By Raymond S. Lance, H. Barton Grossman (auth.), Anthony Atala, Debra Slade (eds.)
In 1996, the nationwide Bladder origin (NBF) used to be based via a devoted workforce of physicians and researchers propeIled via the pressing have to locate higher remedies for bladder sickness. devoted to expanding bladder ailment learn and to assisting its study group, the NBF coordinates and sponsors the foreign Bladder Symposium (IBS) in Washington, DC. Now thought of to be a optimal medical meeting, the IBS brings jointly foreign leaders in bladder illness examine to provide and speak about their findings. it's the in simple terms overseas convention the place all parts of bladder sickness examine are solely lined and the place bladder ailment researchers are supplied with a different chance to proportion their effects and theories. IBS individuals contributed the learn papers incorporated during this e-book in 2000 and 2001. AIl immense components of bladder illness examine are addressed, together with oncology and ceIlular biology, neurophysiology, neurogenic bladder and incontinence, immunology, irritation and an infection, muscle, matrix and obstruction, and new frontiers and remedies of the bladder. Assembled in a single book, those papers and their findings show the excessive clinical quality of the devoted researchers during this box and the possibility of major discoveries in remedies within the subsequent decade.
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Additional info for Bladder Disease, Part A: Research Concepts and Clinical Applications
24. 31 Bradford MM: A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem, 72:248, 1976. Damell Jr lE, Kerr 1M, Stark GR: Jak-ST AT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins. Science, 264: 1415, 1994. Deiss LP, Feinstein E, Berissi H, Cohen 0, Kimchi A: Identification of a novel serine/threonine kinase and a novel 15-kd protein as potential mediators of the ginterferon-induced cell death.
Both STATl and ST AT2 levels were low in 5637 cells compared to the other 2 TCCs (Fig. 5B). These results indicate that Tyk-2 was expressed at a very low level in the HTlI97 cell line and that levels of STATl and (A) Jakl - - (8) 5637 HT SUP U4A HT 5637 TAT! S P UIA HT 5637 - UP 2fT -- 3A U6A 5637 S P HT 2fT Tyk2 STAT2 - Figure 5. Low levels ofSTATl. STAT2, and Tyk-2 expressions in TCCs. Equal amounts of protein from TCCSUP (SUP), HTJ197 (HT), and 5637 cellular extracts were subjected to Western blot analysis with A: Jakl and Tyk-2 antibodies and B: STAT] and STAT2 antibodies.
The p48 protein is known to be upregulated by IFN-y treatment, so if the defect is in the regulatory region within this gene, or mutations are present in the coding region so that the functional protein is not expressed, then treatment with IFN-y will not induce the functional protein However, treatment of 5637 cells with IFN-y resulted in an increased and easily detectable level in p48 expression. Therefore, in 5637 cells, the p48 protein is not expressing but is inducible by IFN-y treatment. Results indicate that lack of ISGF3 formation is due to undetectable levels of p48 protein in 5637 cells and that p48 is inducible by IFN-y treatment.
Bladder Disease, Part A: Research Concepts and Clinical Applications by Raymond S. Lance, H. Barton Grossman (auth.), Anthony Atala, Debra Slade (eds.)