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Health News - Cancer

Village of Weston works to avoid direct smoking ban legislation (Wausau Daily Herald)
WESTON -- The villages work on a smoking ordinance -- which includes players typically on opposite sides of the issue -- is partially motivated by the possibility that if officials dont act, citizens will.



Delaying The Evolution Of Drug Resistance
Keeping germs from cooperating can delay the evolution of drug resistance more effectively than killing germs one by one with traditional drugs such as antibiotics, according to new research from The University of Arizona in Tucson. John W. Pepper proposes a new strategy in the arms race between humans and germs -- targeting the teamwork within gangs of germs.

Texas Invests Record $3.5 Million In Startup Cofounded By UT's Mauro Ferrari For Cancer Technology
NanoMedical Systems Inc., (NMS), an Austin-based startup cofounded by Mauro Ferrari, Ph.D., of The University of Texas Health Science Center at Houston (UTHSC-Houston), to improve the effectiveness of anti-cancer agents and other medications, has received a record $3.5 million Commercialization Award through the Texas Emerging Technology Fund (ETF). NMS was one of six companies that received the ETF awards, which were announced by Texas Gov. Rick Perry on Tuesday, Nov. 18.

Stop Smoking Hypnotherapy
If you've already tried a variety of the stop smoking aids, and you've tried quitting smoking without any help at all, you may think it's just not meant to be. If you haven't tried quit smoking hypnosis, you should take a minute to consider the possibility.

ErbB3 is required for ductal morphogenesis in the mouse mammary gland
IntroductionThe receptor ErbB3/HER3 is often overexpressed in human breast cancers, frequently in conjunction with overexpression of the proto-oncogene ERBB2/HER2/NEU. Although the prognostic/predictive value of ErbB3 expression in breast cancer is unclear, ErbB3 is known to contribute to therapeutic resistance. Understanding ErbB3 functions in the normal mammary gland will help explain its role in cancer etiology and as a modulator of signalling responses to the mammary oncogene ERBB2. Methods: To investigate the roles of ErbB3 in mouse mammary gland development, we transplanted mammary buds from ErbB3-/- embryos into the cleared mammary fat pads of wild-type immunocompromised mice. Effects on ductal outgrowth were analyzed at 4 weeks, 7 weeks and 20 weeks post-transplantation for total ductal outgrowth, branch density and number and area of terminal end buds. Sections of glands containing terminal end buds were analyzed for number and epithelial area of terminal end buds. Terminal end buds were also analyzed for presence of mitotic figures, apoptotic figures, BrdU incorporation, and expression of E-cadherin, P-cadherin, alpha-smooth muscle actin, and cleaved caspase-3. Results: The mammary ductal trees developed from ErbB3-/- buds only partly filled the mammary fat pad. In contrast to similar experiments with ErbB2-/- mammary buds, this phenotype was maintained through adulthood, pregnancy, and parturition. In addition, in contrast to similar work with ErbB4-/- mammary buds, lobuloalveolar development of ErbB3-/- transplanted glands was normal. The ErbB3-/- mammary outgrowth defect was associated with a decrease in the size of the terminal end buds, and increases in branch density, the number of terminal end buds, and in the number of luminal spaces. Proliferation rates were not affected by the lack of ErbB3, but there was an increase in apoptosis in ErbB3-/- terminal end buds. Conclusions: Endogenous ErbB3 regulates morphogenesis of mammary epithelium.

Interleukin-17 expression by breast cancer associated macrophages: IL-17 promotes invasiveness of breast cancer cell lines
IntroductionInterleukin (IL)-17 plays an important role in autoimmunity, promoting auto-immunity, inflammation and invasion in multiple sclerosis, rheumatoid arthritis and type-I diabetes. However, its role in cancer is unclear as there are few studies examining IL-17 protein expression in cancer. Therefore, we examined IL-17 protein expression in human breast cancer and modelled its potential biological significance in vitro. Methods: Immunohistochemistry was used to determine IL-17 expression in breast cancers. Matrigel invasion assays were employed to examine the effect of IL-17 on cancer cell invasion by a panel of breast cancer cell lines. The role of matrix metalloproteinases (MMPs) was investigated with selective antagonists and immunoassays for MMPs-2, 3, 9 and tissue inhibitor of MMP (TIMP1). Results: IL-17 expressing cells with macrophage morphology were identified in the peri-tumoural area of a proportion of patients (8/19). Macrophages were confirmed by CD68 staining on serial sections. With the exception of occasional lymphocytes, one patient with rare multinucleate giant cells and one patient with occasional expression of IL-17 in tumour cells, no other IL-17+ cells were detected. Addition of IL-17 to cell lines in vitro stimulated marked invasion of Matrigel. In contrast, IL-17 did not promote the invasion of MCF7 or T47D cell lines. Invasion was initially thought to be dependent on MMPs as evidenced by the broad-spectrum MMPs inhibitor, GM6001, and selective antagonists of MMP2/9 and MMP3. However measurement of MMPs-2, 3 and 9 and TIMP1 secretion failed to reveal any changes in expression following IL-17 exposure. In contrast, tumour necrosis factor (TNF) promoted secretion of MMPs but IL-17 did not augment TNF, indicating that IL-17 acts via an independent mechanism. Conclusions: This is the first study to describe in situ expression of IL-17 protein in human breast tumours and propose a direct association between IL-17 and breast cancer invasion. The precise effectors of IL-17 dependent invasion remain to be characterised but could include a range of proteases such as a disintegrin and metalloproteinase (ADAM) or astacins. Nevertheless, this work identifies a novel potential mechanism for breast cancer invasion and tumour progression, the prognostic implication of which is currently under investigation.

Quit Smoking today
There's no doubt that smoking is bad for your health, but is it reason enough to give up smoking? The answer, according to a general consensus by health officials everywhere is a resounding "yes." Never smoking is one of the best things you can do for yourself, but stopping smoking (even after years of dependency) is next on the list.

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