Mediaboss Marketing

Home

Calcutta News.Net Wednesday 28th March, 2012 (IANS)

Cervical cancer is the leading cause of cancer deaths among women in India with mortality being three times higher in rural areas than in urban areas, a study by the medical journal Lancet said Wednesday.

'The study found that 17 percent of cancer deaths among women were due to cervical cancer, followed by 14 percent due to stomach cancer and 10 percent due to breast cancer. The study spanned across geographical and social variation in specific cancers, and the degree to which the cancers might be avoided by controlling their risk factors or causative agents,' said Prabhat Jha, co-author of the study released in Mumbai said.

'The rate of cervical cancer deaths was nearly the same in rural and urban areas. A similar pattern of mortality rate was seen for breast cancer in both the areas,' Jha, director of the Toronto-based Centre for Global Health Research, added.

The study found cancer mortality in 2010 in India to be at a high 71 percent (3,95,400) deaths in people between 30 and 69 years. The authors assessed cancer mortality in the Million Death Study (MDS), led by the Office of the Registrar General of India.

According to the World Health Organisation (WHO), which has been advocating early detection and prevention among women, personal hygiene and public health education are keys for early diagnosis of cervical cancer.

'Cervical cancer is the leading cause of cancer death in Indian women, killing more than 33,000 women every year in India. The risk of a woman dying from cervical cancer is higher than her risk of dying during child birth (0.8 percent vs 0.6 percent respectively),' Poonam Khetrapal Singh, deputy regional director at the WHO regional office for Southeast Asia in New Delhi, told IANS.

Cervical cancer starts in the cervix, the lower part of the uterus (womb), caused by human papilloma virus (HPV). The virus spreads through unsafe sexual intercourse. Routine pap smear tests are advised so the disease is diagnosed at an early stage.

Reacting to the study, the WHO official said: 'Public health education advocating personal hygiene and periodic screening can reduce cervical cancer deaths. Early detection of treatable cancers would save many lives in India, particularly in the rural areas which are under served by cancer screening and treatment.'

Read more here:
Cervical cancer leading cancer-killer among Indian women

The advent of highly resistant bacteria or "superbugs" was one of the issues discussed at the Society for General Microbiology's Spring Conference currently being held in Dublin between 26-29 March. An important aspect of the meet was to bring forth new research that focused on combating the advent of superbugs or drug-resistant bacterial strains.

A logic proposed was to use viruses called bacteriophages to wipe out bacterial strains that are resistant to the current crop of antibiotics. The growing menace of accelerated antibiotic resistance has added to the woes of the medical fraternity in combating bacterial diseases that remain resistant to existing antibiotics.

This has reduced the number of potent antibiotics for treating drug-resistant diseases. The novel bacteriophage therapy could be the answer to the growing "superbug" malady. New research has re-investigated the characteristics of bacteriophages as the potential "killer" virus that has the ability to infect drug-resistant bacteria by multiplying within the bacterial cells and breaking them down.

Like us on Facebook

In the process, the virus itself enhances its own inner mechanism to deal better with other bacterial strains. The bacteriophages are widely present in the environment such as rivers, water, soil, the human body and sewage. The new idea is to tap these viruses.

"Each bacteriophage is highly specific to a certain type of bacteria and needs the right bacterial host cell in order to multiply. The more bacterial targets there are, the quicker they grow by killing the host cells. Therefore it seems very likely that infections harboring high numbers of bacteria will benefit most from bacteriophage therapy - for example chronically infected ears, lungs and wounds," explained Dr. David Harper at the the Dublin meet. He is the Chief Scientific Officer at AmpliPhi Bioscience, Bedfordshire, that has conducted clinical trials on bacteriophages since 2005.

"For these types of infection, only a tiny dose of the virus is needed - as small as one thousandth of a millionth of a gram. This can usually be administered directly to the site of infection in a spray, drops or a cream. The major advantage to bacteriophages is that they don't infect human cells so seem likely to be very safe to use," Harper added.

Bacteriophages, discovered initially in 1915, were seen as mere anti-bacterial therapeutic agents but a lack of understanding on their mode of action failed to pave the way for future investigations as anti-bacterial agents. With the advent of new-age chemical variants of anti-bacterial drugs, the viral impact on bacteria remained ignored.

"The rate of new antibiotics coming onto the market does not match the rate of increasing drug-resistance. The need for new approaches to counter such high resistance is both urgent and vital. New approaches will save lives," added Harper.

Harper is positive on the results of clinical trials and said that once regulatory issues are taken care of and enough funds are generated to secure this area of research on bacteriophages, the development of the novel viral-based antibacterial agents would be a step to curb the prevailing crisis of drug-resistant antibiotics.

Follow this link:
New Study Explores Virus To Fight Superbugs

Genetic test could reveal those most at risk from next influenza pandemic

By Daily Mail Reporter

PUBLISHED: 02:49 EST, 26 March 2012 | UPDATED: 02:50 EST, 26 March 2012

A genetic discovery could help explain why flu makes some people seriously ill or kills them, while others seem able to bat it away with little more than a few aches, coughs and sneezes.

British and American researchers said they had found for the first time a human gene that influences how people respond to flu infections, making some people more susceptible than others.

A genetic clue may explain why some people experience mild flu symptoms while others are hospitalised

The finding helps explain why during the 2009/2010 pandemic of H1N1 or 'swine flu', the vast majority of people infected had only mild symptoms, while others - many of them healthy young adults - got seriously ill and died.

In future, the genetic discovery could help doctors screen patients to identify those more likely to be brought down by flu, allowing them to be selected for priority vaccination or preventative treatment during outbreaks, the researchers said.

It could also help develop new vaccines or medicines against potentially more dangerous viruses such as bird flu.

Read the rest here:
Genetic flaw discovered that turns flu into a killer

The following editorial appeared in the Chicago Tribune on March 19:

Late last year came word that a Dutch scientist had genetically tweaked one of the worlds most deadly bird flu viruses to make it more contagious to humans. In other words, a doomsday virus in a sneeze that could kill more than half of the people who caught it.

That chilling revelation set off an international furor over whether the details of that study and a similar one done by researchers at the University of Wisconsin at Madison should be published in scientific journals.

Scientists argued that researchers need those details to better detect and fight a possible epidemic of the virus, known as H5N1. Security experts argued compellingly that the studies should be expunged of key details, lest terrorists use that information to unleash a devastating biological weapon.

Another fear if those details escape the lab: There are thousands of do-it-yourself biologists who can buy sophisticated devices to duplicate segments of DNA on eBay. Might they be tempted to recreate the killer virus, known as H5N1, in their garage labs, just for kicks?

So far, the journals Science and Nature have not published the studies, at the behest of the National Science Advisory Board for Biosecurity, a panel of experts that advises federal health officials.

But that could change soon. A panel of biologists assembled by the World Health Organization recommended recently that the full details of the experiments eventually be released, although WHO didnt set a timetable.

Talk about publish and perish.

We know that some researchers believe it is already too late, that enough details have circulated among scientists for them to deduce the recipe for the virus. We also know many researchers argue that censoring this study makes it harder to identify changes that might signal a virus is developing the ability to cause a pandemic Thats a powerful argument.

We oppose government censorship. Science works best when information flows freely.

Link:
Guest editorial: Publish and perish?

On my way to give a keynote talk at a genome meeting in California, I noticed in the Hartford airport that the April issue of Wired is on the newsstand. And in that issue is a feature I wrote about fighting viruses, based on visits and interviews with scientists exploring new ways of doing battle with these invisible foes. Its not yet on Wireds web site yet (Ill post a link when it goes online), but heres the introduction for a taste:

Theres a moment in the history of medicine thats so cinematic its a wonder no one has put it in a movie. The scene is a London laboratory. The year is 1928. Alexander Fleming, a British microbiologist, is back from a vacation and is cleaning up his workspace. He notices that a speck of mold has invaded one of his cultures of Staphylococcus bacteria. It isnt just spreading through the culture, though. It is killing the bacteria surrounding it.

Fleming rescued the culture and carefully isolated the mold. He ran a series of experiments that confirmed it made a Staphylococcus-killing molecule. And Fleming then discovered it could kill many other species of infectious bacteria as well. I had a clue that here was something good, but I could not possibly know how good it was, he later said.

No one at the time could have known how good it was. In 1928, something as minor as a scraped knee could be a death sentence, because doctors were mostly helpless to stop bacteria infections. Fleming was the first scientist to recognize an antibiotica discovery for which hed later win the Nobel Prize. Penicillin saved countless lives, killing off a wide range of pathogens while causing few side effects. Flemings work also led other scientists to discover more antibiotics, which collectively changed the rules of medicine. Now doctors could prescribe drugs that effectively wiped out most bacteria, without even knowing what kind of bacteria was making their patients sick.

Of course, even if all the bacteria in the world were eradicated, we would still get sick. Viruseswhich cause their own panoply of diseases from colds and the flu to AIDS and Ebolaare profoundly different from bacteria, and so they dont present the same targets for a drug to hit. Penicillin interferes with the growth of bacteria cell walls, for example, but viruses dont have cell walls, because they arent even cells; theyre just genes packed into protein shells. Other antibiotics, such as streptomycin, attack the factories inside bacteria that make new proteins, known as ribosomes. A virus doesnt have ribosomes, but instead uses the ribosome inside its host cell to make new copies of itself.

We do currently have antiviral drugs, but theyre a pale shadow of their counterparts that fight bacteria. Typically, antivirals will drive down the number of virus particles in the body, but they cant wipe the virus out completely. People infected with HIV (for example) can avoid developing AIDS by taking a cocktail of antiviral drugs. But if they stop taking antivirals, the virus will rebound to its former levels in a matter of weeks. They have to keep taking the drugs for the rest of their lives to prevent the viruses from wiping out their immune system.

And antivirals have a limited scope of attack. You can treat your flu with Tamiflu, but it wont cure you of dengue fever or Japanese encephalitis. Scientists have to develop antivirals one disease at a timea labor that can take many years. As a result, we still have no antivirals for many of the worlds nastiest viruses, like Lassa fever and Ebola. We can expect new viruses to leap from animals to our own species in the future, and when those new viruses begin to spread, theres a good chance we wont have any antivirals to help stop them.

Virologists, in other words, are still waiting for their Penicillin Moment. But they might not have to wait forever. Buoyed by advances in molecular biology, a handful of researchers in labs around the US and Canada are trying to engineer a new and unprecedented type of antiviral: a broad-spectrum virus-killer, one that could wipe out viral infections with the same ruthless efficiency that penicillin and Cipro bring to the fight against bacteria. If they succeed, future generations may struggle to imagine a time when we were at the mercy of viruses, just as we struggle to imagine life before Flemings moldy dish.

Excerpt from:
Waiting for the Penicillin Moment: my new feature on antiviral drugs for Wired | The Loom