Surviving the shift: College student satisfaction with emergency online learning during COVID-19 pandemic.

BACKGROUND: The coronavirus disease 2019 (COVID-19) epidemic disrupted education systems by forcing systems to shift to emergency online leaning. Online learning satisfaction affects academic achievement. Many factors affect online learning satisfaction. However there is little study focused on personal characteristics, mental status, and coping style when college students participated in emergency online courses. AIM: To assess factors related to satisfaction with emergency online learning among college students in Hebei province during the COVID-19 pandemic. METHODS: We conducted a cross-sectional survey of 1600 college students. The collected information included demographics, psychological aspects of emergent public health events, and coping style. Single factor, correlation, and multiple linear regression analyses were performed to identify factors that affected online learning satisfaction. RESULTS: Descriptive findings indicated that 62.9% (994/1580) of students were satisfied with online learning. Factors that had significant positive effects on online learning satisfaction were online learning at scheduled times, strong exercise intensity, good health, regular schedule, focusing on the epidemic less than one hour a day, and maintaining emotional stability. Positive coping styles were protective factors of online learning satisfaction. Risk factors for poor satisfaction were depression, neurasthenia, and negative coping style. CONCLUSION: College students with different personal characteristics, mental status, and coping style exhibited different degrees of online learning satisfaction. Our findings provide reference for educators, psychologists, and school administrators to conduct health education intervention of college students during emergency online learning.

Expression of CYP76C6 Facilitates Isoproturon Metabolism and Detoxification in Rice.

Agricultural chemical residues in farmland and crops is one of the serious public issues that constantly threatens crop production, food security, and human health. Understanding their decay mechanism in crops for accelerating their degradative metabolism is important. In this study, a rice uncharacterized cytochrome P450 gene encoding CYP76C6 was functionally identified in rice exposed to isoproturon (IPU). To verify the role of CYP76C6 in rice resistance to IPU toxicity, CYP76C6 overexpression (OEs) and knockout mutant rice by CRISPR/Cas9 were generated through genetic transformation and gene-editing technologies. Assessment of growth and physiological responses revealed that the growth of OE lines was improved, the IPU-induced cellular damage was attenuated, and IPU accumulation was significantly repressed, whereas the Cas9 lines displayed a contrasting phenotype compared to the wild-type. Both relative contents of IPU metabolites and conjugates in OE lines were reduced and those in Cas9 line were increased, suggesting that CYP76C6 plays a critical role in IPU degradation. Our study unveils a new regulator, together with its mechanism for IPU decay in rice crops, which will be used in reality to reduce environmental risks in food safety and human health.

Identification of a novel function of a component in the jasmonate signaling pathway for intensive pesticide degradation in rice and environment through an epigenetic mechanism.

Developing a biotechnical system with rapid degradation of pesticide is critical for reducing environmental, food security and health risks. Here, we investigated a novel epigenetic mechanism responsible for the degradation of the pesticide atrazine (ATZ) in rice crops mediated by the key component CORONATINE INSENSITIVE 1a (OsCOI1a) in the jasmonate-signaling pathway. OsCOI1a protein was localized to the nucleus and strongly induced by ATZ exposure. Overexpression of OsCOI1a (OE) significantly conferred resistance to ATZ toxicity, leading to the improved growth and reduced ATZ accumulation (particularly in grains) in rice crops. HPLC/Q-TOF-MS/MS analysis revealed increased ATZ-degraded products in the OE plants, suggesting the occurrence of vigorous ATZ catabolism. Bisulfite-sequencing and chromatin immunoprecipitation assays showed that ATZ exposure drastically reduced DNA methylation at CpG context and histone H3K9me2 marks in the upstream of OsCOI1a. The causal relationships between the DNA demethylation (hypomethylatioin), OsCOI1a expression and subsequent detoxification and degradation of ATZ in rice and environment were well established by several lines of biological, genetic and chemical evidence. Our work uncovered a novel regulatory mechanism implicated in the defense linked to the epigenetic modification and jasmonate signaling pathway. It also provided a modus operandi that can be used for metabolic engineering of rice to minimize amounts of ATZ in the crop and environment.

Comprehensive analyses of degradative enzymes associated with mesotrione-degraded process in rice for declining environmental risks.

Mesotrione (MTR) is a highly effective pesticide widely used for weeding in farmland. Overload of MTR in agricultural soils may result in environmental problems. To evaluate the potential contamination of MTR in environments, a better understanding of the MTR degradation process and mechanisms in crops is required. This study investigated the impact of MTR on growth and toxicological responses in rice (Oryza sativa). The growth of rice tissues was significantly compromised with increasing MTR concentrations. RNA-sequencing combined with HRLC-Q-TOF-MS/MS analysis identified many transcriptional components responsible for MTR degradation. Four libraries composed of root and shoot tissues exposed to MTR were RNA-sequenced in biological triplicate. Compared to -MTR, treatment with environmentally realistic MTR concentration upregulated 1995 genes in roots and 326 genes in shoots. Gene enrichment revealed many MTR-degradative enzymes functioning in resistance to environmental stress and molecular metabolism of xenobiotics. Specifically, many differentially expressed genes are critical enzymes like cytochrome P450, glycosyltransferases, methyltransferase, glutathione S-transferases and acetyltransferase involved in the process. To evidence MTR degradative metabolisms, HRLC-Q-TOF-MS/MS was used to characterize eight metabolites and five conjugates in the pathways involving hydrolysis, reduction, glycosylation, methylation or acetylation. The precise association between the specific MTR-degraded products and enhanced activities of its corresponding enzymes was established. This study advanced our understanding of the detailed MTR degradative mechanisms and pathways, which may help engineer genotypes to facilitate MTR degradation in the paddy crop.

A Comparison of Intracerebral Transplantation of RMNE6 Cells and MSCs on Ischemic Stroke Models.

BACKGROUND: Cell therapy using stem cells is promising for stroke patients; however, stem cell therapy faces many problems. RMNE6 cells, a new stem cell line, are superior to other stem cell lines. Mesenchymal stem cells (MSCs) appear to be a promising candidate for stroke patients. In the current study, we determined the therapeutic effects of RMNE6 cells on a middle cerebral artery occlusion (MCAO) model of rats and identified the differences between RMNE6 cells and MSCs with respect to therapeutic effects. MATERIAL AND METHODS: RMNE6 and Enhanced green fluorescent protein (EGFP)-labeled MSCs were transplanted into the ischemic brains of MCAO rats. The behavior of rats was examined using the rotarod test with neuroradiologic assessment using magnetic resonance imaging (MRI). Four weeks after cell transplantation, the rats were investigated by immunofluorescence staining to explore the fates of the graft cells. RESULT: After transplantation, RMNE6 cells and MSCs survived and migrated toward the injured area without differentiation. There was tumorigenesis in the brains transplanted with RMNE6 cells. Cell transplantation had no effects on the size of the ischemic volume. The behavior of the model animals showed no significant improvement. CONCLUSION: MSCs are still the preferred cells for cell replacement in stroke therapy, while RMNE6 cells need to be modified.

Effect of neuron-derived neurotrophic factor on rejuvenation of human adipose-derived stem cells for cardiac repair after myocardial infarction.

The decline of cell function caused by ageing directly impacts the therapeutic effects of autologous stem cell transplantation for heart repair. The aim of this study was to investigate whether overexpression of neuron-derived neurotrophic factor (NDNF) can rejuvenate the adipose-derived stem cells in the elderly and such rejuvenated stem cells can be used for cardiac repair. Human adipose-derived stem cells (hADSCs) were obtained from donors age ranged from 17 to 92 years old. The effects of age on the biological characteristics of hADSCs and the expression of ageing-related genes were investigated. The effects of transplantation of NDNF over-expression stem cells on heart repair after myocardial infarction (MI) in adult mice were investigated. The proliferation, migration, adipogenic and osteogenic differentiation of hADSCs inversely correlated with age. The mRNA and protein levels of NDNF were significantly decreased in old (>60 years old) compared to young hADSCs (<40 years old). Overexpression of NDNF in old hADSCs significantly improved their proliferation and migration capacity in vitro. Transplantation of NDNF-overexpressing old hADSCs preserved cardiac function through promoting angiogenesis on MI mice. NDNF rejuvenated the cellular function of aged hADSCs. Implantation of NDNF-rejuvenated hADSCs improved angiogenesis and cardiac function in infarcted mouse hearts.

Uptake of atrazine in a paddy crop activates an epigenetic mechanism for degrading the pesticide in plants and environment.

There is a rising public concern on accumulation of harmful pesticides in environment and crops. Epigenetic alteration caused by environmental contaminants is one of the key factors in the etiology of environmentally-associated diseases. Growing evidence shows that harmful pesticide atrazine (ATZ) has a profound effect on DNA methylation in human genome, however, little is known about the epigenetic mechanism underlying ATZ accumulation and degradation in plants, particularly in edible plants growing in the ATZ-contaminated areas. This study investigated the atrazine elimination that was mediated by DNA methylation and histone modification in the food crop rice. Studies with two mutant Osmet1-1/2 defective in the genomic CG DNA methylation show significantly lower accumulation of atrazine than its wild-types. Profiling methylome and transcriptome of ATZ-exposed Osmet1 and wild-type identified many differentially methylated loci (≥2 fold change, p < 0.05), which were associated with activation of genes responsible for atrazine degradation in plants. Three demethylated loci OsGTF, OsHPL1 and OsGLH were expressed in eukaryotic yeast cells and found to eliminate a marked proportion of ATZ in growth environments by 48%, 43% and 32%, respectively, whereas the increased ATZ-degraded products were characterized using UPLC/Q-TOF-MS/MS. These results suggest that activation of the loci mediated by ATZ-induced hypomethylation could be responsible for the removal of ATZ in rice. Our work helps understand a new regulatory mechanism underlying the atrazine degradation in crops which may potentially reduce the environmental risks to human health through food chain.

Aged Human Multipotent Mesenchymal Stromal Cells Can Be Rejuvenated by Neuron-Derived Neurotrophic Factor and Improve Heart Function After Injury.

Reduced regenerative capacity of aged stem cells hampers the benefits of autologous cell therapy for cardiac regeneration. This study investigated whether neuron-derived neurotrophic factor (NDNF) could rejuvenate aged human bone marrow (hBM)- multipotent mesenchymal stromal cells (MSCs) and whether the rejuvenated hBM-MSCs could improve cardiac repair after ischemic injury. Over-expression of NDNF in old hBM-MSCs decreased cell senescence and apoptosis. Engraftment of NDNF over-expressing old hBM-MSCs into the ischemic area of mouse hearts resulted in improved cardiac function after myocardial infarction, while promoting implanted stem cell survival. Our findings suggest NDNF could be a new factor to rejuvenate aged stem cells and improve their capability to repair the aged heart after injury.

Knockdown of SIRT6 Enables Human Bone Marrow Mesenchymal Stem Cell Senescence.

Autologous bone marrow mesenchymal stem cell (BM-MSC) transplantation is a novel strategy for treating ischemic heart disease. However, limited benefits have been reported in aging patients. Rejuvenation of aged human BM-MSCs (hBM-MSCs) could be a means to improve the efficacy of stem cell transplantation in older patients. While it has been shown that sirtuin 6 (SIRT6) is an important antiaging factor in various cells, the role of SIRT6 in hBM-MSCs remains unknown. The hBM-MSCs from different ages were cultured for quantifying SIRT6 expression by mRNA and Western blotting. The cell proliferative and migration abilities were evaluated by BrdU staining, cell growth curves, and scratch assay. Senescence-associated ß-galactosidase (SA-ß-Gal) activity and aging-associated p16 (cyclin-dependent kinase inhibitor 2A) expression were also quantified. The knockdown of SIRT6 in hBM-MSCs was used to investigate its impact on aging. SIRT6 expression increased with age, while the proliferative and migration abilities of aged hBM-MSCs were decreased compared with young cells. Knockdown of SIRT6 impaired the proliferative, migration, and oxidative stress resistance potentials of BM-MSCs. SA-ß-Gal activity and p16 expression were increased in aged cells compared with young ones and in siRNA SIRT6 knockdown cells compared with their controls. Aging results in compensatory overexpression of SIRT6 in hBM-MSCs. Downregulation of SIRT6 in these cells resulted in less cell proliferation and migration but increased SA-ß-Gal activity and p16 expression. These results suggest that SIRT6 regulates the aging process in hBM-MSCs and could serve as a target for their rejuvenation.