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Effects of the hot-isostatic pressing (HIP) temperature (1280,1300,1320℃) on microstructures and mechanical properties of a second generation single crystal superalloy DD6 were investigated. The results show that the HIP treatment significantly decrease the cast porosity number of DD6 compared with standard treated specimens. Especially, the cast porosity volume fraction is deceased from 0.31% to 0.04% after the HIP treatment of 1300℃/100MPa, 4h. The cast eutectic volume fractions are remarkably reduced with increasing HIP temperature. The HIP treatments nearly unchanged the creep lives, While they greatly promote the low cycle fatigue lives. The elimination of cast microspores using the HIP treatment of 1300℃/100MPa, 4h result in the inhibition of crack initiation during fatigue and improve the low cycle fatigue lives one order of magnitude larger than that after standard heat treatment.

The efficient conversion of CO2 to value‐added products represents one of the most attractive solutions to mitigate climate change and tackle the associated environmental issues. In particular, electrochemical CO2 reduction to fuels and chemicals has garnered tremendous interest over the last decades. Among all products from CO2 reduction, formic acid is considered one of the most economically vital CO2 reduction products. P‐block metals (especially Bi, Sn, In, and Pb) have been extensively investigated and recognized as the most efficient catalytic materials for the CO2 electroreduction to formate. Despite remarkable progress, the future implementation of this technology at the industrial‐scale hinges on the ability to solve remaining roadblocks. In this review, the current research status, challenges, and prospects of p‐block metal‐based catalysts primarily for CO2 electroreduction to formate are comprehensively reviewed. The rational design and nanostructure engineering of these p‐block metal catalysts for the optimization of their electrochemical performances are discussed in detail. Subsequently, the recent progress in the development of state‐of‐the‐art operando characterization techniques together with the design of advanced electrochemical cells to uncover the intrinsic catalysis mechanism is discussed. Lastly, a perspective on future directions including tackling critical challenges to realize its early industrial implementation is presented. [ABSTRACT FROM AUTHOR]

Objective: Mesencephalic astrocyte-derived neurotrophic factor (MANF) expressions are dramatically up-regulated in injured brain tissues, thereby conferring neurological protective effects. We intended to determine significance of serum MANF as a prognostic biomarker of intracerebral hemorrhage (ICH). Methods: In this prospective, observational study done from February 2018 to July 2021, 124 patients with new-onset primary supratentorial ICH were consecutively enrolled. Also, a group of 124 healthy individuals constituted controls. Their serum MANF levels were detected using the Enzyme-Linked Immunosorbent Assay. National Institutes of Health Stroke Scale (NIHSS) and hematoma volume were designated as the two severity indicators. Early neurologic deterioration (END) was referred to as an increase of 4 or greater points in NIHSS scores or death at post-stroke 24 h. Post-stroke 90-day modified Rankin scale (mRS) scores of 3–6 was considered as a poor prognosis. Serum MANF levels were analyzed using multivariate analysis with respect to its association with stroke severity and prognosis. Results: Patients, in comparison to controls, displayed markedly elevated serum MANF levels (median, 24.7 versus 2.7 ng/ml; P < 0.001), and serum MANF levels were independently correlated with NIHSS scores (beta, 3.912; 95% confidence interval (CI), 1.623-6.200; VIF = 2.394; t = 3.385; P = 0.002), hematoma volumes (beta, 1.688; 95% CI, 0.764–2.612; VIF = 2.661; t = 3.617; P = 0.001) and mRS scores (beta, 0.018; 95% CI, 0.013–0.023; VIF = 1.984; t = 2.047; P = 0.043). Serum MANF levels significantly predicted END and poor 90-day prognosis with areas under receiver operating characteristic curve at 0.752 and 0.787 respectively. END and prognostic predictive abilities were similar between serum MANF levels and NIHSS scores plus hematoma volumes (all P > 0.05). Combination of serum MANF levels with NIHSS scores and hematoma volumes had significantly higher prognostic capability than each of them (both P < 0.05). Serum MANF levels above 52.5 ng/ml and 62.0 ng/ml distinguished development of END and poor prognosis respectively with median-high sensitivity and specificity values. Using multivariate analysis, serum MANF levels > 52.5 ng/ml predicted END with odds ratio (OR) value of 2.713 (95% CI, 1.004–7.330; P = 0.042) and > 62.0 ng/ml predicted a poor prognosis with OR value of 3.848 (95% CI, 1.193–12.417; P = 0.024). Using restricted cubic spline, there was a linear correlation between serum MANF levels and poor prognosis or END risk (both P > 0.05). Nomograms were well established to predict END and a poor 90-day prognosis. Under calibration curve, such combination models were comparatively stable (using Hosmer & Lemeshow test, both P > 0.05). Conclusion: Increased serum MANF levels after ICH, in independent correlation with disease severity, independently distinguished risks of END and 90-day poor prognosis. Therefore, serum MANF may be a potential prognostic biomarker of ICH. [ABSTRACT FROM AUTHOR]

Background: Emerging evidence manifests that cyclin‐dependent kinase 6 (CDK6) plays an essential part in the initiation and progression of several types of human cancer, and its descending expression is correlated with an adverse prognosis. However, the precise role of CDK6 in Pancreatic cancer (PC) remains obscure. Aims: To identify the potential ceRNA regulatory axis of CDK6 in PC and explore its relationship with immune cells and immune checkpoints. Materials & Methods: Using The Cancer Genome Atlas TCGA and GTEx data analyze the expression and survival of CDK6 in patients in pan‐cancer, and cellular experiments were performed to verify the effect of CDK6 on cell function. Using GEPIA and STARBASE databases to analyze prognosis, expression and survival, and identify non coding RNA (ncRNA) that mediates CDK6 overexpression. The TIMER 2.0 database was used for immune correlation analysis. Results: We revealed CDK6 might be an oncogene in PC, and the HOXA11‐AS /NR2F1‐AS1‐ miR‐454‐3p axis was identified as the possible upstream ncRNA‐associated pathway of CDK6 in PC. In addition, CDK6 show significant association with three immune checkpoints (PD‐L1, PD‐L2, and HAVCR2), the infiltration level of immune cells, and immunity biomarkers. Discussion: We discussed some applications of CDK6 in breast cancer, melanoma, and hemorrhagic malignancies. The role of miR‐15a‐5p, HOXA11‐AS and NR2F1‐AS1 in tumor development was also discussed based on existing studies. The potential mechanism of CDK6 affecting immune cells in pancreatic cancer was discussed. Conclusions: Overall, these results established that nc‐RNA‐mediated high expression of CDK6 is associated with patient outcomes and immune invasion in pancreatic cancer. [ABSTRACT FROM AUTHOR]