Coexistence of Superconductivity and Nontrivial Band Topology in Monolayered Cobalt Pnictides on SrTiO₃

As an intrinsically layered material, FeSe has been extensively explored for potentially revealing the underlying mechanisms of high transition temperature (high-Tc) superconductivity and realizing topological superconductivity and Majorana zero modes. Here we use first-principles approaches to identify that the cobalt pnictides of CoX (X = As, Sb, Bi), none of which is a layered material in bulk form. Nevertheless, all can be stabilized as monolayered systems either in freestanding form or supported on the SrTiO3(001) substrate. We further show that each of the cobalt pnictides may potentially harbor high-Tc superconductivity beyond the Cu- and Fe-based superconducting families, and the underlying mechanism is inherently tied to their isovalency nature with the FeSe monolayer. Most strikingly, each of the monolayered CoX’s on SrTiO3 is shown to be topologically nontrivial, and our findings provide promising new platforms for realizing topological superconductors in the two-dimensional limit

Table_1_TGF-β-Containing Small Extracellular Vesicles From PM2.5-Activated Macrophages Induces Cardiotoxicity.XLSX

Numerous epidemiological and experimental studies have demonstrated that the exposure to fine particulate matter (aerodynamic diameter 2.5) was closely associated with cardiovascular morbidity and mortality. Our previous studies revealed that PM2.5 exposure induced cardiac dysfunction and fibrosis. However, the corresponding underlying mechanism remains largely unaddressed. Here, PM2.5-induced cardiotoxicity is presented to directly promote collagen deposition in cardiomyocytes through the transforming growth factor-β (TGF-β)-containing small extracellular vesicles (sEV). The sEV transition may play an important role in PM2.5-induced cardiac fibrosis. Firstly, long-term PM2.5 exposure can directly induce cardiac fibrosis and increase the level of serum sEV. Secondly, PM2.5 can directly activate macrophages and increase the release of tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), and TGF-β-containing sEV. Thirdly, TGF-β-containing sEV increases the expression of α-smooth muscle actin (α-SMA), collagen I, and collagen III in mouse cardiac muscle HL-1 cells. Finally, TGF-β-containing sEV released from PM2.5-treated macrophages can increase collagen through the activation of the TGF-β-Smad2/3 signaling pathway in HL-1 cells from which some fibroblasts involved in cardiac fibrosis are thought to originate. These findings suggest that TGF-β-containing sEV from PM2.5-activated macrophages play a critical role in the process of increasing cardiac collagen content via activating the TGF-β-Smad2/3 signaling pathway.</p

IMR902912 Supplemental Material2 - Supplemental material for Intravenous transfusion of iron sucrose reduces blood transfusions and improves postoperative anaemia after a second thoracotomy: a propensity-score matching study

Supplemental material, IMR902912 Supplemental Material2 for Intravenous transfusion of iron sucrose reduces blood transfusions and improves postoperative anaemia after a second thoracotomy: a propensity-score matching study by Chentao Luo, Yunqing Shi, Yi Lin, Runhua Ma, Qi Xia and Wenjun Ding in Journal of International Medical Research</p

Data_Sheet_1_TGF-β-Containing Small Extracellular Vesicles From PM2.5-Activated Macrophages Induces Cardiotoxicity.docx

Numerous epidemiological and experimental studies have demonstrated that the exposure to fine particulate matter (aerodynamic diameter 2.5) was closely associated with cardiovascular morbidity and mortality. Our previous studies revealed that PM2.5 exposure induced cardiac dysfunction and fibrosis. However, the corresponding underlying mechanism remains largely unaddressed. Here, PM2.5-induced cardiotoxicity is presented to directly promote collagen deposition in cardiomyocytes through the transforming growth factor-β (TGF-β)-containing small extracellular vesicles (sEV). The sEV transition may play an important role in PM2.5-induced cardiac fibrosis. Firstly, long-term PM2.5 exposure can directly induce cardiac fibrosis and increase the level of serum sEV. Secondly, PM2.5 can directly activate macrophages and increase the release of tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), and TGF-β-containing sEV. Thirdly, TGF-β-containing sEV increases the expression of α-smooth muscle actin (α-SMA), collagen I, and collagen III in mouse cardiac muscle HL-1 cells. Finally, TGF-β-containing sEV released from PM2.5-treated macrophages can increase collagen through the activation of the TGF-β-Smad2/3 signaling pathway in HL-1 cells from which some fibroblasts involved in cardiac fibrosis are thought to originate. These findings suggest that TGF-β-containing sEV from PM2.5-activated macrophages play a critical role in the process of increasing cardiac collagen content via activating the TGF-β-Smad2/3 signaling pathway.</p

IMR902912 Supplemental Material1 - Supplemental material for Intravenous transfusion of iron sucrose reduces blood transfusions and improves postoperative anaemia after a second thoracotomy: a propensity-score matching study

Supplemental material, IMR902912 Supplemental Material1 for Intravenous transfusion of iron sucrose reduces blood transfusions and improves postoperative anaemia after a second thoracotomy: a propensity-score matching study by Chentao Luo, Yunqing Shi, Yi Lin, Runhua Ma, Qi Xia and Wenjun Ding in Journal of International Medical Research</p

DataSheet_1_Aspirin Alleviates Particulate Matter Induced Asymptomatic Orchitis of Mice via Suppression of cGAS-STING Signaling.pdf

As an important source of air pollutant, airborne particulate matter (PM) has become a major threat to public health. Orchitis is characterized by acute or chronic testicular inflammation and is a primary cause of male infertility. Although accumulating evidence indicates that PM exposure is associated with increased male infertility rates, the mechanism by which PM is involved is not well understood. Here, we found that short-term PM exposure activated NF-κB signaling in mouse Leydig cells and testes and leading to asymptomatic orchitis. Analyzing the mitochondrial abundance and cGAMP levels in PM exposed mouse Leydig cells, we found that PM exposure induced mitochondrial injury and mtDNA release, leading to inflammation via the cGAS-STING axis. We also found that aspirin-induced acetylation of cGAS inhibited the inflammation in mice after PM exposure, especially in the testes. Moreover, aspirin pretreatment rescued offspring growth in PM-exposed mice. In summary, our study not only provides evidence that PM-induced asymptomatic orchitis in mice may be amenable to aspirin pre-treatment by acetylating cGAS, but also provides a potential explanation for male infertility caused by air pollutants.</p

Image_1_Aspirin Alleviates Particulate Matter Induced Asymptomatic Orchitis of Mice via Suppression of cGAS-STING Signaling.tiff

As an important source of air pollutant, airborne particulate matter (PM) has become a major threat to public health. Orchitis is characterized by acute or chronic testicular inflammation and is a primary cause of male infertility. Although accumulating evidence indicates that PM exposure is associated with increased male infertility rates, the mechanism by which PM is involved is not well understood. Here, we found that short-term PM exposure activated NF-κB signaling in mouse Leydig cells and testes and leading to asymptomatic orchitis. Analyzing the mitochondrial abundance and cGAMP levels in PM exposed mouse Leydig cells, we found that PM exposure induced mitochondrial injury and mtDNA release, leading to inflammation via the cGAS-STING axis. We also found that aspirin-induced acetylation of cGAS inhibited the inflammation in mice after PM exposure, especially in the testes. Moreover, aspirin pretreatment rescued offspring growth in PM-exposed mice. In summary, our study not only provides evidence that PM-induced asymptomatic orchitis in mice may be amenable to aspirin pre-treatment by acetylating cGAS, but also provides a potential explanation for male infertility caused by air pollutants.</p

Polymorphisms in the Interleukin 18 Receptor 1 Gene and Tuberculosis Susceptibility among Chinese

<div><p>Tuberculosis (TB), an infectious disease caused by infection of <i>Mycobacterium tuberculosis</i>, is a major public health challenge globally. Genetic epidemiological evidence suggests a genetic basis for TB, but the molecular mechanism for a genetic predisposition to TB remains largely unknown. Thirty-five tag single-nucleotide polymorphisms (SNPs) across 11 candidate cytokines and related genes, including IL-12/IFN-γ axis genes (<i>IL12B</i>, <i>IL12RB1</i>, <i>IL18R1</i>, <i>IL27, IFNGR1</i>, <i>IFNGR2</i> and <i>STAT1</i>), the <i>TNF</i> gene locus (<i>TNF</i> and <i>LTA</i>), <i>IL10</i>, and <i>CCL2</i>, were genotyped using Sequenom's iPLEX assays in 1,032 patients with TB and 1,008 controls of Chinese Han origin. We did not find that any of the 35 tag SNPs individually or as haplotypes was significantly associated with susceptibility to TB, on the basis of multivariable logistic regression analysis with adjustment for age and sex. However, stratification analyses showed that, in those with age 46 years or older, carrying the rs1974675 T allele in the <i>IL18R1</i> gene had a significantly decreased susceptibility to TB occurrence compared with carrying the C/C genotype (OR = 0.57, <i>P</i> = 5.0×10⁻⁴). Further analysis indicated that a SNP in absolute linkage disequilibrium with rs1974675, rs3755276, is located within a CpG dinucleotide and showed hypomethylation in controls than in patients (19.6% vs. 31.4%; <i>P</i> = 1.0×10⁻⁴) and genotype-specific DNA methylation at the <i>IL18R1</i> promoter and <i>IL18R1</i> mRNA levels. In addition, DNA methylation levels were significantly inversely correlated with mRNA levels. Thus, decreased mRNA levels of <i>IL18R1</i> due to rs3755276 may partially mediate the increased susceptibility to TB risk.</p></div

SNPs in the <i>IL18R1</i> gene, DNA methylation at the <i>IL18R1</i> promoter and <i>IL18R1</i> mRNA levels.

<p>(A) The upper panel indicates the tag SNPs across the <i>IL18R1</i> gene and the linkage disequilibrium (LD) structure in the Chinese case-control population. Pairwise LD (measured by <i>r</i>²) between SNPs is indicated by the color of individual squares in the triangular graphic, the squares with the deepest color have <i>r</i>² = 1. The lower panel indicates the five CpG sites at the <i>IL18R1</i> promoter (−814, −662, −660, −592, and −516 bp), where a SNP in absolute LD with rs1974675 (<i>r²</i> = 1 in CHB), rs3755276, is located within the second CpG site (−662 bp). Position +1 is determined by the start codon. (B) Correlation between methylation status at two CpG sites next to each other (−662 and −660 bp) and genotypes at rs3755276 in 18 patients with TB and 18 controls. DNA methylation was analysed using the EpiTYPER platform (Sequenom) which recognizes the two CpG sites (−662 and −660 bp) as one methylation signal. (C) Correlation between methylation status of the CpG site at −662 bp and genotypes at rs3755276 in additional 30 healthy controls. DNA methylation was analysed at a single nucleotide level by quantitative pyrosequencing in a Biotage PSQ 96MA system. (D) Correlation between <i>IL18R1</i> mRNA levels and genotypes at rs3755276 in the 30 healthy controls. (E) Correlation between <i>IL18R1</i> mRNA levels and DNA methylation at −662 bp (rs3755276) in the 30 healthy controls. A Pearson's test was used, and the correlation coefficient (<i>ρ</i>) and the two-tailed significance are shown. Outliers are marked with a circle on the boxplot. Error bars indicate means ±SD.</p

Age-stratified association of rs1974675 and rs6758936 in the <i>IL18R1</i> gene with TB risk among Chinese TB patients and controls.

<p>Due to genotyping failure, the actual sample size for rs1974675 is 1,017 and 998 for the cases and controls, respectively; the actual sample size for rs6758936 is 1,010 and 987 for the cases and controls, respectively. OR, odds ratio; CI, confidence interval.</p>a<p>The ORs and <i>P</i> values were calculated by logistic regression and adjusted for age and sex where appropriate within the strata.</p>b<p>For difference in ORs within each stratum.</p><p>Age-stratified association of rs1974675 and rs6758936 in the <i>IL18R1</i> gene with TB risk among Chinese TB patients and controls.</p