Summary Circulating neutrophil phenotype and function are altered during neutrophilia associated with acute inflammatory states, however, the contribution of bone marrow neutrophil release to these changes has been difficult to quantify in humans. Accelerated release of neutrophils, with potentially distinct attributes, from the bone marrow and their dilution within the circulating pool may produce these apparent changes. Unfortunately selective analysis of these newly emergent neutrophils is difficult given their morphologic similarity to those already in the circulation and the coincident effect of soluble inflammatory mediators on circulating neutrophil phenotype and function. Using whole blood flow cytometry and cardiac surgery as an inflammatory stimulus, we demonstrate the emergence of a unique subpopulation of circulating neutrophils characterised as CD10−/CD16low, indicative of active bone marrow neutrophil release peri‐operatively. CD10−/CD16low neutrophils emerge at the same operative stages as band forms and a left shift, yet represent over 40% of circulating neutrophils postoperatively, and generate a greater stimulus‐induced [Ca2+]i flux than their CD10+ counterparts. We conclude that CD10−/CD16low neutrophils represent a significant proportion of the circulating pool after cardiac surgery and that bone marrow release, a major contributor to neutrophilia, influences the phenotype and functional activity of circulating neutrophils following this acute inflammatory stimulus.

Context Androgen abuse impairs male reproductive and cardiac function, but the rate, extent, and determinants of recovery are not understood. Objective To investigate recovery of male reproductive and cardiac function after ceasing androgen intake in current and past androgen abusers compared with healthy non-users. Methods Cross-sectional, observational study recruited via social media 41 current and 31 past users (≥3 months since last use, median 300 days since last use) with 21 healthy, eugonadal non-users. Each provided a history, examination, and serum and semen sample and underwent testicular ultrasound, body composition analysis, and cardiac function evaluation. Results Current abusers had suppressed reproductive function and impaired cardiac systolic function and lipoprotein parameters compared with non- or past users. Past users did not differ from non-users, suggesting full recovery of suppressed reproductive and cardiac functions after ceasing androgen abuse, other than residual reduced testicular volume. Mean time to recovery was faster for reproductive hormones (anti-Mullerian hormone [AMH], 7.3 months; luteinizing hormone [LH], 10.7 months) than for sperm variables (output, 14.1 months) whereas spermatogenesis (serum follicle-stimulating hormone [FSH], inhibin B, inhibin) took longer. The duration of androgen abuse was the only other variable associated with slower recovery of sperm output (but not hormones). Conclusion Suppressed testicular and cardiac function due to androgen abuse is effectively fully reversible (apart from testis volume and serum sex hormone binding globulin) with recovery taking between 6 to 18 months after ceasing androgen intake with possible cumulative effects on spermatogenesis. Suppressed serum AMH, LH, and FSH represent convenient, useful, and underutilized markers of recovery from androgen abuse.

Individual patient response to effective therapies for pulmonary hypertension (PAH) is variable and difficult to quantify. Consequently, management decisions regarding initiation and continuation of therapy are highly dependent on the results of investigations. Registry data show that changes in cardiac index, mean right atrial pressure, and mean pulmonary artery pressure have the greatest influence on survival. It is recognized that pulmonary artery pressure (PASP) responses to PAH-specific drugs are heterogeneous. However, follow-up testing is strongly focused on assessing changes in PASP and functional status (6-min walk). The goals of therapy, which should be highlighted in follow-up imaging, include not only reduction of PASP, decrease in pulmonary vascular resistance, and improvements in right ventricular function, cardiac output, and tricuspid regurgitation. This paper reviews the echocardiographic follow-up of pulmonary hypertension, and especially focuses on right ventricular function-a major determinant of outcome, for which reliable echocardiographic assessment has become more feasible.