Background Very low levels of cardiac troponin T associate with increased risk of cardiovascular death in patients with stable chronic coronary disease. Whether high-sensitivity cardiac troponin T (hsTnT) levels associate with adverse cardiovascular outcomes in individuals without cardiovascular disease (CVD) has not been well studied. Methods and Results Utilizing two complementary study designs, we evaluated the relationship between baseline cardiac troponin and incident CVD events among diabetic and non-diabetic participants in the Women’s Health Study (median follow-up 12.3 years). All diabetic women with blood specimens were included in a cohort study (n=512 diabetic women, n=65 events) and non-diabetic women were sampled for inclusion in a case-cohort analysis (n=564 comprising the subcohort, n=479 events). HsTnT was detectable (≥0.003 μg/L) in 45.5% of diabetic women and 30.3% of non-diabetic women (P<0.0001). In models adjusted for traditional risk factors and hemoglobin A1c, detectable hsTnT was associated with subsequent CVD (myocardial infarction, stroke, cardiovascular death) in diabetic women (adjusted HR 1.79, 95% CI 1.04-3.07, P=0.036), but not non-diabetic women (adjusted HR 1.13, 95% CI 0.82-1.55, P=0.46). Further adjustment for NT-proBNP and estimated renal function did not substantially alter this relationship among diabetic women (HR 1.76, 95% CI 1.00-3.08, P=0.0499), which appeared to be driven by a threefold increase in CVD death that was not observed in non-diabetic women. Conclusions Very low but detectable levels of cardiac troponin T associate with total CVD and CVD death in women with diabetes. Among healthy non-diabetic women, detectable compared to undetectable troponin was not associated with CVD events.

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Abstract. [Purpose] This study was performed to investigate the effects of trunk stability exercise using the proprioceptive neuromuscular facilitation (PNF) technique on stroke patients' muscle activation and their results in the functional reach test (FRT).[Subjects] Adult hemiplegia patients (n=40) were randomly allocated to two groups: an experimental group and a control group.[Methods] The experimental group performed a trunk stability exercise using the PNF, while the control group performed only a general exercise program for 6 weeks (5 times a week). Pre-and post-experiment measurements were made of the FRT. For measuring muscle activation, the quadriceps, hamstring, tibialis anterior, and soleus muscles were recorded by electromyography (EMG) in the FRT. [Results] The results of this study show that after performing the therapeutic exercise program, the experimental group showed significant improvements in FRT, activities of quadriceps, hamstring, and soleus muscles on the affected side, and activities of the quadriceps, and soleus muscles on the non-affected side, the control group showed significant improvements only in activities of the quadriceps, and soleus muscles on the non-affected side.[Conclusion] These results indicate that trunk stabilizing exercises using PNF performed by stroke patients were effective at improving FRT and the muscle activities of the soleus and quadriceps.

Glucocorticoids (GCs) are potent anti-inflammatory drugs, the secretion of which is mediated and controlled by the hypothalamic–pituitary–adrenal axis. However, they are also secreted de novo by peripheral tissues for local use. Several tissues express 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1), including the skin. The inactive GC cortisone is converted by 11β-HSD1 to active GC cortisol, which is responsible for delayed wound healing during a systemic excess of GC. However, the role of 11β-HSD1 in inflammation is unclear. We assessed whether 11β-HSD1 affects the development of atopic dermatitis (AD) in vitro and in vivo. The expression of 11β-HSD1 in the epidermis of AD lesions was higher than that in the epidermis of healthy controls. Knockdown of 11β-HSD1 in human epidermal keratinocytes increased the production of thymic stromal lymphopoietin. In an oxazolone-induced mouse model of AD, localized inhibition of 11β-HSD1 aggravated the development of AD and increased serum cytokine levels associated with AD. Mice with whole-body knockout (KO) of 11β-HSD1 developed significantly worse AD upon induction by oxazolone. We propose that 11β-HSD1 is a major factor affecting AD pathophysiology via suppression of atopic inflammation due to the modulation of active GC in the skin.