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Biomedical subjects

R M Grant

Publications and source records attributed to R M Grant.

63 records · Page 4Linked to original sources
PubMed1971

Liver metastases--an experimental study.

The effect of the Walker 256 rat carcinoma, growing at a site remote from the liver, on liver glycogen synthesis has been determined. Although the mechanism has not been defined it has been shown that the deposition of liver glycogen in response to a glucose load is inhibited in tumour bearing rats. It has been further demonstrated that, by comparison with the normal liver, the liver depleted of glycogen is more susceptible to the development of metases from circulating cancer cells.

Animals↗
PubMedDate not supplied

Parallel evolution of CCR5-null phenotypes in humans and in a natural host of simian immunodeficiency virus.

The C-C chemokine receptor CCR5 in humans and rhesus macaques (Macaca mulatta) serves as the primary coreceptor for cellular entry by macrophagetropic strains of human immunodeficiency virus type 1 (HIV-1) and all reported strains of simian immunodeficiency virus (SIV) [1-6]. Humans homozygous for a 32 bp deletion allele of CCR5, resulting in a null phenotype, are highly resistant to infection by HIV-1 [7-9], prompting development of therapies and vaccines targeting CCR5. We now report a novel deletion allele of CCR5, with an allele frequency of 0.04, in sooty mangabey monkeys (Cercocebus torquatus atys), a natural host of SIV (SIVsmm) [10]. The mutant protein was not expressed at the cell surface and accordingly did not function as a viral coreceptor. Primary activated lymphocytes from mangabeys heterozygous for the deletion allele expressed significantly less CCR5 on the cell surface. Moreover, SIV seroprevalence and viremia were comparable among CCR5 heterozygotes and wild-type animals. Parallel evolution of CCR5-null alleles in humans and sooty mangabeys suggests that similar negative selection pressures have acted against CCR5, as would occur during epidemics of infectious agents that require CCR5 for pathogenesis. Sooty mangabeys bred to homozygosity for the deletion allele will be useful for experimental studies on the context-dependent role of CCR5 in host defense and microbial pathogenesis.

Animals↗
PubMedDate not supplied

The high prevalence of genital herpes among patients with genital ulcer disease in Uganda.

BACKGROUND: Genital ulcer disease is a risk factor for transmission of human immunodeficiency virus. One-hundred consecutive Ugandan patients (median age, 25 years) with genital ulcer disease were examined to determine the prevalence of genital herpes and its relationship to human immunodeficiency virus seropositivity. GOAL OF THIS STUDY: To improve management, prevention, and control of genital ulcer disease, thus reducing human immunodeficiency virus infections attributable to genital ulcer disease. STUDY DESIGN: This was a prevalence study of genital herpes in a consecutive sample of an urban sexually transmitted disease clinic population. RESULTS: Forty-nine percent (48/98) of the patients had genital herpes (36% by direct fluorescent antigen and 13% by history of recurrent vesicles). There was a trend toward larger lesions in patients who were human immunodeficiency virus seropositive. Twelve percent (11/89) of patients had syphilis, and 30% (30/100) remained sexually active, despite the presence of active genital ulcer disease. Sixty-five percent of 89 patients tested had antibodies to human immunodeficiency virus. CONCLUSIONS: Genital herpes is a common cause of genital ulcer disease in patients attending sexually transmitted disease clinics in Uganda, and herpes ulcers may be more extensive among those who are infected with human immunodeficiency virus.

Adult↗
PubMedDate not supplied

Sign of progress.

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Humans↗
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Scheduled and unscheduled combination chemotherapy in the treatment of squamous cell lung cancer (cyclophosphamide, adriamycin, vincristine and bleomycin, with and without cis-platinum).

Fifty four patients with squamous cell lung cancer, treated with Cyclophosphamide (750 mg/m2), Adriamycin (50 mg/m2), Vincristine (1.5 mg/m2) and Bleomycin (30 mg) (CAVB) in a 2 day scheduled regime, showed an overall median survival time (MST) of 32 weeks (28 weeks for non-responders and 46.5 weeks for responders--a non-significant difference). The response rate was 24%, the median duration of response being 23 weeks. Bone marrow toxicity was not a major problem. A further 21 patients received the same drugs but in a single bolus (unscheduled regime). Comparison of their results with the 25 patients randomised to the scheduled regime showed no significant difference in MST or toxicity. The addition of Cis-platinum (50 mg/m2) to the unscheduled CAVB regime (CAVBP) in a further 22 patients did not result in an improvement either in survival or response, but added to the toxicity.

Adult↗