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Biomedical subjects

J Strong

Publications and source records attributed to J Strong.

51 records · Page 3Linked to original sources
PubMed1984

A third example of haemolytic auto-anti-Vel.

A non-transfused, 43 year old Caucasian female presented with acute haemolytic anaemia and splenomegaly. Sections of bone marrow showed erythroid hyperplasia. The patient's red blood cells gave a negative reaction with polyspecific antiglobulin serum, but a positive reaction with specific anti-IgM. A heat eluate prepared from her red cells showed anti-Vel specificity. Her serum agglutinated only Vel-positive cells including her own. All papain pre-treated red cells including her own and Vel-negative cells were completely haemolysed at 37 degrees C. The percentage of haemolysis of Vel-positive cells was greater than that of Vel-negative cells.

Adult↗
PubMed1983

Flux through the de novo pyrimidine pathway in vivo. Effect of N-phosphonacetyl-L-aspartate, a potent inhibitor of aspartate transcarbamylase.

The activity of the de novo pyrimidine biosynthetic pathway has been measured in resistant and sensitive murine tumors in vivo following a single intraperitoneal dose of N-phosphonacetyl-L-aspartate (PALA) (400 mg/kg). For these studies, we utilized a gas chromatograph-mass spectrometric technique which enabled measurement of 13C incorporation from 13CO2 into the uracil nucleotide pool (sigma uracil) of tumors in situ. Flux through the de novo pathway was 75-85% inhibited 1 h after PALA treatment in both sensitive (Lewis lung carcinoma) and the resistant (L1210) tumors, but there was a lag time before this inhibition was reflected in reduced sigma uracil pools. The activity of the pathway in the Lewis lung carcinoma tumors remained maximally depressed (5-15% of control activity) for up to 48 h after the dose of PALA. In contrast, flux through the pathway of L1210 tumors remained 80% inhibited for up to 4 h following PALA administration, but recovered to 70% of control activity between 4 and 12 h after PALA treatment. Recovery of the remaining 30% of control activity in the L1210 tumor was at a much slower rate requiring between 12 and 48 h after PALA treatment to regain full activity of the pathway. This recovery of flux through the de novo pyrimidine biosynthetic pathway did not correlate with the measurement of recovery of aspartate transcarbamylase activity in similarly treated tumors. These data argue strongly in favor of the importance of the de novo biosynthetic pathway, rather than salvage mechanisms, for determining in vivo sensitivity or resistance of these tumors to PALA treatment.

Animals↗
PubMed1983

Regional [14C]misonidazole distribution in experimental RT-9 brain tumors.

Regional [14C]misonidazole-derived radioactivity (MISO) was measured by quantitative autoradiography in experimental RT-9 brain tumors 0.5, 2, and 4 hr after an i.v. bolus (25 mg) and constant infusion (10 mg/hr). Misonidazole (MISO) concentration in plasma and brain was also measured by high-pressure liquid chromatography; the brain/plasma MISO ratio ranged between 0.5 and 0.7. MISO equivalents were calculated from tissue or plasma 14C radioactivity and [14C]MISO specific activity data. The MISO/MISO equivalents ratio, which represents the nonmetabolized fraction of [14C]MISO, fell gradually in plasma (0.89 at 4 hr) and more rapidly in brain (0.67 at 4 hr) and tumor (0.30 at 4 hr). MISO distributed uniformly throughout the brain at all three time periods. In contrast, MISO distribution in tumor was variable, and tumor concentrations relative to that in brain increased with time. The average tumor/brain MISO ratio was 1.3, 1.7, and 2.6 at 0.5, 2, and 4 hr, respectively, which suggests tumor uptake and binding of MISO or, more likely, MISO-derived 14C-labeled metabolites. In addition, MISO distribution in tumor tissue was strikingly heterogeneous at 4 hr, resulting in an average high/low tumor activity ratio of 4/1 and an average high tumor/brain ratio of 5/1. Tumor regions with high MISO activity correlated in part to viable-appearing cells around necrotic foci.

Animals↗
PubMed1982

Activation of misonidazole by rat liver microsomes and purified NADPH-cytochrome c reductase.

Rat liver microsomes and purified NADPH-cytochrome c reductase metabolized [14C]misonidazole anaerobically to a reactive intermediate that covalently binds to tissue macromolecules. Air strongly inhibited the binding whereas carbon monoxide had no effect, indicating that misonidazole is activated via reduction and not by cytochrome P-450-dependent oxidation. Both systems showed an absolute requirement for NADPH and were stimulated by flavine (FAD) and paraquat. The apparent Km for misonidazole binding to microsomal protein was 0.74 mM the apparent Vmax was 0.64 nmole 14C bound . mg-1 . min-1. At a single substrate concentration, nitrofurantoin, nitrofurazone and desmethylmisonidazole inhibited the covalent binding of misonidazole to microsomal protein by 47, 26, and 38% respectively. The effect of nitrofurantoin on the kinetics of misonidazole binding gave a complex interaction indicative of uncompetitive inhibition. Glutathione reduced the binding of misonidazole to microsomal protein below the level observed for boiled microsomes while ascorbic acid had no effect. Compared to nitrofurantoin and paraquat, misonidazole was a poor stimulator of superoxide production as measured by adrenochrome formation.

Animals↗
PubMed1978

Initiation of light adaptation in barnacle photoreceptors.

Intracellular recordings were used to measure the action spectrum of light adaptation in barnacle photoreceptors. The action spectrum closely resembles the absorption spectrum of rhodopsin (lambdamax at 530 nanometers) and is clearly different from that of metarhodopsin (lambdamax at 495 nanometers). These results suggest that absorption of light by rhodopsin initiates both excitation and light adaptation. The previously reported antagonistic process initiated by metarhodopsin does not appear to play a role at moderate light intensities.

Adaptation, Physiological↗
PubMed1978

Comparison of two radioimmunoassays and a microbiologic assay for bleomycin.

Recently two radioimmunoassays have been independently developed for determination of bleomycin levels. In this study these assays are compared with each other and with a standard microbiologic assay for bleomycin. Bleomycin levels were determined in serum and urine samples obtained at varying intervals following intramuscular bleomycin injection. There were systematic differences between the assays. One radioimmunoassay indicated bleomycin levels lower than the levels indicated by the microbiologic assay with serum samples. With urine samples, both radioimmunoassays indicated bleomycin levels greater than the microbiologic assay.

Antibody Specificity↗
PubMed1977

Bleomycin serum pharmacokinetics as determined by a radioimmunoassay and a microbiologic assay in a patient with compromised renal function.

Serum and plasma bleomycin concentrations were determined in a patient with renal dysfunction at two creatinine clearances. The results obtained with a new radioimmunoassay and the microbiologic assay were compared. It was shown: 1) that the clearance of bleomycin from the blood is markedly retarded in severe renal dysfunction, 2) that clearance of bleomycin varies with creatinine clearance, 3) that bleomycin is probably not dialyzable, 4) that determinations on serum and plasma were equivalent, and 5) that the radioimmunoassay and microbiologic assays gave equivalent results (P less than 0.001).

Acute Kidney Injury↗
PubMedDate not supplied

Development, reliability, and concurrent validity of the modified inventory of potential reconstructive needs.

Documentation of burn sequelae can be a difficult and time-consuming task. To date a reliable and systematic format for recording postburn trauma is lacking. The purpose of this research was two-fold: first, to develop a Modified Inventory of Potential Reconstructive Needs from the original Inventory of Potential Reconstructive Needs to allow methodical documentation of functional and cosmetic burn sequelae in all body surface areas of children with burns and, second, to establish interrater reliability and concurrent validity of the instrument, thus allowing its clinical application. Two raters scored the Modified Inventory of Potential Reconstructive Needs on 41 children with a range of burns types and severity. Excellent interrater reliability was demonstrated for both total (intraclass correlation coefficient = 0.996) and subsection inventory scores. Concurrent validity was also established with total scores showing strong positive correlations (0.73-0.76) with three indicators of burn severity. These findings provide initial support for the tool's clinical applicability, particularly in relation to rehabilitative planning and documentation.

Adolescent↗
PubMedDate not supplied

Effect of hepatic microsomal enzyme inducers on the metabolism of misonidazole in rats.

Pretreatment of rats with the hepatic microsomal enzyme inducers, phenobarbital or phenytoin, increased the metabolism of the hypoxic cell radiosensitizer, misonidazole. The increase was reflected in the ratio of O-demethylated metabolite to unchanged drug in the 24-hour urine collection and was more extensive with phenobarbital. No inducement was observed after pretreatment with dexamethasone or misonidazole. Such pretreatment with inducers prior to misonidazole therapy would be clinically important since the incidence of neurotoxicity may be reduced without impairment of the radiosensitizing effect.

Animals↗