ABSTRACT Introduction: Inflammatory and immunological factors play pivotal roles in the prognosis of acute type A aortic dissection. We aimed to evaluate the prognostic values of immune-inflammatory parameters in acute type A aortic dissection patients after surgery. Methods: A total of 127 acute type A aortic dissection patients were included. Perioperative clinical data were collected through the hospital’s information system. The outcomes studied were delayed extubation, reintubation, and 30-day mortality. Multivariate logistic regression analysis and receiver operating characteristic analysis were used to screen the risk factors of poor prognosis. Results: Of all participants, 94 were male, and mean age was 51.95±11.89 years. The postoperative prognostic nutritional indexes were lower in delayed extubation patients, reintubation patients, and patients who died within 30 days. After multivariate regression analysis, the postoperative prognostic nutritional index was a protective parameter of poor prognosis. The odds ratios (95% confidence interval) of postoperative prognostic nutritional index were 0.898 (0.815, 0.989) for delayed extubation and 0.792 (0.696, 0.901) for 30-day mortality. Low postoperative fibrinogen could also well predict poor clinical outcomes. The odds ratios (95% confidence interval) of postoperative fibrinogen were 0.487 (0.291, 0.813) for delayed extubation, 0.292 (0.124, 0.687) for reintubation, and 0.249 (0.093, 0.669) for 30-day mortality. Conclusion: Postoperative prognostic nutritional index and postoperative fibrinogen could be two promising markers to identify poor prognosis of acute type A aortic dissection patients after surgery. Introduction immuneinflammatory immune inflammatory surgery Methods 12 included hospitals hospital s system 30day day mortality Results participants 9 male 51951189 51 95 11 89 51.95±11.8 years 3 days 95% (95 interval 0898 0 898 0.89 0.815, 0815 815 (0.815 0.989 0989 989 0792 792 0.79 0.696, 0696 696 (0.696 0.901 0901 901 0487 487 0.48 0.291, 0291 291 (0.291 0.813 0813 813 0292 292 0.29 0.124, 0124 124 (0.124 0.687 0687 687 0249 249 0.24 0.093, 0093 093 (0.093 0.669 0669 669 Conclusion 1 5195118 5 8 51.95±11. (9 089 0.8 0.815 081 81 (0.81 0.98 098 98 079 79 0.7 0.696 069 69 (0.69 0.90 090 90 048 48 0.4 0.291 029 29 (0.29 0.81 0.2 0.124 012 (0.12 0.68 068 68 024 24 0.093 009 09 (0.09 0.66 066 66 519511 51.95±11 ( 08 0. (0.8 0.9 07 7 0.69 06 6 (0.6 04 4 02 2 (0.2 0.12 01 (0.1 0.6 0.09 00 (0.0 51951 51.95±1 (0. 0.1 0.0 5195 51.95± (0 519 51.95 51.9 51.

In this study, we aimed to explore the relationship among miR-22, deep cerebral microbleeds (CMBs), and post-stroke depression (PSD) 1 month after ischemic stroke. We consecutively recruited 257 patients with first-ever and recurrent acute cerebral infarction and performed PSD diagnosis in accordance with the Diagnostic and Statistical Manual IV criteria for depression. Clinical information, assessments of stroke severity, and imaging data were recorded on admission. We further detected plasma miR-22 using quantitative PCR and analyzed the relationship among miR-22, clinical data, and PSD using SPSS 23.0 software. Logistic regression showed that deep (OR=1.845, 95%CI: 1.006-3.386, P=0.047) and brain stem CMBs (OR=2.652, 95%CI: 1.110–6.921, P=0.040), as well as plasma miR-22 levels (OR=2.094, 95%CI: 1.066–4.115, P=0.032) were independent risk factors for PSD. In addition, there were significant differences in baseline National Institutes of Health Stroke Scale scores (OR=1.881, 95%CI: 1.180–3.011, P=0.007) and Widowhood scores (OR=1.903, 95%CI: 1.182–3.063, P=0.012). Analysis of the receiver operating curve (AUC=0.723, 95%CI: 0.562–0.883, P=0.016) revealed that miR-22 could predict PSD one month after ischemic stroke. Furthermore, plasma miR-22 levels in brainstem and deep CMBs patients showed an upward trend (P=0.028) relative to the others. Patients with acute ischemic stroke, having brainstem and deep cerebral microbleeds, or a higher plasma miR-22 were more likely to develop PSD. These findings indicate that miR-22 might be involved in cerebral microvascular impairment and post-stroke depression.

The microstructure in the Z-Y surface of Inconel 718 alloys fabricated by selective laser melting (SLM) shows the relatively homogeneous and irregular fine grain structure after the heat treatment process of 1050ºC solid solution + double ageing. A large number of bulk precipitates were observed on the grain boundary, and the typical dendritic crystallization and Laves phases disappeared. It is possible that a large number of δ phases (NbNi3) were precipitated on the grain boundary since the enrichment effect of element Nb. The hardness in the Z-Y surface increased from 350HV to 500HV, and the residual stress was transformed from the tensile stress to compressive stress.

ABSTRACTPurpose:RNA activation (RNAa) is a mechanism of gene activation triggered by promoter-targeted small double stranded RNAs (dsRNAs), also known as small activating RNAs (saRNAs). Myogenic regulatory factor MyoD is regarded as the master activator of myogenic differentiation cascade by binding to enhancer of muscle specific genes. Stress urinary incontinence (SUI) is a condition primarily resulted from urethral sphincter deficiency. It is thus expected that by promoting differentiation of adipose-derived stem cells (ADSCs) into myoblasts by activating MyoD gene through RNAa may offer benefits to SUI.Materials and Methods:Rats ADSCs were isolated, proliferated in vitro, and identified by flow cytometry. Purified ADSCs were then transfected with a MyoD saRNA or control transfected. Real-time polymerase chain reaction (RT-PCR) and western blotting were used to detect MyoD mRNA and protein expression, respectively. Immunocytochemical staining was applied to determine the expression of desmin protein in transfected cells. Cell viability was measured by using CellTiter 96® AQueous One Solution Cell Proliferation Assay kit.Results:Transfection of a MyoD saRNA (dsMyoD) into ADSCs significantly induced the expression of MyoD at both the mRNA and protein levels, and inhibited cell proliferation. Desmin protein expression was detected in dsMyoD treated ADSCs 2 weeks later.Conclusion:Our findings show that RNAa mediated overexpression of MyoD can promote transdifferentiation of ADSCs into myoblasts and may help treat stress urinary incontinence (SUI)–a condition primarily resulted from urethral sphincter deficiency.