Low plasma zinc and androgen in insulin-dependent diabetes mellitus

Plasma zinc and pituitary and testicular hormone concentrations were measured in two groups of male adolescents. One group comprised insulin-dependent diabetes mellitus patients, aged 14-19 years; the other, as control, included 12 healthy youngsters aged 13-19 years. Plasma concentration of zinc, prolactin, testosterone, and dihydrotestosterone were lower in diabetics than in controls, whereas the ratios of androstenedione and androstenedione to testosterone + dihydrotestosterone were higher. Plasma FSH and LH were normal. These results suggest a diminished conversion of androstenedione to testosterone and relate zinc with the 17-beta-hydroxysteroid dehydrogenase enzyme activity.     

Ultrastructural myocardial preservation during coronary artery surgery: a controlled, prospective, randomized study in humans

Potassium cardioplegia was compared with normothermic, intermittent ischemic arrest in 30 patients undergoing multiple coronary artery bypass grafts. Group 1 comprised 15 patients in whom cold potassium cardioplegia with St. Thomas' Hospital solution was used. In Group 2 were 15 patients who underwent intermittent ischemic arrest during the construction of the distal anastomoses. Two myocardial transmural left ventricular biopsies were done in each patient. There was no operative mortality. Electron microscopical examination showed normal myocardial ultrastructure in both groups. In particular, mitochondria were well preserved in all samples. The postoperative electrocardiogram demonstrated a new Q wave in 1 patient in Group 2 whose level of the myocardial isoenzyme of creatine phosphokinase (CPK-MB) was within the normal range. The peak CPK-MB release in Group 1 was 23.2 +/- 20.1 IU and in Group 2, 19.9 +/- 15.1 IU. This difference was not statistically significant. The mean period of anoxic arrest in Group 1 was 49.5 +/- 15 minutes and in Group 2, 25.5 +/- 8 minutes (p less than 0.001). Total cardiopulmonary bypass time in Group 1 was 114.5 +/- 20 minutes and in Group 2, 90.2 +/- 16 minutes (p less than 0.01). It is concluded that both techniques can preserve myocardial subcellular architecture during multiple coronary artery bypass grafting in patients with normal left ventricular function.     

Long-term follow-up of patients with persistent/recurrent,isolated haematuria: A Hungarian multicentre study

A retrospective multicentre study of 341 children with persistent/recurrent, isolated haematuria is described. The haematuria was isolated for at least 6 months at the beginning of observation. The duration of follow-up was 2–5 years in 201, 5–10 years in 119, 10–15 years in 19, and over 15 years in 2 cases. Of these patients 47.8% became symptom-free. In 18.4% the haematuria remained isolated; in 13.8% it was combined with proteinuria over 250 mg/day more than 2 years later. The occurrence of associated proteinuria increased progressively with time. It was 8.6% between the 3rd and 5th years, and 37.0% after the 5th year. Renal biopsy was performed because of the symptoms of glomerular disease in 47 cases at an average time of 12 months following the appearance of proteinuria. Proteinuria appeared after a 2–5, 5–10, 10–15 and more than 15 years follow-up period in 16, 23, 6, and 2 patients respectively; 14 of them had Alport's nephropathy. The percentage of more serious azotaemia was 1.7 (creatinine clearance: 10–50 ml/min per 1.73 m²) and 0.3 (creatinine clearance: < 10 ml/min per 1.73 m²). Mortality was 0.58%. Most of the patients who developed severe azotaemia had persistent microscopic haematuria at the beginning. The prevalence of hypertension was only 1.2%. The time of its appearance was above 5 years in 2 and below 5 years in 2 cases. All these patients had chronic glomerulonephritis. The haematuria was associated with hypercalciuria in 19.9%. In 14.3% of the overall group of patients urolithiasis developed 2–15 years after onset. All of these had hypercalciuria. Our findings suggest that symptoms of isolated haematuria may last for a longterm period and need systematic control. When proteinuria and/or hypertension is associated with haematuria a worse prognosis can be expected.Participating paediatric hospitals and university departments: Second Department of Paediatrics, I. Semmelweis Medical University of Budapest (M. Visy); Department of Paediatrics, University Medical School of Pécs (V. Jászai); Department of Paediatrics, A. Szent-Györgyi Medical University of Szeged (I. Haszon, S. Túri); County Children's Hospital, Miskolc (Á. Vissy); P. Heim Children's Hospital, Budapest (Z. Czirbesz); County Children's Hospital, Györ (Zs. Szelid); Buda-Children's Hospital, Budapest (I. Ferkis); I. Apáthy Hospital, Budapest (J. Kisbán); János Hospital, Budapest (I. Marosváry); Hospital of Hungarian State Railway, Budapest (J. Fehér); L. Madarász Hospital, Budapest (F. Kalmár); South Pest Hospital, Budapest (G. Halász); County Children's Hospital, Pécs (E. Kolman); County Children's Hospital, Gyula (P. Sipos); County Children's Hospital, Szolnok (I. Jaksics); County Children's Hospital, Debrecen (Á. Miskolczi); County Children's Hospital, Tatabánya (I. Kiss); County Children's Hospital, Eger (M. Frank, E. Ladányi); County Children's Hospital, Nyíregyháza (E. Bujdosó); County Children's Hospital, Szombathely (M. Andics); Kerepestarcsa Hospital, Budapest (M. Marcell); Komárom Hospital, Komárom (J. Kecskés)     

Acute toxicity of ammonia to Artemia sp.]

The acute toxicity of total ammonia-N, (NH3 + NH4+), and un-ionized ammonia-N, NH3-N, on newly hatched Artemia nauplii and Artemia adults was measured in 24, 48, 72, and 96-h semi-static bioassays system. There was a significant difference (P < 0.05) in medial lethal concentrations (LC50) obtained during the tests. The LC50 values on nauplii ranged from 650 mg/l, in 24-h, to 399.1 mg/l total ammonia-N, in 96-h, while the LC50 values on adults ranged from 1290.4 mg/l to 600.5 mg/l total ammonia-N, in the same period. Two methods for calculations of un-ionized ammonia toxicity are analyzed and discussed.     

Relationship between digestive and killing abilities of neutrophils against Paracoccidioides brasiliensis.

Peripheral blood neutrophils (PMN) from patients with paracoccidioidomycosis killed and digested Paracoccidioides brasiliensis much less than did PMN from normal individuals or from patients with other diseases. However, deficiency in killing ability was less specific than digestive deficiency and correlated poorly with it. We conclude that the capacities of PMN to digest and kill P. brasiliensis are not intimately related phenomena, and that in paracoccidioidomycosis the key deficiency of neutrophil function is that of digestion of P. brasiliensis.     

Truncation mutants define and locate cytoplasmic barriers to lateral mobility of membrane glycoproteins.

The lateral mobility of cell membrane glycoproteins is often restricted by dynamic barriers. These barriers have been detected by measurements of fluorescence photobleaching and recovery (FPR) and barrier-free path (BFP). To define the location and properties of the barriers, we compared the lateral mobility, measured by FPR and BFP, of wild-type class I major histocompatibility complex (MHC) membrane glycoproteins with the lateral mobility of mutant class I MHC glycoproteins truncated in their cytoplasmic domains. Mutants with 0 or 4 residues in the cytoplasmic domain were as mobile as lipid-anchored class I MHC molecules, molecules whose lateral mobility is relatively unrestricted by barriers. In contrast, mobility of class I MHC molecules with 7-residue cytoplasmic domains was as restricted as mobility of class I molecules with full-length, 31-residue cytoplasmic domains. Though some of the difference between the mobilities of mutants with 4- or 0-residue domains and the other class I molecules may be due to differences in the net charge of the cytoplasmic domain, FPR measurements of the mobility of molecules with 7-residue domains show that length of the cytoplasmic domain has an important influence on the lateral mobility. Model calculations suggest that the barriers to lateral mobility are 2-3 nm below the membrane bilayer.