Human stem cells engineered to seek out and kill HIV

In a major breakthrough in the fight against AIDS, scientists claim to have for the first time shown that human stem cells can be genetically engineered to seek out and kill HIV-infected cells in a living organism.

The study demonstrates f

or the first time that engineering stem cells to form immune cells that target HIV is effective in suppressing the virus in living tissues in an animal model, said lead scientist Scott G Kitchen.

He added: “We believe that this study lays the groundwork for the potential use of this type of an approach in combating HIV infection in infected individuals, in hopes of eradicating the virus from the body.”

In their previous research, the scientists took CD8 cytotoxic T lymphocytes — the “killer” T cells that help fight infection — from an HIV-infected individual and identified the molecule known as the T cell receptor, which guides T cell in recognising and killing HIV-infected cells.

In their latest research, the scientists at California University similarly engineered human blood stem cells and found that they can form mature T cells that can attack HIV in tissues where the virus resides and replicates.

They did so by using a surrogate model, the humanised mouse, in which HIV infection closely resembles the disease and its progression in humans.

In a series of tests on the mice’s peripheral blood, plasma and organs conducted two weeks and six weeks after introducing the engineered cells, the scientists found that the number of CD4 “helper” T cells — which become depleted as a result of HIV infection — increased, while levels of HIV in the blood decreased.

CD4 cells are white blood cells that are an important component of immune system, helping to fight off infections.

These results indicated that the engineered cells were capable of developing and migrating to the organs to fight infection there, the PLoS Pathogens journal reported.

“We believe that this is the first step in developing a more aggressive approach in correcting the defects in the human T cell responses that allow HIV to persist in infected people,” Mr. Kitchen said.

Keywords: HIV-AIDS, stem cells research

Residents of Pak’s Bara district flee homes following Lashkasr’s warning

Landi Kotal (Pakistan), Sep 19 (ANI): Following a warning issued by the leader of a terrorist organization, hundreds of Bara residents fled their houses to move to safer places before the last day of Eidul Fitr festivities.

On Friday morning, Lashkar-i-Islam (LI) chief Mangal Bagh issued a warning over his illegal FM radio station, saying that people should take cover as his armed outfit was about to retaliate the military operation in Bara, The Dawn reports.

Earlier, the militant leader had said that his private miltia would not resist the operation in the area.

Traders and shopkeepers of Bara bazaar have shifted their merchandise to safer places, it has been learned.

Meanwhile, the bullet-riddled body of Wahid son of Hanan, who was kidnapped by Lashkar activists a day earlier, was found in Jamrud Khwar area.

A note was found with the dead body saying that anyone found assisting the security forces would meet the similar fate.

Earlier, the FC media cell had appealed the locals to help security forces in their operation against militants. (ANI)

Four Nepali women being sent to Muscat detained at Gorakhpur

Gorakhpur, Sept 19 (ANI): Volunteers of a social service organisation and the personnel of the Anti-Human Trafficking Cell of Uttar Pradesh Police at Gorakhpur detained four Nepalese women.

Reportedly, as per the statement of the women who were taken into custody at the Gorakhpur Railway Station, they were intending to go to Muscat.

These women had entered India through the Sanauli border post.

Although all the four women had their respective passports with them, only two of them could show their endorsed visas for Muscat.

“Our team visited the railway station along with a Nepali counsellor. When she saw these women and spoke to them, they gave some wrong information, which in turn sounded fishy and made us to suspect something was amiss. When we asked them where they were heading, initially they said Oman and again changed their statement saying, New Delhi. When our counsellor asked them for their passports, some said they had it while others said they didn’t. So, we found them suspicious,” said Gyan Kumar, co-ordinator, Maanava Sewa Sansthan, Gorakhpur.

Amidst such confusing utterances by the women, the police believe that one of the women named Dilmaya was trying to send the other three to Muscat by bringing them from Nepal.

She claimed that they were going to Muscat because they had their relatives residing and working there.

“These people held us for interrogation. We asked them either to let us go to Nepal or else allow us to go to Muscat. We have our relatives there,” said Dilmaya.

A couple of months ago, police officials of Gorakhpur had detained five women who were allegedly being trafficked to Gulf countries for flesh trade.

Reportedly, a pimp was escorting these women to Mumbai from where they were to be sent to certain destinations in the Middle East. (ANI)

Catalyst simulations for fuel cells may make clean cars a reality

Washington, Sep 18 (ANI): University of Wisconsin-Madison researchers are working towards developing better catalyst for fuel cells in a bid to make clean cars a reality.

If successful, the researchers could make a car that runs on hydrogen from solar power, and produces water instead of carbon emissions.

Materials science and engineering assistant professor Dane Morgan and Ph.D. student Edward (Ted) Holby have developed a computational model that could optimise an important component of fuel cells, making it possible for the technology to have a more widespread use.

The researchers investigated how particle size is related to the overall stability of a material, and showed with their model that increasing the particle size of a fuel cell catalyst decreases degradation and therefore increases the useful lifetime of a fuel cell.

Fuel cells are electrochemical devices that facilitate a reaction between hydrogen and oxygen, producing electrical power and forming water.

In the type of fuel cells Morgan is researching, called proton exchange membrane fuel cells (PEMFCs), hydrogen is split into a proton and electron at one side of the fuel cell (the anode).

The proton moves through the device while the electron is forced to travel in an external circuit, where it can perform useful work, while at the other side of the fuel cell (the cathode), the protons, electrons and oxygen combine to form water, which is the only waste product.

One of the many hurdles to producing efficient fuel cells for widespread use is the catalyst added to aid the reaction between protons, electrons and oxygen at the cathode.

Current fuel cells use platinum and platinum alloys as a catalyst. While platinum can withstand the corrosive fuel cell environment, it is expensive and not very abundant.

Thus, to maximize platinum use, researchers use catalysts made with platinum particles as small as two nanometers, which are approximately 10 atoms across.

These tiny structures have a large surface area on which the fuel cell reaction occurs.

However, platinum catalysts this small degrade very quickly, which means that the fuel cell doesn’t last long.

The researchers have found a possible solution to the rapid degradation problem-when it comes to catalyst particle size, sometimes smaller isn’t better.

In their modelling work, they showed that if the particle size of a platinum catalyst is increased to four or five nanometers, which is approximately 20 atoms across, the level of degradation significantly decreases.

This means the catalyst and the fuel cell as a whole can continue to function for much longer than if the particle size was only two or three nanometers.

“Fuel cells are just one of many energy technologies – solar, battery, etc. – with enormous potential to reduce our dependence on oil and our carbon emissions. Computer simulation offers a powerful tool to understand and develop new materials at the heart of these energy technologies,” said Morgan. (ANI)

Genes controlling insulin ‘alter’ body clock

Washington, Sept 18 (ANI): Scientists at University of California, San Diego have identified certain insulin-regulating genes that can also alter the timing of the body clock.

They said that the findings can lead to new approaches to treating disorders such as metabolic syndrome that can result, at least in part, from chronic disruption of the sleep-wake cycle.

“People knew that the clock regulates many different processes, but what they didn’t realize what that when you tweak those processes, it feeds back and alters the clock,” said Steve Kay, Dean of the Division of Biological Sciences at the University of California, San Diego, who led the study along with John Hogenesch of the University of Pennsylvania.

A molecular clock controls daily physiological rhythms in many types of cells, even cells grown in culture.

By engineering cultured cells to glow yellow when a particular clock gene switched on, the team made the cycle visible. They then interfered with every human gene to see which would shift the clock. They found that hundreds altered the timing.

“We just suddenly discovered 350 new genes that affect the clock that weren’t known before,” Kay said.

However, subsequent screening to confirm the genes’ effect on a second clock gene narrowed the list to 200.

Seven genes involved in insulin control also influenced the rhythms of the clock.

“What came out very strongly was this close relationship between circadian regulation and insulin signalling. There’s a reciprocal relationship between circadian dysfunction and metabolic dysfunction,” said Kay.

The researchers suggest that genetically altered mice with malfunctioning clocks become obese and develop diet-induced diabetes.Understanding this close relationship between circadian regulation and metabolic homeostasis should provide novel ways of identifying new therapies for metabolic disease,” Kay added.

The study appears in journal Cell. (ANI)

Stem cell transplantation may correct rare genetic disorder in kids

Washington, Sep 18 (ANI): Scripps Research Institute scientists have offered new hope for parents whose children suffer from the rare genetic disorder ‘cystinosis’ by showing through an experiment on mice that stem cell transplantation can successfully correct the defect.

“After meeting the children who suffer from this disease, like an 18-year-old who has already had three kidney transplants, and the families who are desperately searching for help, our team is committed to moving toward a cure for cystinosis, a lysosomal storage disorder. This study is an important step toward that goal,” said principal investigator Stephanie Cherqui.

In the study, the researchers used bone marrow stem cell transplantation to address symptoms of cystinosis in a mouse model.

The procedure virtually halted the cystine accumulation responsible for the disease, and the cascade of cell death that follows.

Cystine is a by-product of the break down of cellular components the body no longer needs in the cell’s “housekeeping” organelles, called lysosomes.

Normally, cystine is shunted out of cells, but in cystinosis a gene defect of the lysosomal cystine transporter causes it to build up, forming crystals that are especially damaging to the kidneys and eyes.

Cystinosis is a rare but devastating disease affecting children as young as six months, who begin to suffer renal dysfunction, which grows progressively worse with time. Other symptoms include diabetes, muscular disease, neurological dysfunction, and retinopathy.

The only available drug to treat cystinosis, cysteamine, while slowing the progression of kidney degradation, does not prevent it, and end-stage kidney failure is inevitable.

In the new study, the researchers found that transplanted bone marrow stem cells carrying the normal lysosomal cystine transporter gene abundantly engrafted into every tissue of the experimental mice.

This led to an average drop in cystine levels of about 80 percent in every organ.

Not only it prevented kidney dysfunction, there was less deposition of cystine crystals in the cornea, less bone demineralization, and an improvement in motor function.

“The results really surprised and encouraged us. Because the defect is present in every cell of the body, we did not expect a bone marrow stem cell transplant to be so widespread and effective,” says Cherqui.

Cherqui said that adult bone marrow stem cell therapy is particularly well suited as a potential treatment for cystinosis because these cells target all types of tissues.

In addition, stem cells reside in the bone marrow for the duration of a patient’s life, becoming active as needed, a particular benefit for a progressive disease like cystinosis.

The study has been published in the journal Blood. (ANI)

Green tea may help improve bone health

Washington, Sept 17 (ANI): Green tea may help improve bone health, researchers in Hong Kong have reported.

The boffins found that the tea contains a group of chemicals that can stimulate bone formation and help slow its breakdown.

The study has been published in ACS’ Journal of Agricultural and Food Chemistry, a bi-weekly publication.

In the study, Ping Chung Leung and colleagues noted that many scientific studies have linked tea to beneficial effects in preventing cancer, heart disease, and other conditions.

To reach the conclusion, scientists exposed a group of cultured bone-forming cells (osteoblasts) to three major green tea components – epigallocatechin (EGC), gallocatechin (GC), and gallocatechin gallate (GCG) – for several days. They found that one in particular, EGC, boosted the activity of a key enzyme that promotes bone growth by up to 79 percent. EGC also significantly boosted levels of bone mineralization in the cells, which strengthens bones.

The scientists also showed that high concentrations of ECG blocked the activity of a type of cell (osteoclast) that breaks down or weakens bones. The green tea components did not cause any toxic effects to the bone cells, they noted. (ANI)

Gene linked to male infertility identified

Washington, Sept 16 (ANI): Scientists from Virginia Commonwealth University have identified a gene that may contribute to male infertility.

The research team hopes that the new findings would lead to new approaches to male contraception.

Sperm are produced in the testicles through a three-step process called spermatogenesis.

During the final stage, known as spermiogenesis, a lot of changes take place, including the packaging of DNA into the sperm head and the formation of the sperm tail, which propels the sperm cell toward the egg.

The study conducted using mouse model showed that mice lacking a protein called meiosis expressed gene 1, or MEIG1, were sterile as a result of impaired spermiogenesis – the process that encompasses changes in the sperm head and the formation of the tail.

The team also found that MEIG1 associates with the Parkin co-regulated gene protein, or PACRG protein, and that testicular PACRG protein is reduced in MEIG1-deficient mice.

PACRG is thought to play a key role in assembly of the sperm tail, and the reproductive phenotype of PACRG -deficient mice mirrors that of the MEIG1-mutant mice.

“We discovered that MEIG1 is essential for male fertility. Moreover, our findings reveal a critical role for the MEIG1/PACRG partnership in the function of a structure that is unique to sperm, the manchette. The absence of a normal manchette in mice lacking MEIG1 totally disrupts the maturation process of sperm,” said Dr Jerome F. Strauss III, dean in the VCU School of Medicine.

“In addition to having an impact on fertility, the discovery identifies a new target for drug discovery for a much needed reversible male method of contraception,” he added.

The study is published in the Early Edition of the Proceedings of the National Academy of Sciences. (ANI)

Popular diabetes drug may help fight breast cancer

Washington, Sept 15 (ANI): A popular diabetes drug called metformin has been found to be effective in fighting breast cancer.

The findings of the study from Harvard Medical School showed that metformin, along with conventional chemotherapy, shows promise for treating and delaying recurrence of breast cancer.

“We have found a compound selective for cancer stem cells,” said senior author Kevin Struhl, the David Wesley Gaiser professor of biological chemistry and molecular pharmacology at HMS.

“What’s different is that ours is a first-line diabetes drug,” he added.

The drug seemed to work independently of its ability to improve insulin sensitivity and lower blood sugar and insulin levels, all of which are also associated with better breast cancer outcomes.

“There is a big desire to find drugs specific to cancer stem cells,” said Struhl.

“The cancer stem cell hypothesis says you cannot cure cancer unless you also get rid of the cancer stem cells. From a purely practical point of view, this could be tested in humans. It’s already used as a first-line diabetes drug,” he added.

Lead researchers Heather Hirsch and Dimitrios Iliopoulos found that the combination of metformin and the cancer drug doxorubicin killed human cancer stem cells and non-stem cancer cells in culture.

In mice, pre-treatment with the diabetes drug prevented the otherwise dramatic ability of human breast cancer stem cells to form tumours.

In cases where tumours were allowed to take hold for 10 days, the dual therapy also reduced tumour mass more quickly and prevented relapse for longer than doxorubicin alone.

“This is an exciting study,” said Jennifer Ligibel, a medical oncologist at Dana-Farber Cancer Institute and an HMS instructor in medicine, who was not involved in the study.

“There is a lot of interest in studying metformin in breast cancer, but so far we do not have direct evidence that metformin will improve outcomes in patients,” Ligibel said. “That’s what this trial is for.”

The findings appear online in the journal Cancer Research. (ANI)

Scientists make first high-resolution 3D images of a polymer solar cell’s insides

Washington, September 14 (ANI): Researchers from the Eindhoven University of Technology and the University of Ulm in Germany have made the first high-resolution 3D images of the inside of a polymer solar cell.

This gives them important new insights in the nanoscale structure of polymer solar cells and its effect on the performance.

The investigations shed new light on the operational principles of polymer solar cells.

These solar cells do not have the high efficiencies of their silicon counterparts yet. Polymer cells, however, can be printed in roll-to-roll processes, at very high speeds, which makes the technology potentially very cost-effective.

Added to that, polymer cells are flexible and lightweight, and therefore suitable to be used on vehicles or clothing or to be incorporated in the design of objects.

In these hybrid solar cells, a mixture of two different materials, a polymer and a metal oxide are used to create charges at their interface when the mixture is illuminated by the sun.

The degree of mixing of the two materials is essential for its efficiency.

Intimate mixing enhances the area of the interface where charges are formed but at the same time obstructs charge transport because it leads to long and winding roads for the charges to travel.

Larger domains do exactly the opposite.

The vastly different chemical nature of polymers and metal oxides generally makes it very difficult to control the nanoscale structure.

The Eindhoven researchers have been able to largely circumvent this problem by using a precursor compound that mixes with the polymer and is only converted into the metal oxide after it is incorporated in the photoactive layer.

This allows better mixing and enables extracting up to 50 percent of the absorbed photons as charges in an external circuit.

The importance of the degree of mixing was clearly demonstrated by visualization of the structure of these blends in three dimensions.

Traditionally such visualization has been extremely challenging, but by using 3D electron tomography, the team has been able to resolve the mixing with unprecedented detail on a nanoscale.

From these images, the researchers at the Institute of Stochastics in Ulm have been able to extract typical distances between the two components, relating to the efficiency of charge generation, and analyze the percolation pathways, that is, how much of each component is connected to the electrode.

These quantitative analyses of the structure matched perfectly with the observed performance of the solar cells in sunlight. (ANI)

Master gene that switches on disease-fighting cells identified

London, Sep 14 (ANI): British scientists have identified the master gene, called E4bp4, that causes blood stem cells to turn into disease-fighting ‘Natural Killer’ (NK) immune cells.

The discovery, by researchers at Imperial College London, UCL and the Medical Research Council’s National Institute for Medical Research, could one day help scientists boost the body’s production of these frontline tumour-killing cells, creating new ways to treat cancer.

By ‘knocking out’ E4bp4 in a mouse model, the researchers created the world’s first animal model entirely lacking NK cells, but with all other blood cells and immune cells intact.

The breakthrough model should help solve the mystery of the role that Natural Killer cells play in autoimmune diseases, such as diabetes and multiple sclerosis.

According to many scientists, these diseases are a result of malfunctioning NK cells that turn on the body and attack healthy cells, which cause disease instead of fighting it.

They believe that clarifying NK cells’ role could lead to new ways of treating these conditions.

Natural Killer cells – a type of white blood cell – are a major component of the human body’s innate, quick-response immune system, providing a fast frontline defence against tumours, viruses and bacterial infections.

The gene E4bp4 is the ‘master gene’ for NK cell production, which means it is the primary driver that causes blood stem cells in the bone marrow to differentiate into NK cells.

Led by Dr Hugh Brady, the researchers are hoping to progress with a drug treatment for cancer patients which reacts with the protein expressed by their E4bp4 gene, causing their bodies to produce a higher number of NK cells than normal, to increase the chances of successfully destroying tumours.

“If increased numbers of the patient’s own blood stem cells could be coerced into differentiating into NK cells, via drug treatment, we would be able to bolster the body’s cancer-fighting force, without having to deal with the problems of donor incompatibility,” Nature quoted Brady as saying.

The researchers proved the pivotal role E4bp4 plays in NK production when they knocked the gene out in a mouse model.

Without E4bp4 the mouse produced no NK cells whatsoever but other types of blood cell were unaffected.

“Now finally, with our discovery of the NK cell master gene and subsequent creation of our mouse model, we will be able to find out if the progression of these diseases is impeded or aided by the removal of NK cells from the equation. This will solve the often-debated question of whether NK cells are always the ‘good guys’, or if in certain circumstances they cause more harm than good,” said Brady.

The study has been published in Nature Immunology. (ANI)

New method to monitor early sign of oxidative stress that triggers cancer

Washington, Sept 12 (ANI): Scientists from University of Michigan have developed a new method to monitor early sign of oxidative stress that triggers cancer spread.

Lead researcher Kate Carroll suggests that being able to monitor a marker of oxidative stress that is associated with the activation of tumor cell growth pathways, particularly at an early stage, and then tailor treatments accordingly would allow for more targeted studies and might improve the odds of success with antioxidants and pro-oxidants.

The new method detects sulfenic acid in proteins-a tip off to early oxidative stress and to a specific protein modification associated with cell growth pathways.

Sulfenic acid is produced when a particular oxidant, hydrogen peroxide, reacts with the protein building block cysteine. But because the chemical modification involved is so small and transient, it has been difficult to detect.

To get around that problem, Carroll and Seo used a chemical probe that “traps” sulfenic acid and tags it for recognition by an antibody.

The antibody is labeled with a fluorescent dye that glows when observed with a fluorescence microscope.

The researchers then used the method to assess sulfenic acid levels as a marker of oxidative stress in several systems, including a panel of breast cancer cell lines.

“For each line, we saw a very distinct pattern of sulfenic acid modifications,” indicating different oxidative stress levels and hinting at differences in the underlying molecular events associated with tumor growth,” said Carroll, assistant professor of chemistry and a research assistant professor in the Life Sciences Institute.

“Whether the patterns we see will correlate with response to antioxidant treatment or other therapies that modulate oxidative stress level remains to be seen, but now we at least have a way to investigate that question,” the expert added.

The study appears in Proceedings of the National Academy of Sciences. (ANI)

Why pandemic swine flu causes more severe symptoms than seasonal flu

London, September 11 (ANI): Scientists at Imperial College London have warned that pandemic swine flu can infect cells deeper in the lungs than seasonal flu can.

They write in a research paper that this may help understand why people infected with the pandemic strain of swine-origin H1N1 influenza are more likely to suffer more severe symptoms than those infected with the seasonal strain of H1N1.

The researchers have also stressed the need for monitoring the current pandemic H1N1 influenza virus for any changes in the way it infects cells, which may make infections more serious.

Generally, influenza viruses infect cells by attaching to bead-like molecules on the outside of the cell, known as receptors. If a virus cannot find its specific receptors, it cannot get into the cell.

Seasonal influenza viruses attach to receptors found on cells in the nose, throat and upper airway, enabling them to infect a person’s respiratory tract.

In the current study, the researchers have found that pandemic H1N1 swine flu can also attach to a receptor found on cells deep inside the lungs, which can result in a more severe lung infection.

They say that the pandemic influenza virus’s ability to stick to the additional receptors may explain why the virus replicates, and spreads between cells more quickly.

“Most people infected with swine-origin flu in the current pandemic have experienced relatively mild symptoms. However, some people have had more severe lung infections, which can be worse than those caused by seasonal flu. Our new research shows how the virus does this – by attaching to receptors mostly found on cells deep in the lungs. This is something seasonal flu cannot do,” Nature Biotechnology quoted Professor Ten Feizi, from the Division of Medicine at Imperial College London, as having writte in the research paper.

The researchers found that pandemic H1N1 influenza bound more weakly to the receptors in the lungs than to those in the upper respiratory tract, which is why most people infected with the virus have experienced mild symptoms.

However, the researchers are concerned that the virus could mutate to bind more strongly to these receptors.

“If the flu virus mutates in the future, it may attach to the receptors deep inside the lungs more strongly, and this could mean that more people would experience serious symptoms. We think scientists should be on the lookout for these kinds of changes in the virus so we can try to find ways of minimising the impact of such changes,” said Prof. Feizi.

“Receptor binding determines how well a virus spreads between cells and causes an infection. Our new study adds to our understanding of how swine-origin influenza H1N1 virus is behaving in the current pandemic, and shows us changes we need to look out for,” added Prof. Feizi.

The financial assistance for the study came from the Wellcome Trust, the Medical Research Council and the Engineering and Physical Sciences Research Council. (ANI)

Exposure to second-hand tobacco smoke linked to liver disease

Washington, September 11 (ANI): People can develop liver disease even when they are exposed to second-hand tobacco smoke, according to a study.

Scientists at the University of California, Riverside (UCR) have found that exposure to second-hand tobacco smoke can lead to non-alcoholic fatty liver disease (NAFLD), a common disease and rising cause of chronic liver injury wherein fat accumulates in the liver of people who drink little or no alcohol.

For their study, the researchers exposed some mice to second-hand cigarette smoke for a year in the lab, and observed fat build-up in their liver cells, a sign of NAFLD that eventually leads to liver dysfunction.

The researchers focused on two key regulators of lipid (fat) metabolism that are found in many human cells as well: SREBP (sterol regulatory element-binding protein) that stimulates synthesis of fatty acids in the liver, and AMPK (adenosine monophosphate kinase) that turns SREBP on and off.

They found that second-hand smoke exposure inhibits AMPK activity, which, in turn, causes an increase in activity of SREBP.

More active SREBP results in more fatty acids getting synthesized, they say.

The result is NAFLD induced by second-hand smoke, according to the researchers.

“Our study provides compelling experimental evidence in support of tobacco smoke exposure playing a major role in NAFLD development,” said Manuela Martins-Green, a professor of cell biology, who led the study.

“Our work points to SREBP and AMPK as new molecular targets for drug therapy that can reverse NAFLD development resulting from second-hand smoke. Drugs could now be developed that stimulate AMPK activity, and thereby inhibit SREBP, leading to reduced fatty acid production in the liver,” Martins-Green added.

A research article describing the study has been published in the Journal of Hepatology. (ANI)

Suspected Jakarta bombing ‘mastermind’ was trained in Pak

Jakarta, Sep.9 (ANI): In yet another case which determines that terror is Pakistan’s principle export, it has been revealed that the prime suspect of the July 2009 Jakarta hotel attacks received military training in Pakistan.

Indonesia’s national police chief General Bambang Hendarso Danuri disclosed that Mohamad Jibril, who allegedly provided funds for the terror group responsible for the bombings, received training in Pakistan during 1999-2000.

“Jibril received military training from several Jemaah Islamiyah activists for about a year, from 1999- 2000,” Bambang told the House of Representatives.

“The training was conducted in Pakistan while he was studying there,” he added.

Mohamad Jibril alias Mohamad Rizky Ardhan alias Muhammad Jibriel Abdul Rahman was arrested two weeks ago.

He is believed to have played a key role in raising funds for the terrorist group led by Noordin Top, who belongs to Malaysia.

The Indonesian police suspect that the money was coming from Middle Easte countries such as Saudi Arabia and Yemen, however, it is yet to arrive on any conclusion.

Officials said they are still working to find more solid evidence against Jibril, who was nabbed after his cell phone number was found in Ali Muhammad bin Abdullah’s mobile phone.

Ali is a Saudi Arabian who was arrested a few days before Jibril, the jihadwatch.org reports.

It has also been revealed that Jibril’s uncle, Irfan S Awwas, was the chairman of a radical Islamic organization , Indonesia Mujahidin Council (MMI). (ANI)

Pak Telecom authority denies planning to snoop on all phone calls, e-mails, sms’

Islamabad, Sep.9 (ANI): The Pakistan Telecommunication Authority (PTA) has rejected reports regarding it forming a regulation committee to monitor telecom traffic including phones calls, e-mails and text messages, The Daily Times reports.

Commenting on the reports regarding the PTA’s plans of having a monitoring cell to keep tab of all telecommunication traffic, a PTA spokesperson said monitoring cyber and telecom traffic does not come under the authority’s mandate.

The spokesperson, however, said the PTA has installed latest filters to check illegal telecommunication traffic coming into the country.

Earlier, it was reported that the PTA has drafted a plan to monitor all telecommunication traffic, including landlines, mobile services and emails.

It was also reported that the PTA has already prepared a code of conduct for monitoring. (ANI)

Engineered human fusion protein stops HIV-1 replication in mice

Washington, September 9 (ANI): Inspired by New World owl monkeys’ ability to make a fusion protein that potently blocks HIV-1 infection, scientists at the University of Geneva in Switzerland have engineered a human HIV-1 inhibitor.

Lead researcher Jeremy Luban points out that owl monkeys make AoT5Cyp, and that the human genome encodes the equivalent of the two components of this fusion protein, namely TRIM5 and cyclophilin A.

However, adds the researcher, humans do not make the T5Cyp fusion protein.

In their new study, Luban and colleagues have engineered a human HIV-1 inhibitor modeled after AoT5Cyp, by fusing human cyclophilin A to human TRIM5 (hT5Cyp).

The researchers said that the human fusion protein blocked HIV-1 infection of human macrophage and T cell lines, without disrupting normal cell function.

During the study, the researchers engineered some mice to lack B, T, and NK immune cells, so that the animals would not reject grafts of human material.

The team then engrafted with human CD4+ T cells engineered to contain hT5Cyp.

HIV-1 replication was potently inhibited in these animals.

Based on their findings, the researchers came to the conclusion that hT5Cyp is a robust inhibitor of HIV-1 replication, and a promising anti-HIV-1 gene therapy candidate.

The study has been published in the Journal of Clinical Investigation. (ANI)

Novel biosensor can detect typhoid bacteria instantly

Washington, Sept 9 (ANI): Scientists from Rovira i Virgili University (URV) in Tarragona have come up with a novel biosensor that can instantly detect Salmonella typhi, the bacteria that causes typhoid fever.

The technique uses carbon nanotubes and synthetic DNA fragments that activate an electric signal when they link up with the pathogen.

“We have developed a new biosensor that can detect extremely low concentrations of bacteria immediately, easily and reliably”, F. Xavier Rius, lead author of the study and a professor in the Chemometrics, Qualimetrics and Nanosensors research group in the Analytical Chemistry and Organic Chemistry Department of the URV, told SINC.

The new biosensor functions using a method, which involves carbon nanotubes with inbuilt aptamers providing electrochemical readings.

According to the researchers, the aptamers are small fragments of artificial DNA or RNA designed to attach themselves specifically to a particular molecule, cell or micro organism, in this case Salmonella.

If the bacteria are not present, the aptamers remain on the walls of the carbon nanotubes.

However, if they detect bacteria, they become activated and stick to it, and the carbon nanotubes generate an electric signal that is picked up by a simple potentiometer connected to the biosensor.

“The presence of the bacteria sparks a change in the interaction between the aptamers and the nanotubes, which takes place in a few seconds and creates an increase in the voltage of the electrode”, said Ruis, who led the research along with researcher Jordi Riu.

“This technique means small quantities of micro organisms can be detected simply and practically in real time, just the same as measuring the pH of water”, Ruis added.

The study appears in the scientific journal Angewandte Chemie International Edition. (ANI)

Over-expressed protein may make non-invasive breast cancer invasive

Washington, Sep 9 (ANI): An over-expressed protein can convert active but non-invasive breast cancer into a different cell type, and thereby turn it into invasive breast cancer, according to scientists at The University of Texas M. D. Anderson Cancer Center.

The researchers say that overexpression of the protein 14-3-3? (zeta) launches a molecular cascade that removes bonds that tie the pre-malignant cells together, and hold them in place, converting them from stationary epithelial cells to highly mobile mesenchymal-like cells.

This epithelial-to-mesenchymal transition (EMT) is recognized as a crucial step in metastasis, the spread of cancer to distant organs that causes 90 percent of all cancer deaths.

“We have discovered a key molecular mechanism for the deadly transition of non-invasive breast cancer into invasive disease,” said senior author Dr. Dihua Yu.

The researchers have shown that the zeta protein teams up with the oncoprotein ErbB2, also known as HER2, in a two-hit process to convert normal mammary cells to invasive cancer cells.

The findings of the study also provided a biomarker in zeta to identify high-risk patients for more aggressive treatment before their noninvasive breast cancer converts to invasive disease.

The researchers also got new therapeutic targets among the components of the molecular pathway launched by zeta.

According to Yu, some drugs already aim at these targets.

In addition, they found a solution to a puzzling mystery about how a subset of non-invasive breast cancer with excessive presence of an ErbB2/HER2 develops into invasive breast cancer.

Earlier, the researchers showed that zeta is over-expressed in many other cancer types, like lung, liver, uterine, stomach cancers.

“Our findings might have broader implications relating to the mechanism of invasion and metastasis in other types of cancer,” Yu said.

The researchers said that it would be very challenging to target zeta by drugs because it also regulates other important proteins in normal cellular processes.

The study has been published in the journal Cancer Cell. (ANI)

Turning off oncogene may inhibit lung cancer stem cells’ growth

Washington, Sep 9 (ANI): A lung cancer oncogene, called PKCiota, is necessary for the proliferation of lung cancer stem cells, and turning it off could act as a key for the treatment of this deadly disease, according to scientists at the Mayo Clinic campus in Florida.

These stem cells are rare and powerful master cells that manufacture the other cells that make up lung tumours, and are resistant to chemotherapy treatment.

The study also shows that an agent, aurothiomalate, being tested at Mayo Clinic in a phase I clinical trial substantially inhibits growth of these cancer stem cells.

“Our data indicate that PKCiota is required for the earliest steps in the development of lung cancer, which is the expansion of tumor-initiating cells or cancer stem cells,” said the study’s senior author, Dr. Alan Fields.

“Lung cancer stem cells appear to be the major drivers in many common lung cancers, and in order for a therapeutic treatment to be effective, it has to disrupt these cancer stem cells. We show that aurothiomalate, the agent now being tested in lung cancer patients, can, in fact, target these cells,” he added.

While aurothiomalate was once used to treat rheumatoid arthritis, the researchers have now discovered that it can also target PKCiota.

Currently, the agent is being tested in patients at Mayo Clinic’s sites in Minnesota and Arizona and, based on this phase I trial, a phase II human clinical trial is planned to combine aurothiomalate with agents targeted at other molecules involved in cancer growth.

“We had previously shown that PKCiota is required to maintain tumor growth, but what this study sought to determine is whether PKCiota is involved in the initial steps of lung cancer development,” said Fields.

Fields said that, in mice, an oncogene known as Kras is thought to transform normal lung stem cells into cancer stem cells, thereby initiating lung cancer.

In the present study, the researchers established a strain of mice in which Kras can be activated at the same time that the PKCiota gene is inactivated.

They found that when the PKCiota gene is inactivated, Kras was unable to cause errant growth and expansion of lung stem cells in mice, the process that initiates tumour formation.

“What this told us is that Kras requires PKCiota to transform the lung stem cells and make them proliferate. In other words, PKCiota is downstream from Kras, and is necessary for Kras to initiate lung tumor formation,” said Fields.

After discovering that aurothiomalate disables PKCiota, the researchers tested whether this agent is effective against lung cancer that develops due to Kras mutation.

“The drug showed potent inhibitory effects on the Kras-dependent proliferation of lung cancer stem cells both in cell culture and in animals,” said Fields.

“That further suggests that a drug like aurothiomalate could have an effect on tumors that are dependent on either Kras or PKCiota for growth and survival, and that is potentially a lot of cancers.

Aurothiomalate appears to be one of the few drugs available that can effectively target these critical cancer stem cells. In the clinic, however, it is likely that aurothiomalate will be most effective when combined with other agents designed to target other tumor survival pathways,” he added.

The study has been published in Cancer Research. (ANI)