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Background: Sarcoidosis has been considered to be associated with many autoimmune diseases (ADs), but the cause-and-effect relationship between these two diseases has not been fully explored. Therefore, the objective of this study is to explore the possible genetic association between sarcoidosis and ADs. Methods: We conducted a bidirectional Mendelian randomization (MR) study using genetic variants associated with ADs and sarcoidosis (4,041 cases and 371,255 controls) from the FinnGen study. The ADs dataset comprised 96,150 cases and 281,127 controls, encompassing 44 distinct types of autoimmune-related diseases. Subsequently, we identified seven diseases within the ADs dataset with a case size exceeding 3,500 and performed subgroup analyses on these specific diseases. Results: The MR evidence supported the causal association of genetic predictors of ADs with an increased risk of sarcoidosis (OR = 1.79, 95% CI = 1.59 to 2.02, P IVW-FE = 1.01 × 10-21), and no reverse causation (OR = 1.05, 95% CI 0.99 to 1.12, P IVW-MRE = 9.88 × 10-2). Furthermore, subgroup analyses indicated that genetic predictors of type 1 diabetes mellitus (T1DM), celiac disease, and inflammatory bowel disease (IBD) were causally linked to an elevated risk of sarcoidosis (All P < 6.25 × 10-3). Conversely, genetic predictors of sarcoidosis showed causal associations with a higher risk of type 1 diabetes mellitus (P < 6.25 × 10-3). Conclusion: The present study established a positive causal relationship between genetic predictors of ADs (e.g. T1DM, celiac disease, and IBD) and the risk of sarcoidosis, with no evidence of reverse causation.
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Doenças Autoimunes , Predisposição Genética para Doença , Análise da Randomização Mendeliana , Sarcoidose , Humanos , Sarcoidose/genética , Sarcoidose/epidemiologia , Doenças Autoimunes/genética , Doenças Autoimunes/epidemiologia , Polimorfismo de Nucleotídeo Único , Estudos de Casos e Controles , Estudo de Associação Genômica AmplaRESUMO
Previous studies have shown that alertness is closely related to executive control function, but its impact on components of post-error adjustment is unknown. This study applied the Attentional Networks Test and the Four-choice Flanker task with three response stimulus intervals (RSIs) to explore the correlation between alertness and post-error adjustment. The linear mixed-effects model of alertness and RSI on the post-error processing indicators showed a significant negative correlation between the alertness and post-error slowing (PES) under 200â¯ms RSI , as well as between alertness and post-error improvement in accuracy (PIA) under both 700 ms RSI and 1200 ms RSI. Participants with lower alertness showed larger post-error slowing in the early stages, while those with higher alertness had smaller PIA in later stages. This study revealed the effects of alertness on different processing components of post-error adjustment. The control strategies utilized by individuals with high and low levels of alertness differed in preparation for performance monitoring. Alertness improved post-error response speed in a task-unspecific manner, but not post-error adaptation.
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Atenção , Função Executiva , Desempenho Psicomotor , Tempo de Reação , Humanos , Masculino , Feminino , Atenção/fisiologia , Adulto Jovem , Tempo de Reação/fisiologia , Função Executiva/fisiologia , Adulto , Desempenho Psicomotor/fisiologia , Adaptação Psicológica/fisiologiaRESUMO
PURPOSE: Loneliness disproportionately affects people with mental disorders, but associations with mental health outcomes in groups affected remain less well understood. METHOD: A cohort of patients receiving mental healthcare on 30th June 2012 was assembled from a large mental health records database covering a south London catchment area. Recorded loneliness within the preceding 2 years was extracted using natural language processing and outcomes were measured between 30th June 2012 until 30th December 2019, except for survival which applied a censoring point of 6th December 2020 according to data available at the time of extraction. The following mental healthcare outcomes: (i) time to first crisis episode; (ii) time to first emergency presentation; (iii) all-cause mortality; (iv) days active to service per year; and (v) face-to-face contacts per year. RESULTS: Loneliness was recorded in 4,483 (16.7%) patients in the study population and fully adjusted models showed associations with subsequent crisis episode (HR 1.17, 95% CI 1.07-1.29), emergency presentation (HR 1.30, 1.21-1.40), days active per year (IRR 1.04, 1.03-1.05), and face-to-face contacts per year (IRR 1.28, 1.27-1.30). Recorded loneliness in patients with substance misuse problems was particularly strongly associated with adverse outcomes, including risk of emergency presentation (HR 1.68, 1.29-2.18) and mortality (HR 1.29, 1.01-1.65). CONCLUSION: Patients receiving mental healthcare who are recorded as lonely have a higher risk of several adverse outcomes which may require a need for higher service input.
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Recent research has hinted at a potential connection between silicosis, a fibrotic lung disease caused by exposure to crystalline silica particles, and cuproptosis. The aim of the study was to explore how cuproptosis-related genes (CRGs) may influence the development of silicosis and elucidate the underlying mechanisms. An analysis of genes associated with both silicosis and cuproptosis was conducted. Key gene identification was achieved through the application of two machine learning techniques. Additionally, the correlation between these key genes and immune cell populations was explored and the critical pathways were discerned. To corroborate our findings, the expression of key genes was verified in both a publicly available silica-induced mouse model and our own silicosis mouse model. A total of 12 differentially expressed CRGs associated with silicosis were identified. Further analysis resulted in the identification of 6 CRGs, namely LOX, SPARC, MOXD1, ALB, MT-CO2, and AOC2. Elevated immune cell infiltration of CD8 T cells, regulatory T cells, M0 macrophages, and neutrophils in silicosis patients compared to healthy controls was indicated. Validation in a silica-induced pulmonary fibrosis mouse model supported SPARC and MT-CO2 as potential signature genes for the prediction of silicosis. These findings highlight a strong association between silicosis and cuproptosis. Among CRGs, LOX, SPARC, MOXD1, ALB, MT-CO2, and AOC2 emerged as pivotal players in the context of silicosis by modulating CD8 T cells, regulatory T cells, M0 macrophages, and neutrophils.
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Dióxido de Silício , Silicose , Silicose/genética , Silicose/imunologia , Silicose/patologia , Animais , Dióxido de Silício/toxicidade , Camundongos , Masculino , Camundongos Endogâmicos C57BL , Humanos , Modelos Animais de Doenças , Pulmão/patologia , Pulmão/imunologia , Pulmão/efeitos dos fármacos , Fibrose Pulmonar/genética , Fibrose Pulmonar/induzido quimicamente , Fibrose Pulmonar/imunologia , Fibrose Pulmonar/patologia , Aprendizado de Máquina , Osteonectina/genéticaRESUMO
Tetrandrine (TET) is a bisbenzylisoquinoline alkaloid derived from Stephania tetrandra S. Moor, known for its potential use in attenuating the progression of silicosis. However, the precise effects and underlying mechanisms of TET remain controversial. In this study, we aimed to elucidate the pharmacological mechanism of TET using a network pharmacology approach, while also evaluating its effect on silica-induced lung fibrosis in mice and TGF-ß1-stimulated pulmonary fibroblasts in vitro. We employed network pharmacology to unravel the biological mechanisms through which TET may exert its therapeutic effects on pulmonary fibrosis and silicosis. In a silica-induced mouse model of lung fibrosis, TET was administered orally either during the early or late stage of fibrotic progression. Additionally, we examined the effects of TET on fibroblasts stimulated by TGF-ß1 in vitro. Through the analysis, we identified a total of 101 targets of TET, 7,851 genes associated with pulmonary fibrosis, and 80 overlapping genes. These genes were primarily associated with key pathways such as epidermal growth factor receptor tyrosine kinase inhibitor resistance, the vascular endothelial growth factor signaling pathway, and the phosphatidylinositol 3 kinase (PI3K)-protein kinase B (PKB or AKT) signaling pathway. Furthermore, molecular docking analysis revealed the binding of TET to AKT1, the catalytic subunit of phosphatidylinositol-3 kinase, and KDR. In vivo experiments demonstrated that TET significantly alleviated silica-induced pulmonary fibrosis and reduced the expression of fibrotic markers. Moreover, TET exhibited inhibitory effects on the migration, proliferation, and differentiation of TGF-ß1-induced lung fibroblasts in vitro. Notably, TET mitigated silica-induced pulmonary fibrosis by suppressing the PI3K/AKT pathway. In conclusion, our findings suggest that TET possesses the ability to suppress silica-induced pulmonary fibrosis by targeting the PI3K/AKT signaling pathway. These results provide valuable insights into the therapeutic potential of TET in the treatment of pulmonary fibrosis and silicosis.
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Benzilisoquinolinas , Farmacologia em Rede , Proteínas Proto-Oncogênicas c-akt , Fibrose Pulmonar , Transdução de Sinais , Dióxido de Silício , Animais , Fibrose Pulmonar/induzido quimicamente , Fibrose Pulmonar/tratamento farmacológico , Fibrose Pulmonar/metabolismo , Benzilisoquinolinas/farmacologia , Benzilisoquinolinas/uso terapêutico , Proteínas Proto-Oncogênicas c-akt/metabolismo , Camundongos , Dióxido de Silício/toxicidade , Transdução de Sinais/efeitos dos fármacos , Fosfatidilinositol 3-Quinases/metabolismo , Fibroblastos/efeitos dos fármacos , Fibroblastos/metabolismo , Silicose/tratamento farmacológico , Silicose/metabolismo , Silicose/patologia , Masculino , Fator de Crescimento Transformador beta1/metabolismo , Camundongos Endogâmicos C57BLRESUMO
BACKGROUND: Acute-on-chronic liver failure (ACLF) is a refractory disease with high mortality, which is characterized by a pathophysiological process of inflammation-related dysfunction of energy metabolism. Jieduan-Niwan formula (JDNWF) is a eutherapeutic Chinese medicine formula for ACLF. However, the intrinsic mechanism of its anti-ACLF effect still need to be studied systematically. PURPOSE: This study aimed to investigate the mechanism of JDNWF against ACLF based on altered substance metabolic profile in ACLF the expression levels of related molecules. MATERIALS AND METHODS: The chemical characteristics of JDNWF were characterized using ultra performance liquid chromatography (UPLC) coupled with triple quadrupole mass spectrometry. Wistar rats subjected to a long-term CCL4 stimulation followed by a combination of an acute attack with LPS/D-GalN were used to establish the ACLF model. Liver metabolites were analyzed by LC-MS/MS and multivariate analysis. Liver function, coagulation function, histopathology, mitochondrial metabolic enzyme activity and mitochondrial damage markers were evaluated. The protein expression of mitochondrial quality control (MQC) was investigated by western blot. RESULTS: Liver function, coagulation function, inflammation, oxidative stress and mitochondrial enzyme activity were significantly improved by JDNWF. 108 metabolites are considered as biomarkers of JDNWF in treating ACLF, which were closely related to TCA cycle. It was further suggested that JDNWF alleviated mitochondrial damage and MQC may be potential mechanism of JDNWF improving mitochondrial function. CONCLUSIONS: Metabolomics revealed that TCA cycle was impaired in ACLF rats, and JDNWF had a regulatory effect on it. The potential mechanism may be improving the mitochondrial function through MQC pathway, thus restoring energy metabolism.
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Purpose: Chronic obstructive pulmonary disease (COPD) is the main cause of mortality world widely. Non-coding RNAs (lncRNAs) and associated competitive endogenous RNAs (ceRNAs) networks were recently proved to lead to mRNA gene expression downregulation but were still unclear in COPD. This study aims to investigate and elucidate the mechanisms underlying the involvement of ceRNA co-expression networks in COPD pathogenesis. Methods: Obtained expression signature of data from the Gene Expression Omnibus database and compared the differentially expression of mRNAs and miRNAs between COPD patients and healthy smokers. Predicted the miRNA-lncRNA and miRNA-mRNA interaction using online library and employed CIBERSORT to measure the proportions of the 22 immune cells in the COPD and control groups. Results: Established a ceRNA-network comprising 11 lncRNAs, 5 miRNAs, and 16 mRNAs. Using the weighted correlation network analysis method, we identified hub genes and hub miRNAs and obtained one core sub-network, XIST, FGD5-AS1, KCNQ1OT1, HOXA11-AS, LINC00667, H19, PRKCQ-AS1, NUTM2A-AS1/has-mir-454-3p/ZNF678, PRRG4. COPD patients had different proportions of immune cells than controls, and these variations were associated with the magnitude of pulmonary function parameters. Conclusion: The ceRNA-network, particularly the core sub-network, may be a putative goal for COPD, in which specific immune cells were involved.
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MicroRNAs , Doença Pulmonar Obstrutiva Crônica , RNA Longo não Codificante , Humanos , RNA Longo não Codificante/genética , Redes Reguladoras de Genes , Doença Pulmonar Obstrutiva Crônica/diagnóstico , Doença Pulmonar Obstrutiva Crônica/genética , MicroRNAs/genética , MicroRNAs/metabolismo , RNA Mensageiro/genética , RNA Mensageiro/metabolismoRESUMO
BACKGROUND: Gene variants have been identified in patients with familial or sporadic idiopathic pulmonary fibrosis (IPF). These variants may partially account for the genetic risk of IPF. The aim of this study was to identify potential genes involved in both familial and sporadic IPF. METHODS: A Han family in northern China with four members diagnosed with IPF was investigated in this observational study. Whole-exome sequencing (WES) was used to identify germline variants underlying disease phenotypes in five members of this family. Candidate rare variants were validated by Sanger sequencing in samples from 16 family members and 119 patients with sporadic IPF. The plasma levels of proteins encoded by the above candidate genes were also examined in 16 family members, 119 other patients with sporadic IPF and 120 age- and sex-matched healthy controls. RESULTS: In a Chinese Han family, MMP19 c.1222 C > T was identified in all familial IPF patients and six offspring from generations III and IV. This variant introduces a premature stop codon, which may damage protein function. Sanger sequencing revealed that 7.6% (9/119) of sporadic IPF patients harbored three MMP19 variants. The genetic risk analysis for pulmonary fibrosis showed that MMP19 c.1499 C > T and c.1316G > A were significantly associated with an increased risk of IPF (OR 3.66, p = 0.028 and OR 8.64, p < 0.001, respectively). The plasma levels of MMP19 were significantly higher in patients with sporadic or familial IPF than in healthy controls (all p < 0.001). CONCLUSIONS: MMP19 variants were identified in familial or sporadic IPF, thus providing a potential new clue into IPF pathogenesis.
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Fibrose Pulmonar Idiopática , Humanos , China/epidemiologia , Fibrose Pulmonar Idiopática/genética , Fatores de RiscoRESUMO
Chronic pain (CP) and mental illness (MI) are leading causes of years lived with disability and commonly co-occur. However, it remains unclear if available interventions are effective in improving pain outcomes in patients with co-existing CP and MI. This systematic review synthesised evidence for the effectiveness of interventions to improve pain outcomes for people with comorbid CP and clinically diagnosed MI. Ten electronic databases were searched from inception until May 2023. Randomised controlled trials (RCTs) were included if they evaluated interventions for CP-related outcomes among people with comorbid CP and clinically diagnosed MI. Pain-related and mental health outcomes were reported as primary and secondary outcomes, respectively. 26 RCTs (2,311 participants) were included. Four trials evaluated the effectiveness of cognitive-behavioural therapy, 6 mindfulness-based interventions, 1 interpersonal psychotherapy, 5 body-based interventions, 5 multi-component interventions, and 5 examined pharmacological-based interventions. Overall, there was considerable heterogeneity in sample characteristics and interventions, and included studies were generally of poor quality with insufficient trial details being reported. Despite the inconsistency in results, preliminary evidence suggests interventions demonstrating a positive effect on CP may include cognitive-behavioural therapy for patients with depression (with a small to medium effect size) and multi-component intervention for people with substance use disorders (with a small effect size). Despite the high occurrence/burden of CP and MI, there is a relative paucity of RCTs investigating interventions and none in people with severe MI. More rigorously designed RCTs are needed to further support our findings. PERSPECTIVE: This systematic review presents current evidence evaluating interventions for CP-related and MH outcomes for people with comorbid CP and clinically diagnosed MI. Our findings could potentially help clinicians identify the most effective treatments to manage these symptoms for this vulnerable patient group.
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Background: Asbestos exposure is closely related to the occurrence and development of various malignancies. This prospective cohort study aimed to evaluate the incidence rate and potential risk factors in a cohort of asbestosis patients in China. Methods: The incidence of malignancies was determined in patients who had been exposed to chrysotile asbestos and diagnosed with asbestosis sequentially at Beijing Chaoyang Hospital from 1 January 2007 to 31 December 2019. Cox regression analyses were used to analyze the correlations between clinical variables and asbestosis combined with malignancies. Results: A total of 618 patients with asbestosis were identified, of whom 544 were eligible for analysis. Among them, 89 (16.36%) were diagnosed with various malignancies. The standardized incidence ratios (SIRs) of patients with asbestosis combined with malignancies were 16.61, 175, 5.23, and 8.77 for lung cancer, mesothelioma, breast cancer, and endometrial carcinoma, respectively. The risks of all malignancies and lung cancer increased with initial exposure before 17 years old, longer asbestos exposure, and smoking. Conclusions: The SIRs of patients with asbestosis-related malignancies were significantly increased in lung cancer, mesothelioma, breast cancer, and endometrial carcinoma in a hospital-based Chinese cohort. Smoking and the duration of asbestos exposure increased the risk of lung cancer.
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OBJECTIVE: To describe the prevalence, clinical features and potential risk factors of pneumoconiosis in combination with connective tissue disease (CTD) or positive autoantibodies. DESIGN: Cross-sectional study. SETTING: A retrospective study of adults recruited in China between December 2016 and November 2021. PARTICIPANTS: A total of 931 patients with pneumoconiosis at Beijing Chao-Yang Hospital were enrolled in this study; of these, 580 patients were included in the final analysis. MAIN OUTCOME MEASURES: Pneumoconiosis combined with CTD or positive autoantibodies was a major adverse outcome. RESULTS: In total, 13.8% (80/580) of the patients had combined pneumoconiosis with CTD, among whom the prevalence of CTD was 18.3% (46/251) in asbestosis and 11.4% (34/298) in silicosis/coal mine workers' pneumoconiosis. In comparison to the general Chinese adult population, the relative risk of various CTD in pneumoconiosis, including rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, primary Sjögren's syndrome, idiopathic inflammatory myopathy and antineutrophil cytoplasmic antibodies-associated vasculitis, were 11.85, 12.12, 127.40, 4.23, 9.94 and 644.66, respectively. Multivariate analysis revealed that female sex (OR 2.55, 95% CI 1.56 to 4.17) and a later stage of pneumoconiosis (OR 2.04, 95% CI 1.24 to 3.34) were the independent risk factors for CTD in patients with pneumoconiosis (all p<0.050). CONCLUSION: CTD is highly prevalent in patients with pneumoconiosis, especially in patients of asbestosis, and silicosis/coal mine workers' pneumoconiosis. Female sex and later stages of pneumoconiosis are associated with an increased risk of combined with CTD.
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Asbestose , Doenças do Tecido Conjuntivo , Pneumoconiose , Silicose , Adulto , Humanos , Feminino , Estudos Transversais , Asbestose/etiologia , Estudos Retrospectivos , Pneumoconiose/complicações , Pneumoconiose/epidemiologia , Doenças do Tecido Conjuntivo/complicações , Doenças do Tecido Conjuntivo/epidemiologia , Silicose/complicações , Silicose/epidemiologia , Autoanticorpos , Carvão Mineral , China/epidemiologiaRESUMO
Paclitaxel (PTX) resistance is a key cause of chemotherapy failure in patients with triple negative breast cancer (TNBC). The aim of this study is to investigate the effect and mechanism of long non-coding RNA (lncRNA) on the PTX resistance of TNBC cells through autophagy. MDA-MB-231 cells are used to induce the PTX-resistant TNBC cell line MDA-MB-231.PR (MDR) by increasing dose intermittently. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to validate the mRNA levels of phosphoinositide-3-kinase class 3 (PIK3C3), miR-361-5p and lncRNA PRKCQ-AS1 in the cells, and Western blot analysis was used to detect the protein expressions of PIK3C3, autophagy-related, drug-resistant and apoptosis-related genes. MDC staining detected the formation of autophagic vacuoles. The interactions between miR-361-5p and PIK3C3 and between lncRNA PRKCQ-AS1 and miR-361-5p were verified by dual-luciferase assay. Cell viability, apoptosis, migration and invasion were assessed by performing MTT, flow cytometry assay, and transwell assay. The mRNA level of miR-361-5p and the autophagy and drug resistance levels of TNBC PTX-resistant cells were significantly up-regulated. miR-361-5p could target autophagy-related gene PIK3C3, and overexpression of miR-361-5p could down-regulate PIK3C3 protein expression and autophagy level and PTX resistance of MDR cells. LncRNA PRKCQ-AS1 was selected through bioanalysis, and miR-361-5p could target lncRNA PRKCQ-AS1. In addition, lncRNA PRKCQ-AS1 level was up-regulated in TNBC PTX-resistant cells, and knockdown of lncRNA PRKCQ-AS1 could weaken autophagy and drug resistance level and could promote cell apoptosis. Overexpression of lncRNA PRKCQ-AS1 reversed the pro-apoptotic effect and down-regulation of autophagy and resistance levels was induced by miR-361-5p. In vivo experiments were performed to verify the role of lncRNA PRKCQ-AS1. We demonstrate that down-regulation of lncRNA PRKCQ-AS1 weakened PTX resistance and promoted cell apoptosis by miR-361-5p/PIK3C3 mediated autophagy.
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MicroRNAs , RNA Longo não Codificante , Neoplasias de Mama Triplo Negativas , Humanos , MicroRNAs/genética , RNA Longo não Codificante/genética , Neoplasias de Mama Triplo Negativas/genética , Proteína Quinase C-theta/genética , Proteína Quinase C-theta/metabolismo , Paclitaxel/farmacologia , Proliferação de Células , Linhagem Celular Tumoral , Autofagia , RNA Mensageiro , Regulação Neoplásica da Expressão GênicaRESUMO
Silicosis is an irreversible, progressive, fibrotic lung disease caused by long-term exposure to dust-containing silica particles at the workplace. Despite the precautions enforced, the rising incidence of silicosis continues to occur globally, particularly in developing countries. A better understanding of the disease progression and potential metabolic reprogramming of silicosis is warranted. The low- or high-dose silica-induced pulmonary fibrosis in mice was constructed to mimic chronic or accelerated silicosis. Silica-induced mice lung fibrosis was analyzed by histology, lung function, and computed tomography scans. Non-targeted metabolomics of the lung tissues was conducted by ultra-high-performance liquid chromatography-mass spectrometry to show the temporal metabolic trajectory. The low-dose silica-induced silicosis characterized inflammation for up to 42 days, with the onset of cellular silicon nodules. Conversely, the high-dose silica-induced silicosis characterized inflammation for up to 14 days, after which the disease developed rapidly, with a large volume of collagen deposition, presenting progressive massive fibrosis. Both low- and high silica-induced fibrosis had aberrant lipid metabolism. Combined with the RNA-Seq data, this multiomics study demonstrated alterations in the enzymes involved in sphingolipid metabolism. Time-dependent metabolic reprogramming revealing abnormal glycerophospholipid metabolism was intimately associated with the process of inflammation, whereas sphingolipid metabolism was crucial during lung fibrosis. These findings suggest that lipid dysregulation, especially sphingolipid metabolism, was involved in the process of silicosis.
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Fibrose Pulmonar , Silicose , Camundongos , Animais , Fibrose Pulmonar/metabolismo , Dióxido de Silício/toxicidade , Pulmão/patologia , Silicose/patologia , Fibrose , Inflamação/induzido quimicamente , Esfingolipídeos/toxicidade , Lipídeos , Modelos Animais de DoençasRESUMO
BACKGROUND: People with serious mental illness (SMI) experience higher mortality partially attributable to higher long-term condition (LTC) prevalence. However, little is known about multiple LTCs (MLTCs) clustering in this population. METHODS: People from South London with SMI and two or more existing LTCs aged 18+ at diagnosis were included using linked primary and mental healthcare records, 2012-2020. Latent class analysis (LCA) determined MLTC classes and multinominal logistic regression examined associations between demographic/clinical characteristics and latent class membership. RESULTS: The sample included 1924 patients (mean (s.d.) age 48.2 (17.3) years). Five latent classes were identified: 'substance related' (24.9%), 'atopic' (24.2%), 'pure affective' (30.4%), 'cardiovascular' (14.1%), and 'complex multimorbidity' (6.4%). Patients had on average 7-9 LTCs in each cluster. Males were at increased odds of MLTCs in all four clusters, compared to the 'pure affective'. Compared to the largest cluster ('pure affective'), the 'substance related' and the 'atopic' clusters were younger [odds ratios (OR) per year increase 0.99 (95% CI 0.98-1.00) and 0.96 (0.95-0.97) respectively], and the 'cardiovascular' and 'complex multimorbidity' clusters were older (ORs 1.09 (1.07-1.10) and 1.16 (1.14-1.18) respectively). The 'substance related' cluster was more likely to be White, the 'cardiovascular' cluster more likely to be Black (compared to White; OR 1.75, 95% CI 1.10-2.79), and both more likely to have schizophrenia, compared to other clusters. CONCLUSION: The current study identified five latent class MLTC clusters among patients with SMI. An integrated care model for treating MLTCs in this population is recommended to improve multimorbidity care.
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Multimorbidade , Esquizofrenia , Masculino , Humanos , Estudos de Coortes , Londres/epidemiologia , Análise de Classes LatentesRESUMO
BACKGROUND: Evidence on the association of low physical activity (PA) with depression or anxiety is well established. Yet, evidence on the association between PA and comorbid anxiety/depression remains scarce, especially in low- and middle-income countries (LMICs). Thus, this study explored this relationship among adults aged ≥18 years from 46 LMICs. METHODS: Cross-sectional, community-based data were analyzed from the World Health Survey (WHS). Multivariable multinomial logistic regression analysis was conducted to examine the association between low PA and comorbid anxiety/depression with no anxiety or depression as the base category. RESULTS: 237,023 participants [mean (SD) age = 38.4 (16.0) years; 50.8 % female] were included in the analysis. Low PA was significantly associated with depression alone (OR = 1.33; 95%CI = 1.12-1.57) and anxiety alone (OR = 1.37; 95%CI = 1.23-1.53), while the OR was highest among those with comorbid anxiety/depression (OR = 1.75; 95%CI = 1.52-2.01). CONCLUSION: Low PA is associated with particularly increased odds for comorbid anxiety/depression. Increasing PA may have a beneficial effect on the prevention of comorbid anxiety/depression. However, future longitudinal research establishing the direction of this relationship is warranted.
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Depressão , Países em Desenvolvimento , Humanos , Adulto , Feminino , Adolescente , Masculino , Depressão/epidemiologia , Estudos Transversais , Exercício Físico , Comorbidade , PrevalênciaRESUMO
OBJECTIVE: The purpose of this study was to use the MR method to explore the causal relationship between 211 gut microbiota and male reproductive and sexual health. METHODS: The MiBioGen alliance published genome-wide association study (GWAS) related genetic variation data was used as instrumental variables (IVs) for gut microbiota, and the Finngen biobank GWAS related genetic variation data was used as IVs for male infertility, abnormal sperm, sexual dysfunction, erectile dysfunction, and testicular dysfunction. The inverse variance-weighted (IVW) method was used as the MR analysis method, the results were evaluated according to the odds ratio and 95% confidence interval of the effect measures, and data sensitivity analysis was performed. RESULTS: The results showed that 6 types of gut microbiota were related to male infertility, 12 types were related to abnormal sperm, 5 types were related to sexual dysfunction, 4 types were related to erectile dysfunction, and 4 types were related to testicular dysfunction. And there was no abnormality in the data sensitivity analysis. CONCLUSION: The intestinal microbiota is closely related to male reproductive and sexual health.
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Disfunção Erétil , Microbioma Gastrointestinal , Infertilidade Masculina , Saúde Sexual , Doenças Testiculares , Masculino , Humanos , Estudo de Associação Genômica Ampla , Sêmen , Disfunção Erétil/etiologia , Infertilidade Masculina/genéticaRESUMO
Conspiracy theories can have particularly harmful effects by negatively shaping health-related behaviours. A significant number of COVID-19 specific conspiracy theories emerged in the immediate aftermath of the pandemic outbreak. The aim of this study was to systematically review the literature on conspiracy theories related to COVID-19 during the first year of the pandemic (2020), to identify their prevalence, their determinants and their public health consequences. A comprehensive literature search was carried out in PubMed and PsycINFO to detect all studies examining any conspiracy theory related to COVID-19 between January 1st 2020, and January 10th 2021. Forty-three studies were included with a total of 61,809 participants. Between 0.4 and 82.7% of participants agreed with at least one conspiracy belief. Certain sociodemographic factors (young age, female gender, being non-white, lower socioeconomic status), psychological aspects (pessimism, blaming others, anger) and other qualities (political conservatism, religiosity, mistrust in science and using social media as source of information) were associated with increased acceptance of conspiracy theories. Conspiracy beliefs led to harmful health-related behaviours and posed a serious public health threat. Large-scale collaborations between governments and healthcare organizations are needed to curb the spread of conspiracy theories and their adverse consequences.