No abstract

Background High-grade inflammation may play a pivotal role in the pathogenesis of left ventricular (LV) dysfunction. Evidence to support a role of systemic inflammation in mediating impaired LV function in experimental models of rheumatoid arthritis (RA) remains limited. The aim of the present study was to determine the effects of high-grade systemic inflammation on LV diastolic and systolic function in collagen-induced arthritis (CIA).

The skin is a protective barrier, and an endocrine, sensory and thermoregulatory organ. We investigated whether the skin of local pigs had beneficial anatomical traits compared to exotic pigs to withstand the increased heat loads predicted under future climate change scenarios. Full-thickness skin specimens were obtained from the dorsal interscapular, lateral thoraco-abdominal and ventral abdominal regions of intact boars (age 6–8 months) of two local breeds of pigs (Windsnyer [n = 5] and Kolbroek [n = 4]) and an exotic pig breed (Large White [n = 7]). The skin sections were stained with a one-step Mallory–Heidenhain stain and Fontana stain (melanin). Sweat gland perimeter was measured using Image J software. The Windsnyer breed had the thinnest dermis layer while the Large White had the thickest dermis layer across all the three body regions (analysis of variance [ANOVA]; p < 0.001). The Windsnyers had widely spaced dermal pegs compared to the other breeds. The Windsnyers had significantly more superficial and larger (~1 mm depth; 4.4 mm perimeter) sweat glands than the Kolbroek (~3 mm depth; 2.2 mm perimeter) and Large White (~4 mm depth; 2.0 mm perimeter) pigs (ANOVA; p < 0.001). The Windsnyers had visibly more melanin in the basal layer, the Kolbroek pigs had very little and the Large Whites had none. The functionality of the sweat glands of the Windsnyer breed needs to be established. The skin from the Windsnyer breed possesses traits that may confer a protective advantage for the increased solar radiation and ambient temperatures predicted with climate change.

Abstract-Although the profibrotic inflammatory substance galectin-3 predicts outcomes in the general population, the mechanisms responsible for this effect are uncertain. We aimed to determine whether circulating galectin-3 concentrations are associated with carotid femoral (aortic) pulse wave velocity and aortic reflective wave index (applanation tonometry and SphygmoCor software) in 966 randomly selected participants from a community sample. Galectin-3 concentrations were not independently associated with office (n=966) or 24-hour (n=661) systolic (P=0.88-0.92) or diastolic (P=0.65-0.94) blood pressure. In contrast, with adjustments for age, sex (in all participants), office or 24-hour mean arterial pressure (or systolic blood pressure and pulse pressure), pulse rate, body mass index, regular smoking, regular alcohol intake, total cholesterol concentrations, diabetes mellitus or an glycohemoglobin >6.1%, treatment for hypertension, and estimated glomerular filtration rate, galectin-3 was independently associated with aortic pulse wave velocity in all participants (partial r=0.15, P<0.0001) and reflective wave index in men (partial r=0.13, P<0.02). In 745 participants who had never received antihypertensive therapy, galectin-3 concentrations were similarly independently associated with pulse wave velocity in all participants (partial=0.16, P<0.0001) and reflective wave index in men (partial r=0.15, P<0.02). The blood pressureindependent relations between galectin-3 concentrations and aortic hemodynamics persisted with further adjustments for C-reactive protein concentrations (pulse wave velocity in all participants: partial r=0.14, P<0.0001; reflective wave index in men: partial r=0.12, P<0.05). In conclusion, despite a lack of independent association with brachial blood pressure, the profibrotic inflammatory substance galectin-3 may contribute toward adverse outcomes through an effect on aortic stiffness, an effect that cannot be attributed to general inflammatory changes. (Hypertension. 2015;65:1356-1364.

Resistin is independently and directly associated with aortic stiffness and these effects occur beyond BP, insulin resistance, and general inflammation.