BioCryst Initiates a Phase 2 Study of BCX4208 Alone and in Combination with Allopurinol in Patients with Gout

BIRMINGHAM, Ala.–(Business Wire)–
BioCryst Pharmaceuticals, Inc. (NASDAQ: BCRX) today announced it is initiating a
Phase 2 study of BCX4208 alone and in combination with allopurinol in patients
with gout. BioCryst recently reported positive results from part one of its
Phase 2 monotherapy study of BCX4208 in patients with gout and is now moving
forward as planned with an additional Phase 2 trial of BCX4208.

This randomized, double-blind, multi-center, placebo-controlled study is
designed to evaluate the urate-lowering activity and safety of several doses of
BCX4208 alone and in combination with selected doses of allopurinol administered
once-daily in patients with gout for 21 days. The enrollment target for this
study is approximately 80 patients. The study utilizes a factorial design,
evaluating BCX4208 at doses of 20 mg, 40 mg and 80 mg administered as
monotherapy or in combination with allopurinol at doses of 100 mg, 200 mg and
300 mg. Allopurinol administered at 300 mg is the most common treatment dose for
patients with gout. The doses of BCX4208 selected for this study have been found
to be generally safe and well-tolerated in patients with psoriasis or gout.
Further details regarding this Phase 2 study design is available at
clinicaltrials.gov at the following link:

http://clinicaltrials.gov/ct2/show/NCT01129648

“We are pleased to initiate this Phase 2 study of BCX4208, a highly potent and
selective PNP inhibitor, as it will help to determine whether the inhibition of
xanthine oxidase and PNP together has additive or synergistic effects in
reducing uric acid levels in patients with gout,” said Dr. William P. Sheridan,
Chief Medical Officer at BioCryst. “We expect to complete this study during 2010
and look forward to providing top-line data in the fourth quarter.”

About BCX4208

BCX4208 is a next generation purine nucleoside phosphorylase (PNP) inhibitor
with the potential for once-a-day dosing suitable for chronic administration.
Previous studies have shown that BCX4208 may have utility in diseases dependent
on T-cells, B-cells or uric acid. With its novel mechanism of action, BCX4208
has the potential to address unmet medical needs across a broad spectrum of
inflammatory diseases, including gout.

About Gout

Gout is an inflammatory arthritis that affects up to five million people in the
U.S. Gout is caused by higher-than-normal uric acid in the blood, (a condition
known as hyperuricemia) that may lead to the buildup of uric acid in synovial
fluid around joints and the formation of monosodium urate crystals that result
in painful joint inflammation. More information regarding gout and hyperuricemia
is available at: http://www.cdc.gov/arthritis/basics/gout.htm

About BioCryst

BioCryst Pharmaceuticals designs, optimizes and develops novel small-molecule
pharmaceuticals that block key enzymes involved in infectious diseases, cancer
and inflammatory diseases. BioCryst has progressed two novel compounds that are
in late-stage pivotal clinical trials; peramivir, an anti-viral for influenza,
and forodesine, a purine nucleoside phosphorylase (PNP) inhibitor forcutaneous
T-cell lymphoma (CTCL). Additionally, BioCryst has a third product candidate,
BCX4208-a next generation PNP inhibitor-in mid-stage trials for the treatment of
gout. Utilizing crystallography and structure-based drug design, BioCryst
continues to discover additional compounds and to progress others through
pre-clinical and early development to address the unmet medical needs of
patients and physicians. For more information, please visit the Company’s Web
site at www.biocryst.com.

Forward-Looking Statements

This press release contains forward-looking statements, including statements
regarding future results, performance or achievements. These statements involve
known and unknown risks, uncertainties and other factors which may cause our
actual results, performance or achievements to be materially different from any
future results, performances or achievements expressed or implied by the
forward-looking statements. These statements reflect our current views with
respect to future events and are based on assumptions and subject to risks and
uncertainties. Given these uncertainties, you should not place undue reliance on
these forward-looking statements. Some of the factors that could affect the
forward-looking statements contained herein include: that we or our licensees
may not be able to enroll the required number of subjects in planned clinical
trials of our product candidates and that such clinical trials may not be
successfully completed; that our product candidates may not receive required
regulatory clearances from the FDA; that ongoing and future preclinical or
clinical development and commercialization of our product candidates, including
peramivir, forodesine, BCX4208 and other PNP inhibitor and hepatitis C
development programs, may not have positive results; that we or our licensees
may not be able to continue future development of our current and future
development programs; that our development programs may never result in future
product, license or royalty payments being received by BioCryst; that BioCryst
may not be able to retain its current pharmaceutical and biotechnology partners
for further development of its product candidates or it may not reach favorable
agreements with potential pharmaceutical and biotechnology partners for further
development of its product candidates; that BioCryst may not have sufficient
cash to continue funding the development, manufacturing, marketing or
distribution of its products and that additional funding, if necessary, may not
be available at all or on terms acceptable to BioCryst. Please refer to the
documents BioCryst files periodically with the Securities and Exchange
Commission, specifically BioCryst’s most recent Annual Report on Form 10-K,
Quarterly Reports on Form 10-Q, and current reports on Form 8-K, all of which
identify important factors that could cause the actual results to differ
materially from those contained in our projections and forward-looking
statements.

BCRXW

BioCryst Pharmaceuticals
Robert Bennett, +1-919-859-7910
or
WeissComm Group
Catherine Collier Kyroulis, +1-212-301-7174 (Media)

Copyright Business Wire 2010

Binge drinking weakens body’s ability to fight infections

Washington, Sept 18 (ANI): Binge drinking can weaken body’s ability to fight off infections for at least 24 hours afterwards, finds a new study.

Stephen Pruett, currently at the College of Veterinary Medicine at Mississippi State University, USA and Ruping Fan of Louisiana State University Health Sciences Centre, USA, focused their study on the effect of heavy drinking on toll-like receptor 4 (TLR4), a protein that has an important role in immune system activation.

Previous research has shown that too much alcohol inhibits the body’s production of pro-inflammatory cytokines, which are signalling molecules that launch the inflammatory response to infection.

The new study conducted over mouse model has confirm that acute alcohol exposure prevents the body from producing certain key pro-inflammatory cytokines.

The researchers found that ethanol molecules suppress TLR4′s usual ability to send signals that would normally trigger the production of inflammatory cytokines.

Alcohol’s effects continue long after the party is over: some cytokines were still not on full duty guarding against infection 24 hours after the binge.

“The time frame during which the risk of infection is increased might be at least 24 hours,” said Pruett.

“A persistent effect of ethanol on cells is indicated, such that inhibition of the response of some cytokines occurs even after the ethanol is cleared,” he added.

The study is published in the open access journal BMC Immunology. (ANI)

Aspirin ‘cuts colorectal cancer death risk’

Washington, Aug 12 (ANI): Taking aspirin on a regular basis after being diagnosed with colon cancer has been found to reduce the chances of dying from the disease, reveals a new study.

Numerous prospective, observational studies have shown that regular aspirin use is linked to a lower risk of colorectal adenoma (a benign tumour) or cancer.

However, the influence of aspirin on survival after diagnosis of colorectal cancer has been unknown.

Dr. Andrew Chan of Massachusetts General Hospital and Harvard Medical School in Boston and colleagues studied aspirin use in 1,279 men and women with colorectal cancer that had not spread to other parts of the body.

They found that people who took aspirin regularly after their diagnosis were nearly 29 percent less likely to die from their cancer than people who did not take aspirin. These people also were 21 percent less likely to die for any reason while they were in the study lasting more than two decades.

“These results suggest that aspirin may influence the biology of established colorectal tumours in addition to preventing their occurrence,” Chan said.

Aspirin is likely, at least in part, to prevent colorectal neoplasia (tumour growth) through inhibition of cyclooxygenase-2 (COX-2; an enzyme), which promotes inflammation and cell proliferation, and is overexpressed in the majority of human colorectal cancers, according to background information in the article.

The study has been published in the August 12 issue of JAMA. (ANI)

Locusts’ brains may provide clues to curing migraines, stroke

Washington, July 4 (ANI): Queen’s University biologists have revealed that insight into the locust’s brain may offer a novel way to manipulate human brain to stave off diseases like migraines, stroke, and epilepsy.

The researchers said that a similarity in brain disturbance between the insect and human sufferers of migraines, stroke, and epilepsy could open pathways for development of new drug therapies.

The study showed that the ability of the insect to resist entering the coma, and the speed of its recovery, can be manipulated using drugs that target one of the cellular signalling pathways in the brain.

“This suggests that similar treatments in humans might be able to modify the thresholds or severity of migraine and stroke,” said Gary Armstrong, who is completing his PhD research in Biology professor Mel Robertson’s laboratory.

“What particularly excites me is that in one of our locust models, inhibition of the targeted pathway completely suppresses the brain disturbance in 70 per cent of animals,” Dr. Robertson added.

The same researchers previously showed that locusts go into a coma as a way of shutting down and conserving energy, when conditions are dangerous.

The cellular responses in the locust are similar to the response of brain cells at the onset of a migraine. (ANI)

A thirst for blood sparks toxic algal blooms

Washington, July 1 (ANI): Scientists at the University of Gothenburg in Sweden have suggested that toxic algal blooms are created when aggressive algae kill and injure their competitors in order to absorb the nutrients they contain.

“The behaviour of the algae can be compared to that of blood-sucking insects,” said Per Jonsson of the Department of Marine Ecology.

The blooming of toxic algae in the oceans and lakes is a familiar health risk and causes problems every summer, leading to increased costs for water cleaning, water consumption and the tourist industry.

Scientists still do not know why algal blooms arise, and what it is that causes certain species of microalgae to multiply and form dense blooms.

Scientists within the research platform MARICE (Marine Chemical Ecology) at the Faculty of Science, the University of Gothenburg, present a new possible explanation of why algal blooms arise in a study.

Current theory postulates that the algae produce toxins not only in order to inhibit the growth of competing species, but also to protect themselves from predators.

The strategy of inhibiting competitors, however, is difficult to explain from an evolutionary perspective.

The turbulent ocean surface means, quite simply, that it is difficult for one algal species to obtain exclusive rights on the effect of a toxin that inhibits competitors.

The production of the toxin must be explained by other factors.

Marine ecologist Per Jonsson and his colleagues suggest that the inhibition of competitors that previous research had found is only a side-effect of a considerably more aggressive behaviour: toxic algae injure or kill competing algae in order to gain access to the nutrients in their cells.

“The way the algae absorb food is similar to that of blood-sucking insects, such as mosquitoes. Our study shows that this theft of nutrients may be an important mechanism in the formation of blooms of toxic plankton,” said Per Jonsson.

“The results will lead to several further experimental studies, and we hope that these will eventually contribute to solving the mystery of how algal blooms arise,” he added. (ANI)

New discovery may offer potential strategy for therapies to clear HIV

Washington, June 26 (ANI): Gladstone scientists have identified a key that regulates HIV latency – a discovery that may lead to eradication of HIV from infected patients who have been on antiretroviral therapy.

The real cure for HIV has been elusive because the virus can “hide” in a latent form in resting CD4-T cells.

By understanding this “latency” effect, researchers can identify ways to reactivate the virus and enable complete clearance by current or future therapies.

The study showed that methylation of cytosine in the DNA of infected cells is associated with HIV latency and inhibition of DNA methylation causes the reactivation of latent HIV.

“While HIV-1 latency is likely to be a multifactorial process, we have shown that inhibiting the methylation of the provirus contributes to an almost complete reactivation of latent HIV-1,” said lead author Steven E. Kauder.

In addition to finding that DNA methylation is a mechanism of latency, the scientists also discovered that a host protein, called methlyl-CpG binding domain protein 2 (MBD2) binds to the methylated HIV DNA and is an important mediator of latency.

“Interfering with methylation greatly potentiates the reactivation of HIV,” said Kauder.

In this study, the researchers found that the drug 5-aza-2′deoxycytidine (aza-CdR) can inhibit HIV methylation and cause the virus to reactivate.

“Combined with other areas of our investigation into HIV latency, this research provides important new knowledge about the process and opens many new pathways for future study,” said GIVI Associate Director Eric Verdin, MD, senior author of the study.

The discovery was reported in the current edition of PloS Pathogens. (ANI)

Key protein may explain how dietary restriction contributes to longevity, cancer prevention

Washington, May 22 (ANI): An Indian-origin researcher says that studying a protein that plays a key role in tumour formation, oxygen metabolism, and inflammation may help understand the anti-aging and anti-cancer benefits of dietary restriction, say researchers.

Dr. Pankaj Kapahi, of the Buck Institute for Age Research, has revealed that the protein is called hypoxia-inducible factor 1 (HIF-1), which helps cells survive by “turning on” when oxygen levels are low, and is also active in some forms of human cancer.

He further highlights the fact that HIF-1 overexpression is frequently detected in solid tumours, and that its inhibition has been proved to be an efficient way to prevent cancer growth.

He says that the current study has shown that HIF-1 is also a key player in dietary restriction.

The researcher says that HIF-1 is involved in a molecular pathway known to regulate cell growth and metabolism in response to nutrients and growth factors.

“Previous studies on HIF-1 have mainly focused on its roles in oxygen metabolism and tumor development,” he said.

Dr. Kapahi says that his study encourages the investigation of HIF-1 in nutrient sensing pathways.

“The data in this study also points to HIF-1 as a likely target for regulating the protective effects of dietary restriction in mammals. Dietary restriction is one of the most robust methods for extending lifespan and delaying age-related disease among various species,” he said.

According to the researcher, the molecular mechanisms involved in how dietary restriction slows cancer and extends lifespan have been largely unknown.

“This study gets us closer to understanding that process and gives us better targets for both designing and testing drugs which could mimic the effects of dietary restriction in humans,” he said.

For their study, the researchers genetically altered nematode worms to both under and over-express HIF-1.

The animals, which are the most-often used model to study aging, were fed different diets.

The researchers said that the animals that were designed to over-express HIF-1 did not get the benefit of lifespan extension, even though their diets were restricted.

They further revealed that the animals that under-expressed HIF-1 lived longer, even when they had a nutrient-rich diet.

The research team also observed the lifespan extension resulting from dietary restriction required activity in signalling pathways in the endoplasmic reticulum, the part of the cell involved in processing and the proper folding of proteins.

This finding supports the theory that aging stems from the effects of misfolded proteins, and opens up a rich area of investigation to examine the mechanisms by which stress in the endoplasmic reticulum affects lifespan.

The study has been published in the on-line journal PLoS Genetics. (ANI)

Chinese mind-body training technique improves attention, reduces stress

Washington, May 20 (ANI): Just five days of practicing a newly emerging mind-body technique may produce effective changes in attention and stress reduction, say Chinese researchers.

Now undergraduates at the University of Oregon are being taught the practice-called integrative body-mind training (IBMT)-which was adapted from traditional Chinese medicine in the 1990s in China, where it is practiced by thousands of people.

In a 2007 study, the researchers had reported that doing IBMT prior to a mental math test led to low levels of the stress hormone cortisol among Chinese students, along with lower levels of anxiety, depression, anger and fatigue than students in a relaxation control group.

“The previous paper indicated that IBMT subjects showed a reduced response to stressWhy after five days did it work so fast?” said UO professor Yi-Yuan Tang.

He says that the new findings point to how IBMT alters blood flow and electrical activity in the brain, breathing quality and even skin conductance, allowing for “a state of ah, much like in the morning opening your eyes, looking outside the grass and sunshine, you feel relaxed, calm and refresh without any stress, this is the meditation state.”

Using several technologies, the researchers conducted two experiments involving 86 undergraduate students at Dalian University of Technology and analyzed the data collected.

“We were able to show that the training improved the connection between a central nervous system structure, the anterior cingulate, and the parasympathetic part of the autonomic nervous system to help put a person into a more bodily state. The results seem to show integration-a connectivity of brain and body,” said UO psychologist Michael Posner.

In each experiment, participants who had not previously practiced relaxation or meditation received either IBMT or general relaxation instruction for 20 minutes a day for five days.

After conducting single photon emission computed tomography (SPECT), the researchers found that both groups experienced some benefit from the training-those in IBMT showed dramatic differences based on brain-imaging and physiological testing.

Physiological tests also revealed that IBMT subjects had lower heart rates and skin conductance responses, increased belly breathing amplitude, and decreased chest respiration rates as compared with the relaxation group.

Finally, the researchers noted that IBMT subjects had more high-frequency heart-rate variability than their relaxation counterparts, indicating “successful inhibition of sympathetic tone and activation of parasympathetic tone (in the autonomic nervous system).”

IBMT avoids struggles to control thought, and instead relies on a state of restful alertness, allowing for a high degree of body-mind awareness while receiving instructions from a coach.

The study has been published online ahead of regular publication in PNAS. (ANI)

Why eczema often leads to asthma

Washington, May 19 (ANI): Many young children who get a severe skin rash develop asthma later. Now, researchers from Washington University have shed light on what leads to progression from eczema, or atopic dermatitis, to breathing problems.

The doctors call this progression the atopic march.

In the new study, researchers have shown that a substance secreted by damaged skin circulates through the body and triggers asthmatic symptoms in allergen-exposed laboratory mice.

Early treatment of skin rash and inhibition of the trigger substance might block asthma development in young patients with eczema.

“Over the years, the clinical community has struggled to explain atopic march,” said study author Dr Raphael Kopan, professor of developmental biology and of dermatology.

“So when we found that the skin of mice with an eczema-like condition produced a substance previously implicated in asthma, we decided to investigate further.

“We found that the mice also suffered from asthma-like responses to inhaled allergens, implicating the substance, called TSLP, as the link between eczema and asthma,” he added.

The researchers found that cells in damaged skin can secrete TSLP (thymic stromal lymphopoietin), a compound capable of eliciting a powerful immune response.

And because the skin is so effective in secreting TSLP into the blood system, the substance travels throughout the body. When it reaches the lungs, it triggers the hypersensitivity characteristic of asthma.

“We are excited because we’ve narrowed down the problem of atopic march to one molecule,” said Kopan.

“We’ve shown that skin can act as a signalling organ and drive allergic inflammation in the lung by releasing TSLP. Now it will be important to address how to prevent defective skin from producing TSLP. If that can be done, the link between eczema and asthma could be broken,” he added.

The findings are published in Public Library of Science Biology. (ANI)

New way to reduce tumour-risk factor in stem cell therapy unveiled

Washington, May 7 (ANI): Paving the way for advancement in the field of stem cell therapy, scientists have discovered a method to potentially eliminate the tumour-risk factor in utilizing human embryonic stem cells.

Human embryonic stem cells are theoretically capable of differentiation to all cells of the mature human body, and are hence defined as “pluripotent”.

The above capability, along with the ability to remain undifferentiated indefinitely in culture, make regenerative medicine using human embryonic stem cells a potential tool for the treatment of various diseases, including diabetes, Parkinson’s disease and heart failure.

However, the biggest hurdle in using stem cells is their tendency to grow into a specific kind of tumour, called teratoma, when they are implanted in laboratory experiments into mice.

And scientists have thought that the tumorigenic feature will be manifested upon transplantation to human patients as well.

Thus the development of tumours from embryonic stem cells is especially puzzling, keeping in mind that these cells start out as completely normal cells.

So, researchers at the Stem Cell Unit in the Department of Genetics at the Silberman Institute of Life Sciences at the Hebrew University analysed the genetic basis of tumour formation from human embryonic stem cells, and identified a key gene that is involved in this unique tumorigenicity.

The gene called survivin is expressed in most cancers and in early stage embryos, but it is almost completely absent from mature normal tissues.

The gene is especially highly expressed in undifferentiated human embryonic stem cells and in their derived tumours.

The researchers could neutralise the activity of survivin in the undifferentiated cells as well as in the tumours, and thus managed to initiate programmed cell death (apoptosis) in those cells.

The inhibition of this gene just before or after transplantation of the cells could minimize the chances of tumour formation.

But the researchers have warned that a combination of strategies may be needed to address the major safety concerns regarding tumour formation by human embryonic stem cells. (ANI)

Novel target for depression treatment identified

Washington, Apr 29 (ANI): US researchers claim that a brain protein involved in fear behavior and anxiety may represent a new target for depression therapies.

The study, by researchers at the University of Iowa and the Iowa City Veterans Affairs Medical Center, has appeared in the April 29 issue of the Journal of Neuroscience.

Depression can be severely disabling. However, the causes of depression are not well understood.

The UI research team found that disrupting ASIC1a, an ion channel protein found in the brain, produced an antidepressant-like effect in mice. The effect was similar to that produced by currently available antidepressant drugs, but the team also showed that ASIC1a’s effect arose through a new and different biological mechanism.

“The mechanism issue is important because if a patient doesn’t respond to one drug, the chances of them responding to another drug that works through the same mechanism are low,” said study investigator John Wemmie, M.D., Ph.D., associate professor of psychiatry and neurosurgery at the UI Carver College of Medicine and a staff physician and researcher at the Iowa City Veterans Affairs Medical Center.

“We need antidepressants with new mechanisms of action to help those people who don’t respond to what is currently available,” the expert said.

Wemmie added that although there is no immediate therapy available based on the new findings, the results suggest that ASIC1a inhibition represents a new approach to antidepressant therapy. The channel can be blocked pharmacologically. (ANI)

Novel target for migraine prevention identified

Washington, Apr 29 (ANI): Researchers have found a potential target for developing new treatment for acute migraine attacks.

The new research by Addex Pharmaceuticals showed that targeting glutamate receptor ‘mGluR5′, the most common neurotransmitter in the brain, could prevent migraines.

The research team suggest that mGluR5 could play a role in the “migraine circuit,” a positive feedback loop that generates the symptoms of a migraine attack.

During the study, the researchers conducted trials with the help og potential drug candidate ADX10059, a negative mGluR5 allosteric modulator.

It showed efficacy in treating acute migraine attacks and provides evidence that inhibition of this glutamate receptor subtype could play a role in stopping migraine attacks before they start.

In the study involving 129 migraine patients, the researchers found that more patients taking ADX10059 than those taking placebo were pain-free two hours after dosing.

ADX10059 administration yielded better pain improvement at all time points up to two hours after treatment of a migraine attack.

“Medication is available to prevent migraine but these treatments are often secondary uses of the drug and come with potentially limiting side-effects,” said Dr. Peter Goadsby of the UCSF Headache Center.

“New therapies specifically developed for migraine prevention are urgently needed especially for the substantial proportion of migraine sufferers who have frequent attacks and have significant disability in their daily lives.

“Targeting mGluR5 signaling with ADX10059 is an interesting approach that is showing significant promise in early clinical evaluation.

“The clinical trial data for ADX10059 proved the concept that by terminating acute attacks in some patients, mGluR5 inhibition plays a role in migraine pathophysiology.

The study was presented at annual meeting of the American Academy of Neurology. (ANI)

Molecule that raises cardiac insufficiency risk identified

Washington, Apr 25 (ANI): Researchers from Center for Applied Medical Research (CIMA) of the University of Navarra have found a key enzyme in the development of cardiac insufficiency.

The enzyme is involved in the accumulation of fibrous tissues in the hearts of patients with chronic cardiac diseases and deterioration of heart functions.

The research project, published in the journal Hypertension, is part of a project of the “Red Europea de Excelencia en Hipertensisn y Enfermedades Cardiovasculares” [European Network of Excellence in Hypertension and Cardiovascular Diseases], in which research groups from Belgium, the Netherlands, Italy, Great Britain, France, Germany, Finland and Poland are all participating.

The accumulation of fibrosis in the heart has been proven to have a significant influence on the development of cardiac insufficiency among patients with chronic heart disease.

The research team from the CIMA analyzed the expression of Llysyl oxidase, an enzyme which regulates the amount of fibrous tissue in cardiac muscle.

“By means of molecular and histological methods, we have found that the cardiac muscle in patients with cardiac insufficiency contains an excess of this enzyme as well as collagen fiber (which it produces). These factors are associated with the deterioration of cardiac functions,” explained Dr. Begoqa Lspez, Lead Researcher of the project.

According to the researchers, this project shows that some drugs prescribed for patients with cardiac insufficiency do not actually inhibit the enzyme lysyl oxidase, nor do they reduce fibrosis or improve heart functions. Other drugs however, which are less commonly used, do have these beneficial qualities.

“Our work opens new possibilities for treating patients with heart disease through the inhibition of the enzyme. The development of cardiac insufficiency could thus be impeded,” said Begoqa Lspez. (ANI)

How smoking relieves stress

Washington, April 24 (ANI): Smoking to relieve stress is nothing new. But a new study has shown just how nicotine calms people down.

The study, conducted by a team of researchers at the University of California, suggests that nicotine may alter the activity of brain areas that are involved in the inhibition of negative emotions such as anger.

The research team, led by Jean Gehricke, studied the effect of nicotine patches on the subjects’ tendency to retaliate in response to anger provocation.

The subjects played a computer game and could see a video screen of another player who they believed to be their opponent, although, in fact, they were playing alone.

After each round, the victor could give his opponent a burst of unpleasant noise – at a duration and volume set by the winner.

In some of the subjects, nicotine was associated with a reduced tendency to retaliate, even after provocation by the ‘opponent’.

“Participants who showed nicotine-induced changes in anger task performance also showed changes in brain metabolism. Nicotine-induced reductions in length of retaliation were associated with changes in brain metabolism in response to nicotine in brain areas responsible for orienting, planning and processing of emotional stimuli,” Gehricke said.

The researchers said that their findings support the idea that people of an angry disposition are more susceptible to nicotine’s effects, and are therefore more likely to become addicted to cigarettes.

“Novel behavioral treatments that affect the cortical and limbic brain areas, like anger management training, may aid smoking cessation efforts in anger provoking situations that increase withdrawal and tobacco cravings, the authors said. (ANI)

New technique shrinks size of circuitry used in nanotechnology devices

Washington, April 17 (ANI): A University of Colorado at Boulder team, US, has developed a new method of shrinking the size of circuitry used in nanotechnology devices like computer chips and solar cells by using two separate colors of light.

Like current methods in the nanoengineering field, one color of light inscribes a pattern on a substrate, according to CU-Boulder Assistant Professor Robert McLeod of the electrical, computer and energy engineering department.

But, the new system developed by McLeod’s team uses a second color to “erase” the edges of the pattern, resulting in much smaller structures.

“The team used tightly focused beams of blue light to record lines and dots thousands of times smaller than the width of a human hair into patterned lithography on a substrate,” said McLeod.

The researchers then “chopped off the edges” of the lines using a halo of ultraviolet light, trimming the width of the lines significantly.

“We are essentially drawing a line with a marker on a nanotechnology scale and then erasing its edges,” said McLeod.

The method offers potential new approaches in the search for ways to shrink transistor circuitry, a process that drives the global electronic market that is pursuing smaller, more powerful microchips, he added.

For the project, McLeod and his team used a tabletop laser to project tightly focused beams of visible blue light onto liquid molecules known as monomers.

A chemical reaction initiated a bonding of the monomers into a plastic-like polymer solid.

If the beam was focused in one place, it inscribed a small solid dot. If the beam was moving the focus through the material, it created a thin thread, or line.

The researchers then added a second ultraviolet laser focused into a halo, or donut, which surrounded the blue light.

The special monomer formulation was designed to be inhibited by the UV light, shutting down its transformation from a liquid to a solid.

This “halo of inhibition” prevented the edges of the spot or line from developing, resulting in a much finer final structure.

According to McLeod, the new technology has the potential to lead to the construction of a variety of nanotechnology devices, including “nanomotors”.

“We now have a set of new tools. We believe this is a new way to do nanotechnology,” he said. (ANI)

Our eyes seek new targets while searching for something

Washington, April 15 (ANI): People’s attention does not return time and again to the objects they have already seen while searching for something, but they tend to shift their eyes to previously fixated locations when performing other visual tasks, according to a study.

Psychologists Michael D. Dodd from the University of Nebraska – Lincoln, Stefan Van der Stigchel of Utrecht University, and Andrew Hollingworth from the University of Iowa tracked eye movements of volunteers as they viewed various scenes, and recorded the location where the eyes were focused at each moment.

The volunteers were divided into four groups, with each group receiving different instructions for scene viewing.

They were told to search the scenes for a specific target, memorize each scene, rate how pleasant the scenes were, or free-view the scenes.

A target appeared in the scene during viewing, and the participants shifted their eyes as quickly as possible to the target. The target either appeared in an old location or a new location.

The researchers observed that the participants’ attention was less likely to return to objects they had already viewed during visual search tasks, but not during other visual tasks.

They said that the volunteers in the search group were slower to shift their eyes to previously fixated locations than to new locations.

However, the subjects in the other three groups exhibited the opposite pattern of eye movements: they were faster to shift their eyes to previously fixated locations than to new locations.

Based on their observations, the researchers came to the conclusion that the “facilitation of return” effect might be “the default setting of the visual system, with inhibition of return representing an exception implemented during visual search.”

The study has been reported in the journal Psychological Science. (ANI)

Curing Alzheimer’s disease would need combination therapy

Washington, March 18 (ANI): Researchers at the University of Illinois at Chicago College of Medicine say that a potential cure for Alzheimer’s disease may require a combination therapy, which will target the malformations of the proteins that characterise this condition.

Alzheimer’s disease is characterized by two distinctive protein malformations: amyloid plaques, which are sticky deposits made up of a short protein called amyloid beta, and tau tangles, which are made of short filaments of the tau protein.

Referring to a previous study, the researchers highlight the fact that tau tangles work together with amyloid beta to create a perfect storm that destroys neural function and memory.

They, however, insist that no study to date has been able to show as to how amyloid beta and the tau tangles wreak their damage on the nervous system.

Scott Brady, professor and head of anatomy and cell biology at the UIC College of Medicine, points out that when short assemblies of amyloid, rather than the long-chain plaques, get inside neurons, they interfere with the cells’ transport system.

This, according to him, limits their ability to send vital proteins and vesicles to where they are needed within the cell, and interferes with the synaptic connections to other nerve cells.

Brady says that the new study has shown that the short assemblies of amyloid activate a transport-regulatory enzyme called CK2, which causes the motor protein to drop its cargo.

His team have also found that inhibition of CK2 is sufficient to prevent the effects of amyloid on transport.

An earlier study by the same researchers showed that tau tangles halt transport to the neuron periphery through other regulatory enzymes, by causing the motor protein to release the microtubule track.

The new study shows that the CK2 activated by amyloid also works as a primer for one of the enzymes activated by tau tangles, GSK3.

“Now we have the perfect storm. Both amyloid and tau tangles cause problems. But when you put them together, you exacerbate the problems, creating the cascade of events that cause Alzheimer’s loss of neural connections,” said Brady.

“It makes sense of why both have to be present to have Alzheimer’s.

“It is also telling us that treating one is not going to be sufficient. We’re going to have to think in terms of combination therapies that will allow us to address many targets at once. This may explain why attempts to manipulate one or the other haven’t been successful in patients,” he added.

A research article on the current study appears in the online edition of Proceedings of the National Academy of Sciences. (ANI)

Genetic mutations linked to high levels of ‘good’ cholesterol

Washington, Mar 17 (ANI): A new study from the University of Pennsylvania has shown that high levels of HDL cholesterol (HDL-C), also known as “good” cholesterol, could be tied to genetic mutations.

Individuals with high plasma HDL-C levels have a decreased risk of developing coronary artery disease.

Lead researcher Daniel Rader has identified a gene called LIPG, which when mutated result in high plasma HDL-C levels.

During the study, the researchers looked at 585 subjects of European ancestry, and identified 10 people with previously unreported rare mutated forms of this gene that were unique to subjects with very high HDL-C levels

Further analysis revealed that mutations in the LIPG gene that cause loss of endothelial lipase activity were the cause of increased plasma HDL-C levels.

These data provide important human genetic evidence that inhibition of endothelial lipase is likely to raise HDL-C levels in humans. (ANI)

Buckyballs can be used to keep water pipes clear from clogging

Washington, March 5 (ANI): Engineers at Duke University, US, have found that microscopic particles of carbon known as buckyballs may be able to keep water pipes clear in the same way clot-busting drugs prevent arteries from clogging up.

The research team found that buckyballs hinder the ability of bacteria and other microorganisms to accumulate on the membranes used to filter water in treatment plants.

This attribute leads the researchers to believe that coating pipes and membranes with these nanoparticles may prove to be an effective strategy for addressing one of the major problems and costs of treating water.

“Just as plaque can build up inside arteries and reduce the flow of blood, bacteria and other microorganisms can over time attach and accumulate on water treatment membranes and along water pipes,” said So-Ryong Chae, post-doctoral fellow in Duke’s environmental and civil engineering department.

“As the bacteria build up on these surfaces, they attract other organic matter, creating a biofilm that slowly builds up over time,” Chae added.

According to Chae, “The results of our experiments in the laboratory indicate that buckyballs may be able to prevent this clogging, known as biofouling.”

The only other options to address biofouling are digging up the pipes and replacing the membranes, which can be expensive and inconvenient.

A buckyball, or C60, is one shape within the family of tiny carbon shapes known as fullerenes. They are named after Richard Buckminster Fuller, the inventor of the geodesic dome, since their shape resembles his famous structure.

The addition of buckyballs to treatment membranes had a two-fold effect.

First, treated membranes showed less bacterial attachment than non-treated membranes. After three days, the membranes treated with buckyballs had on average 20 colony forming units, the method by which bacterial colonies are counted.

“In contrast, the number of bacterial colonies on the untreated membrane was too numerous to count,” Chae said.

Chae also found that the presence of the buckyballs inhibited respiration, or the ability of the bacteria to use oxygen to fuel its activities.

“As the concentration of buckyballs increased, so did the inhibition of respiration,” Chae said. “This respiratory inhibition and anti-attachment suggests that this nanoparticle may be useful as an anti-fouling agent to prevent the biofouling of membranes or other surfaces,” he added. (ANI)