Methylmercury: bacterial degradation in lake sediments

During the first 50 days of a long-term period of incubation of lake sediments with inorganic mercury (Hg(2+)), low concentrations of methylinercury were observed to build up. Upon continued incubation there was a rapid decrease in amount of methylmercury in the system and a concomitant evolution of volatile inorganic mercury (Hg(0)). Transfer of the mixed culture to growth media containing methylmercury resulted in the degradation of methylmercury and the volatilization of Hg(0). Four bacterial isolates were obtained from the mixed culture which, in pure culture, rapidly degraded methylmercury to methane and Hg(0). The presence of methane in head space gases was confirmed by flameionization gas chromatography, and the presence of Hg(0) in head space gases was confirmed by mass spectrometry.     

Acephate toxicity,metabolism, and anticholinesterase activity in Heliothis virescens (F.) and Anthonomus grandis grandis (Boheman)

The toxicity (72 hr) of acephate and methamidophos to fourth-instar larvae of the tobacco budworm, Heliothis virescens (F.), was nearly equivalent. In contrast, toxicity (72 hr) of methamidophos to adult boll weevils, Anthonomus grandis grandis (Boheman), was substantially greater than that of acephate. The internal accumulation of acephate was greater for A. grandis grandis than for H. virescens at 24 and 48 hr post-treatment, as was excretion. Acephate was metabolized to methamidophos both in vivo and in vitro by H. virescens but not by A. grandis grandis. In vitro acetylcholinesterase inhibition by methamidophos was greater than that of acephate, but less than that of paraoxon for H. virescens, A. grandis grandis, and the electric eel. Treatment of H. virescens larvae with acephate resulted in increased in vivo acetylcholinesterase inhibition between 24 and 72 hr post-treatment, which was associated with a large increase in mortality. H. virescens treated with methamidophos showed greater mortality and greater acetylcholinesterase inhibition at earlier time periods than those treated with acephate. However, by 72 hr post-treatment, in vivo acetylcholinesterase inhibition by LD₅₀ doses of acephate and methamidophos were approximately equivalent. These results indicate that, for H. virescens, toxicity of acephate is directly related to its metabolism to methamidophos and subsequent acetylcholinesterase inhibition. Likewise, the differential toxicity of acephate and methamidophos to A. grandis grandis adults appears to be due to their inability to metabolize acephate to methamidophos.     

The distribution of ventilation-perfusion ratios in the lungs of a dysmature foal

The distribution of ventilation-perfusion (VA/Q) ratios, before and after 100 per cent oxygen, was studied in an induced-premature foal at 4 h and again at eleven days of age, using the multiple inert gas elimination technique. The major finding was an absence of low VA/Q ratios when breathing air, indicating that low PaO2 in the neonatal period was totally attributable to the right-to-left shunt. At 4 h of age the PaO2 was 5.48 kPa and the right-to-left shunt represented 33.4 per cent of the cardiac output. At eleven days of age the PaO2 was 9.76 kPa and right-to-left shunt was 10.1 per cent of cardiac output. At both ages there was a separate high mode where ventilation was greatly in excess of blood flow but at neither age were units with low VA/Q ratios present. Oxygen breathing for 40 mins did not increase the right-to-left shunt, but at eleven days right-to-left shunt decreased when 100 per cent oxygen was administered.     

Acute lung injury and acute respiratory distress syndromes in veterinary medicine: consensus definitions: The Dorothy Russell Havemeyer Working Group on ALI and ARDS in Veterinary Medicine

Background: As veterinary medicine has become more sophisticated, with greater numbers of veterinary patients receiving intensive care, more patients with an acute respiratory distress (ARDS)‐like syndrome have been recognized. Methods: A consensus definition meeting was held for the purpose of developing veterinary‐specific definitions for acute lung injury (ALI) and ARDS. Results/conclusions: Three clinically based definitions for acute lung injury and acute respiratory distress‐like syndromes occurring in veterinary patients were described. Neonatal equine respiratory distress syndrome (NERDS) was defined separately due to the specific requirement for primary developmental surfactant dysfunction and lack of an inflammatory component. Five diagnostic criteria categories were established for Veterinary ALI/ARDS (Vet ALI/ARDS) with 4 required and a fifth highly recommended criteria. A strong consensus was reached that onset of respiratory distress must have been acute and that known risk factors must be present. Additional criteria included evidence of pulmonary capillary leak with no evidence of increased pulmonary capillary pressure, evidence of inefficient gas exchange and, finally, evidence of inflammation. Some features of ALI/ARDS in the neonatal horse were recognized as unique, therefore, equine neonatal ALI/ARDS (EqNALI/EqNARDS) was similarly defined but with a graded gas exchange inefficiency table to allow for normal developmental changes in gas exchange. Use of these definitions in planning prospective studies of these problems in veterinary patients should allow for more direct comparisons of studies and clinical trials, with a larger goal of improving outcome in veterinary patients.