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The benefits and safety of intravenous recombinant tissue plasminogen activator (IV-tPA) for patients with mild ischaemic stroke (MIS) are still unclear. The objective of this meta-analysis was to evaluate the efficacy and safety of IV-tPA as treatment for patients with MIS. We performed a systematic literature search across MEDLINE, Embase, Central, Global Health and Cumulative Index to Nursing and Allied Health Literature (CINAHL), from inception to 10 November 2016, to identify all related studies. Where possible, data were pooled for meta-analysis with odds ratio (OR) and corresponding 95% confidence interval (CI) using the fixed-effects model. MIS was defined as having National Institutes of Health Stroke Scale score of ≤6. We included seven studies with a total of 1591 patients based on the prespecified inclusion and exclusion criteria. The meta-analysis indicated a high odds of excellent functional outcome based on the modified Rankin Scale or Oxfordshire Handicap Score 0–1 (OR=1.43; 95% CI 1.14 to 1.79; P=0.002, I2=35%) in patients treated with IV-tPA compared with those not treated with IV-tPA (74.8% vs 67.6%). There was a high risk of symptomatic intracranial haemorrhage (sICH) with IV-tPA treatment (OR=10.13; 95% CI 1.93 to 53.02; P=0.006, I2=0%) (1.9% vs 0.0%) but not mortality (OR=0.78; 95% CI 0.43 to 1.43; P=0.43, I2=0%) (2.4% vs 2.9%). Treatment with IV-tPA was associated with better functional outcome but not mortality among patients with MIS, although there was an increased risk of sICH. Randomised trials are warranted to confirm these findings.

Abstract. advanced glycation end-products (aGes) contribute to the pathogenesis of diabetes mellitus and atherosclerosis by promoting vascular endothelial cell proliferation, migration, damage and death. in this study, we examined the role of autophagy in HUVECs exposed to AGE-modified bovine serum albumin (aGe-BSa). HuVecs incubated with aGe-BSa for 6 h showed an increase in the formation of acidic vesicular organelles and autophagosomes. aGe-BSa-induced upregulation of microtubule associated protein 1 light chain 3-ii (lc3-ii), a marker of autophagy, was abolished by pretreatment with the autophagy inhibitor 3-methyladenine (3-Ma), and was increased by rapamycin, an autophagy inducer. The increase of lactate dehydrogenase (ldH) leakage induced by aGe-BSa was increased by 3-Ma, but not rapamycin. an oxidative inhibitor, α-tocopherol, decreased not only the aGe-BSa-induced increase of reactive oxygen species, but also the upregulation of lc3-ii protein levels. These results suggest that aGe-BSa increases the level of autophagy, which is protective against HuVec injury, and that roS play a role in this activation of autophagy.

IntroductionRight ventricular (RV) function has increasingly being recognized as an important predictor for morbidity and mortality in patients with pulmonary arterial hypertension (PAH). The increased RV after-load increase RV work in PAH. We used time-resolved 3D phase contrast MRI (4D flow MRI) to derive RV kinetic energy (KE) work density and energy loss in the pulmonary artery (PA) to better characterize RV work in PAH patients.Methods4D flow and standard cardiac cine images were obtained in ten functional class I/II patients with PAH and nine healthy subjects. For each individual, we calculated the RV KE work density and the amount of viscous dissipation in the PA.ResultsPAH patients had alterations in flow patterns in both the RV and the PA compared to healthy subjects. PAH subjects had significantly higher RV KE work density than healthy subjects (94.7±33.7 mJ/mL vs. 61.7±14.8 mJ/mL, p = 0.007) as well as a much greater percent PA energy loss (21.1±6.4% vs. 2.2±1.3%, p = 0.0001) throughout the cardiac cycle. RV KE work density and percent PA energy loss had mild and moderate correlations with RV ejection fraction.ConclusionThis study has quantified two kinetic energy metrics to assess RV function using 4D flow. RV KE work density and PA viscous energy loss not only distinguished healthy subjects from patients, but also provided distinction amongst PAH patients. These metrics hold promise as imaging markers for RV function.

A low LDL-C/HDL-C ratio was independently associated with an increased risk of all-cause mortality at three months in patients with ICH. Moreover, the LDL-C/HDL-C ratio appeared to be a best lipid predictor of all-cause mortality than traditional lipid profiles.

Key Points Question Is there characteristic microbiota in nasopharyngeal carcinoma (NPC) tissues and, if so, is it associated with prognosis? Findings In this multicenter cohort study including 802 patients with NPC, we confirmed the existence of microbiota within NPC tissues, which mainly originated from the nasopharynx. Intratumoral bacterial load was associated with poor survival in patients with NPC and was negatively associated with T-lymphocyte infiltration. Meaning The results suggest that the intratumoral bacterial load may be a reliable prognostic indicator for patients with NPC.

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Objectives: Oxidized low-density lipoprotein (ox-LDL) may induce autophagy, apoptosis, necrosis or proliferation of cultured endothelial cells depending on the concentration and exposure time. Our previous studies found that ox-LDL exposure for 6 h increases the autophagic level of human umbilical vein endothelial cells (HUVECs) in a concentration-dependent manner. The present study investigates the relationship between autophagy and apoptosis in HUVECs exposed to ox-LDL. Methods: Flow cytometry and Western blot were used to study the apoptotic and autophagic phenomena. The contribution of autophagic and apoptotic mechanisms to ox-LDL-induced upregulation of MAP1-LC3, beclin1 and p53 protein levels were assessed by pretreatment with the autophagic inhibitors 3-MA and Atg5 small interfering (si)RNA, as well as z-vad-fmk, an apoptosis inhibitor. Results: ox-LDL induced the apoptosis of HUVECs in a concentration-dependent way. The increased expression of the autophagic proteins, LC3-II and beclin1, can be reversed by 3-MA and z-vad-fmk pretreatment. 3-MA and Atg5 siRNA increased the ox-LDL-induced increases of the p53 protein level and the annexin V-positive staining, which was decreased by z-vad-fmk. Conclusion: These results suggest thatoverstimulation of ox-LDL can induce autophagy and apoptosis in HUVECs. Inhibition of apoptosis leads to an inhibition of autophagy induced by ox-LDL. However, inhibition of autophagy leads to an increase in the ox-LDL-induced apoptosis.