Hereditary characteristics of enzyme deficiency and dermatoglyphics in congenital color blindness

The hereditary characteristics of enzyme deficiency and dermatoglyphics in congenital color blindness (CCB) were studied. We propose that there is a linkage between the two loci on the X-chromosome determining CCB and glucose-6-phosphate dehydrogenase (G6PD), based on our study of a high incidence of G6PD deficiency in 156 male cases with CCB. The CCB gene is closely linked with that of G6PD deficiency from our pedigree investigations. The rise in the frequency of eight or more whorls, the low value of atd angle and the presenting rate of real palmar patterns of the thenar, hypothenar and I, areas presented the hereditary traits of congenital color blindness.     

Biological activity of fluorinated 3,4-dihydroisoquinolines

Translated from Khimiko-farmatsevticheskii Zhurnal, Vol. 26, No. 1, pp. 44–45, January, 1992.     

N-unsubstituted glucosamine residues and other modifications in murein of the obligatory chemolithotroph Thiobacillus neapolitanus.

Purified murein from Thiobacillus neapolitanus was poorly digested by lysozyme. It's sensitivity to the enzyme greatly increased after N-acetylation. The murein was found to contain 30 to 35% glucosamine residues lacking N-acetyl groups. It also contained phosphomuramic acid. Further modifications included amidation of diaminopimelic acid in the peptide side chains and a low alanine content. None of these modifications were found in the murein of another sulphur bacterium, Thiobacillus versutus.     

Differential modulation by dopamine of responses evoked by excitatory amino acids in human cortex.

The responses of human neocortical neurons to iontophoretic application of excitatory amino acids and their modulation by dopamine (DA) were studied in vitro. Brain slices were obtained from children undergoing surgery for intractable epilepsy. Application of N-methyl-D-aspartate (NMDA) to the slices induced slow depolarizations accompanied by decreased input conductances and sustained action potentials in cortical neurons. Glutamate produced rapid depolarizations and firing with few changes in input conductances. Quisqualate also induced depolarization and firing, but input conductances increased during the rising phase of the membrane depolarization. Iontophoretic application of DA alone produced no change in membrane potential or input conductance. However, when DA was applied in conjunction with the excitatory amino acids, it produced contrasting effects. With either bath application of DA or when iontophoresis of DA preceded application of NMDA, the amplitude of the membrane depolarizations and the number of action potentials were increased, whereas the latency of these responses decreased. In contrast, DA decreased the amplitude of the depolarizations and the number of action potentials evoked by glutamate or quisqualate. The fact that DA affects responses to NMDA and glutamate or quisqualate in opposite directions is of considerable importance to the understanding of cellular mechanisms of neuromodulation and the role of DA in cognitive processing and in epilepsy.     

Arterial oxygen consumption after hemorrhagic shock: the effect of beta-adrenergic agonist.

Oxygen consumption of the rabbit femoral artery after hemorrhagic shock was studied. Hemorrhagic shock was initiated and maintained at 60 mm Hg of systolic blood pressure for 2 hours. A significant reduction in femoral artery oxygen consumption was observed after hemorrhagic shock (1.64 +/- 0.14 microliter/g/hr) when compared to oxygen consumption in the normal condition (2.52 +/- 0.22 microliter/g/hr). Application of the beta-agonist isoproterenol significantly increased oxygen consumption in the isolated femoral artery after hemorrhagic shock (2.66 +/- 0.20 microliter/g/hr), but did not exceed the normal values recorded without stimulation. Also, isoproterenol significantly increased oxygen consumption in the femoral artery of nonhemorrhagic condition (4.84 +/- 0.42 microliter/g/hr). The increase in oxygen consumption conditioned by isoproterenol was significantly lower after hemorrhagic shock compared with values in the nonhemorrhagic state. The data suggest that oxygen consumption is regulated by beta-adrenergic receptors, and the phenomenon of diminished oxygen consumption after hemorrhagic shock probably occurs because of changes in beta-adrenergic receptors, causing the appearance of change in the mechanism of oxygen consumption.     

Treatment of acute destructive pancreatitis

The authors analyse observations over 113 patients (1978-1988) with destructive pancreatitis; there were 54 males and 59 females, whose ages ranged from 18 to 85 years. Complex nonoperative treatment was effective only in 17 patients. Cholecystectomy, cholecystostomy or choledochotomy was performed in 7 patients after their condition had improved. Eighty-eight patients underwent operation in the acute period. Total lethality was 71.6%. In summarizing the results the authors came to the conclusion that operative interventions should be postponed in clinical practice. The optimal time for the operation is 6-9 days after the onset of the disease.