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Biomedical subjects

D S Rowe

Publications and source records attributed to D S Rowe.

At least 19 recordsLinked to original sources
PubMed1983

Physician turnover in eight New England prepaid group practices: an analysis.

The objectives of this questionnaire study of all primary care physicians (N = 154) who had ever worked in eight New England prepaid group practices (PGPs) include 1) calculation of turnover rates, 2) comparison of those who stayed in (stayers) versus those who left (leavers) the PGPs, and 3) description of reasons given for leaving. An annual turnover rate of 3.9 to 6.3 per cent, depending upon the measure, was within the range reported by others. Factors associated with stayer-leaver status were experiences before and during the physician's PGP tenure. Leavers reported pre-PGP experience in fee-for-service, hospital-based, and academic positions, and while in the PGPs, they reported constraints on autonomy, independence, and professional development. Leavers reported higher incomes and longer working hours in their new practices. They cited the potential for greater autonomy as the reason for leaving. The findings and study limitations are discussed.

Attitude of Health Personnel↗
PubMed1979

Purulent ocular discharge in neonates: significance of Chlamydia trachomatis.

We obtained cultures for bacteria and chlamydiae from 100 infants with conjunctivitis that began during the first month of life. Sixty-nine infants were evaluated during well-child visits (group A); 31 were seen specifically for the ocular discharge (group B). Potentially pathogenic bacteria, predominantly Staphylococcus aureus, were cultured from one third of the infants in each group. Chlamydia trachomatis was recovered from three infants (4%) in group A and from ten (32%) in group B. Three infants with chlamydial conjunctivitis (two in group A, one in group B) had only mild inflammation. Initial treatment with topical antibiotics was unsuccessful in eliminating the organism from seven of 11 infants.

Conjunctivitis↗
PubMed1977

Mechanisms of protective immunity in experimental cutaneous leishmaniasis of the guinea-pig. III. Inhibition of leishmanial lesion in the guinea-pig by delayed hypersensitivity reaction to unrelated antigens.

The purpose of this investigation was to determine whether prior induction of a non-specific delayed reaction at a site of leishmanial infection could modify the course of infection. Groups of animals were made hypersensitive to either DNCB or BCG and a delayed reaction was elicited by corresponding antigen in one or both ears when an infective dose of L. enriettii was inoculated. With various experimental designs the following results were obtained: (a) induction of delayed reaction by DNCB or BCG inhibited the development of leishmanial lesions; (a) the protection was effective only when delayed reaction occurred at the site of infection; (c) to be effective, the reaction had to be continuously present at the site of infection for at least 3--4 weeks; (d) lesions developed normally, in the absence of delayed reaction, in DNCB-tolerant animals treated with DNCB; (E) a protective delayed reaction did not completely eliminate the parasites from the host tissues, since metastatic lesions appeared later at ectopic areas; (f) the suppressed development of a lesion did not confer resistance to reinfection dose of the parasite. It is concluded that cell-mediated immunity plays an important role in healing leishmanial lesions in the guinea-pig and that the final effector mechanism may be sought in the non-specific microbicidal capacity of activated macrophages. The relevance of leishmania-specific delayed reaction in the course of the disease is discussed.

Animals↗
PubMed1975

Antibody-induced movement of protozoan surface membrane antigens.

Direct and indirect immunofluorescence techniques were used to study the effects of host antibodies on surface membrane antigens of viable Leishmania parasites in vitro. Antisera to L. enriettii and L. tropica caused surface membrane antigens of these parasites to aggregate, move toward the poles of the parasite, and to eventually disappear. This sequence did not occur at low temperature or in the presence of some metabolic inhibitors. Antigen subsequently reappeared on the parasite membrane. These phenomena appear to be similar to those described in mammalian cells. Antibodies may therefore effect an alteration in the surface membrane structure of living protozoan parasites.

Animals↗
PubMed1975

Mechanisms of protective immunity in experimental cutaneous leishmaniasis of the guinea-pig. II. Selective destruction of different Leishmania species in activated guinea-pig and mouse macrophages.

Macrophages activation as the effector mechanism in destroying L. enriettii in the guinea-pig, and L. tropica in the mouse, was tested in vitro. Activated guinea-pig macrophages, with enhanced anti-Listeria capacity had no effect on the survival of intracellular L. enriettii, irrespective of the antigen used. Activated mouse macrophages, on the other hand, destroyed ingested L. enriettii within 24-48 hr but had no effect on L. tropica during the same time period. It is suggested that the pathogenicity of a Leishmania parasite in a given host depends on the ability of the parasite to survive in the host's activated macrophages. The possible mechanisms by which L. enriettii evades destruction in activated guinea-pig macrophages are discussed.

Animals↗
PubMed1975

Mechanisms of protective immunity in experimental cutaneous leishmaniasis of the guinea-pig. I. Lack of effects of immune lymphocytes and of activated macrophages.

Leishmania enriettii is an obligatory intracellular protozoan parasite which infects guinea-pigs and resides in macrophages. Subcutaneous inoculation produces a skin infection which heals spontaneously and leaves the animal immune to reinfection. Experiments have been performed to explore the mechanisms of parasite destruction in the recovering and immune animal. Using quantitative techniques to assess parasite survival it was found that L. enriettii is not killed in vitro in macrophages from immune guinea-pigs. Inocubation of monolayers of parasitized macrophages with lymphocytes from Leishmania-immune animals had no effect on the intracellular parasites. Finally, macrophages activated to destroy Listeria monocytogenes did not impair intracellular survival of L. enriettii. The possible significance of these findings in explaining the course of infection is discussed.

Animals↗
PubMed1974

Antibody-induced movement of membrane components of Leishmania enriettii.

Incubation in vitro of viable Leishmania enriettii with antibodies from infected or immune guinea pigs and a fluorescein-labeled antiguinea pig Ig conjugate induced aggregation of surface antigens to form a "cap" over the anterior pole of the amastigote and over both the anterior and posterior poles of the promastigote form of the parasite. Cap formation occurred only with optimum quantities of guinea pig antibodies and was inhibited by low temperature and the metabolic inhibitors, sodium azide and iodoacetamide. The aggregated antigens were rapidly lost from the surface of the parasite but reappeared after 3 h of incubation at 23 degrees C. This phenomenon of ligand-induced membrane antigen movement is apparently similar to that described in mammalian cells, and may represent the first stage of the interaction between host antibodies and the surface membrane of protozoal parasites.

Amides↗
PubMed1973

Immunoglobulin D as a lymphocyte receptor.

A large proportion of the human peripheral blood lymphocytes of adults and newborns having IgD were found also to have IgM on their membranes and vice versa. A few lymphocytes had one of these classes only. IgD and IgM could be capped independently on the same cell. The possibility that IgD was acquired by a cytophilic process was excluded by the finding that IgD-bearing cells were of one light chain type only, and by the direct demonstration of reappearance of IgD on the lymphocyte membrane during incubation in an IgD-free culture medium. On the basis of these findings, it is proposed that IgD functions as a lymphocyte antigen receptor.

Adult↗