Chronic scrotal heat stress causes testicular interstitial inflammation and fibrosis: An experimental study in mice.

Background: Chronic heat stress is a risk factor that adversely affects the reproduction system. Inflammation and fibrosis are 2 important response processes to damaged tissues. Objective: This study investigates the association of chronic scrotal heat stress with testicular interstitial inflammation and fibrosis in mice. Materials and Methods: For all experiments, 8-10 wk old male Swiss mice (Mus musculus) (20-23 gr) were divided into 3 groups (n = 10/each). The heat-stress groups were submerged in a water bath at 37 C and 40 C, while the control group was treated at 25 C. The testicular tissues underwent hematoxylin and eosin staining, picro sirius red staining, and immunohistochemistry for intercellular adhesion molecule-1, fibroblast-specific protein 1, F4/80, collagen I, and Ki-67 staining to determine the testicular interstitial inflammation and fibrosis. Results: Chronic scrotal heat stress impairs spermatogenesis and reverses testicular histological structure. In this study, heat stress significantly induced increased interstitial cell proliferation and upregulation of intercellular adhesion molecule-1 expression in the interstitial testicular tissue. In the interstitial testicular tissue, the number of F4/80-positive macrophages and the number of fibroblast-specific protein 1-positive fibroblasts were significantly increased in the heat-exposed groups compared to those in the control group. The heat exposed groups had substantially increased extracellular matrix collagen accumulation in their testicular interstitial tissues. Conclusion: Heat stress adversely affects the testicular structure and spermatogenesis, causes inflammation, and leads to testicular interstitial fibrosis.

Asia-Pacific consensus statement on the optimal use of high-sensitivity troponin assays in acute coronary syndromes diagnosis: focus on hs-TnI.

OBJECTIVE: High-sensitivity troponin (hs-Tn) assays need to be applied appropriately to improve diagnosis and patient outcomes in acute coronary syndromes (ACS). METHODS: Experts from Asia Pacific convened in 2015 to provide data-driven consensus-based, region-specific recommendations and develop an algorithm for the appropriate incorporation of this assay into the ACS assessment and treatment pathway. RESULTS: Nine recommendations were developed by the expert panel: (1) troponin is the preferred cardiac biomarker for diagnostic assessment of ACS and is indicated for patients with symptoms of possible ACS; (2) hs-Tn assays are recommended; (3) serial testing is required for all patients; (4) testing should be performed at presentation and 3 hours later; (5) gender-specific cut-off values should be used for hs-Tn I assays; (6) hs-Tn I level >10 times the upper limit of normal should be considered to 'rule in' a diagnosis of ACS; (7) dynamic change >50% in hs-Tn I level from presentation to 3-hour retest identifies patients at high risk for ACS; (8) where only point-of-care testing is available, patients with elevated readings should be considered at high risk, while patients with low/undetectable readings should be retested after 6 hours or sent for laboratory testing and (9) regular education on the appropriate use of troponin tests is essential. CONCLUSIONS: We propose an algorithm that will potentially reduce delays in discharge by the accurate 'rule out' of non-ACS patients within 3 hours. Appropriate research should be undertaken to ensure the efficacy and safety of the algorithm in clinical practice, with the long-term goal of improvement of care of patients with ACS in Asia Pacific.