Single crystal growth of and hyperfine couplings in the spin-triplet superconductor K2_2Cr3_3As3_3

We report single crystal growth of strongly-correlated compound K$_2$Cr$_3$As$_3$ with superconducting temperature $T_{\textrm c}$=6.2 K, and the measurements of magnetic susceptibility $\chi$ above $T_{\textrm c}$. We determined the hyperfine coupling constants directly from the relation between the Knight shift ($K$) and susceptibility ($K$-$\chi$ plot) and obtained the orbital contribution $K_{\textrm{orb}}$. Our results of $K_{\textrm{orb}}$ is in fairly good agreement with the previous estimate using a novel method, and reinforce the conclusion that K$_2$Cr$_3$As$_3$ is a spin-triplet superconductor

Associations between Comorbidities and Acute Exacerbation of Interstitial Lung Disease after Primary Lung Cancer Surgery

Acute exacerbation (AE) of interstitial lung disease (ILD) is a severe complication of lung resection in lung cancer patients with ILD (LC-ILD). This study aimed to assess the predictive value of comorbidities other than ILD for postoperative AE in patients with LC-ILD. We retrospectively evaluated 68 patients with LC-ILD who had undergone lung resection. We classified them into two groups: those who had developed postoperative AE within 30 days after resection and those who had not. We analyzed patient characteristics, high-resolution computed tomography findings, clinical data, pulmonary function, and intraoperative data. The incidence of postoperative AEs was 11.8%. In univariate analysis, performance status (PS), honeycombing, forced vital capacity (FVC), and high hemoglobin A1c (HbA1c) levels without comorbidities were significantly associated with postoperative AE. Patients were divided into two groups according to cutoff levels of those four variables as determined by receiver operating characteristic curves, revealing that the rates of patients without postoperative AE differed significantly between groups. The present results suggested that preoperative comorbidities other than ILD were not risk factors for postoperative AE in patients with LC-ILD. However, a high preoperative HbA1c level, poor PS, low FVC, and honeycombing may be associated with postoperative AE of LC-ILD

Lack of impact of the ALDH2 rs671 variant on breast cancer development in Japanese BRCA1/2‐mutation carriers

The aldehyde degrading function of the ALDH2 enzyme is impaired by Glu504Lys polymorphisms (rs671, termed A allele), which causes alcohol flushing in east Asians, and elevates the risk of esophageal cancer among habitual drinkers. Recent studies suggested that the ALDH2 variant may lead to higher levels of DNA damage caused by endogenously generated aldehydes. This can be a threat to genome stability and/or cell viability in a synthetic manner in DNA repair-defective settings such as Fanconi anemia (FA). FA is an inherited bone marrow failure syndrome caused by defects in any one of so far identified 22 FANC genes including hereditary breast and ovarian cancer (HBOC) genes BRCA1 and BRCA2. We have previously reported that the progression of FA phenotypes is accelerated with the ALDH2 rs671 genotype. Individuals with HBOC are heterozygously mutated in either BRCA1 or BRCA2, and the cancer-initiating cells in these patients usually undergo loss of the wild-type BRCA1/2 allele, leading to homologous recombination defects. Therefore, we hypothesized that the ALDH2 genotypes may impact breast cancer development in BRCA1/2 mutant carriers. We genotyped ALDH2 in 103 HBOC patients recruited from multiple cancer centers in Japan. However, we were not able to detect any significant differences in clinical stages, histopathological classification, or age at clinical diagnosis across the ALDH2 genotypes. Unlike the effects in hematopoietic cells of FA, our current data suggest that there is no impact of the loss of ALDH2 function in cancer initiation and development in breast epithelium of HBOC patients

Sex- and Age-Related Differences in Morbidity Rates of 2009 Pandemic Influenza A H1N1 Virus of Swine Origin in Japan

BACKGROUND: The objective of the present study was to determine whether the morbidity rates of the 2009 pandemic influenza A H1N1 virus (pdmH1N1) varied by age and/or sex. METHODS AND FINDINGS: Retrospective analysis of 2,024,367 cases of pdmH1N1 was performed using the national surveillance data from influenza sentinel points in Japan. The male-to-female morbidity ratios (M/F ratios) in nineteen age groups were estimated as the primary outcome. The M/F ratios for pdmH1N1 influenza were: >1 in age groups <20 years and ≥80 years (p<0.001); <1 in age groups 20-79 years (p<0.001). This data suggests that males <20 years of age may be more likely to suffer from pdmH1N1 influenza than females in the same age categories. When the infection pattern for pdmH1N1 was compared with that of seasonal influenza outbreaks between 2000 and 2008, the M/F ratio for pdmH1N1 influenza was higher in ages 3-29 years and lower in ages 40-79 years. Because the present study was based on the national surveillance, it was impossible to estimate the morbidity rate for the Japanese population. It is also likely that the data did not capture asymptomatic or mild infections. CONCLUSIONS: Although exposure to the pdmH1N1 virus is assumed to be similar in both boys and girls, M/F ratios were >1 in those younger than 20 years. The subsequent reversal of the M/F ratio in the adult generation could be due to several possibilities, including: greater immunity among adult males, more asymptomatic infections among males, less reporting of illness by males, or differences in exposure to the virus and probability of visiting a clinic. These results suggest that the infection and virulence patterns of pdmH1N1 are more complex than previously considered

Exophiala dermatitidis coinfection with nontuberculous mycobacteria: A case report and literature review

Abstract Six years ago, a 60‐year‐old man presented to our hospital with a cough and sputum. Upon suspicion of nontuberculous mycobacterial (NTM) infection, he was followed up at our hospital. Because the abnormal shadows in the bilateral lung fields deteriorated slightly over 6 years, bronchoscopy was performed. Exophiala dermatitidis and Mycobacterium intracellulare were detected in the bronchial lavage fluid. The patient underwent follow‐up examinations without drug administration. Currently, the patient's condition remains stable. E. dermatitidis is regulatory found in the lungs of patients with cystic fibrosis, but only rarely is it found in respiratory samples from patients without cystic fibrosis. However, NTM complications have been reported more frequently in recent years. Due to the increasing number of NTM patients, E. dermatitidis pulmonary infections may also increase. Additional research is required to develop strategies for treating this infection

Cell Stress Induces Upregulation of Osteopontin via the ERK Pathway in Type II Alveolar Epithelial Cells

<div><p>Osteopontin (OPN) is a multifunctional protein that plays important roles in cell growth, differentiation, migration and tissue fibrosis. In human idiopathic pulmonary fibrosis and murine bleomycin-induced lung fibrosis, OPN is upregulated in type II alveolar epithelial cells (AEC II). However, the mechanism of OPN induction in AEC II is not fully understood. In this study, we demonstrate the molecular mechanism of OPN induction in AEC II and elucidate the functions of OPN in AEC II and lung fibroblasts. Human lung adenocarcinoma cells (A549) and mouse alveolar epithelial cells (MLE12), used as type II alveolar epithelial cell lines for in vitro assays, and human pulmonary alveolar epithelial cells (HPAEpiC) were treated with either bleomycin, doxorubicin or tunicamycin. The mechanism of OPN induction in these cells and its function as a pro-fibrotic cytokine on A549 and lung fibroblasts were analyzed. The DNA damaging reagents bleomycin and doxorubicin were found to induce OPN expression in A549, MLE12 and HPAEpiC. OPN expression was induced via activation of the extracellular signal-regulated protein kinase (ERK)-dependent signaling pathway in A549 and MLE12. The endoplasmic reticulum (ER) stress-inducing reagent tunicamycin induced <i>OPN</i> mRNA expression in A549, MLE12 and HPAEpiC, and <i>OPN</i> mRNA expression was induced via activation of the ERK-dependent signaling pathway in A549 and MLE12. Another ER stress-inducing reagent thapsigargin induced the expression of <i>OPN</i> mRNA as well as the subsequent production of OPN in A549 and MLE12. Furthermore, OPN promoted the proliferation of A549 and the migration of normal human lung fibroblasts. Inhibition of OPN by small interference RNA or neutralizing antibody suppressed both of these responses. The results of this study suggest that cell stress induces the upregulation of OPN in AEC II by signaling through the ERK pathway, and that upregulated OPN may play a role in fibrogenesis of the lung.</p></div

Effect of thapsigargin on OPN expression.

<p>(A) A549 were exposed to 10 nM thapsigargin or DMSO for 48 h. Western blotting was used to detect BiP and β-actin. (B and C) A549 were exposed to 10 nM thapsigargin or DMSO for 48 h. (B) <i>OPN</i> mRNA was assessed by qRT-PCR. (C) OPN concentrations in cell culture media were determined by ELISA. Data are presented as mean ± S.E. *, P<0.05; **, P<0.01.</p

Effect of bleomycin on OPN expression in type II alveolar epithelial cell lines.

<p>(A) A549 were exposed to 1 µg/mL bleomycin for 0, 6, 12, 24 and 48 h. <i>OPN</i> mRNA was assessed by qRT-PCR. (B) MLE12 were exposed to 1 µg/mL bleomycin for 0, 6, 12, 24 and 48 h. <i>Opn</i> mRNA was assessed by qRT-PCR. (C) A549 were exposed to 0, 1 and 10 µg/mL bleomycin for 48 h. <i>OPN</i> mRNA was assessed by qRT-PCR. (D) MLE12 were exposed to 0, 1 and 10 µg/mL bleomycin for 48 h. <i>Opn</i> mRNA was assessed by qRT-PCR. (E, F and G) A549 were exposed to 1 µg/mL bleomycin. (E) The cells were lysed at 0, 2, 4 and 6 d. OPN concentrations in cell lysates were determined by ELISA. (F) The cell culture supernatants were collected at 0, 2, 4 and 6 d. OPN concentrations in cell culture media were determined by ELISA. (G) Total OPN concentrations in cell lysates and cell culture media were determined by ELISA. Data are presented as mean ± S.E. *, P<0.05; **, P<0.01.</p

Molecular mechanism of OPN induction after exposure to bleomycin.

<p>(A) A549 were exposed to 10 µg/mL bleomycin or PBS for 24 h. Western blotting was used to detect phospho-specific ERK1/2, ERK1/2, phospho-specific SAPK/JNK, SAPK/JNK, phospho-specific p38 MAPK and p38 MAPK. (B) A549 were pretreated with PD98059 (50 µM) or DMSO for 1 h, and subsequently exposed to 10 µg/mL bleomycin for 48 h. Western blotting was used to detect phospho-specific ERK1/2 and ERK1/2. (C) A549 were pretreated with U0126 (50 µM) or DMSO for 1 h, and subsequently exposed to 10 µg/mL bleomycin for 48 h. Western blotting was used to detect phospho-specific ERK1/2 and ERK1/2. (D) A549 were pretreated with PD98059 (50 µM) or DMSO for 1 h, and subsequently exposed to 10 µg/mL bleomycin or PBS for 48 h. <i>OPN</i> mRNA was assessed by qRT-PCR. (E) A549 were pretreated with U0126 (50 µM) or DMSO for 1 h, and subsequently exposed to 10 µg/mL bleomycin or PBS for 48 h. <i>OPN</i> mRNA was assessed by qRT-PCR. (F) A549 were pretreated with PD98059 (50 µM) or DMSO for 1 h, and subsequently exposed to 10 µg/mL bleomycin or PBS for 48 h. OPN concentrations in cell culture media were determined by ELISA. (G) A549 were pretreated with U0126 (50 µM) or DMSO for 1 h, and subsequently exposed to 10 µg/mL bleomycin or PBS for 48 h. OPN concentrations in cell culture media were determined by ELISA. Data are presented as mean ± S.E. *, P<0.05; **, P<0.01.</p