A pot belly increases your risk of bowel cancer

That beer belly or a “muffin top” your friends find cute is more dangerous than it appears—it can dramatically increase the risk ofbowel cancer, according to a study.

A shocking study revealed that for every inch above a healthy waist measurement, the likelihood of the fatal disease rises by three per cent.

While the link between excess fat and the chances of bowel cancer is known but the new study provides the strongest evidence so far that waist size is a significant contributing factor.

According to researchers, even slim people whose weight is normal are still at risk if they carry a bulge.

They say a healthy waist measurement is less than 31.5in for women, less than 37in for white and black men and under 35in for Asian men.

Scientists have recommended that people should try to stay as slim as possible without becoming underweight.

They estimate this could prevent more than 2,700 cases of bowel cancer in the UK every year.

“As well as confirming the link between body fat and bowel cancer, this study has strengthened the evidence that where we carry the fat is also important. This means that people with large waists should try to lose that flab even if they are otherwise in the normal body mass index range,” the Daily Express quoted Professor Martin Wiseman of the WorldCancer Research Fund, which paid for the study, as saying

“In fact, scientists now say that, after not smoking, maintaining a healthy weight is the most important thing for cancer prevention,” he added.

Experts at Imperial College London and the University of Leeds reviewed seven research papers, all of which showed tummy fat as a predictor for bowel cancer.

Dr Teresa Norat, lead researcher, said: “This study indicates that people should pay attention to abdominal fatness even if they are in the normal range of weight and it confirms that being overweight increases the risk of this type of cancer. “More research is needed to understand how abdominal fatness can be prevented.”

The results will be presented at an international conference in London. (ANI)

Pacemaker implanted in brain at Delhi hospital

 Doctors in a Delhi hospital implanted a pacemaker in the brain of a woman suffering from a psychiatric disorder - probably performing the unusual surgery for the first time in Asia.

The pacemaker implant in the brain for the 48-year-old woman suffering from obsessive compulsive disorder (OCD) was performed bydoctors in Vimhans hospital here.

"The 48-year-old patient from New Delhi who suffered from the disease for 21 years became the first OCD patient who has been implanted a brain pacemaker," hospital officials said.

"The patient had an obsession of being contaminated by drain water, doubts that she may be dirty, and performed elaborate rituals while cleaning herself and while cooking. She preferred to stay immobile when her family were away, not even going to toilet as she feared contamination," he added.

According to doctors, one to three percent of the world's population suffers from OCD. In India, OCD is one of the common psychiatric disorder. However, the awareness about the disease,symptoms and treatment options is extremely low. Since patients feel embarrassed about the disease, they refuse to acknowledge it. (IANS)

After 4 years of silence, Fatima can hear herself

Doctors at a Delhi hospital Monday succesfully operated on a four-year-old Iraqi girl suffering from deafness since birth to restore her hearing. The girl was responding to sounds after the surgery.

A doctors at the Apollo Hospitals, where Fatima Ali underwent the surgery, said: "The girl was born without the auditory nerve, the tool of hearing. We have carried out an operation to put an electronic device in her brain to restore hearing sensation."

"It takes at least two months before the brain can respond to the chip and can be switched on," senior surgeon of the Apollo Hospitals Ameet Kishore, who conducted the surgery, told IANS.

The internal chip’s electrodes stimulate the brain to produce sounds.

A team of surgeons and neurologists conducted the operation, the average cost of which ranges from Rs. 10 lakh to Rs. 15 lakh depending on the price of the equipment. (IANS)

Chances of cancer begin even before conception

A person's chances of developing cancer begins even before his or her conception.Medical experts have long linked cancer risk with their genes and lifestyles as adults.

But Professor Rocardo Uauy claims that factors of a mother's life such as whether she smokes, drinks, or is overweight all play key roles.

It is believed that environmental factors that encourage obesity and weight-gain in children can increase their risk of getting cancer, reports the Daily Mail.

"Someone's risk of developing cancer starts from before the time of conception. The risk factors are already operating in the mother's eggs before conception," said Uauy in The Observer newspaper.

"Yes, cancer is a genetic disease, but your chances of getting cancer are affected by the environment in which you live. So it's not just about if you smoked from the age of 12."

"But did your mother smoke? What was the water like that she drank? Is she exposed to toxins such as dioxins, which are found in the environment, and did she pass them on to her baby through her breast milk?"

Uauy has been a leading advisor to the United Nations and the World Heath Organisation for several years and is believed to have compiled one of the most detailed pictures of cancer prevention yet.

He recommends that parents reduce their baby's cancer risk by eating less tinned food and reducing exposure to certain cancer-causing chemicals.

Women should stop smoking before they conceive as cigarettes can increase the risk of children having a low birth weight.

Research suggests that underweight children put on weight quickly around their middles in early years which adds to the risk of cancer later on.

He added: "Mothers-to-be only need to consume an extra 150 calories a day during the nine months of pregnancy and should not eat for two."

Uauy recently highlighted the growing evidence of how early-life factors affect cancer risk at a World Cancer Research Fund conference.(IANS)

Study finds mothers' education levels affect child mortality

A study published in the journal Lancet on Friday found that "a mother's education level has a huge, if indirect, effect on the health of her children," the Washington Post reports.

"Half the reduction in child mortality over the past 40 years can be attributed to the better education of women, according to the analysis ... Worldwide, there were 8.2 million fewer deaths in 2009 among children younger than 5 than there were in 1970. Of those 'averted deaths,' 4.2 million were the result of better-educated mothers," the newspaper writes (Bown, 9/16).

The study, conducted by researchers from the Institute for Health Metrics and Evaluation (IHME) at the University of Washington, "shows that education is rising in every region. Most dramatically, average years of schooling for women of reproductive age (ages 15 to 44) in developing countries have grown from 2.2 years to 7.2 years," states an IHME press release. At the same time, according to the release, in "six countries - Afghanistan, Burkina Faso, Chad, Mali, Niger, and Yemen-women receive less than one year of schooling" (9/16). 

Researchers obtained results by using "915 censuses and surveys from 175 countries tracking education, economic growth, HIV rates and child deaths from 1970 to 2009," the Associated Press reports (Cheng, 9/16).Study co-author Christopher Murray explained that a mother's education affects the health of her children in many ways, the Washington Post writes. "According to Murray, better-educated women are more likely to understand disease-prevention measures such asvaccines and mosquito nets, and to use them. They are more likely to take a sick child to a clinic early and to follow treatment instructions. They are more likely to understand germ theory and set clean water and sanitation as household priorities. With more schooling, women tend to have fewer children and space births more widely, both of which also reduce child mortality."

Al Bartlett, a child health expert at USAID, said the findings are not unexpected, "but the magnitude is impressive." Bartlett added, "It clearly justifies what many have been saying for a long time - that one of the investments we need to make is girls' education" (9/16).

AP notes that "not everyone was convinced that the study's conclusions were right."

"Education is not much good if the health facilities and infrastructure don't exist," said Philip Stevens, a senior fellow at the International Policy Network. "If a country is massively misgoverned, like Sierra Leone, no amount of education is going to put bread on the table for children."

William Easterly, an economics professor at New York University, said, "It sounds plausible that education is related to child mortality, but finding a correlation does not prove causation."

H1N1 influenza increases neurological complications in children: Study

A recent study by researchers at the University of Utah determined that the 2009 pandemic influenza A (H1N1) caused a higher rate of neurological complications in children than the seasonal flu. The most common complications observed were seizures and encephalopathy. Full details of the study, the most extensive evaluation of neurological complications following H1N1 flu in children, are published in the September issue of Annals of Neurology, a journal of the American Neurological Association.

The H1N1 virus (swine flu) was identified in Mexico and the U.S. in April 2009 and quickly spread worldwide, prompting the World Health Organization (WHO) to declare the novel influenza A virus a pandemic. According to estimates from the Centers for Disease Control and Prevention (CDC), 43 million to 89 million Americans were infected with H1N1 between April 2009 and April 10, 2010, with approximately 14 million to 28 million of those cases in children 17 years of age and younger. On August 10, 2010 the WHO International Health Regulations Emergency Committee officially declared an end to the 2009 H1N1 pandemic.In their retrospective study, Josh Bonkowsky, M.D., Ph.D., and colleagues examined neurological complications in children with H1N1 compared to the seasonal flu. Children (younger than 19 years of age) who were hospitalized with H1N1 and neurological complications between April 1 and November 30, 2009 were included in the study. In the comparison group, the research team used records of children hospitalized with seasonal flu and neurological complications from July 1, 2004-June 30, 2008. Neurological complications observed included seizures, febrile seizures, status epilepticus, encephalopathy, encephalitis, myositis, myalgia, aphasia, ataxia, neuropathy, Gullain-Barre syndrome, or other focal neurological complaints.

Researchers identified 303 children who were hospitalized with 2009 H1N1 of which 18 experienced neurological complications. Eight-three percent of these pediatric patients had an underlying medical condition-primarily neurological issues (66%). The research team found the most common neurologic symptoms in this group were seizures (67%) and encephalopathy (50%). More than half of those children who experienced seizures presented in a life-threatening state known as status epilepticus, where continuous seizure activity occurs for more than 5 to 30 minutes1.

The comparison group included 234 children who were hospitalized for seasonal flu with 16 patients experiencing neurological issues. In the seasonal flu cohort only 25% patients had underlying medical conditions. The researchers also noted that none of the patients with seasonal flu and neurological complications had encephalopathy, aphasia, or focal neurological deficits.

Compared to seasonal influenza, patients with H1N1 were more likely to have abnormal electroencephalogram (EEG) findings. "We found that more pediatric H1N1 patients had neurological deficits and required ongoing treatment with anti-epileptic medications upon discharge from the hospital," commented Dr. Bonkowsky.

Additionally, researchers found the use of steroids or intravenous immunoglobulin was not beneficial in the treatment of encephalopathy. "The absence of proven treatments for influenza-related neurological complications underlines the importance of vaccination," said Dr. Bonkowsky. For protection against the flu, the CDC recommends yearly flu vaccination and the U.S. 2010-2011 seasonal influenza vaccine will protect against an H3N2 virus, influenza B, and the 2009 H1N1 virus.

Manganese in water can harm children’s IQ: Study

A team of researchers led by Maryse Bouchard, adjunct professor at the Center for Interdisciplinary Research in Biology, Health, Environment and Society (CINBIOSE) of the Universit- du Qu-bec - Montr-al and a researcher at Sainte-Justine University Hospital, and Donna Mergler, professor emerita in the Department of Biological Sciences and a member of CINBIOSE, recently completed a study showing that children exposed to high concentrations of manganese in drinking water performed worse on tests of intellectual functioning than children with lower exposures. Their results are published in the prestigious scientific journal Environmental Health Perspectives, in an article entitled "Intellectual Impairment in School-Age Children Exposed to Manganese from Drinking Water".

Manganese: toxic in the workplace but harmless in water?

The neurotoxic effects of manganese exposure in the workplace are well known. This metal is naturally occurring in soil and in certain conditions is present in groundwater. In several regions of Quebec and Canada and in other parts of the world, the groundwater contains naturally high levels of manganese. Does it pose a danger? What effect might it have on children's health? This is the first study to focus on the potential risks of exposure to manganese in drinking water in North America.

An international consortium of scientists has discovered new genetic variants in five regions of the genome that affect the risk of ovarian cancer in the general population, according to two separate studies published today (Sunday), online in Nature Genetics.

The consortium, including scientists from the U.S., Europe, Canada and Australia, based the new work on their earlier research comparing 10,283 women withovarian cancer to 13,185 women without the disease. That effort had found a stretch of DNA on chromosome 9 containing single DNA letter variations (SNPs) associated with ovarian cancer risk.

The researchers have now found additional stretches of DNA on chromosomes 2, 3, 8, 17 and 19 after grouping patients according to the type of ovarian cancer they had developed. Four out of five of the new DNA variations were more common in women who had developed the most common and aggressive form of disease, known as serous ovarian cancer.

Andrew Berchuck, MD, professor of gynecologic oncology at Duke University Medical Center and head of the steering committee of the international Ovarian CancerAssociation Consortium (OCAC), says the associations of these genetic variants withovarian cancer were discovered using genome-wide association studies (GWAS).

"Since the critical validation of these findings was performed by a large consortium of investigators from around the world, we see this research as a triumph of science without borders for the benefit of women everywhere."

Ovarian cancer is the fifth most common cancer among women in developed countries, and often detected in later stages when the chances of cure are small. As a result, the disease claims more lives in the U.S. than all other gynecological cancers combined. Every year, about 13,000 women in the U.S. and 130,000 worldwide die from the disease.

Scientists develop microscopic gas-filled spheres of silica to locate breast cancers

A new material could help surgeons more accurately locate breast cancers, reduce the need for second surgeries and minimize pre-surgical discomfort for patients. Microscopic gas-filled spheres of silica, a porous glass, can mark the location of early-stage tumors to show their position using ultrasound imaging in the operating room.

A team of chemists, radiologists and surgeons at the University of California, San Diego, created the new material, which they describe in a forthcoming issue of the journal MedChemComm.

The X-rays used to make mammograms reveal calcium deposits associated with breast cancer even in tumors too small to be felt. But surgeons can't use X-rays while operating. Instead, radiologists place guide wires into tumors hours or even the day before surgery. The wires don't mark depth well and can shift. Patients find them both uncomfortable and unsettling.

As an alternative, the researchers created spheres of silica and filled them with perfluoropentane, a gas that has been used before in short-lived contrast materials for medical imaging. The rigid silica shells help the new material last longer.

"These little gas-filled microbubbles stick to human breast tissue for days and can be seen with ultrasound," said William Trogler, professor chemistry. "If doctors placed them in early stage breast cancer, which is difficult to see during surgery, they could help surgeons remove all of it in the first operation."

Improper biological clocks tend to develop diabetes and obesity: Research

Biologists have found that a key protein that regulates the biological clocks of mammals also regulates glucose production in the liver and that altering the levels of this protein can improve the health of diabetic mice.

Their discovery, detailed in this week's advanced online publication of the journal Nature Medicine, provides an entirely new biochemical approach for scientists to develop treatments forobesity and type 2 diabetes. It also raises the interesting possibility that some of the rise in diabetes in the U.S. and other major industrialized countries could be a consequence of disturbances in sleep-wake cycles from our increasingly around-the-clock lifestyles.

"We know that mice that don't have good biological clocks tend to develop diabetesand obesity," said Steve Kay, Dean of the Division of Biological Sciences at UC San Diego and one of the lead authors of the research study. "And we know that mice that have developed diabetes and obesity tend not to have very good biological clocks. This reciprocal relationship between circadian rhythm and the maintenance of a constant supply of glucose in the body had been known for some time. But what we found that's so significant is that a particular biological clock protein, cryptochrome, is actually regulating how the hormone that regulates glucose production in the liver works in a very specific way."

"We used to think that our metabolism was regulated primarily by hormones that are released from the pancreas during fasting or feeding. This work shows that the biological clock determines how well these hormones work to regulate metabolism," says Marc Montminy, a professor in the Clayton Foundation Laboratories for Peptide Biology at the Salk Institute for Biological Studies. "The study may explain why shift workers, whose biological clocks are often out of kilter, also have a greater risk of developing obesity and insulin resistance."

Cryptochrome was first discovered by scientists as a key protein regulating the biological clocks of plants. It was later found to have the same function in fruit flies and mammals. But its role in regulating glucose production in the liver came as a complete surprise to the UCSD and Salk team, which included scientists from theGenomics Institute of the Novartis Research Foundation in San Diego, the University of Memphis and the Chinese Academy of Sciences in Shanghai.

Research Could Improve Detection Of Liver Damage

Research at the University of Liverpool could lead to faster and more accurate diagnoses of liver damage. 

The team used paracetamol as the basis for the study: research indicates that paracetamol can place temporary stress on the liver in around a third of people who take a normal dose (4g per day) but the liver returns to normal when the drug has left the system. Overdoses of the drug are a major cause of liver failure in both the UK and US. 

Scientists have discovered that the presence of specific proteins in the blood are indicative of early liver cell damage and can determine the point at which cell death occurred, the type of cell death, and the extent of any damage. This could lead to liver damage being assessed faster and more accurately in the future - information which could prove valuable when treating people following drug overdoses. 

The current blood test used by clinicians to assess liver function simply indicates whether liver enzymes leaking from dying cells can be detected in the blood. The test is not always reliable because positive results are often, but not always, an indicator of serious underlying liver problems. 

Scientists induced a mild paracetamol overdose in mice and discovered that proteins released by cells in the liver - HMGB1 and keratin 18 - provided a detailed picture of the level of cell damage. The release of HMGB1 was associated with necrosis - a process in which a cell bursts and dies - while the release of different types of keratin 18 was associated with both apoptosis - a process of normal cell renewal - and necrosis. This latter combination of both types of cell death is significantly less traumatic for the liver than necrosis alone in paracetamol overdose. 

Pharmacologist, Dr Dominic Williams, from the University's Medical Research Council Centre for Drug Safety Science, said: "The findings are significant because knowing how the cells die will allow development of medicines to help them survive, and may also distinguish patients who have severe injury and require intensive care from those who have mild injury. 

"The research has implications for determining how much stress has been placed on the liver in patients who are worried about an accidental overdose, as well as the more serious overdose cases." 

For Leukemia Patients A Scientific Breakthrough Could Be The First Step In A Better Treatment

A discovery made by Dr. Tarik Moroy, President and Scientific Director and Director of the Hematopoiesis and Cancer research unit at the Institut de recherches cliniques de Montreal (IRCM), and his team was recently published in Blood, the official journal of the American Society of Hematology. The researchers found that a protein can regulate certain characteristics of blood stem cells, which could lead to a better treatment for leukemia patients. Dr. Cyrus Khandanpour, medical doctor and postdoctoral fellow in Dr. Moroy's laboratory, is the study's first author. 

The transplantation of blood stem cells in used worldwide as a therapy for patients suffering from leukemia and other blood diseases. "The blood stem cells given to leukemia patients are capable of renewing the entire blood producing system and all its blood cells, including white cells, red cells and platelets," explains Dr. Möröy. 

Patients with leukemia or a blood disease are initially treated with chemotherapy, which destroys their entire blood forming system along with the disease. Blood stem cells can then be used in two different ways. The first is to harvest them from the patient before chemotherapy, and give the patient his/her own stem cells back after the treatment so they can rebuild blood cells. "One of the problems with this therapy is that blood stem cells normally reside in a niche between the bone and surrounding cells, and are in a dormant state," explains Dr. Khandanpour. "To obtain a sufficient number of stem cells, they have to be mobilized from their bone marrow niche so they can enter the bloodstream where they can be readily collected." 

The second possibility is to harvest blood stem cells from a healthy donor and give them to a patient following the chemotherapy treatment. These foreign cells will then rebuild the patient's blood system and regenerate its blood cells. "However, this therapy still fails in about 10% to 20% of cases," adds Dr. Khandanpour. "Among other reasons, these patients die because the transplanted stem cells do not generate new blood cells quickly enough, which leads to infection and death." 

"We have found a protein (called Gfi1b) that seems to regulate the stem cells' activity level and where they reside in the bone," says Dr. Khandanpour. "In our mouse model, we were able to turn off the gene coding for Gfi1b. When we did this, the stem cells became activated, started expanding drastically, left their bone marrow niche and entered the bloodstream without losing their function. The ability to manipulate blood stem cells in this manner would significantly increase the efficiency of stem cell therapy." 

According to the researchers, the inactivation of Gfi1b in the transplanted stem cells could accelerate the production of new blood cells, thus making stem cell therapy more efficient and less dangerous for the patient. However, the mechanisms regulating stem cell dormancy and mobilization are not well understood. 

"Our next goal is to investigate the precise molecular mechanisms achieved by the ablation of Gfi1b, and to study in more detail how Gfi1b regulates the location and activation of blood stem cells," adds Dr. Möröy. "Our project will contribute to a better understanding of the biology of stem cell mobilization and dormancy, which could lead to the design of better treatment regimens for transplant donors and patients." 

According to The Leukemia & Lymphoma Society of Canada, one person is diagnosed with a blood cancer every four minutes and someone dies from a blood cancer every 10 minutes. This statistic represents over 54,000 people per year. Leukemia causes more deaths than any other cancer among children and young adults under the age of 20. 

Research Into Chronic Pain, The Winning Project Of The Pharmacology Award Presented By Almirall And The Spanish Pharmacology Society

The 9th Pharmacology Award, given jointly by Almirall and the Spanish Pharmacology Society (SEF) was presented today. The award aims to promote research in the Pharmacology area and is the only award in Spain that recognises the quality of a future research project in this field rather than an already completed work. The award was announced during the 32nd SEF Congress, which was held in León from 15 to 17 September.

The winning project this year was "Mechanisms involved in the protective action of citoquines belonging to the family of Transforming-beta growth factors in the development of chronic pain", by Dr. María Amor Hurlé from the University of Cantabria. The prize, of 9,000 euros, is for research in the project during the period 2010-2011.

The jury was made up of doctors Teresa Tejerina (President of the SEF and Professor of Pharmacology at the University Complutense Madrid), Pilar D'Ocon (Professor of Pharmacology at the University of Valencia and member of the Board of Directors of the SEF) and Amadeu Gavaldà (Head of Integrative Pharmacology at Almirall). Dr. Gavaldà commented: "After nine years this award has become a reference point in the Pharmacology area in Spain. It has facilitated important contributions to treat pathologies such as Parkinson's disease, hypertension or hyperlipidemia, which affect a large number of people in our society. This year the winning project by Dr. Hurlé will study progress in the treatment of chronic pain, which has a negative impact on all vital aspects of sufferers. It is estimated that around 19-37% (1) of the Spanish population experiences moderate to severe chronic pain".

Breast Cancer Risk Linked To Other Genes

A large international team of researchers led by the Mayo Clinic in the US has discovered that some individuals whose risk ofbreast cancer may be increased by carrying a variant of the BRCA1 gene may also possess other gene variants that can modify that risk, bringing closer the day when it will be possible to determine individual risk for breast cancer in carriers of BRCA1.

You can read about the findings that led to this discovery, and other insights, in a paper published online on 19 September in the journal Nature Genetics. 

Among the 180 co-authors who contributed as individuals and as members of several consortia are first author Dr Antonis Antoniou of the Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care at the University of Cambridge in the UK, and senior study investigator Dr Fergus Couch of the Department of Laboratory Medicine and Pathology, at the Mayo Clinic in Rochester, Minnesota, in the US.

People who carry certain mutations of the BRCA1 gene are known to have a higher risk of developing breast cancer. 

Couch told the media that their findings should be "useful in helping determine individual risk for breast cancer in BRCA1 carriers". 

"It also provides insights into hormone-receptor-negative breast cancer in the general population," he added.

For the study, Couch and colleagues conducted four phases of genome-wide association studies (GWAS) that altogether involved 20 research centers in 10 North American and European countries and Israel.

For the first phase, to identify candidate gene variants, they scanned the genomes of 1,193 carriers of BRCA1 mutations who were under 40 and had invasive breast cancer and compared them to scans of about the same number of controls: BRCA1 carriers of similar age who did not have breast cancer.

In comparing the genomes from the two populations the researchers examined over half a million genetic alterations. They found 96 pieces of DNA called SNPs, or "snips", short for single nucleotide polymorphisms, that they thought would be likely candidates because they differed between the two populations.

To narrow down the list, they moved into the second phase of the study, where they looked at just the 96 SNPs in another two groups: one of about 3,000 BRCA1 carriers with breast cancer and a matched group of carriers without breast cancer. From this second phase they narrowed the 96 SNPs down to five linked to breast cancer. The five SNPs were all in a region of chromosome 19p13.

In a third phase, where the researchers examined the genomes of 6,800 breast cancer patients who did not have the cancer-linked BRCA1 mutations, they found links between the newly discovered five SNPs and estrogen-receptor-negative (ER-) disease (ER- cancer is where the tumors don't possess estrogen receptors).


And in a fourth phase, the researchers found that the same five SNPs were also linked to another aggressive form of breast cancer known as triple-negative breast cancer, which occurs in around 12 per cent of breast cancers. For this phase they scanned the genomes of 2,300 triple-negative cases and 3,949 controls. (Triple negative breast cancer tumors don't express genes for estrogen or progesterone receptors or Her2/neu).

The researchers also determined that the five SNPs were not linked to higher risk ofovarian cancer among carriers of the breast cancer-prone variants of BRCA1.

The researchers concluded that by identifying these five SNPs, we are in a better position to understand the mechanisms behind the development of breast cancer, and if further risk-modifying SNPs are found (the team is continuing the search), it may one day be possible to identify which BRCA1 carriers are at lower risk of developing breast cancer, and who may be at higher risk, giving them the opportunity to change their approach to cancer prevention.