Longitudinal association of spirituality with depressive symptom trajectories among older adults in mainland China.

OBJECTIVES: The relationship between spirituality and depressive symptoms among the Chinese elderly is not well known. The current study explores this relationship using longitudinal data and trajectory modeling of depressive symptoms. METHODS: A longitudinal study design was used to measure depressive symptoms repeatedly from 2012 to 2021 using the Geriatric Depression Scale (GDS). Group-based trajectory modeling analysis was conducted to determine the trajectories of depressive symptoms, and multiple logistic regression was used to explore the association between spirituality and depressive symptom trajectories. RESULTS: A total of 2333 participants completed at least two GDS measures, and these were included in the Group-based trajectory modeling analysis. An optimal model of three trajectories was derived: no depressive symptoms group (75.2%), new-onset depressive symptoms group (14.4%), and persistent depressive symptoms group (10.4%). Logistic regression modeling revealed that higher spirituality was associated with a lower risk of both new-onset depressive symptoms (OR = 0.68, 95% CI = 0.49-0.93) and persistent depressive symptoms (OR = 0.32, 95% CI = 0.23-0.45). CONCLUSIONS: Spirituality predicts a lower risk of new-onset depressive symptoms and persistent symptoms among older adults in mainland China.

Silver nanoparticles induce endothelial cytotoxicity through ROS-mediated mitochondria-lysosome damage and autophagy perturbation: The protective role of N-acetylcysteine.

Silver nanoparticles (AgNPs) are used increasingly often in the biomedical field, but their potential deleterious effects on the cardiovascular system remain to be elucidated. The primary aim of this study was to evaluate the toxic effects, and the underlying mechanisms of these effects, of AgNPs on human umbilical vein endothelial cells (HUVECs), as well as the protective role of N-acetylcysteine (NAC) against cytotoxicity induced by AgNPs. In this study, we found that exposure to AgNPs affects the morphology and function of endothelial cells which manifests as decreased cell proliferation, migration, and angiogenesis ability. Mechanistically, AgNPs can induce excessive cellular production of reactive oxygen species (ROS), leading to damage to cellular sub-organs such as mitochondria and lysosomes. More importantly, our data suggest that AgNPs causes autophagy defect, inhibits mitophagy, and finally activates the mitochondria-mediated apoptosis signaling pathway and evokes cell death. Interestingly, treatment with ROS scavenger-NAC can effectively suppress AgNP-induced endothelial damage.Our results indicate that ROS-mediated mitochondria-lysosome injury and autophagy dysfunction are potential factors of endothelial toxicity induced by AgNPs. This study may provide new evidence for the cardiovascular toxicity of AgNPs and serve as a reference for the safe use of nanoparticles(NPs) in the future.

Sodium Selenite Ameliorates Silver Nanoparticles Induced Vascular Endothelial Cytotoxic Injury by Antioxidative Properties and Suppressing Inflammation Through Activating the Nrf2 Signaling Pathway.

Silver nanoparticles (AgNP) are the dominant nanomaterials in commercial products and the medical field, but the widespread occurrence of AgNP has become a global threat to human health. Growing studies indicate that AgNP exposure can induce vascular endothelial toxicity by excessive oxidative stress and inflammation, which is closely related to cardiovascular disease (CVD), but the potential intrinsic mechanism remains poorly elucidated. Thus, it has been crucial to control the toxicological effects of AgNP in order to improve their safety and increase the outcome of their applications.Multiple researches have demonstrated that sodium selenite (Se) possesses the capability to counteract the toxicity of AgNP, but the functional role of Se in AgNP-induced CVD is largely unexplored. The aim of this study was to explore the potential protective effect of Se on AgNP-induced vascular endothelial lesion and elucidate the underlying mechanisms. An in vivo model of toxicity in animals was established by the instillation of 200 µL of AgNP into the trachea of rats both with (0.2 mg/kg/day) and without Se treated. In vitro experiments, human umbilical vein endothelial cells (HUVECs) were incubated with AgNP (0.3 µg/mL ) and Se for a duration of 24 h. Utilizing transmission electron microscopy, we observed that the internalization of AgNP-induced endothelial cells was desquamated from the internal elastic lamina, the endoplasmic reticulum was dilated, and the medullary vesicle formed. Se treatment reduced the levels of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), inhibited the release of pro-inflammatory cytokines (specifically tumor necrosis factor (TNF)-α, interleukin (IL)-1ß and IL-6), improved endothelial cell permeability, integrity, and dysfunction, and prevented damage to the aortic endothelium caused by AgNP. Importantly, we found that Se showed the capacity against AgNP with biological functions in guiding the intracellular reactive oxygen species (ROS) scavenging and meanwhile exhibiting anti-inflammation effects. Se supplementation decreased the intracellular ROS release and suppressed NOD-like receptor protein 3 (NLRP3) and nuclear factor kappa-B (NF-κB) mediated inflammation within AgNP-intoxicated rats and HUVECs. The anti-oxidant stress and anti-inflammatory effects of Se were at least partly dependent on nuclear factor erythroid 2-related factor 2 (Nrf2). Overall, our results indicated that the protectiveness of Se against AgNP-induced vascular endothelial toxicity injury was at least attributed to the inhibition of oxidative ROS and pro-inflammatory NF-κB/NLRP3 inflammasome by activating the Nrf2 and antioxidant enzyme (HO-1) signal pathway.

Recent advances of artificial intelligence in melanoma clinical practice.

Skin melanoma is a lethal cancer. The incidence of melanoma is increasing rapidly in all regions of the world. Despite significant breakthroughs in melanoma treatment in recent years, precise diagnosis of melanoma is still a challenge in some cases. Even specialized physicians may need time and effort to make accurate judgments. As artificial intelligence (AI) technology advances into medical practice, it may bring new solutions to this problem based on its efficiency, accuracy, and speed. This paper summarizes the recent progress of AI in melanoma-related applications, including melanoma diagnosis and classification, the discovery of new medication, guiding treatment, and prognostic assessment. The paper also compares the effectiveness of various algorithms in melanoma application and suggests future research directions for AI in melanoma clinical practice.

Effects of multi-organ crosstalk on the physiology and pathology of adipose tissue.

In previous studies, adipocytes were found to play an important role in regulating whole-body nutrition and energy balance, and are also important in energy metabolism, hormone secretion, and immune regulation. Different adipocytes have different contributions to the body, with white adipocytes primarily storing energy and brown adipocytes producing heat. Recently discovered beige adipocytes, which have characteristics in between white and brown adipocytes, also have the potential to produce heat. Adipocytes interact with other cells in the microenvironment to promote blood vessel growth and immune and neural network interactions. Adipose tissue plays an important role in obesity, metabolic syndrome, and type 2 diabetes. Dysfunction in adipose tissue endocrine and immune regulation can cause and promote the occurrence and development of related diseases. Adipose tissue can also secrete multiple cytokines, which can interact with organs; however, previous studies have not comprehensively summarized the interaction between adipose tissue and other organs. This article reviews the effect of multi-organ crosstalk on the physiology and pathology of adipose tissue, including interactions between the central nervous system, heart, liver, skeletal muscle, and intestines, as well as the mechanisms of adipose tissue in the development of various diseases and its role in disease treatment. It emphasizes the importance of a deeper understanding of these mechanisms for the prevention and treatment of related diseases. Determining these mechanisms has enormous potential for identifying new targets for treating diabetes, metabolic disorders, and cardiovascular diseases.

Ameliorative Effect of Sodium Selenite on Silver Nanoparticles-Induced Myocardiocyte Structural Alterations in Rats.

BACKGROUND: The application of silver nanoparticles (AgNPs) is growing exponentially, and its potential damage to the cardiac remains to be elucidated. The purpose of this study was to investigate the ameliorative effect of sodium selenite on silver nanoparticles-induced myocardiocyte structural alterations in rats. MATERIALS AND METHODS: Forty male Sprague-Dawley (SD) rats were randomly divided into four groups: control group, AgNPs group, Se control group, and AgNPs + Se group. SD rats were administered AgNPs through a single intratracheal instillation, and sodium selenite was given by intraperitoneal injection for seven days. Cardiac function was determined by echocardiography and hemodynamic, ultrastructural changes by transmission electron microscopy examination. Mitochondrial fission and autophagy markers were measured by Western blotting. RESULTS: AgNPs caused a significant decrease in cardiac contraction, diastolic dysfunction, fragmentation, and lysis of the myofibrils, the formation of stenosis in the capillary, damaging the mitochondria membrane and cristae. AgNPs significantly increased mitochondrial fission markers dynamin-related protein 1 (Drp1), phospho-Drp1 (p-Drp1), and mitochondrial fission protein 1 (Fis1), as well as autophagy marker LC3 II/I (P<0.05). Treatment with sodium selenite is capable of protecting cardiac function from AgNPs toxicity through attenuating ultrastructural alterations, stabilizing mitochondrial dynamic balance and blocking mitochondrial autophagy. CONCLUSION: We conclude that the protection of sodium selenite against silver nanoparticles-induced myocardiocyte structural alterations is associated with stabilizing mitochondrial dynamic balance and mitophagy.

Silver Nanoparticle Exposure Causes Pulmonary Structural Damage and Mitochondrial Dynamic Imbalance in the Rat: Protective Effects of Sodium Selenite.

BACKGROUND: With the increased application of Silver nanoparticles (AgNP), its potential concerns to the health of human beings remain to be defined. This study aims to explore the harmful effects of AgNP on lung tissue in animals and to examine the mechanisms of protection achieved by sodium selenite. METHODS: Sprague-Dawley(SD) rats were exposed to AgNP (200 µL,1mg/mL) through a single intratracheal instillation. Sodium selenite (0.2mg/kg) was i.p. injected. Malondialdehyde (MDA) and glutathione (GSH) were measured using a spectrophotometer. Histological outcomes and ultrastructural changes were assessed by hematoxylin and eosin (HE) staining and electronic microscopy. Caspases and mitochondrial fission and fusion markers were measured by Western blotting. RESULTS: The histopathologic findings showed that AgNP significantly increased the thickness of alveolar septa, accumulation of macrophage, and the formation of pulmonary bullae and pulmonary consolidation. Ultrastructural studies showed localization of AgNP inside the mitochondria, hyperplasia and vacuolation of type I and type II alveolar cells, lysis of osmiophilic lamellar bodies, and swollen of the mitochondria. AgNP elevated MDA and reduced GSH levels. AgNP activated caspases-3, increased mitochondrial fission markers Dynamin-related protein 1 (Drp1) and phospho-Drp1(p-Drp1), and decreased fusion proteins optic atrophy 1 (Opa1) and mitofusins 2 (Mfn2). Treatment with sodium selenite for 7 days corrected the AgNP-caused alterations in morphological, ultrastructural, oxidative stress, caspase-3 activation and mitochondrial dynamic imbalance. CONCLUSION: We conclude that the exposure of AgNP causes lung tissue damage by enhances oxidative stress, activates caspases-3, and triggers mitochondrial dynamic imbalance towards fission. Sodium selenite effectively detoxifies the AgNP-induced damage to the lung tissue by preventing the above alterations.

Hyperhomocysteinemia induces vascular calcification by activating the transcription factor RUNX2 via Krüppel-like factor 4 up-regulation in mice.

One of the main characteristics of atherosclerosis is vascular calcification, which is linked to adverse cardiovascular events. Increased homocysteine (Hcy), a feature of hyperhomocysteinemia, is correlated with advanced vascular calcification and phenotypic switching of vascular smooth muscle cells (VSMCs). Oxidative stress and high phosphate levels also induce VSMC calcification, suggesting that the Krüppel-like factor 4 (KLF4) signaling pathway may also contribute to vascular calcification. In this study, we investigated this possibility and the role and mechanisms of Hcy in vascular calcification. We found that in atherosclerotic apolipoprotein E-deficient (ApoE-/-) mice, Hcy significantly increases vascular calcification in vivo, as well as VSMC calcification in vitro Of note, the Hcy-induced VSMC calcification was correlated with elevated KLF4 levels. Hcy promoted KLF4 expression in calcified atherosclerotic lesions in vivo and in calcified VSMCs in vitro shRNA-mediated KLF4 knockdown blocked the Hcy-induced up-regulation of runt-related transcription factor 2 (RUNX2) and VSMC calcification. RUNX2 inhibition abolished Hcy-induced VSMC calcification. Using ChIP analysis, we demonstrate that KLF4 interacts with RUNX2, an interaction promoted by Hcy stimulation. Our experiments also revealed that the KLF4 knockdown attenuates Hcy-induced RUNX2 transactivity, indicating that KLF4 is important in modulating RUNX2 transactivity. These findings support a role for Hcy in regulating vascular calcification through a KLF4-RUNX2 interaction and indicate that Hcy-induced, enhanced RUNX2 transactivity increases VSMC calcification. These insights reveal possible opportunities for developing interventions that prevent or manage vascular calcification.

Silver nanoparticle exposure induced mitochondrial stress, caspase-3 activation and cell death: amelioration by sodium selenite.

Silver nanoparticles (AgNP), one of the most commonly used engineered nanomaterial for biomedical and industrial applications, has shown a toxic potential to our ecosystems and humans. In this study, murine hippocampal neuronal HT22 cells were used to delineate subcellular responses and mechanisms to AgNP by assessing the response levels of caspase-3, mitochondrial oxygen consumption, reactive oxygen species (ROS), and mitochondrial membrane potential in addition to cell viability testing. Selenium, an essential trace element that has been known to carry protecting property from heavy metals, was tested for its ameliorating potential in the cells exposed to AgNP. Results showed that AgNP reduced cell viability. The toxicity was associated with mitochondrial membrane depolarization, increased accumulation of ROS, elevated mitochondrial oxygen consumption, and caspase-3 activation. Treatment with sodium selenite reduced cell death, stabilized mitochondrial membrane potential and oxygen consumption rate, and prevented accumulation of ROS and activation of caspase-3. It is concluded that AgNP induces mitochondrial stress and treatment with selenite is capable of preventing the adverse effects of AgNP on the mitochondria.

Religious involvement and mental disorders in mainland china.

PURPOSE: The present study aims to examine the association between religious involvement and mental disorder (anxiety disorder, mood disorder, alcohol use disorder) in a general Chinese population, and explore connections between religious belief and mental disorders in the Hui and Han ethnic groups. METHOD: Data were examined from a representative sample of 2,770 community-dwelling adults in the province of Ningxia located in western China. Self-reported religious attendance and the importance of religious in daily life were measured. The WHO Composite International Diagnostic Interview was used to diagnose mental disorders. RESULTS: In the overall sample, the importance of religious affiliation was positively associated with mental disorders (especially anxiety) (p<0.01). No association was found between any religious characteristic and mood disorders or alcohol use disorders. With regard to analyses within different ethnic groups, religious affiliation was positively associated with mental disorder in Han ethnicity (p<0.01), but not in Hui ethnicity. When stratified by age and ethnic group, religious affiliation was associated positively with mental disorder in younger Han (p<0.01); whereas high religiosity was associated positively with mental disorder in older Hui (p<0.05). Among older Hui, however, religious affiliation was inversely associated with mood disorder (p<0.05). CONCLUSIONS: In contrast to most previous studies in Western populations, religious involvement is less likely to be inversely related to mental disorder in Mainland China, although this association varies by age and ethnic group.

Religious involvement, suicidal ideation and behavior in mainland China.

OBJECTIVE: Little is known about relations between religious involvement and suicidal behaviors in mainland China. This study aims to examine the association between religious involvement and suicidal ideation, planning, and attempts within a general community population controlling for socio-demographic, physical, and mental health factors. METHOD: Data were examined from a population-based sample of 2,769 community-dwelling adults in the province of Ningxia China, where nearly 40% are Muslim, 11% other religious affiliations, and 49% no religion. Four separate logistic regression models examined correlations between religious involvement and self-reported suicidal thoughts, plans, and attempts. Analyses were also stratified by Muslim affiliation (n = 1103) and no religion (n = 1,366). RESULTS: Bivariate analyses in the overall sample demonstrated that higher personal religiosity scores (χ(2) = 6.8, p < 0.01) and total religiosity scores (χ(2) = 5.1, p < 0.05) were positively correlated with developing a suicidal plan, which disappeared after controlling for demographic characteristics. Otherwise, no significant correlations were found between any religious characteristic and suicidal ideation, plan, or attempt in either Muslims or those with no religion. CONCLUSIONS: In contrast to most previous studies, religious involvement plays less of a role in suicidal behaviors in at least one province of mainland China.

The Association between Apolipoprotein E Gene Polymorphism and Mild Cognitive Impairment among Different Ethnic Minority Groups in China.

The association, in different ethnic groups, of apolipoprotein E (apoE) gene polymorphism with mild cognitive impairment (MCI) has been unclear. Few studies have examined the association in Chinese minorities. The current study explores the association between apoE gene polymorphism and MCI in one of the biggest ethnic groups-the Hui-and compares it with the Han. The Minimental State Exam, Activities of Daily Living Scale, and Geriatric Depression Scale were administered to 306 ethnic Hui and 618 ethnic Han people aged ≥55 years. ApoE genotypes were determined using the high resolution melting curve method. The distribution of the apoE genotype and the frequency of alleles ε2, ε3, and ε4 were similar in the Hui and Han groups. In analyses adjusted for age, gender, and education level, the ε4 allele was a risk factor for MCI in both the Hui group (OR = 2.61, 95% CI: 1.02-6.66) and the Han group (OR = 2.36, 95% CI: 1.19-4.67), but the apoE ε2 allele was protective for MCI only in the Han group (OR = 0.48, 95% CI: 0.38-0.88). The association of some apoE genotypes with MCI may differ in different ethnic groups in China. Further studies are needed to explore this effect among different populations.

Water-soluble coenzyme q10 inhibits nuclear translocation of apoptosis inducing factor and cell death caused by mitochondrial complex I inhibition.

The objectives of the study were to explore the mechanism of rotenone-induced cell damage and to examine the protective effects of water-soluble Coenzyme Q10 (CoQ10) on the toxic effects of rotenone. Murine hippocampal HT22 cells were cultured with mitochondrial complex I inhibitor rotenone. Water-soluble CoQ10 was added to the culture media 3 h prior to the rotenone incubation. Cell viability was determined by alamar blue, reactive oxygen species (ROS) production by dihydroethidine (DHE) and mitochondrial membrane potential by tetramethyl rhodamine methyl ester (TMRM). Cytochrome c, caspase-9 and apoptosis-inducing factor (AIF) were measured using Western blotting after 24 h rotenone incubation. Rotenone caused more than 50% of cell death, increased ROS production, AIF nuclear translocation and reduction in mitochondrial membrane potential, but failed to cause mitochondrial cytochrome c release and caspase-9 activation. Pretreatment with water-soluble CoQ10 enhanced cell viability, decreased ROS production, maintained mitochondrial membrane potential and prevented AIF nuclear translocation. The results suggest that rotenone activates a mitochondria-initiated, caspase-independent cell death pathway. Water-soluble CoQ10 reduces ROS accumulation, prevents the fall of mitochondrial membrane potential, and inhibits AIF translocation and subsequent cell death.