{"title":"Plasma coagulation proteases, proteolytic inhibitors, and their interaction with platelets.","authors":"A K Rao, A H Schmaier, R W Colman","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76307,"journal":{"name":"Pathobiology annual","volume":"12 ","pages":"35-64"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17251646","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}
{"title":"Natural killer cells and naturally occurring antibodies as representatives of natural tumor immunity.","authors":"R Ehrlich, I P Witz","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76307,"journal":{"name":"Pathobiology annual","volume":"12 ","pages":"85-113"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17251647","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}
{"title":"The pathobiology of lymphocyte transformation.","authors":"C R Taylor","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76307,"journal":{"name":"Pathobiology annual","volume":"12 ","pages":"65-84"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17814938","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}
{"title":"Biology of cardiac overload.","authors":"B. Swynghedauw, C. Delcayre","doi":"10.1093/eurheartj/17.suppl_2.3","DOIUrl":"https://doi.org/10.1093/eurheartj/17.suppl_2.3","url":null,"abstract":"Mechanical overload in the heart induces two different types of adaptational mechanisms. (a) From a qualitative point of view, the maximum speed of shortening is depressed in relation to a myosin isoenzymic change responsible for decreased ATPase and, although the relaxation appears normal from a physiological point of view, the existence of an abnormality in Ca2+ uptake in the sarcoplasmic reticulum has been well documented. Both of these processes appear to improve efficiency by decreasing the heat produced per gram of tension. The existence of a large broadening of the action potential has now been well established, but it remains unexplained at the biochemical level. The functioning of mitochondria is rather controversial, and although it has been shown that they are both more abundant and smaller, the reason why their respiratory index changes remains unknown. (b) From a quantitative point of view, the adult heart adapts to overload by increasing its mass. This is mainly a consequence of a hypertrophy of the myocytes and a mitotic multiplication of nonmuscular cells. Data suggest that myocyte amitotic divisions may occur, at least in humans, and perhaps in very sizeable experimental hypertrophy. To this phenomenon has been added the development of polyploidy of myocyte nuclei, which seems to be specific to certain species. The stimulation of protein synthesis occurs very soon after pressure overload, and is delayed in volume overload; protein lysis also increases, although this is controversial. The process occurs whatever the proteins. This is accompanied by increased nuclear activity and a stimulation in RNA synthesis, which is especially precocious for messenger RNA. Among the very early events which could be potential signals for protein synthesis, attention has been focused on polyamine, RNA polymerase, and uridine kinase. The trigger mechanism, of course remains hypothetical. As a trigger for protein synthesis, several data suggest an increase in wall stress and stretch; a drop in efficiency is suggested as a trigger for qualitative changes.","PeriodicalId":76307,"journal":{"name":"Pathobiology annual","volume":"12 1","pages":"137-83"},"PeriodicalIF":0.0,"publicationDate":"1982-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/eurheartj/17.suppl_2.3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"60877850","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}
{"title":"Parathyroid hormone: chemistry and structure-activity relations.","authors":"M Rosenblatt","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Peptide synthesis and the application of a wide range of biological assays have permitted intensive and detailed study of structure-activity relations for parathyroid hormone. Within the structure of the hormone molecule reside largely distinct domains critical for receptor binding or activation of adenylate cyclase in addition to receptor binding. Subtle modifications of hormonal structure can cause striking changes in hormone potency or in the nature of the biological properties displayed by such analogs. For parathyroid hormone, structure-activity studies have identified several discrete regions of the molecule that are responsible for independent biological functions. It was determined that these separate functions are displayed in an almost linear fashion along the primary sequence of the hormone--a conceptual framework that has greatly facilitated synthesis of parathyroid hormone analogs. The amino-terminal region of the initially biosynthesized precursor form of parathyroid hormone, pre-proparathyroid hormone, - 31 through - 7, contains a leader or signal sequence. Despite differences in sequence of the parathyroid hormone signal region and other precursor-specific sequences, this region of the molecule possesses biological properties related to intracellular transport and metabolism that appear to be universal for precursor forms of many, if not all, peptide hormones and other secreted proteins. In contrast, the amino-terminal portion of the secreted form of the molecule, sequence region 1-34, has an amino acid sequence that is homologous to that of several peptide hormones, including ACTH, alpha-MSH, beta-MSH, and beta-lipotropin. Yet the biological \"message\" conveyed by this peptide sequence appears unique to parathyroid hormone. Directions have now been established for the design of hormone inhibitors and for analogs of enhanced biological activity and perhaps even analogs possessing an altered spectrum of biological properties. The rapid advances that are occurring in techniques for peptide synthesis, purification, and analysis; in the variety, sensitivity, and specificity of the increasing number of bioassays; and in the elucidation of peptide and protein conformation may provide further important new directions for analog design. Extension of these investigations of structure and function over the next several years should yield a more sophisticated understanding of the mode of hormone action. In such studies lies the promise of generating highly refined and perhaps clinically useful analogs of parathyroid hormone.</p>","PeriodicalId":76307,"journal":{"name":"Pathobiology annual","volume":"11 ","pages":"53-86"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17339233","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}
{"title":"Tamm-Horsfall uromucoprotein and the pathogenesis of casts, reflux nephropathy, and nephritides.","authors":"R E Wenk, B S Bhagavan, J Rudert","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This chapter is an attempt to organize and summarize a diverse literature concerning Tamm-Horsfall uromucoprotein. Importance of examination of urine sediment for casts and diagnostic classification of casts have been discussed. Despite a lack of understanding of its biologic function, clinicopathologic study of T-HM has implicated it as a component of a variety of disease states. It binds a number of proteins, including those on surfaces of bacteria and viruses. It inactivates enzymes of those organisms, possibly by reacting with ionic cofactors, such as divalent metals. Ionic binding of monovalent cations (e.g., Na+) and repulsion of anions, such as Cl-, suggest a role for T-HM in renal salt and water balance. The combination of T-HM with ions, including H+, and other materials that enhance gel formation may indicate an ion-exchange function. Gel (cast) formation in the lower nephron, however, may produce obstruction, which, following calcification, infection, or inflammation, could go on to produce stones, increase scarring, and augment reflux nephropathy. Pathogenetic roles in autoimmunity and disorders of mucus metabolism have also been speculated on.</p>","PeriodicalId":76307,"journal":{"name":"Pathobiology annual","volume":"11 ","pages":"229-57"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17239102","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}
{"title":"Complement mediated inflammatory reactions.","authors":"S L Kunkel, J C Fantone, P A Ward","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76307,"journal":{"name":"Pathobiology annual","volume":"11 ","pages":"127-54"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17239234","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}