M. Valente, Fiorella Calabrese, G. Thiene, A. Angelini, C. Basso, A. Nava, L. Rossi
{"title":"In vivo evidence of apoptosis in arrhythmogenic right ventricular cardiomyopathy.","authors":"M. Valente, Fiorella Calabrese, G. Thiene, A. Angelini, C. Basso, A. Nava, L. Rossi","doi":"10.1093/eurheartj/17.suppl_5.589","DOIUrl":"https://doi.org/10.1093/eurheartj/17.suppl_5.589","url":null,"abstract":"Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a primary heart muscle disease characterized by progressive atrophy of the right ventricular myocardium with fibro-fatty replacement and the risk of electrical instability and sudden death. The disease is often familial and the aetiopathogenesis is still unknown. Recently apoptosis (genetically determined cell death) was postulated to account for progressive loss of myocardium. To establish whether apoptosis is present in ARVC, right ventricular endomyocardial biopsies from 20 patients with clinical and histological diagnosis of ARVC were examined by electron microscopy and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling method (TUNEL). Apoptotic index was calculated as the percentage of positive nuclei in sections stained by TUNEL. Cell proliferation activity was also assessed by argyrophilic staining of the nucleolar organizer region (AgNOR) and MIB-1 antibody analysis. Twenty biopsies taken from patients during monitoring of cardiac transplantation (grade 0 rejection) served as control. Occurrence of apoptosis was correlated with clinical history duration and the presence of acute symptoms and signs like angina, pyrexia, erythrocyte sedimentation rate and creatine phosphokinase elevation, as well as ST segment elevation on basal electrocardiogram. Electron microscopy and TUNEL revealed presence of apoptotic myocytes in seven cases (35%) with a mean apoptotic index of 24.4+/-9.8. The remaining 13 patients and all of the 20 controls were negative both at the electron microscopy and TUNEL. Presence of apoptosis appeared to be significantly related to clinical history duration of less than 6 months (P < 0.001) and presence of acute symptoms and signs (P = 0.007). AgNOR staining and MIB-1 antibody analysis ruled out cell proliferation activity. In conclusion, apoptosis is present in endomyocardial biopsies of patients with ARVC, especially in the early symptomatic phase of disease. Myocardial destruction with replacement by fat may be episodic rather than gradual and continuous.","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"19 1","pages":"479-84"},"PeriodicalIF":0.0,"publicationDate":"1998-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75308239","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 kidneys of mice with autoimmune disease acquire a hypofibrinolytic/procoagulant state that correlates with the development of glomerulonephritis and tissue microthrombosis.","authors":"Koji Yamamoto, D. Loskutoff","doi":"10.1016/S0268-9499(97)80175-0","DOIUrl":"https://doi.org/10.1016/S0268-9499(97)80175-0","url":null,"abstract":"","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"48 1","pages":"725-34"},"PeriodicalIF":0.0,"publicationDate":"1997-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72867591","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}
C. Werner, H. Döhner, S. Joos, L. Trümper, M. Baudis, T. Barth, G. Ott, P. Möller, P. Lichter, Martin Bentz
{"title":"High-level DNA amplifications are common genetic aberrations in B-cell neoplasms.","authors":"C. Werner, H. Döhner, S. Joos, L. Trümper, M. Baudis, T. Barth, G. Ott, P. Möller, P. Lichter, Martin Bentz","doi":"10.5167/UZH-18928","DOIUrl":"https://doi.org/10.5167/UZH-18928","url":null,"abstract":"Gene amplification is one of the molecular mechanisms resulting in the up-regulation of gene expression. In non-Hodgkin's lymphomas, such gene amplifications have been identified rarely. Using comparative genomic hybridization, a technique that has proven to be very sensitive for the detection of high-level DNA amplifications, we analyzed 108 cases of B-cell neoplasms (42 chronic B-cell leukemias, 5 mantle cell lymphomas, and 61 aggressive B-cell lymphomas). Twenty-four high-level amplifications were identified in 13% of the patients and mapped to 15 different genomic regions. Regions most frequently amplified were bands Xq26-28, 2p23-24, and 2p14-16 as well as 18q21 (three times each). Amplification of several proto-oncogenes and a cell cycle control gene (N-MYC (two cases), BCL2, CCND2, and GLI) located within the amplified regions was demonstrated by Southern blot analysis or fluorescence in situ hybridization to interphase nuclei of tumor cells. These data demonstrate that gene amplifications in B-cell neoplasms are much more frequent than previously assumed. The identification of highly amplified DNA regions and genes included in the amplicons provides important information for further analyses of genetic events involved in lymphomagenesis.","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"179 1","pages":"335-42"},"PeriodicalIF":0.0,"publicationDate":"1997-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76659677","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":"Tumor cell and connective tissue cell interactions in human colorectal adenocarcinoma. Transfer of platelet-derived growth factor-AB/BB to stromal cells.","authors":"C. Sundberg, M. Branting, B. Gerdin, K. Rubin","doi":"10.1007/978-3-540-47648-1_5535","DOIUrl":"https://doi.org/10.1007/978-3-540-47648-1_5535","url":null,"abstract":"","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"216 1","pages":"479-92"},"PeriodicalIF":0.0,"publicationDate":"1997-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77121576","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}
N. Okamoto, T. Tobe, S. Hackett, H. Ozaki, M. A. Vinores, W. L. Rochelle, D. Zack, P. Campochiaro
{"title":"Transgenic mice with increased expression of vascular endothelial growth factor in the retina: a new model of intraretinal and subretinal neovascularization.","authors":"N. Okamoto, T. Tobe, S. Hackett, H. Ozaki, M. A. Vinores, W. L. Rochelle, D. Zack, P. Campochiaro","doi":"10.1097/00006982-199805000-00034","DOIUrl":"https://doi.org/10.1097/00006982-199805000-00034","url":null,"abstract":"Vascular endothelial growth factor (VEGF) has been implicated in retinal neovascularization (NV), but it has been difficult to produce retinal NV with exogenous VEGF. We investigated the effect of increased VEGF expression in the retina using tissue-specific, gain-of-function transgenic mice in which the bovine rhodopsin promoter is coupled to the gene for human VEGF. Three founder mice were obtained and used to generate transgenic lines. One of the lines shows increased expression of VEGF in the retina by reverse transcription coupled to polymerase chain reaction and Northern blots, and the VEGF is localized to photoreceptors by immunohistochemistry. These mice demonstrate new vessels originating from the deep capillary bed of the retina that extend beneath the photoreceptor layer into the subretinal space where they form clumps of blood vessels surrounded by proliferated retinal pigmented epithelial cells. The appearance is similar to subretinal NV seen in some patients, except that the blood vessels originate from the retinal vasculature rather than the choroidal vasculature. One of the other two lines of mice did not show increased expression of VEGF and did not have NV; the other line showed retinal degeneration. This study demonstrates that over-expression of VEGF in the retina is sufficient to cause intraretinal and subretinal NV and provides a valuable new animal model.","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"100 1","pages":"281-91"},"PeriodicalIF":0.0,"publicationDate":"1997-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80648410","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":"Index of Authors","authors":"J. V. D. Veen, Abbams","doi":"10.3109/02699050903466110","DOIUrl":"https://doi.org/10.3109/02699050903466110","url":null,"abstract":"Abreu, B. C., see Temple, R. O. Ada, L., Sherrington, C., Canning, C. G., Dean, C. M. and Scianni, A., Computerized tracking to train dexterity after cerebellar tumour: A single-case experimental study, 702 af Geijerstam, J.-L., see Lannsjö, M. Aguayo, C., see Bonilla, C. Al-Adawi, S., Hoaglin, H., Vesali, F., Dorvlo, A. S. S. and Burke, D. T., Effect of amantadine on the sleep–wake cycle of an inpatient with brain injury, 559 Al-Lawati, Z., see Srinivasan, L. Alexandersen, A., Dalen, K. and Brønnick, K., Prediction of driving ability after inconclusive neuropsychological investigation, 313 Alin, J., see Tenovuo, O. Allouard, Y., see Rousseau, M.-C. Amaro, E., see Nucci-da-Silva, M. P. Amaya-Villar, R., see Muñoz-Sánchez, M. A. Amicuzi, I., see Barca, L. Amiri, S., see Ghotbi, N. Andelic, N., see Sigurdardottir, S. Anderson, M. I., Simpson, G. K., Morey, P. J., Mok, M. M. C., Gosling, T. J. and Gillett, L. E., Differential pathways of psychological distress in spouses vs. parents of people with severe traumatic brain injury (TBI): Multi-group analysis, 931 Andriessen, T. M. J. C., de Jong, B., Jacobs, B., van der Werf, S. P. and Vos, P. E., Sensitivity and specificity of the 3-item memory test in the assessment of post traumatic amnesia, 345 Ansari, N. N., see Ghotbi, N. Ansari, N. N., Naghdi, S., Hasson, S. and Rastgoo, M., Efficacy of therapeutic ultrasound and infrared in the management of muscle spasticity, 632 Aouani, E., see Sebai, H. Apicella, M. G., see Barca, L. Arango-Lasprilla, J. C., see Gary, K. W. Arciniegas, D. B., see Silver, J. M. Ashman, T., see Carlson, N. E. Azouvi, P., see Vallat-Azouvi, C.","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"39 1","pages":"2196 - 2215"},"PeriodicalIF":0.0,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85745404","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}
Maomi Li, Zuo‐Feng Zhang, V. Reuter, C. Cordon-Cardo
{"title":"Chromosome 3 allelic losses and microsatellite alterations in transitional cell carcinoma of the urinary bladder.","authors":"Maomi Li, Zuo‐Feng Zhang, V. Reuter, C. Cordon-Cardo","doi":"10.1007/978-3-319-40618-3_62","DOIUrl":"https://doi.org/10.1007/978-3-319-40618-3_62","url":null,"abstract":"","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"9 1","pages":"229-35"},"PeriodicalIF":0.0,"publicationDate":"1996-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82797896","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}
T. Morimoto, T. Ide, Y. Ihara, A. Tamura, T. Kirino
{"title":"Transient ischemia depletes free ubiquitin in the gerbil hippocampal CA1 neurons.","authors":"T. Morimoto, T. Ide, Y. Ihara, A. Tamura, T. Kirino","doi":"10.1007/978-3-642-60546-8_12","DOIUrl":"https://doi.org/10.1007/978-3-642-60546-8_12","url":null,"abstract":"","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"61 1","pages":"249-57"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77806517","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}
B. Criado, A. Barros, R. Suijkerbuijk, D. Weghuis, R. Seruca, E. Fonseca, S. Castedo
{"title":"Detection of numerical alterations for chromosomes 7 and 12 in benign thyroid lesions by in situ hybridization. Histological implications.","authors":"B. Criado, A. Barros, R. Suijkerbuijk, D. Weghuis, R. Seruca, E. Fonseca, S. Castedo","doi":"10.1016/0165-4608(94)90396-4","DOIUrl":"https://doi.org/10.1016/0165-4608(94)90396-4","url":null,"abstract":"","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"62 1","pages":"136-44"},"PeriodicalIF":0.0,"publicationDate":"1995-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90565993","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":"A case of right ventricular dilated cardiomyopathy.","authors":"E Okada, K Okuda","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This paper presents a sudden death case of 16-year-old girl. She is assumed to have died of ventricular arrhythmia clinically. On autopsy, the right cardiac ventricle was markedly dilated due to extensive infiltration of fibroadipose tissue and resultant depletion of the myocytes, but there was no full thickness disappearance of the contractile element in any part. Considerable parts of remaining myocytes showed degenerative changes similar to those of dilated cardiomyopathy. The left ventricle was moderately dilated. It showed similar significant degenerative changes to the right ventricle, but the degree was less extensive than the right. These findings do not fill the diagnostic requirements of neither Uhl's anomaly nor parchment heart, which reveal almost total depletion of the right ventricular myocytes. However, the findings were consistent with arrhythmogenic right ventricular dysplasia, in case the concept of the entity is extended, we concluded that it would be better to adopt a term--cardiomyopathy--to this case rather than dysplasia. Because, there were considerable histological evidence of myocardial degeneration suggesting primary myocardial disease rather than congenital defect in nature. We diagnosed, therefore, this case as right ventricular dilated cardiomyopathy, comprising a type of dilated cardiomyopathy whose myocardial lesions predominate in the right compared to the left ventricle.</p>","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"5 1","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19805634","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}