Clinical study on the effect of Bi-level positive airway pressure therapy on COPD complicated with Anxiety and Depression.

Objectives: To investigate the effect of bi-level positive airway pressure (BIPAP) therapy on chronic obstructive pulmonary disease (COPD) complicated with anxiety and depression. Methods: This is a retrospective study. One hundred patients with COPD complicated with anxiety and depression who were admitted to the Respiratory Department of The First Affiliated Hospital of Hebei North University from August 2021 to August 2022 were selected and randomly divided into two groups. Patients in the control group were given conventional symptomatic treatment, while those in the observation group were given BIPAP therapy in addition to the treatment in the control group. The two groups were compared and analyzed in terms of respiratory function indicators, the changes in the scores of St. George's Hospital Respiratory Questionnaire (SGRQ) and COPD assessment test (CAT), blood gas analysis indicators, the levels of serum neurokinin A (NKA), serum interleukin-6 (IL-6), and serum serotonin (5-HT), as well as the changes in the scores of Hamilton Anxiety Scale (HAMA) and Hamilton Depression Scale (HAMD). Results: After treatment, the levels of lung function indicators in both groups increased, SGRQ and CAT scores decreased, and pH levels remained unchanged. In addition, PaO2 levels increased, PCO2, 5-HT, NKA and IL-6 levels decreased, and HAMA and HAMD scores decreased. The improvement degree of each indicator in the observation group was superior to that in the control group. Conclusion: In the clinical treatment of COPD complicated with anxiety and depression, BIPAP boasts effective amelioration of lung function and relief of anxiety and depression symptoms, and its mechanism of action may have a close bearing on ameliorating the levels of 5-HT, NKA, and IL-6 in patients.

eEF-2K knockdown synergizes with STS treatment to inhibit cell proliferation, migration, and invasion via the TG2/ERK pathway in A549 cells.

Emerging research has suggested the anticancer potential of tanshinone IIA, the bioactive ingredient isolated from the traditional Chinese herb Salvia miltiorrhiza. However, the molecular mechanism of sodium tanshinone IIA sulfonate (STS) antilung cancer effect is not very clear. In this study, our purpose is to investigate the roles of STS and elongation factor-2 kinase (eEF-2K) in regulating the proliferation, migration, and invasion of A549 cells and explore the implicated pathways. We found that STS suppressed A549 cell survival and proliferation in a time- and xdose-dependent manner. Knockdown of eEF-2K and treatment with STS synergistically exerted antiproliferative, -migratory, and -invasive effects on A549 cells. These effects were caused by attenuation of the extracellular signal-regulated kinase (ERK) pathway via inhibition of tissue transglutaminase (TG2). In summary, the inhibition of eEF-2K synergizes with STS treatment, exerting anticancer effects on lung adenocarcinoma cells through the TG2/ERK signaling pathway, which provides a potential therapeutic target for treating lung adenocarcinoma.

Cucurbitacin B regulates lung cancer cell proliferation and apoptosis via inhibiting the IL-6/STAT3 pathway through the lncRNA XIST/miR-let-7c axis.

CONTEXT: Lung cancer, the most common type of cancer, has a high mortality rate. Cucurbitacin B (CuB), a natural compound extracted from Cucurbitaceae plants, has antitumor effects. OBJECTIVE: We investigated the role of CuB on lung cancer and its potential mechanisms. MATERIALS AND METHODS: A549 cells were treated with 0.1, 0.3, 0.6, and 0.9 µM CuB for 12, 24, and 48 h or untreated. Gene and protein levels were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting. Enzyme-linked immunosorbent assay (ELISA) detected inflammatory factors levels (TNF-α and IL-10). 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, and colony formation assays measured cell viability, apoptosis, and proliferation. The interaction between miR-let-7c and long non-coding RNA X inactive-specific transcript (XIST) or interleukin-6 (IL-6) was verified by dual-luciferase reporter assays. RESULTS: CuB treatment inhibited the proliferation of lung cancer cells and promoted cell apoptosis, and increased the expression of Bax and cleaved caspase3, decreased cyclin B1 and Bcl-2 expression. CuB suppressed XIST and IL-6 expression, and enhanced miR-let-7c expression. XIST silencing enhanced the inhibitory effect of CuB on cell proliferation and the promotion effect on apoptosis via upregulating miR-let-7c. Moreover, XIST targeted miR-let-7c to activate the IL-6/STAT axis. MiR-let-7c overexpression enhanced the regulatory effect of CuB on proliferation and apoptosis via suppressing the IL-6/STAT3 pathway. DISCUSSION AND CONCLUSION: CuB regulated cell proliferation and apoptosis by inhibiting the XIST/miR-let-7c/IL-6/STAT3 axis in lung cancer. These findings indicate CuB may have the possibility of clinical application in lung cancer treatment.

Exosomal miR-132-3p from mesenchymal stem cells alleviated LPS-induced acute lung injury by repressing TRAF6.

Exosomes isolated from mesenchymal stem cells (MSC) had shown beneficial effect on acute lung injury (ALI). However, the effective components in MSC-derived exosomes need further investigation. ALI mice model was established by lipopolysaccharide (LPS) injection. In vitro inflammatory model was established by LPS stimulation of MLE-12 cells. The cell proliferation was evaluated by EdU assay. TUNEL and Annexin V/PI were applied to evaluate the apoptosis of tissue and cell respectively. HE staining was performed to evaluate the lung injury. Transmission electronic microscope was used to observe isolated exosomes. Level of cytokines, MDA, KGF were determined by ELISA kit. Direct interaction of miR-132-3p and TRAF6 were verified by dual luciferase assay. The level of mRNA or proteins were determined by qRT-PCR or western blots respectively. TRAF6 was upregulated while miR-132-3p was downregulated in LPS-stimulated ALI model. MiR-132-3p negatively regulated TRAF6 by direct binding. MiR-132-3p potentiated proliferation and suppressed apoptosis of LPS-induced MLE-12 cells at least partly dependent on targeting TRAF6. Treatment of exosome alleviated the LPS-induced ALI in mice and LPS-induced inflammatory response in MLE-12 cells. Moreover, overexpression of miR-132-3p promoted the protective effect of exosomes in LPS-induced MLE-12 cells injury and LPS-induced ALI. Mechanically, it was suggested that miR-132-3p inactivated PI3K/Akt signalling via targeting TRAF6. In the present study, our results indicated that miR-132-3p mediated protective effect of MSC-derived exosomes on LPS-induced ALI. Exosomal miR-132-3p ameliorated LPS-induced ALI via targeting TRAF6 and inactivating PI3K/Akt signalling.

Relationships Between Internet Use and Sleep Duration in Chinese Adults: A Cross-Sectional Study.

PURPOSE: Most studies that examined the relationship between internet use and sleep were conducted mainly in children and adolescents, and we know little about the use of internet among adults. The purpose of this study is to understand the internet use patterns of Chinese adults and to measure their associations with sleep duration from variety, frequency and type. METHODS: A total of 19,730 samples were selected from 2018 data of the China Health and Retirement Longitudinal study. Internet usage was obtained by specific questions, and the range of sleep period was grouped according to recommendations from the National Sleep Foundation. Kruskal-Wallis H-test and the chi-squared test were used for basic descriptive analysis, and multinomial logistic regression was used to analyze the relationships between internet use and sleep duration. Stata version 15.0 was used for data cleaning, and SPSS version 20.0 was used for statistics analysis. RESULTS: After screening, a total of 6346 persons were included in the analysis, of which 3148 (49.61%) were males and 3198 (50.39%) were females. Age ranged from 21 to 95 years, most persons were over 45 years old, with the median age of 56 years. Only 1180 (18.59%) participants used the internet, and almost all of them used mobile phones (1137, 96.36%), the other three types were desktop computer (232, 19.66%), laptop computer (69, 5.85%) and tablet (73, 6.19%). There were 912 (77.28%) and 268 (22.71%) participants who used only one and two or more types, respectively. In the unadjusted model, both short sleep and long sleep were associated with internet use compared with normal sleep duration (0.806 [0.708-0.918] p = 0.001; 0.345 [0.251-0.475] p < 0.000). After adjusting for all covariates, the association between long sleep and internet use still persisted (0.612 [0.433-0.865] p = 0.005), but no significant difference was found in short sleep (0.929 [0.803-1.075] p = 0.325). CONCLUSION: Internet use was found to be closely associated with sleep and the duration of sleep negatively affected, which may provide new ideas for sleep hygiene recommendations and healthy media use. This conclusion needs more evidence to support.

Mobile Phone Addiction Mediates the Relationship Between Alexithymia and Learning Burnout in Chinese Medical Students: A Structural Equation Model Analysis.

BACKGROUND: Learning burnout is a passive mental state among students. It is a common phenomenon that can cause many bad outcomes in Chinese medical students, such as mental disorders and suicide, and its causes are complex. PURPOSE: To analyze the relationship between alexithymia and learning burnout, as well as the mediating effect of mobile phone addiction, and provide clues for future interventions to deal with learning burnout among Chinese medical students. METHODS: In this cross-sectional study, convenience cluster sampling was used to produce a sample of 1200 medical universities in Chongqing, China. The Toronto Alexithymia Scale (TAS-20), Mobile Phone Addiction Tendency Scale (MPATS), and Learning Burnout Questionnaire (LBQ) were used to examine participants. Hierarchical regression was used to analyze the effect of alexithymia and mobile phone addiction on learning burnout. A structural equation model (SEM) with maximum likelihood was used to evaluate the mediating effect of mobile phone addiction on the relationship between alexithymia and learning burnout. The bootstrap method was used to confirm the significance of this mediating effect. RESULTS: The final sample size was 1062, with a valid response rate of 88.5%. The prevalence of learning burnout among Chinese medical students was 39.6%. Results of hierarchical regression revealed that alexithymia (ΔR2=0.198, P<0.01) and mobile phone addiction (ΔR2=0.021, P<0.01) were independent factors of learning burnout; the SEM revealed that the mediating effect of mobile phone addiction between alexithymia and learning burnout accounted for 25.16% of the total effect of alexithymia on learning burnout; the bootstrap method revealed that the bounds of the CI did not contain 0, confirming the significance of this mediating effect. CONCLUSION: Of the medical students, 39.6% had learning burnout. Alexithymia can positively predict learning burnout, and this relationship is partially mediated by mobile phone addiction.

Prevalence and Patterns of Comorbidity Among Middle-Aged and Elderly People in China: A Cross-Sectional Study Based on CHARLS Data.

INTRODUCTION: Under the background of the accelerated aging of the population, comorbidity in the elderly has gradually become a social problem. At present, the related studies on chronic diseases are mainly focused on a single disease. This study aimed to investigate the prevalence of common chronic diseases, the conditions and patterns of comorbidity in middle-aged and elderly people in China. METHODS: We extracted the data from China Health and Retirement Longitudinal Study (CHARLS). A total of 14 diseases were included, and the prevalence was assessed by self-report. We calculate different disease combinations and perform descriptive statistics analysis of chronic disease and comorbidity status. RESULTS: Among the 6754 subjects, 2833 (42.0%) people had at least one chronic disease, and 1138 (17.0%) people had two or more diseases at the same time. The top three diseases of prevalence were hypertension (15.4%), arthritis or rheumatism (11.0%), and stomach or digestive diseases (9.3%). Common dual disease combinations were hypertension and dyslipidemia, hypertension and arthritis or rheumatism, arthritis or rheumatism and stomach or digestive diseases. CONCLUSION: Comorbidity is common in the population, and the pattern of chronic disease comorbidity is complex. Hypertension exists in a variety of comorbidity patterns, and its screening and prevention should be strengthened.

Dihydroquercetin attenuates lipopolysaccharide-induced acute lung injury through modulating FOXO3-mediated NF-κB signaling via miR-132-3p.

BACKGROUND: Dihydroquercetin (DHQ) is a potent flavonoid which has been demonstrated to have multiple biological activities including anti-inflammation activity, antioxidant activity as well as anti-cancer activity etc. Recently, many studies have focused on the antioxidant activity of DHQ. However, the use of the anti-inflammation activity of DHQ in acute lung injury (ALI) has not been reported. METHODS: Cell viability was examined by CCK-8 assay. The relative expression of miR-132-3p, FOXO3 were detected by qPCR. The levels of TNF-α, IL-6 and IL-1ß were detected using enzyme-linked immunosorbent assay. The amount of apoptosis cells was detected by flow cytometry. The protein levels of Bcl-2, Bax, p-p65 and p-IκBα were measured by western blot. RESULTS: We found that DHQ-induced the expression of miR-132-3p in LPS-induced ALI. Overexpression of miR-132-3p resulted in the inhibition of FOXO3 expression and then suppressed FOXO3-activated NF-κB pathway, attenuating LPS-induced inflammatory response and apoptosis. CONCLUSION: We demonstrated FOXO3 to be a target of miR-132-3p, and DHQ could induce the expression of miR-132-3p, relieving LPS-induced ALI via miR-132-3p/FOXO3/NF-κB axis, providing a promising therapeutic target for ALI.

Psychological Capital Mediating the Relationship Between Childhood Trauma and Alexithymia in Chinese Medical Students: A Cross-Sectional Study.

PURPOSE: A much higher prevalence of alexithymia has been found in medical students compared with the general population. This study aimed to test the potential mediating effect of psychological capital on the relationship between childhood trauma and alexithymia in Chinese medical students, thereby providing clues for future interventions aimed at dealing with alexithymia in this population. METHODS: Convenience cluster sampling was used to recruit 1200 medical students in Chongqing, China. This cross-sectional study utilised the Childhood Trauma Questionnaire Short Form, the Toronto Alexithymia Scale, and the Psychological Capital Questionnaire. A structural equation model with maximum likelihood was used to study the mediating effect presented in the aim, and the significance of the mediating effect was examined by the bootstrap method. Multiple-group invariance analyses were also conducted to confirm the stability of the model. RESULTS: A total of 1018 were identified to have valid responses with a rate of 84.83%. 38.4% were males, 61.6% were females. The prevalence of alexithymia was 16.5%. Results of structural equation model showed that childhood trauma was positively related to alexithymia, with a standard path coefficient of 0.219 (C.R.=6.644, P<0.001). The partial mediating effect of psychological capital was 0.060 (P<0.001), accounting for 21.51% of the total effect of childhood trauma on alexithymia. Results of bootstrap method showed that the lower and upper bounds of the 95% confidence interval did not contain 0, and the multiple-group invariance analyses showed that the p values of the changes in the degrees of freedom and chi-square value were greater than 0.05, thus confirming the stability of the model. CONCLUSION: Childhood trauma was a direct predictor of alexithymia among Chinese medical students, and the relationship between these two was partially mediated by psychological capital. Therefore, interventions aimed at enhancing psychological capital in this population may be effective at diminishing alexithymia.

LncRNA-CASC7 enhances corticosteroid sensitivity via inhibiting the PI3K/AKT signaling pathway by targeting miR-21 in severe asthma.

BACKGROUND: Asthma, a common chronic inflammatory disease, is treated with corticosteroid in most cases, but corticosteroid resistance in severe asthma patients seriously impairs the therapeutic effects. LncRNA-CASC7 inhibits cell proliferation and enhances drug sensitivity, but the molecular mechanisms of corticosteroid resistance in severe asthma are still unknown. METHODS: Airway smooth muscle cells (ASMCs) from healthy and severe asthmatic subjects were used in this study. The expression of CASC7 and miR-21 were modified by transfection with the pcDNA3.1-CASC7, miR-21 mimics and inhibitor. MTT assay was conducted to measure cell proliferation. ELISA assay was used to determine the secretion of CCL5, CCL11 and IL-6. The phosphorylation of glucocorticoid receptor (GR) and the PI3K/AKT signaling were assessed by western blotting assays. qRT-PCR was used to analyze the expression of CASC7, miR-21 and PTEN. Dual-luciferase reporter assay was used to assess the interaction among CASC7, miR-21 and PTEN. RESULTS: Compared with AMSCs from severe asthma patients, dexamethasone inhibited cytokines (CCL5, CCL11 and IL-6) and promoted the phosphorylation of GR more significantly in normal AMSCs. CASC7 expression was suppressed while miR-21 expression and AKT activity were promoted in ASMCs from severe asthma patients. CASC7 promoted PTEN expression via directly inhibiting miR-21 expression. Overexpression of CASC7 suppressed the PI3K/AKT signaling pathway and promoted the inhibition effects of dexamethasone on cell proliferation and cytokines secretion via targeting miR-21. CONCLUSION: CASC7 increased corticosteroid sensitivity by inhibiting the PI3K/AKT signaling pathway via targeting miR-21, which provided a promising potential target for designing novel therapeutic strategy for severe asthma.

[Influence of S-nitrosoglutathione on the membrane glycoprotein of frozen platelets].

This study was purposed to explore the influence of S-nitrosoglutathione (GSNO) on membrane glycoprotein of frozen platelet. The levels of membrane glycoprotein on fresh liquid platelets, frozen platelets and frozen platelets with GSNO were measured by flow cytometry. The results showed that the GSNO obviously decreased platelet aggregation, the PAC-1 change in the three groups was not significant. The changes of CD42b and CD62P in fresh liquid platelet group, frozen platelet group and frozen platelets with GSNO were significant different. The change of membrane glycoprotein in above-mentioned three group was not significant. It is concluded that the GSNO inhibits platelet aggregation, maintains the function of platelets and may be used as a cryoprotectant. When frozen platelets were added with GSNO, the molecular rearrangement, structure change and other mechanism may occur in platelets.

[Important role of nitric oxide in stored red blood cells -- review].

The efflux of nitro oxide (NO) in the duration of storing red blood cells (RBCs) was the main reason resulting in decrease and even loss of vasodilatory activity, cell deformability and ability of carrying oxygen (O2) in the stored RBCs. The deep understanding physical functions and acting ways of NO in circulatory system, as well as transformations and balance control of S-Nitrosohemoglobin (SNO-Hb) has an important significance for ensuring sure safety and efficacy of transfusion. In this article, the physical functions, acting ways, retaining and transferring form of nitro oxide, and SNO-Hb adjusting, as well as effects of SNO-Hb concentration on change on stored red blood cells were reviewed.

[Detection and analysis of CD271, CD133 and CD34 expressions in bone marrow cells by flow cytometry with three color fluorescence labelling].

This study was purposed to detect the expressions of CD271, CD133 and CD34, and to analyze the correlation of CD271 with CD133 and CD133 with CD34 expressions. The human bone marrow cells (BMCs) and mononucleated cells (MNCs) were detected by flow cytometry with CD45-PerCP, CD271-FITC, CD133-PE and CD34-FITC labelling according to different combinations of design, cells were located and selected repeatedly by FSC, SSC and CD45 after acquirement, then the expressions of CD271, CD133 and CD34 were detected by flow cytometry. The results showed that the expressions of CD271, CD133 and CD34 in BMCs were 0.16%, 0.20% and 0.43% respectively, while their expressions were 0.49%, 0.47% and 1.07% respectively after isolation of MNCs. The co-expressions of CD271(+)CD133(+) before and after isolation of MNCs were (0.02 +/- 0.01)% and (0.03 +/- 0.02)% respectively. The co-expression of CD133(+) and CD34(+) before and after isolation of MNCs were (0.18 +/- 0.11)% and (0.42 +/- 0.23)% respectively (p < 0.01); meanwhile about 90% of cells with CD133(+) expressed CD34 and 40% of cells with CD34(+) expressed CD133. It is concluded that the established method of detection using flow cytometry with three color fluorescence labelling can be used to detect expression of CD271, CD133 and CD34 in BMCs. The cells with CD271 are different from cells with CD133 and CD34, which suggests that the CD271 may be of important role in evaluating and guiding the clinical application of BM MSCs.