Proceedings of the Association of American Physicians最新文献_第2页

Predictors and outcomes of cardiac complications following elective coronary bypass grafting. 择期冠状动脉旁路移植术后心脏并发症的预测因素和结果。

Proceedings of the Association of American Physicians Pub Date : 1999-11-01 DOI: 10.1046/j.1525-1381.1999.99130.x

M Charlson, K H Krieger, J C Peterson, J Hayes, O W Isom

{"title":"Predictors and outcomes of cardiac complications following elective coronary bypass grafting.","authors":"M Charlson, K H Krieger, J C Peterson, J Hayes, O W Isom","doi":"10.1046/j.1525-1381.1999.99130.x","DOIUrl":"https://doi.org/10.1046/j.1525-1381.1999.99130.x","url":null,"abstract":"Our objective was to determine the predictors of cardiac complications among a cohort of elective coronary artery bypass graft (CABG) surgery patients and to determine the relationship of such complications to subsequent quality of life and symptoms. A total of 248 patients were enrolled and 237 completed 6 month follow-up. The combined rate of both major and minor cardiac complications was 9.7% (n = 24). Patients in this study were evaluated preoperatively, monitored intraoperatively, followed immediately postoperatively and at 6 months. Major cardiac complications accounted for 3.6% (n = 9) and minor complications for 6% (n = 15). Using multivariable logistic regression analysis, the predictors of major cardiac complications were receiving diuretics preoperatively (p = .01) and increased time during cross-clamping (p = .006). At 6 months after surgery, 19% of the patients with postoperative cardiac complications experienced worsening of symptoms, in contrast to only 8% of those without cardiac complications (p = .03). We concluded that patients who were on preoperative diuretics and those who had longer cross-clamp times were at higher risk of cardiac complications. The majority of patients who had acute cardiac complications had improved function and symptoms at 6 months postoperatively.","PeriodicalId":20612,"journal":{"name":"Proceedings of the Association of American Physicians","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21448989","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}

引用次数: 14

Physiology and pathophysiology of nitric oxide in chronic renal disease. 慢性肾脏疾病中一氧化氮的生理和病理生理。

Proceedings of the Association of American Physicians Pub Date : 1999-11-01 DOI: 10.1046/j.1525-1381.1999.99256.x

M Noris, G Remuzzi

{"title":"Physiology and pathophysiology of nitric oxide in chronic renal disease.","authors":"M Noris, G Remuzzi","doi":"10.1046/j.1525-1381.1999.99256.x","DOIUrl":"https://doi.org/10.1046/j.1525-1381.1999.99256.x","url":null,"abstract":"Nitric oxide (NO), an L-arginine derivative, exerts a variety of renal and extrarenal physiological and pathophysiological effects. NO is generated by three isoforms of nitric oxide synthases (NOS): two acutely responsive, constitutive isoforms, neuronal NOS (nNOS) and endothelial NOS (ecNOS), and the slower, more persistent, inducible NOS (iNOS). NO regulates glomerular ultrafiltration; tubular reabsorption, and intrarenal renin secretion. A number of recent studies, most of them in the experimental model of renal mass reduction (RMR) in rats, have raised the hypothesis that an impaired NO synthetic pathway could have a key role in mediating the complex renal hemodynamic and nonhemodynamic disorders associated with the progression of renal disease. Thus, kidneys from rats with RMR produce less NO than normal rats, and NO generation negatively correlates with markers of renal damage. The abnormality is due to a defect in iNOS in the kidney. Data are also available showing that drugs capable of enhancing renal NO activity may be renoprotective in a variety of experimental renal diseases, particularly those characterized by derangements of glomerular hemodynamics. Fewer studies are available in humans and these have shown less than conclusive results.","PeriodicalId":20612,"journal":{"name":"Proceedings of the Association of American Physicians","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21448990","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}

引用次数: 46

Human retroviruses: their role in cancer. 人类逆转录病毒:它们在癌症中的作用

Proceedings of the Association of American Physicians Pub Date : 1999-11-01 DOI: 10.1046/j.1525-1381.1999.99210.x

W A Blattner

{"title":"Human retroviruses: their role in cancer.","authors":"W A Blattner","doi":"10.1046/j.1525-1381.1999.99210.x","DOIUrl":"https://doi.org/10.1046/j.1525-1381.1999.99210.x","url":null,"abstract":"Viruses are etiologically linked to approximately 20% of all malignancies worldwide. Retroviruses account for approximately 8%-10% of the total. For human T-cell leukemia virus 1 (HTLV-I), the viral regulatory tax gene product is responsible for enhanced transcription of viral and cellular genes that promote cell growth by stimulating various growth factors and through dysregulation of cellular regulatory suppressor genes, such as p53. After a long latent period, adult T-cell leukemia/lymphoma (ATL) occurs in 1 per 1000 carriers per year, resulting in 2500-3000 cases per year worldwide and over half of the adult lymphoid malignancies in endemic areas. Human immunodeficiency virus 1 (HIV-1) accounts for a significant cancer burden, and its transactivating regulatory protein Tat enhances direct and indirect cytokine and immunological dysregulation to cause diverse cancers. Kaposi's sarcoma (KS) is a very rare tumor except after HIV-1 infection, when its incidence is greatly amplified reaching seventy thousand-fold in HIV-infected homosexual men. Human herpesvirus 8 (HHV-8), which is also known as Kaposi's sarcoma-associated virus (KSHV), is a necessary but not sufficient etiological factor in KS. The dramatic decline of KS since the introduction of highly active antiretroviral therapy (HAART) could be due to suppression of HIV-1 tat. B-cell non-Hodgkin's lymphoma occurs as their first acquired immunodeficiency syndrome-defining diagnosis in 3%-4% of HIV-infected patients. Hodgkin's lymphoma is also associated with HIV infection but at a lower risk. Human papillomaviruses are linked to invasive cervical cancer and anogenital cancers among HIV-infected patients. Human retroviruses cause malignancy via direct effects as well as through interactions with other oncogenic herpesviruses and other viruses.","PeriodicalId":20612,"journal":{"name":"Proceedings of the Association of American Physicians","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21449062","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}

引用次数: 76

Heme oxygenase: recent advances in understanding its regulation and role. 血红素加氧酶的调控及其作用的研究进展。

Proceedings of the Association of American Physicians Pub Date : 1999-09-01

K K Elbirt, H L Bonkovsky

{"title":"Heme oxygenase: recent advances in understanding its regulation and role.","authors":"K K Elbirt, H L Bonkovsky","doi":"","DOIUrl":"","url":null,"abstract":"Heme oxygenase (HO) is responsible for the physiological breakdown of heme into equimolar amounts of biliverdin, carbon monoxide, and iron. Three isoforms (HO-1, HO-2, and HO-3) have been identified. HO-1 is ubiquitous and its mRNA and activity can be increased several-fold by heme, other metalloporphyrins, transition metals, and stimuli that induce cellular stress. HO-1 is recognized as a major heat shock/stress response protein. Recent work from our laboratory has demonstrated several potential consensus regulatory elements in the 5'-untranslated region (UTR) of HO-1, including activator protein 1 (AP-1), metal responsive element (MRE), oncogene c-myc/max heterodimer binding site (Myc/Max), antioxidant response element (ARE), and GC box binding (Sp1) sites. Using deletion-reporter gene constructs, we have mapped sites that mediate the arsenite-dependent induction of HO-1, and we have shown that components of the extracellular signal-regulated kinase (ERK) and p38 (a homologue of the yeast HOG1 kinase), but not c-jun N-terminal kinase (JNK), mitogen-activated protein (MAP) kinase pathways are involved in arsenite-dependent upregulation. In contrast, HO-2 is present chiefly in the brain and testes and is virtually uninducible. HO-3 has very low activity; its physiological function probably involves heme binding. Products of the HO reaction have important effects: carbon monoxide is a potent vasodilator, which is thought to play a key role in the modulation of vascular tone, especially in the liver under physiological conditions, and in many organs under \"stressful\" conditions associated with HO-1 induction. Biliverdin and its product bilirubin, formed in most mammals, are potent antioxidants. In contrast, \"free\" iron increases oxidative stress and regulates the expression of many mRNAs (e.g., DCT-1, ferritin, and transferrin receptor) by affecting the conformation of iron regulatory protein (IRP)-1 and its binding to iron regulatory elements (IREs) in the 5'- or 3'-UTRs of the mRNAs.","PeriodicalId":20612,"journal":{"name":"Proceedings of the Association of American Physicians","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21380740","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}

引用次数: 0

Presentation of the Kober Medal for 1999 to Jean D. Wilson physician-scientist exemplar. 1999年颁发Kober奖章给Jean D. Wilson医生-科学家典范。

Proceedings of the Association of American Physicians Pub Date : 1999-09-01 DOI: 10.1111/paa.1999.111.5.469

J L Goldstein, M S Brown

引用次数: 0

Heme oxygenase: recent advances in understanding its regulation and role. 血红素加氧酶的调控及其作用的研究进展。

Proceedings of the Association of American Physicians Pub Date : 1999-09-01 DOI: 10.1111/PAA.1999.111.5.438

K. Elbirt, H. Bonkovsky

{"title":"Heme oxygenase: recent advances in understanding its regulation and role.","authors":"K. Elbirt, H. Bonkovsky","doi":"10.1111/PAA.1999.111.5.438","DOIUrl":"https://doi.org/10.1111/PAA.1999.111.5.438","url":null,"abstract":"Heme oxygenase (HO) is responsible for the physiological breakdown of heme into equimolar amounts of biliverdin, carbon monoxide, and iron. Three isoforms (HO-1, HO-2, and HO-3) have been identified. HO-1 is ubiquitous and its mRNA and activity can be increased several-fold by heme, other metalloporphyrins, transition metals, and stimuli that induce cellular stress. HO-1 is recognized as a major heat shock/stress response protein. Recent work from our laboratory has demonstrated several potential consensus regulatory elements in the 5'-untranslated region (UTR) of HO-1, including activator protein 1 (AP-1), metal responsive element (MRE), oncogene c-myc/max heterodimer binding site (Myc/Max), antioxidant response element (ARE), and GC box binding (Sp1) sites. Using deletion-reporter gene constructs, we have mapped sites that mediate the arsenite-dependent induction of HO-1, and we have shown that components of the extracellular signal-regulated kinase (ERK) and p38 (a homologue of the yeast HOG1 kinase), but not c-jun N-terminal kinase (JNK), mitogen-activated protein (MAP) kinase pathways are involved in arsenite-dependent upregulation. In contrast, HO-2 is present chiefly in the brain and testes and is virtually uninducible. HO-3 has very low activity; its physiological function probably involves heme binding. Products of the HO reaction have important effects: carbon monoxide is a potent vasodilator, which is thought to play a key role in the modulation of vascular tone, especially in the liver under physiological conditions, and in many organs under \"stressful\" conditions associated with HO-1 induction. Biliverdin and its product bilirubin, formed in most mammals, are potent antioxidants. In contrast, \"free\" iron increases oxidative stress and regulates the expression of many mRNAs (e.g., DCT-1, ferritin, and transferrin receptor) by affecting the conformation of iron regulatory protein (IRP)-1 and its binding to iron regulatory elements (IREs) in the 5'- or 3'-UTRs of the mRNAs.","PeriodicalId":20612,"journal":{"name":"Proceedings of the Association of American Physicians","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77856225","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}

引用次数: 296

Thematic review series. IX: New therapeutic targets for the treatment of heart failure. Introduction. 专题评论系列。九:治疗心力衰竭的新靶点。介绍。

Proceedings of the Association of American Physicians Pub Date : 1999-09-01 DOI: 10.1111/paa.1999.111.5.396

J Ross

引用次数: 0

Voltage-gated T-type Ca2+ channels and heart failure. 电压门控t型Ca2+通道与心力衰竭。

Proceedings of the Association of American Physicians Pub Date : 1999-09-01 DOI: 10.1111/paa.1999.111.5.429

J P Clozel, E A Ertel, S I Ertel

{"title":"Voltage-gated T-type Ca2+ channels and heart failure.","authors":"J P Clozel, E A Ertel, S I Ertel","doi":"10.1111/paa.1999.111.5.429","DOIUrl":"https://doi.org/10.1111/paa.1999.111.5.429","url":null,"abstract":"In the cardiovascular system, two types of voltage-gated Ca2+ channels are present: the L-type and the T-type. Under normal conditions, T-type Ca2+ channels are involved in the maintenance of vascular tone and cardiac automaticity but, since they are not present in contractile myocardial cells, they do not contribute significantly to myocardial contraction. In experimental models of cardiac hypertrophy, myocardial T-type Ca2+ channels are upregulated, which could contribute to the increased incidence of ventricular arrhythmia. In addition, T-type Ca2+ channels participate in the regulation of cell proliferation and neurohormonal secretion; through these pathways, T-type Ca2+ channels might participate in myocardial remodeling. The pathophysiological role of T-type Ca2+ channels in heart failure has been investigated using mibefradil, a Ca2+ antagonist that is 10-50 times more potent at blocking T-type than L-type Ca2+ channels. In contrast with classic L-type Ca2+ channel antagonists, miberfradil appears beneficial in many animal models of heart failure; in particular, it does not exert negative inotropic effects nor does it stimulate the neurohormonal system. Furthermore, in the Pfeffer rat model, blockade of T-type Ca2+ channels with mibefradil is associated with an improved survival rate. In humans, however, major metabolic drug interactions independent of T-type Ca2+ channel blockade made it impossible to determine the efficacy of mibefradil in treating heart failure; indeed, these interactions led to the withdrawal of the drug from the market.","PeriodicalId":20612,"journal":{"name":"Proceedings of the Association of American Physicians","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/paa.1999.111.5.429","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21380768","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}

引用次数: 43

Myeloperoxidase. 髓过氧物酶。

Proceedings of the Association of American Physicians Pub Date : 1999-09-01 DOI: 10.1111/paa.1999.111.5.383

S J Klebanoff

{"title":"Myeloperoxidase.","authors":"S J Klebanoff","doi":"10.1111/paa.1999.111.5.383","DOIUrl":"https://doi.org/10.1111/paa.1999.111.5.383","url":null,"abstract":"Phagocytes respond to stimulation with a burst of oxygen consumption, and much, if not all, of the extra oxygen consumed in the respiratory burst is converted first to the superoxide anion and then to hydrogen peroxide (H2O2). Myeloperoxidase (MPO), which is released from cytoplasmic granules of neutrophils and monocytes by a degranulation process, reacts with the H2O2 formed by the respiratory burst to form a complex that can oxidize a large variety of substances. Among the latter is chloride, which is oxidized initially to hypochlorous acid, with the subsequent formation of chlorine and chloramines. These products of the MPO-H2O2-chloride system are powerful oxidants that can have profound biological effects. The primary function of neutrophils is the phagocytosis and destruction of microorganisms, and the release of MPO and H2O2 into the phagosome containing the ingested microorganism generally leads to a rapid microbicidal effect. Neutrophils from patients with chronic granulomatous disease (CGD) have a microbicidal defect that is associated with the absence of a respiratory burst and, thus, H2O2 production. Neutrophils from patients with a hereditary MPO deficiency, who lack MPO, also have a microbicidal defect, although it is not as severe as that seen in CGD. MPO and H2O2 also can be released to the outside of the cell where a reaction with chloride can induce damage to adjacent tissue and, thus, contribute to the pathogenesis of disease. It has been suggested that pulmonary injury, renal glomerular damage, and the initiation of atherosclerotic lesions may be caused by the MPO system.","PeriodicalId":20612,"journal":{"name":"Proceedings of the Association of American Physicians","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/paa.1999.111.5.383","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21380762","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}

引用次数: 11

Oxygen-independent microbicidal mechanisms of phagocytes. 吞噬细胞不依赖氧的杀微生物机制。

Proceedings of the Association of American Physicians Pub Date : 1999-09-01 DOI: 10.1111/paa.1999.111.5.390

T Ganz

引用次数: 33