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Dr Jeevani Hasantha Testimonials-eczema
Eczema patient describes how homeopathy cured him compleately with a very short period at Sajeevi Healing Home.

By: jeevani hasantha

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Dr Jeevani Hasantha Testimonials-eczema - Video

PUBLIC RELEASE DATE:

9-Jan-2014

Contact: Linda Huynh linda.huynh@nih.gov 301-402-1663 NIH/National Institute of Allergy and Infectious Diseases

A study reports the development of a new mouse model for atopic dermatitis, an inflammatory skin disorder commonly known as eczema. The findings, published in Cell Reports, suggest that mast cells, a type of immune cell, are critical for both spontaneous and allergen-induced eczema. The study, led by researchers at the La Jolla Institute for Allergy and Immunology, was supported in part by the National Institute of Allergy and Infectious Diseases (NIAID), a component of the National Institutes of Health.

Eczema is estimated to affect approximately one in five infants and one in fifty adults in the United States. The causes underlying the disorder are unclear. Previous research has suggested a role for imbalanced immune responses and impaired skin defenses, as well as overproduction of thymic stromal lymphopoietin (TSLP), a protein that promotes inflammation. While different mouse models for eczema have been developed, research examining how they are linked to human disease is still ongoing.

In the current study, researchers show that mice lacking phospholipase C-3 (PLC- 3), an enzyme that helps regulate inflammation, develop a skin disorder similar to human eczema, with high levels of TSLP. In this model, disease progression depends on the accumulation of mast cells and the activity of a signaling protein called Stat5. This role for mast cells and Stat5 in eczema was not previously known. The researchers also examined skin lesions of eczema patients and found that some had accumulation of mast cells expressing active Stat5. They identified changes, or polymorphisms, in genes that regulate PLC- 3 and Stat5 that are more common in patients with eczema. With these links to human disease, the targets identified in the mouse model may offer potential new strategies for treating this common disorder in people.

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ARTICLE: T. Ando et al. Critical role for mast-cell Stat5 activity in skin inflammation. Cell Reports. DOI: 10.1016/j.celrep.2013.12.029 (2014).

Marshall Plaut, M.D., chief of the Food Allergy, Atopic Dermatitis and Allergic Mechanisms Section in NIAID's Division of Allergy, Immunology and Transplantation, is available to discuss the findings.

To schedule interviews, please contact Linda Huynh, (301) 402-1663, linda.huynh@nih.gov.

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NIH-funded scientists develop mouse model for atopic dermatitis

PUBLIC RELEASE DATE:

9-Jan-2014

Contact: Bonnie Ward contact@liai.org 619-303-3160 La Jolla Institute for Allergy and Immunology

SAN DIEGO (January 9th, 2014) Researchers from the La Jolla Institute for Allergy and Immunology have revealed a critical player in the cellular interactions leading to eczema a chronic inflammatory skin condition affecting more than 14 million U.S. children and adults.

In a study published today, Toshiaki Kawakami, M.D., Ph.D., and his research team provide information which supports for the first time in humans the long-held theory that mast cells are a key culprit in causing eczema, also known as atopic dermatitis. Further, the team showed that a cellular protein, known as STAT5, plays a pivotal role by triggering major increases in mast cells in the skin of some eczema sufferers. The discovery opens the door to creating new therapies to prevent or better treat eczema based on blocking STAT5 in mast cells.

The team conducted its studies using skin samples from eczema patients. "We found that the number of mast cells, which we have previously shown to be important in mouse atopic dermatitis, is increased in human patients," says Kawakami. "We also showed that these mast cells contain high levels of the active form of STAT5."

Kawakami says the researchers also tested their theory on STAT5's importance in mice. "When STAT5 is knocked out in the mast cells (of specially engineered mice), the mice become resistant to atopic dermatitis," says Kawakami. "This indicates that STAT5 regulatory mechanisms in mast cells are important for the pathogenesis of this disease."

The findings were published online in Cell Reports in a paper entitled "Critical role for mast-cell Stat5 activity in skin inflammation." The study was supported in part by the National Institute of Allergy and Infectious Diseases (NIAID), a component of the National Institutes of Health, under contract number N01 AI40030.

Eczema is a condition in which the skin becomes inflamed or irritated and is marked by redness, itchiness and dry, cracked skin. The exact cause of eczema is unknown, but it's thought to be linked to an overactive response by the body's immune system to allergens and irritants, similar to other allergic diseases such as asthma and food allergy. Eczema is more common in children than adults, since it sometimes resolves with age. About 10.7 percent of U.S. children and 3 percent of adults are estimated to be affected.

Kawakami says this finding is a continuation of his nearly 10-year effort to pinpoint the cascade of key cellular actions involved in eczema. Initially working in mice, his latest study enabled human confirmation of his key findings. "We now know that, in eczema, the mechanisms we found in mice are also operative in human disease," says Kawakami. Along with showing that mast cells and STAT5 drive the eczema process in humans, this study also found an enzyme -- Phospholipase C-beta3 (PLC-3) that can block the activation. PLC-3 has a calming effort on STAT5 and can prevent it from driving up the mast cell numbers, explains Kawakami. "The mast cell numbers are inversely correlated with PLC-3 levels," he says. "The more PLC-3, the fewer the mast cells."

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La Jolla Institute scientist identifies pivotal cellular protein underlying eczema