The American journal of cardiovascular pathology最新文献

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Osteoprotective Effects of IL-33/ST2 Link to Osteoclast Apoptosis. IL-33/ST2与破骨细胞凋亡相关的骨保护作用
The American journal of cardiovascular pathology Pub Date : 2015-12-01 DOI: 10.1016/j.ajpath.2015.08.013
Izabella L A Lima, S. Macari, M. Madeira, L. F. D. Rodrigues, P. M. Colavite, G. Garlet, F. Soriani, M. Teixeira, S. Fukada, T. Silva
{"title":"Osteoprotective Effects of IL-33/ST2 Link to Osteoclast Apoptosis.","authors":"Izabella L A Lima, S. Macari, M. Madeira, L. F. D. Rodrigues, P. M. Colavite, G. Garlet, F. Soriani, M. Teixeira, S. Fukada, T. Silva","doi":"10.1016/j.ajpath.2015.08.013","DOIUrl":"https://doi.org/10.1016/j.ajpath.2015.08.013","url":null,"abstract":"","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"43 1","pages":"3338-48"},"PeriodicalIF":0.0,"publicationDate":"2015-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89440908","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: 29
Tumors stimulate platelet delivery of angiogenic factors in vivo: an unexpected benefit. 肿瘤刺激血小板输送血管生成因子在体内:一个意想不到的好处。
The American journal of cardiovascular pathology Pub Date : 2008-12-01 DOI: 10.2353/ajpath.2008.080474
G. Pietramaggiori, S. Scherer, D. Cervi, G. Klement, D. Orgill
{"title":"Tumors stimulate platelet delivery of angiogenic factors in vivo: an unexpected benefit.","authors":"G. Pietramaggiori, S. Scherer, D. Cervi, G. Klement, D. Orgill","doi":"10.2353/ajpath.2008.080474","DOIUrl":"https://doi.org/10.2353/ajpath.2008.080474","url":null,"abstract":"The interaction between platelets and the tumor microenvironment results in the modulation of angiogenesis, although the mechanisms governing this regulation remain unclear. This study explores the differences in the communication between wounded tissues and healthy, tumor-conditioned, and frozen platelets. Platelet-rich plasma obtained from healthy (PRP) or tumor-bearing (TPRP) mice was applied to dorsal, full-thickness wounds on diabetic mice. Wound healing was evaluated using macroscopic criteria and a staging system based on angiogenesis and stromal cell proliferation. Proteomic analysis was used to compare the levels of angiogenic proteins contained in the platelet preparations. TPRP-treated wounds reached 90% wound closure 5.6 to 9.5 days earlier than PRP-treated and nontreated wounds, respectively. TPRP induced a fourfold increase in stromal cell proliferation compared with nontreated wounds, and a 2.5-fold increase compared with PRP-treated wounds. TPRP induced the highest stimulation of angiogenesis with a fourfold increase compared with nontreated controls. On day 21, wounds treated with TPRP showed a typical architecture with thick collagen bundles. Although the levels of angiogenesis regulators detected via SELDI-ToF were similar between the PRP and TPRP treatment regimens, the enhanced healing capacity of TPRP suggests improved platelet delivery as indicated by frozen TPRP preparations that had lost most of their pro-angiogenic drive. In conclusion, these results show that intact tumor-conditioned platelets display an improved ability to deliver angiogenesis regulators to wounded tissues.","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"3 1","pages":"1609-16"},"PeriodicalIF":0.0,"publicationDate":"2008-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85442583","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: 44
Cyclophilin A as a novel biphasic mediator of endothelial activation and dysfunction. 亲环蛋白A作为内皮细胞激活和功能障碍的新型双相介质。
The American journal of cardiovascular pathology Pub Date : 2004-05-01 DOI: 10.1016/J.CARPATH.2004.03.284
Se-hwa Kim, S. Lessner, Y. Sakurai, Z. Galis
{"title":"Cyclophilin A as a novel biphasic mediator of endothelial activation and dysfunction.","authors":"Se-hwa Kim, S. Lessner, Y. Sakurai, Z. Galis","doi":"10.1016/J.CARPATH.2004.03.284","DOIUrl":"https://doi.org/10.1016/J.CARPATH.2004.03.284","url":null,"abstract":"","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"40 1","pages":"1567-74"},"PeriodicalIF":0.0,"publicationDate":"2004-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85743026","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: 125
Expression of myopodin induces suppression of tumor growth and metastasis. myopodin的表达可以抑制肿瘤的生长和转移。
The American journal of cardiovascular pathology Pub Date : 2003-09-24 DOI: 10.1016/S1569-9056(03)90524-0
Ling Jing, Lijun Liu, Y. Yu, R. Dhir, Marie Acquafondada, D. Landsittel, K. Cieply, A. Wells, Jian-Hua Luo
{"title":"Expression of myopodin induces suppression of tumor growth and metastasis.","authors":"Ling Jing, Lijun Liu, Y. Yu, R. Dhir, Marie Acquafondada, D. Landsittel, K. Cieply, A. Wells, Jian-Hua Luo","doi":"10.1016/S1569-9056(03)90524-0","DOIUrl":"https://doi.org/10.1016/S1569-9056(03)90524-0","url":null,"abstract":"","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"39 1","pages":"1799-806"},"PeriodicalIF":0.0,"publicationDate":"2003-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88355454","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: 36
The cytoplasmic domain of tissue factor contributes to leukocyte recruitment and death in endotoxemia. 内毒素血症中组织因子的细胞质结构域参与白细胞募集和死亡。
The American journal of cardiovascular pathology Pub Date : 2003-07-01 DOI: 10.1111/j.1538-7836.2003.tb04442.x
L. Sharma, E. Melis, M. Hickey, C. Clyne, J. Erlich, L. Khachigian, P. Davenport, E. Morand, P. Carmeliet, P. Tipping
{"title":"The cytoplasmic domain of tissue factor contributes to leukocyte recruitment and death in endotoxemia.","authors":"L. Sharma, E. Melis, M. Hickey, C. Clyne, J. Erlich, L. Khachigian, P. Davenport, E. Morand, P. Carmeliet, P. Tipping","doi":"10.1111/j.1538-7836.2003.tb04442.x","DOIUrl":"https://doi.org/10.1111/j.1538-7836.2003.tb04442.x","url":null,"abstract":"Tissue factor (TF) is an integral membrane protein that binds factor VIIa and initiates coagulation. The extracellular domain of TF is responsible for its hemostatic function and by implication in the dysregulation of coagulation, which contributes to death in endotoxemia. The role of the cytoplasmic domain of tissue factor in endotoxemia was studied in mice, which lack the cytoplasmic domain of TF (TF(deltaCT/deltaCT)). These mice develop normally and have normal coagulant function. Following i.p injection with 0.5 mg of lipopolysaccharide (LPS), TF(deltaCT/deltaCT) mice showed significantly greater survival at 24 hours compared to the wt mice (TF(+/+)). The serum levels of TNF-alpha and IL-1beta were significantly lower at 1 hour after LPS injection and IL-6 levels were significantly lower at 24 hours in TF(deltaCT/deltaCT) mice compared to TF(+/+)mice. Neutrophil recruitment into the lung was also significantly reduced in TF(deltaCT/deltaCT) mice. Nuclear extracts from tissues of endotoxemic TF(deltaCT/deltaCT) mice also showed reduced NFkappaB activation. LPS induced leukocyte rolling, adhesion, and transmigration in post-capillary venules assessed by intravital microscopy was also significantly reduced in TF(deltaCT/deltaCT) mice. These results indicate that deletion of the cytoplasmic domain of TF impairs the recruitment and activation of leukocytes and increases survival following endotoxin challenge.","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"43 1","pages":"331-40"},"PeriodicalIF":0.0,"publicationDate":"2003-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81992596","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: 48
Frequent CpG island methylation in serrated adenomas of the colorectum. 结直肠锯齿状腺瘤中常见的CpG岛甲基化。
The American journal of cardiovascular pathology Pub Date : 2003-03-01 DOI: 10.1016/S0016-5085(03)81193-9
Seun-Ja Park, A. Rashid, Jaehyuk Lee, S. Kim, S. Hamilton, Tsung-Teh Wu
{"title":"Frequent CpG island methylation in serrated adenomas of the colorectum.","authors":"Seun-Ja Park, A. Rashid, Jaehyuk Lee, S. Kim, S. Hamilton, Tsung-Teh Wu","doi":"10.1016/S0016-5085(03)81193-9","DOIUrl":"https://doi.org/10.1016/S0016-5085(03)81193-9","url":null,"abstract":"","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"50 1","pages":"815-22"},"PeriodicalIF":0.0,"publicationDate":"2003-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86017225","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: 228
Endothelin-1 suppresses plasma membrane Ca++-ATPase, concomitant with contraction of hepatic sinusoidal endothelial fenestrae. 内皮素-1抑制质膜Ca++- atp酶,伴肝窦内皮窗收缩。
The American journal of cardiovascular pathology Pub Date : 2003-02-01 DOI: 10.1016/S0016-5085(03)83656-9
H. Yokomori, M. Oda, M. Ogi, K. Yoshimura, M. Nomura, Kayo Fujimaki, Y. Kamegaya, N. Tsukada, H. Ishii
{"title":"Endothelin-1 suppresses plasma membrane Ca++-ATPase, concomitant with contraction of hepatic sinusoidal endothelial fenestrae.","authors":"H. Yokomori, M. Oda, M. Ogi, K. Yoshimura, M. Nomura, Kayo Fujimaki, Y. Kamegaya, N. Tsukada, H. Ishii","doi":"10.1016/S0016-5085(03)83656-9","DOIUrl":"https://doi.org/10.1016/S0016-5085(03)83656-9","url":null,"abstract":"","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"58 1","pages":"557-66"},"PeriodicalIF":0.0,"publicationDate":"2003-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91219708","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: 18
A critical involvement of oxidative stress in acute alcohol-induced hepatic TNF-alpha production. 氧化应激在急性酒精诱导的肝脏tnf - α生成中的关键参与。
The American journal of cardiovascular pathology Pub Date : 2003-01-01 DOI: 10.1016/S0270-9139(03)80963-1
Zhanxiang Zhou, Lipeng Wang, Zhenyuan Song, J. Lambert, C. McClain, Y. J. Kang
{"title":"A critical involvement of oxidative stress in acute alcohol-induced hepatic TNF-alpha production.","authors":"Zhanxiang Zhou, Lipeng Wang, Zhenyuan Song, J. Lambert, C. McClain, Y. J. Kang","doi":"10.1016/S0270-9139(03)80963-1","DOIUrl":"https://doi.org/10.1016/S0270-9139(03)80963-1","url":null,"abstract":"","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"19 1","pages":"1137-46"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73216986","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: 111
Hemoglobin-vesicles as oxygen carriers: influence on phagocytic activity and histopathological changes in reticuloendothelial system. 血红蛋白囊泡作为氧载体:对网状内皮系统吞噬活性和组织病理学改变的影响。
The American journal of cardiovascular pathology Pub Date : 2001-09-01 DOI: 10.2302/KJM.52.SUPPLEMENT1_44
H. Sakai, H. Horinouchi, K. Tomiyama, E. Ikeda, S. Takeoka, K. Kobayashi, E. Tsuchida
{"title":"Hemoglobin-vesicles as oxygen carriers: influence on phagocytic activity and histopathological changes in reticuloendothelial system.","authors":"H. Sakai, H. Horinouchi, K. Tomiyama, E. Ikeda, S. Takeoka, K. Kobayashi, E. Tsuchida","doi":"10.2302/KJM.52.SUPPLEMENT1_44","DOIUrl":"https://doi.org/10.2302/KJM.52.SUPPLEMENT1_44","url":null,"abstract":"Hemoglobin-vesicles (HbV) have been developed for use as artificial oxygen carriers (particle diameter, 250 nm) in which a purified Hb solution is encapsulated with a phospholipid bilayer membrane. The influence of HbV on the reticuloendothelial system was studied by carbon clearance measurements and histopathological examination. The HbV suspension ([Hb] = 10 g/dl) was intravenously infused in male Wistar rats at dose rates of 10 and 20 ml/kg, and the phagocytic activity was measured by monitoring the rate of carbon clearance at 8 hours and at 1, 3, 7, and 14 days after infusion. The phagocytic activity transiently decreased one day after infusion by about 40%, but it recovered and was enhanced at 3 days, showing a maximum of about twice the quiescent level at 7 days, and then returned to the normal value at 14 days. The initial transient decreased activity indicates a partly, but not completely, suppressed defensive function of the body. The succeeding increased phagocytic activity corresponds to the increased metabolism of HbV. The histopathological examination with anti-human Hb antibody, hematoxylin/eosin, and oil red O stainings showed that HbV was metabolized within 7 days. Hemosiderin was very slightly confirmed with Berlin blue staining at 3 and 7 days in liver and spleen, though they completely disappeared at 14 days, indicating that the heme metabolism, excretion or recycling of iron proceeded smoothly and iron deposition was minimal. Electron microscopic examination of the spleen and liver tissues clearly demonstrated the particles of HbV with a diameter of about 1/40 of red blood cells in capillaries, and in phagosomes as entrapped in the spleen macrophages and Kupffer cells one day after infusion. The vesicular structure could not be observed at 7 days. Even though the infusion of HbV modified the phagocytic activity for 2 weeks, it does not seem to cause any irreversible damage to the phagocytic organs. These results offer important information for evaluating the safety issues of HbV for clinical use.","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"159 3 1","pages":"1079-88"},"PeriodicalIF":0.0,"publicationDate":"2001-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81788924","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: 104
Direct thrombin inhibition reduces lung collagen, accumulation, and connective tissue growth factor mRNA levels in bleomycin-induced pulmonary fibrosis. 在博莱霉素诱导的肺纤维化中,直接凝血酶抑制可降低肺胶原蛋白、积累和结缔组织生长因子mRNA水平。
The American journal of cardiovascular pathology Pub Date : 2001-08-01 DOI: 10.1042/CS101020PA
David C. J. Howell, Neil R. Goldsack, Richard P. Marshall, R. McAnulty, Richard Starke, Gordon Purdy, Geoffrey J. Laurent, R. Chambers
{"title":"Direct thrombin inhibition reduces lung collagen, accumulation, and connective tissue growth factor mRNA levels in bleomycin-induced pulmonary fibrosis.","authors":"David C. J. Howell, Neil R. Goldsack, Richard P. Marshall, R. McAnulty, Richard Starke, Gordon Purdy, Geoffrey J. Laurent, R. Chambers","doi":"10.1042/CS101020PA","DOIUrl":"https://doi.org/10.1042/CS101020PA","url":null,"abstract":"Dramatic activation of the coagulation cascade has been extensively documented for pulmonary fibrosis associated with acute and chronic lung injury. In addition to its role in hemostasis, thrombin exerts profibrotic effects via activation of the major thrombin receptor, protease-activated receptor-1. In this study, we examined the effect of the direct thrombin inhibitor, UK-156406 on fibroblast responses in vitro and on bleomycin-induced pulmonary fibrosis in rats. UK-156406 significantly inhibited thrombin-induced fibroblast proliferation, procollagen production, and connective tissue growth factor (CTGF) mRNA levels when used at equimolar concentration to the protease. Thrombin levels in bronchoalveolar lavage fluid and expression of thrombin and protease-activated receptor-1 in lung tissue were increased after intratracheal instillation of bleomycin. The characteristic doubling in lung collagen in bleomycin-treated animals (38.4 +/- 2.0 mg versus 17.1 +/- 1.4 mg, P < 0.01) was preceded by significant elevations in alpha1(I) procollagen and CTGF mRNA levels (3.0 +/- 0.4-fold and 6.3 +/- 0.4-fold respectively, (P < 0.01), and total inflammatory cell number. UK-156406, administered at an anticoagulant dose, attenuated lung collagen accumulation in response to bleomycin by 35 +/- 12% (P < 0.05), inhibited alpha1(I) procollagen and CTGF mRNA levels by 50% and 35%, respectively (P < 0.05), but had no effect on inflammatory cell recruitment. This is the first report showing that direct thrombin inhibition abrogates lung collagen accumulation in bleomycin-induced pulmonary fibrosis.","PeriodicalId":77408,"journal":{"name":"The American journal of cardiovascular pathology","volume":"16 1","pages":"1383-95"},"PeriodicalIF":0.0,"publicationDate":"2001-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89119183","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: 188
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