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Abstract Background Previous observational studies have shown that people with dental scaling (DS) had decreased risk of stroke. However, limited information is available on the association between DS and poststroke outcomes. The present study aimed to evaluate the effects of regular DS on the complications and mortality after stroke. Methods We conducted a retrospective cohort study of 49,547 hospitalized stroke patients who received regular DS using 2010–2017 claims data of Taiwan’s National Health Insurance. Using a propensity-score matching procedure, we selected 49,547 women without DS for comparison. Multiple logistic regressions were used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) of poststroke complications and in-hospital mortality associated with regular DS. Results Stroke patients with regular DS had significantly lower risks of poststroke pneumonia (OR 0.58, 95% CI 0.54–0.63), septicemia (OR 0.58, 95% CI 0.54–0.63), urinary tract infection (OR 0.68, 95% CI 0.66–0.71), intensive care (OR 0.81, 95% CI 0.78–0.84), and in-hospital mortality (OR 0.66, 95% CI 0.62–0.71) compared with non-DS stroke patients. Stroke patients with regular DS also had shorter hospital stays (p

Abstract Background Little was know about the association between the CHA2DS2-VASc score and postoperative outcomes. Our purpose is to evaluate the effects of CHA2DS2-VASc score on the perioperative outcomes in patients with atrial fibrillation (AF). Methods We identified 47,402 patients with AF over the age of 20 years who underwent noncardiac surgeries between 2008 and 2013 from claims data of the National Health Insurance in Taiwan. The CHA2DS2-VASc score was used to evaluate postoperative complications, mortality and the consumption of medical resources by calculating adjusted odds ratios (ORs) and 95% confidence intervals (CIs). Results Compared with patients with a CHA2DS2-VASc score of 0, patients with scores ≥ 5 had an increased risk of postoperative septicemia (OR 2.76, 95% CI 2.00–3.80), intensive care (OR 2.55, 95% CI 2.12–3.06), and mortality (OR 2.04, 95% CI 1.14–3.64). There was a significant positive correlation between risk of postoperative complication and the CHA2DS2-VASc score (P

Abstract Background This study investigated whether lipopolysaccharide (LPS) increase protease-activated receptor-2 (PAR-2) expression and enhance the association between PAR-2 expression and chemokine production in human vascular endothelial cells (ECs). Methods The morphology of ECs was observed through microphotography in cultured human umbilical vein ECs (EA. hy926 cells) treated with various LPS concentrations (0, 0.25, 0.5, 1, and 2 μg/mL) for 24 h, and cell viability was assessed using the MTT assay. Intracellular calcium imaging was performed to assess agonist (trypsin)-induced PAR-2 activity. Western blotting was used to explore the LPS-mediated signal transduction pathway and the expression of PAR-2 and adhesion molecule monocyte chemoattractant protein-1 (MCP-1) in ECs. Results Trypsin stimulation increased intracellular calcium release in ECs. The calcium influx was augmented in cells pretreated with a high LPS concentration (1 μg/mL). After 24 h treatment of LPS, no changes in ECs viability or morphology were observed. Western blotting revealed that LPS increased PAR-2 expression and enhanced trypsin-induced extracellular signal-regulated kinase (ERK)/p38 phosphorylation and MCP-1 secretion. However, pretreatment with selective ERK (PD98059), p38 mitogen-activated protein kinase (MAPK) (SB203580) inhibitors, and the selective PAR-2 antagonist (FSLLRY-NH2) blocked the effects of LPS-activated PAR-2 on MCP-1 secretion. Conclusions Our findings provide the first evidence that the bacterial endotoxin LPS potentiates calcium mobilization and ERK/p38 MAPK pathway activation and leads to the secretion of the pro-inflammatory chemokine MCP-1 by inducing PAR-2 expression and its associated activity in vascular ECs. Therefore, PAR-2 exerts vascular inflammatory effects and plays an important role in bacterial infection-induced pathological responses.