Experiments were designed to establish whether mercuric chloride administered to rainbow trout (Salmo gairdneri Rich.) through the gills or by way of the mouth is converted in vivo to methylmercury. The mercury was measured by atomic absorption spectrophotometry and methylmercury determinations were performed by extraction and gas chromatography. The experiments show that while mercuric chloride administered by either method increased the total mercury content of kidney, liver, intestine, and muscle tissues, no evidence was found to support the hypothesis that mercuric chloride was methylated in fish to form methylmercury.

Pericardial effusion can dangerously precipitate patient’s hemodynamic stability and requires prompt intervention in case of tamponade. We investigated potential predictors of in-hospital mortality, a composite outcome of in-hospital mortality, pericardiocentesis-related complications, and the need for emergency cardiac surgery and all-cause mortality in patients undergoing percutaneous pericardiocentesis. This is an observational, retrospective, single-center study on patients undergoing percutaneous pericardiocentesis (2010–2019). We enrolled 81 consecutive patients. Median age was 71.4 years (interquartile range [IQR] 58.1–78.1 years) and 51 (63%) were male. Most of the pericardiocentesis were performed in an urgency setting (76.5%) for cardiac tamponade (77.8%). The most common etiology was idiopathic (33.3%) followed by neoplastic (22.2%). In-hospital mortality was 14.8% while mortality during follow-up (mean 17.1 months) was 44.4%. Only hemodynamic instability (i.e., cardiogenic shock, hypotension refractory to fluid challenge therapy and inotropes) was associated with in-hospital mortality at the univariate analysis (odds ratio [OR] 7.2; 95% confidence interval [CI] 1.76–29.4). Non-neoplastic/non-idiopathic etiology and hemodynamic instability were associated with the composite outcome of in-hospital mortality, need for emergency cardiac surgery, or pericardiocentesis-related complications (OR 5.75, 95% CI 1.65–20.01, and OR 5.81, 95% CI 2.11–15.97, respectively). Multivariate Cox regression analysis adjusted for possible confounding variables (age, coronary artery disease, and hemodynamic instability) showed that neoplastic etiology was independently associated with medium-term mortality (hazard ratio [HR] 4.05, 95% CI 1.45–11.36). In a real-world population treated with pericardiocentesis for pericardial effusion, in-hospital adverse outcomes and medium-term mortality are consistent, in particular for patients presenting with hemodynamic instability or neoplastic pericardial effusion.

2-Mercaptopropionylglycine (2-MPG) transformed normal red blood cells (RBCs) into paroxysmal nocturnal haemoglobinuria (PNH)-like RBCs in vitro, depending on the concentration, pH and time of incubation. The incorporation of radioactive choline in the presence of acetylcholine was reduced, as in RBCs treated with aminoethylisothiouronium salt (AET). In contrast, the uptake in the presence of choline differed when the RBCs were incubated with the two compounds, being reduced in AET-treated RBCs and increased in 2-MPG-treated ones. As true PNH RBCs incorporated to a higher extent the radioactivity in the presence of both acetylcholine and choline, 2-MPG-treated RBCs seemed to resemble the PNH RBCs better than the AET-treated ones. Present results suggest the possibility of modifying selectively the activity of acetylcholinesterase and the transport of choline through the cell membrane.

Analogies and differences between the growth-promoting action of fusicoccin (FC), the toxic agent produced by Fusicoccum amygdali, and of indole-3-acetic acid (IAA) in etiolated pea internode segments were further investigated. It was confirmed that the effect of FC, at optimal concentration, on growth by cell enlargement is markedly higher (ca. 70%) than that of IAA. The lack of an inhibitory effect of FC at high concentrations corresponds to a lack of capacity of the toxin to induce ethylene synthesis. When FC and IAA are present together at suboptimal concentrations, the effects of the two substances are clearly additive. Growth stimulation by a mixture of FC and IAA at optimal concentrations is equal to that by FC alone. NaF, 2,4-DNP, actinomycin D, and cycloheximide strongly depress FC-induced stimulation of cell enlargement. These data are in agreement with the hypothesis that FC promotes growth through some effect on cell-wall extensibility probably identical to the one mediating auxin-induced growth, while the primary site of action of FC is different from that of the natural and synthetic auxins.