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Introduction: Type 2 diabetes mellitus (T2DM) is a metabolic disease characterized by diminished insulin secretion and hyperglycemia leading to damage of multiple organs. The present study is aimed to test the association between type 2 diabetes vascular complications and K469E variant (rs5498) of the intercellular adhesion molecule-1 (ICAM1) gene. Methods: Online databases were searched to retrieve all publications relating to the ICAM1 rs5498 variant in human diabetic vascular complications. In the present meta-analysis, we included all eligible studies and calculated the pooled results using MetaGenyo web tool. Results: Studies concerning ICAM1 gene K469E variant association with either type 2 diabetes or diabetes related vascular complications were included in this meta-analysis. Fifteen articles were included in this analysis (n=10 for T2DM; n=5 for diabetes nephropathy; n=8 for diabetes retinopathy). ICAM1 K469E variant significantly increased the risk of T2DM in the allelic (OR = 1.10, 95% CI: 1.01-1.20, P = 0.032) and recessive models (OR = 1.27, 95% CI: 1.08-1.49, P = 0.004). However, the ICAM1 gene K469E variant is not associated with diabetic nephropathy or diabetic retinopathy. No noticeable evidence of publication bias was detected. Conclusion: In summary, our study indicated that ICAM1 K469E variant was significantly associated with the increased risk of diabetes but not with the diabetic vascular complications.

Velocardiofacial syndrome (VCFS) is one of the most common genetic disorders that affect every major system in the body. The worldwide frequency of VCFS is 1 in 2000 live births. A search using the terms and variants of velo-cardio facial syndrome, VCFS, and disabilities within PubMed, Embase, and Scopus was carried out and restricted to human studies published in English. Further, reference lists were checked to identify relevant studies. The phenotypic spectrum of VCFS overlaps with that of DiGeorge syndrome and includes physical, cognitive, behavioral, and neurological disabilities. The VCFS is caused by hemizygous deletions on chromosome 22q11.2 and usually diagnosed at childhood. Several approaches, such as fluorescence in situ hybridization and polymerase chain reaction-based techniques, have been applied to analyze deleted regions. As majority of the VCFS children have multiple diagnoses, it may need more time to find appropriate combination of medications that will work for them. Treatment for VCFS is always depended on child's age, overall health, medical history, and child's tolerance for specific medications, procedures, or therapies, and parents' opinion or preference.

Introduction: Endothelial nitric oxide synthase (eNOS) genes have been implicated in renal hemodynamics as potent regulators of vascular tone and blood pressure. It has been linked to a reduction in plasma nitric oxide levels. Several studies have recently been conducted to investigate the role of NOS3 gene polymorphisms and end-stage renal disease (ESRD). However, the results are still unclear and the mechanisms are not fully defined. As a result, we conducted a meta-analysis to examine the relationship between NOS3 gene polymorphism and ESRD in autosomal polycystic kidney disease (ADPKD) patients., Methods: To assess the relationship between NOS3 gene polymorphism and ESRD, relevant studies published between September 2002 and December 2020 were retrieved from the PubMed (Medline), EMBASE, Google Scholar, and Web of Science databases. The pooled odds ratio (OR) and 95 % confidence interval (CI) were calculated using a fixed-effect model. To assess the heterogeneity of studies, we used Cochrane's Q test and the Higgins and Thompson I2 statistics., Results: Our meta-analysis of 13 studies showed that the presence of the two NOS3 gene polymorphisms significantly increased ESRD risk in ADPKD patients with 4a/b gene polymorphism (aa+ab vs. bb: OR=1.95, 95% CI=1.24-3.09, p=0.004). In addition, no significant association was found between the NOS3 894G>T (Glu298Asp) polymorphism and the risk of ESRD in ADPKD patients (GT+TT vs. GG: OR=1.21, 95% CI=0.93-1.58, p=0.157). There was no evidence of publication bias., Conclusions: The findings of the current meta-analysis suggest that NOS3 intron 4a/b polymorphism plays a vital role in the increasing risk of ESRD in ADPKD patients.