Pub Date : 1997-09-01DOI: 10.1016/S0197-1859(00)80017-5
D.V.M., Ph.D. Rustin M. Moore (Diplomate American College of Veterinary Surgeons), D.V.M., M.S. Thomas L. Seaborn (Diplomate American College of Veterinary Internal Medicine)
Nitric oxide is a simple molecule that exerts complex physiologic and pathophysiologic effects in mammalian biologic systems. The biosynthesis of NO is controlled by the availability of the substrate and enzyme, L-arginine and NOS, respectively. Nitric oxide derived from cNOS is principally involved in cytoprotective functions including vasodilatation, inhibition of platelet aggregation and adhesion, inhibition of neutrophil adhesion and emigration, and non vascular smooth muscle relaxation. On the other hand, iNOS-derived NO is involved with cytoxicity via the synthesis of peroxynitrite through the reaction of NO with superoxide. The cNOS-derived NO exerts a predominanty anti-inflammatory effect during acute gastrointestinal tract inflammation such as intestinal I-R injury, whereas iNOS-derived NO serves principally as a pro-inflammatory agent during chronic gastrointestinal tract inflamamtion such as IBD. Administration of NO donors during early stages and selective iNOS inhibitors during later stages of of gastrointestinal inflammation appear to have therapeutic potential.
{"title":"Cytoprotective vs. Cytotoxic effects of nitric oxide in ischemic and inflammatory bowel disease","authors":"D.V.M., Ph.D. Rustin M. Moore (Diplomate American College of Veterinary Surgeons), D.V.M., M.S. Thomas L. Seaborn (Diplomate American College of Veterinary Internal Medicine)","doi":"10.1016/S0197-1859(00)80017-5","DOIUrl":"10.1016/S0197-1859(00)80017-5","url":null,"abstract":"<div><p>Nitric oxide is a simple molecule that exerts complex physiologic and pathophysiologic effects in mammalian biologic systems. The biosynthesis of NO is controlled by the availability of the substrate and enzyme, L-arginine and NOS, respectively. Nitric oxide derived from cNOS is principally involved in cytoprotective functions including vasodilatation, inhibition of platelet aggregation and adhesion, inhibition of neutrophil adhesion and emigration, and non vascular smooth muscle relaxation. On the other hand, iNOS-derived NO is involved with cytoxicity via the synthesis of peroxynitrite through the reaction of NO with superoxide. The cNOS-derived NO exerts a predominanty anti-inflammatory effect during acute gastrointestinal tract inflammation such as intestinal I-R injury, whereas iNOS-derived NO serves principally as a pro-inflammatory agent during chronic gastrointestinal tract inflamamtion such as IBD. Administration of NO donors during early stages and selective iNOS inhibitors during later stages of of gastrointestinal inflammation appear to have therapeutic potential.</p></div>","PeriodicalId":100270,"journal":{"name":"Clinical Immunology Newsletter","volume":"17 9","pages":"Pages 125, 131-139"},"PeriodicalIF":0.0,"publicationDate":"1997-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0197-1859(00)80017-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85181333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1997-09-01DOI: 10.1016/S0197-1859(00)80016-3
M.D., Ph.D. John C. Reed
Chronic lymphocytic leukemia (CLL) represents a quintessential example of a human malignancy which is caused principally by defects that prevent cell turnover due to programmed cell death rather than by alterations in cell cycle regulation. In the vast majority of patients, CLL cells are predominantly G0 quiescent lymphocytes that gradually accumulate in the patient's body not because they are dividing more rapidly than normal, but because they are surviving too long. Investigations of the genetics of CLL therefore seem likely to teach us much about the molecular mechanisms that regulate programmed cell death (PCD). Moreover, since defects in the pathway for PCD can render neoplastic cells resistant to the cytotoxic effects of chemotherapeutic drugs and radiation, investigations of the aberrant regulation of cell death in CLL may also prove informative for gaining a better understanding of drug- and radiation-resistance mechanisms. In this review, I summarize current knowledge about the cytogenetic abnormalities associated with CLL and the role of deregulated cell death in the pathogenesis of this most common of the adult leukemias.
{"title":"Chronic lymphocytic leukemia: A disease of dysregulated programmed cell death","authors":"M.D., Ph.D. John C. Reed","doi":"10.1016/S0197-1859(00)80016-3","DOIUrl":"10.1016/S0197-1859(00)80016-3","url":null,"abstract":"<div><p>Chronic lymphocytic leukemia (CLL) represents a quintessential example of a human malignancy which is caused principally by defects that prevent cell turnover due to programmed cell death rather than by alterations in cell cycle regulation. In the vast majority of patients, CLL cells are predominantly G<sub>0</sub> quiescent lymphocytes that gradually accumulate in the patient's body not because they are dividing more rapidly than normal, but because they are surviving too long. Investigations of the genetics of CLL therefore seem likely to teach us much about the molecular mechanisms that regulate programmed cell death (PCD). Moreover, since defects in the pathway for PCD can render neoplastic cells resistant to the cytotoxic effects of chemotherapeutic drugs and radiation, investigations of the aberrant regulation of cell death in CLL may also prove informative for gaining a better understanding of drug- and radiation-resistance mechanisms. In this review, I summarize current knowledge about the cytogenetic abnormalities associated with CLL and the role of deregulated cell death in the pathogenesis of this most common of the adult leukemias.</p></div>","PeriodicalId":100270,"journal":{"name":"Clinical Immunology Newsletter","volume":"17 9","pages":"Pages 125-130"},"PeriodicalIF":0.0,"publicationDate":"1997-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0197-1859(00)80016-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75666695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1997-08-01DOI: 10.1016/S0197-1859(00)80015-1
D.V.M, M.S. Thomas L. Seahorn, D.V.M., Ph.D. Rustin M. Moore
{"title":"Nitric oxide as a pulmonary inflammatory mediator","authors":"D.V.M, M.S. Thomas L. Seahorn, D.V.M., Ph.D. Rustin M. Moore","doi":"10.1016/S0197-1859(00)80015-1","DOIUrl":"10.1016/S0197-1859(00)80015-1","url":null,"abstract":"","PeriodicalId":100270,"journal":{"name":"Clinical Immunology Newsletter","volume":"17 8","pages":"Pages 118-122"},"PeriodicalIF":0.0,"publicationDate":"1997-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0197-1859(00)80015-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84312060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1997-07-01DOI: 10.1016/S0197-1859(97)80319-6
Susan E. Sparks , Donna King
{"title":"Bone marrow and the GH/IGF-I Axis: Bone remodeling and immune function","authors":"Susan E. Sparks , Donna King","doi":"10.1016/S0197-1859(97)80319-6","DOIUrl":"10.1016/S0197-1859(97)80319-6","url":null,"abstract":"","PeriodicalId":100270,"journal":{"name":"Clinical Immunology Newsletter","volume":"17 7","pages":"Pages 93, 99-102"},"PeriodicalIF":0.0,"publicationDate":"1997-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0197-1859(97)80319-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77428975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1997-07-01DOI: 10.1016/S0197-1859(97)80320-2
Chong-kil Lee , Kyungjae Kim , Kathrin Muegge , Scott K. Durum
{"title":"Thymocytes Expressing Both αβ and γδ TCRs: Implications for Models of Lineage Commitment","authors":"Chong-kil Lee , Kyungjae Kim , Kathrin Muegge , Scott K. Durum","doi":"10.1016/S0197-1859(97)80320-2","DOIUrl":"10.1016/S0197-1859(97)80320-2","url":null,"abstract":"","PeriodicalId":100270,"journal":{"name":"Clinical Immunology Newsletter","volume":"17 7","pages":"Pages 102-107"},"PeriodicalIF":0.0,"publicationDate":"1997-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0197-1859(97)80320-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79796418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}