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Objective@#To describe the prevalence and the association of sleep quality trajectory, social jetlag and comorbid symptoms of anxiety and depression among college students, in order to provide a theoretical basis for improving the comorbid symptoms of anxiety and depression in college students.@*Methods@#A questionnaire survey was conducted among 1 135 college students from two universities in Shangrao, Jiangxi Province and Hefei, Anhui Province from April to May 2019, and were followed up once every one year for a total of three times, with a valid sample size of 1 034 individuals after matching with the baseline survey. A selfassessment questionnaire was used to investigate the social jetlag of college students, the Generalized Anxiety Disorder-7 (GAD-7) and Patient Health Questionnaire 9 (PHQ-9) were used to evaluate anxiety and depression symptoms, respectively, while the Pittsburgh Sleep Quality Index (PSQI) was used to assess sleep quality. College students with GAD-7 score ≥5 and PHQ-9 score ≥5 were defined as having comorbid anxiety and depression symptoms. Latent class growth model (LCGM) was employed to analyze the sleep quality trajectory of college students, and binary Logistic regression was used to analyze the relationship between social jetlag, sleep quality trajectory and comorbid symptoms of anxiety and depression.@*Results@#The detection rate of comorbid symptoms of anxiety and depression among college students was 16.9%, and the detection rate of social jetlag ≥2 h was 13.8%. The sleep quality showed an overall improvement trend, and the two trajectories were good sleep quality (81.6%) and poor sleep quality (18.4%). Binary Logistic regression model showed that poor sleep quality and social jetlag ≥2 h were positively correlated with comorbid symptoms of anxiety and depression (OR=5.94, 1.84, P<0.05).@*Conclusions@#Poor sleep quality and social jetlag ≥2 h in college students increase the risk of comorbid symptoms of anxiety and depression. Early screening and intervention of sleep quality and reduction of social jetlag are crucial for enhancing the mental health of college students.
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Background The senescence of alveolar type II epithelial cells is an important driving factor for the progression of silicotic fibrosis, and the regulatory effects of oxamate on the senescence of alveolar type II epithelial cells is still unclear. Objective To explore whether lactate dehydrogenase inhibitor oxamate can alleviate silicotic fibrosis in mice by inhibiting senescence of alveolar type II epithelial cellsMethods This study was divided into two parts: in vivo experiments and in vitro experiments. In the first part, forty SPF C57BL/6J male mice were randomly divided into four groups with 10 in each group: control group, silicosis model group, low-dose oxamate treatment group, and high-dose oxamate treatment group. The silicotic mouse model was established by intratracheal instillation of 50 μL SiO2 suspension (100 mg·mL−1). The treatment models were prepared by intraperitoneal injection of 100 μL oxamate (225 mmol·L−1 and 1125 mmol·L−1). In the second part, induction of MLE-12 mouse alveolar type II epithelial cells was conducted with SiO2. The in vitro experimental groups were ① SiO2 induction groups: control group, 50 μg·mL−1 SiO2 group, 100 μg·mL−1 SiO2 group, and 200 μg·mL−1 SiO2 group, and ② oxamate treatment groups: control group, SiO2 group (100 μg·mL−1), low-dose oxamate (25 mmol·L−1) treatment group, and high-dose oxamate (50 mmol·L−1) treatment group. Pathological morphology of lung tissues was evaluated after hematoxylin-eosin (HE) staining; deposition of collagen in lung tissues was evaluated after sirius red staining; positive co-expression of prosurfactant protein C (Pro-SPC) and β-galactosidase was detected by immunofluorescence staining; positive expression of β-galactosidase in MLE-12 cells was detected by immunofluorescence staining. The protein expression levels of collagen type I (CoL I), fibronectin1 (FN1), hexokinase 2 (HK2), pyruvate kinase isozyme type M2 (PKM2), lactate dehydrogenase A (LDHA), p-ataxia telangiectasia and Rad3-related kinase (ATR), and cyclin-dependent kinase inhibitors p21, and p16 were detected by Western blotting. Results Compared with the control group, the protein expression levels of HK2, PKM2, LDHA, p-ATR, p21, and p16 were significantly upregulated in the silicosis model group and the SiO2-induced MLE-12 cells (P<0.05). The in vivo studies showed that, compared with the control group, the silicon nodule area, the collagen deposition area, the proportion of β-galactosidase positive cells, and the protein expression levels of CoL I, FN1, LDHA, p-ATR, p21, and p16 were significantly upregulated in the silicosis model group (P<0.05). Compared with the silicosis model group, the oxamate treatment groups showed significant downregulation of the silicon nodule area, the collagen deposition area, the proportion of β-galactosidase positive cells, and the the CoL I, FN1, LDHA, p-ATR, p21, and p16 protein expression levels, and the high-dose oxamate treatment group showed a higher efficacy on these indicators than the low-dose oxamate treatment group (P<0.05). The in vitro studies showed that, compared with the control group, the proportion of β-galactosidase positive cells and the protein expression levels of p-ATR, p21, and p16 were significantly upregulated in the SiO2-induced group (P<0.05). Compared with the SiO2 group, the proportion of β-galactosidase positive cells and the LDHA, p-ATR, p21 and p16 protein expression levels were significantly downregulated in the oxamate treatment groups, and the high-dose oxamate treatment group showed a higher efficacy on these indicators than the low-dose oxamate treatment group (P<0.05). Conclusion Lactate dehydrogenase inhibitor oxamate can alleviate silicotic fibrosis in mice by inhibiting the senescence of alveolar type II epithelial cells.
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Background Pneumoconiosis is the most serious occupational disease in China, and silicosis accounts for about half of it. Any intervention effect of physical exercise as the key and core of lung rehabilitation training on silicosis is still unclear. Objective To explore potential intervention effect of physical exercise on silicotic mice. Methods Forty SPF C57BL/6 male mice were randomly divided into four groups, 10 in each group, including a control group, a physical exercise group, a silicosis model group, and a silicosis model + physical exercise intervention group. Silicotic mouse model was established by using 50 μL SiO2 suspension (200 mg·mL−1). A treadmill was used to prepare mice receiving physical exercise at 0° inclination, 12.3 m·min−1, 60 min·d−1, 5 d·week−1 for 4 weeks. Pathological morphology of lung tissues was evaluated after hematoxylin-eosin (HE) staining; deposition of collagen in lung tissues was evaluated after Van Gieson (VG) staining; expression of p-protein kinase R-like endoplasmic reticulum kinase (PERK) was detected by immunofluorescence staining; expressions of cyclin dependent kinase inhibitors (p21) and p-p38 mitogen activated protein kinase (p38) were detected by immunohistochemistry. The protein expressions of endoplasmic reticulum stress signal factors [p-inositol-requiring enzyme-1α (p-IRE-1α), p-PERK, and p-eukaryotic initiation factor-2α (p-eIF-2α)], senescence signal factors (p-p53, p21, and p16), mitogen-activated protein kinase (MAPK) signal factors [p-p38, p-extracellular regulated protein kinases (p-ERK), and p-stress-activated protein kinase (p-JNK)] were detected by Western blotting. Results After designed acute SiO2 exposure, the images of micro computed tomography (CT) showed high density shadows in lung tissues of the silicotic mice and less shadows in lung tissues of the physical exercise intervention mice. After HE staining, the proportions of silicotic nodule area in lung tissues was (18.67±3.89) % in the silicosis model group, and significantly decreased to (8.78±1.05) % in the silicosis model + physical exercise intervention group (P<0.05). After VG staining, the proportion of collagen fiber area of lung tissues was (10.37±2.18) % in the silicosis model group, and significantly decreased to (4.35±0.89) % in the silicosis model + physical exercise intervention group (P<0.05). The results of immunofluorescence staining showed that in the silicosis model group, the expression of p-PERK increased at the location of silicotic nodules, while in the silicotic model + physical exercise intervention group, the expression of p-PERK decreased. The immunohistochemical staining results showed that the expression of p21 and p-p38 increased in the lung tissues of the silicosis model group; the expression of p21 and p-p38 decreased in the lung tissues of the silicosis model + physical exercise intervention group. The results of Western blotting showed that compared with the control group, the expression levels of p-IRE-1α (0.11±0.03), p-PERK (0.95±0.40), p-eIF-2α (3.53±0.91), p-p53 (1.78±0.07), p21 (1.98±0.10), p16 (1.26±0.17), p-p38 (0.41±0.09), p-ERK (0.42±0.05), and p-JNK (3.20±1.23) of the silicosis model group were all upregulated (P<0.05). Compared with the silicosis model group, the expression levels of p-IRE-1α (0.03±0.01), p-PERK (0.31±0.12), p-eIF-2α (0.30±0.06), p-p53 (0.76±0.08), p21 (0.18±0.11), p16 (0.70±0.24), p-p38 (0.03±0.00), p-ERK (0.19±0.03), and p-JNK (0.46±0.21) of the silicosis model + physical exercise intervention group were downregulated (P<0.05). Conclusion Physical exercise may alleviate pulmonary fibrosis in silicotic mice, and inhibit abnormal expressions of endoplasmic reticulum stress signal, MAPK signal, and senescent signal.
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Cognitive impairment can be attributed to various causes.Its main manifestations include declines in learning, memory, understanding and executive function, and may be accompanied by varying degrees of psychiatric symptoms.Dementia is characterized by progressive deterioration in multiple cognitive domains that is severe enough to interfere with daily functioning.The pathogenesis of dementia is still unclear.In addition to the mainstream Aβ amyloid cascade hypothesis, recent research increasingly points to an association of microbial dysbiosis with many brain disorders.There is a direct or indirect link between gut bacteria and the central nervous system and consequently a new concept, the gut-brain axis, has been proposed.This paper will review recent advances in research on gut microbiota and cognitive function in the past five years, aiming to provide strategies for disease prevention and treatment.
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Trichoderma spp. is a kind of filamentous fungi with important biocontrol value. Twelve strains of Trichoderma spp. were isolated from the soils of different types of crops in Shaoxing, Zhejiang and Foshan, Guangdong. The antagonistic resistance to Fusarium oxysporum was compared by plate confrontation test. The further analysis of volatile secondary metabolites for two strains were carried out using HS-SPME-GC-MS analysis. The results showed that T. asperellum ZJSX5003 and GDFS1009 had fast growth ability, and the inhibition effects on F. oxysporum were 73% and 74% respectively. Six identical volatile metabolites were detected as follows 2-Methyl-1-propanol, 3-Methyl-1-butanol, 3-Methyl-3-buten-1-ol, Acetyl methyl carbinol, Butane-2,3-diol and 6-n-pentyl-2H-pyran-2-one (6-PAP). Among them, 6-PAP was validated to have a higher inhibitory effect on F. oxysporum in vitro. This study will provide basis for the development of biocontrol agents with metabolites of Trichoderma, such as 6-PAP.
Subject(s)
Antibiosis , Antifungal Agents , Pharmacology , Fusarium , Physiology , Gas Chromatography-Mass Spectrometry , Trichoderma , Chemistry , MetabolismABSTRACT
To study the functional mechanism of thioredoxin-interacting protein (TXNIP) in delaying Alzheimer's disease (AD) by estrogen. Methods: After estradiol (E2) treatment in Aβ-induced AD cell model, reactive oxygen species (ROS), TXNIP, and apoptosis levels were detected. After lentiviral infection with TXNIP overexpression, the effect of E2 on ROS and apoptosis were observed. In the AD rat model, the learning and memory ability and the expression of TXNIP in the hippocampus were observed in the presence of E2. After overexpressing TXNIP, the effect of E2 on the learning and memory ability of AD rat model was observed. Results: ROS, TXNIP and apoptosis levels were enhanced in AD cell model, while E2 treatment reduced ROS, TXNIP and apoptosis levels in AD cell model. After enhancing TXNIP, E2 treatment reduced ROS and apoptosis levels in AD cell model. Similar to the cell experiment, E2 enhanced the learning and memory ability in the AD rat model and inhibited the expression of TXNIP in brain, while TXNIP overexpression attenuated the effect of E2 on learning and memory ability in the AD rats. Conclusion: Estrogen can inhibit the expression of TXNIP in nerve tissue, reduce nerve damage, and delay the development of AD.
Subject(s)
Animals , Rats , Alzheimer Disease , Carrier Proteins , Cell Cycle Proteins , Estrogens , Hippocampus , Oxidative Stress , Reactive Oxygen SpeciesABSTRACT
OBJECTIVE: To observe the clinical efficacy of Jianpi shoushen decoction in the treatment of cases of impaired glucose tolerance with Qi deficiency and phlegm-dampness constitution. METHODS:62 Patients with impaired glucose tolerance with Qi deficiency and phlegm-dampness constitution were randomized into 2 groups, i.e. trial group were treated with Jianpi shoushen decoction q.d for 3months (p.o.,n=31); control group were treated with 50 mg Acarbose tablet t.i.d for 3 months (p.o.,n=31). Patients in two groups were all received healthy education such as diet guide and sport instruction. The effective rate, glycemic index and weight index of two groups were observed. RESULTS: The rate of hypoglycemic efficacy and weight lose efficacy in trial group were better than in control group(P