Dimapur, June 7 (MExN): The Legislators’ Forum on AIDS, Nagaland Assembly, today clarified to reported statements made by Nagaland’s Health & Family Welfare minister that the government has no knowledge or check over funds meant for the HIV/AIDS health sector in Nagaland.
The coordinator of the forum Dr. Vinito L Chishi issued a statement today saying that the comments “has been brought out of context.” The clarification said that the minister for Health & Family Welfare was surprised to see the context in which he had reacted to queries from the Press ‘has been brought out-of context’. “The honorable minister regrets that his statement has been misquoted from what he intended and wishes to put the record straight in regard to the headlines: ‘Government unaware of HIV/AIDS budget’; ‘No mechanism to check utilization of HIV/AIDS funds’; ‘Selection of NGOs and utilization of fund by the NGOs’.”
“This has cast aspersion on the NGOs as well as NSACS. In this regard, the minister wishes to put it clear that he was quoted out of context. The reply was given to mean that LFA has no mechanism to control the funds or their utilizations which are channelised through NSACS. However, apologies are hereby extended to the NGOs and NSACS if this has hurt their sentiments,” the forum said.
The forum said the minister is fully aware that the funds received by local NGOs through the NSACS from the NACO are “utilized strictly as per Operational Guideline of the Financial Management issued by NACO-GOI; in this regard, the chairman–cum–Commissioner & Secretary of Health & Family Welfare has also clarified that NACO has one of the strictest monitoring mechanism for checking the fund utilization,” the forum asserted.
Nagaland has 68 NGOs which are funded by NACO through NSACS; the process of contracting these NGOs is through a tedious process of evaluation mechanism prescribed by NACO, the forum said. “The utilization of fund by the concern NGOs has been very specific and strict that diversion and mis-utilization of the fund is restricted by constant monitoring through comparison of the Physical and Financial achievements. Furthermore, the Annual Action Plan of NSACS is taken up to the Executive Committee for approval.”
The Legislators’ Forum added that the minister “is happy” that the HIV prevalence (Adult HIV prevalence per NACO technical brief) is in “downward trend”: 2003 – 1.83%, 2004 – 1.62%, 2005 – 1.45%, 2006 – 1.26% and 1.20% in 2007. “Further the population based survey has revealed that the prevalence is showing a further downward trend. This has been made possible because of the joint efforts of all concerned, especially the NGOs and stakeholders,” the forum said and extended its appreciation.

In a surprising discovery that someday may lead to new treatments for many inflammatory diseases, University of Utah scientists found that a hormone involved in iron metabolism can save mice from deadly acute inflammation.

"It's well recognized that the hormone hepcidin helps regulate iron balance. This study shows it has an additional, brand-new, unexpected role in reducing inflammation," says the study's principal author, Jerry Kaplan, a pathology professor and assistant vice president for basic sciences at the University of Utah Health Sciences Center.

The findings by Kaplan and his fellow molecular biologists were scheduled for publication online Monday, June 7 in The Journal of Clinical Investigation and in the print issue dated July 1. The research was funded by the National Institutes of Health.

The study reveals that "hepcidin has an anti-inflammatory effect, reducing the consequences of inflammation," says the study's first author, Ivana De Domenico, an assistant professor of internal medicine.

Coauthor Diane Ward, an associate professor of pathology, adds: "This could mean that hepcidin might be considered as a therapy for a wide range of acute inflammatory conditions such bacterial infections; inflammation from surgery, injury or burns; organ transplantation; and rare cases of inflammation from blood transfusions."

Toxic shock and fever also might be subject to hepcidin treatment, Kaplan says.

"Clinical trials in humans are required to determine if hepcidin is effective at treating human inflammatory conditions - and that will be a few years away," he adds.

Hepcidin Rescues Cells and Mice from Fatal Inflammation

In the study's key experiments, mice were given one of three substances in doses that cause fatal inflammation: (1) Lipopolysaccharide or LPS, a toxin on the outside of bacteria and recognized as "foreign" by the immune system, inducing inflammation; (2) Poly I:C, which is found in viruses and also provokes inflammation; (3) Turpentine, a solvent used historically to provoke and study inflammation.

Cells called macrophages were cultured in the lab and exposed to LPS. Some cell cultures were pretreated with hepcidin. The untreated cells showed high levels of inflammatory proteins, while the treated cells had lower levels.

"When your body sees either that LPS coating or the bacteria, your innate immune system signals to make cytokines, which are proteins that cause inflammation," Ward says. "That inflammation response makes immune cells like macrophages and neutrophils converge on the invading bacteria and kill them."

But the "big release of inflammatory agents can cause septic shock, which can be fatal," she adds. "Your temperature drops, there's inactivity and eventually you can die."

So in the key experiments, "we took mice and either preinjected them with hepcidin or just saline as a control, and then two hours later we injected them with LPS [or one of the two other inflammatory substances] to provoke inflammation," says Ward.

"In animals injected with saline before the inflammatory substance, the animals' temperatures dropped, their cytokines and inflammation increased and they became so sick they couldn't move. If mice were injected with hepcidin prior to the inflammatory substance, they showed less inflammation, only minor illness and remained mobile."

It has been known for at least a decade that hepcidin is released into the bloodstream in response to inflammation. It also has been known that hepcidin attacks bacteria and kills them. And increased hepcidin reduces iron in the blood, which also has an antibacterial effect, since infectious agents require iron, says Ward.

"The new finding is that the presence of hepcidin in the blood actually reduces inflammation," she says.

Kaplan and colleagues cautioned that they showed only that hepcidin works against acute inflammation. It did not help mice who suffered chronic bowel inflammation and resulting sepsis or blood poisoning.

They speculated larger hepcidin doses might combat chronic inflammation, but only during some limited time window, say, early in the inflammation process.

Hepcidin: Maintaining Iron Balance in Your Body

Kaplan says iron balance in the human body is regulated by hepcidin, which is a peptide hormone secreted to help metabolize iron that we eat. Hepcidin attaches or "binds" to a substance named ferroportin, which exports iron from cells into the blood.

"High levels of hepcidin in the blood results in the loss of ferroportin from cells, leading to decreased export of iron from cells to blood," Kaplan says.

If too little iron in the blood persists, a person has anemia.

"Usually when you take an iron pill or you get a bacterial infection that is self-limiting, you'll get an increase in hepcidin, which in time will decrease," says Kaplan. "As hepcidin binds to ferroportin, it removes ferroportin from the blood and also removes hepcidin from the blood. Both are degraded in the cells."

The opposite of anemia is iron overload, and "most diseases of iron overload result from not enough hepcidin to remove ferroportin from cells," he adds. Ferroportin brings iron from our diet into the blood, so without enough hepcidin, too much iron accumulates in the blood.

"Hepcidin monitors your body's iron status," Kaplan says. "When you have too much iron, hepcidin increases to help prevent more iron from coming in. When you need more iron, hepcidin levels decrease, permitting more iron to come into the body from your diet and from iron stored in your cells, particularly your spleen."

In a series of previous studies, Kaplan and colleagues worked out how hepcidin causes ferroportin to be carried into cells and degraded.

They discovered an enzyme named Jak2 changes or "phosphorylates" ferroportin so it can be carried into cells to be degraded.

In the new study, they showed the same Jak2 enzyme also phosphorylates or adds a phosphate molecule to Stat3, which is a protein that turns various genes on or off. In other words, Jak2 makes it possible for Stat3 to turn genes on or off.

The new study shows that "among the genes that are turned on are genes that reduce inflammation," Kaplan says.

Yet only a couple of the genes activated by Stat3 involve inflammation. What the rest of them do isn't known. So it's possible the iron metabolism process involving hepcidin, ferroportin, Jak2 and Stat3 may be involved in other processes in the body.

A Mystery of Evolution

Why would a hormone that regulates iron balance also combat inflammation?

"Our view is that this is a feedback system, so anytime in your body when you turn on a gene, there's always a mechanism by which you can turn it off or limit it," Kaplan says. "So here's a case where bacteria come in, turn on inflammation, and this hepcidin pathway we discovered is a way of limiting that. Inflammation is good, but too much inflammation is bad. So here is a way of regulating inflammation."

But, he adds, "How an antibacterial agent got to regulate iron and then got to reduce inflammation is one of the mysteries of evolution."

In addition to Kaplan, De Domenico and Ward, the study's coauthors are medical students Tian Zhang and Nyall London; physician Curry Koening, an assistant professor of rheumatology; Ryan Branch, a high school student who worked as a lab aide; Eric Lo, a lab technician; Raymond Daynes, a professor of pathology; James Kushner, a professor of hematology; and cardiologist Dean Li, a professor of internal medicine.

Source
University of Utah Health Sciences

London, United Kingdom (AHN) - Tighter immigration notwithstanding, the United Kingdom's National Health Service is being forced to recruit hundreds of physicians from India to overcome a shortage of junior doctors in the country.

Due to strict immigration rules, which were made even stricter after the Conservative-Liberal Democrat Coalition took charge last month, a significant number of overseas medical professionals had to leave the UK. This, combined with European regulations on doctors' working hours and childcare breaks, has led to dozens of hospitals facing a severe deficit in the number of doctors.

A range of specialties like obstetrics, gynecology, pediatrics, accident and emergency are facing a shortage of junior doctors and are struggling to fill the vacancies. The situation has led many in the medical fraternity to believe that the government might have "pulled the plug on overseas recruitment far too quickly."

Medical training schools across the UK are busy recruiting manpower from India and are expected to continue this recruitment drive over the coming year. The major schools that are looking to fill up their vacancies out of India are from Wales, Severn, the West Midlands and Northern Ireland.

Reports suggest that it is the hospitals in major cities that are facing the shortage crunch the most after the European Working Time Directive was introduced into the NHS in August 2009. Moreover, British doctors were not willing to serve in the shortage areas while the Indian doctors were ready to do that and even work for longer hours.

The problem could have been solved earlier if the UK Department of Health (DoH) had had a free hand in handling fulfillment of vacancies. With the UK Home Office not ready to concede on its current two-year limit for overseas doctors, the shortage has remained unresolved.

The British Association of Physicians of Indian Origin (BAPIO) had agreed to help with the DoH's recruitment drive but it wanted the two-year limit increased to three and four years, which the Home Office would not agree to.

The DoH is reportedly going ahead with its recruitment drive in India at least. In order to plug the shortage of medicos in the country, UK health officials held interviews of potential candidates in Kolkata last week. The doctors, if selected, will join duty by August.

Read more: http://www.allheadlinenews.com/articles/7018885779#ixzz0prbxqJjB

Aarti Dhar

NEW DELHI: Confronted with a number of complaints about corruption in grant of recognition to medical colleges, Union Health and Family Welfare Minister Ghulam Nabi Azad has cautioned the institution managements of strict action if they are found to be involved in malpractices.

Mr. Azad will also write to the Board of Governors that has superseded the Medical Council of India (MCI) to be transparent in their dealings.

'Action against touts and colleges'

"I have cautioned the managements that action would not only be taken against the touts who indulge in corruption by name-dropping but also against them for using touts to get their jobs done," he told journalists here on Monday.

"Instead of waiting to get their work done through unfair means using touts, they [managements] should use the money for creating infrastructure and faculty for improving the institution so that it gets recognition on merit," Mr. Azad said.

In February, Mr. Azad wrote to the deans and principals of all medical colleges, urging them to be vigilant against touts using his or any Health Ministry official's name to get recognition for medical colleges through the MCI.

The malpractice was expected to end after the MCI was superseded by the six-member Board of Governors, and its president Ketan Desai arrested by the CBI on charges of corruption.

"The Board of Governors has been given the final powers for approval from the MCI through the Ordinance and the cases need not come to the Ministry," Mr. Azad said.

However, with the recognition process at its peak before the new academic session starts, unscrupulous elements are said to be in action again assuring clearance in lieu of money.

80 complaints

The Ministry had received close to 80 complaints of malpractices since February from southwest India, where 80 per cent of the country's private medical colleges were situated.

Action was initiated against these after the complaints were forwarded to the respective Chief Ministers and heads of police departments, Mr. Azad said.

The Minister asked students to come forward with their complaints regarding lack of infrastructure or faculty in their college.

On the Board of Governors seeking more time for clearing pending cases, Mr. Azad said the panel would also look into complaints received by it regarding undue favour or malpractices in refusing recognition.

US immunologists have developed a prototype breast cancer vaccine that targets a protein that is only present in breast cells when a woman is lactating or when she has breast cancer: they found it provided protection against breast cancer in mice and suggest it could be developed to protect women against the disease in their post-childbearing years.

You can read how lead investigator Dr Vincent Tuohy, and colleagues from the Cleveland Clinic's Lerner Research Institute in Cleveland, Ohio, conducted their research in an online before print issue of their study that appeared in Nature Medicine on 30 May.

In a statement, the researchers said enrolling for human trials could start next year, and if successful, this could be the first vaccine to prevent breast cancer.

Tuohy told the press that:

"We believe that this vaccine will someday be used to prevent breast cancer in adult women in the same way that vaccines have prevented many childhood diseases."

"If it works in humans the way it works in mice, this will be monumental. We could eliminate breast cancer," he added.

The vaccine targets α-lactalbumin, a protein found in the majority of breast cancers, and only present in healthy women when they are lactating, that is when their breasts are producing milk.

The challenge of developing a vaccine against cancer is that cancer is not like a virus that the immune system readily recognizes as alien: cancer cells are no more than over-produced variations of healthy cells, and trying to vaccinate against cancer cells risks destroying healthy tissue as well.

The key is therefore to find something that is present in and necessary for cancer cells to survive, but targeting it does not wipe out healthy cells at the same time: it revs up the immune system, but only targets the protein necessary for tumor formation.

So Tuohy and colleagues decided to try for α-lactalbumin, because this would fit with a strategy of vaccinating women over 40, when breast cancer risk begins to rise and pregnancy is less likely. (They explained that if a woman receiving this vaccine did fall pregnant then her breasts would feel sore and she would probably have to opt not to breast feed).

For the study, they tested the effect of the vaccine in mice genetically bred to be prone to breast cancer: usually such mice develop breast tumors at the age of 10 months.

They injected six 2-month old cancer-prone mice with a vaccine that contained the α-lactalbumin antigen and an adjuvant (a chemical that boosts the immune system to help the vaccine), and another six had a dummy injection that did not contain the antigen. None of the mice had cancer when they were injected.

After 10 months, all the mice that had not received the antigen had developed large breast tumors, while none of the mice that had received the antigen showed signs of breast tumors.

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The authors wrote also that "vaccination-induced prophylaxis occurs without any detectable inflammation in normal nonlactating breast tissue", and concluded:

"Thus, α-lactalbumin vaccination may provide safe and effective protection against the development of breast cancer for women in their post-child-bearing, premenopausal years, when lactation is readily avoidable and risk for developing breast cancer is high."

The researchers also found that the vaccine inhibited tumor growth when injected in mice that already had breast cancer tumors.

There are already two cancer-prevention vaccines approved for use in the US, one against cervical cancer and the other against liver cancer, but these target viruses, the human papillomavirus (HPV) and the Hepatitis B virus (HBV), and not the cancer itself.

Dr Joseph Crowe, Director of the Breast Center at Cleveland Clinic, said because Tuohy was an immunologist rather than a cancer specialist he approached the problem from a different angle: attack the tumor itself.

"It's a simple concept, yet one that has not been explored until now," said Crowe.

Tuohy said he thinks their findings go beyond breast cancer, and give us a glimpse of how we might develop vaccines against other types of cancer.

For instance, in line with these findings, scientists could search for antigens for other cancers; they would have to meet the same criteria, which are: must be over-expressed in the majority of targeted tumors and must not be present in normal tissue, except under specific avoidable conditions (such as lactation).