Botox - popular for its ability to smooth wrinkles when injected into the face, may have another use that goes beyond the cosmetic, say Johns Hopkins researchers.

Botox is a toxin that works by weakening or paralyzing certain nerves and muscles.

In the new study, the researchers found that patients with a painful and debilitating nerve compression disorder called thoracic outlet syndrome (TOS), reported a significant reduction in short-term pain after receiving a single, low-dose injection of Botox in a muscle located in the neck.

Though the study, was small, researchers say it suggests Botox is a safe, noninvasive alternative to the syndrome's treatment of last resort: surgery to remove the first rib and sever one of the muscles in the neck.

"There haven't been many alternatives to the use of surgery to treat this syndrome," says Paul J. Christo, an assistant professor of anesthesiology and critical care medicine at the Johns Hopkins University School of Medicine and the study's lead author.

"Botox seems to be an effective treatment that avoids surgery's obvious drawbacks, such as its invasive nature and long recovery time," he adds.

The study has been published in the April issue of the journal Pain Medicine.

NEW DELHI: Radiotherapy for breast cancer patients could soon be a single dose 30-minute affair, instead of the tedious present-day regimen lasting over six weeks.

In a major breakthrough, a team of British doctors headed by University College London's Dr Jayant S Vaidya -- an Indian from Goa -- has succesfully created and tested a new technique that will blast the remnants of a tumour inside the breast in just one shot, lasting half an hour. The team used radiation on areas just around the tumour rather than the whole breast, as is done presently.

A 10-year trial of this Targeted Intraoperative Radiotherapy (TIR), conducted in nine countries involving over 2,200 women, confirmed that radiation targeting a specific area of the breast was as effective as whole-breast radiation in reducing breast cancer recurrence in women.

The results of this trial was published in the latest edition of the medical journal 'The Lancet'.

So, while a patient is still under anaesthesia following the removal of the tumour, a series of gentle X-rays are administered to destroy any remaining tumour cells at the cancer site. The technique is highly convenient, requiring just one session of radiation, making it less time consuming and less costly than whole-breast treatment.

"TARGIT trial can change two fundamental principles in the treatment of breast cancer: whole breast radiotherapy can be replaced by a targeted one-time shot and a much smaller dose of radiation may be adequate," Dr Vaidya told TOI from UK. Several hospitals in India, including Breach Candy in Mumbai and AIIMS in Delhi, have expressed interest in his work, he added.

"Breast cancer usually recurs around the area where the tumour was detected the first time. So it's logical to give concentrated dose of radiation to the tissues at highest risk of cancer coming back rather than the whole breast," he added.

Dr Vaidya said that since 2000, the team started delivering TIR to patients. A special machine called Intrabeam administered radiation from inside the breast to the exact site of the cancer, instead of the present-day external beam radiotherapy.

"Our decade-long TARGIT trial has now confirmed that old and new methods are as good as each other," Dr Vaidya said.

The therapy, however, has a few limitations at present. It can be done on patients over the age of 45 and the tumour should not be bigger than 3cm. "Our trials till now tried this technique on women above age of 45. So we don't know how effective it will be in stopping recurrence of cancer on younger women. Trials to find this are going to start soon," he said.

Dr Vaidya launched the TARGIT trial on March 24, 2000. In this randomized trial, women aged 45 years or older with breast cancer undergoing breast-conserving surgery were enrolled from 28 centres in nine countries. Patients were randomly assigned in a 1:1 ratio to receive TIR or whole-breast external beam radiotherapy.

The study said, "At four years, there were six local recurrences in the intraoperative radiotherapy group and five in the external beam radiotherapy group. Recurrence in the conserved breast at four years was 1.2% in the targeted intraoperative radiotherapy and 0.95% in the external beam radiotherapy group. Radiotherapy toxicity was lower in the TIR group."

Prof Michael Baum, professor emeritus of surgery at University College London who carried out the first procedure using intraoperative radiotherapy in 1998 said, "Many women specially in the developing world who live hundreds of miles from a radiotherapy unit will be spared six weeks of treatment going back and forth to the radiotherapy centre."

* Targeted Intraoperative Radiotherapy (TIR) has a comparable recurrence rate of around 1% with presently used external beam radiation
* Radiotherapy toxicity were four times lower, with an incidence rate of 0.5% compared with 2% from EBR
* The new technique involves an intense blast of radiation to the tumour site extending to a radius of 2 cm lasting 30 minutes
* It takes place after the surgeon has taken out the tumour and before the wound is closed
* TIR completely avoided irradiation of the heart, lung and oesophagus causing no damage to these structures
* It is currently only available to women taking part in clinical trials

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