Ekonomi kreatif dan pariwisata

BACKGROUND High carbon dioxide (CO2) level from indoor environments, such as classrooms and offices, might cause sick building syndrome. Excessive indoor CO2 level increases CO2 level in the blood, and over-accumulation of CO2 induces an adaptive response that requires modulation of gene expression. This study aimed to investigate the adaptive transcriptional response toward hypoxia and oxidative stress in human peripheral blood mononuclear cells (PBMCs) exposed to elevated CO2 level in vitro and its association with cell viability. METHODS PBMCs were treated in 5% CO2 and 15% CO2, representatives a high CO₂ level condition for 24 and 48 hours. Extracellular pH (pHe) was measured with a pH meter. The levels of reactive oxygen species were determined by measuring superoxide and hydrogen peroxide with dihydroethidium and dichlorofluorescin-diacetate assay. The mRNA expression levels of hypoxia-inducible factor (HIF)-1α, HIF-2α, nuclear factor (NF)-κB, and manganese superoxide dismutase (MnSOD) were analyzed using a real-time reverse transcriptase-polymerase chain reaction (qRT-PCR). Cell survival was determined by measuring cell viability. RESULTS pHe increased in 24 hours after 15% CO₂ treatment, and then decreased in 48 hours. Superoxide and hydrogen peroxide levels increased after the 24- and 48-hour of high CO₂ level condition. The expression levels of NF-κB, MnSOD, HIF-1α, and HIF-2α decreased in 24 hours and increased in 48 hours. The increased antioxidant mRNA expression in 48 hours showed that the PBMCs were responsive under high CO2 conditions. Elevated CO2 suppressed cell viability significantly in 48 hours. CONCLUSIONS After 48 hours of high CO₂ level condition, PBMCs showed an upregulation in genes related to hypoxia and oxidative stress to overcome the effects of CO2 elevation.

Objective: To describe expected endoscopic and histological changes at gastro-esophageal junction (GEJ) and define diagnostic paradigms for Barrett esophagus (BE) post-sleeve gastrectomy (SG). Summary Background Data: De novo incidence of BE post-SG was reported as high as 18.8%. A confounding factor is the lack of standardized definition of BE post-SG, which may differ from the general population due to procedure-induced alterations of GEJ.Methods: Part 1 involved evaluating endoscopic changes of GEJ post-SG (N ¼ 567) compared to pre-SG (N ¼ 320), utilizing protocolized pre-operative screening, post-operative surveillance and synoptic reporting. Part 2 involved dedicated studies examining causes of altered anatomical and mucosal GEJ appearance using histopathology (N ¼ 55) and high-resolution manometry (HRM) (N ¼ 15). Results: Part 1 -A characteristic tubularized cardia segment projecting supra-diaphragmatically was identified and almost exclusive to post-SG (0.6%vs.26.6%, p < 0.001). True BE prevalence was low (4.1%pre-SG vs. 3.8%post-SG, p ¼ 0.756), esophagitis was comparable (32.1%vs.25.9%, p ¼ 0.056). Part 2 -Histologically-confirmed BE was found in 12/55 patients, but 70.8% had glandular-type gastric mucosa implying tubularized cardia herniation. HRM of tubularized cardia demonstrated concordance of supra-diaphragmatic cardia herniation between endoscopy and HRM (3cmvs.3.2 cm, p ¼ 0.168), with frequent elevated isobaric intraluminal pressurizations in supra-and infra-diaphragmatic cardia compartments. Conclusion: A novel appearance of tubularized cardia telescoping supradiaphragmatically with flattening of gastric folds is common post-SG, likely associated with isobaric hyper-pressurization of proximal stomach. Incidence of true BE post-SG is low in short-intermediate term. These provided a clear framework for approaching endoscopic screening and surveillance, with correct anatomical and mucosal identifications, and clarified key issues of SG and BE.