Restenosis after carotid endarterectomy.
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Biomedical subjects
Publications and source records attributed to C Lattimer.
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Intramural thrombosis is a consistent finding in the arteries of patients who die following coronary angioplasty. This thrombosis is thought to have a role in restenosis, which is a common complication of coronary angioplasty. It has been hypothesised that antithrombotics such as hirudin or tissue-type plasminogen activator (tPA), may be therapeutically useful following angioplasty. This report describes the bioavailability of both agents following subcutaneous (sc) injection in cholesterol-fed rabbits. Intravenously delivered tPA has a half-life of 3-5 minutes. The half-life of intravenously administered hirudin is less than one hour in many species. In order to prolong the duration of action recombinant hirudin was conjugated to polyethylene glycol (PEG). Polyethylene glycol conjugated recombinant hirudin (PEG-rH) (0.7 mg/kg) antigen and activity were measurable after just 1 hr, reaching a maximum (663 and 884 ng/ml respectively) at 12 hours. Significant levels were present in rabbit plasma 24 hours after injection. Subcutaneously delivered recombinant (r-tPA) (1 mg/kg) was present in significant amounts 1 hr after injection, reaching a maximum (92 IU/ml) at 2 hours. Levels of tPA at 9 hours were approximately 80x normal circulating levels. High and constant levels of functional activity of both PEG-rH and r-tPA in rabbit plasma are achieved by subcutaneous delivery.
Hepatitis A antibody was detected by specific immune adherence and complement-fixation tests in a study involving 473 serum specimens from 20 patients who had viral hepatitis, Type A. In all 20 patients who had no detectable immune adherence antibody (less than 1:5) before onset of hepatitis high levels (greater than or equal to 1:1024) developed one to four weeks later, occasionally reaching peak levels exceeding greater than or equal to 1:81,920 several months thereafter. Five to 10 years later the immune adherence antibody levels ranged between 1:640 and 1:20,480. In general, the complement-fixation test was not as sensitive or as specific as the immune adherence test. These findings indicate that the immune adherence test should be a valuable tool for diagnosis, for epidemiologic surveys, for identification of susceptible and immune persons, for quantitative assays of gamma globulin and for identification of hepatitis A virus in attempts to propagate the virus in cell culture.
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Seven population groups were tested by radioimmunoassay for the presence of hepatitis A antibody (anti-HAV), hepatitis B surface antigen (HBsAg) and antibody to HBsAg (anti-HBs). Detection of anti-HAV was indicative of past hepatitis A infection and presence of HBsAg or anti-HBs indicated past hepatitis B infection. The results of tests of 680 serum specimens from the seven groups were as follows: (1) of 100 newly admitted children to Willowbrook where hepatitis A and B were hyperendemic, 32% had anti-HAV and 4% had anti-HAV and 4% had HBsAg (1%) plus anti-HBs (3%); (2) of 100 Willowbrook residents who lived in the institution about three or more years, 97% had anti-HAV and 90% had HBsAg (32%) plus anti-HBs (58%); (3) of 100 new Willowbrook employees, 50% had anti-HAV and 13% had anti-HBs; (4) of 100 Willowbrook employees who worked in the institution more than three years, 75% had anti-HAV and 30% had HBsAg (3%) plus anti-HBs (27%); (5) of 80 house staff physicians, 27.5% had anti-HAV and 10% had anti-HBs; (6) of 100 student 34% had anti-HAV and 6% had anti-HBs; and (7) of 100 suburban teenagers 4% had anti-HAV and 5% had anti-HBs. This study confirmed the variability of the prevalence of hepatitis A and B markers among different population groups and the effect of socioeconomic status and environmental factors on the incidence of past infection caused by hepatitis A and B viruses.