Depression and anxiety of medical students at Kunming Medical University during COVID-19: A cross-sectional survey.

An isolation strategy was used to control the transmission and rapid spread of COVID-19 in Yunnan. As a result, students were supposed to stay at home and disrupted their outside activities. It led to a detrimental influence on students' mental health. The purpose of this study was to investigate the prevalence and risk factors of depression and anxiety among medical students and to provide ideas for the prevention of depression and anxiety in medical students. A cross-sectional survey was conducted among 2,116 medical students at Kunming Medical University from July 8 to July 16, 2020. Participants' demographic and living conditions were collected. Depression and anxiety were measured using the Patient Health Questionnaire 9 and General Anxiety Disorder-7, respectively. Uni- and multivariate logistic regression analyses were performed to detect risk factors associated with depression and anxiety. The prevalence rates of depression and anxiety among medical students were 52.5 and 29.6%, respectively. Depression was more likely to be caused by low grades, lack of physical exercise, drug use, irregular diet, extensive screen time on mobile phones, being greatly affected by the COVID-19 pandemic, and inadaptability to offline courses. Anxiety was more likely to be caused by lack of physical exercise, drug use, irregular diet, and inadaptability to offline courses. Depression and anxiety are highly comorbid. Our study showed predictive factors for depression and anxiety and identified a major mental health burden on medical students during the COVID-19 outbreak. More targeted measures should be taken to improve the mental state of students to reduce the incidence of depression and anxiety.

Deletion of YJL218W reduces salt tolerance of Saccharomyces cerevisiae.

The YJL218W open reading frame may be involved in peroxisomal biogenesis. However, whether it mediates salt tolerance is unclear. We found that after knockdown of YJL218W in Saccharomyces cerevisiae (S. cerevisiae), its salt tolerance was reduced and cell death was increased. Transcriptome sequencing and analysis further revealed that YJL218W knockdown mediated significant changes in the expression of 1432 messenger RNA (mRNAs), of which 603 were upregulated. KEGG enrichment analysis and polymerase chain reaction (PCR) assay indicated that YJL218W mediated the regulation of peroxisome-related genes. Therefore, YJL218W may regulate salt stress in S. cerevisiae by regulating peroxisome assembly.

Transcriptome Analysis Reveals that MAPK Signaling Pathway Mediates Salt Tolerance of YMR253C ORF in Saccharomyces cerevisiae.

The YMR253C open reading frame encodes a membrane protein that is highly expressed in NaCl-resistant Saccharomyces cerevisiae mutants. Whether it mediates NaCl tolerance is unclear. By knocking out YMR253C in S. cerevisiae, we found that the salt tolerance of yeast was reduced, the integrity of the cell wall was impaired, and cell death was induced; transcriptome analysis further revealed that YMR253C gene knockout mediates significant changes of 1291 genes, and YMR253C mediates the regulation of MAPK signal pathways. Therefore, the transmembrane protein YMR253C may regulate the MAPK signaling pathway to regulate the salt stress of S. cerevisiae.

The Ubiquitin Proteasome System and Skin Fibrosis.

The ubiquitin proteasome system (UPS) is a highly conserved way to regulate protein turnover in cells. The UPS hydrolyzes and destroys variant or misfolded proteins and finely regulates proteins involved in differentiation, apoptosis, and other biological processes. This system is a key regulatory factor in the proliferation, differentiation, and collagen secretion of skin fibroblasts. E3 ubiquitin protein ligases Parkin and NEDD4 regulate multiple signaling pathways in keloid. Tumor necrosis factor (TNF) receptor-associated factor 4 (TRAF4) binding with deubiquitinase USP10 can induce p53 destabilization and promote keloid-derived fibroblast proliferation. The UPS participates in the occurrence and development of hypertrophic scars by regulating the transforming growth factor (TGF)-ß/Smad signaling pathway. An initial study suggests that TNFα-induced protein 3 (TNFAIP3) polymorphisms may be significantly associated with scleroderma susceptibility in individuals of Caucasian descent. Sumoylation and multiple ubiquitin ligases, including Smurfs, UFD2, and KLHL42, play vital roles in scleroderma by targeting the TGF-ß/Smad signaling pathway. In the future, drugs targeting E3 ligases and deubiquitinating enzymes have great potential for the treatment of skin fibrosis.

Ginsenoside Rb1 exerts antidepressant-like effects via suppression inflammation and activation of AKT pathway.

Depression-like behaviors caused by chronic stress are related to inflammation and microglia activation. Antidepressant therapy may contribute to inhibiting inflammation responses and microglia activation. Ginsenoside Rb1 (GRb1) is known to display antidepressant-like effect on chronic unpredictable mild stress-induced depressive rats. However, the antidepressant-like effects of GRb1 on chronic restraint stress (CRS) mice and the potential anti-inflammatory mechanisms are unclear. Here, we focused on the molecular mechanisms related to inhibition of inflammation response and the protection on microglia. Our results showed that GRb1 had an antidepressant effects via relieving the depression-like behaviors in CRS model. Furthermore, GRb1 increased the protein expressions of brain-derived neurotrophic factor and phospho- protein kinase B/ protein kinase B (p-AKT/AKT), and decreased the protein expressions of interleukin-1ß (IL-1ß), tumor necrosis factor α (TNF-α) and ionized calcium binding adapter molecule 1 in hippocampus, reduced the levels IL-1ß and TNF-α in serum. Finally, GRb1 lowered the protein expressions of IL-1ß and TNF-α in BV-2 microglia induced by lipopolysaccharides. Taken together, the results indicate that GRb1 prevents CRS-induced depression-like behaviors in mice, which may be related to anti-inflammatory effects in hippocampus, serum and microglia and activation of AKT pathway.

Depressive Symptoms, Sleep Quality and Diet During the 2019 Novel Coronavirus Epidemic in China: A Survey of Medical Students.

The psychological condition of medical students may be influenced by the 2019 novel coronavirus (COVID-19) outbreak. This study investigated the prevalence and influencing factors of depressive symptoms, poor sleep quality and poor diet in students at Kunming Medical University during the early part of the COVID-19 outbreak. A cross-sectional study was used from a questionnaire survey in February 2020. Of a total of 1,026 study participants, the prevalence of depressive symptoms, poor sleep quality, and poor diet was, respectively, 22.4, 33.2, and 17.4%. Male students and students with a low degree of focus on COVID-19 had a high risk of depressive symptoms. A high percentage of females and students in the fifth grade, as well as students with high levels of concern about the negative impact of COVID-19 on their education or employment, comprised those with poor sleep quality. Students in the fifth grade and students with high levels of concern about the negative impact of COVID-19 on their education or employment were more likely to report poor diet. This study suggests the importance of monitoring medical students' depressive state during the COVID-19 outbreak, and universities are encouraged to institute policies and programs to provide educational counseling and psychological support to help students to cope with these problems.

Panax notoginsenoside Rb1 Restores the Neurotrophic Imbalance Following Photothrombotic Stroke in Rats.

Mature brain-derived neurotrophic factor (mBDNF) has neuroprotection in cerebral ischemia. Conversely, the precursor of brain-derived neurotrophic factor (proBDNF) has the opposite function to its mature form, inducing apoptosis. However, whether the neuroprotection of Panax notoginsenoside Rb1 (PNS-Rb1) on ischemic stroke is due to, at least partially, its modulation of suppressing proBDNF/P75NTR/sortilin or upregulation of mBDNF is not clear. To test this hypothesis, rats induced by photothrombotic stroke were treated with PNS-Rb1 100 mg/kg or nimodipine 1 mg/kg twice a day until 3, 7, and 14 days. Our data indicate that PNS-Rb1 significantly reduced cerebral infarction rate, proBDNF/P75NTR/sortilin, and plasminogen activator inhibitor-1 (PAI-1) protein levels, and improved sensorimotor dysfunctions induced by ischemic stroke, upregulation of BDNF/TrkB levels, and its processing enzymes (tissue plasminogen activator, tPA) in a time-dependent manner. Taken together, our findings indicate that the improvement of sensorimotor dysfunctions by PNS-Rb1 following ischemic stroke is made, at least partially, by activating the BDNF/TrkB and inhibiting proBDNF/sortilin/P75NTR.

[Relationship between cytoplasmic phospholipase A2 and nuclear factor κB in one lung ventilation-induced lung injury in rabbits].

OBJECTIVE: To elucidate the mechanisms of up regulated expression of cytoplasmic phospholipase A2 (CPLA2) induced by one lung ventilation (OLV) by investigating the interactions between nuclear factor kappaB (NF-κB) and C-PLA2. METHODS: Forty-eight healthy Japanese white rabbits were randomized into control group, solvent treatment group (group S), NF-κB inhibitor (PDTC)/solvent treatment group ( group PS), C-PLA2 inhibitor (AACOCF3)/solvent treatment group (group AS), OLV group (group O), solvent treatment plus OLV group (SO group), NFκB inhibitor (PDTC)/solvent treatment plus OLV group (group PSO) and CPLA2 inhibitor (AACOCF3)/solvent treatment plus OLV group (group ASO). ELISA was used to detect arachidonic acid (AA) content in the lung tissues, and NFκB and CPLA2 expressions were detected by Western blotting and quantitative PCR. Lung injuries were assessed based on the lung histological score, and the polymorphonuclear leukocyte count in the bronchial alveolar lavage fluid, myeloperoxidase (MPO) content in the lung tissues, and lung wet/dry weight (W/D) raito were determined. RESULTS: Treatment of the rabbits with the solvent did not produce any adverse effects. OLV caused obvious lung injury in the rabbits and up regulated the expressions of CPLA2 and NFκB in the lung tissues (P<0.05). In rabbits without OLV, treatment with AACOCF3 or PDTC significantly down regulated both CPLA2 and NFκB expressions without affecting the other parameters. In rabbits with OLV, treatment with AACOCF3 or PDTC obviously lowered CPLA2 and NFκB expressions and lessened the OLV-induced lung injuries. CONCLUSION: Both C-PLA2 and NF-κB play important roles and show interactions in OLV-induced lung injury in rabbits.

Effects of delaying transplanting on agronomic traits and grain yield of rice under mechanical transplantation pattern.

A delay in the mechanical transplantation (MT) of rice seedlings frequently occurs in Huanghuai wheat-rice rotation cropping districts of China, due to the late harvest of wheat, the poor weather conditions and the insufficiency of transplanters, missing the optimum transplanting time and causing seedlings to age. To identify how delaying transplanting rice affects the agronomic characteristics including the growth duration, photosynthetic productivity and dry matter remobilization efficiency and the grain yield under mechanical transplanting pattern, an experiment with a split-plot design was conducted over two consecutive years. The main plot includes two types of cultivation: mechanical transplanting and artificial transplanting (AT). The subplot comprises four japonica rice cultivars. The results indicate that the rice jointing, booting, heading and maturity stages were postponed under MT when using AT as a control. The tiller occurrence number, dry matter weight per tiller, accumulative dry matter for the population, leaf area index, crop growth rate, photosynthetic potential, and dry matter remobilization efficiency of the leaf under MT significantly decreased compared to those under AT. In contrast, the reduction rate of the leaf area during the heading-maturity stage was markedly enhanced under MT. The numbers of effective panicles and filled grains per panicle and the grain yield significantly decreased under MT. A significant correlation was observed between the dry matter production, remobilization and distribution characteristics and the grain yield. We infer that, as with rice from old seedlings, the decrease in the tiller occurrence, the photosynthetic productivity and the assimilate remobilization efficiency may be important agronomic traits that are responsible for the reduced grain yield under MT.

The null polymorphism of the GSTM1/T1 gene is not associated with susceptibility to systemic lupus erythematosus: a meta-analysis.

Previous studies have suggested that the null polymorphism of the glutathione S-transferases M1/T1 (GSTM1/T1) gene may be associated with the risk of developing systemic lupus erythematosus (SLE). We further explored this potential association using a meta-analysis. A systematic literature search was carried out in the scientific literature databases and we used odds ratios (OR) and 95 % confidence intervals (CIs) to evaluate the strength of this association. All statistical analyses were calculated using Stata software 11.0, and Bonferroni correction was used to adjust the p values. Nine eligible articles with 1,850 patients and 2,826 controls were identified. Our results showed the null polymorphism of the GSTM1 gene was associated with SLE in East Asians (OR 1.32, 95 % CI 1.04-1.69, p = 0.024), but not in Europeans and Africans. However, when Bonferroni corrections were applied (p = 0.05/2 = 0.025), we could not be sure of this association. We further analysed the associations between the GSTT1 gene null polymorphism and the risk of SLE. The results of this investigation showed that this null polymorphism was not associated with susceptibility to SLE in all included populations. In conclusion, the null polymorphism of GSTM1/T1 gene may not be associated with the risk of SLE. More studies are needed to confirm this lack of association between key oxidative defense genes and susceptibility to SLE in the future.