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BMC Cardiovascular Disorders Jun 2024Stent restenosis is a relatively common phenomenon among patients with coronary heart disease undergoing percutaneous coronary intervention (PCI). It seems that a set of...
BACKGROUND
Stent restenosis is a relatively common phenomenon among patients with coronary heart disease undergoing percutaneous coronary intervention (PCI). It seems that a set of clinical, laboratory, and even genetic factors make people susceptible to such a phenomenon and in fact, this is multi-factorial. We aimed to first determine the underlying clinical and laboratory risk factors for the occurrence of stent re-stenosis after PCI based on a systematic review study, and after that, through a bioinformatics study, to evaluate the related genes and microRNAs with the occurrence of stent re-stenosis.
MAIN TEXT
In the first step, the manuscript databases including Medline, Web of Knowledge, Google Scholar, Scopus, and Cochrane were deeply searched by the two blinded investigators for all eligible studies based on the considered keywords to introduce clinical and laboratory determinants of stent re-stenosis. In the bioinformatic phase, and following a review of the literature to identify genes and microRNAs involved in restenosis, the interaction of each gene with other genes associated with stent re-stenosis was determined by GeneMANIA network analysis and Cytoscape software. Overall, 67 articles (including 40,789 patients) on clinical and biochemical predictors for stent restenosis and 25 articles on genetic determinants of this event were eligible for the final analysis. The predictors for this event were categorized into four subgroups patient-based parameters including traditional cardiovascular risk profiles, stent-based parameters including type and diametric characteristics of the stents used, coronary lesion-based parameters including several two target lesions and coronary involvement severity and laboratory-based parameters particularly related to activation of inflammatory processes. In the bioinformatic phase, we uncovered 42 genes that have been described to be involved in such a phenomenon considering a special position for genes encoding inflammatory cytokines. Also, 12 microRNAs have been pointed to be involved in targeting genes involved in stent re-stenosis.
CONCLUSIONS
The incidence of stent re-stenosis will be the result of a complex interaction of clinical risk factors, laboratory factors mostly related to the activation of inflammatory processes, and a complex network of gene-to-gene interactions.
Topics: Humans; Percutaneous Coronary Intervention; Coronary Restenosis; Stents; Risk Factors; Computational Biology; Coronary Artery Disease; MicroRNAs; Risk Assessment; Genetic Predisposition to Disease; Treatment Outcome; Female; Male; Gene Regulatory Networks; Middle Aged; Aged
PubMed: 38877398
DOI: 10.1186/s12872-024-03955-3 -
Frontiers in Oral Health 2024The association between chronic oral diseases and other major systemic health conditions, commonly referred to as the oral-systemic health connection, has been...
BACKGROUND
The association between chronic oral diseases and other major systemic health conditions, commonly referred to as the oral-systemic health connection, has been previously studied with several underlying common risk factors and pathways linking both groups of diseases. Psychosocial factors contribute to an increased susceptibility to chronic oral and non-oral diseases. The aim of this review is to summarize the current state of knowledge on the role of psychosocial stress in chronic oral and systemic diseases.
METHODS
A search strategy was built and a literature search was conducted using four databases (CINAHL, Embase, Medline, PsycINFO). A combination of search terms related to psychosocial stress, systemic disease, and oral conditions were used. Studies were eligible for inclusion if they included human adults (aged 18 years and older), included psychosocial factors as an exposure measure, and outcome measures of both an oral and systemic condition. Only English-language articles were considered. Pilot testing of the data extraction form and calibration were conducted and data were extracted independently by one researcher.
RESULTS
A total of fifteen articles out of eighty full-text articles screened were determined to be eligible for inclusion in this review. Periodontal disease was the most commonly studied oral disease, measured in 53% of included articles, with the most commonly studied systemic diseases being of mental health conditions (40%) and diabetes (47%). Psychosocial stress was measured using a range of psychometric indicators and/or biomarkers, including perceived stress, individual behaviours, childhood adversity, and cortisol. In total, fourteen studies found a positive association between measures of psychosocial stress and oral-systemic health.
CONCLUSION
Psychosocial stress may be a common contributor to both chronic oral and non-oral diseases.
PubMed: 38872985
DOI: 10.3389/froh.2024.1378467 -
BMC Genomics Jun 2024The association between Apolipoprotein A5 (APOA5) genetic polymorphisms and susceptibility to metabolic syndrome (MetS) has been established by many studies, but there... (Meta-Analysis)
Meta-Analysis
BACKGROUND
The association between Apolipoprotein A5 (APOA5) genetic polymorphisms and susceptibility to metabolic syndrome (MetS) has been established by many studies, but there have been conflicting results from the literature. We performed a meta-analysis of observational studies to evaluate the association between APOA5 gene polymorphisms and the prevalence of MetS.
METHODS
PubMed, Web of Science, Embase, and Scopus were searched up to April 2024. The random effects model was used to estimate the odds ratios (ORs) and 95% confidence intervals (CI) of the association between APOA5 gene polymorphisms and the prevalence of MetS development. The potential sources of heterogeneity were evaluated by subgroup analyses and sensitivity analyses.
RESULTS
A total of 30 studies with 54,986 subjects (25,341 MetS cases and 29,645 healthy controls) were included. The presence of rs662799 and rs651821 polymorphisms is associated with an approximately 1.5-fold higher likelihood of MetS prevalence (OR = 1.42, 95% CI: 1.32, 1.53, p < 0.001; I = 67.1%; P-heterogeneity < 0.001; and OR = 1.50, 95% CI: 1.36-1.65, p < 0.001), respectively. MetS is also more prevalent in individuals with the genetic variants rs3135506 and rs2075291. There was no evidence of a connection with rs126317.
CONCLUSION
The present findings suggest that polymorphisms located in the promoter and coding regions of the APOA5 gene are associated with an increased prevalence of MetS in the adult population. Identifying individuals with these genetic variations could lead to early disease detection and the implementation of preventive strategies to reduce the risk of MetS and its related health issues. However, because the sample size was small and there was evidence of significant heterogeneity for some APOA5 gene polymorphisms, these results need to be confirmed by more large-scale and well-designed studies.
Topics: Metabolic Syndrome; Apolipoprotein A-V; Humans; Genetic Predisposition to Disease; Polymorphism, Single Nucleotide; Odds Ratio
PubMed: 38867151
DOI: 10.1186/s12864-024-10493-x -
Turkish Journal of Obstetrics and... Jun 2024Endometriosis is a common condition among women and can cause complications such as abdominal pain, dysmenorrhea, and infertility. One of the potential causes of this...
Endometriosis is a common condition among women and can cause complications such as abdominal pain, dysmenorrhea, and infertility. One of the potential causes of this disease is autoimmunity. However, evidence regarding the role of autoimmunity is conflicting and inconclusive. The aim of this study was to investigate whether autoantibodies, a sign of autoimmunity, are present in people suffering from endometriosis. Relevant studies up to April 14, 2023 were identified by systematically searching Scopus, PubMed, Web of Science, Embase, and Google Scholar. This meta-analysis includes all qualified case-control studies of human populations that analyzed the association between serum autoantibodies and endometriosis. The odd ratios and 95% confidence intervals were calculated. In addition, heterogeneity and publication bias were examined, and subgroup analyses were performed based on region and target antigens. Forty-one studies were included, comparing 2,825 endometriosis patients with 4,158 healthy controls. The meta-analysis findings indicated a significant association between the presence of autoantibodies in the serum and an increased susceptibility to endometriosis (odds ratio: 4.242, confidence interval 95%: 3.824-4.706, p<0.001). In addition, there was a significant correlation between the presence of endometriosis and serum levels of anti-nuclear antibodies, B2 glycoprotein 1, CA125, carbonic anhydrase 1, cardiolipin, endometrial, laminin-1, smooth muscle, and syntaxin autoantibodies. Upon further analysis, it was found that the serum levels of these autoantibodies were higher in patients with endometriosis from North America than in those from other regions (p=0.001). The study revealed a significant correlation between serum autoantibodies and susceptibility to endometriosis, highlighting autoimmunity as a potential cause.
PubMed: 38853493
DOI: 10.4274/tjod.galenos.2024.77489 -
Frontiers in Cellular and Infection... 2024The microbiota-gut-lung axis has elucidated a potential association between gut microbiota and idiopathic pulmonary fibrosis (IPF). However, there is a paucity of...
BACKGROUND
The microbiota-gut-lung axis has elucidated a potential association between gut microbiota and idiopathic pulmonary fibrosis (IPF). However, there is a paucity of population-level studies with providing robust evidence for establishing causality. This two-sample Mendelian randomization (MR) analysis aimed to investigate the causal relationship between the gut microbiota and IPF as well as lung function.
MATERIALS AND METHODS
Adhering to Mendel's principle of inheritance, this MR analysis utilized summary-level data from respective genome-wide association studies (GWAS) involving 211 gut microbial taxa, IPF, and lung function indicators such as FEV, FVC, and FEV/FVC. A bidirectional two-sample MR design was employed, utilizing multiple MR analysis methods, including inverse variance-weighted (IVW), weighted median, MR-Egger, and weighted mode. Multivariable MR (MVMR) was used to uncover mediating factors connecting the exposure and outcome. Additionally, comprehensive sensitivity analyses were conducted to ensure the robustness of the results.
RESULTS
The MR results confirmed four taxa were found causally associated with the risk of IPF. (OR=0.773, 95% CI: 0.610-0.979, p=0.033), (OR=0.773, 95% CI: 0.610-0.979, p=0.033), and (OR=0.793, 95% CI: 0.652-0.965, p=0.020) exerted protective effects on IPF, while (OR=1.349, 95% CI: 1.021-1.783, p=0.035) promote the development of IPF. Several taxa were causally associated with lung function, with those in , and being the most prominent beneficial microbiota, while those in , and were associated with impaired lung function. As for the reverse analysis, MR results confirmed the effects of FEV and FVC on the increased abundance of six taxa (, and ) with a boosted level of evidence. MVMR suggested monounsaturated fatty acids, total fatty acids, saturated fatty acids, and ratio of omega-6 fatty acids to total fatty acids as potential mediating factors in the genetic association between gut microbiota and IPF.
CONCLUSION
The current study suggested the casual effects of the specific gut microbes on the risk of IPF and lung function. In turn, lung function also exerted a positive role in some gut microbes. A reasonable dietary intake of lipid substances has a certain protective effect against the occurrence and progression of IPF. This study provides novel insights into the potential role of gut microbiota in IPF and indicates a possible gut microbiota-mediated mechanism for the prevention of IPF.
Topics: Humans; Mendelian Randomization Analysis; Idiopathic Pulmonary Fibrosis; Gastrointestinal Microbiome; Genome-Wide Association Study; Lung; Respiratory Function Tests; Genetic Predisposition to Disease
PubMed: 38841114
DOI: 10.3389/fcimb.2024.1348685 -
Journal of Hazardous Materials Aug 2024Existing studies on the most impactful component remain controversial, hindering the optimization of future air quality standards that concerns particle composition. We... (Meta-Analysis)
Meta-Analysis Review
Existing studies on the most impactful component remain controversial, hindering the optimization of future air quality standards that concerns particle composition. We aimed to summarize the health risk associated with PM components and identify those components with the greatest health risk. We performed a meta-analysis to quantify the combined health effects of PM components, and used the meta-smoothing to produce the pooled concentration-response (C-R) curves. Out of 8954 initial articles, 80 cohort studies met the inclusion criteria, including a total of 198.08 million population. The pooled C-R curves demonstrated approximately J-shaped association between total mortality and exposure to BC, and NO, but U-shaped and inverted U-shaped relationship withSO and OC, respectively. In addition, this study found that exposure to various elements, including BC,SONO, NH, Zn, Ni, and Si, were significantly associated with an increased risk of total mortality, with Ni presenting the largest estimate. And exposure to NO, Zn, and Si was positively associated with an increased risk of respiratory mortality, while exposure to BC, SO, and NO showed a positive association with risk of cardiovascular mortality. For health outcome of morbidity, BC was notably associated with a higher incidence of asthma, type 2 diabetes and stroke. Subgroup analysis revealed a higher susceptibility to PM components in Asia compared to Europe and North America, and females showed a higher vulnerability. Given the significant health effects of PM components, governments are advised to introduce them in regional monitoring and air quality control guidelines. ENVIRONMENTAL IMPLICATION: PM is a complex mixture of chemical components from various sources, and each component has unique physicochemical properties and uncertain toxicity, posing significant threat to public health. This study systematically reviewed cohort studies on the association between long-term exposure to 13 PM components and the risk of morbidity and mortality. And we applied the meta-smoothing approach to establish the pooled concentration-response associations between PM components and mortality globally. Our findings will provide strong support for PM components monitoring and the improvement of air quality-related regulations. This will aid in helping to enhance health intervention strategies and mitigating public exposure to detrimental particulate matter.
Topics: Particulate Matter; Humans; Air Pollutants; Environmental Exposure; Cohort Studies; Cardiovascular Diseases; Air Pollution
PubMed: 38838524
DOI: 10.1016/j.jhazmat.2024.134715 -
Technology in Cancer Research &... 2024Exploring the relationship between the hOGG1 rs1052133 polymorphism and the occurrence of nasopharyngeal carcinoma (NPC). PubMed, Web of Science, Scopus, CNKI,... (Meta-Analysis)
Meta-Analysis
Exploring the relationship between the hOGG1 rs1052133 polymorphism and the occurrence of nasopharyngeal carcinoma (NPC). PubMed, Web of Science, Scopus, CNKI, Wanfangdata, and VIP were used to search for studies and the NOS evaluation scale was used to evaluate the quality. All studies were grouped according to different genotypes. The Cochrane's Q test and I test were used for heterogeneity evaluations. If heterogeneity was small, the fixed effects model was used, and conversely, the random effects model was used. Publication bias was also detected. P < .05 in all results indicated statistically significant. We ultimately included 6 studies with 2021 NPC patients in the study group and 2375 healthy populations in the control group. After meta-analysis, it was found that the total OR value of the "Ser/Cys (CG) vs Ser/Ser (CC)" group was 1.00 (95% CI: 0.85-1.18) and the "Cys/Cys (GG) vs Ser/Ser (CC)" group was 1.06 (95% CI: 0.87-1.28). These results were not statistically significant (P > .05). Furthermore, the integrated total OR values of each group were not statistically significant with or without the smoking history, even in other genotype models (Allele, Dominant, Recessive, and Additive) (P > .05). There is no clear correlation between the hOGG1 rs1052133 polymorphism and the occurrence of NPC, even with or without the smoking history.
Topics: Humans; Nasopharyngeal Carcinoma; Genetic Predisposition to Disease; Polymorphism, Single Nucleotide; DNA Glycosylases; Genotype; Alleles; Nasopharyngeal Neoplasms; Odds Ratio; Genetic Association Studies; Publication Bias; Case-Control Studies
PubMed: 38836311
DOI: 10.1177/15330338241246457 -
BJS Open May 2024Diverticulosis is a normal anatomical variant of the colon present in more than 70% of the westernized population over the age of 80. Approximately 3% will develop...
BACKGROUND
Diverticulosis is a normal anatomical variant of the colon present in more than 70% of the westernized population over the age of 80. Approximately 3% will develop diverticulitis in their lifetime. Many patients present emergently, suffer high morbidity rates and require substantial healthcare resources. Diverticulosis is the most common finding at colonoscopy and has the potential for causing a significant morbidity rate and burden on healthcare. There is a need to better understand the aetiology and pathogenesis of diverticular disease. Research suggests a genetic susceptibility of 40-50% in the formation of diverticular disease. The aim of this review is to present the hypothesized functional effects of the identified gene loci and environmental factors.
METHODS
A systematic literature review was performed using PubMed, MEDLINE and Embase. Medical subject headings terms used were: 'diverticular disease, diverticulosis, diverticulitis, genomics, genetics and epigenetics'. A review of grey literature identified environmental factors.
RESULTS
Of 995 articles identified, 59 articles met the inclusion criteria. Age, obesity and smoking are strongly associated environmental risk factors. Intrinsic factors of the colonic wall are associated with the presence of diverticula. Genetic pathways of interest and environmental risk factors were identified. The COLQ, FAM155A, PHGR1, ARHGAP15, S100A10, and TNFSF15 genes are the strongest candidates for further research.
CONCLUSION
There is increasing evidence to support the role of genomics in the spectrum of diverticular disease. Genomic, epigenetic and omic research with demographic context will help improve the understanding and management of this complex disease.
Topics: Humans; Risk Factors; Epigenesis, Genetic; Genetic Predisposition to Disease; Diverticular Diseases; Gene-Environment Interaction; Obesity
PubMed: 38831715
DOI: 10.1093/bjsopen/zrae032 -
Clinical Immunology (Orlando, Fla.) May 2024Rheumatoid arthritis (RA) is a systemic chronic autoimmune disease that primarily affects the joints and surrounding soft tissues, characterized by chronic inflammation... (Review)
Review
Rheumatoid arthritis (RA) is a systemic chronic autoimmune disease that primarily affects the joints and surrounding soft tissues, characterized by chronic inflammation and proliferation of the synovium. Various immune cells are involved in the pathophysiology of RA. The complex interplay of factors such as chronic inflammation, genetic susceptibility, dysregulation of serum antibody levels, among others, contribute to the complexity of the disease mechanism, disease activity, and treatment of RA. Recently, the cytokine storm leading to increased disease activity in RA has gained significant attention. Interleukin-33 (IL-33), a member of the IL-1 family, plays a crucial role in inflammation and immune regulation. ST2 (suppression of tumorigenicity 2 receptor), the receptor for IL-33, is widely expressed on the surface of various immune cells. When IL-33 binds to its receptor ST2, it activates downstream signaling pathways to exert immunoregulatory effects. In RA, IL-33 regulates the progression of the disease by modulating immune cells such as circulating monocytes, tissue-resident macrophages, synovial fibroblasts, mast cells, dendritic cells, neutrophils, T cells, B cells, endothelial cells, and others. We have summarized and analyzed these findings to elucidate the pathways through which IL-33 regulates RA. Furthermore, IL-33 has been detected in the synovium, serum, and synovial fluid of RA patients. Due to inconsistent research results, we conducted a meta-analysis on the association between serum IL-33, synovial fluid IL-33, and the risk of developing RA in patients. The pooled SMD was 1.29 (95% CI: 1.15-1.44), indicating that IL-33 promotes the onset and pathophysiological progression of RA. Therefore, IL-33 may serve as a biomarker for predicting the risk of developing RA and treatment outcomes. As existing drugs for RA still cannot address drug resistance in some patients, new therapeutic approaches are needed to alleviate the significant burden on RA patients and healthcare systems. In light of this, we analyzed the potential of targeting the IL-33/ST2-related signaling pathway to modulate immune cells associated with RA and alleviate inflammation. We also reviewed IL-33 and RA susceptibility-related single nucleotide polymorphisms, suggesting potential involvement of IL-33 and macrophage-related drug-resistant genes in RA resistance therapy. Our review elucidates the role of IL-33 in the pathophysiology of RA, offering new insights for the treatment of RA.
PubMed: 38825072
DOI: 10.1016/j.clim.2024.110264 -
Schizophrenia Bulletin Jun 2024The high co-occurrence of tobacco smoking in patients with schizophrenia spectrum disorders (SSD) poses a serious health concern, linked to increased mortality and worse...
BACKGROUND AND HYPOTHESIS
The high co-occurrence of tobacco smoking in patients with schizophrenia spectrum disorders (SSD) poses a serious health concern, linked to increased mortality and worse clinical outcomes. The mechanisms underlying this co-occurrence are not fully understood.
STUDY DESIGN
Addressing the need for a comprehensive overview of the impact of tobacco use on SSD neurobiology, we conducted a systematic review of neuroimaging studies (including structural, functional, and neurochemical magnetic resonance imaging studies) that investigate the association between chronic tobacco smoking and brain alterations in patients with SSD.
STUDY RESULTS
Eight structural and fourteen functional studies were included. Structural studies show widespread independent and additive reductions in gray matter in relation to smoking and SSD. The majority of functional studies suggest that smoking might be associated with improvements in connectivity deficits linked to SSD. However, the limited number of and high amount of cross-sectional studies, and high between-studies sample overlap prevent a conclusive determination of the nature and extent of the impact of smoking on brain functioning in patients with SSD. Overall, functional results imply a distinct neurobiological mechanism for tobacco addiction in patients with SSD, possibly attributed to differences at the nicotinic acetylcholine receptor level.
CONCLUSIONS
Our findings highlight the need for more longitudinal and exposure-dependent studies to differentiate between inherent neurobiological differences and the (long-term) effects of smoking in SSD, and to unravel the complex interaction between smoking and schizophrenia at various disease stages. This could inform more effective strategies addressing smoking susceptibility in SSD, potentially improving clinical outcomes.
PubMed: 38824451
DOI: 10.1093/schbul/sbae088