A simplified technique for revascularization of homografts of the liver with a variant right hepatic artery from the superior mesenteric artery

A simplified technique for conversion of a complex hepatic arterial supply into a common channel is described. This technique permits single vessel anastomosis in the recipient of a liver transplant

Liver rejection and its differentiation from other causes of graft dysfunction.

Numerous causes can lead to hepatic dysfunction following orthotopic liver transplantation. The most common cause is rejection, which is usually nonpreventable. The clinical presentation, time of onset, and even treatment are variable. Other causes, such as perioperative ischemic injury, vascular thrombosis, and complications of bile duct reconstruction may be preventable with good surgical technique. Infections can also be minimized by careful adjustment of immunotherapy, avoidance overimmunosuppression, and the judicious use of antibiotics. Hepatic dysfunction following orthotopic liver transplantation requires rapid assessment and proper treatment in order to prevent serious and possibly fatal complications

Influence of selected patient variables and operative blood loss on six-month survival following liver transplantation.

A group of 118 adults who underwent primary, orthotopic transplantation of the liver over a 4-year period served as the subjects of a detailed examination of their ability to survive the first 6 months as a function of their preoperative condition. As a result, a scoring system was developed empirically in an attempt to separate very high-risk from relatively low-risk patients. The scoring method is based on the high degree of correlation between survival probability and various patient characteristics. It allows for additional scoring to account for the dramatic effect of operative blood loss on the eventual outcome. The curve that best describes the relationship between patient scores and survival probability is sigmoidal in shape. Many patients will have scores located on the curve between the inflection points. They represent a group whose relative risk is difficult to estimate but for whom operative blood loss or the occurrence of surgical complications may prove particularly telling

The acute toxicity of thallium to freshwater organisms: Implications for risk assessment.

The acute toxicity of Tl(I) to the microalga, Pseudokirchneriella subcapitata, the planktonic crustaceans, Daphnia magna and Daphnia pulex, and early-life stage of the zebrafish, Danio rerio, has been studied according to OECD protocols. Toxicological end-point concentrations for the microalga ranged from 17 μg l(-1) for a 72 h EyC25 (yield inhibition) to 80 μg l(-1) for a 72 h ErC50 (growth inhibition). Daphnia were less sensitive to Tl, with 48 h EC50s of about 1000 μg l(-1) and 1200 μg l(-1) for D. magna and D. pulex, respectively; however, end-point concentrations were reduced considerably (to about 510 μg l(-1) and 730 μg l(-1), respectively) when experiments were repeated in dechlorinated Plymouth tap water (rather than OECD medium). The 96 h LC50 for D. rerio was 870 μg l(-1) but a variety of sub-lethal effects, including enlargement of yolk sac and reduction in heart beat rate, were observed when larvae were exposed to lower concentrations. Based on these results, a predicted no effect concentration (PNEC) for Tl in freshwaters of 0.087 μg l(-1) is proposed. The PNEC is an order of magnitude lower than the only (Canadian) water quality guideline for Tl that appears to exist, and is lower than Tl concentrations reported in freshwaters impacted by historical or contemporary metal mining. Our results are also consistent with previous studies that employ different organisms and end-points in that Tl toxicity is dependent on the concentration of K+, the biogeochemical analogue of Tl+. Accordingly, regulation of Tl in the freshwater environment should factor in the relative abundance of K