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In order to reduce the energy consumption of the reaction, the magnesium alloy samples were immersed directly into three conversion solutions and reacted for 9 hours at 60 ℃ and pH=12.0 used the chelating agent-assisted method by adding three chelating agents, ethylenediaminetetraacetic acid tetrasodium (EDTA-4Na), sodium citrate (SC) and potassium sodium tartrate (PST) to aluminum nitrate (Al(NO3)3) solution, and Mg-Al layered double hydroxides (LDHs) films doped with different chelating agents can be prepared on the surface of magnesium alloys. The microstructure, phase composition, and corrosion resistance of each LDHs film were analyzed by SEM, XRD, FT-IR, etc. The results show that the chelating agent-assisted method can successfully prepare LDHs films with typical layered structure on the surface of magnesium alloys under normal pressure and 60 ℃ environment; and three kinds of Mg-Al LDHs films obtained can effectively improve the corrosion resistance of magnesium alloys. Then, by comparing the structural properties of three different LDHs film layers, it is found that the Mg-Al-PST LDHs film prepared by adding PST has the highest density and the largest thickness, reaching up to 1.4 μm. The improvement effect of three coatings on the corrosion resistance of magnesium alloys is as follows: Mg-Al-PST LDHs > Mg-Al-SC LDHs > Mg-Al-EDTA LDHs; The magnesium alloy covered with the Mg-Al-PST LDHs film compared to the blank magnesium alloy, the corrosion current density decreases by about two orders of magnitude, and the total corrosion resistance increases by about one order of magnitude. And based on the analysis of the structure and properties of the obtained LDHs films, it can be seen that the chelating agent-assisted method can prepare Mg-Al LDHs films with better corrosion resistance in-situ on the surface of magnesium alloys under the lower energy consumption condition. The reason may be that the carboxyl group in the chelating agent can accelerate the deposition of Al3+ on the magnesium substrate and promote the substitution of some Mg2+ in Mg (OH)2 by Al3+ to form LDHs.

Pontine autosomal dominant microangiopathy and leukoencephalopathy (PADMAL) is a rare hereditary cerebral small vessel disease. We report a novel collagen type IV alpha 1 (COL4A1) gene mutation in a Chinese family with PADMAL. The index case was followed up for 6 years. Neuroimaging, whole-exome sequencing, skin biopsy, and pedigree analysis were performed. She initially presented with minor head injury at age 38. MRI brain showed chronic lacunar infarcts in the pons, left thalamus, and right centrum semiovale. Extensive workup was unremarkable except for a patent foramen ovale (PFO). Despite anticoagulation, PFO closure, and antiplatelet therapy, the patient had recurrent lacunar infarcts in the pons and deep white matter, as well as subcortical microhemorrhages. Whole-exome sequencing demonstrated a novel c.*34G > T mutation in the 3' untranslated region of COL4A1 gene. Skin biopsy subsequently demonstrated thickening of vascular basement membrane, proliferation of endothelial cells, and stenosis of vascular lumen. Three additional family members had gene testing and 2 of them were found to have the same heterozygous mutation. Of the 18 individuals in the pedigree of 3 generations, 12 had clinical and MRI evidence of PADMAL. The mechanisms of both ischemic and hemorrhagic stroke are likely the overexpression of COLT4A1 in the basement membrane and frugality of the vessel walls. Our findings suggest that the novel c.*34G > T mutation appears to have the same functional consequences as the previously reported COL4A1 gene mutations in patients with PADMAL and multi-infarct dementia of Swedish type.

In order to analyze the influence of unsteady diffusion characteristics of tectonic coal on energy instability, the steady and unsteady gas diffusion models were used to establish the functional relationship between the initial gas diffusion coefficient and pressure of intact coal and tectonic coal. Based on the existing energy formula, the calculation models of adsorbed gas and free gas expansion energy were established. The relationship between buried depth and outburst energy was analyzed, and the instability tendency of outburst energy in coal under different buried depths was discussed. The critical buried depth of outburst in the tectonic coal seam was 190 m, and the field gas dynamic phenomenon also verified the conclusion.

Background and objectiveSurvival of patients with pancreatic adenocarcinoma is limited and few prognostic factors are known. We conducted a two-stage genome-wide association study (GWAS) to identify germline variants associated with survival in patients with pancreatic adenocarcinoma.MethodsWe analysed overall survival in relation to single nucleotide polymorphisms (SNPs) among 1005 patients from two large GWAS datasets, PanScan I and ChinaPC. Cox proportional hazards regression was used in an additive genetic model with adjustment for age, sex, clinical stage and the top four principal components of population stratification. The first stage included 642 cases of European ancestry (PanScan), from which the top SNPs (p≤10(-5)) were advanced to a joint analysis with 363 additional patients from China (ChinaPC).ResultsIn the first stage of cases of European descent, the top-ranked loci were at chromosomes 11p15.4, 18p11.21 and 1p36.13, tagged by rs12362504 (p=1.63×10(-7)), rs981621 (p=1.65×10(-7)) and rs16861827 (p=3.75×10(-7)), respectively. 131 SNPs with p≤10(-5) were advanced to a joint analysis with cases from the ChinaPC study. In the joint analysis, the top-ranked SNP was rs10500715 (minor allele frequency, 0.37; p=1.72×10(-7)) on chromosome 11p15.4, which is intronic to the SET binding factor 2 (SBF2) gene. The HR (95% CI) for death was 0.74 (0.66 to 0.84) in PanScan I, 0.79 (0.65 to 0.97) in ChinaPC and 0.76 (0.68 to 0.84) in the joint analysis.ConclusionsGermline genetic variation in the SBF2 locus was associated with overall survival in patients with pancreatic adenocarcinoma of European and Asian ancestry. This association should be investigated in additional large patient cohorts.

The tumorigenic mechanism for pancreatic ductal adenocarcinoma (PDAC) is not clear, although chronic inflammation is implicated. Here, we identified an inflammatory cytokine-regulated transfer RNA- derived (tRNA-derived) fragment, tRF-21VBY9PYKHD (tRF-21), as a tumor suppressor in PDAC progression. We found that the biogenesis of tRF-21 could be inhibited by leukemia inhibitory factor and IL-6 via the splicing factor SRSF5. Reduced tRF- 21 promoted AKT2/1-mediated heterogeneous nuclear ribonucleoprotein L (hnRNP L) phosphorylation, enhancing hnRNP L to interact with dead-box helicase 17 (DDX17) to form an alternative splicing complex. The provoked hnRNP L-DDX17 activity preferentially spliced Caspase 9 and mH2A1 pre-mRNAs to form Caspase9b and mH2A1.2, promoting PDAC cell malignant phenotypes. The tRF-21 levels were significantly lower in PDACs than in normal tissues, and patients with low tRF-21 levels had a poor prognosis. Treatment of mouse PDAC xenografts or patient-derived xenografts (PDXs) with tRF-21 mimics repressed tumor growth and metastasis. These results demonstrate that tRF-21 has a tumor-suppressive effect and is a potential therapeutic agent for PDAC., Introduction Pancreatic ductal adenocarcinoma (PDAC) is the most lethal malignancy, with a 5-year survival rate of less than 9% (1, 2). Most PDAC tumors are already in an advanced stage [...]