Chlorambucil in histiocytosis X: a Southwest Oncology Group study.
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Biomedical subjects
Publications and source records attributed to R Iyer.
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Patients with acute pancreatitis were studied by arginine infusion at 48--72 h. 7--10 days, and 18--21 days after onset of their illness. Plasma glucose, insulin, and glucagon values were determined. Acute pancreatitis was characterized by fasting hyperglycemia and hyperglucagonemia, associated with relative hyoinsulinemia. Arginine stimulation early in the disease (48--72 h) demonstrated hyperglycemia and hyperglucagonemia, which normalized by 18--21 days. Both phases of the normal biphasic insulin response to arginine were decreased during the initial arginine infusion. By 18--21 days, although the first phase was completely normal, the second phase of insulin secretion remained depressed. Acute pancreatitis is associated with damage to both the endocrine and exocrine pancreas. Glucose intolerance seen with this disease appears to be the result of hyperglucagonemia and relative hypoinsulinemia. Although the healing process at 3 wk is associated with return of plasma glucose and glucagon concentrations to normal, the impaired second phase insulin secretion persists.
Plasmids of the N incompatibility group have been found to decrease or virtually eliminate the synthesis of the 36,500 dalton outer membrane matrix protein of their Escherichia coli B/r hosts (Iyer, R. (1977) Biochim. Biophys. Acta 470, 258--272 and Iyer, R., Darby, V. and Holland, I.B. (1978) FEBS Lett. 85, 127--132) or modify its composition. Although the 34,000 dalton tol G protein is slightly increased in some strains, it is identical in composition to the homologous protein from the plasmidless host. In three of five N+ strains the synthesis of the modified matrix proteins depends on the temperature of cultivation of the strains in which they occur. The alterations to the matrix proteins are non-identical and do not affect the expression of several plasmid-coded functions including those of sensitivity to the N plasmid-specific filamentous bacteriophage IKe (Khatoon, H. and Iyer, R. (1971) Can. J. Microbiol. 17, 669--675), or their interbacterial transfer via conjugation to appropriate recipient strains. Thus, although the significance of the variant matrix proteins in N+ strains with respect to plasmid-mediated functions remains unclear, N plasmids nevertheless provide a convenient system which might be used to elucidate the events that precede the insertion of this protein into the outer membrane of E. coli B/r hosts.
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ITP in childhood is most often of the acute, self-limited variety, with spontaneous recovery occurring within a matter of days or weeks. In many of these children, acute thrombopenic purpura follows in the wake of a viral infection. While the pathogenesis is not entirely clear, it seem probable that the platelet membrane is altered by virus or by soluble viral antigen-antibody complexes; platelets thus damaged become susceptible to rapid destruction by the RES. Management remains somewhat controversial. While almost all agree that corticosteroid should not be used in all cases of acute childhood purpura, there are still no clear-cut indications for their use, and no real evidence that they are of benefit in reducing the risk of the one rare but serious complication of childhood ITP, namely, intracranial hemorrhage (ICH). In approximately 5-10% of children, ITP ultimately proves to be of the chronic variety, and is in all probability the same condition that is seen in adults. Splenectomy is the treatment of choice, Another small subgroup of children have ITP of the recurrent acute variety; there is some evidence that this entity may also have an autoimmune pathogenesis. Infants born to mothers who have (or have had) ITP often manifest thrombopenia, with or without purpura and other bleeding. While this is generally a benign, self-limited process, requiring no treatment, ICH occurs in a small but significant number of affected infants and probably results from head trauma during delivery.
At least 3 minor proteins have been detected by sodium dodecyl sulfate polyacrylamide gel electrophoresis in the unseparated (31 000 daltons) and inner membranes (53 000 and 86 000 daltons) of a non-piliated strain of E. coli K12 bearing the phage IKe-specific resistance plasmid RM98 (Tra+); these proteins are lacking in its Tra- derivative and in the plasmidless host. In contrast, in another K12 host carrying each of different IKe-specific colicinogenic factors, an extra 30 000 dalton protein is observed in the outer membranes; a number of minor proteins seen in the inner membranes appear to be different from those observed in the RM98+ strain. The evidence suggests that the 30 000-31 000 dalton protein is transfer function specific.
Of 148 children with acute lymphoblastic leukemia (ALL) 34 had bilateral interstitial pneumonia (BIP). Their records were reviewed retrospectively to evaluate the incidence of this pneumonia and delineate the various etiologic factors involved. All but 1 were in remission; 82% of the episodes occurred within the first 6 months, the majority of these occurring during the first 3 months of diagnosis of ALL; 16 were receiving methotrexate (MTX), and 14 were receiving combination chemotherapy with vincristine, prednisone and 6-mercaptopurine (6-Mp) and 4 were on no systemic therapy. Thirty patients with 35 episodes recovered within an average period of 18 days, including clearance of radiologic findings; 4 died. Four had open lung biopsies without complications. There was a single case of pneumocystis carinii infection diagnosed postmortem. Laboratory data and histopathologic findings (of 4 biopsies and 3 remaining autopsies) were suggestive of a viral etiology. The incidence of BIP in ALL at Children's Hospital of Michigan is 22.9% with a mortality rate of 10.3%. The incidence of pneumocystis carinii infection appeared to be low. Hypersensitivity to MTX was not substantiated.
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The relationship between cigarette yields (of nicotine, tar, and carbon monoxide), puffing patterns, and smoke intake was studied by determining puffing patterns and measuring blood concentrations of nicotine and carboxy-haemoglobin (COHb) in a sample of 55 smokers smoking their usual brand of cigarette. Regression analyses showed that the total volume of smoke puffed from a cigarette was a more important determinant of peak blood nicotine concentration than the nicotine or tar yield of the cigarette, its length, or the reported number of cigarettes smoked on the test day. There was evidence of compensation for a lower tar yield over and above any compensation for nicotine. When nicotine yield was controlled for, smokers of lower-tar cigarettes not only puffed more smoke from their cigarettes than smokers of higher-tar cigarettes but they also had higher plasma nicotine concentrations, suggesting that they were compensating for the reduced delivery of tar by puffing and inhaling a greater volume of smoke. The results based on the COHb concentrations were consistent with this interpretation. If an adequate intake of tar proves to be one of the main motives for smoking, then developing a cigarette that is acceptable to smokers and also less harmful to their health will be much more difficult.
A double blind randomized placebo controlled clinical trial was carried out to assess the efficacy and safety of L-carnitine in patients suffering from acute anterior wall myocardial infarction with respect to left ventricular function. Sixty patients (34 men, 26 women, mean age 56+11 yr.) with acute anterior wall myocardial infarction were randomized to placebo and L-carnitine. All the patients were given intravenous L-carnitine / placebo in the dose of 6gm/day for the first seven days followed by oral L-carnitine / placebo 3 gm/day in three divided doses for a period of three months. Echocardiography was performed for regional wall motion abnormality, left ventricular end systolic volume (ESV), end diastolic volume (EDV) and ejection fraction (EF) on admission, after seven days and after three months of the infarction. Forty-four patients completed the study. There were three deaths, two in the placebo and one in the L-carnitine group (p>0.05). Thirteen patients were lost to follow up. Echo parameters in both groups were comparable (p>0.05). The duration of chest pain prior to initiation of the I.V. L-carnitine was 7.5 + 5.2 hrs in the L-carnitine group and 7 + 4 hrs in the placebo group (p>0.05). There was no statistical difference in the EF, ESV and EDV on admission, at discharge and after three months in the L-carnitine and the placebo groups (p>0.05). No significant adverse effects were noted. L-carnitine, though a safe drug, does not affect the left ventricular function in patients with myocardial infarction.
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