Previous studies on the in vitro transport capacity ofmedian eminence demonstrated the existence of two separate active mechanisms for the uptake of neutral amino acids and thyroxine (T4). Although the nature of the transport systems could be characterized, the cellular component responsible for accumulation remained unknown. In order to resolve this question, median eminence was placed in organ culture for 8 days. After this time, degeneration of nerve fibers and terminals is complete as evidenced by morphological criteria; moreover, the reuptake mechanism for catecholamines is virtually absent. Transport studies with α-amino-isobutyric acid (AIB) and T4 show that the surviving tissue possesses the active transport systems for both compounds. For both substances, the apparent intracellular concentration is increased twofold over that of fresh tissue. The modifying effects of TSH on T4 transport as seen in fresh tissue were also demonstrable in the organ cultured material. These data further support the belief that ependymal components in median eminence are responsible for the major portion of AIB and T4 accumulation and that the effect of TSH on the latter is mediated, at least in part, directly on these cells.
Levels of antibodies to six major structural proteins of human immunodeficiency virus type 1 (gp120, gp41, p66, p31, p24, and p17) were assessed in serial samples from 22 persons with severe hemophilia (16 asymptomatic and 6 who developed acquired immunodeficiency syndrome [AIDS] or AIDS-related complex) with an automated dot blot assay using purified recombinant antigens. High and sustained levels of antibody to gp120, gp41, and p31 were found in all patients irrespective of their clinical condition for 4 to 6 years after seroconversion. In contrast, immune response to p66 and p17 was significantly lower in symptomatic patients. Over time, the levels of these two antibodies, as well as anti-p24, decreased and tended to become undetectable. Abnormal immune response and low levels of antibody to p66 and p17 are early indications of rapid clinical progression.
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