inosinic-acid and Gout

inosinic-acid has been researched along with Gout* in 6 studies

Reviews

3 review(s) available for inosinic-acid and Gout

ArticleYear
Molecular nature of enzyme regulation in purine biosynthesis.
    Ciba Foundation symposium, 1977, Issue:48

    Topics: Amidophosphoribosyltransferase; Animals; Female; Glucosephosphate Dehydrogenase Deficiency; Glutamine; Gout; Humans; Inosine Monophosphate; Kinetics; Liver; Molecular Weight; Nucleotidases; Pentosyltransferases; Phosphoribosyl Pyrophosphate; Phosphotransferases; Placenta; Pregnancy; Purine Nucleotides; Ribose-Phosphate Pyrophosphokinase; Ribosemonophosphates; Xanthine Oxidase

1977
Molecular variation in relation to purine metabolism.
    Journal of clinical pathology. Supplement (Royal College of Pathologists), 1974, Volume: 8

    Topics: Amidophosphoribosyltransferase; Chemical Phenomena; Chemistry; Glucosephosphate Dehydrogenase Deficiency; Glutathione Reductase; Gout; Humans; Inosine Monophosphate; Lesch-Nyhan Syndrome; Phosphoribosyl Pyrophosphate; Purine-Pyrimidine Metabolism, Inborn Errors; Purines; Uric Acid; Xanthine Oxidase; Xanthines; Xeroderma Pigmentosum

1974
Uric acid metabolism in normal man and in primary gout.
    The New England journal of medicine, 1965, Aug-05, Volume: 273, Issue:6

    Topics: Arthritis, Gouty; Gout; Humans; Hyperuricemia; Inosine Monophosphate; Male; Quaternary Ammonium Compounds; Uric Acid

1965

Other Studies

3 other study(ies) available for inosinic-acid and Gout

ArticleYear
A pharmacy practice laboratory exercise to apply biochemistry concepts.
    American journal of pharmaceutical education, 2010, Oct-11, Volume: 74, Issue:8

    To develop exercises that allow pharmacy students to apply foundational knowledge discussed in a first-professional year (P1) biochemistry course to specific disease states and patient scenarios.. A pharmacy practice laboratory exercise was developed to accompany a lecture sequence pertaining to purine biosynthesis and degradation. The assignment required students to fill a prescription, provide patient counseling tips, and answer questions pertaining to the disease state, the underlying biochemical problem, and the prescribed medication.. Students were graded on the accuracy with which they filled the prescription, provided patient counseling, and answered the questions provided. Overall, students displayed mastery in all of these areas. Additionally, students completed a course survey on which they rated this exercise favorably, noting that it helped them to integrate basic science concepts and pharmacy practice.. A laboratory exercise provided an opportunity for P1 students to apply foundational pharmacy knowledge to a patient case and can serve as a template for the design of additional exercises.

    Topics: Adenosine Monophosphate; Biochemistry; Counseling; Curriculum; DNA; Drug Prescriptions; Drug Therapy; Education, Pharmacy; Educational Measurement; Gout; Guanosine Monophosphate; Humans; Hyperuricemia; Inosine Monophosphate; Professional Practice; Purines; Students, Pharmacy

2010
A method for the determination of 5-phosphoribosyl 1-pyrophosphate concentrations in erythrocytes using high-performance liquid chromatography.
    Analytical biochemistry, 1987, Feb-01, Volume: 160, Issue:2

    A method for the measurement of erythrocyte 5-phosphoribosyl 1-pyrophosphate (PP-ribose-P) using HPLC is described. Inosinic acid formed from the enzyme-catalyzed reaction of hypoxanthine and PP-ribose-P using partially purified hypoxanthine-guanine phosphoribosyltransferase is measured after chromatography on an ion-exchange column (Partisil 10 SAX). The average recovery of PP-ribose-P added to erythrocytes was 96.6%. Normal values found were 1.3 +/- 0.6 nmol PP-ribose-P/ml packed RBC (20 individuals). Replication experiments gave a coefficient of variation of 4.4%. Elevated levels in the range 4.4-7.9 nmol PP-ribose-P/ml packed RBC were found in four patients with gout and partial deficiency of the enzyme hypoxanthine-guanine phosphoribosyltransferase.

    Topics: Chromatography, High Pressure Liquid; Erythrocytes; Gout; Humans; Hypoxanthine Phosphoribosyltransferase; Inosine Monophosphate; Male; Pentosephosphates; Phosphoribosyl Pyrophosphate

1987
Enzyme defect in primary gout.
    Lancet (London, England), 1979, Mar-17, Volume: 1, Issue:8116

    The rate-limiting step in the degradation of adenine nucleotides in the liver is the conversion of adenosine monophosphate (A.M.P.) to inosine monophosphate by A.M.P. deaminase, which is normally 95% inhibited. When the inhibition is released, uric acid is formed in large excess, and the biosynthesis of purines is increased. We therefore propose that congenital hyperuricaemia is caused by the presence of an abnormal A.M.P. deaminase, which is less sensitive to its physiological inhibitors. Verification of the hypothesis depends upon the availability of liver tissue from patients with congenital hyperuricaemia for kinetic analysis of A.M.P. deaminase. A call for collaboration is addressed to the medical community.

    Topics: AMP Deaminase; Deamination; Gout; Humans; Inosine Monophosphate; Liver; Nucleotide Deaminases; Purine Nucleotides; Purines; Uric Acid

1979