Association of greenspaces exposure with cardiometabolic risk factors: a systematic review and meta-analysis.

BACKGROUND: Cardiometabolic conditions are major contributors to the global burden of disease. An emerging body of evidence has associated access to and surrounding public open spaces (POS) and greenspace with cardiometabolic risk factors, including obesity, body mass index (BMI), hypertension (HTN), blood glucose (BG), and lipid profiles. This systematic review aimed to synthesize this evidence. METHODS: This systematic review was conducted based on the PRISMA guidelines. Four electronic databases including Web of Science, PubMed, Scopus, and Google Scholar were searched for eligible articles published until July 2023. All observational studies which assessed the association of greenspace and POS with cardiometabolic risk factors including obesity, BMI, HTN, BG, and lipid profiles were included and reviewed by two authors independently. Heterogeneity between studies was assessed using the I2 index and Cochrane's Q test. Random/fixed effect meta-analyses were used to combine the association between greenspace exposure with cardiometabolic risk factors. RESULTS: Overall, 118 relevant articles were included in our review. The majority of the articles were conducted in North America or Europe. In qualitative synthesis, access or proximity to greenspaces or POS impacts BMI and blood pressure or HTN, BG, and lipid profiles via various mechanisms. According to the random effect meta-analysis, more access to greenspace was significantly associated with lower odds of HTN (odds ratio (OR): 0.81, 95% confidence intervals (CIs): 0.61-0.99), obesity (OR: 0.83, 95% CIs: 0.77-0.90), and diabetes (OR:0.79, 95% CI: 0.67,0.90). CONCLUSIONS: Findings of this systematic review and meta-analysis suggested that greenspace accessibility is associated with some cardiometabolic risk factors. Improving greenspace accessibility could be considered as one of the main strategies to reduce cardiometabolic risk factors at population level.

Compound Heterozygous Mutations Presented with Quadriparesis and Menopause. A Case Report.

Mitochondrion regulates cellular metabolism with the aid of its respiratory complexes; any defect within these complexes can result in mitochondrial malfunction and various conditions. One such mutation can occur in SLC25A10, resulting in mitochondrial DNA depletion syndrome. It should be noted that the pattern of inheritance of this syndrome is autosomal recessive. However, we present a case with compound heterozygous mutations within this gene resulting in disease. An 18-year-old female was referred to our clinic due to menopause with a medical history of hearing loss, spasticity, hypotonia and quadriparesis. The child's birth and development were uneventful until the initiation of movement reduction and hypotonia when she was 12 months old. Afterward, the hypotonia progressed to quadriparesis and spasticity throughout the years. Our patient became completely quadriplegic up to the age of 3 and became completely deaf at 10. Her puberty onset was at the age of 9, and no significant event took place until she was 17 years old when suddenly her periods, which were regular until that time, became irregular and ceased after a year; hence, a thorough evaluation began, but similar to her previous evaluations all tests were insignificant. Nonetheless, we suspected an underlying metabolic or genetic defect; thus, we ordered a whole-exome sequencing (WES) workup and found simultaneous heterozygous mutations within SLC25A10, HFE and TTN genes that could explain her condition. When all other tests fail, and we suspect an underlying genetic or metabolic cause, WES can be of great value.

Aberrant methylation of miR-124 upregulates DNMT3B in colorectal cancer to accelerate invasion and migration.

The dysregulation of microRNA expression is significantly associated with the initiation and development of CRC. miR-124 is markedly downregulated in colorectal cancer. In the present study, the effects of methylation, over expression and downregulation of miR-124 and its target gene DNMT3B on the proliferation, migration and invasion of colorectal cell line were investigated. The promoter methylation status of miR-124 in the CRC was investigated by methylation specific PCR (MSP). The potential role of miR-124 expression in CRC cells was investigated using the demethylation reagent 5-Aza-CdR and transfection of miR-124 mimic/antimir. MSP revealed that miR-124 promoter region was hypermethylated, result in its significant downregulation in tumour tissues. We showed miR-124 expression was upregulated following 5-AZA-CdR treatment. Transfected Hct-116 cell line with miR-124 leads to decreased DNMT3B expression, cell proliferation, migration and invasion of HCT-116. In conclusion, our data indicate that miR-124 suppress colorectal cancer proliferation, migration and invasion through downregulating DNMT3B level.