Exploring Candidate Gene Studies and Alexithymia: A Systematic Review.

BACKGROUND: Alexithymia is a trait involving difficulties in processing emotions. Genetic association studies have investigated candidate genes involved in alexithymia's pathogenesis. Therefore, the aim of the present study was to perform a systematic review of the genetic background associated with alexithymia. METHODS: A systematic review of genetic studies of people with alexithymia was conducted. Electronic databases including PubMed, Scopus, and Web of Science were searched for the study purpose. We used the words "Alexithymia", "gene", "genetics", "variants", and "biomarkers". The present systematic review was performed following the Preferred Reporting Items for Systematic reviews and Meta-Analyses statement. We found only candidate gene studies. A total of seventeen studies met the eligibility criteria, which comprised 22,361 individuals. The candidate genes associated with alexithymia were the serotoninergic pathway genes solute carrier family 6 member 4 (SLC6A4), serotonin 1A receptor (HTR1A), and serotonin 1A receptor (HTR2A); the neurotransmitter metabolism genes dopamine receptor D2 (DRD2), ankyrin repeat and kinase domain containing 1 (ANKK1), catechol-o-methyltransferase (COMT), brain-derived neurotrophic factor (BDNF), and oxytocin receptor (OXTR); and other pathway genes, vitamin D-binding protein (VDBP), tumor protein P53 regulated apoptosis inducing protein 1 (TP53AIP1), Rho GTPase Activating Protein 32 (ARHGAP32), and transmembrane protein 88B (TMEM88B). CONCLUSION: The results of this study showed that only case-control gene studies have been performed in alexithymia. On the basis of our findings, the majority of alexithymia genes and polymorphisms in this study belong to the serotoninergic pathway and neurotransmitter metabolism genes. These data suggest a role of serotoninergic neurotransmission in alexithymia. Nevertheless, more and future research is required to learn about the role of these genes in alexithymia.

Effects of IL-6/IL-6R axis alterations in serum, plasma and cerebrospinal fluid with the schizophrenia: an updated review and meta-analysis of 58 studies.

Studies investigating the association between IL-6/IL-6R axis and schizophrenia (SZ) susceptibility found inconsistent data. To reconcile the results, a systematic review followed by a meta-analysis was performed to assess the associations. This study followed the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. A comprehensive search of the literature was carried out in July 2022 using electronic databases PubMed, EBSCO, Science Direct, PsychInfo, and Scopus. Study quality was assessed by the Newcastle-Ottawa scale. Pooled standard mean difference (SMD) with 95% confidence interval (CI) was calculated by fixed-effect or random-effect model analysis. Fifty-eight studies were identified, including 4,200 SZ patients and 4,531 controls. Our meta-analysis results showed an increase of IL-6 levels in plasma, serum, or CSF and decreased IL-6R levels in serum in patients under treatment. Further studies are needed to better elucidate the correlation between the IL-6/IL-6R axis and the schizophrenia.

The association of cytokines genes (IL-6 and IL-10) with the susceptibility to schizophrenia: A systematic review and meta-analysis.

Cytokines are among the important effectors and messenger molecules for restoring the homeostasis tissue after an inflammatory response. The association between IL-6 and IL-10 genes polymorphisms with the schizophrenia susceptibility have yielded controversial results. To reconcile the results, a systematic review followed by meta-analysis was performed to assess the association. We carried out literature searches of PubMed, Scopus, EBSCO, and Web of Sciences databases. Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated to assess the strength of the association. Subgroup analysis, heterogeneity analyses, and publication bias were also calculated in the meta-analysis. A total of 22 case-control studies, consisting of 4,993 schizophrenic patients and 5,195 healthy controls, were included in the meta-analysis. The meta-analysis suggests that the IL-6 rs1800795 polymorphism displays a protective role against schizophrenia, while the IL-10 rs1800896 and rs1800872 polymorphisms confer an increased risk of schizophrenia. Similar results were found in subgroup analysis by ethnicity. We did not find association between IL-10 rs1800871 polymorphism and schizophrenia susceptibility. Finally, this meta-analysis suggested that the dysregulation of cytokines could lead to the pathogenesis of the schizophrenia.

High Serum Levels of IL-6 Are Associated with Suicide Attempt but Not with High Lethality Suicide Attempts: A Preliminary Case-Control Study.

Suicide attempts are an emerging health problem around the world. Increased levels of IL-6 have been associated with suicidal behavior. Therefore, the aims of this study were to evaluate the serum levels of IL-6 in individuals with suicide attempts and a comparison group and to associate the IL-6 levels with the lethality of the suicide attempt. Additionally, we associated the rs2228145 polymorphism of the IL6R gene with suicide attempts or with the IL-6 serum levels. Suicide attempts and their lethality were evaluated using the Columbia Suicide Severity Rating Scale. The serum concentrations of IL-6 were measured by the ELISA technique in individuals with suicide attempts and then compared to a control group. The rs2228145 polymorphism of the IL6R gene was analyzed by real-time polymerase chain reaction. We found elevated serum levels of IL-6 in the suicide attempt group when compared to the control group (F = 10.37, p = 0.002). However, we found no differences of the IL-6 levels between high and low lethality. The IL6R gene polymorphism rs2479409 was not associated with suicide attempts. Our data suggest that IL-6 serum is increased in individuals with suicide attempts.

Abdominal Surgical Site Infection Incidence and Risk Factors in a Mexican Population.

OBJECTIVE: To investigate possible predictors and prevalence of surgical site infections (SSIs) in a group of Mexican patients who underwent open abdominal surgery. METHODS: This retrospective study included all patients (N = 755) who underwent elective or emergency open abdominal surgeries from October 2011 to March 2012. MAIN OUTCOME MEASURE: Sociodemographic and clinical characteristics were collected through preoperative and postoperative examinations by the infection surveillance team. The relationship among variables (age, gender, body mass index, comorbidities, smoking habit, antimicrobial prophylaxis, hair removal, American Society of Anesthesiologists classification, type of operation, duration of operation, and SSI classification) was analyzed by odds ratio and χ tests. MAIN RESULTS: Of the 755 patients, 91 (12%) suffered from SSI. Several variables were associated with SSI: American Society of Anesthesiologists classification (P = .001) and receiving preoperative prophylactic antimicrobials (P < .0001), among other factors. Isolated pathogens were mostly enterobacteria (60%). CONCLUSIONS: Surveillance plays an important role in the control and prevention of SSI. Providers must implement appropriate procedures to reduce SSI after abdominal surgery.

Association between CRP and TNF-α genes Variants and Cardiovascular Heart Disease in a Mexican Population: Protocol for a Case-Control Study.

BACKGROUND: The C-reactive protein (CRP) and the tumor necrosis factor-alpha (TNF-α) are considered markers of inflammation and have been shown to predict the risk of incident cardiovascular events. However, few studies have undertaken a comprehensive examination of SNPs (single nucleotide polymorphisms) of the CRP and TNF-α genes; due to this, we will present a protocol study to evaluate the role of the CRP and TNF-α genes in Mexican individuals. METHODS/DESIGN: we will perform a case-control study to explore the CRP and TNF-α genotype distribution as well as the serum influence of rs1800947, rs1130864, rs2794521 and rs1205 (polymorphisms of the CRP gene) and rs361525, rs1800629, rs1799724, rs1800630, rs1799964 (of the TNF-α gene) in Mexican individuals who present coronary artery disease. ETHICS AND DISSEMINATION: a written informed consent will be obtained from all the participating subjects. An article detailing the results of the study will be submitted for publication in an international peer-reviewed journal, in accordance with STROBE criteria.

Association of G308A and G238A Polymorphisms of the TNF-α Gene with Risk of Coronary Heart Disease: Systematic Review and Meta-analysis.

BACKGROUND AND AIMS: It is widely acknowledged that coronary heart disease (CHD) has a genetic influence. One of the most promising candidate genes is tumor necrosis factor-alpha (TNF-α). Although there have been several positive studies associating the TNF-α gene and CHD, the evidence is not entirely consistent. The aim of the study was to evaluate the role of the TNF-α gene in CHD using combined evidence by generating a meta-analysis and a systematic review of all published data. METHODS: Meta-analysis and systematic review were conducted using 27 articles of genetic association studies of the TNF-α gene variants (G308A and G238A) and CHD. To analyze the association we used allelic, additive, dominant and recessive models. Moreover, we conducted a subanalysis by populations using the same four models. RESULTS: TNF-α variant G308A showed a significant association with CHD but only when the analysis comprised the whole population. In addition, the variant G238A yielded the same outcome in the Asian population. CONCLUSIONS: Genetic polymorphisms at positions -308 and -238 in the promoter region of the TNF-α gene may be useful as predictive factors for CHD.

The role of gene variants of the inflammatory markers CRP and TNF-α in cardiovascular heart disease: systematic review and meta-analysis.

It is widely acknowledged that cardiovascular heart disease (CHD) has a genetic influence. Several studies have investigated the role of inflammatory markers like C-reactive protein (CRP) and tumor necrosis factor α (TNF-α) in the causation of cardiovascular diseases. Although there have been several positive studies associating CRP and TNF-α genes with CHD, the evidence is not entirely consistent. Therefore, we performed a meta-analysis to gain a better understanding into this issue. The meta-analysis was conducted with 22 articles of genetic association studies of CRP (G1059C rs1800947, C1444T rs1130864, C717T rs2794521 and G3872A rs1205) and TNF-α (C857T rs1799724, C863A rs1800630 and T1031C rs1799964) genes. To analyze the association of these variants with CHD we used the following models: allelic, additive, dominant and recessive. In addition, we performed a sub-group analysis by Caucasian population using the same four models. CRP and TNF-α gene polymorphisms showed a positive significant association with CHD. This study provides evidence that rs2794521 of the CRP gene and rs1799724, rs1800630 and rs1799964 of the TNF-α gene polymorphisms may be risk factors to manifest CHD. The analysis of rs1800947 and rs1205 of the CRP gene yielded a protective effect in the pathogenesis of this disease. Only the analysis of the rs1130864 polymorphism showed a lack of association with CHD. To have conclusive outcomes it is necessary to integrate more studies to confirm our findings.