Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The overgrowth of cells of the vessel wall, especially of the smooth muscle cells (SMCs), contributes to the pathogenesis of coronary atherosclerosis and wound repair after coronary angioplasty. However, the association between cellular proliferation in coronary lesions and clinical pathophysiology remains to be clarified in humans. Thus, we investigated proliferative activity in coronary tissues obtained from patients with coronary ischemia. The proliferative activity in tissues obtained by using directional coronary atherectomy (DCA) from 87 coronary lesions was assessed by immunohistochemical staining for the proliferating cell nuclear antigen (PCNA). The lesions were divided into 34 primary lesions and 53 postangioplasty lesions. The 34 primary tissue samples were obtained from 9 patients with stable angina pectoris (SAP) and 25 patients with acute coronary syndromes (ACS). Collectively, the 53 postangioplasty tissue samples were obtained from 37 patients with SAP and 16 patients with ACS. The PCNA labeling index (LI) was quantified as the mean percentage of PCNA-positive cells in the 3 most positive high-power fields (x 200). The mean LIs were high in the primary ACS samples [8.9 +/- 2.1% (p = 0.01)] and postangioplasty samples [2.3 +/- 0.8% (p = 0.08) in SAP cases and 4.1 +/- 2.4% (p = 0.06) in ACS cases] compared with the primary SAP samples (0.2 +/- 0.2%). Intimal hyperplasia, a random proliferation of SMCs (alpha-actin positive) was marked in the primary ACS samples (76%) as well as in the postangioplasty SAP (92%) and ACS (81%) samples, as compared with the primary SAP samples (33%) (p < 0.01). PCNA expression was mainly evident in the nucleus of the SMCs and CD68-positive macrophages. Many PCNA-positive cells were localized in plaque areas, as follows: intimal hyperplasia, neovascularized lesions, lesions with macrophage clusters, and lesions near areas of disrupted internal elastic lamina. The levels of PCNA expression in coronary lesions were not associated with the subsequent development of restenosis after DCA. Our findings suggest that the excessive proliferation of vascular wall cells, especially SMCs, is involved in the pathogenesis of ACS and in the process of wound repair after angioplasty in humans.
 ...
PMID:Comparison of proliferative activity in coronary plaques from patients with coronary ischemia. Histopathological and immunohistochemical analysis. 911 65

Gunshot wounds to the brain usually lead to acute respiratory arrest or death after a brief survival period, even in cases involving only slight direct tissue damage. It can be assumed therefore that the damage extends beyond the zone of recognizable destruction and hemorrhages. To determine the true extent of the tissue injury resulting from gunshot wounds to the brain, we carried out microscopic investigations for reactive changes (emigration of leukocytes and macrophages, axonal expression of beta-amyloid precursor protein (beta-APP) in 10 cases of gunshot wound to the narrow channel of the brain with survival times >2h. Demonstration of leukocytes expressing naphthol AS-D chloroacetate esterase activity in the brain tissue at the border of the missile track established the vitality of the gunshot effect. The presence of macrophages (CD68-epitope) allowed demarcation of a 1-2mm wide necrotic zone around the permanent cavity. Within this zone and beyond, beta-APP showed an initial increase followed by a decline in the number of injured axons. Three types of beta-APP positive staining could be differentiated. In the immediate vicinity of the missile track beta-APP positive neurons were present at a distance of 2-4mm from the margin of the permanent cavity (type 1) as a result of primary injured neuronal tissue by the gunshot itself. At longer distances from the narrow channel and the permanent cavity single beta-APP positive axons or axon fragments and two additional types were found; type 2 shows a parallel, wave-like arrangement of the damaged fibers, which suggests that the injury was produced by mechanical acceleration of the brain tissue created by the energy the projectile expended within the brain; irregular aggregation of beta-APP positive axons or axon fragments within a local edema represents type 3, which may be attributed to secondary ischemia or edema.
 ...
PMID:Brain injury after survived gunshot to the head: reactive alterations at sites remote from the missile track. 1107 74

In general, massive pulmonary embolism induces severe right ventricular overload, but pathological changes in the right ventricle due to pulmonary embolism is rarely seen. In this report, we describe two autopsy cases of massive pulmonary embolism without pre-existing cardiopulmonary disease. Both cases were accompanied by myocarditis-like changes in the right ventricle and infiltration of a number of polymorphonuclear neutrophils and mononuclear cells into the dilated right ventricular wall. Transmural or subendocardial coagulation necrosis was not apparent. Almost all of the mononuclear cells were immunohistochemically revealed to be CD68-positive macrophages. We speculated that these findings resulted from ischemia due to massive pulmonary embolism.
 ...
PMID:Two cases of right ventricular ischemic injury due to massive pulmonary embolism. 1118 71

Microglia are a major glial component of the central nervous system (CNS), play a critical role as resident immunocompetent and phagocytic cells in the CNS, and serve as scavenger cells in the event of infection, inflammation, trauma, ischemia, and neurodegeneration in the CNS. Studies of human microglia have been hampered by the difficulty of obtaining sufficient numbers of human microglia. One way to circumvent this difficulty is to establish permanent cell lines of human microglia. In the present study we report the generation of immortalized human microglial cell line, HMO6, from human embryonic telencephalon tissue using a retroviral vector encoding myc oncogene. The HMO6 cells exhibited cell type-specific antigens for microglia-macrophage lineage cells including CD11b (Mac-1), CD68, CD86 (B7-2), HLA-ABC, HLA-DR, and ricinus communis agglutinin lectin-1 (RCA), and actively phagocytosed latex beads. In addition, HMO6 cells showed ATP-induced responses similar to human primary microglia in Ca2+ influx spectroscopy. Both human primary microglia and HMO6 cells showed the similar cytokine gene expression in IL-1beta, IL-6, IL-8, IL-10, IL-12, IL-15, and TNF-alpha. Using HMO6 cells, we investigated whether activation was induced by Amyloid-beta fragments or lipopolysaccharide (LPS). Treatment of HMO6 cells with Amyloid-beta 25-35 fragment (Abeta(25-35)) or Amyloid-beta 1-42 fragment (Abeta(1-42)) led to increased expression of mRNA levels of cytokine/chemokine IL-8, IL-10, IL-12, MIP-1beta MIP-1, and MCP-1, and treatment with LPS produced same results. Expression of TNF-alpha and MIP1-alpha was not detected in unstimulated HMO6 cells, but their expression was later induced by long-term exposure to Abeta(25-35) or Abeta(1-42.) ELISA assays of spent culture media showed increased protein levels of TNF-alpha and IL-8 in HMO6 cells following treatment with Abeta(25-35) or LPS. Taken together, our results demonstrate that treatment of human primary microglia and HMO6 immortalized human microglia cell line with Abeta(25-35), Abeta(1-42) and LPS upregulate gene expression and protein production of proinflammatory cytokines and chemokines in these cells. The human microglial cell line HMO6 exhibits similar properties to those documented in human microglia and should have considerable utility as an in vitro model for the studies of human microglia in health and disease.
 ...
PMID:Generation and characterization of immortalized human microglial cell lines: expression of cytokines and chemokines. 1174 1

To clarify the mechanism of muscle fiber destruction in sarcoid myopathy, muscle biopsy specimens were examined from patients with sarcoid myopathy, polymyositis, or dermatomyositis. In sarcoid myopathy, noncaseating granulomatous lesions were located in the perimysium or endomysium or both. Little fiber atrophy, caused by mechanical compression of the granuloma, was seen, and there was no evidence of ischemia-induced changes (i.e., perifascicular atrophy) due to microangiopathy in muscles. Immunoreactivity for membrane-associated cytoskeletal proteins such as dystrophin and merosin was detected homogeneously along the surface of many small granulomas in intrafascicular lesions. These granulomas showed a characteristic phenotypic cellular distribution: CD68(+) and CD4(+) cells were present in the center, and some CD8(+) cells were found at the periphery, indicating typical sarcoid granuloma formation in each muscle fiber. Strong expression of proteases such as cathepsin B, calpain II and ubiquitin-proteasome was observed in macrophages and epithelioid cells but not in lymphocytes in granulomas within muscle fibers or those in the endomysium or perimysium. The expression intensity was stronger in premature-stage granulomas than in late-stage granulomas. Weak expression of these proteases was detected mainly in some muscle fibers invaded by epithelioid cells and macrophages and in a few atrophic or necrotic fibers adjacent to inflammatory foci but not in fibers of fascicles without granuloma formation or in fibers in perifascicular areas. Our results suggest that muscle fiber destruction in sarcoid myopathy is caused mainly by direct invasion of granulomatous inflammatory cells into muscle fibers during the process of granuloma formation rather than by mechanical compression or ischemia. Furthermore, the proteases derived from epithelioid cells and macrophages may play an important role in muscle fiber destruction.
 ...
PMID:Cellular distribution of proteolytic enzymes in the skeletal muscle of sarcoid myopathy. 1207 Jun 62

A-25-year-old man was admitted because of a painless tumor of the scrotum. The patient denied a history of exogenous material injection and trauma in the scrotum. Physical and radiological examination revealed a mass in the scrotum, and blood laboratory tests showed no significant findings except for mild eosinophilia (5.6%). Resection of the mass was performed. The mass was isolated and located in the subcutaneous tissue of the scrotum. The mass was rectangular and symmetrical, and measured 65 x 45 x 15 mm. Histologically, the mass was composed of adipose tissue with fibrosis. Many epithelioid granulomas with multinucleated giant cells of foreign body and Langhans' types and heavy infiltrates of lymphocytes and eosinophils were recognized. Characteristically, the lesion showed broad coagulative and lytic necrosis. Congestion and edema suggestive of ischemia were seen in some areas. Special stains for acid-fast bacteria, gram-positive bacteria and fungi failed to detect any microorganisms. Polymerase chain reaction for mycobacterium tuberculosis revealed no reaction products. Immunohistochemically, the majority of lymphocytes were CD45RO-positive T cells, and S-100 protein-positive cells and CD68-positive macrophages were scattered in small amounts. The appearances were typical for sclerosing lipogranuloma except for the necrosis. Although the pathological mechanism of the broad necrosis is unclear, the necrosis might be the result of ischemia. Our case suggests that primary sclerosing lipogranuloma of the scrotum might show broad necrosis, and that T-cell-mediated immune response might play a part in the formation of lipogranuloma.
 ...
PMID:Primary sclerosing lipogranuloma with broad necrosis of the scrotum. 1258 42

We investigated the fate of proliferating cells in the adult monkey brain after global ischemia. We used the thymidine analogue bromodeoxyuridine (BrdU) to label S-phase cells and their progeny in Japanese macaques subjected to global cerebral ischemia for 20 min or to a sham operation. Subsequently, newly generated cells were identified by BrdU immunohistochemistry, and their immunophenotype was determined quantitatively, using specific markers. The ischemic insult significantly increased the number of proliferating cells in the hippocampus and temporal neocortex, where the majority BrdU-labeled cells expressed markers for microglia (Iba1, CD68, and Ham56) or astrocytes (S-100beta and glial fibrillary acidic protein [GFAP]). In contrast, the proliferation level in the parahippocampal region remained unchanged. This discrepancy prompted us to investigate the postischemic response in the olfactory bulb, a well-known site of adult cell generation that is anatomically distant from the above-mentioned regions but that is also subjected to the global ischemic insult. The olfactory bulb contained clusters of proliferating cells expressing markers for neural (Musashi1 and Nestin) and/or neuronal (class III beta-tubulin) progenitors; these were immunophenotypically distinct from other cell types. Their number and distribution were unaltered by ischemia. Our results demonstrate that cell proliferation and differentiation in the adult macaque brain and olfactory bulb are differentially affected by a common insult.
 ...
PMID:Differential proliferative response in the postischemic hippocampus, temporal cortex, and olfactory bulb of young adult macaque monkeys. 1267 28

ELR(+) CXC chemokines including IL-8 are known to be involved in the ischemia-reperfusion injuries in various organs including rodent brain. However, the roles of these chemokines during the ischemia-reperfusion injuries of the primate brain still remain unknown. Here, we studied expressions of CXC chemokines and their receptor CXCR2 in monkey hippocampus known to develop total CA1 neuronal loss on day 5 after 20-min ischemia and reperfusion. ELR(+) chemokines and their receptor CXCR2 were not detected in the hippocampus of non-ischemic monkeys. On the contrary, at 30-60 min after the start of reperfusion, CD68-positive microglial cells increased significantly in the hippocampal CA1 sector, but there was negligible infiltration of neutrophils. These microglial cells expressed simultaneously growth regulated oncogene (Gro)-alpha and other ELR(+) CXC chemokines. Moreover, CD68-positive microglial cells also expressed the receptor for ELR(+) CXC chemokines. On day 4, capillary endothelial cells were significantly increased in the CA1 sector. Considering that ELR(+) CXC chemokines have potent angiogenic activities, the coordinate expression of ELR(+) CXC chemokines and their receptor CXCR2 in microglial cells may be related not only to the ischemic brain injuries but also to the microglial and capillary proliferation in the monkey hippocampus.
 ...
PMID:Accumulation of microglial cells expressing ELR motif-positive CXC chemokines and their receptor CXCR2 in monkey hippocampus after ischemia-reperfusion. 1270 61

To investigate the pathological changes in the heart induced by pulmonary embolism, 20 autopsy cases of pulmonary embolism and 10 control cases of acute death from traumatic injury were examined. Adding to the routine hematoxylin-eosin (HE) staining, immunostaining with CD68 pan-macrophage marker was performed on the specimens obtained from both right and left ventricular walls. The number of macrophages was counted semi-quantitatively in 100 random high-power fields (HPF). Although typical pathological findings of myocardial infarction was not observed in any of the cases, 16 of the 20 pulmonary embolism cases showed an increase in the number of macrophages, mainly in the right ventricular wall. Four cases showed massive macrophage infiltration in the entire right ventricular wall. It is speculated that ischemia due to pulmonary embolism may be connected to its pathogenesis.
 ...
PMID:Right ventricular damage due to pulmonary embolism: examination of the number of infiltrating macrophages. 1285 Apr 10

A review is given summarizing different methods that have been applied to the specific forensic neuropathological question of brain hypoxia/ischemia. On the microscopic level the authors applied routine stains and immunohistochemistry (MAP2, ALZ 50, GFAP, CD68, beta-APP) for characterization of the functional activity of neurons as well as of different cell types in various brain areas. Moreover, using molecular techniques for evaluation of the mitochondrial 4977-bp deletion in correlation to hypoxia and to age brain tissue and single cell analyses are described. The demonstrated scope of methods and results give evidence of the wide spectrum of possibilities to visualize hypoxic brain injuries for determining the cause (and matter) of death and for reconstructing the time-dependent process.
 ...
PMID:Methodical approach to brain hypoxia/ischemia as a fundamental problem in forensic neuropathology. 1460 62


1 2 3 4 5 6 7 8 Next >>