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J Maher

Publications and source records attributed to J Maher.

At least 73 records · Page 4Linked to original sources
PubMed1986

The membrane proteins of the methanol-induced peroxisome of Candida boidinii. Initial characterization and generation of monoclonal antibodies.

Peroxisomes are massively induced when methylotrophic yeasts are cultured on methanol as the sole carbon and energy source. An analysis of the protein composition of the peroxisomal membrane and the generation of probes against two peroxisomal membrane proteins (PMPs) have been undertaken. Peroxisomes from Candida boidinii were obtained from sucrose gradients as previously described or from a novel one-step purification of the organelle on a Percoll gradient. The protein composition of the membranes from these two preparations was virtually identical. About 10 proteins comprise nearly all of its protein mass. The most prominent proteins have molecular masses of 120, 100, 47, 31-32 (a triplet), and 20 kDa; significant amounts of alcohol oxidase and dihydroxyacetone synthase, the two abundant matrix proteins, also remain associated with the membrane. Glycosylation of the membrane proteins could not be detected. Exposure of the membrane to chaotropes shows that PMPs 100 and 20 are the most easily removable, whereas PMP 47 appears to be the most tightly associated. Mice were injected with peroxisomal membrane, and hybridoma lines were isolated that produced antibody against PMP 20, PMP 47, and dihydroxyacetone synthase. Indirect immunofluorescence with these monoclonal antibodies confirmed that all three proteins are localized to the peroxisomal cluster. Immunoblotting experiments demonstrated that peroxisomal membrane as well as matrix proteins are induced by methanol.

Antibodies, Monoclonal↗
PubMed1984

Nurses in need.

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Crisis Intervention↗
PubMed1984

The response of human neutrophils to a chemotactic tripeptide (N-formyl-methionyl-leucyl-phenylalanine) studied by microcinematography.

A quantitative microcinematographic technique for the measurement of cellular motion in response to chemical influences is described. The data are analyzed by using a magnetic digitizer connected to a computer, permitting comparison of several characteristics of such motion. When human granulocytes are placed in a gradient of formyl-methionyl-leucyl-phenylalanine (fMLP) (concentration 10(-6)-10(-8) mol/L) against buffer, the motion of the cells is increased in velocity (chemokinesis) and is directed toward the chemoattractant, as measured by the orientation of the vector of motion. This directionality is confirmed by positive values for the McCutcheon index and analysis of directed linear displacement. Concentrations of fMLP below 10(-9) mol/L did not result in chemokinesis or chemotaxis, presumably due to insufficient stimulus. Concentrations of 10(-6) mol/L fMLP and greater resulted in marked stimulation of the cell surface but reduced directionality and velocity of motion compared with cells in a more optimal gradient. Motion of the unstimulated cells tended to be ortholinear , and this was not increased by the presence of a gradient of fMLP. Hence, as previously shown, the Random Walk analysis, which does not give weight to the direction of motion, is not useful in the analysis of the response of these cells to a chemotaxin in this system.

Cell Movement↗
PubMed1983

Studies on fractionated hyperthermia in experimental animals systems III. Uneven daily doses.

The effect of daily hyperthermia on the murine normal and tumor tissues was investigated. Tumors were early generation isotransplants of a fibrosarcoma (FSa-II) and a mammary carcinoma (MCa) in C3Hf/Sed mice. Hyperthermia was given by immersing animal feet into a water bath at 45.5 degrees C. Tumor response was studied by TG time assay (determination of the time required for half of the treated animals' tumors to reach 1000 mm3 from the treatment day). Average peak foot reaction was also investigated to compare the therapeutic effectiveness of various fractionation regimens. In the first experiment the first dose (D1) of 10 min was followed by 10, 20, or 30 min daily doses. The treatment regimen "D1 of 10 min + daily 30 min" resulted in a significant therapeutic gain. The smaller doses were unable to overcome the repopulation of surviving tumor cells and the increasing magnitude of thermal resistance. To overcome tumor cell repopulation and thermal resistance, a regimen of increasing daily doses was attempted without success. These results indicated that doses following a D1 of 10 min must be as large as 30 min to obtain a therapeutic gain. Any fractionation regimens for MCa tumors, which developed the greatest thermal resistance among our animal tumors tested, failed to result in a therapeutic gain.

Animals↗
PubMed1981

Thermal resistance in a spontaneous murine tumour.

Resistance to subsequent hyperthermia as a result of prior heating was investigated using a spontaneous murine tumour implanted into the feet of C3H/Sed mice. Tumours were treated by immersing the tumour-bearing foot into a constant-temperature hot water bath set at 45.5 degrees C and were given single and split doses of heat. Response was assessed using a tumour-growth time assay. Three aspects of thermally-induced resistance were particularly considered: the time course of development and decay; the importance of the magnitude of the priming dose and the influence of the size of the tumour at the time of treatment. Substantial resistance was induced in this tumour by short priming doses at 45.5 degrees C, rising rapidly 1-2 days after the first treatment and then starting to decay. There was no significant difference in the kinetics of thermal resistance induced in tumours treated at 4mm and those treated at 8 mm in size, although the large tumours were more sensitive to single doses of heat. Increasing the magnitude of the priming dose of heat resulted in an increase in the magnitude of resistance to the second dose. The results of this study are compared with results of similar studies in this and other laboratories using murine normal tissues and cells in culture. Possible clinical implications are considered.

Animals↗
PubMed1981

Integrity of perfused rat liver at different heat loads.

Isolated rat livers were perfused for 90 minutes at temperatures from 37 degrees to 43 degrees C. to evaluate the effects of heat alone on bile production, alanine aminotransferase, and asparate aminotransferase release, and light and electron microscopic structure. Bile production reached a plateau after 45 minutes at 43 degrees C. and after 60 minutes at 42 degrees C. At temperatures between 39 degrees and 41 degrees C., bile production was not significantly different from that produced at 37 degrees C. The timing and levels of alanine aminotransferase and aspartate aminotransferase released into the perfusates were similar, with increases after 45 minutes at 43 degrees C., after 60 minutes at 41 degrees and 42 degrees C. and after 75 minutes at 39 degrees and 40 degrees C. At the end of the 90-minute perfusion, light microscopy indicated vacuolization and severe dissociation of hepatocytes at 42 degrees and 43 degrees C., and pronounced centrilobular vacuolization at 41 degrees C. Electron microscopy demonstrated that hepatocytes had sustained extensive damage at 41 degrees to 43 degrees C. Mild focal and probably reversible damage occurred at 39 degrees and 40 degrees C. Since pH and O2 levels were regulated in a nonrecirculating system and perfusion rates were constant, neither acidosis, hypoxia, nor circulatory inadequacy were responsible for the alterations. Therefore, changes were attributed to the direct effects of heat, reflected a continuum from no detectable damage at 37 degrees C. to occasional necrosis of individual cells at 39 degrees to 40 degrees C. and culminated in widespread necrosis at 41 degrees to 43 degrees C. with a 90-minute exposure. These results reflect a time/temperature relationship over a range of temperatures. A hypothesis for the sequence of events in the pathogenesis of heat-induced hepatic injury is described.

Alanine Transaminase↗
PubMed1980

Cimetidine vs. placebo in prepyloric gastric ulcer therapy. Six week controlled double blind investigation without any antacid therapy.

We studied the healing efficacy of cimetidine or placebo on 24 endoscopically proven prepyloric gastric ulcer outpatients in randomized controlled prospective double blind trial. There were 11 patients in the cimetidine (1,200 mg daily) treatment group and 13 patients in the placebo treated group. No antacid was allowed, but a placebo antacid with no neutralizing capacity was given as needed for pain. The incidence of complete endoscopic healing at 2, 4, and 6 weeks was 45%, 64%, and 73% in the cimetidine treated patients and 0%, 15%, and 62% in the placebo treated patients. There was a statistically significant difference (p less than .05) in complete prepyloric gastric ulcer healing between both treatment groups after 2 and. 4 weeks of therapy, but there was no significant difference at the 6 week observation period. The results of this study demonstrate that in prepyloric gastric ulcer outpatients treated for 6 weeks 1) cimetidine accelerates the rate of prepyloric gastric ulcer healing during the first 4 weeks of treatment; 2) more than 60% of prepyloric gastric ulcers will spontaneously heal during a 6 week observation period which is not statistically modified by cimetidine treatment.

Cimetidine↗