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Background: Hospital staff are vulnerable and at high risk of novel coronavirus disease (COVID-19) infection. The aim of this study was to monitor the psychological distress in hospital staff and examine the relationship between the psychological distress and possible causes during the COVID-19 epidemic. Methods: An online survey was conducted from February 1 to February 14, 2020. Hospital staff from five national COVID-19 designated hospitals in Chongqing participated. Data collected included demographics and stress responses to COVID-19: 1) the impact of event scale to measure psychological stress reactions; 2) generalized anxiety disorder 7 to measure anxiety symptoms; 3) Patient Health Questionnaire 9 to measure depression symptoms; 4) Yale-Brown Obsessive-Compulsive Scale to measure obsessive-compulsive symptoms (OCS); and 5) Patient Health Questionnaire 15 to measure somatization symptoms. Multiple logistic regression analysis was used to identify factors that were correlated with psychological distress. Results: Hospital staff that participated in this study were identified as either doctors or nurses. A total of 456 respondents completed the questionnaires with a response rate of 91.2%. The mean age was 30.67 ± 7.48 years (range, 17 to 64 years). Of all respondents, 29.4% were men. Of the staff surveyed, 43.2% had stress reaction syndrome. The highest prevalence of psychological distress was OCS (37.5%), followed by somatization symptoms (33.3%), anxiety symptoms (31.6%), and depression symptoms (29.6%). Univariate analyses indicated that female subjects, middle aged subjects, subjects in the low income group, and subjects working in isolation wards were prone to experience psychological distress. Multiple logistic regression analysis showed “Reluctant to work or considered resignation” (odds ratio [OR], 5.192; 95%CI, 2.396–11.250; P < .001 ), “Afraid to go home because of fear of infecting family” (OR, 2.099; 95%CI, 1.299–3.391; P = .002 ) “Uncertainty about frequent modification of infection and control procedures” (OR, 1.583; 95%CI, 1.061–2.363; P = .025 ), and“Social support” (OR, 1.754; 95%CI, 1.041–2.956; P = .035 ) were correlated with psychological reactions. “Reluctant to work or considered resignation” and “Afraid to go home because of fear of infecting family” were associated with a higher risk of symptoms of Anxiety (OR, 3.622; 95% CI, 1.882–6.973; P < .001 ; OR, 1.803; 95% CI, 1.069–3.039; P = .027), OCS (OR, 5.241; 95% CI, 2.545–10.793; P < .001 ; OR, 1.999; 95% CI, 1.217–3.282; P = .006 ) and somatization (OR, 5.177; 95% CI, 2.595–10.329; P ...

Air pollution has been classified as Group 1 carcinogenic to humans, but the underlying tumorigenesis remains unclear. In Xuanwei City of Yunnan Province, the lung cancer incidence is among the highest in China attributed to severe air pollution generated by combustion of smoky coal, providing a unique opportunity to dissect lung carcinogenesis of air pollution. Here we analyzed the somatic mutations of 164 non-small cell lung cancers (NSCLCs) from Xuanwei and control regions (CR) where smoky coal was not used. Whole genome sequencing revealed a mean of 289 somatic exonic mutations per tumor and the frequent C:G → A:T nucleotide substitutions in Xuanwei NSCLCs. Exome sequencing of 2010 genes showed that Xuanwei and CR NSCLCs had a mean of 68 and 22 mutated genes per tumor, respectively (p < 0.0001). We found 167 genes (including TP53, RYR2, KRAS, CACNA1E) which had significantly higher mutation frequencies in Xuanwei than CR patients, and mutations in most genes in Xuanwei NSCLCs differed from those in CR cases. The mutation rates of 70 genes (e.g., RYR2, MYH3, GPR144, CACNA1E) were associated with patients' lifetime benzo(a)pyrene exposure. This study uncovers the mutation spectrum of air pollution-related lung cancers, and provides evidence for pollution exposure–genomic mutation relationship at a large scale.

Histone deacetylase 9 (HDAC9), a member of class II HDACs, regulates a wide variety of normal and abnormal physiological functions. We found that HDAC9 is over-expressed in prognostically poor glioblastoma patients. Knockdown HDAC9 decreased proliferation in vitro and tumor formation in vivo. HDAC9 accelerated cell cycle in part by potentiating the EGFR signaling pathway. Also, HDAC9 interacted with TAZ, a key downstream effector of Hippo pathway. Knockdown of HDAC9 decreased the expression of TAZ. We found that overexpressed TAZ in HDAC9-knockdown cells abrogated the effects induced by HDAC9 silencing both in vitro and in vivo. We demonstrated that HDAC9 promotes tumor formation of glioblastoma via TAZ-mediated EGFR pathway activation, and provide the evidence for promising target for the treatment of glioblastoma.

A key aspect of VQA models that are interpretable is their ability to ground their answers to relevant regions in the image. Current approaches with this capability rely on supervised learning and human annotated groundings to train attention mechanisms inside the VQA architecture. Unfortunately, obtaining human annotations specific for visual grounding is difficult and expensive. In this work, we demonstrate that we can effectively train a VQA architecture with grounding supervision that can be automatically obtained from available region descriptions and object annotations. We also show that our model trained with this mined supervision generates visual groundings that achieve a higher correlation with respect to manually-annotated groundings, meanwhile achieving state-of-the-art VQA accuracy.

Background Cerebral ischemia-reperfusion injury (CIRI) refers to a secondary brain injury that can occur when the blood supply to the ischemic brain tissue is restored. However, the mechanism underlying such injury remains elusive. Methods The 150 male C57 mice underwent middle cerebral artery occlusion (MCAO) for 1 h and reperfusion for 24 h, Among them, 50 MCAO mice were further treated with Mitochondrial division inhibitor 1 (Mdivi-1) and 50 MCAO mice were further treated with N-acetylcysteine (NAC). SH-SY5Y cells were cultured in a low-glucose culture medium for 4 h under hypoxic conditions and then transferred to normal conditions for 12 h. Then, cerebral blood flow, mitochondrial structure, mitochondrial DNA (mtDNA) copy number, intracellular and mitochondrial reactive oxygen species (ROS), autophagic flux, aggresome and exosome expression profiles, cardiac tissue structure, mitochondrial length and cristae density, mtDNA and ROS content, as well as the expression of Drp1-Ser616/Drp1, RIP1/RIP3, LC3 II/LC3 I, TNF-α, IL-1β, etc., were detected under normal or Drp1 interference conditions. Results The mtDNA content, ROS levels, and Drp1-Ser616/Drp1 were elevated by 2.2, 1.7 and 2.7 times after CIRI (P < 0.05). However, the high cytoplasmic LC3 II/I ratio and increased aggregation of p62 could be reversed by 44% and 88% by Drp1 short hairpin RNA (shRNA) (P < 0.05). The low fluorescence intensity of autophagic flux and the increased phosphorylation of RIP3 induced by CIRI could be attenuated by ROS scavenger, NAC (P < 0.05). RIP1/RIP3 inhibitor Necrostatin-1 (Nec-1) restored 75% to a low LC3 II/LC3 I ratio and enhanced 2 times to a high RFP-LC3 after Drp1 activation (P < 0.05). In addition, although CIRI-induced ROS production caused no considerable accumulation of autophagosomes (P > 0.05), it increased the packaging and extracellular secretion of exosomes containing p62 by 4 – 5 times, which could be decreased by Mdivi-1, Drp1 shRNA, and Nec-1 (P < 0.05). Furthermore, TNF-α and IL-1β increased in CIRI-derived exosomes could increase RIP3 phosphorylation in normal or oxygen–glucose deprivation/reoxygenation (OGD/R) conditions (P < 0.05). Conclusions CIRI activated Drp1 and accelerated the p62-mediated formation of autophagosomes while inhibiting the transition of autophagosomes to autolysosomes via the RIP1/RIP3 pathway activation. Undegraded autophagosomes were secreted extracellularly in the form of exosomes, leading to inflammatory cascades that further damaged mitochondria, resulting in excessive ROS generation and the blockage of autophagosome degradation, triggering a vicious cycle.

We demonstrate a centimeter-scale optomechanical magnetometer based on a crystalline whispering gallery mode resonator. The large size of the resonator allows high magnetic field sensitivity to be achieved in the hertz to kilohertz frequency range. A peak sensitivity of 131 pT Hz −1/2 is reported, in a magnetically unshielded non-cryogenic environment and using optical power levels beneath 100 µW. Femtotesla range sensitivity may be possible in future devices with further optimization of laser noise and the physical structure of the resonator, allowing applications in high-performance magnetometry.