New Delhi, June 7 (IANS) India Sunday reported two fresh cases of swine flu taking the total number of confirmed people infected with the virus to 10 so far, health officials said.

Those who tested positive for influenza A (H1N1) include a 25-year-old man who sat in close proximity to a techie who had returned from the US May 31 with the infection.

'The man travelled with the techie by British Airways flight BA 277 May 31. All his close contacts are being traced and would be quarantined,' said a health ministry official.

Of the 10 cases, seven are from Hyderabad, which also reported the first case in the country May 16.

A 35-year-old man who reached Delhi from New York June 2 has also tested positive for the flu.

'He developed flu like symptoms two days after reaching Delhi and tested positive for it. The man is on home quarantine and his contacts have been provided with medicine,' the official said.

The 28-year-old techie who arrived from Philadelphia May 31 had gone home after his arrival at the airport. He later developed high fever and approached the Chest Hospital in Hyderabad June 2. The next day he tested positive for H1N1 influenza.

India reported its first swine flu infection May 16 - that of a 23-year-old man who travelled by Emirates Airline from New York to Hyderabad via Dubai. He has now been discharged after treatment.

Meanwhile three suspect cases -- one each at Cochin, Delhi and Kolkata - have been isolated at the identified health facility.

Health screening of passengers coming from the affected countries is continuing at 21 international airports and over 1.3 million passengers have been screened so far.

Samples of 176 persons have been tested of which 10 have been tested positive for Influenza A (H1N1). The Central Rapid Response Team is assisting Andhra Pradesh for instituting public health measures that need to be taken in the event of a cluster reporting.

The WHO has reported about 21,940 confirmed cases of influenza A(H1N1) infection from 69 countries and 125 deaths till June 5.

Your immune system plays an important function in your health - it protects you against viruses, bacteria, and other toxins that can cause disease. In autoinflammatory diseases, however, the immune system goes awry, causing unprovoked and dangerous inflammation. Now, researchers from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), part of the National Institutes of Health, and other institutions have discovered a new autoinflammatory syndrome, a rare genetic condition that affects children around the time of birth. The findings appear in the current issue of the New England Journal of Medicine.

The scientists have termed the new autoinflammatory syndrome DIRA (deficiency of the interleukin-1 receptor antagonist). Children with the disorder display a constellation of serious and potentially fatal symptoms that include swelling of bone tissue; bone pain and deformity; inflammation of the periosteum (a layer of connective tissue around bone); and a rash that can span from small individual pustules to extensive pustulosis that covers most of the patient's body. Most of the children begin to have symptoms from birth to 2 weeks of age.

"The beauty of this discovery is that the symptoms of this devastating disease can now be treated," said NIAMS director and immunodermatologist, Stephen I. Katz, M.D., Ph.D. "The abnormal inflammatory pathways seen in this disease may also help us understand other common diseases that share clinical features, such as psoriasis, as well as other autoinflammatory disorders."

"We knew when we saw these children that we were dealing with a previously unrecognized autoinflammatory syndrome. The clinical characteristics were distinct from other diseases we had seen before," said NIAMS researcher and lead author Raphaela Goldbach-Mansky, M.D., M.H.S. When her colleague, Dr. Ivona Aksentijevich, tested the first patient for genetic abnormalities, their suspicions were confirmed, and ultimately abnormalities were found in a number of other cases.

All the children had inherited mutations in IL1RN, a gene that encodes a protein known as interleukin-1 receptor antagonist (IL-1Ra). IL-1Ra binds to the same cell receptors as the inflammatory protein interleukin-1, and acts as a brake on this inflammatory protein. Without IL-1Ra, the children's bodies cannot control systemic inflammation that can be caused by interleukin-1.

The scientists identified nine patients from six families with DIRA in the Canadian province of Newfoundland, the Netherlands, Lebanon, and Puerto Rico. Those who were alive at the time of diagnosis - six in all - were treated with anakinra, a drug that is normally used for rheumatoid arthritis and is a synthetic form of human IL-1Ra. Although the patients were resistant to other medications such as steroids, most responded successfully and immediately to anakinra. "Our first patient had been unresponsive to several treatments, and his health care team had almost given up. But with anakinra, he was out of the hospital in 10 days and his symptoms resolved," Dr. Goldbach-Mansky said.

US researchers found that a drug made from the root of the hydrangea plant, which has for centuries been used in Chinese medicine, showed promising results in treating autoimmune disorders such as rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease, type 1 diabetes, eczema and psoriasis.

The study was the work of researchers from the Program in Cellular and Molecular Medicine and the Immune Disease Institute at Children's Hospital Boston (PCMM/IDI), together with the Harvard School of Dental Medicine and is published in the 5 June issue of the journal Science.

An exciting new area in the field of autoimmune disease research is learning about the role of a particular immune system cell called the T helper 17 (Th17) which is genetically different from other types of CD4+ T cell like the Th1, Th2 and T-regulatory cells and appears to play a unique role in the part of the immune system that causes harm when it over-reacts.

The immune system is a complex of delicately balanced "seek and destroy" systems that recognize when something is wrong in the body and then trigger a response to repair the damage or eliminate foreign agents. However, when this delicate balance is disturbed, the responses switch on when there is nothing wrong, causing the immune system essentially to "attack" healthy tissue.

This is what happens in rheumatoid arthritis, where the overactive inflammatory response eventually destroys cartilage in the joints and even healthy tissue in places like the lungs or under the skin. Exactly how and why this happens is still a mystery, but the more scientist look into it, the more they discover that immune cells like the Th17 are involved in unique ways.

In this study, the authors report how a small molecule called halofuginone (extracted from hydrangea root) selectively stops Th17 cells being made, without affecting the other CD4+ T cells, thus showing how it might be possible to stop the immune system from over-producing harmful Th17 cell responses.

They also showed that halofuginone reduced disease symptoms in mice bred with autoimmune disorders.

In the body, cytokines cause Th17 cells to differentiate from other CD4+ T cells, but when the researchers collected cultured mouse CD4+ T cells along with the cytokines, they found that adding halofuginone made levels of Th17 go down significantly but not Th1, Th2 or T regulatory cells.

They also found a similar effect in cultured human CD4+ T-cells: halofuginone selectively stopped production of IL-17, the principal cytokine made by Th17 cells.

The reason this discovery is important is because there are currently no good treatments for autoimmune disorders because you can't get in there and turn down just the inflammatory process without also turning down the protective processes that for instance protect patients from infections.

The main treatments currently rely on antibodies that neutralize cytokines, the chemical messengers that T cells use to control immune fuction and inflammatory responses.

But antibodies are expensive, have to be injected and/or infused, and don't actually solve the root cause of the problem, they just mop up cytokines rather than stop them being produced in the first place. So patients have to keep coming back for infusions to keep the inflammation under control.

As a last resort you can give patients drugs that completely suppress the immune system but for obvious reasons this is very risky.

Mice lacking the fat hormone leptin or the ability to respond to it become morbidly obese and severely diabetic - not to mention downright sluggish. Now, a new study in the June Cell Metabolism shows that blood sugar control in those animals can be completely restored by returning leptin sensitivity to a single class of neurons in the brain, which account for only a small fraction of those that normally carry the hormone receptors.

"Just the receptors in this little group of neurons are sufficient to do the job," said Christian Bjorbaek of Harvard Medical School.

What's more, animals with leptin receptors only in the so-called pro-opiomelanocortin (POMC) neurons spontaneously increase their physical activity levels despite the fact that they remain profoundly obese. While understanding exactly how the POMC neurons act on other organs remains a future challenge, the discovery suggests that drugs designed to tap into the pathway - turning up or down the dial, so to speak - might have benefit for those with severe diabetes and obesity, according to the researchers.

Such drugs might even encourage obese individuals to get moving. "This gives us the opportunity to search for drugs that might induce the desire or will to voluntarily exercise," Bjorbaek said.

Leptin was first identified 15 years ago and made famous for its ability to curb appetite and lead to weight loss. It is known to play a pivotal role in energy balance through its effects on the central nervous system, specifically by acting on a hypothalamic brain region known as the arcuate nucleus (ARC). The ARC contains two types of leptin-responsive neurons, the POMC neurons, which cause a loss of appetite, and the so-called Agouti-related peptide (AgRP) neurons, which do the opposite.

Studies had also revealed a role for leptin in blood sugar control and activity level, also via effects on the ARC. However, scientists still didn't know which neurons were responsible, until now.

When the researchers restored leptin receptor activity in POMC neurons of otherwise leptin-resistant, obese, and diabetic mice, the animals began eating about 30 percent fewer calories and lost a modest amount of weight. Remarkably, the researchers report, their blood sugar levels returned to normal independently of any change in their eating habits or weight. The animals also doubled their activity levels.

Whether this particular bunch of neurons also plays a similarly important role in animals that are lean remains uncertain, Bjorbaek said. "It may be that in the context of severe obesity and diabetes, these neurons do something they don't normally do," he said. But, he added, even if that were the case, it may not matter when it comes to its potential as a therapeutic target.

Achieving a world first, scientists in China have induced cells from pigs to become pluripotent stem cells, which like embryonic stem cells are able to develop into any cell of the body.

The study, which is to published early June in the newly launched Journal of Molecular Cell Biology, was the work of principal investigator Dr Lei Xiao, who leads the stem cell lab at the Shanghai Institute of Biochemistry and Cell Biology, and colleagues.

This is the first time anyone in the world has made pluripotent stem cells from somatic cells (as opposed to germline cells such as sperm and eggs) from an ungulate (an animal that has hooves).

The researchers hope this opens the door to making human disease models, engineering animals as sources of organs for transplant into humans, and developing pigs that are resistant to diseases like swine flu.

Quoted in a separate statement, Xiao said:

"Pig pluripotent stem cells would be useful in a number of ways, such as precisely engineering transgenic animals for organ transplantation therapies."

"The pig species is significantly similar to humans in its form and function, and the organ dimensions are largely similar to human organs," added Xiao.

Xiao and colleagues took cells from the ears and bone marrow of pigs and using transcription factors introduced by a virus they reprogrammed them and coaxed them to develop into colonies of induced pluripotent stem cells (iPS cells) which are very similar to embryonic stem cells, regarded as the "gold standard" of stem cell research.

Further tests showed that like embryonic stem cells, the new iPS pig cells were capable of differentiating into the types of cells that form the endoderm, mesoderm and ectoderm layers of an embryo.

Working with iPS cells in this way also gives information that should make it easier to develop embryonic stem cells (ES cells) from pig or other ungulate embryos, said the researchers.

"We could use embryonic stem cells or induced stem cells to modify the immune-related genes in the pig to make the pig organ compatible to the human immune system," explained Xiao, adding that the pigs could then be used as organ donors for human patients without their immune system having an adverse reaction.

Another application could be to create models for human diseases, for many of them are caused by a disorder of gene expression.

"We could modify the pig gene in the stem cells and generate pigs carrying the same gene disorder so that they would have a similar syndrome to that seen in human patients," explained Xiao, adding that it would then be possible to use the pig model to develop treatments.

And another use could be to breed gene-modified pigs with resistance to diseases like swine flu.

"We would do this by first, finding a gene that has anti-swine flu activity, or inhibits the proliferation of the swine flu virus; second, we can introduce this gene to the pig via pluripotent stem cells, a process known as gene knock-in," said Xiao.

Another way they could make pigs resistant to swine flu would be to knock out the pig cell membrane receptor that the virus uses to gain access to cells. Doing this would stop the virus invading cells and using their contents to replicate itself.

"We could knock out this receptor in the pig via gene targeting in the pig induced pluripotent stem cell," explained Xiao.

There could also be applications to farming, not only by helping to breed healthier and more disease resistant pigs, but also by improving the way that pigs grow.