers at UCSD will report in the Dec. 27 issue of Proceedings of the National Academy of Sciences (PNAS) that Escherichia coli doesn’t gamble with its metabolism. In a surprise about E. coli that may offer clues about how human cells operate, the PNAS paper reports that only a handful of dominant metabolic states are found in E. coli when it is “grown” in 15,580 different environments in computer simulations.
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Researchers at Columbia University Medical Center have identified an inherent feature of stem and progenitor cells that may promote initiation and progression of cancerous tumors.

In a study published in the December issue of Cancer Cell, the team showed that stem and progenitor cells are susceptible to a specific error during cell division that can result in severe chromosomal defects. This susceptibility may explain how a tumor-initiating cell, also known as a cancer stem cell, arises from a normal cell. It may also explain how a cancer stem cell acquires additional mutations that increase tumor malignancy.

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Work on the world’s first human-made species is well under way at a research complex in Rockville, Md., and scientists in Canada have been quietly conducting experiments to help bring such a creature to life.

Robert Holt, head of sequencing for the Genome Science Centre at the University of British Columbia, is leading efforts at his Vancouver lab to play a key role in the production of the first synthetic life form — a microbe made from scratch.

The project is being spearheaded by U.S. scientist Craig Venter, who gained fame in his former job as head of Celera Genomics, which completed a privately-owned map of the human genome in 2000.
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Virtual reality that allows doctors to visualise the heart in three dimensions could help in the diagnosis of heart conditions. A pilot study published today in the open access journal Cardiovascular Ultrasound reveals that doctors can diagnose heart conditions quickly and easily from virtual three-dimensional animated images or ’holograms’ of the heart. Three-dimensional (3D) holograms allow doctors to ’dive’ into the beating heart and see interior parts of the organ.
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Reminiscent of the 1966 sci-fi thriller Fantastic Voyage, where a surgical team is miniaturized and injected into a dying man, researchers from Harvard Medical School have used injectable self-assembling peptide nanofibers loaded with the pro-survival factor PDGF-BB to protect rat cardiomyocytes from injury and subsequent heart failure.
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Mayo Clinic researchers have challenged the conventional teaching about a common cancer trait and in doing so, discovered how cells are naturally “cancer proofed.”

The researchers investigated aneuploidy (AN-u-ploy-dee), the state in which a cell has an abnormal number of chromosomes that creates cellular instability, giving rise to tumors. They discovered two key proteins that help prevent aneuploidy, and also found how the proteins work to “cancer proof” a cell: by preventing premature segregation of duplicated chromosomes during (nuclear) cell division.

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Researchers have known for some time that a long, fibrous coil grown by a single-cell protozoan is, gram for gram, more powerful than a car engine. Now, researchers at Whitehead Institute have found that this coil is far stronger than previously thought. In addition, the researchers have discovered clues into the mechanism behind this microscopic powerhouse.

Cell based nano machine.jpg

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Researchers suggest that the traditional view of cancer as a group of diseases with markedly different biological properties arising from a series of alterations within a cell’s nuclear DNA may have to give way to a more complicated view. In the January issue of Nature Reviews Genetics, available online Dec. 21,scientists suggest that cancers instead begin with “epigenetic” alterations to stem cells.
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A gene therapy research team at Cedars-Sinai Medical Center has developed a new method of signaling therapeutic genes to turn “off” or “on,” a mechanism that could enable scientists to fine-tune genetic- and stem cell-based therapies so that they are safer, more controllable and more effective.

Although other similar signaling systems have been developed, the Cedars-Sinai research is the first to give physicians the flexibility to arbitrarily turn the gene expression on or off even in the presence of an immune response to adenovirus, as would be present in most patients undergoing clinical trials. This has been a major obstacle in bringing the testing of genetic therapies to humans in a clinical setting.
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In experiments with mice, scientists from Johns Hopkins’ Institute for Cell Engineering have discovered the steps required to integrate new neurons into the brain’s existing operations.

For more than a century, scientists thought the adult brain could only lose nerve cells, not gain them, but in fact, new neurons do form during adulthood in all mammals, including humans, and become a working part of the adult brain in mice at the very least.

In the first study to show how these “baby” neurons are integrated into the brain’s existing networks, the Johns Hopkins researchers show that a brain chemical called GABA readies baby neurons to make connections to old ones. The discovery is described in the Dec. 11 advance online section of Nature.
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Chromosome ends, or telomeres, are repetitive stretches of DNA that protect chromosomes in much the same way as plastic tips on shoelaces prevent the fabric from fraying. Each time a cell divides, its chromosome ends get a little shorter, and eventually the cell can no longer divide because its critical genetic information is exposed. In stem cells, however, a protein called telomerase normally maintains the telomeres’ length, allowing the cells to divide indefinitely.

Now, the Hopkins researchers report that mice engineered to have just half the normal amount of telomerase can’t maintain their stem cells’ chromosome ends, showing that a little telomerase isn’t enough. In these “half-telomerase” mice, their telomeres shortened over time, bringing an early demise to stem cells that replenish the blood supply, immune system and intestine, the researchers report. Moreover, offspring of these mice bred to have normal levels of telomerase still exhibited early loss of stem cells, the researchers report in the Dec. 16 issue of Cell.
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For many years, scientists thought gene activity was relatively straightforward: Genes were transcribed into messenger RNA, which was processed and translated into the proteins of the body. Certainly, there were many factors governing the transcription process, but gene control happened at the level of the DNA

In the past few years, however, evidence for a more nuanced understanding of the total genetic system has steadily accumulated. Researchers at The Wistar Institute and elsewhere have been teasing out the details of a process called RNA editing, in which messenger RNA sequence is altered after transcription by editing enzymes, so that a single gene can produce a number of related but distinct variant proteins. Most recently, scientists have discovered an extensive family of small molecules called microRNAs, or miRNAs, that appear to target and inactivate particular messenger RNAs. This targeted gene silencing is now seen as one of the body’s primary strategies for regulating its genome.
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A common additive found in food and cosmetics has been found to inhibit the activity of sirtuins, enzymes associated with lifespan control in yeast and other organisms, according to a new study led by researchers at the University of California, Berkeley.

The study, to be published Friday, Dec. 16, in the online journal Public Library of Science (PLoS) Genetics, found that in lab tests, dihydrocoumarin (DHC), a compound found naturally in sweet clover and synthetically manufactured for use in foods and cosmetics, inhibited the activity of Sir2p and SIRT1, forms of sirtuin found in yeast and humans, respectively.
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University of North Carolina at Chapel Hill scientists have demonstrated in a living organism that cancers may cause surrounding supportive cells to evolve and ultimately promote cancer growth.

The new research offers what is believed to be the first evidence that mutations within cancer cells can signal surrounding tissue cells to alter their molecular composition in ways that promote tumor growth and proliferation. Moreover, the findings also suggest that cell mutations that promote cancer progression may arise in cells other than the predominant cancer cell.
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Scientists have finally managed to take an extensive look at the genetic makeup of one of the most famous beasts of the last ice age. This week, an international team of researchers reports using a new technology to sequence a staggering 13 million basepairs of both nuclear and mitochondrial DNA from a 27,000-year-old frozen Siberian mammoth. Also this week, another team reports using a souped-up version of more conventional methods to sequence a mammoth’s entire mitochondrial genome.

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Uncoiled strands of DNA, organized in precise patterns, one day might become the backbone of biologically based electronics and medical devices, according to L. James Lee, professor of chemical and biomolecular engineering at Ohio State University. His team of scientists has made the first step in creating the nanowires of the future by uncoiling and organising long strands of DNA.

In the early online edition of the Proceedings of the National Academy of Sciences, Lee and postdoctoral researcher Jingjiao Guan describe how they used a tiny rubber comb to pull DNA strands from drops of water and stamp them onto glass chips.
Other labs have formed very simple structures with DNA, and those are now used in devices for gene testing and medical diagnostics. But Lee and Guan are the first to coax strands of DNA into structures that are at once so orderly and so complex that they resemble stitches on a quilt.
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FDA approved Nexavar, a drug that officials described as “a major advance” in treating kidney cancer.
The manufacturer of Nexavar, Bayer, used X-rays to determine that the drug doubled the time, to 167 days from 84, before tumors grew substantially in number or size, a finding called “progression-free survival.”
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New research on living neurons has clarified how the brain refreshes the supply of molecules it needs to make new memories.
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Evolution has been the foundation and guiding theory of biology since Darwin gave the theory its proper scientific debut in 1859. But Darwin probably never dreamed that researchers in 2005 would still be uncovering new details about the nuts and bolts of his theory — how does evolution actually work in the world of influenza genes and chimpanzee genes and stickleback fish armor? Studies that follow evolution in action claim top honors as the Breakthrough of the Year, named by Science and its publisher AAAS, the nonprofit science society.
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Neuroscientists at Princeton University have developed a new way of tracking people’s mental state as they think back to previous events — a process that has been described as “mental time travel.”

The findings, detailed in the Dec. 23 issue of Science, will aid efforts to learn more about how people mine the recesses of memory and could have a wide-ranging impact in the field of neuroscience, including studies of brain disorders such as Alzheimer’s disease.
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A cancer-fighting virus has eliminated malignant brain tumors and prolonged survival in mice with a single injection.

Reporting in the journal Cancer Research, Canadian scientists from Calgary and London, Ontario have shown for the first time that myxoma virus, a poxvirus, kills human brain tumors in mice.
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A dense bed of light-sensitive bacteria has been developed as a unique kind of photographic film. Although it takes 4 hours to take a picture and only works in red light, it also delivers extremely high resolution.

The “living camera” uses light to switch on genes in a genetically modified bacterium that then cause an image-recording chemical to darken. The bacteria are tiny, allowing the sensor to deliver a resolution of 100 megapixels per square inch.
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Fruit flies can live significantly longer, and remain healthy, when activity of the fly version of the tumor-suppressing protein p53 is reduced in nerve cells. Published in Current Biology, the results shed important new light on the role this “protector of the genome” plays in aging and point to p53 as a viable target for anti-aging drugs.

The p53 gene plays a critical role in the body. It protects human cells by producing a protein that triggers apoptosis, or cell suicide, when DNA is badly damaged. This prevents the spread of genetic mutations and the formation of cancer. When the p53 gene is damaged or missing, cancer may result. In fact, more than 50 percent of human cancers carry p53 mutations.
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Researchers at the University of Washington have found a genetic pathway linking nutrient response and the aging process, they report in the Nov. 18 issue of the journal Science. Scientists have long known that dramatically reducing food intake boosts the lifespan of model organisms such as mice, but the new results point to a possible mechanism through which drastic calorie restriction affects aging.
As scientists learn more about the biochemical processes that affect lifespan, they might one day be able to target those processes to reduce the effects of age-related diseases like heart disease or diabetes.
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A counterintuitive experiment has resulted in one of the longest recorded life-span extensions in any organism and opened a new door for anti-aging research in humans.

Scientists have known for several years that an extra copy of the SIR2 gene can promote longevity in yeast, worms and fruit flies. That finding was covered widely and incorporated into anti-aging drug development programs at several biotechnology companies. Now, molecular geneticists at the University of Southern California suggest that SIR2 instead promotes aging.
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The researchers and scientists at Rensselaer Polytechnic Institute and the University of Illinois, Urbana-Champaign have achieved a major breakthrough in utilizing nanotechnology. The team of researchers has been successful in combining a DNA-based enzyme with a carbon nanotube; they have successfully combined the DNA based enzyme and have converting Carbon Nanotubes into RNA-Degrading Nano-Enzymes. Thus they have created a nanoscale device capable of degrading specific sequences of RNA.

Such a device is capable of providing a novel approach to treat cancer. This device would be quite a beneficial instrument in cancer therapy as it would be enabling researchers to block a cancer cell’s production of proteins needed to maintain a cancerous state.

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A breakthrough in stem cell research could eventually lead to cures for debilitating diseases such as Alzheimer’s or Parkinson’s. According to the latest issue of the Proceedings of National Academy of Sciences, researchers now firmly believe that one day stem cells, by transmuting into healthy tissue cells to replace rotten ones, could become a remedy for the brain diseases.
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I like to provide some idea on how I choose the stories posted in this blog.

First, I try to find discoveries that are real breakthroughs and not just incremental increases in knowledge, typically published in high profile, high impact science journals.

Second, I limit my blogs to several key technological areas, which I believe will have the greatest impact towards biosingularity, such as: Tissue, genetic and gadget oriented bioengineering, application of nanotechnology to biology, programming biological systems (stem cells, synthetic biology, biohacking, neuroprogramming).

I also focus on general medical and biological advances on understanding genetic code, stem cell biology, aging, immune system, nervous system, infectious organisms and cancer. I will also less frequently I will also post other major breakthroughs in other medical fields.

I believe breakthroughs in these fields will help us better to decode the biological programs and provide tools to reprogram or engineer biological systems. I also have better knowledge in these topics, which allows me to better judge the importance of the advances.

Of course as new technologies lead to new fields I will expand the categories that will encompass wider range of biological topics.

In addition, I hope to post both my commentaries or opinions regarding biological advances and about issues such as human life extension and transhumanism.

Using a new form of microscopy to penetrate living lymph nodes, UCSF scientists have for the first time viewed immune cells at work, helping clarify how T cells control autoimmunity.

The technique, known as two-photon laser-scanning microscopy, was able to focus deep within the lymph node of a diabetic mouse, allowing the researchers to show that immune cells known as T regulatory, or Treg, cells control the destructive action of rogue autoimmune cells when each of the two cell types interact with a third kind of cell.
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A team of scientists at Yale University has completed the first comprehensive map of the proteins and kinase signaling network that controls how cells of higher organisms operate, according to a report this week in the journal Nature.

The study is a breakthrough in understanding mechanisms of how proteins operate in different cell types under the control of master regulator molecules called protein kinases. Although protein kinases are already important targets of cancer drugs including Gleevec and Herceptin, until recently, it has been difficult to identify the proteins regulated by the kinases.
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Dr. Ralph Weissleder at Harvard Medical School and his colleagues are developing nanoparticles that can emit either magnetic or optical signals. The hope is to coat these nanoparticles with compounds that help guide their way toward specific cells. Such coated nanoparticles could then single out tumor cells to help physicians detect where they are in the body, even if they are few in number and otherwise unnoticeable.

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Researchers at the University of Utah have discovered that when a gene called smedwi-2 is silenced in the adult stem cells of planarians, the quarter-inch long worm is unable to carry out a biological process that has mystified scientists for centuries: regeneration.

Elimination of smedwi-2 not only leads to an inability to mount a regenerative response after amputation, but also to the eventual demise of unamputated animals along a reproducible series of events, that is, regression of the head tip, curling of the body and tissue disintegration. These defects are very similar to what is observed after the planarian stem cells are destroyed by lethal doses of irradiation. The key difference, however, is that the irradiation-like defects observed in animals devoid of smedwi-2 occur even though the stem cells are still present in the organism.
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