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Biomedical subjects

M J Droller

Publications and source records attributed to M J Droller.

At least 109 records · Page 6Linked to original sources
PubMed1978

An approach to the control of massive hemorrhage in cyclophosphamide-induced cystitis by intravenous vasopressin: a case report.

Massive bleeding owing to cyclophosphamide-induced hemorrhagic cystitis was not affected by intravesical instillation of 4 per cent formalin or 1 per cent silver nitrate. After initiation of a continuous systemic infusion of vasopressin hematuria and transfusion requirements diminished markedly. Adverse reactions were mild. Intravenous vasopressin was a safe and effective means to control temporarily life-threatening hemorrhagic cystitis.

Adolescent↗
PubMed1976

Thrombin-induced platelet prostaglandin and cyclic AMP production and a possible intrinsic modulation of platelet function.

In previous studies, we observed an increase in intracellular cyclic AMP in platelets during thrombin-induced nucleotide and calcium release. Our present work suggests that platelet prostaglandins are directly involved in this phenomenon. Washed human platelets were incubated at 37 degrees C with human thrombin for times ranging between 5 s and 5 min. The release of nucleotides and calcium in response to thrombin, determined spectrophotometrically, reached 40-60% of maximal plateau levels by 5 s, 70-80% by 10 s, and 90-100% by 15 s. The production and secretion of prostaglandin E (PGE), measured by radioimmunoassay, parelleled this rapid time course. After 10 s, however, the amount of extracellular PGE began to decrease, continuing to do so through 5 min of incubation. Intracellular cyclic AMP accumulation, determined by radioimmunoassay, lagged behind the time course of nucleotide and calcium release, and that of PGE secretion, by several seconds. This lag in cyclic AMP accumulation appeared to correlate closely with the disappearance of PGE from the supernate in the same platelet samples. In view of the inhibitory effects of cyclic AMP and PGE on platelet release and aggregation, these interrelated time course curves suggest the existence within platelets of a mechanism for the modulation of platelet activity.

Blood Platelets↗
PubMed1976

Clinical and laboratory studies into the pathogenesis of malacoplakia.

Three cases of malacoplakia are described. Electron microscopic studies revealed intact bacteria or bacteria in varying states of degradation within phagolysosomes of the malacoplakic macrophages. Michaelis-Gutmann bodies arise within the phagolysosomes. These findings suggest that the bacteria incorporated within the phagolysosomes persist as dense amorphous aggregates which later become encrusted with calcium phosphate crystals to form the laminated Michaelis-Gutmann bodies. Possible explanations for the unusual macrophage response in malacoplakia are: (1) infection with an unusual strain of bacteria, (2) an immunological abnormality affecting intracellular killing of organisms, and (3) an abnormality affecting intracellular digestion of organisms. In considering each of the possibilities, we have been unable to detect any unusual strain of infecting organisms in association with malacoplakia, and in vitro studies have revealed normal T lymphocyte response to mitogen and normal monocyte bactericidal capacity. According to the history, each patient had reason to have a compromised immune status; in only one, however, was this demonstrated.

Adult↗
PubMed1976

Differences in adenylate cyclase activities in murine normal cells and bladder tumor cells in tissue culture.

Cyclic AMP may be involved in the modulation of cell growth. The present work sought to further define differences between normal cells and tumor cells in their cyclic AMP system. Mouse embryo fibroblasts and murine bladder transitional epithelium tumor cells were grown in vitro; at various times, adenyl cyclase activity was assayed by measuring the conversion of [alpha32P]ATP to cyclic AM32P; stimulation by prostaglandin E1 or sodium fluoride was also determined. Base line and fluoride-stimulated enzyme activity were significantly greater in normal cells than tumor cells (P less than 0.01), and reached a peak at day 2; at confluency, levels in both systems decreased. Prostaglandin E1-stimulated levels, in contrast, were greater in tumor cells, there being a 10 fold greater relative stimulation in these cells compared to normal cells (P less than 0.01). Findings of a possibly greater sensitivity in these tumor cells may be important in a therapeutic modulation of tumor growth.

Adenylyl Cyclases↗
PubMed1975

A role for the macrophage in in vivo and in vitro resistance to murine bladder tumor cell growth.

Studies were performed to determine the role of macrophages in inhibition of growth of the same tumor cell type both in vitro and in vivo. Bladder transitional epithelium tumor cells were injected s.c. into Toxoplasma-infected mice, previously shown to contain activated macrophages, and into uninfected controls. The subsequent growth of a solid tumor was significantly less in the Toxoplasma-infected animals. Bladder tumor cells from the same cell line were grown in vitro either alone or in the presence of peritoneal lymphocytes and/or macrophages from oxoplasma-infected and control, uninfected mice. [3H]Thymidine incorporation by the tumor cells was inhibited only in the presence of macrophages from the Toxoplasma-infected animals. Lymphocytes alone did not appear to be cytotoxic under the conditions used. Moreover, lymphocytes from Toxoplasma-infected mice did not convey cytotoxicity to macrophages from control animals under the experimental conditions used.

Animals↗