Studies on the synthesis of proinsulin. 3. Synthesis of polypeptides related to the connecting peptide segment of bovine proinsulin.
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Amino Acid Sequence↗
Biomedical subjects
N Sakura
Publications and source records attributed to N Sakura.
Synthesis of polypeptides related to porcine proinsulin.
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Amino Acid Sequence↗
Isolation of "myocardial depressant factor(s)" from the ultrafiltrate of heart failure patients with acute renal failure.
Cardiac function improvement seen with hemofiltration may be attributable to "cardiac depressant factor(s)" removal. The authors have attempted "factor" isolation. Initial 12 hr hemofiltrate was obtained from: 4 patients with acute congestive heart failure (cardiac index: 2.02 +/- 0.48) and acute renal failure (blood urea nitrogen [BUN] 97.7 +/- 32.7; serum creatinine [SCr] 6.2 +/- 3.4 mg%) (Group I); 8 patients with chronic congestive heart failure (CI: 2.69 +/- 1.3) and mild renal failure (BUN 48.8 +/- 31.4; SCr 3.5 +/- 2.4 mg%) (Group II); and 8 patients with end-stage renal disease and no congestive heart failure (Group III). Crude samples were passed through C18Sep-Pak, and eluted with methanol/water mixtures, and 50% methanol samples were fractionated by high pressure liquid chromatography. Inotropic response was studied by injecting samples (in Krebs-Hensleit buffer) into a Langendorff rat heart preparation. The effect of pH, acetate, salts, and adding propranolol on the inotropic response also was tested. Myocardial depression followed all vehicle and preparatory elements: 0.1 M HCl (-47%); 0.08 M acetic acid (-75%); Na acetate (-25%); 0.1 M NaHCO3 (-11%); Na citrate (-84%); and Na glutarate (-14%). Group I had biphasic responses, the positive inotropism accorded to catecholamines, whereas negative inotropism was equal in each patient (-40.3%). Group II had a biphasic response with negative (-15%) inotropism noted. Group III was weakly biphasic. The data indicate there was myocardial depressive activity, most pronounced in Groups I and II, after method interference was corrected.
Acute Kidney Injury↗
Markedly increased omega-oxidation of valproate in fulminant hepatic failure.
Using gas chromatography-mass spectrometry, we showed that the urinary metabolite profile of valproate (VPA) in a subject receiving VPA and phenobarbital (PB) who died of fulminant hepatic failure was quite different from those of reported patients with Reye's syndrome or fatal hepatic failure. Only 2-n-propylglutarate, the end product of omega-oxidation of VPA, was excreted in markedly increased amounts, while other VPA metabolites were undetectable. Although the primary cause of fulminant hepatitis and the mechanism of enhanced VPA metabolism by the hepatic P-450 system in this patient are not clear, our findings suggest that P-450-mediated reactions become the predominant metabolic pathway of VPA in a stage of fulminant hepatic failure.
Chemical and Drug Induced Liver Injury↗
Asthma as the first presenting symptom of complex glycerol kinase deficiency.
Two patients presenting with asthma as the first clinical symptom of a mild form of Addison crisis were found to have complex glycerol kinase deficiency (CGKD). They had been treated with bronchodilators prior to the exact diagnosis. Asthma may appear in a mild form of Addison crisis in a patient with CGKD. Pediatricians should be aware of this unusual presentation of CGKD.
Addison Disease↗