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Biomedical subjects

H S Kantor

Publications and source records attributed to H S Kantor.

12 recordsLinked to original sources
PubMed1988

Nosocomial transmission of tuberculosis from unsuspected disease.

Tuberculosis remains an occupational hazard for hospital employees. A case of acute generalized tuberculosis occurring in a patient with a malignancy who had received corticosteroids was undetected during life and during a gross autopsy examination. Histologic examination of tissue performed one month later was necessary to establish the diagnosis. Of susceptible hospital staff members who were exposed to the index case, infection developed in nine of 56 (16 percent) compared with three of 333 (0.9 percent) unexposed personnel with similar risk but no known exposure (p less than 0.001). This was a 17.8-fold increase in the infection rate for the exposed group. Three employees infected had evidence of active disease: two had pleural effusions and one had cavitary pulmonary infiltrates; six were asymptomatic. The high rate of infection was associated with inadequate air ventilation and exposure to uncontained infectious aerosol. Preventive therapy with isoniazid, high-change-ventilating systems, ultraviolet radiation, and primary barrier systems are recommended methods to reduce the infection risk.

Air Microbiology↗
PubMed1987

Survey of multiply resistant Providencia stuartii in a chronic care unit.

Providencia stuartii was cultured over a 4-year period from the urinary tract, throat, perineum, axilla and stools of patients in a long-term chronic care unit, the most common site of colonization being the urinary tract. A total of 17 patients had Prov. stuartii bacteraemia and manipulation of the urinary tract preceded bacteraemia in 10 cases. Eighty-two per cent of the patients had long-term urinary tract colonization from 1 month to 4 years. Although most isolates were resistant to all aminoglycosides except amikacin, the organisms were all susceptible to thienamycin, ceftazidime, cefotaxime, ceftizoxime and moxalactam.

Adult↗
PubMed1980

Nosocomial multiply resistant Providencia stuartii: a long-term outbreak with multiple biotypes and serotypes at one hospital.

A long-term outbreak of urinary tract-associated multiply resistant Providencia stuartii occurred in a large medical facility that included a 513-bed chronic care unit. The unique characteristics of this outbreak were that from within a single medical facility, P. stuartii with multiple serotypes, biotypes, and antibiograms could be identified. The organisms isolated had five different biotypes, seven different antibiograms, and two major serotypes. All of the organisms were susceptible to amikacin, cefamandole, and cefoxitin. Application of standard infection control measures impeded the spread of this outbreak, and it slowly terminated 16 months later.

Anti-Bacterial Agents↗
PubMed1975

Enterotoxins of Escherichia coli and vibriocholerae: tools for the molecular biologist.

With the independent discovery in several different laboratories that Vibrio cholerae and heat-labile Escherichia coli enterotoxins activated an enzyme (adenylate cyclase) in small intestinal epithealial cells to cause an enhanced intestinal secretion mediated by cyclic adenosine 3',5'-monophosphate (cyclic AMP), a molecular mechanism was provided for these disease states. As agents that also elevate intracellular concentrations of cyclic AMP in virtually every mammalian tissue tested, the enterotoxins are potentially invaluable tools in investigation of the molecular sequence of events of all cyclic AMP-related cellular phenomena. Cyclic AMP has been known for some time to be the central regulator in the cellular expression of the effects of hormones and has become known more recently as an agent that controls cellular growth by corrdinately influencing several biochemical processes related to rate of cell division. Successful application of the enterotoxins as cellular probes in the areas of regulation of cell division, determination of the reaction mechanism of adenylate cyclase, and elucidation of the relationship between prostaglandin and adenylate cyclase, both in this laboratory and in those of others, is reviewed.

Adenylyl Cyclases↗
PubMed1974

Kinetic evidence for the presence of two prostaglandin receptor sites regulating the activity of intestinal adenylate cyclase sensitive to Escherichia coli enterotoxin.

Kinetic behavior most consistent with the presence of two independent, but simultaneously acting, regulatory effector sites for prostaglandins has been presented for adenylate cyclase (EC 4.6.1.1) of rabbit intestinal epithelial cells. One site regulates activation of the catalytic site, while the other site regulates inhibition. A synthetic prostaglandin analogue, 7-oxa-13-prostynoic acid, is recognized at both sites in a concentration-dependent manner. At concentrations of 7-oxa-13-prostynoic acid less than 45 mug/ml, activation is seen, while at higher concentrations, inhibition is seen. Different naturally occurring prostaglandins appear to be site-specific. Prostaglandin E(1) gives only activation of the cyclase, while prostaglandin A(1) gives only inhibition of the activated cyclase. When saturating concentrations of prostaglandin E(1) are used to activate adenylate cyclase, no further activation by 7-oxa-13-prostynoic acid can be elicited, indicating that both molecules activate at the same site. The similarity of inhibition constants for both 7-oxa-13-prostynoic acid and prostaglandin A(1) suggests that the mode of binding is the same for both compounds and that they probably inhibit by acting at the same site. The inhibition by 7-oxa-13-prostynoic acid and by prostaglandin A(1) overrides enzyme activation produced by either Escherichia coli enterotoxin, prostaglandin E(1), or sodium fluoride, suggesting that in intestinal adenylate cyclase this site is the primary regulatory site (i.e., primary allosteric effector site) for enzyme activity. These data suggest that sites exist on adenylate cyclase which would allow prostaglandins to serve as the intracellular messengers by which the cell controls its adenylate-cyclase-mediated response to extracellular stimulation, as with hormones.

Adenylyl Cyclase Inhibitors↗
PubMed1974

Action of Escherichia coli enterotoxin: adenylate cyclase behavior of intestinal epithelial cells in culture.

Heat-labile enterotoxin preparations obtained from two enteropathogenic strains of Escherichia coli of porcine and human origin were shown to stimulate adenylate cyclase activity of human embryonic intestinal epithelial cells in culture. Comparable results were also obtained when cholera toxin was used. The degree of enzyme stimulation was proportional to the concentration of enterotoxin. Similar preparations from two strains of non-enterotoxigenic E. coli had no effect on adenylate cyclase activity. Cells exposed to enterotoxin could be washed after 1 min of contact time without altering the subsequent course of maximum adenylate cyclase activity, which was maintained for at least 18 h at 37 C. During long periods (18 h) of tissue culture incubation, the determination of adenylate cyclase activity was 200- to 300-fold more sensitive than quantitating fluid accumulation in the adult rabbit ileal loop model. Decreasing the incubation time appreciably reduced the sensitivity of the epithelial cells to enterotoxin. E. coli enterotoxin is an effective activator of nonintestinal adenylate cyclase systems. Treatment of KB and HEp-2 cell lines with enterotoxin also resulted in significant enzyme stimulation. The intestinal epithelial cell tissue culture model provides a sensitive homogenous biological system for studying the response of intestinal adenylate cyclase to enterotoxin while eliminating the numerous cellular and tissue components present in the ligated ileal loop model.

Adenosine Triphosphate↗