PubMed Health⌕ Search

Biomedical subjects

J E May

Publications and source records attributed to J E May.

At least 19 recordsLinked to original sources
PubMed1989

Prevalence of dyskinesia and related movement disorders in a developmentally disabled population.

The prevalences and inter-relationships of five types of movement disorders were evaluated in a large, developmentally disabled (DD) population (n = 1227); prevalence was evaluated with regard to severity, age, gender and antipsychotic-drug (APD) exposure. Dyskinesia was found in 48% of the sample, dystonia in 29%, akathisia in 13%, Parkinsonism in 3% and paroxysms in 4%. Many persons had more than one symptom so that 72% had one or more of the five target symptoms. Although the five movement-disorder categories were not mutually exclusive, analysis supported the individuality of the categories as defined in this study. The prevalences of dyskinesia and Parkinsonism were considerably greater than those in the general population. On the other hand, the prevalence of dyskinesia was similar to that reported for psychiatric and institutionalized geriatric populations. Parkinsonism increased with age and male gender, while dyskinesia increased with age and female gender. APD-exposure was significantly correlated only with akathisia.

Adolescent↗
PubMed1988

Dyskinesia, antipsychotic-drug exposure and risk factors in a developmentally-disabled population.

The relation between antipsychotic drug (APD) exposure and the prevalence of dyskinesia (DK) was examined in a large, developmentally-disabled (DD) population. Using qualitative data in a cross-sectional, retrospective design, the drug-exposed group was systematically compared with a non-drug-exposed group, controlling for age and gender. When the population was evaluated with no regard to APD-exposure, age and female gender were significant risk factors, as in many prior studies. When APD-exposure was considered, it proved to be a complex variable dependent on the recency of exposure to APD, and the outcome depended on the method of analysis: when APD-exposure was considered as a binomial variable (yes/no), the relationship between APD and DK was not significant; when APD-exposure was controlled for recency of exposure, however, a significant relationship between APD and DK was demonstrated (p less than 0.01) although the relationship accounted for less than 3% of the variance. Analysis of the relation between DK-prevalence and recency-of-APD-exposure revealed a pattern of diminished prevalence during APD use and increased prevalence during early withdrawal.

Adolescent↗
PubMed1977

Urachal remnants: benign or malignant?

Two cases are presented with cystoscopically visible cystic urachal remnants. The initial clinical findings, including bladder biopsies, were remarkably similar. Partial cystectomy with removal of the urachal cord alone clarified the actual disease. The inability to separate the malignant and the benign urachal lesion by other means suggests the necessity of total surgical extirpation. Perhaps this approach may result in an improvement in the generally poor prognosis for urachal carcinoma.

Adenocarcinoma↗
PubMed1975

Studies of the biologic effects of selective C4 deficiency.

The role of the several pathways of complement activation in mediating a number of the biologic activities of complement has been examined in an animal model, the C4-deficient guinea pig. It has been shown that the presence of an intact classic pathway (C1, 4, 2) is requisite for damage of antibody-sensitized mammalian cell membranes and for the development of thrombocytopenia and the hypercoagulable state following in vivo endotoxin administration. Both the classic and alternate pathways participate in defense against the lethal effects of endotoxin, in opsonization and lysis of bacteria and in mediation of the events of inflammation.

Antigen-Antibody Complex↗
PubMed1973

A new complement-mediated cytolytic mechanism--the C1-bypass activation pathway.

A new cytolytic pathway is described whereby cells sensitized with cytotoxic antibody can be specifically lysed in the complete absence of intact, classical complement pathway function. Evaluation of this model with sera deficient in the 4th (C4), 2nd (C2), and 6th (C6) components of complement has revealed that this new lytic mechanism, termed the C1-bypass activation pathway, is initiated by the antibody-mediated activation of C1. Utilizing components of the previously described alternate complement pathway, this pathway bypasses C4 and C2 to activate the third to ninth components of complement (C3-9) with induction of membrane damage.

Animals↗
PubMed1973

Interactions of the classical and alternate complement pathway with endotoxin lipopolysaccharide. Effect on platelets and blood coagulation.

The contributions of the classical and alternate pathways of complement activation to the biological effects of endotoxin have been examined in the guinea pig, with particular reference to thrombocytopenia, leukopenia, and the development of the hypercoagulable state. Injection of endotoxin into normal guinea pigs led to a 95% fall in the level of circulating platelets within 15 min as well as a fall in circulating granulocytes. C4-deficient guinea pigs, known to have a complete block in the activity of the classical complement pathway, but with the alternate pathway intact, sustained no fall in platelets. The development of granulocytopenia proceeded normally. Endotoxin did activate the alternate complement pathway in C4D guinea pigs, as evidenced by the fall in C3-9 titers. With restoration of serum C4 levels, endotoxin-induced thrombocytopenia was observed in C4D animals. Thus, function of the classical complement pathway was an absolute requirement for the development of thrombocytopenia. Experiments performed in cobra venom factor (CVF)-treated normal guinea pigs, with normal levels of C1, C4, and C2, but with less than 1% of serum C3-9 demonstrated the importance of the late components in the development of thrombocytopenia but not leukopenia.C4-deficient guinea pigs had normal clotting times demonstrating that C4 was not required for normal clotting. In addition, development of the hypercoagulable state, evidenced by a marked shortening of the clotting time, was not observed on injection of endotoxin into C4D animals. Therefore, development of the hypercoagulable state paralleled the development of thrombocytopenia and required function of the classical complement pathway. Again, the importance of the late components of complement was emphasized by the failure of CVF-treated normal animals to develop hypercoagulability. These results demonstrate that endotoxin is capable of activating both the classical and alternate complement pathways in guinea pigs but that function of the classical pathway is an absolute requirement for the development of thrombocytopenia and the hypercoagulable state.

Animals↗