Early and late clinical and angiographic outcomes following terumo coronary stent implantation

The Terumo stent is a new, balloon-expandable, stainless-steel device with a unique multicellular design to provide robust radial force and end-stoppers to prevent dislodgement. We evaluated the early and late clinical and angiographic outcomes of Terumo coronary stent implantation in native coronary arteries using an open, nonrandomized 3-center registry. From July 1998 to June 1999, a total of 118 Terumo stents were implanted in 105 patients (mean age, 58 +/- 10 years). A significant proportion of patients suffered from diabetes (34%), prior myocardial infarction (MI; 43%) and unstable angina (31%). Most target lesions (48%) had unfavorable morphological characteristics (type B2 or C); mean reference luminal diameter was 2.76 +/- 0.41 mm and lesion length was 11.4 +/- 5.3 mm. Primary success in stent deployment was achieved in 103 patients (98%). There was 1 patient with acute stent thrombosis in whom 2 overlapping stents were deployed. Following stenting, the minimal luminal diameter increased from 1.04 +/- 0.48 mm to 2.39 +/- 0.33 mm. Six-month angiography was performed in 97 patients (92%), and the binary angiographic restenosis (> or = 50% narrowing) rate was 16%. Late loss index was 0.50 +/- 0.43. By 6 months, two patients (1.9%) died, two patients (1.9%) had Q-wave MI and 9 patients (8.4%) required repeat coronary interventions. Therefore, our study shows that the Terumo stent is potentially safe and efficacious in the treatment of coronary narrowings, even in the presence of unfavorable clinical conditions and complex lesion morphological characteristics.     

Anti-platelet antibodies in patients with systemic lupus erythematosus and the primary antiphospholipid antibody syndrome: their relationship with the observed thrombocytopenia

The role of antiphospholipid antibodies in the pathogenesis of the thrombocytopenia observed during primary antiphospholipid antibody syndrome (APAS) and systemic lupus erythematosus (SLE) remains controversial. We have used the MAIPA test to examine the frequency and specificity of anti-platelet antibodies directed against the major platelet membrane glycoproteins (GP IIb–IIIa, GP Ib–IX, GP Ia–IIa and GP IV) in patients where SLE and APAS were associated or not with thrombocytopenia. Results were compared with a series of 26 ITP patients, 46% of whom were shown to possess anti-platelet antibodies directed against one or more of the platelet surface glycoproteins. When APAS was associated with thrombocytopenia, 7/10 patients possessed antibodies against GP IIb–IIIa and/or GP Ib–IX. For SLE patients with thrombocytopenia, 6/10 patients were shown to have antiplatelet antibodies against GP IIb–IIIa, GP Ib–IX or GP IV. In contrast, for APAS ( n =11) and SLE patients ( n =11) without thrombocytopenia, only one patient had an antibody directed against GP IIb–IIIa and one patient had an antibody to GP IV. Our results suggest that antibodies directed against major platelet membrane glycoproteins may play a role in the thrombocytopenia that is seen during SLE and APAS.     

居家安宁疗护对晚期癌症患者生活质量和情绪影响的Meta分析

目的 系统评价居家安宁疗护对晚期癌症患者生活质量和情绪的影响,为相关研究提供循证依据。 方法 计算机检索中国知网、万方数据库、维普数据库、中国生物医学文献数据库、CINAHL、CENTRAL、PubMed、Web of Science、Embase中关于居家安宁疗护对晚期癌症患者的随机对照试验,并追踪参考文献,检索时限为建库至2020年11月13日。由2名研究者独立筛选文献并交叉核对纳入文献质量,按照Cochrane评价手册5.1.0的质量评价方法评价纳入文献质量。采用RevMan 5.3软件进行Meta分析。 结果 共纳入10篇文献,包括1 720例晚期癌症患者。Meta分析结果显示,居家安宁疗护可以改善晚期癌症患者的生活质量[SMD=0.41,95%CI（0.30,0.51）,Z=7.44,P<0.001],减轻抑郁情绪[SMD=-0.29,95%CI（-0.45,-0.14）,Z=3.68,P<0.001],尚不能认为居家安宁疗护能够减轻晚期癌症患者的焦虑情绪[SMD=-0.15,95%CI（-2.12,1.82）,Z=0.15,P=0.880]。 结论 居家安宁疗护能够提高晚期癌症患者的生活质量,减轻患者的抑郁情绪,暂未发现能够减轻患者的焦虑情绪,需高质量、大样本研究进一步探讨居家安宁疗护对患者的影响。     

Elevated antigen-specific Th2 type response is associated with the poor prognosis of hand,foot and mouth disease

The immunopathogenesis of severe hand, foot and mouth disease (HFMD) remains elusive. This study revealed that enterovirus 71 (EV71) epitope-specific CD4+ T cell responses of HFMD patients were skewed toward a Th2 cytokine profile. Patients that demonstrated higher levels of IL-4 expression in their CD4 T cells following antigen stimulation in vitro tended to have a more prolonged period of high fevers and a longer duration of illness. Thus, an increase of EV71 epitope-specific Th2 type response may portend the poor prognosis for some HFMD patients.     

DNA hypermethylation of SFRP2 influences the pathology of rheumatoid arthritis through the canonical Wnt signaling in model rats

Abstract

In this work, the expression of secreted frizzled related protein 2 (SFRP2) in rheumatoid arthritis (RA) model rats and the mechanisms of SFRP2 on the RA pathogenesis were investigated. Data suggested that SFRP2 was significantly down-regulated in RA model rats compared with normal control, and overexpression of SFRP2 suppressed the RA pathogenesis and the canonical Wnt signaling in fibroblast-like synovial cells (FLS) from RA model rats, whereas knockdown of SFRP2 got an opposite observation. Interestingly, 5-azadC treatment up-regulated the SFRP2 expression, inhibited the FLS proliferation, suppressed the expression of IL-6 and IL-8 and the fibronectin production, suggesting that the decreased SFRP2 in RA model rats was due to the DNA methylation. Furthermore, DNMT1 knockdown up-regulated the SFRP2 expression, DNMT1 overexpression inhibited the SFRP2, and the quantitative methylation-specific PCR (qMSP) confirmed that the DNMT1 has direct methylation roles for the SFRP2 promoter, leading to a regulation of FLS proliferation and fibronectin expression in RA model rats. In addition, up-regulated MeCP2 was involved in the SFRP2 regulation and the pathogenesis of RA model rats, and MeCP2 and DNMT1 have synergistic inhibition roles in the SFRP2 expression. Combination of DNMT1 and DNA methylation may be a promising treatment strategy for individuals with RA in which SFRP2 is down-regulated.     

Galectin-1 ameliorates perioperative neurocognitive disorders in aged mice

IntroductionThe incidence of perioperative neurocognitive disorders (PND) is higher in the elderly patients undergoing surgery. Microglia activation‐mediated neuroinflammation is one of the hallmarks of PND. Galectin‐1 has been identified as a pivotal modulator in the central nervous system (CNS), while the role of galectin‐1 in PND induced by microglia‐mediated neuroinflammation is still undetermined.MethodsAn exploratory laparotomy model anesthetized with isoflurane was employed to investigate the role of galectin‐1 on PND in aged mice. Open field test and Morris water maze were used to test the cognitive function 3‐ or 7‐days post‐surgery. The activation of microglia in the hippocampus of aged mice was tested by immunohistochemistry. Western blot, enzyme‐linked immunosorbent assay (ELISA), and quantitative real‐time polymerase chain reaction (qRT‐PCR) were employed to elucidate the underlying mechanisms.ResultsGalectin‐1 attenuated the cognitive dysfunction induced by surgery in aged mice and inhibited microglial activity. Moreover, galectin‐1 decreased the expression level of inflammatory proteins (interleukin‐1β, interleukin‐6, and tumor necrosis factor‐α), and prevented neuronal loss in the hippocampus. Galectin‐1 inhibited the inflammation of BV2 microglial cells induced by lipopolysaccharide via decreasing the translocation of NF‐κB p65 and c‐Jun, while this kind of inhibition was rescued when overexpressing IRAK1.ConclusionOur findings provide evidence that galectin‐1 may inhibit IRAK1 expression, thus suppressing inflammatory response, inhibiting neuroinflammation, and improving ensuing cognitive dysfunction. Collectively, these findings unveil that galectin‐1 may elicit protective effects on surgery‐induced neuroinflammation and neurocognitive disorders.