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Biomedical subjects

A Qureshi

Publications and source records attributed to A Qureshi.

68 records · Page 4Linked to original sources
PubMed1988

Investigational study of iodine-124 with a positron camera.

A case is presented where I-124 produced by a clinical cyclotron was used with a positron emission tomography camera for clinical usage. This represents the first report of the utilization of this modality with this radionuclide. We feel the increased spatial resolution of PET should be of value in looking at thyroid disease.

Carcinoma↗
PubMed1986

Increasing the thermosensitivity of a mammary tumor (CA755) through dietary modification.

Disruption of the integrity of tumor cellular membranes has been proposed as an initiating event in hyperthermic cell death. Thermosensitivity measured by the shift in the harmonic mean of tumor regrowth delay of CA755 mammary adenocarcinomas grown in the hind legs of male BDF1, mice increased 22% when the hosts were fed a diet enriched in polyunsaturated fatty acids. Although the diet elicited the anticipated increase in tumor membrane phospholipid polyunsaturated fatty acids, the proportion of total unsaturated fatty acids decreased and the proportion of membrane-rigidifying saturated fatty acids increased. Concomitantly, the concentrations of cholesterol and phospholipid phosphorus increased and the ratio of phosphatidylethanolamine to phosphatidylcholine decreased, presumably to counter the effect of the change in the fatty acid pattern. In host liver membranes, the diet-mediated increase in proportion of polyunsaturated fatty acids was not accompanied by an increase in the proportion of rigidifying saturated fatty acids. Instead, the homeoviscous adaptation consisted of decreases in monounsaturated fatty acids and cholesterol concentration and an increase in the phosphatidylethanolamine-phosphatidylcholine ratio. Addition of a natural inhibitor of cholesterol biosynthesis to the polyunsaturated fatty acid enriched-diet reversed the diet-mediated increase in the phosphatidylethanolamine-phosphatidylcholine ratio of host liver membranes. Tumor membrane lipids from hosts fed the combined dietary factors were characterized by the formentioned rigidifying increase in saturated fatty acids and compensatory decrease in the phosphatidylethanolamine-phosphatidylcholine ratio. The inhibitor reversed the compensatory increases in cholesterol and phospholipid phosphorus concentrations. As a consequence the thermosensitivity of tumors bearing this perturbed membrane was increased.

Adenocarcinoma↗
PubMed1986

Regression of rat primary mammary tumors following dietary d-limonene.

The effects of d-limonene on rat mammary tumors were investigated. Following the appearance of mammary tumors induced by 7,12-dimethylbenz[a]anthracene in female (W/Fu X F344)F2 rats, animals were assigned to pairs in which 1 rat was fed a diet containing 10% d-limonene and the other was pair fed an isocaloric diet containing 10% cellulose. There was a highly significant increase in the regression of the first tumors in the rats fed d-limonene. In addition, d-limonene given at this time inhibited the formation of subsequent multiple tumors in these rats.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1984

Inhibition of DMBA-induced mammary cancer by the monoterpene d-limonene.

We investigated whether the addition of d-limonene to the diets of rats would modify the process of mammary tumor induction by 7,12-dimethylbenz[a]anthracene (DMBA). When diets containing 1000 or 10 000 p.p.m. d-limonene were fed to rats from one week before DMBA administration to the end of the experiment (27 weeks post DMBA treatment), a significant reduction in mammary carcinogenesis was observed at each level. The inhibition of carcinogenesis was mainly due to an increase in latency; however, major differences in incidence could be seen during the follow-up period. For example, rats fed 10 000 p.p.m. of d-limonene had a 72% reduction in mammary tumors when compared to controls at 18 weeks post DMBA treatment. In addition to inhibiting the appearance of mammary tumors, d-limonene was also found to cause the regression of frank mammary tumors. No toxicity was evident in these rats even at the highest d-limonene dose. Control and all treated rats gained weight at the same rate throughout the experiment. In addition, no differences were found in their peripheral blood counts (Hct, total white cell and differential count).

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1983

Production of formaldehyde and acetone by hydroxyl-radical generating systems during the metabolism of tertiary butyl alcohol.

t-Butyl alcohol is not a substrate for alcohol dehydrogenase or for the peroxidatic activity of catalase and, therefore, it is used frequently as an example of a non-metabolizable alcohol. t-Butyl alcohol is, however, a scavenger of the hydroxyl radical. The current report demonstrates that t-butyl alcohol can be oxidized to formaldehyde plus acetone by hydroxyl radicals generated from four different systems. The systems studied were: (a) two chemical systems, namely, the iron catalyzed oxidation of ascorbic acid and the Fenton reaction between H2O2 and iron; (b) an enzymatic system, the coupled oxidation of xanthine by xanthine oxidase; and (c) a membrane-bound system, NADPH-dependent microsomal electron transfer. The oxidation of t-butyl alcohol appeared to be mediated by hydroxyl radicals, or by a species with the oxidizing power of the hydroxyl radical, because the production of formaldehyde plus acetone was (a) inhibited by competing scavengers of the hydroxyl radical; (b) stimulated by the addition of iron-EDTA; and (c) inhibited by catalase. The last observation suggests that H2O2 served as the precursor of the hydroxyl radical in all three systems. A possible mechanism is hydrogen abstraction to form the alkoxyl radical [CH3)3-C-O.), spontaneous fission of the alkoxyl radical to produce acetone and the methyl radical (CH3.), interaction of the methyl radical with O2 to form the methyl peroxy radical (CH300.), and decomposition of the later to formaldehyde. These results extend the alcohol oxidizing capacity of the microsomal alcohol oxidizing system to a tertiary alcohol. Since t-butyl alcohol is not a substrate for alcohol dehydrogenase or catalase, the ability of microsomes to oxidize t-butyl alcohol lends further support for a role for hydroxyl radicals in the microsomal alcohol oxidation system. In view of the production of formaldehyde, and the reactivity as well as further metabolism of this aldehyde, caution should be used in interpreting experiments in which t-butyl alcohol is used as a presumed "non-metabolizable" alcohol. t-Butyl alcohol may be a valuable probe for the detection of hydroxyl radicals in intact cells and in vivo.

Acetone↗
PubMed1982

Role of catalase and hydroxyl radicals in the oxidation of methanol by rat liver microsomes.

In view of the presence of adventitious catalase in isolated microsomes, and the requirement for H2O2, it has been suggested that NADPH-dependent oxidation of methanol by rat liver microsomes was mediated exclusively by the peroxidatic activity of catalase. However, H2O2 may also serve as a precursor of the hydroxyl radical, and methanol reacts with hydroxyl radicals to produce formaldehyde. Inhibition of H2O2 production should therefore decrease methanol oxidation by either a hydroxyl radical-dependent pathway or a catalase-dependent pathway. To attempt to clarify some of the controversies concerning the roles of H2O2 and catalase in the microsomal pathway of oxidation of short chain alcohols, studies were carried out to determine the nature of the pathway responsible for methanol oxidation by isolated microsomes. In the absence of the catalase inhibitor azide, methanol may be oxidized primarily by the peroxidatic activity of catalase since there was little effect on methanol oxidation by competing hydroxyl radical scavengers. Azide, which inhibited catalase activity greater than 95%, inhibited NADPH-dependent oxidation of methanol by 30-50%. The azide-insensitive (catalase-independent) pathway of methanol oxidation was inhibited by scavengers of hydroxyl radicals. The inhibition of the scavengers reflected the rate constant for interaction with hydroxyl radicals and was greater at lower concentrations of methanol than at higher concentrations, suggesting competition between the scavengers and methanol. The addition of H2O2 stimulated the oxidation of methanol in the presence of azide; H2O2 may serve as a precursor of the hydroxyl radical. Iron-EDTA, which is known to increase hydroxyl radical production, stimulated the oxidation of methanol in the absence and presence of azide. The stimulation by iron-EDTA was blocked by the competing hydroxyl radical scavengers even in the absence of azide, suggesting that the added iron-EDTA favorably with microsomal catalase for H2O2 to produce hydroxyl radicals (or a species with the oxidizing power of the hydroxyl radical). These results suggest that in microsomes, depending on the absence or presence of azide, methanol may be oxidized by two primary pathways, one involving the peroxidatic activity of catalase, and the other in which hydroxyl radicals, generated from microsomal electron transfer, play a role. In view of the crucial role played by H2O2 in both pathways, inhibition of H2O2 formation should not be interpreted solely as evidence for a role for catalase in the microsomal oxidation of alcohols.

Animals↗
PubMed1976

Solid-phase radioimmunoassay for antibodies to flavivirus structural and nonstructural proteins.

A micro-solid-phase radioimmunoassay (SPRIA) is described for quantitation of antibodies to purified flaviviruses as well as to the purified envelope glycoprotein and 80,000-molecular-weight viral nonstructural protein. Sera from mice experimentally infected with Saint Louis encephalitis (SLE) virus or from humans after a primary SLE virus infection reacted more specifically with the major viral envelope protein in the SPRIA test than with antigens conventionally used in the complement fixation (CF) and hemagglutination inhibition tests. A high degree of correlation (P is less than 0.05) was observed between SPRIA anti-immunoglobulin G binding values with the 80,000-molecular-weight nonstructural protein of SLE virus and antibody titers obtained by plaque reduction neutralization and CF with the nonstructural protein. In five of seven human sera in which CF antibody titers to the nonstructural protein were 4 or less, SPRIA testing revealed significant titers of IgG immunoglobulin reactive with this viral protein. The SPRIA test for antibodies reactive with group B togavirus nonstructural protein is as specific and sensitive as the plaque reduction neutralization test for titrating viral antibody in human and animal sera. Antibodies reactive with viral envelope proteins are broadly cross-reactive by the Spria technique, demonstrating both group- and complex-reactive antigenic determinants. The SPRIA test, using wells precoated with antigen, can be completed in 1 day, providing a rapid, highly sensitive test which can be adapted to use in testing a large number of sera.

Animals↗
PubMedDate not supplied

The impact of automatic prescriptions on reducing low-density lipoprotein cholesterol levels.

CONTEXT: Compliance with the National Cholesterol Education Program (NCEP) guidelines for secondary prevention of atherosclerotic disease has been poor. OBJECTIVE: To determine whether an automatic prescription would improve compliance with NCEP guidelines on low-density lipoprotein (LDL) cholesterol for secondary prevention of atherosclerotic disease. DESIGN: Observational study in which physicians chose whether to use an automatic prescription system. PATIENTS: 126 patients with established coronary or cerebrovascular disease whose LDL cholesterol level was greater than 100 mg/dL. INTERVENTION: By signing the automatic prescription, physicians allowed the study team (medical director and pharmacist) to change lipid-lowering medications. One member of the team then contacted the patient, advising him or her of any changes to medications and treatment. The patient was told that his or her doctor was recommending this change on the basis of recent laboratory tests. OUTCOME MEASURES: The proportion of patients reaching the LDL cholesterol goal of 100 mg/dL or less. RESULTS: Physicians used the automatic prescription for 25 patients. Eighteen of the 25 patients in the intervention group (72.0%) achieved the LDL cholesterol goal compared with only 43 of the 101 controls (42.6%) (P = 0.004). After adjustment for differences in age, sex, triglyceride levels, total cholesterol levels, high-density lipoprotein cholesterol levels, and preintervention LDL cholesterol levels, the likelihood of achieving the LDL cholesterol goal was 1.74 times higher in the automatic prescription group than in the control group (P = 0.025). CONCLUSION: An automatic prescription can help physicians comply with the NCEP guidelines.

Anticholesteremic Agents↗