By Icon Health Publications
This can be a 3-in-1 reference e-book. It offers a whole scientific dictionary protecting thousands of phrases and expressions on the subject of bilirubin. It additionally offers wide lists of bibliographic citations. ultimately, it presents details to clients on the way to replace their wisdom utilizing a number of web assets. The e-book is designed for physicians, clinical scholars getting ready for Board examinations, scientific researchers, and sufferers who are looking to get to grips with learn devoted to bilirubin. in case your time is efficacious, this publication is for you. First, you won't waste time looking the web whereas lacking loads of proper info. moment, the booklet additionally saves you time indexing and defining entries. ultimately, you won't waste money and time printing countless numbers of websites.
Read or Download Bilirubin - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References PDF
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Additional resources for Bilirubin - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References
Significance: Characterization of the mechanisms by which estrogens decrease Mrp2/MRP2 function and expression can lead to 1) improved drug therapy for women in pregnancy, 2) development of therapeutic measures to increase MRP2 function in cholestatic liver disease, and 3) methods to screen for cholestatic toxicity in drugs under development. Generate_Screen • Project Title: HYPOXIC RESPONSES OF VASCULAR SMOOTH MUSCLE Principal Investigator & Institution: Kourembanas, Stella; Associate Professor of Pediatrics; Children's Hospital (Boston) Boston, Ma 021155737 Timing: Fiscal Year 2002; Project Start 06-SEP-1996; Project End 31-AUG-2003 Summary: (Verbatim from Investigator's Abstract): Abnormal vascular smooth muscle cell (VSMC) proliferation is a key feature of vascular diseases such as pulmonary hypertension and atherosclerosis.
Furthermore, bilirubin (rapidly formed from biliverdin by the enzyme biliverdin reductase) has been shown to be a potent antioxidant which confers neuroprotection against oxidative damage. However, the role of CO as a neurotransmitter remains controversial because H02 has not been shown to be activated by a signal transduction pathway. The specific aims of this project are as follows: 1) We will determine the functional effects of various protein kinases on the enzymatic activity of H02 and determine the molecular mechanisms by which H02 is activated in vivo by signal transduction pathways.
Due to properties of HO-1 and its products, it is believed that HO-1 may play an important role in protecting cells and tissues in the settings of increased oxidative stress, such as during endotoxemia. Studies from our laboratory using HO-1 null (-/-) mice confirmed this hypothesis by showing that endotoxemia produced increased oxidative stress, end-organ damage, and death in mice lacking HO-1 compared with wild-type mice. This detrimental outcome did not correlate with the blood pressure response, as HO-1-/- mice had a significantly higher systolic blood pressure in the setting of increased mortality.
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