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Jan 25
Drinking mate tea may help prevent colon cancer
Mate tea, which has long been consumed in South America for its medicinal properties, may help prevent colon cancer, a new study has suggested.

University of Illinois scientists found that that human colon cancer cells die when they are exposed to the approximate number of bioactive compounds present in one cup of this brew.

"The caffeine derivatives in mate tea not only induced death in human colon cancer cells, they also reduced important markers of inflammation," said Elvira de Mejia, a U of I associate professor of food chemistry and food toxicology.

That's important because inflammation can trigger the steps of cancer progression, she said.

In the in vitro study, de Mejia and former graduate student Sirima Puangpraphant isolated, purified, and then treated human colon cancer cells with caffeoylquinic acid (CQA) derivatives from mate tea. As the scientists increased the CQA concentration, cancer cells died as a result of apoptosis.

"Put simply, the cancer cell self-destructs because its DNA has been damaged," she said.

The ability to induce apoptosis, or cell death, is a promising tactic for therapeutic interventions in all types of cancer, she said.

de Mejia said they were able to identify the mechanism that led to cell death. Certain CQA derivatives dramatically decreased several markers of inflammation, including NF-kappa-B, which regulates many genes that affect the process through the production of important enzymes.

Ultimately cancer cells died with the induction of two specific enzymes, caspase-3 and caspase-8, de Mejia said.

"If we can reduce the activity of NF-kappa-B, the important marker that links inflammation and cancer, we'll be better able to control the transformation of normal cells to cancer cells," she added.

The results of the study strongly suggest that the caffeine derivatives in mate tea have potential as anti-cancer agents and could also be helpful in other diseases associated with inflammation, she said.

But, because the colon and its microflora play a major role in the absorption and metabolism of caffeine-related compounds, the anti-inflammatory and anti-cancer effects of mate tea may be most useful in the colon.

"We believe there's ample evidence to support drinking mate tea for its bioactive benefits, especially if you have reason to be concerned about colon cancer. Mate tea bags are available in health food stores and are increasingly available in large supermarkets," she added.

Jan 25
Why many don't quit smoking despite cancer
A substantial number of lung and colorectal cancer patients continue to smoke after being diagnosed, a new study has revealed. When a patient receives a cancer diagnosis, the main focus is to treat the disease. But stopping smoking after a cancer diagnosis is also important because
continuing to smoke can negatively affect patients responses to treatments, their subsequent cancer risk, and, potentially, their survival.

A team led by Elyse R. Park, PhD, MPH, of the Massachusetts General Hospital/Harvard Medical School in Boston, studied how many patients quit smoking around the time of a cancer diagnosis, and which smokers were most likely to quit.

The investigators determined smoking rates around the time of diagnosis and five months after diagnosis in 5,338 lung and colorectal cancer patients.

At diagnosis, 39 percent of lung cancer patients and 14 percent of colorectal cancer patients were smoking, five months later, 14 percent of lung cancer patients and 9 percent of colorectal cancer patients were still smoking.

These results indicate that a substantial minority of cancer patients continue to smoke after being diagnosed. Also, although lung cancer patients have higher rates of smoking at diagnosis and following diagnosis, colorectal cancer patients are less likely to quit smoking following diagnosis.

Factors and characteristics that predicted continued smoking differed by cancer type. Lung cancer patients who continued smoking tended to have Medicare or other public health insurance, have a lower body mass index, have low emotional support, not have received chemotherapy, not have had surgery, have had prior heart disease, and have smoked a high number of cigarettes per day at some point during their lives.

Colorectal cancer patients who continued to smoke tended to be male, have completed less education, be uninsured, not have had surgery, and have once smoked a high number of cigarettes per day.

"These findings can help cancer clinicians identify patients who are at risk for smoking and guide tobacco counseling treatment development for cancer patients," said Dr. Park.

Jan 24
Advanced Cell Technology: Stem cell retinal implants safe
Early results from the world's first human trial using embryonic stem cells to treat diseases of the eye suggest the method is safe, say researchers.

US firm Advanced Cell Technology told The Lancet how two patients who had received the retinal implants were doing well, four months on.

Trials of the same technique have now started at London's Moorfields Eye Hospital.

But experts say it will be years before these treatments are proven.

The aim of these first human studies is to establish that the treatment is safe to use.

The treatment takes healthy immature cells from a human embryo, which are then manipulated to grow into the cells that line the back of the eye - the retina.

Experts hope that by injecting these cells into a diseased eye, they will be able to restore vision for people with currently incurable conditions such as Stargardt's disease - one of the main causes of blindness in young people.
The study involved one elderly patient in her 70s with dry age-related macular degeneration - the leading cause of blindness in the developed world - and another female patient in her 50s with Stargardt's disease.

Both had very poor vision and were registered blind.

Each patient was given an injection containing 50,000 of the retinal pigment epithelium cells into one of their diseased eyes.

After surgery, structural evidence confirmed the cells had attached to the eye's membrane as hoped, and continued to survive throughout the next 16 weeks of the study.

Furthermore, the procedure appeared to be safe, causing no signs of rejection or abnormal cell growth.
Ethical concerns

Although this study is not designed to see if the procedure actually works, the researchers say their results do suggest that their patients' vision has improved slightly.

But they say it is still too soon to make any firm conclusions and that many more years of investigation will be needed to confirm that the treatment is both safe and effective.

They told The Lancet: "The ultimate therapeutic goal will be to treat patients earlier in the disease processes, potentially increasing the likelihood of photoreceptor and central visual rescue."

But even if this does become possible, such treatments would face stiff opposition by critics who say it is ethically wrong to use human embryonic tissue.

Dr Dusko Ilic, Senior Lecturer in Stem Cell Science at Kings College London, said that these early findings did not necessarily hint towards a viable treatment.

"We should keep in mind that people are not rats.

"The number one priority of initial clinical trial is always patient safety. If everyone expects that the blind patients will see after being treated with human embryonic stem cell-derived retinal pigment epithelium, even if the treatment ends up being safe (which is what Advanced Cell Technology are trying to determine in this trial), they risk being unnecessarily disappointed."."

Jan 24
How the brain decides whether to 'Sell Out' : Study
An Emory University neuro-imaging study shows that personal values that people refuse to disavow, even when offered cash to do so, are processed differently in the brain than those values that are willingly sold.

"Our experiment found that the realm of the sacred - whether it's a strong religious belief, a national identity or a code of ethics - is a distinct cognitive process," says Gregory Berns, director of the Center for Neuropolicy at Emory University and lead author of the study. The results were published in Philosophical Transactions of the Royal Society.

Sacred values prompt greater activation of an area of the brain associated with rules-based, right-or-wrong thought processes, the study showed, as opposed to the regions linked to processing of costs-versus-benefits.

Berns headed a team that included economists and information scientists from Emory University, a psychologist from the New School for Social Research and anthropologists from the Institute Jean Nicod in Paris, France. The research was funded by the U.S. Office of Naval Research, the Air Force Office of Scientific Research and the National Science Foundation.

"We've come up with a method to start answering scientific questions about how people make decisions involving sacred values, and that has major implications if you want to better understand what influences human behavior across countries and cultures," Berns says. "We are seeing how fundamental cultural values are represented in the brain."

The researchers used functional magnetic resonance imaging (FMRI) to record the brain responses of 32 U.S. adults during key phases of an experiment. In the first phase, participants were shown statements ranging from the mundane, such as "You are a tea drinker," to hot-button issues such "You support gay marriage" and "You are Pro-Life." Each of the 62 statements had a contradictory pair, such as "You are Pro-Choice," and the participants had to choose one of each pair.

At the end of the experiment, participants were given the option of auctioning their personal statements: Disavowing their previous choices for actual money. The participants could earn as much as $100 per statement by simply agreeing to sign a document stating the opposite of what they believed. They could choose to opt out of the auction for statements they valued highly.

"We used the auction as a measure of integrity for specific statements," Berns explains. "If a person refused to take money to change a statement, then we considered that value to be personally sacred to them. But if they took money, then we considered that they had low integrity for that statement and that it wasn't sacred."

The brain imaging data showed a strong correlation between sacred values and activation of the neural systems associated with evaluating rights and wrongs (the left temporoparietal junction) and semantic rule retrieval (the left ventrolateral prefrontal cortex), but not with systems associated with reward.

"Most public policy is based on offering people incentives and disincentives," Berns says. "Our findings indicate that it's unreasonable to think that a policy based on costs-and-benefits analysis will influence people's behavior when it comes to their sacred personal values, because they are processed in an entirely different brain system than incentives."

Research participants who reported more active affiliations with organizations, such as churches, sports teams, musical groups and environmental clubs, had stronger brain activity in the same brain regions that correlated to sacred values. "Organized groups may instill values more strongly through the use of rules and social norms," Berns says.

The experiment also found activation in the amygdala region, a brain region associated with emotional reactions, but only in cases where participants refused to take cash to state the opposite of what they believe. "Those statements represent the most repugnant items to the individual," Berns says, "and would be expected to provoke the most arousal, which is consistent with the idea that when sacred values are violated, that induces moral outrage."

The study is part of a special issue of the Philosophical Transactions of the Royal Society, titled "The Biology of Cultural Conflict." Berns edited the special issue, which brings together a dozen articles on the culture of neuroscience, including differences in the neural processing of people on the opposing sides of conflict, from U.S. Democrats and Republicans to Arabs and Israelis.

"As culture changes, it affects our brains, and as our brains change, that affects our culture. You can't separate the two," Berns says. "We now have the means to start understanding this relationship, and that's putting the relatively new field of cultural neuroscience onto the global stage."

Future conflicts over politics and religion will likely play out biologically, Berns says. Some cultures will choose to change their biology, and in the process, change their culture, he notes. He cites the battles over women's reproductive rights and gay marriage as ongoing examples.

Jan 23
Paracetamol cannot kill, say doctors
Denying that a paracetamol shot can kill a person, health officials at Theni, said they are awaiting the post-mortem lab reports to ascertain the exact cause for the death of a 10-month-old infant on Saturday, after allegedly being administered with the paracetamol dose.

"Paracetamol in reality cannot kill a person when administered and the actual cause of death can be revealed only when the lab reports of drug samples collected from the body reach us," V Shanmugasundaram, deputy director of health (Madurai), who is holding additional in charge for Theni district said.

The 10-month-old infant, son of Suresh and Annapackiam from Erathimakkalpatti was taken to the primary health care centre at M Subbalapuram near Andipatti, as he was suffering from fever and cough. The duty doctor at PHC, Uma Balan instructed the nurse, Mariammal to administer paracetamol injection to the infant. However, the baby fainted after the injection.

In the same way, two others, aged 10 and eight years, both children of one Selvaraj from the same village also developed fainting symptoms. The three were rushed to the Theni Medical College GH, where the infant was declared dead, while the other two children were admitted for treatment.

Irked by the death of the child, villagers of Erathimakkalpatti picketed the road in front of medical college. Andipatti DSP, K R Vijayabaskaran and MLA, Thangatamilselvan pacified the villagers and assured them that action would be taken once the post-mortem report is out. The villagers dispersed from the spot after their assurances.

Shanmugasundaram said that the infant was administered paracetamol and setron, the regular dose for fever and cough.

"The drug samples collected from the child's body has been sent to the lab at Chennai. Further action will be taken once the reports are in hand, which will take a week's time," he said. He also suspected the possibility of anaphylaxis, serious allergic reaction to any drug, which is rapid and causes death. Departmental action will also be initiated if need be after ascertaining the reports, he added.

The condition of other two children admitted in the hospital is stable and improving, sources said.

Jan 23
Genes responsible for 40% of lifetime intelligence
We inherit 40 percent of our lifetime intelligence while the environment we grow up in impacts the rest 60 percent, researchers say.

Scientists at University of Queensland, Australia studied a unique group of nearly 2000 unrelated people in Scotland who were tested for their intelligence, using the same test, at age 11 and again at age 65, 70 or 79 years.

Most people who began life with above average intelligence were above average when they were older, while others who had below average intelligence tended to stay below average, a website reported.

However, the researchers did notice that there were some whose intelligence improved and some whose got worse compared to others.

They also took genetic samples and quantified the role genes play in determining how much transformation there is in intelligence as we age.

"We estimate roughly a quarter to a third of that change is genetic," Professor Peter Visscher, lead author of the study said in a statement.

"Measuring detailed environmental factors over a person's entire life course is very difficult."

The study revealed that overall, environment contributes more than genes to determining intelligence, although, both play an important role.

Jan 21
Indian-origin scientists lead fundamental malaria discovery
A team led by Indian-origin scientists has made a fundamental discovery in understanding how malaria parasites cause the deadly disease.

The researchers led by Kasturi Haldar and Souvik Bhattacharjee of the University of Notre Dame's Center for Rare and Neglected Diseases revealed how parasites target proteins to the surface of the red blood cell that enables sticking to and blocking blood vessels.

Strategies that prevent this host-targeting process will block disease.

Malaria is a blood disease that kills nearly 1 million people each year. It is caused by a parasite that infects red cells in the blood. Once inside the cell, the parasite exports proteins beyond its own plasma membrane border into the blood cell.

These proteins function as adhesins that help the infected red blood cells stick to the walls of blood vessels in the brain and cause cerebral malaria, a deadly form of the disease that kills over half a million children each year.

In all cells, proteins are made in a specialized cell compartment called the endoplasmic reticulum (ER) from where they are delivered to other parts of the cell.

Haldar and Bhattacharjee and collaborators Robert Stahelin at the Indiana University School of Medicine- South Bend (who also is an adjunct faculty member in Notre Dame's Department of Chemistry and Biochemistry), and David and Kaye Speicher at the University of Pennsylvania's Wistar Institute discovered that for host-targeted malaria proteins the very first step is binding to the lipid phosphatidylinositol 3-phosphate, PI(3)P, in the ER.

This was surprising for two reasons. Previous studies suggested an enzyme called Plasmepsin V that released the proteins into the ER was also the export mechanism.

However, the team discovered that binding to PI(3)P lipid which occurs first is the gate keeper to control export and that export can occur without Plasmepsin V action.

Further, in higher eukaryotic cells (such as in humans), the lipid PI(3)P is not usually found within the ER membrane but rather is exposed to the cellular cytoplasm.

The research findings appear in the Jan. 20 edition of the journal Cell, the leading journal in the life sciences.

Jan 21
Origins of esophageal cancer unfolded
We just read a study regarding a fluorescent dye to be used for the diagnosis of esophageal cancer. Now, this report by scientists from the Columbia University has unfolded the origins of throat cancer.

The team accessed a new genetically programmed mouse prototype of chronic esophageal inflammation, also called esophagitis, in this research. They stumbled upon varied molecular changes occurring during the development of Barrett's esophagus and esophageal adenocarcinoma (EAC) in the mouse model.

"All told, the findings present a new model for the pathogenesis of Barrett's esophagus and esophageal adenocarcinoma," specified research leader Timothy C. Wang.

The researchers found that higher proportions of a molecule called interleukin 1 apparently led to esophagitis and growth of progenitor cells, which were maintained by the Notch signaling pathway. So far, scientists believed that physiological alterations seen in Barrett's esophagus begin in the lower esophagus. However, the findings showed that the aforesaid condition supposedly took place in a region called gastric cardia.

The latter is a region lying between the lower portion of the esophagus and the upper part of the stomach secreting acids. Another belief that these changes usually happen in goblet cells appeared to be untrue. These alterations occurred principally in columnar-like epithelial cells.

The scientists concluded that inhibition of the notch signaling pathway is likely to impede the survival and growth of pre-malignant cells. This could be used as a new strategy in patients suffering from Barrett's esophagus and who are at high risk for cancer.

Jan 20
Origins of Esophageal Cancer Identified
The critical early cellular and molecular events that give rise to a type of esophageal cancer has been identified by scientists. The findings challenge conventional wisdom regarding the origin and development of this deadly cancer and its precursor lesion, Barrett's esophagus, and highlight possible targets for new clinical therapies.

Lacking a good animal model of esophageal adenocarcinoma (EAC), researchers have been hard pressed to explain exactly where and how this cancer arises. What is known is that EAC is usually triggered by gastro-esophageal reflux disease (GERD), in which bile acid and other stomach contents leak backwards from the stomach to the esophagus, the muscular tube that moves food from the mouth to the stomach.

Over time, acid reflux can irritate and inflame the esophagus, leading to Barrett's esophagus, an asymptomatic precancerous condition in which the tissue lining the esophagus is replaced by tissue similar to the lining of the intestine. A small number of people with Barrett's esophagus eventually go on to develop EAC.

Using a new genetically engineered mouse model of esophagitis, the CUMC researchers have clarified critical cellular and molecular changes that occur during the development of Barrett's esophagus and EAC. In human patients, acid reflux often leads to over expression of a molecule called interleukin-1 beta, an important mediator of the inflammatory response. A transgenic mouse was created in which interleukin-1 beta was over expressed in the esophagus.

Over expression of interleukin-1 beta in the mouse esophagus resulted in chronic esophageal inflammation (esophagitis) and expansion of progenitor cells that were sustained by the notch signaling pathway.

Notch is a fundamental signaling system used by neighboring cells to communicate with each other in order to assume their proper developmental role. "When we inhibited notch signaling, that blocked proliferation and survival of the pre-malignant cells, so that's a new possible clinical strategy to use in Barrett's patients at high risk for cancer development," noted Dr. Wang.

For decades, investigators thought that the physiological changes associated with Barrett's esophagus originate in the lower esophagus. "However, our study shows that Barrett's esophagus actually arises in the gastric cardia, a small region between the lower part of the esophagus and the upper, acid-secreting portion of the stomach," said the concerned doctor. "What happens is that the bile acid and inflammatory cytokines activate stem cells at this transition zone, and they begin migrating up toward the esophagus, where they take on this intestinal-like appearance."

The researchers also demonstrated that these changes occur primarily in columnar-like epithelial cells, rather than in goblet cells, as was previously thought.

"All told, the findings present a new model for the pathogenesis of Barrett's esophagus and esophageal adenocarcinoma," said the concerned doctor.

Barrett's esophagus affects about 1 percent of adults in the United States. Men are affected by Barrett's esophagus twice as frequently as women, and Caucasian men are affected more frequently than men of other races. The average age at diagnosis is 50. At present, there is no way to determine which patients with the condition will develop EAC. EAC is increasing in incidence about 7 to 8 percent a year, making it the most rapidly rising solid tumor in the U.S.

Treatment with acid-reducing drugs can lessen symptoms of GERD and lower the chances of developing Barrett's esophagus and EAC. Low-grade EAC is highly treatable with endoscopic radiofrequency ablation, photodynamic therapy, or surgical resection. Patients with severe disease may require open surgery, in which most of the esophagus is removed. The overall five-year survival rate with advanced disease is about 25 percent.

Jan 20
How anti diabetic drug could help cut cancer risk: Study
In a new study, scientists have tried to solve the mystery surrounding how the anti diabetic drug metformin could reduce the risk of developing cancer and what were the mechanisms involved.

In 2005, news first broke that researchers in Scotland found unexpectedly low rates of cancer among diabetics taking the drug, which is commonly prescribed to patients with Type II diabetes.

Many follow up studies reported similar findings, some suggesting as much as a 50 percent reduction in risk.

Fr the current study, researchers from McGill University and the University of Montreal reported an unexpected finding " they learned that exposure to metformin reduces the cellular mutation rate and the accumulation of DNA damage.

It is well known that such mutations are directly involved in carcinogenesis, but lowering cancer risk by inhibiting the mutation rate has never been shown to be feasible.

"It is remarkable that metformin, an inexpensive, off patent, safe and widely used drug, has several biological actions that may result in reduced cancer risk " these latest findings suggest that it reduces mutation rate in somatic cells, providing an additional mechanism by which it could prevent cancer," Newswise quoted Michael Pollak, professor in McGill's Departments of Medicine and Oncology, researcher at the Lady Davis Institute for Medical Research at the Jewish General Hospital and the study's director.

The study, carried out in collaboration with the laboratory of Dr. Gerardo Ferbeyre at Universite de Montreal's Department of Biochemistry, suggests that metformin reduces DNA damage by reducing levels of reactive oxygen species ROS.

ROS are known to be DNA damaging agents produced as by products when cells generate energy from nutrients. This action appears to take place in mitochondria, the cellular organelles that produce energy in cells by "burning" nutrients.

Past studies have identified the mitochondria as a site of action for metformin related to its anti diabetic function, but those studies had not considered that the drug also acted here to reduce ROS production, thereby reducing the rate at which DNA damage accumulates.

"We found that metformin did not act as a classic antioxidant," Ferbeyre said.

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