Monthly Archives: February 2014

Psoriasis researchers identify molecular changes responsible for skin discoloration

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Itchy, painful rashes -- such as those that occur with psoriasis -- are uncomfortable, but at least they fade when the flare-up subsides. Mostly. Evidence often remains in the form of dark, discolored areas of skin, serving as a reminder of the disease. A new study supported by the Milstein Medical Research Program at The Rockefeller University, however, has uncovered the molecular roots of skin discoloration that is often associated with psoriasis, suggesting the possibility of new treatments for pigmentation changes seen not only in psoriasis, but also in other conditions such as eczema and acne.

In psoriasis, the culprit is a class of immune system molecules known as cytokines. Cytokines play a key role in a signaling process that brings immune cells out to fight off an infection. But two cytokines -- interleukin-17 (IL-17) and tumor necrosis factor (TNF) -- are overexpressed in psoriasis, leading the immune system to attack a person's own skin cells. It's well-known that these two molecules play an important role in causing the painful rashes that are characteristic of the disease, but Claire Q. Wang, a research associate in James Krueger's Laboratory of Investigative Dermatology, wanted to see if IL-17 and TNF might also have something to do with the dark spots that psoriasis leaves behind.

"One of the treatments for psoriasis is light therapy," says Wang. "Patients will receive artificial UVA and UVB light as a way to reduce inflammation, and although the light doesn't cause sunburn, it was still commonly assumed that this was causing the pigmentation changes. Our research showed that this was not the case."

The scientists found that the IL-17 and TNF cytokines were disrupting the pigment production of patients' melanocytes -- the cells that produce melanin, the pigment that gives skin its color. The researchers treated normal human melanocytes with IL-17 and TNF, and found that the two cytokines worked together to suppress melanin production. The researchers also looked at the gene expression of skin cells from people with psoriasis and found decreased expression of the genes involved in pigmentation signaling, correlated with increased amounts of IL-17 and TNF.

The two cytokines were also found to promote the formation of melanocyte clusters and stimulate the production of growth-promoting cytokines. Psoriasis lesions that contained high levels of IL-17 and TNF also had more melanocytes than healthy skin.

"This was very surprising," says Wang. "Melanocytes are believed to only replicate in the initial growth stage of melanocyte tumors, including melanomas. Here, in psoriasis, their numbers were doubled, sometimes tripled, but this was noncancerous skin. This shows us that these cells are not as dormant in healthy individuals as scientists believe."

This finding, together with the inhibition of pigment function in melanocytes, paints a picture of what's happening in the skin when a psoriasis flare-up fades.

"During a flare-up, there can be parts of skin with hypopigmentation -- white spots," says Wang. "Then after it subsides, the spots turn dark. We think the increase in IL-17 and TNF induces this build-up of melanocytes, but prevents them from expressing the melanin until the inflammation settles down. Then the build-up is released, and the skin shows hyperpigmentation -- dark spots."

"Knowing that immune cytokines can change pigment production in melanocytes, while also knowing that chronic inflammation has the potential to increase the number of melanocytes, has clear implications for the design of future therapies to address a set of common skin disorders," says Dr. Krueger, director of Milstein Research Program and D. Martin Carter Professor in Clinical Investigation. "In addition, the results of this study provide new mechanisms for how abnormal pigmentation associated with some melanocytic nevi and melanomas might arise as a result of immune responses to the growths."

Dr. Wang plans to continue studying the effects of TNF and IL-17 on melanocytes, and would like to expand the research to 3D skin models -- fabricated samples of tissue in vitro that behave like human skin -- that would give a better visual of how the melanin production process is being disrupted by these two cytokines during skin inflammation or wound healing.

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Psoriasis researchers identify molecular changes responsible for skin discoloration

Cleaning the Sinew in 10-Day Yoga and Detox with Baba- Goa, India -Family World Travel Blog – Video

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Cleaning the Sinew in 10-Day Yoga and Detox with Baba- Goa, India -Family World Travel Blog
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Cleaning the Sinew in 10-Day Yoga and Detox with Baba- Goa, India -Family World Travel Blog - Video

Axe looms for Socceroos' Cup venue

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Feb. 17, 2014, 10:59 a.m.

World Cup travel plans could be in thrown into chaos as the venue for final game is on the cusp of being withdrawn.

Australia's World Cup travel plans could be in thrown into chaos as the venue for their third and final group stage game is on the cusp of being withdrawn as a host city.

The Arena da Baixada in Curitiba is falling well behind the deadline date for completion, originally for December 31, and could be rescinded from the list of venues for the 2014 World Cup by FIFA, who will make a final decision by Wednesday morning.

Reports surfaced on Monday morning that the venue had been already been axed as a host city though the Football Federation of Australia denied that they had received any notice from FIFA.

The game's governing body will assess the renovations of the stadium over the next two days and must be convinced by the local organising committee in the southern city that the venue will be completed in time before announcing their decision to cancel games held there.

Last week, FIFA secretary-general JeromeValcke would not speculate whether Curitiba had been dropped as a World Cup venue but said a decision will be made this week.

"We will communicate the final decision to the teams as promised (next week)," Valcke said.

The venue was one of the newer stadiums in Brazil, originally built in 1999, though endured problems with the upgrade process highlighted by the suspension of all renovation works in October last year due to safety concerns.

The state government of Parana reportedly sought to borrow up to $100 million from a government bank recently in order to fast-track construction and even hire more workers.

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Axe looms for Socceroos' Cup venue

Axe hovers over Socceroos venue

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Feb. 17, 2014, 10:59 a.m.

World Cup travel plans could be in thrown into chaos as the venue for final game is on the cusp of being withdrawn.

Australia's World Cup travel plans could be in thrown into chaos as the venue for their third and final group stage game is on the cusp of being withdrawn as a host city.

The Arena da Baixada in Curitiba is falling well behind the deadline date for completion, originally for December 31, and could be rescinded from the list of venues for the 2014 World Cup by FIFA, who will make a final decision by Wednesday morning.

Reports surfaced on Monday morning that the venue had been already been axed as a host city though the Football Federation of Australia denied that they had received any notice from FIFA.

The game's governing body will assess the renovations of the stadium over the next two days and must be convinced by the local organising committee in the southern city that the venue will be completed in time before announcing their decision to cancel games held there.

Last week, FIFA secretary-general JeromeValcke would not speculate whether Curitiba had been dropped as a World Cup venue but said a decision will be made this week.

"We will communicate the final decision to the teams as promised (next week)," Valcke said.

The venue was one of the newer stadiums in Brazil, originally built in 1999, though endured problems with the upgrade process highlighted by the suspension of all renovation works in October last year due to safety concerns.

The state government of Parana reportedly sought to borrow up to $100 million from a government bank recently in order to fast-track construction and even hire more workers.

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Axe hovers over Socceroos venue

Axe hovers over Socceroos' World Cup venue in Curitiba

Posted on by

Feb. 17, 2014, 10:59 a.m.

World Cup travel plans could be in thrown into chaos as the venue for final game is on the cusp of being withdrawn.

Australia's World Cup travel plans could be in thrown into chaos as the venue for their third and final group stage game is on the cusp of being withdrawn as a host city.

The Arena da Baixada in Curitiba is falling well behind the deadline date for completion, originally for December 31, and could be rescinded from the list of venues for the 2014 World Cup by FIFA, who will make a final decision by Wednesday morning.

Reports surfaced on Monday morning that the venue had been already been axed as a host city though the Football Federation of Australia denied that they had received any notice from FIFA.

The game's governing body will assess the renovations of the stadium over the next two days and must be convinced by the local organising committee in the southern city that the venue will be completed in time before announcing their decision to cancel games held there.

Last week, FIFA secretary-general JeromeValcke would not speculate whether Curitiba had been dropped as a World Cup venue but said a decision will be made this week.

"We will communicate the final decision to the teams as promised (next week)," Valcke said.

The venue was one of the newer stadiums in Brazil, originally built in 1999, though endured problems with the upgrade process highlighted by the suspension of all renovation works in October last year due to safety concerns.

The state government of Parana reportedly sought to borrow up to $100 million from a government bank recently in order to fast-track construction and even hire more workers.

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Axe hovers over Socceroos' World Cup venue in Curitiba

Researchers rejuvenate stem cell population from elderly mice, enabling muscle recovery

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PUBLIC RELEASE DATE:

16-Feb-2014

Contact: Krista Conger kristac@stanford.edu 650-725-5371 Stanford University Medical Center

STANFORD, Calif. Researchers at the Stanford University School of Medicine have pinpointed why normal aging is accompanied by a diminished ability to regain strength and mobility after muscle injury: Over time, stem cells within muscle tissues dedicated to repairing damage become less able to generate new muscle fibers and struggle to self-renew.

"In the past, it's been thought that muscle stem cells themselves don't change with age, and that any loss of function is primarily due to external factors in the cells' environment," said Helen Blau, PhD, the Donald and Delia B. Baxter Foundation Professor. "However, when we isolated stem cells from older mice, we found that they exhibit profound changes with age. In fact, two-thirds of the cells are dysfunctional when compared to those from younger mice, and the defect persists even when transplanted into young muscles."

Blau and her colleagues also identified for the first time a process by which the older muscle stem cell populations can be rejuvenated to function like younger cells. "Our findings identify a defect inherent to old muscle stem cells," she said. "Most exciting is that we also discovered a way to overcome the defect. As a result, we have a new therapeutic target that could one day be used to help elderly human patients repair muscle damage."

Blau, a professor of microbiology and immunology and director of Stanford's Baxter Laboratory for Stem Cell Biology, is the senior author of a paper describing the research, which will be published online Feb. 16 in Nature Medicine. Postdoctoral scholar Benjamin Cosgrove, PhD, and former postdoctoral scholar Penney Gilbert, PhD, now an assistant professor at the University of Toronto, are the lead authors.

The researchers found that many muscle stem cells isolated from mice that were 2 years old, equivalent to about 80 years of human life, exhibited elevated levels of activity in a biological cascade called the p38 MAP kinase pathway. This pathway impedes the proliferation of the stem cells and encourages them to instead become non-stem, muscle progenitor cells. As a result, although many of the old stem cells divide in a dish, the resulting colonies are very small and do not contain many stem cells.

Using a drug to block this p38 MAP kinase pathway in old stem cells (while also growing them on a specialized matrix called hydrogel) allowed them to divide rapidly in the laboratory and make a large number of potent new stem cells that can robustly repair muscle damage, Blau said.

"Aging is a stochastic but cumulative process," Cosgrove said. "We've now shown that muscle stem cells progressively lose their stem cell function during aging. This treatment does not turn the clock back on dysfunctional stem cells in the aged population. Rather, it stimulates stem cells from old muscle tissues that are still functional to begin dividing and self-renew."

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Researchers rejuvenate stem cell population from elderly mice, enabling muscle recovery

Over 5,000 Cubans receive stem cell treatment: Expert

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Havana, Feb 16 (IANS): More than 5,000 patients have received stem cell treatment in Cuba since its procedure was introduced in 2004, a medical expert said.

Porfirio Hernandez, researcher and vice director at the Hematology and Immunology Institute in Cuba, said the stem cell treatment method has been implemented in 13 of the 15 provinces in Cuba.

As a widely acknowledged pioneer of this practice, Hernandez said that more than 60 percent of patients receiving the treatment had suffered from severe ischemia at lower limbs and other blood vessel related ailments, reported Xinhua.

The therapy has also been used to reduce the sufferings of patients with severe orthopedic and cardiac problems, Hernandez added.

Stem cells are capable of self-renewing, regenerating tissues damaged by diverse disease, traumas, and ageing, and stimulating the creation of new blood vessels.

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Over 5,000 Cubans receive stem cell treatment: Expert