Low-pressure pneumoperitoneum is feasible for LC and minimizes the adverse hemodynamic effects of peritoneal insufflation.

More than 100 different blood and urine biomarkers have been described in sickle cell disease (SCD), with the number increasing rapidly as analytical techniques develop. Nearly all of these biomarkers are abnormal in the steady state, and become more so during complications. The range of abnormalities demonstrates the multisystem nature of SCD and the complex pathophysiology. Some biomarkers indicate damage to specific organs, such as urine albumin:creatinine ratio in nephropathy, whereas others indicate more systemic processes. Biomarkers have been useful in identifying various interrelated pathological mechanisms, including haemolysis, inflammation, hypercoagulability, oxidative stress, reperfusion injury, vasculopathy and endothelial dysfunction. However, most biomarkers correlate closely with other more routine measurements, and also with each other. It is not clear that any provide specific prognostic or clinical information beyond that given by the simple measurement of haemoglobin concentration. The identification of prognostically validated biomarkers in prospective clinical trials would be useful.

Six specific pathogen-free foals shown to be free of equine herpesvirus-1 and 4 (EHV-1 and -4) and lacking in maternally-derived antibodies were used to investigate the pathogenesis of EHV-1 in horses. Following primary intranasal inoculation with EHV-1 all foals showed signs of a mild, self-limiting upper respiratory tract infection. A leucopenia was observed, comprising both a lymphopenia and neutropenia. Virus was isolated from nasal mucus and buffy coat cells over several days during the clinical episode and after the animals became clinically normal. Notwithstanding the mildness of the clinical disease, virus was not eliminated completely and intravenous administration of dexamethasone resulted in reactivation of latent EHV-1 in animals which had received only a single dose of the virus. In a second infection given to four foals, 61 days after the primary inoculation, no clinical signs were observed, haematological changes were minimal and viraemia was absent.

K+ influx and efflux were measured in normal (HbA) and sickle (HbS) red blood cells to investigate the interaction of swelling, H+ ions and urea with O2 (0 to 150 mmHg O2) in the presence of ouabain and bumetanide (both 100 μM). In HbA cells, K+‐Cl− cotransport was O2 dependent. At low oxygen tensions (PO2s) the transporter was inactive and refractory to low pH, swelling or urea. Cl−‐independent K+ influxes in sickle cells were elevated at low PO2s, as previously reported. Cl−‐dependent K+ influxes were large at both high and low PO2s, whether stimulated by swelling, H+ ions or urea. In the absence of O2, Cl−‐dependent K+ influxes were similar in magnitude to those measured at high PO2s. The minimum for Cl−‐dependent K+ influx was observed at PO2s of about 40‐70 mmHg. K+ efflux from HbS cells was stimulated by the addition of urea (500 mM). The rate constants were of similar magnitude whether measured at high PO2 or in the absence of O2, and were predominantly Cl− dependent under both conditions. In HbS red blood cells, reduction of extracellular Ca2+, addition of 1 mM Mg2+ or nitrendipine (10 μM) to the saline had no effect. Inhibitors of K+‐Cl− cotransport, [(dihydroindenyl)oxy] alkanoic acid (DIOA; 100 μM) or calyculin A (0·1 μM), inhibited influxes by a similar magnitude to Cl− substitution. Results are significant for the pathophysiology of sickle cell disease. Low pH and urea are able to stimulate KCl loss from sickle cells, leading to cellular dehydration, even in regions of low PO2.

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