43 research outputs found

    The relationship between stigma and quality of life in hospitalized middle-aged and elderly patients with chronic diseases: the mediating role of depression and the moderating role of psychological resilience

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    ObjectivePatients with chronic diseases may have some psychological problems due to their own or surrounding environmental factors, which can adversely affect the patientā€™s illness and life. Given that the number of chronically ill patients in China is currently increasing every year, more research is needed to determine the best ways to manage changes in psychological status and psychological stress responses in chronically ill patients. The researchers constructed a mediated moderation model to explore the impact of stigma on the quality of life of chronically ill patients, as well as the mediating role of depression and the moderating role of psychological resilience.MethodsA stratified sampling method was used to select 363 middle-aged and old-aged patients with chronic diseases aged 45 years and older from the Affiliated Hospital of Zhejiang University for the study. Data were collected from patients with chronic diseases such as cardiac, respiratory, renal, and other chronic diseases using the Cumulative Illness Rating Scale for Geriatrics (CIRS-G), the Stigma Scale for Patients with Chronic Diseases (SSCI), the Patient Health Questionaire-9 (PHQ-9), the Quality of Life Inventory (SF-12), and the Conner-Davidson Resilience Scale (CD-RISC) were collected from patients with cardiac, respiratory, renal, and other chronic diseases. A descriptive analysis was used to describe the sample. Linear regression was used to evaluate the relationship between the variables. Mediation and moderation analyses were used to explore the mediating role of depression and the moderating role of psychological resilience.ResultsThere was a moderate negative correlation between stigma and quality of life (r = -0.378, P < 0.01). There was a moderate negative correlation between depression and quality of life (r = -0.497, P < 0.01). There was a moderately positive correlation between psychological resilience and quality of life (r = 0.382, P < 0.01). There was a moderate negative correlation between psychological resilience and depression (r = -0.348, P < 0.01). There was a weak negative correlation between psychological resilience and stigma (r = -0.166, P < 0.01). There was a strong positive correlation between stigma and depression (r = 0.607, P < 0.01) The mediation study showed that stigma was a significant predictor of quality of life and that stigma and quality of life were mediated to some extent by depression, with the mediating effect accounting for 67.55% of the total effect. The direct path from stigma to depression is moderated by psychological resilience (Ī² = -0.0018, P < 0.01).ConclusionsDepression mediates the relationship between stigma and quality of life, while psychological elasticity plays a moderating role between stigma and depression, and when the level of psychological elasticity increases, the more significant the role of stigma on depression. As a physiologically and psychologically vulnerable group, patients with chronic diseasesā€™ overall quality of life and mental health should be taken more seriously, and clinical workers should pay timely attention to the psychological and mental conditions of patients with chronic diseases and provide timely and appropriate interventions and therapeutic measures. The relevant results of this study also provide a new perspective for clinical work on psychological intervention for patients with chronic diseases

    Expression of TRPC6 in Renal Cortex and Hippocampus of Mouse during Postnatal Development

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    TRPC6, a member of the TRPC family, attracts much attention from the public because of its relationship with the disease. In both the brain and kidney, TRPC6 serves a variety of functions. The aim of the present study was to observe the expression and effects of TRPC6 in renal cortex and hippocampus during earlyĀ postnatal development ofĀ the mouse. In the present study, immunohistochemistry and Western blotting were used to detect the expression of TRPC6 in the mouse kidney and hippocampus of postnatal day 1, 3, 5, 7, 14, 21, 28 and 49 (P1, P3, P5, P7, P14, P21, P28 and P49). Results showed that the expression of TRPC6 was increased in the mouse hippocampus, and there was a significant increase between P7 and P14 during the postnatal development. Meanwhile, the expression of TRPC6 was also detected in glomerulus and tubules, and a decreased expression was found during postnatal maturation of mouse renal cortex. From these in vivo experiments, we concluded that the expression of TRPC6 was active in the developing mouse kidney cortex, and followed a loss of expression with the development of kidney. Meanwhile, an increased expression was found in the hippocampus with the development. Together, these data suggested that the developmental changes in TRPC6 expression might be required for proper postnatal kidney cortex development, and played a critical role in the hippocampus during development, which formed the basis for understanding the nephrogenesis and neurogenesis in mice and provided a practically useful knowledge to the clinical and related research

    A Spatioā€Temporal Enhanced Graphā€Transformer AutoEncoder embedded pose for anomaly detection

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    Abstract Due to the robustness of skeleton data to human scale, illumination changes, dynamic camera views, and complex backgrounds, great progress has been made in skeletonā€based video anomaly detection in recent years. The spatioā€temporal graph convolutional network has been proven to be effective in modelling the spatioā€temporal dependencies of nonā€Euclidean data such as human skeleton graphs, and the autoencoder based on this basic unit is widely used to model sequence features. However, due to the limitations of the convolution kernel, the model cannot capture the correlation between nonā€adjacent joints, and it is difficult to deal with longā€term sequences, resulting in an insufficient understanding of behaviour. To address this issue, this paper applies the Transformer to the human skeleton and proposes the Spatioā€Temporal Enhanced Graphā€Transformer AutoEncoder (STEGTā€AE) to improve the capability of modelling. In addition, the multiā€memory model with skip connections is employed to provide different levels of coding features, thereby enhancing the ability of the model to distinguish similar heterogeneous behaviours. Furthermore, the STEGTā€AE has a single encoderā€double decoder architecture, which can improve the detection performance by the combining reconstruction and prediction error. The experimental results show that performances of STEGTā€AE is significantly better than other advanced algorithms on four baseline datasets

    Triptolide Inhibited Cytotoxicity of Differentiated PC12 Cells Induced by Amyloid-Betaā‚‚ā‚…ā‚‹ā‚ƒā‚… via the Autophagy Pathway.

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    Evidence shows that an abnormal deposition of amyloid beta-peptide25-35 (AĪ²25-35) was the primary cause of the pathogenesis of Alzheimer's disease (AD). And the elimination of AĪ²25-35 is considered an important target for the treatment of AD. Triptolide (TP), isolated from Tripterygium wilfordii Hook.f. (TWHF), has been shown to possess a broad spectrum of biological profiles, including neurotrophic and neuroprotective effects. In our study investigating the effect and potential mechanism of triptolide on cytotoxicity of differentiated rat pheochromocytoma cell line (the PC12 cell line is often used as a neuronal developmental model) induced by Amyloid-Beta25-35 (AĪ²25-35), we used 3-(4, 5-dimethylthiazol-2-yl)-2, 5- diphenyltetrazolium bromide (MTT) assay, flow cytometry, Western blot, and acridine orange staining to detect whether triptolide could inhibit AĪ²25-35-induced cell apoptosis. We focused on the potential role of the autophagy pathway in AĪ²25-35-treated differentiated PC12 cells. Our experiments show that cell viability is significantly decreased, and the apoptosis increased in AĪ²25-35-treated differentiated PC12 cells. Meanwhile, AĪ²25-35 treatment increased the expression of microtubule-associated protein light chain 3 II (LC3 II), which indicates an activation of autophagy. However, triptolide could protect differentiated PC12 cells against AĪ²25-35-induced cytotoxicity and attenuate AĪ²25-35-induced differentiated PC12 cell apoptosis. Triptolide could also suppress the level of autophagy. In order to assess the effect of autophagy on the protective effects of triptolide in differentiated PC12 cells treated with AĪ²25-35, we used 3-Methyladenine (3-MA, an autophagy inhibitor) and rapamycin (an autophagy activator). MTT assay showed that 3-MA elevated cell viability compared with the AĪ²25-35-treated group and rapamycin inhibits the protection of triptolide. These results suggest that triptolide will repair the neurological damage in AD caused by deposition of AĪ²25-35 via the autophagy pathway, all of which may provide an exciting view of the potential application of triptolide or TWHF as a future research for AD

    Localization of TRPC6 in mouse hippocampus during the postnatal development.

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    <p>The immunohistochemical staining showed that TRPC6 was expressed in all regions of the hippocampus at P1 (B), P3 (C), P5 (D), P7 (E), P14 (F) and P21 (G). The negative control image was shown in (A). Scale bar, 200 Āµm. In suit hybridization of P1 (H) and P5 (I) brain sections showed the expression of TRPC6 in hippocampal neurons. Scale bar, 100 Āµm. The corresponding linear diagram of relative fluorescent intensity in glomeruli was shown in (J). Data were presented as meansĀ±S.D. nā€Š=ā€Š6/group. *<i>P</i><0.05, **<i>P</i><0.01 <i>vs.</i> adjacent age group.</p

    The immunoblot analysis of TRPC6 in mouse hippocampus during the development.

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    <p>Total lysates of tissues treated as indicated blotted with antibodies to TRPC6 at the indicated ages (A). Quantitative determination of TRPC6 expression showed an abrupt increase between P7 and P14 in mouse renal cortex during the development, and expression levels remained higher into adulthood (B). The expression of TRPC6 was normalized to Ī²-actin expression. Data were presented as meansĀ±S.D. *<i>P</i><0.05, **<i>P</i><0.01 <i>vs.</i> adjacent age group.</p

    Localization of TRPC6 in mouse renal cortex during postnatal development.

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    <p>Immunohistochemical staining of TRPC6 showed the expression of TRPC6 in the mouse renal cortex at P1 (B), P3 (C), P5 (D), P7 (E), P14 (F), P21 (G), P28 (H), and P49 (I). The negative control image was from the renal cortex, in which the primary antibody was a species-appropriate IgG (A). The corresponding linear diagram of relative fluorescent intensity in glomeruli was shown in (J). The sections from P1 to P5 showed that TRPC6 mostly expressed in comma-shaped body, S-shaped body and renal corpuscles of stage III (B-D). After P7 the expression was found in renal corpuscles and it was weakly positive (E-F). During the development, tubules were all observed. Scale bar, 100 Āµm. Data were presented as meansĀ±S.D. nā€Š=ā€Š6/group. *<i>P</i><0.05, **<i>P</i><0.01 <i>vs.</i> adjacent age group.</p

    Nursing studentsā€™ emotions, educational concerns, and the impact of study careers and professional futures during the COVID-19 pandemic: a cross-sectional study

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    Abstract Background COVID-19 is a challenge to education systems worldwide. The aim of the study was to explore the impact of COVID-19-pandemic-related emotions and COVID-19-related concern for education on the study careers and professional futures of nursing students. Methods The study was completed between March and June 2023 using a multi-stage sampling design. A total of 1126 nursing students were recruited to complete the questionnaire. The self-administered questionnaire consisted of basic characteristics of the subjects, the COVID-19-pandemic-related emotions scale, the COVID-19-related concern for education scale, and the impact of the COVID-19 on study careers and professional futures scale (SCPFI-19Ā S). One-way ANOVA/t-test, correlation coefficient analysis, and hierarchical linear regression analysis were used to explore factors influencing changes in study careers and professional futures, and the relationship between COVID-19-pandemic-related emotions and COVID-19-related concern for education. Results Univariate analysis of variance indicated that residence, willingness, and whether to engage in nursing after graduation were related to SCPFI-19Ā S (Pā€‰<ā€‰0.05). COVID-19-pandemic-related emotions and COVID-19-related concern for education were significantly and positively associated with SCPFI-19Ā S (rā€‰=ā€‰0.566, Pā€‰<ā€‰0.01; rā€‰=ā€‰0.199, Pā€‰<ā€‰0.01). Stratified multiple regression analysis showed that COVID-19-pandemic-related emotions and COVID-19-related concern for education of nursing students were significant predictors of SCPFI-19Ā S. Conclusion Overall, both COVID-19-pandemic-related emotions and COVID-19-related concern for education were significantly correlated with SCPFI-19Ā S. In future interventions, schools should consider structures and strategies to support studentsā€™ mental health and educational trajectories during current and future epidemics or similar crises

    Immunoblot analysis of EPOR in mouse kidney cortex during the development.

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    <p>The position of 68 kDa molecular size was the expression pattern of EPOR in renal cortex at the indicated ages. Ī²-actin was used as a consult. When the expression of EPOR was normalized to Ī²-actin, the level was found decreased with development.</p

    Overexpression of MicroRNA-16 Alleviates Atherosclerosis by Inhibition of Inflammatory Pathways

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    Background. Our previous study demonstrated that the expression of miR-16 was downregulated in the cell and animal models of atherosclerosis (AS), a main contributor to coronary artery disease (CAD). Overexpression of miR-16 inhibited the formation of foam cells by exerting anti-inflammatory roles. These findings indicated miR-16 may be an anti-atherogenic and CAD miRNA. The goal of this study was to further validate the expression of miR-16 in CAD patients and explore its therapeutic roles in an AS animal model. Methods. A total of 40 CAD patients and 40 non-CAD people were prospectively registered in our study. The AS model was established in ApoE-/- mice fed a high-fat diet. The model mice were randomly treated with miR-16 agomiR (n=10) or miR-negative control (n=10). Hematoxylin-eosin staining was conducted for histopathological examination in thoracic aorta samples. ELISA and immunohistochemistry were performed to determine the expression levels of inflammatory factors (IL-6, TNF-Ī±, MCP-1, IL-1Ī², IL-10, and TGF-Ī²). qRT-PCR and western blotting were carried out to detect the mRNA and protein expression levels of PDCD4, miR-16, and mitogen-activated protein kinase pathway-related genes. Results. Compared with the normal control, miR-16 was downregulated in the plasma and peripheral blood mononuclear cell of CAD patients, and its expression level was negatively associated with IL-6 and the severity of CAD evaluated by the Gensini score, but positively related with IL-10. Injection of miR-16 agomiR in ApoE-/- mice reduced the formation of atherosclerotic plaque and suppressed the accumulation of proinflammatory factors (IL-6, TNF-Ī±, MCP-1, and IL-1Ī²) in the plasma and tissues but promoted the secretion of anti-inflammatory factors (IL-10 and TGF-Ī²). Mechanism analysis showed overexpression of miR-16 might downregulate target mRNA PDCD4 and then activate p38 and ERK1/2, but inactivate the JNK pathway. Conclusions. Our findings suggest miR-16 may be a potential diagnostic biomarker and therapeutic target for atherosclerotic CAD
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