The mutual overlapping impact of stress and infection on mental health problems in adolescents and youths during and after COVID-19 pandemic in China.

BACKGROUND: It is unclear about the mutual impact of COVID-19 related psychological stress and infection on mental health of adolescent and youth students. This study aimed to explore the mutual impact of COVID-19 related psychological stress and infection on mental health problems among students. METHODS: This study was conducted from December 14, 2022 to February 28, 2023 in Sichuan, China. Patient Health Questionnaire-9, Generalized Anxiety Disorder-7, PTSD Checklist for DSM-5, Insomnia Severity Index, and Internet Addiction Test were used. Participants were grouped by COVID-19 infection and psychological stress level. The differences among groups were compared, and logistic regression analysis was used to investigate risk factors for depression, anxiety, PTSD and insomnia among groups. RESULTS: Of 90,118 participants, 82,873 (92.0 %) finished the questionnaires and were included in the study. Of 82,873 participants, 33,314 (40.2 %) reported to be infected with COVID-19. Participants had depression symptoms (38.1 %), anxiety symptoms (31.8 %), PTSD (33.9 %), insomnia (34.0 %), and internet addiction (60.3 %). Compared with participants uninfected with low psychological stress level, the risk for symptoms of depression, anxiety, PTSD and insomnia increased by 9.6 %, 12.3 %, 6.6 %, and 12.0 % in participants infected with low psychological stress level (p < 0.001), 106.8 %, 125.9 %, 125.2 %, and 95.7 % in participants uninfected with high psychological stress level (p < 0.001), and 147.3 %, 161.1 %, 158.7 %, and 141.0 % in participants infected with high psychological stress level (p < 0.001). LIMITATION: This study is a cross-sectional design, and no causal associations should be inferred. Infection status was based on self-report of participants with infectious symptoms. CONCLUSION: COVID-19 related psychological stress and infection per se have mutually overlapping impacts on mental health problems among students. Further health policies and psychosocial interventions should be developed to reduce mutually overlapping impact and improve the long-term mental health among students.

Long Noncoding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 Promotes the Osteoblast Differentiation of Human Bone Marrow-Derived Mesenchymal Stem Cells by Targeting the microRNA-96/Osterix Axis.

OBJECTIVES: To investigate whether and how the long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) sponges microRNA-96 (miR-96) to achieve the osteogenic differentiation of human bone marrow-derived mesenchymal stem cells (hBMSCs). METHODS: Protein levels were detected by Western blot. Mineralized bone matrix formation was studied by alizarin red staining. Metastasis-associated lung adenocarcinoma transcript 1, miR-96, and osteogenesis-related Messenger RNA expression was assessed by Quantitative Real-time Polymerase Chain Reaction (qRT-PCR). The interactions between miR-96 and osterix (Osx), MALAT1, and miR-96 were determined by luciferase reporter assay. RESULTS: The expression of MALAT1 was upregulated whereas that of miR-96 was downregulated in osteogenic hBMSCs. In addition, the expression of MALAT1 significantly decreased whereas that of miR-96 increased in the hBMSCs of osteoporosis (OP) patients. qRT-PCR and alizarin red staining assays showed that MALAT1 silencing or miR-96 overexpression inhibits hBMSC osteogenic differentiation and vice versa. overexpression of miR-96 reversed the promotive effect of MALAT1 on the osteogenic differentiation of hBMSCs. Dual luciferase report assay verified that miR-96 is a regulatory target of MALAT1 and that Osx is a gene target of miR-96. CONCLUSIONS: Taken together, the results demonstrate that MALAT1 promotes the osteogenic differentiation of hBMSCs by regulating the miR-96/Osx axis. Our study provides novel mechanistic insights into the critical role of lncRNA MALAT1 as a microRNA sponge in OP patients and sheds new light on lncRNA-directed diagnostics and therapeutics in OP.

MicroRNA­16/VEGFR2/p38/NF­κB signaling pathway regulates cell growth of human pituitary neoplasms.

The association of microRNA (miRNA) with tumor has gradually become an active medical research field, since its discovery in 1993. The aim of the present study was to clarify how microRNA­16 expression affects the proliferation and survival of pituitary tumor, revealing its potential mechanism. MicroRNA­16 expression of pituitary tumor patients was observably declined, compared with the normal group. A high expression of microRNA­16 showed longer survival in pituitary tumor patients, compared to a low expression of microRNA­16 in pituitary tumor patients. MicroRNA­16 upregulation effectively decreased cell proliferation and induced apoptosis in HP75 cells. MicroRNA­16 overexpression effectively induced p27, Bax protein expression and caspase­3/8 activities, and suppressed phosphorylation-(p)-p38, NF­κB, MMP­9 and VEGFR2 protein expression in HP75 cells. After VEGFR2 suppression, the effects of microRNA­16 overexpression on cell proliferation and apoptosis were significantly inhibited in HP75 cells. Moreover, the effects of microRNA­16 overexpression on p27, Bax protein expression and caspase­3/8 activities were significantly decreased in HP75 cells after p38 suppression. VEGFR2 or NF­κB suppression reduced the effects of microRNA­16 overexpression on p­p38, NF­κB, MMP­9 and VEGFR2 protein expression inhibition in HP75 cells. Our results suggest that microRNA­16 expression affects the proliferation and angiogenesis of pituitary cancer through the VEGFR2/p38/NF­κB signaling pathway.

CCNG2 suppressor biological effects on thyroid cancer cell through promotion of CDK2 degradation.

This study aimed to analyze the expression and clinical significance of cyclin G2 (CCNG2) in thyroid carcinoma and the biological effects of CCNG2 overexpression in a cell line. Immunohistochemistry and Western blotting were used to analyze CCNG2 protein expression in 63 cases of thyroid cancer and normal tissues to allow the relationship with clinical factors to be assessed. CCNG2 lentiviral and empty vectors were transfected into the thyroid cancer K1 cell line. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were applied to detect the mRNA and protein levels of CCNG2. MTT assay and cell cycle were also conducted to assess the influence of up-regulated expression of CCNG2 on K1 cell biology. The level of CCNG2 protein expression was found to be significantly lower in thyroid cancer tissue than normal tissues (P<0.05). Western blot: The relative amount of CCNG2 protein in thyroid cancer tissue was respectively found to be significantly lower than in normal tissues (P<0.05), correlating with lymph node metastasis, clinic stage and histological grade (P<0.05), but not gender, age or tumor size (P>0.05). Loss of CCNG2 expression correlated significantly with poor overall survival time on Kaplan-Meier analysis (P<0.05). The results for biological functions showed that K1 cell transfected CCNG2 had a lower survival fraction, a greater percentage in the G0/G1 phases, and lower cyclin-dependent kinase 2 (CDK2) protein expression compared with K1 cells non-transfected with CCNG2 (P<0.05). CCNG2 expression decreased in thyroid cancer and correlated significantly lymph node metastasis, clinic stage, histological grade and poor overall survival, suggesting that CCNG2 may play important roles as a negative regulator in thyroid cancer K1 cells by promoting degradation of CDK2.

[The relationship of angiotensin I-converting enzyme gene polymorphism with diabetic retinopathy and diabetes myocardial infarction].

OBJECTIVE: To investigate the relationship of angiotensin I-converting enzyme (ACE) gene polymorphism to diabetic retinopathy and diabetes myocardial infarction. METHODS: ACE insertion/deletion(I/D) polymorphism was determined by PCR. RESULTS: No evidence showed that ACE gene was associated with diabetic retinopathy. By comparison of the type 2 diabetes patients with myocardial infarction versus those without-myocardial infarction, it was found that the frequencies of homozygote DD (41.2% versus 33.2%) and of allele D (64.7% versus 55.0%) increased remarkably; the difference was statistically significant (P<0.05). CONCLUSION: Allele D(RR=1.50) and genotype DD(RR=1.33) seemed to be a genetic risk factor for type 2 diabetes myocardial infarction.