Oil droplets that creep purposefully through their watery environment, metabolize fuel, sense their surroundings and perhaps even replicate — could these be precursors to life? That's the claim of a chemist with a controversial approach to modelling how Earth's first organisms scraped themselves together.
Theories about how life started range from fortuitous chemistry around hydrothermal vents on the sea floor to the delivery of precursor molecules from outer space. But there is little hope of finding geological evidence for this momentous event: Earth's crust is continuously being recycled, with the oldest known rocks dating to only 3.8 billion years ago. By that point, life was flourishing and relatively complex.
For more information contact coordinator@nthrys.com
2/28/2011
2/25/2011
Researchers describe the pump that bacteria use to resist drugs
A research team led by Edward Yu of Iowa State University and the Ames Laboratory has identified and described two parts of the three-part system that pumps toxins from bacteria and allows them to resist antibiotics.The discoveries are published in the Feb. 24 issue of the journal Nature.
The paper describes the co-crystal structure of two parts of the three-part efflux pump that recognizes and removes heavy metal toxins from bacteria. A research team led by Yu – an Iowa State associate professor of physics and astronomy, of chemistry, of biochemistry, biophysics and molecular biology and an associate of the U.S. Department of Energy's Ames Laboratory – is working to discover the assembled structure of the entire three-part efflux pump.
Yu said a better understanding of how the three parts work together could help medical researchers find ways to restore the effectiveness of antibiotics.
"These pumps have to assemble together in order to pump out heavy metals and antibiotics," Yu said. "Researchers may be able to use these findings to design an inhibitor so the pump can't be assembled and can't work."
Yu and his research team described the first part of the pump – the inner membrane transporter known as CusA – in the Sept. 23, 2010, issue of the journal Nature.
The current paper describes the inner membrane transporter and how it interacts with the pump's middle adapter, known as CusB. The two parts together are known as the CusBA complex.
The research was supported by grants from the National Institutes of Health. In addition to Yu, the research team includes Robert Jernigan, an Iowa State professor of biochemistry, biophysics and molecular biology and director of Iowa State's Laurence H. Baker Center for Bioinformatics and Biological Statistics; Kanagalaghatta Rajashankar, the operations team leader for the Northeastern Collaborative Access Team facility at Argonne National Laboratory in Argonne, Ill., that's managed by Cornell University in Ithaca, N.Y.; Iowa State post-doctoral researchers Chih-Chia Su and Feng Long; and Iowa State graduate student Michael Zimmermann.
For more information contact coordinator@nthrys.com
The paper describes the co-crystal structure of two parts of the three-part efflux pump that recognizes and removes heavy metal toxins from bacteria. A research team led by Yu – an Iowa State associate professor of physics and astronomy, of chemistry, of biochemistry, biophysics and molecular biology and an associate of the U.S. Department of Energy's Ames Laboratory – is working to discover the assembled structure of the entire three-part efflux pump.
Yu said a better understanding of how the three parts work together could help medical researchers find ways to restore the effectiveness of antibiotics.
"These pumps have to assemble together in order to pump out heavy metals and antibiotics," Yu said. "Researchers may be able to use these findings to design an inhibitor so the pump can't be assembled and can't work."
Yu and his research team described the first part of the pump – the inner membrane transporter known as CusA – in the Sept. 23, 2010, issue of the journal Nature.
The current paper describes the inner membrane transporter and how it interacts with the pump's middle adapter, known as CusB. The two parts together are known as the CusBA complex.
The research was supported by grants from the National Institutes of Health. In addition to Yu, the research team includes Robert Jernigan, an Iowa State professor of biochemistry, biophysics and molecular biology and director of Iowa State's Laurence H. Baker Center for Bioinformatics and Biological Statistics; Kanagalaghatta Rajashankar, the operations team leader for the Northeastern Collaborative Access Team facility at Argonne National Laboratory in Argonne, Ill., that's managed by Cornell University in Ithaca, N.Y.; Iowa State post-doctoral researchers Chih-Chia Su and Feng Long; and Iowa State graduate student Michael Zimmermann.
For more information contact coordinator@nthrys.com
Stop and go: How the cell deals with transcriptional roadblocks
Gene transcription is central to cell function, as it converts the information stored in the DNA into RNA molecules of defined sequence, which then program protein synthesis. The enzyme RNA polymerase II (Pol II) is responsible for this genetic readout, but is prone to transcriptional arrest.The biochemist Professor Patrick Cramer, Director of LMU's Genzentrum, and his research associate Dr. Alan Cheung have now shown for the first time – and captured on film -- what happens when Pol II arrests at a "roadblock". They were even able to observe how transcript is reactivated. Reactivation of arrested transcriptional complexes is a normal part of the readout process, and is therefore of fundamental significance in all cells. Indeed, as Patrick Cramer points out, "It is also utilized to regulate gene activity in stem and tumor cells." (Nature online, 23 February 2011)
For more information contact coordinator@nthrys.com
For more information contact coordinator@nthrys.com
Just like cars, developmental genes have more than 1 way to stop
There's more than one way to silence gene activity, according to a Michigan State University researcher.
Downregulating activity is how healthy genes should shift out of their development cycle. The results, published in this week's Current Biology, discuss how specific repressor proteins – which researchers have named Hairy and Knirps – slow genes during development and how the process is comparable to slowing down a car, says molecular biologist David Arnosti.
The binding of repressor proteins to DNA provides a molecular switch for such regulation. Although the two types of protein have been identified as silencers of gene expression, each one uses a distinct molecular mechanism to halt the process, said Arnosti, director of MSU's Gene Expression in Disease Development initiative.
These mechanisms may hold the keys to explaining how diseases, such as cancer, diabetes and arthritis can be traced to genes that are unable to shift gears properly and can't stop, Arnosti said.
"In automotive terms, a driver can either brake or downshift the transmission to achieve the same result," said Arnosti, who published the paper with Li M. Li, a former MSU doctoral student now working at the University of California, Berkeley. "Similarly, short-range and long-range repressor proteins both interfere with the basic gene expression machinery, but in different ways."
In sequencing the human genome, scientists have assembled a parts list and can point to genes that play a part in disease. Through Li's and Arnosti's research, however, scientists can now begin to see how these genes are regulated through special mechanisms, helping show how an entire organism's genes are controlled.
"Mechanistic studies such as this are giving us the assembly instructions for the genome," Arnosti said. "Basically, it's giving us a way to read genomic control instructions."
Arnosti's research involved fruit flies, which have more genetic similarities to humans than was once thought. Based on these similarities, the team's research could soon lead to advances in human medicine.
"We like to say that fruit flies are like little people with wings; they have the same basic genetic nuts and bolts, including genetic switches and proteins," Arnosti said. "While our work is the first of its kind, it is only a small step for other scientists to begin conducting these same studies on human genes. With regards to disease, this study gives us the basic tools to look at genes in a disease state and understand what is going wrong at the genetic level."
For more information contact coordinator@nthrys.com
Downregulating activity is how healthy genes should shift out of their development cycle. The results, published in this week's Current Biology, discuss how specific repressor proteins – which researchers have named Hairy and Knirps – slow genes during development and how the process is comparable to slowing down a car, says molecular biologist David Arnosti.
The binding of repressor proteins to DNA provides a molecular switch for such regulation. Although the two types of protein have been identified as silencers of gene expression, each one uses a distinct molecular mechanism to halt the process, said Arnosti, director of MSU's Gene Expression in Disease Development initiative.
These mechanisms may hold the keys to explaining how diseases, such as cancer, diabetes and arthritis can be traced to genes that are unable to shift gears properly and can't stop, Arnosti said.
"In automotive terms, a driver can either brake or downshift the transmission to achieve the same result," said Arnosti, who published the paper with Li M. Li, a former MSU doctoral student now working at the University of California, Berkeley. "Similarly, short-range and long-range repressor proteins both interfere with the basic gene expression machinery, but in different ways."
In sequencing the human genome, scientists have assembled a parts list and can point to genes that play a part in disease. Through Li's and Arnosti's research, however, scientists can now begin to see how these genes are regulated through special mechanisms, helping show how an entire organism's genes are controlled.
"Mechanistic studies such as this are giving us the assembly instructions for the genome," Arnosti said. "Basically, it's giving us a way to read genomic control instructions."
Arnosti's research involved fruit flies, which have more genetic similarities to humans than was once thought. Based on these similarities, the team's research could soon lead to advances in human medicine.
"We like to say that fruit flies are like little people with wings; they have the same basic genetic nuts and bolts, including genetic switches and proteins," Arnosti said. "While our work is the first of its kind, it is only a small step for other scientists to begin conducting these same studies on human genes. With regards to disease, this study gives us the basic tools to look at genes in a disease state and understand what is going wrong at the genetic level."
For more information contact coordinator@nthrys.com
Nanoparticles help improve survival after blood loss
Scientists have used tiny particles called nanoparticles to improve survival after life-threatening blood loss.
The advance by scientists at Albert Einstein College of Medicine of Yeshiva University could improve battlefield and trauma care.
Nanoparticles containing nitric oxide (NO) were infused into the bloodstream of hamsters, where they helped maintain blood circulation and protect vital organs.
"The new nanomedicine was developed to address the need for better field treatments for massive human blood loss, which can cause cardiovascular collapse, also known as hemorrhagic shock. This potentially fatal condition is best treated with infusions of refrigerated blood and other fluids. But such treatments are limited to emergency rooms or trauma centers.
"It is highly impractical to pack these supplies for use in rural emergencies, mass-casualty disasters or on the battlefield," said coauthor Joel Friedman, professor of physiology and medicine and of medicine and the Young Men's Division Chair in Physiology at Einstein.
"Our nanoparticle therapy may offer the potential for saving lives in those situations. It's lightweight and compact and doesn't require refrigeration."
For more information contact coordinator@nthrys.com
The advance by scientists at Albert Einstein College of Medicine of Yeshiva University could improve battlefield and trauma care.
Nanoparticles containing nitric oxide (NO) were infused into the bloodstream of hamsters, where they helped maintain blood circulation and protect vital organs.
"The new nanomedicine was developed to address the need for better field treatments for massive human blood loss, which can cause cardiovascular collapse, also known as hemorrhagic shock. This potentially fatal condition is best treated with infusions of refrigerated blood and other fluids. But such treatments are limited to emergency rooms or trauma centers.
"It is highly impractical to pack these supplies for use in rural emergencies, mass-casualty disasters or on the battlefield," said coauthor Joel Friedman, professor of physiology and medicine and of medicine and the Young Men's Division Chair in Physiology at Einstein.
"Our nanoparticle therapy may offer the potential for saving lives in those situations. It's lightweight and compact and doesn't require refrigeration."
For more information contact coordinator@nthrys.com
2/24/2011
New 'thunder-thighs' dinosaur discovered
A new dinosaur named Brontomerus mcintoshi, or "thunder-thighs" after its enormously powerful thigh muscles, has been discovered in Utah, USA. The new species is described in a paper recently published in the journal Acta Palaeontologica Polonica by an international team of scientists from the U.K. and the U.S.
A member of the long-necked sauropod group of dinosaurs which includes Diplodocus and Brachiosaurus, Brontomerus may have used its powerful thighs as a weapon to kick predators, or to help travel over rough, hilly terrain. Brontomerus lived about 110 million years ago, during the Early Cretaceous Period, and probably had to contend with fierce "raptors" such as Deinonychus and Utahraptor.
The fossilised bones of two specimens of Brontomerus mcintoshi – an adult and a juvenile – were rescued from a previously looted and damaged quarry in eastern Utah by researchers from the Sam Noble Museum. Paleontologists speculate that the larger specimen is the mother of the younger and would have weighed around 6 tons, about the size of a large elephant, and measured 14 meters in length. At a third of the size, the smaller specimen would have weighed about 200 kg, the size of a pony, and been 4.5 m long.
The authors classified the new genus based on an incomplete skeleton including bones from the shoulder, hip, ribs, vertebrae and some unidentifiable fragments. They used the bones to identify Brontomerus' unique features, primarily the shape of the ilium (hip bone), which, in the case of Brontomerus, is unusually large in comparison to that of similar dinosaurs. The wide, blade-shaped bone projects forward ahead of the hip socket, providing a proportionally massive area for the attachment of muscles.
The shape of the bone indicates that the animal would likely have had the largest leg muscles of any dinosaur in the sauropod family. This is reflected in the name Brontomerus, which literally means "thunder-thighs." The dinosaur's species name, mcintoshi, was chosen in honor of John "Jack" McIntosh, a retired physicist at Wesleyan University, Conn., and lifelong avocational paleontologist.
"Brontomerus mcintoshi is a charismatic dinosaur and an exciting discovery for us," said first author Mike Taylor, a researcher in the Department of Earth Sciences at University College London. "When we recognised the weird shape of the hip, we wondered what its significance might be, but we concluded that kicking was the most likely. The kick would probably have been used when two males fought over a female, but given that the mechanics were all in place it would be bizarre if it wasn't also used in predator defense."
Other marks on the bones give additional clues to Brontomerus' lifestyle and environment. Co author Matt Wedel, assistant professor of anatomy at Western University of Health Sciences, Pomona, Calif., explained: "The shoulder blade of Brontomerus has unusual bumps that probably mark the boundaries of muscle attachments, suggesting that Brontomerus had powerful forelimb muscles as well. It's possible that Brontomerus mcintoshi was more athletic than most other sauropods. It is well established that far from being swamp-bound hippo-like animals, sauropods preferred drier, upland areas; so perhaps Brontomerus lived in rough, hilly terrain and the powerful leg muscles were a sort of dinosaur four-wheel drive."
While Brontomerus' unusual hip structure and enormous thigh muscles place it on the list of most extreme dinosaurs, it is also a significant find for another reason. It is one more in a number of finds over the past 20 years that challenge the previously held idea that sauropods began to disappear in the Early Cretaceous period.
For more information contact coordinator@nthrys.com
A member of the long-necked sauropod group of dinosaurs which includes Diplodocus and Brachiosaurus, Brontomerus may have used its powerful thighs as a weapon to kick predators, or to help travel over rough, hilly terrain. Brontomerus lived about 110 million years ago, during the Early Cretaceous Period, and probably had to contend with fierce "raptors" such as Deinonychus and Utahraptor.
The fossilised bones of two specimens of Brontomerus mcintoshi – an adult and a juvenile – were rescued from a previously looted and damaged quarry in eastern Utah by researchers from the Sam Noble Museum. Paleontologists speculate that the larger specimen is the mother of the younger and would have weighed around 6 tons, about the size of a large elephant, and measured 14 meters in length. At a third of the size, the smaller specimen would have weighed about 200 kg, the size of a pony, and been 4.5 m long.
The authors classified the new genus based on an incomplete skeleton including bones from the shoulder, hip, ribs, vertebrae and some unidentifiable fragments. They used the bones to identify Brontomerus' unique features, primarily the shape of the ilium (hip bone), which, in the case of Brontomerus, is unusually large in comparison to that of similar dinosaurs. The wide, blade-shaped bone projects forward ahead of the hip socket, providing a proportionally massive area for the attachment of muscles.
The shape of the bone indicates that the animal would likely have had the largest leg muscles of any dinosaur in the sauropod family. This is reflected in the name Brontomerus, which literally means "thunder-thighs." The dinosaur's species name, mcintoshi, was chosen in honor of John "Jack" McIntosh, a retired physicist at Wesleyan University, Conn., and lifelong avocational paleontologist.
"Brontomerus mcintoshi is a charismatic dinosaur and an exciting discovery for us," said first author Mike Taylor, a researcher in the Department of Earth Sciences at University College London. "When we recognised the weird shape of the hip, we wondered what its significance might be, but we concluded that kicking was the most likely. The kick would probably have been used when two males fought over a female, but given that the mechanics were all in place it would be bizarre if it wasn't also used in predator defense."
Other marks on the bones give additional clues to Brontomerus' lifestyle and environment. Co author Matt Wedel, assistant professor of anatomy at Western University of Health Sciences, Pomona, Calif., explained: "The shoulder blade of Brontomerus has unusual bumps that probably mark the boundaries of muscle attachments, suggesting that Brontomerus had powerful forelimb muscles as well. It's possible that Brontomerus mcintoshi was more athletic than most other sauropods. It is well established that far from being swamp-bound hippo-like animals, sauropods preferred drier, upland areas; so perhaps Brontomerus lived in rough, hilly terrain and the powerful leg muscles were a sort of dinosaur four-wheel drive."
While Brontomerus' unusual hip structure and enormous thigh muscles place it on the list of most extreme dinosaurs, it is also a significant find for another reason. It is one more in a number of finds over the past 20 years that challenge the previously held idea that sauropods began to disappear in the Early Cretaceous period.
For more information contact coordinator@nthrys.com
Oldest Fossils of Large Seaweeds, Worm-like Animals Tell Story of Ancient Oxygen
Almost 600 million years ago, before the rapid evolution of life forms known as the Cambrian explosion, a community of seaweeds and worm-like animals lived in a quiet deep-water niche near what is now Lantian, a small village in south China.
Then they simply died, leaving some 3,000 nearly pristine fossils preserved between beds of black shale deposited in oxygen-free and unbreathable waters.
Scientists from the Chinese Academy of Sciences, Virginia Tech in the United States and Northwest University in Xi'an, China report the discovery of the fossils in this week's issue of the journal Nature.
In addition to ancient versions of algae and worms, the Lantian biota--named for its location--included macrofossils with complex and puzzling structures.
In all, scientists have identified some 15 species at the site.
The fossils suggest that structural diversification of macroscopic eukaryotes--the earliest versions of organisms with complex cell structures--may have occurred only tens of millions of years after the Snowball Earth event that ended 635 million years ago.
Snowball Earth proposes that the Earth's surface became almost, or completely, frozen at least once during the planet's history.
For more information on this research project contact coordinator@nthrys.com
Discovery of new gene mutation in schizophrenia offers a new target for drug therapies
Newly identified gene mutation has potential for the development of more effective treatment of Schizophrenia
In a major advance for schizophrenia research, an international team of scientists led by the University of California, San Diego School of Medicine and involving Trinity College Dublin researchers has identified a gene mutation strongly linked to schizophrenia that may be an important new target for the development of drug therapies. The findings are just published in the online issue of the journal Nature.
Schizophrenia is a chronic, severe and disabling brain disorder, with symptoms that include hallucinations, delusions and thought disorder. Schizophrenia is believed to be caused by environmental and genetic factors, most notably the latter: the illness occurs in 1% of the general population, or 10 % of people who have a first-degree relative with the disorder, such as a parent or sibling. Current therapies are only partially effective with little progress being made in identifying effective new treatments over several decades.
In the last three years researchers have discovered that rare mutations at many locations in the human genome resulted in significantly higher risk of schizophrenia. These mutations consisted of copy number variants or CNVs −a type of genetic variation in which the number of copies of a gene differs between individuals. The findings were the first conclusive evidence that rare mutations can cause schizophrenia, but this did not identify the specific genes involved.
Professor Aiden Corvin of the Psychosis Research Group at Trinity College Dublin, funded by Science Foundation Ireland and the Wellcome Trust, and an author on this paper, describes that the latest study goes substantially further.
Researchers scanned for CNVs in the genomes of 8,290 individuals with diagnosed cases of schizophrenia and 7,431 healthy controls. The study confirmed CNVs identified in earlier studies, but uncovered an important new finding: duplications at the tip of chromosome 7q were detected in individuals with schizophrenia at a rate 14 times higher than in healthy individuals. These duplications impact a gene coding for the brain receptor VIPR2.
For more information contact coordinator@nthrys.com
Neuroscientists find overlooked brain area is an important locus of depression
The lateral habenula is hyperactive in rat models of human depression
A team of neuroscientists at Cold Spring Harbor Laboratory (CSHL), Brookhaven National Laboratory (BNL) and UC San Diego (UCSD) has collected evidence suggesting that a previously overlooked portion of the brain could be a prime locus of human depression.
In two rat models of human depression, the scientists have demonstrated that neurons in a tiny area in the central brain called the lateral habenula (LHb) are hyperactive.
Specifically, as the team reports today online ahead of print in the journal Nature, excitatory synaptic inputs onto neurons in the LHb are enhanced in "depressed" animals, a finding they regard significant because this excitation in turn causes the inhibition of "downstream targets" -- including neurons in a part of the brain called the ventral tegmental area (VTA), important in the brain's reward system and heavily populated by dopamine neurons.
Furthermore, the team, which includes Professor Fritz Henn of CSHL and BNL and Assistant Professor Bo Li of CSHL, as well as Professor Roberto Malinow of UCSD, was able to use an analog of deep brain stimulation (DBS), a novel form of electrical stimulation involving the implantation of electrodes into a specific brain area, to reverse depression-like symptoms in the rats.
DBS is an important new experimental modality of treatment for refractory depression in people, as well as a potentially important approach to treat other neurophysiological disorders, most notably Parkinson's disease. The team's results point to the LHb as a potential therapeutic target for DBS. A series of ongoing experiments in depression at other laboratories, which have shown promise in a small number of human patients, have used DBS to target an area of the cingulate cortex called Brodman's Area 25. Henn and colleagues in Germany last year reported fsuccess in treating one case of intractable human depression with DBS, targeting the LHb.
For more information contact coordinator@nthrys.com
Entire T-cell receptor repertoire sequenced revealing extensive and unshared diversity
T-cell receptor diversity in blood samples from healthy individuals has been extensively cataloged for the first time in a study published online in Genome Research (www.genome.org), setting the stage for a better understanding of infectious disease, cancer, and immune system disorders.
Adaptive immunity is mediated by T-cells, a white blood cell that identifies and attacks cells that may be infected with viruses or contain cancer-causing mutations. To recognize a wide array of potentially infectious agents or cancer-causing mutations, gene shuffling creates a highly variable and diverse collection of T-cell receptor sequences.
While the diversity of sequences in immune cell repertoires has been investigated previously, no study had yet been able to capture the entire range present in an individual sample. Now, using next-generation sequencing technology, researchers in Canada have identified essentially all T-cell receptor variants in blood samples, identifying more than one million unique sequences.
Dr. Robert Holt of the BC Cancer Agency and Simon Fraser University, senior author of the report, explained that this study is the first to establish that while there is high T-cell diversity in a standard blood sample, it does not give the entire picture. "This is only part of the diversity that would be present within a person's entire body," Holt said, "but now we know that although the diversity is very large, it is ultimately limited, and it is measureable."
The group found that some T-cell receptor sequences are common, some are rare, and the repertoire can change over time. The individual repertoire was then compared to that of two other individuals, showing that only a minority of sequences is shared between them.
Interestingly, they noted that for sequences that were shared, different gene shuffling events had often generated the same sequence. "This shows that certain sequences are more favored than others, most likely because they are more effective in recognizing specific types of infections or mutations," said Holt.
By cataloging the baseline diversity of the immune repertoire in a healthy individual, Holt explained that future studies would be able to then recognize how the repertoire is disturbed in cases of immune challenge, such as infectious disease or organ transplantation, and furthermore, may assist in the development of new vaccines.
For more information on this contact coordinator@nthrys.com
Adaptive immunity is mediated by T-cells, a white blood cell that identifies and attacks cells that may be infected with viruses or contain cancer-causing mutations. To recognize a wide array of potentially infectious agents or cancer-causing mutations, gene shuffling creates a highly variable and diverse collection of T-cell receptor sequences.
While the diversity of sequences in immune cell repertoires has been investigated previously, no study had yet been able to capture the entire range present in an individual sample. Now, using next-generation sequencing technology, researchers in Canada have identified essentially all T-cell receptor variants in blood samples, identifying more than one million unique sequences.
Dr. Robert Holt of the BC Cancer Agency and Simon Fraser University, senior author of the report, explained that this study is the first to establish that while there is high T-cell diversity in a standard blood sample, it does not give the entire picture. "This is only part of the diversity that would be present within a person's entire body," Holt said, "but now we know that although the diversity is very large, it is ultimately limited, and it is measureable."
The group found that some T-cell receptor sequences are common, some are rare, and the repertoire can change over time. The individual repertoire was then compared to that of two other individuals, showing that only a minority of sequences is shared between them.
Interestingly, they noted that for sequences that were shared, different gene shuffling events had often generated the same sequence. "This shows that certain sequences are more favored than others, most likely because they are more effective in recognizing specific types of infections or mutations," said Holt.
By cataloging the baseline diversity of the immune repertoire in a healthy individual, Holt explained that future studies would be able to then recognize how the repertoire is disturbed in cases of immune challenge, such as infectious disease or organ transplantation, and furthermore, may assist in the development of new vaccines.
For more information on this contact coordinator@nthrys.com
All about addiction
Special issue of Neuron examines the new neuroscience of substance abuse
Addiction is a brain disease that destroys lives, devastates families and tears at the very fabric of society. Effective prevention and treatment of addiction requires a clear understanding of the complex brain mechanisms that underlie addictive behaviors, and research has provided a fascinating view of how substance abuse hijacks neuronal circuits involved in reward and motivation and causes profound and persistent changes in behavior. Now, a special issue of the journal Neuron, published on February 24th by Cell Press, provides new insight into to the most recent advances in addiction research and highlights the complexities associated with the neurobiological and societal impacts of addiction, as well as strategies for the prevention and treatment of substance abuse.
The special issue, made freely available at www.neuron.org through March 31st, contains review articles written by leaders in the field of addiction research that shed light on genetic vulnerability to addiction, the impact of addictive drugs on neuronal transmission, the effects of addictive drugs on reward, risk and decision making, behavioral and pharmacological treatments for addiction and reward mechanisms in obesity. In addition, a series of more societal-focused NeuroViews highlight issues associated with the use of opiates to treat chronic pain, the abuse of cognitive enhancing drugs and why a medical approach is likely to be far more effective at treating addicts than a punitive criminal approach.
For more information contact coordinator@nthrys.com
2/19/2011
HOW MIGHT MARS BECOME A HOME FOR HUMANS?
People can live in inhospitable places in two distinct ways, by changing the local environment, or by carrying a suitable ‘environment’ with them. Desert irrigation for agricultural development is an example of the first, while the life-support systems of lunar landing modules, or orbiting space stations, exemplify the second mode of survival. The latter devices cannot be inhabited indefinitely; for lengthy stays the crews sooner or later become dependent on resupply missions from Earth. Recently, the President of the United States called for the establishment of bases for astronauts on the moon and Mars. The first human outposts in space will, of necessity, be of the second kind, even though some local resources may be exploited by their occupants. Human settlements on other planets can become fully and permanently independent of Earth only of these distant environments are transformed to provide Earth-like living conditions and a local agriculture. The realistic possibilities for this latter type of planetary engineering, carried out on a global scale, are assessed briefly in this essay.
Life is a planetary phenomenon, but Earth is the only living planet in the solar system. Plants and animals are mutually dependent products of Earth’s global ecosystem – the biosphere. All are intricately coupled with each other, and with land, oceans and air by the recycling of water, carbon, oxygen, nitrogen and other inorganic materials needed to maintain life. Humans also are component parts of this complex, ever-changing but to some extent self-regulating, biochemical system. We are exotic products of a planetary engine originally set in motion, and continuously fuelled, by energy from the sun.
On other planets, high and low extremes of atmospheric temperatures and pressures, lack of free oxygen and liquid water, high concentrations of toxic gases, and deadly radiation levels variously preclude the existence of life. Though presently barren, Mars, nonetheless, is a biocompatible planet. Its unalterable physical characteristics (e.g. size, density, gravity, orbit, rotation rate, incident sunlight) and its possible chemical resources are remarkably consistent with life. Indeed, it was the hope that organisms might be found on Mars that made life-detection the top priority for NASA’s Viking missions in 1976. However, all of the ingenious biological experiments carried out by the two robotic landers gave negative results.
The Viking data did reveal that environmental conditions on Mars are more severe than ever had been imagined. At the two ‘temperate zone’ landing sites, local temperatures exhibited wide daily variation averaging 60 degrees below zero celsius. The atmospheric pressure was found to be very low, just over six millibars, which is less than one hundredth of that at Earth’s surface. This thin atmosphere consists of 95% carbon dioxide and 3% nitrogen, with only trace amounts of water vapour, oxygen and other gases. There is no protective ozone layer to shield the planet from the ultraviolet radiation emitted by the sun. Most surprising was the absence from the soil of any detectable organic molecules, the building blocks of life. Even though such materials arrive on Mars in meteorites, they are subsequently destroyed, at least on the surface of the planet. Thus, any organisms which might arrive there unprotected today would be freeze-dried, chemically degraded, and soon reduced to dust. It would not be possible to ‘seed’ Mars just by sprinkling bacteria over its surface.
Despite its presently hostile environment, Mars did once possess a great northern ocean and substantial quantities of flowing water, together with a thick, mostly carbon dioxide, atmosphere. These conditions may have persisted long enough for early stages of chemical and cellular evolution to have occurred. It is largely for these reasons that some scientists have begun to consider whether Mars might ultimately be returned, by human intervention, to a habitable state. A major uncertainty in these discussions is whether there remains on Mars today adequate amounts of carbon dioxide, water and nitrogen to allow such a planetary-scale transformation. If most of Mars’ original endowment of these materials has been lost to space, then the regeneration of a habitable state would be impossible.
Preliminary studies have shown that if the surface crust and polar caps of Mars still possess sufficient and accessible quantities of carbon dioxide, water and nitrogen, and if acceptable planetary engineering techniques can be devised to initiate planetary warming and release these volatile materials from their geological reservoirs, then Mars could support a stable and much thicker carbon dioxide/nitrogen atmosphere than it does at present. This atmosphere would be warm and moist, and water would flow again in the dried up river beds. The average temperature at the surface would rise to about 15 degrees celsius and the atmospheric pressure would be roughly twice that on Earth. Appropriately selected, or genetically engineered, anaerobic microorganisms, and eventually some plants, could grow under these conditions. If future exploration reveals that the necessary volatiles are indeed available then a new home for life might someday be created on our sister planet.
The creation of a self-sustaining ecosystem, or biosphere, on a lifeless planet is called ecopoiesis, a new word which means ‘the making of an abode for life’. On Mars, as was the case on Earth, the earliest biosphere would most likely have to consist of localized microbial ecosystems growing and developing under anaerobic conditions. Obviously, this would not provide an environment in which animals or humans could survive outdoors. All oxygen-dependent organisms transported to Mars would have to remain enclosed in life-support modules or appropriate protective gear. The word ‘terraformation’ is used to describe the formation of specifically Earth-like, aerobic conditions on planets. Such a salubrious environment is only one of many possible long-term and not necessarily inevitable, outcomes of ecopoiesis. If we consider the spontaneous development of Earth’s biosphere as a model for what might be achieved by design on Mars, terraformation would have to be initiated subsequently to ecopoiesis. If we restrict our speculations to plausible, near-term technologies, the time periods required to carry out ecopoiesis and terraformation on Mars are very different. If suitable volatile inventories exist, the thick, warm atmosphere described above might be generated in as little as 200 years. However approximately 100,000 years would be required if an oxygen atmosphere was to be produced as efficiently as it was on Earth, that is, by microbial and green plant photosynthesis. However, it remains possible that presently unimagined, futuristic technologies could be developed to shorten these time estimates considerably.
For many people, including some leading scientists, talk of humanly initiated ecopoiesis and terraformation sounds more like science fiction than any justifiable program in space research. The obstacles posed by present conditions on Mars, quite apart from the costs entailed, seem almost insurmountable. In addition, the prospect of ecopoiesis, as a long-range objective for civilian space agencies, raises many unresolved philosophical, political and even legal questions. For example, do humans have any right to ‘play God’ on another planet?
Migration and the colonization of initially in hospitable environments has been one of the most astonishing historical features of biological evolution. The first living cells were formed at least 3.8 billion years ago, presumably in the darker reaches of the primeval, anerobic seas. At that time much of Earth’s surface environment, and certainly its land areas, would have been extremely hostile, if not downright lethal, to most of the organisms which flourish here today. However, in an amazing biotic diaspora, microrganisms, followed by plants and animals, migrated from marine to fresh water environments and then onto the initially barren land. None of this would have been possible were it not for the evolutionary development, by living cells, of the ‘technology’ of photosynthesis. Essentially all of the free oxygen (and the resulting ozone shield) in Earth’s atmosphere was, and is, generated by photosynthesis. Even though oxygen is poisonous to most anaerobic organisms, its accumulation in the atmosphere created the conditions necessary for the flowering of aerobic life as we know it today.
The slow, chancy processes of genetic variation, natural selection and species diversification have made possible the dispersal of nonhuman life across the globe. In contrast the migration and dispersal of Homo sapiens has not entailed any significant biological evolution, and certainly no speciation, ever since the emergence of ‘modern’ humans with linguistic and tool making capabilities about 100,000 years ago. Rather, it has been the amazingly rapid and efficient processes of social and technological evolution which have facilitated the propagation of our species, across every continent, and most recently into space.
In 1969 astronauts first set foot on the moon. If all goes well, others are scheduled to arrive on Mars in 2019. Against this background it is not just an idle dream to imagine that people might yet "slip the surly bonds of Earth" to pioneer new habitats in the sky. Further exploration of Mars may well reveal that ecopoiesis is feasible on that planet. Such a discovery would provide future generations with a tremendous challenge in life and an exhilarating vision of the role of humankind as a participant in creation. Perhaps however, there are also deep psychological and biological reasons for seeking to enliven Mars: such a vast enterprise would surely be consistent with the Promethean myths of many cultural traditions and the proliferative imperative that animates life itself.
for more information counselor@nthrys.co.in
Eggs' quality control mechanism explained
To protect the health of future generations, body keeps a careful watch on its precious and limited supply of eggs. That's done through a key quality control process in oocytes (the immature eggs), which ensures elimination of damaged cells before they reach maturity. In a new report in the February 18th Cell, a Cell Press publication, researchers have made progress in unraveling how a factor called p63 initiates the deathblow.
In fact, p63 is a close relative of the infamous tumor suppressor p53, and both proteins recognize DNA damage. Because of this heritage it was initially assumed that p63 would also function as a tumor suppressor, but various forms of the protein are now known to be important in development. One in particular, called TAp63a, is responsible for killing off damaged oocytes.
But it seems that plenty of TAp63a is always around, whether oocytes are damaged or not, suggesting that there must be a very special way that the protein is kept under wraps lest it kill off perfectly good cells.
The quality control factor normally exists in oocytes in inactive pairs or dimers, he explained. When double strand breaks to the DNA occur, those dimers are chemically modified by an as-yet unidentified enzyme, allowing them to open up and join forces with a second open pair. The result is an active tetramer that can bind DNA more effectively, leading to the death of the damaged cells.
That activation of TAp63a cannot be undone, they show, even if you reverse the chemical modification that enabled the tetramer formation in the first place. That irreversibility stems from an extra helix structure that keeps the tetramer stable.
For more information on this research contact coordinator@nthrys.com
In fact, p63 is a close relative of the infamous tumor suppressor p53, and both proteins recognize DNA damage. Because of this heritage it was initially assumed that p63 would also function as a tumor suppressor, but various forms of the protein are now known to be important in development. One in particular, called TAp63a, is responsible for killing off damaged oocytes.
But it seems that plenty of TAp63a is always around, whether oocytes are damaged or not, suggesting that there must be a very special way that the protein is kept under wraps lest it kill off perfectly good cells.
The quality control factor normally exists in oocytes in inactive pairs or dimers, he explained. When double strand breaks to the DNA occur, those dimers are chemically modified by an as-yet unidentified enzyme, allowing them to open up and join forces with a second open pair. The result is an active tetramer that can bind DNA more effectively, leading to the death of the damaged cells.
That activation of TAp63a cannot be undone, they show, even if you reverse the chemical modification that enabled the tetramer formation in the first place. That irreversibility stems from an extra helix structure that keeps the tetramer stable.
For more information on this research contact coordinator@nthrys.com
Male fertility is in the bones
Researchers have found an altogether unexpected connection between a hormone produced in bone and male fertility. The study in the February 18th issue of Cell, a Cell Press publication, shows that the skeletal hormone known as osteocalcin boosts testosterone production to support the survival of the germ cells that go on to become mature sperm.The findings in mice provide the first evidence that the skeleton controls reproduction through the production of hormones.
Bone was once thought of as a "mere assembly of inert calcified tubes," the researchers explained. But in the last ten years, scientists have gained a much more dynamic picture of bone as a bona fide endocrine organ with links to energy metabolism and reproduction.
Prior work on skeletal ties to reproduction had focused primarily on the reproductive organs as a regulator of bone remodeling. That led researchers to wonder whether the influence might go the other way as well. Given the links between menopause and osteoporosis, his team anticipated such a connection would more likely turn up in females. But that's not what they found at all.
They found that the bones do control reproduction, but only in males. That was obviously a surprise, but that's the finding.
Osteocalcin produced by the bone-building cells known as osteoblasts induces testosterone production by the testes, but fails to influence estrogen production by ovaries, the researchers report.
Matings between normal females and osteocalcin-deficient males produced smaller and less frequent litters than those between typical males and females. Males lacking a second gene that inhibits osteocalcin's endocrine functions showed just the opposite: larger (though not significantly larger) and more frequent litters.
The researchers further showed that osteocalcin works through a receptor found on testosterone-producing Leydig cells in the testes.
For more information on studies related to bones and fertility contact coordinator@nthrys.com
Bone was once thought of as a "mere assembly of inert calcified tubes," the researchers explained. But in the last ten years, scientists have gained a much more dynamic picture of bone as a bona fide endocrine organ with links to energy metabolism and reproduction.
Prior work on skeletal ties to reproduction had focused primarily on the reproductive organs as a regulator of bone remodeling. That led researchers to wonder whether the influence might go the other way as well. Given the links between menopause and osteoporosis, his team anticipated such a connection would more likely turn up in females. But that's not what they found at all.
They found that the bones do control reproduction, but only in males. That was obviously a surprise, but that's the finding.
Osteocalcin produced by the bone-building cells known as osteoblasts induces testosterone production by the testes, but fails to influence estrogen production by ovaries, the researchers report.
Matings between normal females and osteocalcin-deficient males produced smaller and less frequent litters than those between typical males and females. Males lacking a second gene that inhibits osteocalcin's endocrine functions showed just the opposite: larger (though not significantly larger) and more frequent litters.
The researchers further showed that osteocalcin works through a receptor found on testosterone-producing Leydig cells in the testes.
For more information on studies related to bones and fertility contact coordinator@nthrys.com
How disordered proteins spread from cell to cell, potentially spreading disease
One bad apple is all it takes to spoil the barrel. And one misfolded protein may be all that's necessary to corrupt other proteins, forming large aggregations linked to several incurable neurodegenerative diseases such as Huntington's, Parkinson's and Alzheimer's.
Researchers have shown that the mutant, misfolded protein responsible for Huntington's disease can move from cell to cell, recruiting normal proteins and forming aggregations in each cell it visits. Knowing that this protein spends part of its time outside cells opens up the possibility for therapeutics. Kopito studies how such misfolded proteins get across a cell's membrane and into its cytoplasm, where they can interact with normal proteins. They are also investating how these proteins move between neuronal cells. The ability of these proteins to move from one cell to another could explain the way Huntington's disease spreads through the brain after starting in a specific region. Similar mechanisms may be involved in the progress of Parkinson's and Alzheimer's through the brain.
Not all misfolded proteins are bad. The dogma used to be that all our proteins formed neat, well-folded structures, packed together in complexes with a large number of other proteins. But over the past 20 years, researchers have found that as much as 30 percent of our proteins never fold into stable structures. And even ordered proteins appear to have some disordered parts.
Disordered proteins are important for normal cellular functions. Unlike regular proteins, they only interact with one partner at a time. But they are much more dynamic, capable of several quick interactions with many different proteins. This makes them ideal for a lot of the standard communication that happens within a cell for its normal functioning.
But if some of our proteins are always disordered, how do our cells tell which proteins need to be properly folded, and which don't? It's a big mystery.
Huntington's disease is caused by a specific mutated protein. But the body makes this mutant protein all your life, so why do you get the disease in later adulthood? It's because the body's protective mechanisms stop doing their job as we get older.
But it's clear what happens when these mechanisms stop working – misfolded proteins start recruiting normal versions of the same protein and form large aggregations. The presence of these aggregations in neurons has been closely linked with several neurodegenerative diseases.
Researchers found that the mutant protein associated with Huntington's disease can leave one cell and enter another one, stirring up trouble in each new cell as it progresses down the line. The spread of the misfolded protein may explain how Huntington's progresses through the brain.
This disease, like Parkinson's and Alzheimer's, starts in one area of the brain and spreads to the rest of it. This is also similar to the spread of prions, the self-replicating proteins implicated in mad cow disease and, in humans, Creutzfeldt-Jakob disease. As the misfolded protein reaches more parts of the brain, it could be responsible for the progressive worsening of these diseases.
For more information on Alzeihmers research contact coordinator@nthrys.com
Researchers have shown that the mutant, misfolded protein responsible for Huntington's disease can move from cell to cell, recruiting normal proteins and forming aggregations in each cell it visits. Knowing that this protein spends part of its time outside cells opens up the possibility for therapeutics. Kopito studies how such misfolded proteins get across a cell's membrane and into its cytoplasm, where they can interact with normal proteins. They are also investating how these proteins move between neuronal cells. The ability of these proteins to move from one cell to another could explain the way Huntington's disease spreads through the brain after starting in a specific region. Similar mechanisms may be involved in the progress of Parkinson's and Alzheimer's through the brain.
Not all misfolded proteins are bad. The dogma used to be that all our proteins formed neat, well-folded structures, packed together in complexes with a large number of other proteins. But over the past 20 years, researchers have found that as much as 30 percent of our proteins never fold into stable structures. And even ordered proteins appear to have some disordered parts.
Disordered proteins are important for normal cellular functions. Unlike regular proteins, they only interact with one partner at a time. But they are much more dynamic, capable of several quick interactions with many different proteins. This makes them ideal for a lot of the standard communication that happens within a cell for its normal functioning.
But if some of our proteins are always disordered, how do our cells tell which proteins need to be properly folded, and which don't? It's a big mystery.
Huntington's disease is caused by a specific mutated protein. But the body makes this mutant protein all your life, so why do you get the disease in later adulthood? It's because the body's protective mechanisms stop doing their job as we get older.
But it's clear what happens when these mechanisms stop working – misfolded proteins start recruiting normal versions of the same protein and form large aggregations. The presence of these aggregations in neurons has been closely linked with several neurodegenerative diseases.
Researchers found that the mutant protein associated with Huntington's disease can leave one cell and enter another one, stirring up trouble in each new cell as it progresses down the line. The spread of the misfolded protein may explain how Huntington's progresses through the brain.
This disease, like Parkinson's and Alzheimer's, starts in one area of the brain and spreads to the rest of it. This is also similar to the spread of prions, the self-replicating proteins implicated in mad cow disease and, in humans, Creutzfeldt-Jakob disease. As the misfolded protein reaches more parts of the brain, it could be responsible for the progressive worsening of these diseases.
For more information on Alzeihmers research contact coordinator@nthrys.com
2/18/2011
ChemGenome - ab initio Gene Prediction software
[ http://www.scfbio-iitd.res.in/chemgenome/chemgenomenew.jsp ]
Chemgenome is an ab-intio gene prediction software, which find genes in prokaryotic genomes in all six reading frames. The methodology follows a physico-chemical approach and has been validated on 372 prokaryotic genomes.
For more information on bioinformatics software's and tools contact coordinator@nthrys.com
Chemgenome is an ab-intio gene prediction software, which find genes in prokaryotic genomes in all six reading frames. The methodology follows a physico-chemical approach and has been validated on 372 prokaryotic genomes.
For more information on bioinformatics software's and tools contact coordinator@nthrys.com
Scientists uncover surprising features of bear hibernation
Metabolism independent of body temperature
Black bears show surprisingly large and previously unobserved decreases in their metabolism during and after hibernation according to a paper by scientists at the Institute of Arctic Biology at the University of Alaska Fairbanks and published in the 18 February issue of the journal Science.
In general, an animal's metabolism slows to about half for each 10 degree (Celsius) drop in body temperature. Black bears' metabolism slowed by 75 percent, but their core body temperature decreased by only five to six degrees. The amount of metabolic suppression was a surprise since the decrease in body temperatures of hibernating bears was moderate. Researchers were also surprised when the bears' metabolism remained suppressed for several weeks after the animals emerged from their dens.
Interest in the physiology of human-sized hibernators like black bears extends beyond comparative biology, since application of the mechanisms of metabolic suppression to people in emergency situations could save lives. Quickly reducing metabolic demand in victims of stroke, heart attack or trauma would put them in a stabilized, protected state to provide more time to arrange advanced, medical care.
This is the first study to continuously measure the metabolic rates and body temperatures of black bears as they hibernated during the winter under natural conditions and after they emerged from their dens in spring. Technical limitations have previously prevented continuous long-term monitoring of such large animals.
The study included five American black bears, which were nuisance bears captured in south-central and Interior Alaska by the Alaska Department of Fish and Game.
Researchers implanted radio transmitters into each bear to record its body temperature, heart beats and muscle activity. The bears were kept in structures mimicking dens, away from human disturbance, and monitored via infrared cameras.
Resarchers measured the bears' metabolism by continuously measuring the oxygen and carbon dioxide concentrations of the air entering and leaving the den. The transmitters inside each bear told that the bear's body temperature was not stable, but varied over the winter in slow cycles each lasting several days.
Such large, multi-day fluctuations in core body temperature are unlike those observed in any other mammal before. This detail was missed by past studies, and may have caused overestimation of metabolic rate because bears periodically shiver when they increase their body temperature.
Hibernating bears only breathe one to two times per minute and their heart slows between breaths; sometimes there is 20 seconds between beats. Each time the bear takes a breath, the heart accelerates for a short time to almost that of a resting bear in summer. When the bear breathes out, the heart slows down again and there will be another 30 to 60 seconds until the next breath.
Investigators had expected to find the animals' metabolism returning to normal levels right away when the bears resumed activity and emerged from their dens in spring just like a small hibernator such as the arctic ground squirrel would do. They were surprised to find that the bears' metabolic rates were still only about half of their normal, summer levels even though body temperature had returned to near normal of 37°C.
They continued to monitor the bears' metabolism for another month after emergence and observed that it took the bears two to three full weeks to stabilize at their summer metabolic levels. Free-ranging bears one may encounter out in the woods in early spring may be in a transition state.
Researchers will continue studies to determine the changes in gene expression that accompany transitions in hibernating state in black bears and whether protection of tissues can be activated during the summer.
Nthrys Labs offers interesting projects on dormancy, which are still not published. For more information contact coordinator@nthrys.com
Black bears show surprisingly large and previously unobserved decreases in their metabolism during and after hibernation according to a paper by scientists at the Institute of Arctic Biology at the University of Alaska Fairbanks and published in the 18 February issue of the journal Science.
In general, an animal's metabolism slows to about half for each 10 degree (Celsius) drop in body temperature. Black bears' metabolism slowed by 75 percent, but their core body temperature decreased by only five to six degrees. The amount of metabolic suppression was a surprise since the decrease in body temperatures of hibernating bears was moderate. Researchers were also surprised when the bears' metabolism remained suppressed for several weeks after the animals emerged from their dens.
Interest in the physiology of human-sized hibernators like black bears extends beyond comparative biology, since application of the mechanisms of metabolic suppression to people in emergency situations could save lives. Quickly reducing metabolic demand in victims of stroke, heart attack or trauma would put them in a stabilized, protected state to provide more time to arrange advanced, medical care.
This is the first study to continuously measure the metabolic rates and body temperatures of black bears as they hibernated during the winter under natural conditions and after they emerged from their dens in spring. Technical limitations have previously prevented continuous long-term monitoring of such large animals.
The study included five American black bears, which were nuisance bears captured in south-central and Interior Alaska by the Alaska Department of Fish and Game.
Researchers implanted radio transmitters into each bear to record its body temperature, heart beats and muscle activity. The bears were kept in structures mimicking dens, away from human disturbance, and monitored via infrared cameras.
Resarchers measured the bears' metabolism by continuously measuring the oxygen and carbon dioxide concentrations of the air entering and leaving the den. The transmitters inside each bear told that the bear's body temperature was not stable, but varied over the winter in slow cycles each lasting several days.
Such large, multi-day fluctuations in core body temperature are unlike those observed in any other mammal before. This detail was missed by past studies, and may have caused overestimation of metabolic rate because bears periodically shiver when they increase their body temperature.
Hibernating bears only breathe one to two times per minute and their heart slows between breaths; sometimes there is 20 seconds between beats. Each time the bear takes a breath, the heart accelerates for a short time to almost that of a resting bear in summer. When the bear breathes out, the heart slows down again and there will be another 30 to 60 seconds until the next breath.
Investigators had expected to find the animals' metabolism returning to normal levels right away when the bears resumed activity and emerged from their dens in spring just like a small hibernator such as the arctic ground squirrel would do. They were surprised to find that the bears' metabolic rates were still only about half of their normal, summer levels even though body temperature had returned to near normal of 37°C.
They continued to monitor the bears' metabolism for another month after emergence and observed that it took the bears two to three full weeks to stabilize at their summer metabolic levels. Free-ranging bears one may encounter out in the woods in early spring may be in a transition state.
Researchers will continue studies to determine the changes in gene expression that accompany transitions in hibernating state in black bears and whether protection of tissues can be activated during the summer.
Nthrys Labs offers interesting projects on dormancy, which are still not published. For more information contact coordinator@nthrys.com
Research predicts future evolution of flu viruses
New research from the University of Pennsylvania is beginning to crack the code of which strain of flu will be prevalent in a given year, with major implications for global public health preparedness. The findings will be published on February 17 in the open-access journal PLoS Genetics.
The computational study of 40 years of flu genomes offers a new way of looking at mutations: by cataloging pairs of genetic changes that have occurred in rapid succession, observing that a mutation in one half of the pair can act as an early warning sign of a mutation about to occur in the other.
Tracking single mutations in a vacuum is not always enough to understand how the flu virus evolves. "Sometimes a mutation is functional or adaptive only if it's in the context of a certain genetic background – that is, if the protein already has some other mutation," Plotkin said. The influence such combinations have on an organization's adaptive fitness is known as epistasis.
Because the studied mutations generally affect the surface proteins that determine whether the virus can enter and infect human cells, being able to predict what mutations are likely to happen in the near future has lifesaving applications. Tens of thousands of Americans, and hundreds of thousands worldwide, die of seasonal flu complications every year. Flu vaccine production is labor intensive and time consuming; to have enough supplies ready for the flu season, public health groups like the Centers for Disease Control and the World Health Organization must make an educated guess as to which strain is likely to be the most active several months in advance. Observing the leading site of an epistatic pair could give them a head start.
For more information on flu virus project and study of evolution contact coordinator@nthrys.com
The computational study of 40 years of flu genomes offers a new way of looking at mutations: by cataloging pairs of genetic changes that have occurred in rapid succession, observing that a mutation in one half of the pair can act as an early warning sign of a mutation about to occur in the other.
Tracking single mutations in a vacuum is not always enough to understand how the flu virus evolves. "Sometimes a mutation is functional or adaptive only if it's in the context of a certain genetic background – that is, if the protein already has some other mutation," Plotkin said. The influence such combinations have on an organization's adaptive fitness is known as epistasis.
Because the studied mutations generally affect the surface proteins that determine whether the virus can enter and infect human cells, being able to predict what mutations are likely to happen in the near future has lifesaving applications. Tens of thousands of Americans, and hundreds of thousands worldwide, die of seasonal flu complications every year. Flu vaccine production is labor intensive and time consuming; to have enough supplies ready for the flu season, public health groups like the Centers for Disease Control and the World Health Organization must make an educated guess as to which strain is likely to be the most active several months in advance. Observing the leading site of an epistatic pair could give them a head start.
For more information on flu virus project and study of evolution contact coordinator@nthrys.com
Pollution triggers genetic resistance mechanism in a coastal fish
For 30 years, two General Electric facilities released about 1.3 million pounds of polychlorinated biphenyls (PCBs) into New York's Hudson River, devastating and contaminating fish populations. Some 50 years later, one type of fish—the Atlantic tomcod—has not only survived but appears to be thriving in the hostile Hudson environment.
Researchers from Woods Hole Oceanographic Institution (WHOI) have joined colleagues from New York University (NYU) and NOAA to investigate this phenomenon and report that the tomcod living in the Hudson River have undergone a rapid evolutionary change in developing a genetic resistance to PCBs.
Although this kind of reaction has been seen when insects develop resistance to certain insecticides, and bacteria to antibiotics, "This is really the first demonstration of a mechanism of resistance in any vertebrate population," said Isaac Wirgin of NYU's Department of Environmental Medicine and leader of the study. Moreover, he said, the team has found that "a single genetic receptor has made this quick evolutionary change possible."
The findings, reported online in the Feb. 17 issue of Science, provide a first look at "natural selection going on over a relatively short time, changing the characteristics of a population," said WHOI Senior Scientist Mark E. Hahn, who, together with WHOI biologist Diana Franks, collaborated with Wirgin on the study. "It's an example of how human activities can drive evolution by introducing stress factors into the environment."
Looking at the ability of the fish to respond to the contaminants, the researchers found the primary changes occurred in a receptor gene called AHR2, which is important in mediating toxicity in early life stages and can control sensitivity to PCBs. In his work over the last 16 years in the Acushnet River Estuary near New Bedford, Mass., biologist Hahn has found the same gene involved in controlling other fishes' responses to PCBs.
The AHR2 proteins in the Hudson Rover tomcod, he said, appear to be missing two of the 1,104 amino acids normally found in this protein. This causes the receptor to bind more weakly with PCBs than normal, suggesting a reason why the contaminant does not affect the tomcod in this location as much as it does tomcod in other locations. The Hudson River tomcod "are not as sensitive to PCBs," Hahn said. "The mechanism by which PCBs cause toxicity is dampened in this population."
While this may be good news for the tomcod, it may bode not so well for their predators, and even humans. The tomcod survive but they still accumulate PCBs in their bodies and pass it on to whatever eats them.
For more information on this contact coordinator@nthrys.com
Researchers from Woods Hole Oceanographic Institution (WHOI) have joined colleagues from New York University (NYU) and NOAA to investigate this phenomenon and report that the tomcod living in the Hudson River have undergone a rapid evolutionary change in developing a genetic resistance to PCBs.
Although this kind of reaction has been seen when insects develop resistance to certain insecticides, and bacteria to antibiotics, "This is really the first demonstration of a mechanism of resistance in any vertebrate population," said Isaac Wirgin of NYU's Department of Environmental Medicine and leader of the study. Moreover, he said, the team has found that "a single genetic receptor has made this quick evolutionary change possible."
The findings, reported online in the Feb. 17 issue of Science, provide a first look at "natural selection going on over a relatively short time, changing the characteristics of a population," said WHOI Senior Scientist Mark E. Hahn, who, together with WHOI biologist Diana Franks, collaborated with Wirgin on the study. "It's an example of how human activities can drive evolution by introducing stress factors into the environment."
Looking at the ability of the fish to respond to the contaminants, the researchers found the primary changes occurred in a receptor gene called AHR2, which is important in mediating toxicity in early life stages and can control sensitivity to PCBs. In his work over the last 16 years in the Acushnet River Estuary near New Bedford, Mass., biologist Hahn has found the same gene involved in controlling other fishes' responses to PCBs.
The AHR2 proteins in the Hudson Rover tomcod, he said, appear to be missing two of the 1,104 amino acids normally found in this protein. This causes the receptor to bind more weakly with PCBs than normal, suggesting a reason why the contaminant does not affect the tomcod in this location as much as it does tomcod in other locations. The Hudson River tomcod "are not as sensitive to PCBs," Hahn said. "The mechanism by which PCBs cause toxicity is dampened in this population."
While this may be good news for the tomcod, it may bode not so well for their predators, and even humans. The tomcod survive but they still accumulate PCBs in their bodies and pass it on to whatever eats them.
For more information on this contact coordinator@nthrys.com
Identification of glaucoma gene brightens view for future therapies
Glaucoma – a leading cause of vision loss and blindness worldwide – runs in families. A team of investigators from Vanderbilt University and the University of Florida has identified a new candidate gene for the most common form of the eye disorder, primary open angle glaucoma (POAG).The findings, reported Feb. 17 in the open-access journal PLoS Genetics, offer novel insights into glaucoma pathology and could lead to targeted treatment strategies.
Elevated pressure inside the eye is a strong risk factor for POAG. Pressure increases because of increased resistance to the flow of aqueous humor out of the eye's front chamber (between the cornea and iris). Current treatments for POAG attempt to reduce intraocular pressure by reducing aqueous humor production or by surgically providing a clear "drain." It has been known for decades that the reason the pressure goes up in POAG is because the outflow pathway for aqueous humor is not working. It seems kind of simple – there's a decrease in the rate of aqueous humor flowing out of the eye. The basic mechanisms of aqueous humor outflow at the cellular and molecular level – and how they are disrupted in glaucoma – are not understood. It's a long-standing puzzle in ophthalmology.
So far, three genes have been associated with human glaucoma, but they account for only a small fraction of cases and have not shed much light on the disease process. The Vanderbilt investigators turned to a model with simpler genetics – a canine model of the disease.
For more information contact coordinator@nthrys.com
Elevated pressure inside the eye is a strong risk factor for POAG. Pressure increases because of increased resistance to the flow of aqueous humor out of the eye's front chamber (between the cornea and iris). Current treatments for POAG attempt to reduce intraocular pressure by reducing aqueous humor production or by surgically providing a clear "drain." It has been known for decades that the reason the pressure goes up in POAG is because the outflow pathway for aqueous humor is not working. It seems kind of simple – there's a decrease in the rate of aqueous humor flowing out of the eye. The basic mechanisms of aqueous humor outflow at the cellular and molecular level – and how they are disrupted in glaucoma – are not understood. It's a long-standing puzzle in ophthalmology.
So far, three genes have been associated with human glaucoma, but they account for only a small fraction of cases and have not shed much light on the disease process. The Vanderbilt investigators turned to a model with simpler genetics – a canine model of the disease.
For more information contact coordinator@nthrys.com
2/17/2011
DNASIS® SmartNote
[http://www.miraibio.com/dnasis-smartnote/overview.html]
* Access & edit your notebook from anywhere
* Analyze sequences with dozens of tools
* Share pages and sequences with friends
* Blog your results
A lab notebook that writes itself
As you work, your notebook fills itself with details on sequences used, analyses performed and results returned. Add your own notes and images. Use the built-in search engine to find something you did months ago.
Analyze sequences in batch
Save time and reduce errors by analyzing a batch of sequences all at once using a "sequence tray". Easily navigate results, pass them on to other tools for further analysis, and if you need a tool you don’t see, just ask and we’ll add it.
Find anything, fast
You’ll be amazed how fast you’ll find your sequences, analytical tools and notes with DNASIS SmartNote’s builtin search engine. Tags let you assign sequences to multiple projects and organize them the way you want.
A new way to collaborate
Share sequences and notebook pages securely with colleagues. Blog your results and get feedback from a wider audience. Keep track of the latest papers relevant to your work and your colleagues’ latest results.
For more information contact coordinator@nthrys.com
* Access & edit your notebook from anywhere
* Analyze sequences with dozens of tools
* Share pages and sequences with friends
* Blog your results
A lab notebook that writes itself
As you work, your notebook fills itself with details on sequences used, analyses performed and results returned. Add your own notes and images. Use the built-in search engine to find something you did months ago.
Analyze sequences in batch
Save time and reduce errors by analyzing a batch of sequences all at once using a "sequence tray". Easily navigate results, pass them on to other tools for further analysis, and if you need a tool you don’t see, just ask and we’ll add it.
Find anything, fast
You’ll be amazed how fast you’ll find your sequences, analytical tools and notes with DNASIS SmartNote’s builtin search engine. Tags let you assign sequences to multiple projects and organize them the way you want.
A new way to collaborate
Share sequences and notebook pages securely with colleagues. Blog your results and get feedback from a wider audience. Keep track of the latest papers relevant to your work and your colleagues’ latest results.
For more information contact coordinator@nthrys.com
Xenacoelomorpha – a new phylum in the animal kingdom
Scientists reorganise the animal phylogenetic tree.
An international team of scientists including Albert Poustka from the Max Planck Institute for Molecular Genetics in Berlin has discovered that Xenoturbellida and the acoelomorph worms, both simple marine worms, are more closely related to complex organisms like humans and sea urchins than was previously assumed. As a result they have made a major revision to the phylogenetic history of animals. Up to now, the acoelomate worms were viewed as the crucial link between simple animals like sponges and jellyfish and more complex organisms. It has now emerged that these animals did not always have as simple a structure as they do today.
For more information on this contact coordinator@nthrys.com
Drug therapy shows significant benefit in treating a leading cause of childhood blindness
A readily available, inexpensive drug therapy showed a significant benefit in treating premature infants with the worst and historically most difficult-to-treat cases of retinopathy of prematurity.
The results of a multicenter clinical trial led by researchers at The University of Texas Health Science Center at Houston (UTHealth) are published in the Feb. 17 issue of The New England Journal of Medicine.
Retinopathy of prematurity is a leading cause of childhood blindness worldwide. In the immature retina of babies born before 30 weeks' gestational age, the disease results in disorganized growth of retinal blood vessels, which can lead to scarring and retinal detachment.
In this study, Helen A. Mintz-Hittner, M.D., the Alfred W. Lasher, III, Professor in the Department of Ophthalmology and Visual Science at the UTHealth Medical School, and colleagues compared the use of intravitreal bevacizumab, an anti-vascular endothelial growth factor, to conventional laser treatment. The study investigators treated infants with acute retinopathy of prematurity affecting zone I and posterior zone II – the retinal zones with the highest rate of treatment failure.
For more information on this contact coordinator@nthrys.com
The results of a multicenter clinical trial led by researchers at The University of Texas Health Science Center at Houston (UTHealth) are published in the Feb. 17 issue of The New England Journal of Medicine.
Retinopathy of prematurity is a leading cause of childhood blindness worldwide. In the immature retina of babies born before 30 weeks' gestational age, the disease results in disorganized growth of retinal blood vessels, which can lead to scarring and retinal detachment.
In this study, Helen A. Mintz-Hittner, M.D., the Alfred W. Lasher, III, Professor in the Department of Ophthalmology and Visual Science at the UTHealth Medical School, and colleagues compared the use of intravitreal bevacizumab, an anti-vascular endothelial growth factor, to conventional laser treatment. The study investigators treated infants with acute retinopathy of prematurity affecting zone I and posterior zone II – the retinal zones with the highest rate of treatment failure.
For more information on this contact coordinator@nthrys.com
Researchers open the door to biological computers
Genetically modified cells can be made to communicate with each other as if they were electronic circuits. Using yeast cells, a group of researchers at the University of Gothenburg, Sweden, has taken a groundbreaking step towards being able to build complex systems in the future where the body’s own cells help to keep us healthy. The study was presented recently in an article in the scientific journal Nature. Even though engineered cells can’t do the same job as a real computer, our study paves the way for building complex constructions from these cells.
For more information on this research contact coordinator@nthrys.com
For more information on this research contact coordinator@nthrys.com
Researchers find breast cancer link
The discovery was made through looking at repetitive DNA — small, repeating sequences of genes that appear in over two million places in the genome. has discovered variations in a certain sequence — called estrogen related receptor gamma — which correlates with breast cancer. Three times more frequently, breast cancer patients have a longer version of this sequence, and that’s powerful information,And what it means is that this is a possible marker for your susceptibility for cancer. The important thing about a discovery like this is that there’s potential for its use in being both a diagnostic and a therapeutic.Though the team has already created a simple, standardized lab procedure to test a person’s status for the gene, it must be approved and commercialized before it can be used in hospitals and clinics.
For more information on this article contact coordinator@nthrys.com
For more information on this article contact coordinator@nthrys.com
2/16/2011
Noninvasive test for trisomy 21 closer at hand
In 1980 in the United States, approximately 4.5% of all pregnant women were of advanced maternal age. By 2007 that figure had increased to 14%. Women over 35 are at increased risk of giving birth to babies with trisomy 21.
In this study investigators have taken the next step in evaluating the practical use of fetal DNA sequencing and have shown that it has the potential to be highly accurate in a clinical setting. They have implemented technical improvements that will increase sample throughput and reduce costs. Following completion of an ongoing clinical validation study the above improvements will greatly facilitate introduction into clinical practice.
Because the plasma of pregnant women contains circulating cell-free (ccf) fetal (ccff) DNA the DNA sequencing method is able to identify the extra chromosome 21 material present in a fetus with trisomy 21. Independent of gestational age assessments, this novel approach allows for direct fetal assessment using massively parallel shotgun sequencing to detect missing or extra chromosomes, rather than surrogate biochemical markers that are used today in clinical practice.
Using samples from 449 high-risk pregnant women, the DNA sequencing method correctly identified 39 trisomy 21 samples and 409 normal samples, and misclassified 1 normal sample as trisomy 21. The overall classification showed 100% sensitivity and 99.7% specificity.
The data show that, in the future, a noninvasive prenatal trisomy 21 test from ccff DNA might be used in concert with other clinical assessments, such as ultrasound, and become an option to better identify those women who would, or would not, benefit from confirmatory invasive diagnostic tests.
For more information contact coordinator@nthrys.com
In this study investigators have taken the next step in evaluating the practical use of fetal DNA sequencing and have shown that it has the potential to be highly accurate in a clinical setting. They have implemented technical improvements that will increase sample throughput and reduce costs. Following completion of an ongoing clinical validation study the above improvements will greatly facilitate introduction into clinical practice.
Because the plasma of pregnant women contains circulating cell-free (ccf) fetal (ccff) DNA the DNA sequencing method is able to identify the extra chromosome 21 material present in a fetus with trisomy 21. Independent of gestational age assessments, this novel approach allows for direct fetal assessment using massively parallel shotgun sequencing to detect missing or extra chromosomes, rather than surrogate biochemical markers that are used today in clinical practice.
Using samples from 449 high-risk pregnant women, the DNA sequencing method correctly identified 39 trisomy 21 samples and 409 normal samples, and misclassified 1 normal sample as trisomy 21. The overall classification showed 100% sensitivity and 99.7% specificity.
The data show that, in the future, a noninvasive prenatal trisomy 21 test from ccff DNA might be used in concert with other clinical assessments, such as ultrasound, and become an option to better identify those women who would, or would not, benefit from confirmatory invasive diagnostic tests.
For more information contact coordinator@nthrys.com
New model reveals pesticide-free method that takes a bite out of mosquito-borne disease
Research published in Genetics proposes a system for spreading disease-resisting genes in mosquito populations. Scientists have modeled a system that may be used to control mosquitoes and the diseases they transmit, without the use of pesticides. In the proposed system, mosquitoes are engineered to carry two genes. The first gene causes males to transmit a toxin to females through their semen. The second gene, when expressed in females, makes them immune to this toxin. This research, published in the February 2011 issue of Genetics (http://www.genetics.org), describes a system that can be created using currently available molecular tools and could confine the spread of mosquitoes to isolated populations. It also allows the genes to be recalled if necessary.
The gene transfer system was modeled using mathematical equations that describe how genetic alterations in the mosquitos' DNA are inherited from one generation to the next, and predict how these alterations will either spread or be eliminated from the population. The system has two basic components—a toxin expressed in the semen of transgenic males that either kills female recipients or renders them infertile, and an antidote expressed in females that protects them from the effects of the toxin. An all-male release should result in population suppression because wild females that mate with transgenic males produce no offspring. A release that includes transgenic females propagates the desired gene because females carrying the toxin gene are favored at high population frequencies.
The scientists used simple population genetics models to explore the utility of this gene-transfer system, and found that it can work under a wide range of conditions. It requires a high frequency of gene transfer, which is desirable because it means that genetically altered insects released accidentally are unlikely to persist in the wild. Furthermore, it means that those released intentionally can be spatially confined and that the altered genes can be removed from a population through sustained release of wild-type insects. The scientists found few technical barriers to implementing this system, increasing prospects for engineering and testing in the coming years.
The gene transfer system was modeled using mathematical equations that describe how genetic alterations in the mosquitos' DNA are inherited from one generation to the next, and predict how these alterations will either spread or be eliminated from the population. The system has two basic components—a toxin expressed in the semen of transgenic males that either kills female recipients or renders them infertile, and an antidote expressed in females that protects them from the effects of the toxin. An all-male release should result in population suppression because wild females that mate with transgenic males produce no offspring. A release that includes transgenic females propagates the desired gene because females carrying the toxin gene are favored at high population frequencies.
The scientists used simple population genetics models to explore the utility of this gene-transfer system, and found that it can work under a wide range of conditions. It requires a high frequency of gene transfer, which is desirable because it means that genetically altered insects released accidentally are unlikely to persist in the wild. Furthermore, it means that those released intentionally can be spatially confined and that the altered genes can be removed from a population through sustained release of wild-type insects. The scientists found few technical barriers to implementing this system, increasing prospects for engineering and testing in the coming years.
Researchers hit 'jackpot' linking gene mutations to high blood pressure
Researchers have identified two novel genetic mutations that can trigger hypertension in up to a third of patients suffering from a common cause of severe high blood pressure, they report in the Feb. 11 issue of the journal Science.The findings are a major step in understanding the causes of high blood pressure, which afflicts one out of every three Americans.These findings may lead to a genetic screening test for this common cause of severe hypertension. Five to ten percent of patients with severe hypertension have tumors of the adrenal gland that produce a hormone called aldosterone. Removing these tumors can cure this form of hypertension. Sifting for clues by sequencing all of the genes from these tumors, and comparing their sequences to the patients' normal DNA, the researchers found that either one of two mutations of a single gene were found in 8 of 22 tumors studied. The investigators discovered that these mutations cause both aldosterone release and tumor formation by allowing the encoded protein, a potassium channel, to conduct sodium rather than only allowing potassium to pass through the channel.
For more information contact coordinator@nthrys.com
For more information contact coordinator@nthrys.com
New gene test discovered for inherited neuromuscular disorder
Scientists have identified a new gene which will allow rapid diagnosis and earlier treatment of a debilitating neuromuscular condition.The gene, GFPT1, is crucial in causing a variation of Congenital Myasthenic Syndrome (CMS) which gained media attention recently with the plight of baby RB, who was at the centre of a “right-to-life” legal dispute. CMS is a rare genetic condition affecting the way signals travel between the brain and muscles which can cause paralysis and in some cases death. It affects one in every 500,000 births and the severity of the condition varies, depending on where the fault lies in the complex signals between the nerves and the muscles.
The variation of CMS identified by the team of international researchers, GFPT1, tends to develop in the first ten years of life with patients losing muscle strength and control in their hips and shoulders or arms and legs.
For more information contact coordinator@nthrys.com
The variation of CMS identified by the team of international researchers, GFPT1, tends to develop in the first ten years of life with patients losing muscle strength and control in their hips and shoulders or arms and legs.
For more information contact coordinator@nthrys.com
Gene that regulates immune system linked to preeclampsia
Researchers have discovered that the placentas of women who suffer preeclampsia during pregnancy have an overabundance of a gene associated with the regulation of the body’s immune system. Their discovery may lead to improved screening and prenatal care for these patients and their babies.Preeclampsia occurs in up to 10 percent of all pregnancies, and is responsible for about 15 percent of pre-term births. The disorder is usually marked by a rapid rise in blood pressure that can lead to stroke, seizures or organ failures in the mother. Researchers have recently begun looking at preeclampsia as an autoimmune disorder, in which the mother’s body treats the placenta like an invader, but they weren’t sure of the genetic mechanisms involved.
For more information contact coordinator@nthrys.com
For more information contact coordinator@nthrys.com
Apache software foundation
The ASF is made up of nearly 100 top level projects that cover a wide range of technologies. Chances are if you are looking for a rewarding experience in Open Source, you are going to find it here. [http://www.apache.org/]
For more information on open source software in bioinformatics contact coordinator@nthrys.com
For more information on open source software in bioinformatics contact coordinator@nthrys.com
2/15/2011
Protherm
[http://gibk26.bse.kyutech.ac.jp/jouhou/protherm/protherm.html]
Thermodynamic Database for Proteins and Mutants, Jp.
For more information on databases for you research contact coordinator@nthrys.com
Thermodynamic Database for Proteins and Mutants, Jp.
For more information on databases for you research contact coordinator@nthrys.com
Newly identified proteins critical to FA pathway DNA repair function
Identification of two new proteins in the Fanconi anemia DNA repair pathway may help explain genetic instability in people with Fanconi anemia and how otherwise healthy people are susceptible to cancer from environmentally triggered DNA damage.
For more information contact coordinator@nthrys.com
For more information contact coordinator@nthrys.com
Southern African genomes sequenced
Human genomes from Southern African Bushmen and Bantu individuals have been sequenced by a team of scientists seeking a greater understanding of human genetic variation and its effect on human health. The findings will be published in the journal Nature. The research was completed by scientists from American, African, and Australian research institutions, with support from Penn State University in the United States and from several U.S. companies that market DNAsequencing instruments.
For more information on DNA sequencing contact coordinator@nthrys.com
For more information on DNA sequencing contact coordinator@nthrys.com
Sequence Variation Associated With Earlier Onset Of ER Positive Breast Cancer
The investigator's work highlights how a variation in a person's DNA sequence is associated with an earlier age of onset for breast cancer that is stimulated by the hormone estrogen (estrogen receptor positive). At focus were DNA sequence variations (polymorphisms) in the human enzyme known as HDAC9. Recent studies of this enzyme suggest that its suppression could lead to strategies that would regulate estrogen signaling. This latest research further supports a role for HDAC9 in estrogen signaling in that genetic changes in the HDAC9 gene may modulate onset of ER positive breast cancer and its recurrence.
For more information contact coordinator@nthrys.com
For more information contact coordinator@nthrys.com
Individual types of colorectal cancer revealed through mutation patterns
The fight against colorectal cancer, the third most common form of cancer with one million cases worldwide, is always a race against the clock. Early diagnosis and the identification of the particular type of the disease involved are crucial to the prospects of a successful cure. Because there are different molecular pathways to colorectal cancer, it has become increasingly clear in recent years that information about the type of cancer in question can be found in the patient’s genetic pattern. However, the variety of the changes or mutations in the genome is extensive and the methods available up to now often only enabled a limited interpretation.
For more information on mutation studies contact coordinator@nthrys.com
For more information on mutation studies contact coordinator@nthrys.com
Key information about breast cancer risk and development is found in junk DNA
A new genetic biomarker that indicates an increased risk for developing breast cancer can be found in an individual's "junk" (noncoding) DNA, according to a new study featuring work from researchers.
For more information contact coordinator@nthrys.com
For more information contact coordinator@nthrys.com
Rapid brain evolution and Alzeihmers
Of the millions of animals on Earth, including the relative handful that are considered the most intelligent including apes, whales, crows, and owls only humans experience the severe agerelated decline in mental abilities marked by Alzheimers disease. Research on brain and nervous system proteins is being carried out at Nthrys Labs.
For more information contact coordinator@nthrys.com
For more information contact coordinator@nthrys.com
2/14/2011
Organic solution to sanitation challenges
Bioremediation service provider FBF Organics says it can provide a simple, cost-effective and environment-friendly solution to the wastewater problems the country is currently facing.
The national sewage and effluent infrastructure is currently under stress from overloading and an ageing infrastructure that is in critical need of upgrading and refurbishment.
Essentially, FBF uses a natural product and fermentation technology to improve biological wastewater processes.
How It Works
Biological treatment technology involves the use of bacteria and other micro-organisms to degrade or remove contaminants from wastewater. The FBF Organics programme enhances this rate of degradation or decomposition through bioactivation.
This is the stimulation of existing micro-organisms by speeding up the metabolic activity. This increased metabolic activity is achieved by inoculating effluent ponds with activated effector molecules produced through the fermentation of a natural product in a specially designed bioreactor on site.
Tap water and the bioactivator are continuously fed into the bioreactor, allowing for regulated and effective management of wastewater treatment works (WWTWs).
FBF's solution could improve the bioremediation of wastewater, not only in municipal situations but also in agricultural and industrial applications.
The company has been successful in improving the performance of WWTWs in a wide variety of industries, such as tanneries, distilleries, fiberboards, sugar and paper mills, as well as on municipal sewage sites.
The FBF product has proven to be especially effective in treatment technologies including activated sludge, biofilters, anaerobic digesters, sludge lagoons, oxidation ponds, septic tanks, land fills and rivers.
Benefits of the Bioactivator
The primary benefit that FBF Organics offers is the increased capacity of WWTWs. The increased capacity means that the WWTW's ability to handle shock loads is also increased significantly.
Thus, the prevention of overflowing effluent and future sludge build-up is easily achieved. The product works best in overloaded systems.
FBF also allows clients the opportunity to be more environment friendly and improve their carbon footprint through the effective management of their WWTWs.
The FBF product has the potential to improve river water quality in South Africa and contribute to the achievement of legislation standards. It offers easy installation and operation, as well as being affordable, making it an attractive solution.
For more details contact coordinator@nthrys.com
Source: http://www.engineeringnews.co.za/article/organic-cost-effective-solution-to-sanitation-challenges-2009-03-27
The national sewage and effluent infrastructure is currently under stress from overloading and an ageing infrastructure that is in critical need of upgrading and refurbishment.
Essentially, FBF uses a natural product and fermentation technology to improve biological wastewater processes.
How It Works
Biological treatment technology involves the use of bacteria and other micro-organisms to degrade or remove contaminants from wastewater. The FBF Organics programme enhances this rate of degradation or decomposition through bioactivation.
This is the stimulation of existing micro-organisms by speeding up the metabolic activity. This increased metabolic activity is achieved by inoculating effluent ponds with activated effector molecules produced through the fermentation of a natural product in a specially designed bioreactor on site.
Tap water and the bioactivator are continuously fed into the bioreactor, allowing for regulated and effective management of wastewater treatment works (WWTWs).
FBF's solution could improve the bioremediation of wastewater, not only in municipal situations but also in agricultural and industrial applications.
The company has been successful in improving the performance of WWTWs in a wide variety of industries, such as tanneries, distilleries, fiberboards, sugar and paper mills, as well as on municipal sewage sites.
The FBF product has proven to be especially effective in treatment technologies including activated sludge, biofilters, anaerobic digesters, sludge lagoons, oxidation ponds, septic tanks, land fills and rivers.
Benefits of the Bioactivator
The primary benefit that FBF Organics offers is the increased capacity of WWTWs. The increased capacity means that the WWTW's ability to handle shock loads is also increased significantly.
Thus, the prevention of overflowing effluent and future sludge build-up is easily achieved. The product works best in overloaded systems.
FBF also allows clients the opportunity to be more environment friendly and improve their carbon footprint through the effective management of their WWTWs.
The FBF product has the potential to improve river water quality in South Africa and contribute to the achievement of legislation standards. It offers easy installation and operation, as well as being affordable, making it an attractive solution.
For more details contact coordinator@nthrys.com
Source: http://www.engineeringnews.co.za/article/organic-cost-effective-solution-to-sanitation-challenges-2009-03-27
Nucleic acid Dot plot
[http://arbl.cvmbs.colostate.edu/molkit/dnadot/]
Dot or matrix plots provide an easy and powerful means of sequence analysis, useful for searching out regions of similarity in two sequences and repeats within a single sequence.
For more information contact coordinator@nthrys.com
Dot or matrix plots provide an easy and powerful means of sequence analysis, useful for searching out regions of similarity in two sequences and repeats within a single sequence.
For more information contact coordinator@nthrys.com
'Slick' Gene Helps Cattle Beat The Heat
Pinpointing the chromosomal location of the "slick" gene identified by scientists could help breeders develop cattle with shorter, slick hair that helps keep them cool in the subtropical heat.
For more information contact coordinator@nthrys.com
For more information contact coordinator@nthrys.com
Next-Generation Sequencing Technology Applied to Commercial Cattle in Canada
Scientists have successfully sequenced the genome of two influential bulls, one beef and one dairy, the first animals to have been fully sequenced in Canada.
For more information contact coordinator@nthrys.com
For more information contact coordinator@nthrys.com
Scientists Hope to Cut Years Off Development Time of New Antibiotics
Eliminating tens of thousands of manual lab experiments, two University of Houston (UH) professors are working toward a method to cut the development time of new antibiotics. While current practices typically last for more than a decade, a computerized modeling system being developed at UH will speed up this process.
For further information contact coordinator@nthrys.com
For further information contact coordinator@nthrys.com
2/12/2011
Combine Targeted Agents to Kill Multiple Myeloma Cells
Multiple myeloma is a cancer involving antibody-producing cells in the bone marrow, and, in most cases, is incurable. Targeted therapies work by interfering with biological and biochemical functions critical for cancer cell survival and proliferation. The new treatment strategy combines Src inhibitors, which block the activity of an important group of proteins that regulate cancer cell behavior, with Chk1 inhibitors, which interfere with cancer cells' ability to undergo cell cycle arrest and repair DNA damage."Chk1 inhibitors are currently used primarily in conjunction with conventional DNA-damaging chemotherapeutic agents," "By combining Chk1 inhibitors with another targeted agent, such as Src inhibitors, we were able to induce cell death in multiple myeloma cells while sparing healthy, normal cells."When multiple myeloma cells are subjected to DNA-damaging agents, or even when they are undergoing normal DNA replication, their DNA is subject to breakage. To survive, they must slow down their progression through the cell cycle in order to repair the DNA, or, if the damage is too severe, undergo a form of cell suicide.Chk1 is an enzyme that allows cells to undergo cell cycle arrest, a process required to repair the DNA damage. When cancer cells are exposed to Chk1 inhibitors, they experience DNA damage and, as a consequence, launch another defense mechanism by activating a protein known as ERK1/2."The activation of ERK1/2 explains why multiple myeloma cells are able to survive the lethal effects of Chk1 inhibitors,"."Therefore, here Src inhibitors are used to block the activation of ERK1/2." The results were more promising than even the researchers had hoped.Src inhibitors not only blocked ERK1/2 activation, but also synergized with Chk1 inhibitors to trigger a dramatic increase in cell death. In addition, the combined treatment greatly reduced blood vessel formation, which plays an important role in the maintenance of many tumors, including multiple myeloma. Significantly, the treatment exerted virtually no effects on healthy, normal cells."Here tumors treated with the combined regimen were noticeably smaller and showed signs of a lack of blood supply when compared to tumors from the control group or those treated only with Chk1 inhibitors,"."This study is not only the first to demonstrate that Src inhibitors can dramatically increase the effects of Chk1 inhibitors, but it is also the first to show that preventing blood vessel formation may contribute to the effectiveness of this combination strategy."This study builds upon investigating cell signaling in relation to DNA damage repair and survival pathways involving Src and ERK1/2 proteins. The researchers are now developing more complex experiments as a prelude to clinical trials in multiple myeloma patients. "The approach of combining targeted agents will open up the possibility of developing entirely new therapies for patients with multiple myeloma and potentially other blood cancers,".For further more information contact coordinator@nthrys.com
2/11/2011
Production Of Pyocyanin(Alkaloids) from Pseudomonas Aeruginosa
Alkaloid-containing plants constitute an extremely varied group both taxonomically and chemically, a basic nitrogen being the only unifying factor for the various classes. Alkaloid’ (alkali-like) is somewhat difficult because there is no clear-cut boundary between alkaloids and naturally occurring complex amines. Pyocyanin is a active secondary metabolite that is produced by pseudomonas aeruginosa. Pseudomonas is gram negative capable of producing the water soluble pigment pyocyanin.it has antibiotic activity against bacteria.The purpose of this investigation was to determine the antibaacterial action of P.aeruginosa. The results of our study demonstrate the antimicrobial action of pyocyanin is bactericidal in nature.Pseudomonas aeruginosa, the producer organism, was also essentially unaffected by high concentrations of pyocyanin.
Industry of biotechnology is flourishing day by day. Every day NTHRYS team come up with different kind of Projects and even with new kind of techniques which are helpful in improving the health of many people. In this fast moving world, biotechnology is also accepting the challenges and making progress even faster. The above research Project is carried out at NTHRYS LABS.For more information contact Coordinator@nthrys.com
GeneSplicer
A computational method for splice site prediction. A fast, flexible system for detecting splice sites in the genomic DNA of various eukaryotes. The system has been trained and tested successfully on Plasmodium falciparum (malaria), Arabidopsis thaliana, human, Drosophila, and rice . Training data sets for human and Arabidopsis thaliana are included. Use the GeneSplicer Web Interface to run GeneSplicer directly, or see below for instructions on downloading the complete system including source code.
System requirements
GeneSplicer is released as source code and was tested on Linux RedHat 6.x+, Sun Solaris, and Alpha OSF1, but should work on any Unix system.
Obtaining GeneSplicer. This software is OSI Certified Open Source Software.
For more information contact coordinator@nthrys.com
System requirements
GeneSplicer is released as source code and was tested on Linux RedHat 6.x+, Sun Solaris, and Alpha OSF1, but should work on any Unix system.
Obtaining GeneSplicer. This software is OSI Certified Open Source Software.
For more information contact coordinator@nthrys.com
NCBI launches the Database of Genomic Structural Variations
The National Institutes of Health today announces the launch of a new resource, called the Database of Genomic Structural Variation, or dbVar, to help scientists understand how differences in DNA contribute to human health and disease.
For more information contact coordinator@nthrys.com
For more information contact coordinator@nthrys.com
How body clock synchronizes to day and night cycle
French researchers have unveiled a mechanism that explains how biological clock works in sync with the day and night cycle despite large fluctuations in light intensity during the day and from day to day.Following the identification of two central ‘clock genes’ of a green alga, Ostreococcus tauri, a mathematical model reproducing their daily activity profiles has revealed that their internal clock is influenced by the naturally varying light levels throughout the day only at periods when it needs resetting.
For more information contact coordinator@nthrys.com
For more information contact coordinator@nthrys.com
Mathematical model of red blood cells’ life cycle may predict anemia risk
Scientists have developed a mathematical model reflecting how red blood cells change in size and hemoglobin content during their four-month lifespan.
For more information contact coordinator@nthrys.com
For more information contact coordinator@nthrys.com
Subscribe to:
Posts (Atom)
