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The Global ETD Search service is a free service for researchers
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Showing 1 to 6 of 6 (0.08 seconds)Spelling suggestions: "subject:"enzyme inhibitors -- atherapeutic used"" "subject:"enzyme inhibitors -- btherapeutic used""
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Angiotensin converting enzyme inhibitor alone or in combination with angiotensin II type I receptor blocker in patients with chronicproteinuric nephropathies: a systemic reviewof clinical trialsHo, Kwun-wai., 何冠威. January 2005 (has links)
published_or_final_version / Medical Sciences / Master / Master of Medical Sciences
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Relationships among resident, physician, and facility characteristics, angiotensin-converting enzyme inhibitor use, and hospital utilization in elderly nursing home residents with heart failureChou, Jennie Yu 28 August 2008 (has links)
Not available / text
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Rat angiotensin-converting enzyme : tissue specific expression during pharmacological inhibitionBrice, Edmund Andrew William January 1995 (has links)
The renin-angiotensin system plays a central role in the maintenance of blood pressure. Angiotensin II, the main effector of this system, results from the action of angiotensin-converting enzyme (ACE) on angiotensin I. Angiotensin II, maintains vasomotor tone via its vasoconstrictor action, and also increases salt and water retention by stimulating the release of aldosterone. ACE inhibitors, such as captopril, enalapril and lisinopril, are highly effective in the treatment of hypertension and congestive cardiac failure. Previous studies have suggested that angiotensin converting enzyme (ACE) production may be enhanced during pharmacological inhibition of the enzyme. Little is known, however about the mechanism of this induction. After demonstrating increases in circulating ACE protein in cardiac failure patients receiving the ACE inhibitor captopril, a rat model was used to study this effect. A sensitive enzyme linked immunosorbent assay for rat ACE was developed and a partial cDNA for rat ACE cloned to enable examination of ACE mRNA and protein expression during enzyme inhibition with enalapril. Rat lung ACE mRNA increased by 156% (p<0.05) and ACE protein doubled within 3 hours of administering a single dose of enalapril. Testicular ACE mRNA also increased by 300% (p<0.05) within 2 hours and returned to pretreatment levels by 6 hours. The angiotensin II antagonist saralasin similarly caused a significant (p<0.0001) 800% enhancement of mRNA expression. Aldosterone pretreatment of rats prior to enalapril administration was found to abolish this mRNA induction. These findings indicate that increased ACE expression during inhibition results from reduced levels of angiotensin II with consequent reduced stimulation of the angiotensin 11 receptor and its effects, such as aldosterone release. This suggests that ACE levels are regulated by a negative feedback loop involving the distal components of the renin-angiotensin system, namely angiotensin II and aldosterone. In situ hybridisation and immunohistochemical techniques were employed to localise the site of this inductive response in rat tissue sections. It was found that lung macrophages were markedly induced to produce ACE, as was ACE in seminiferous tubules. ACE induction was also noted in the expected sites of renal tubular epithelium and glomerular tissue. Interestingly, ACE expression was also enhanced in cardiac valves. In these studies it has been conclusively demonstrated that new ACE expression is induced by enzyme inhibitor therapy. A variety of techniques have been developed that will allow futher study of ACE in rat tissues.
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Discovery of novel regulators of aldehyde dehydrogenase isoenzymesIvanova, Yvelina Tsvetanova 30 May 2011 (has links)
Indiana University-Purdue University Indianapolis (IUPUI) / Recent work has shown that specific ALDH isoenzymes can contribute to the underlying pathology of different diseases. Many ALDH isozymes are important in oxidizing reactive aldehydes resulting from lipid peroxidation, and, thus, help maintain cellular homeostasis. Increased expression and activity of ALDH isozymes are found in many human cancers and are often associated with poor prognosis. Therefore, the development of inhibitors of the different ALDH enzymes is of interest as means to treat some of these disease states. Here I describe the results of assays designed to characterize the site of interaction and the mode of inhibition for the unique compounds that function as inhibitors of aldehyde dehydrogenase 2 and determine their respective IC50 values with intent to develop structure-activity relationships for future development.
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Small molecule compounds targeting DNA binding domain of STAT3 for inhibition of tumor growth and metastasisHuang, Wei January 2014 (has links)
Indiana University-Purdue University Indianapolis (IUPUI) / Signal transducer and activator of transcription 3 (STAT3) is constitutively activated in malignant tumors, and its activation is associated with high histological grade and advanced cancer stage. STAT3 has been shown to play important roles in multiple aspects of cancer aggressiveness including proliferation, survival, self-renewal, migration, invasion, angiogenesis and immune response by regulating the expression of diverse downstream target genes. Thus, inhibiting STAT3 promises to be an attractive strategy for treatment of advanced tumors with metastatic potential. We firstly identified a STAT3 inhibitor, inS3-54, by targeting the DNA-binding site of STAT3 using an in-silico screening approach; however, inS3-54 was finally found not to be appropriate for further studies because of low specificity on STAT3 and poor absorption in mice. To develop an effective and specific STAT3 inhibitor, we identified 89 analogues for the structure-activity relationship analysis. By using hematopoietic progenitor cells isolated from wild-type and STAT3 conditional knockout mice, further studies showed that three analogues (A18, A26 and A69) only inhibited STAT3-dependent colony formation of hematopoietic progenitor cells, indicating a higher selectivity for STAT3 than their parental compound, inS3-54. These compounds were found to (1) inhibit STAT3-specific DNA binding activity; (2) bind to STAT3 protein; (3) suppress proliferation of cancer cells harboring aberrant STAT3 signaling; (4) inhibit migration and invasion of cancer cells and (5) inhibit STAT3-dependent expression of downstream targets by blocking the binding of STAT3 to the promoter regions of responsive genes in cells. In addition, A18 can reduce tumor growth in a mouse xenograft model of lung cancer with little effect on body weight. Taken together, we conclude that it is feasible to inhibit STAT3 by targeting its DNA-binding domain for discovery of anticancer therapeutics.
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Chemoprevention for Colorectal CancerKrishnan, K, Ruffin, M T., Brenner, D E. 01 March 2000 (has links)
No description available.
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