169 research outputs found

    Impact of incomplete percutaneous revascularization in patients With multivessel coronary artery disease: a systematic review and meta-analysis

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    Background: Up to half of patients undergoing percutaneous coronary intervention have multivessel coronary artery disease (MVD) with conflicting data regarding optimal revascularization strategy in such patients. This paper assesses the evidence for complete revascularization (CR) versus incomplete revascularization in patients undergoing percutaneous coronary intervention, and its prognostic impact using meta‐analysis. Methods and Results: A search of PubMed, EMBASE, MEDLINE, Current Contents Connect, Google Scholar, Cochrane library, Science Direct, and Web of Science was conducted to identify the association of CR in patients with multivessel coronary artery disease undergoing percutaneous coronary intervention with major adverse cardiac events and mortality. Random‐effects meta‐analysis was used to estimate the odds of adverse outcomes. Meta‐regression analysis was conducted to assess the relationship with continuous variables and outcomes. Thirty‐eight publications that included 156 240 patients were identified. Odds of death (OR 0.69, 95% CI 0.61‐0.78), repeat revascularization (OR 0.60, 95% CI 0.45‐0.80), myocardial infarction (OR 0.64, 95% CI 0.50‐0.81), and major adverse cardiac events (OR 0.63, 95% CI 0.50‐0.79) were significantly lower in the patients who underwent CR. These outcomes were unchanged on subgroup analysis regardless of the definition of CR. Similar findings were recorded when CR was studied in the chronic total occlusion (CTO) subgroup (OR 0.65, 95% CI 0.53‐0.80). A meta‐regression analysis revealed a negative relationship between the OR for mortality and the percentage of CR. Conclusion: CR is associated with reduced risk of mortality and major adverse cardiac events, irrespective of whether an anatomical or a score‐based definition of incomplete revascularization is used, and this magnitude of risk relates to degree of CR. These results have important implications for the interventional management of patients with multivessel coronary artery disease

    Enantioselective reductive multicomponent coupling reactions between isatins and aldehydes

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    A reductive coupling of two different carbonyls via a polar two-electron reaction mechanism was developed and the stereochemical outcome of this multicomponent process is precisely controlled by a chiral triaminoiminophosphorane

    The mechanism of SO2 -induced stomatal closure differs from O3 and CO2 responses and is mediated by nonapoptotic cell death in guard cells.

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    Plants closing stomata in the presence of harmful gases is believed to be a stress avoidance mechanism. SO2 , one of the major airborne pollutants, has long been reported to induce stomatal closure, yet the mechanism remains unknown. Little is known about the stomatal response to airborne pollutants besides O3 . SLOW ANION CHANNEL-ASSOCIATED 1 (SLAC1) and OPEN STOMATA 1 (OST1) were identified as genes mediating O3 -induced closure. SLAC1 and OST1 are also known to mediate stomatal closure in response to CO2 , together with RESPIRATORY BURST OXIDASE HOMOLOGs (RBOHs). The overlaying roles of these genes in response to O3 and CO2 suggested that plants share their molecular regulators for airborne stimuli. Here, we investigated and compared stomatal closure event induced by a wide concentration range of SO2 in Arabidopsis through molecular genetic approaches. O3 - and CO2 -insensitive stomata mutants did not show significant differences from the wild type in stomatal sensitivity, guard cell viability, and chlorophyll content revealing that SO2 -induced closure is not regulated by the same molecular mechanisms as for O3 and CO2 . Nonapoptotic cell death is shown as the reason for SO2 -induced closure, which proposed the closure as a physicochemical process resulted from SO2 distress, instead of a biological protection mechanism

    Coronary angioscopic findings 9 months after everolimus-eluting stent implantation compared with sirolimus-eluting stents

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    AbstractObjectivesWe assessed angioscopic findings after everolimus-eluting stents (EES) implantation, compared with sirolimus-eluting stents (SES).BackgroundCoronary angioscopy (CAS) provides an opportunity to assess neointimal coverage over stent struts, thrombus, and plaque color by direct visualization. CAS is a useful tool for evaluating stent struts after drug-eluting stent implantation. Angioscopic findings after EES implantation have not been reported before.MethodsWe performed CAS in 23 patients who were treated with EES and 41 patients with SES. CAS was performed 8.5 months after stent implantation. We assessed neointimal coverage, thrombus, and plaque color. We classified neointimal coverage in 4 grades: grade 0=struts were completely exposed; grade 1=struts were visible with dull light reflexion; grade 2=there was no light reflexion from slightly visible struts; grade 3=struts were completely covered.ResultsThere was no significant difference in minimum, maximum, dominant grade of neointimal coverage, and heterogeneity index between EES and SES. Thrombus was less frequently observed in EES than SES (4% vs 29%, p=0.02). When we divided study patients into acute coronary syndrome (ACS) or stable angina pectoris (SAP), there was a tendency toward less thrombus in EES than SES, in both ACS and SAP. Maximum color grade of the plaques was less advanced in EES than SES (p<0.01). Yellow plaques of grade 2 or 3 were less frequent in EES than SES (35% vs 76%, p<0.01).ConclusionsThis study suggested that EES were associated with lower risk of thrombus formation than SES

    Clinicopathological significance of platelet-derived growth factor (PDGF)-B and vascular endothelial growth factor-A expression, PDGF receptor-β phosphorylation, and microvessel density in gastric cancer

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    Background: Angiogenesis is important in the growth and metastasis of various kinds of solid tumors, including gastric cancers. The angiogenic process is triggered by several key growth factors, including vascular endothelial growth factor (VEGF)-A and platelet-derived growth factor (PDGF)-B, that are secreted by tumors. Our aim was to define: i) the expression pattern of VEGF-A and PDGF-B in tumor cells and the activation of PDGF receptor (PDGFR)-β tyrosine kinase in stromal cells of human gastric adenocarcinomas; and ii) the relationship between VEGF-A and PDGF-B expression and microvessel density (MVD), to determine if there is a rationale for a new therapeutic strategy.Methods: A series of 109 gastric adenocarcinoma cases that had undergone surgical resection was examined immunohistochemically using antibodies against VEGF-A, PDGF-B, and CD34, followed by further examination of PDGFR-β phosphorylation by immunoblotting analysis.Results: MVD was higher in diffuse-type than intestinal-type cancers (p < 0.001). VEGF-A overexpression correlated to PDGF-B overexpression in both the intestinal-type (p < 0.005) and diffuse-type (p < 0.0001) groups, indicating that VEGF-A and PDGF-B are secreted simultaneously in the same tumor, and may thus play important roles together in angiogenesis. However, several differences between intestinal-type and diffuse-type cancers were observed. In the diffuse-type cancer group, higher MVD was related to the PDGF-B proportion (p < 0.05) and VEGF-A overexpression (p < 0.05), but not to PDGF-B overexpression or the VEGF-A proportion. On the other hand, in the intestinal-type cancer group, higher MVD was correlated to overexpression (p < 0.005), intensity (p < 0.05), and proportion (p < 0.05) of PDGF-B, but not of VEGF-A. In addition, phosphorylation of PDGFR-β was correlated with depth of cancer invasion at statistically significant level.Conclusions: Our results indicate that PDGF-B, which is involved in the maintenance of microvessels, plays a more important role in angiogenesis in intestinal-type gastric carcinomas than VEGF-A, which plays a key role mainly in the initiation of new blood vessel formation. In contrast, VEGF-A has a critical role for angiogenesis more in diffuse-type cancers, but less in those of intestinal type. Thus, a therapy targeting the PDGF-B signaling pathway could be effective for intestinal-type gastric carcinoma, whereas targeting VEGF-A or both VEGF-A and PDGF-B signaling pathways could be effective for diffuse-type gastric carcinomas. © 2010 Suzuki et al; licensee BioMed Central Ltd
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