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Biomedical subjects

H Berger

Publications and source records attributed to H Berger.

At least 325 records · Page 18Linked to original sources

PH-dependent changes of 2,3-bisphosphoglycerate in human red cells during transitional and steady states in vitro.

A systematic study of the pH-dependent changes in the range 6.6--7.4 of 2,3-bisphosphoglycerate and the adenine nucleotides was performed in the presence and absence of glucose during transitional and steady states. 1. The results indicatethat 2,3-gisphosphoglycerate phosphatase breaks down 2,3-bisphosphoglycerate nearly independent of pH at a rate of 480 mumol 2,3-bisphosphoglycerate x1 cells-1xh-1.2,3-Bisphosphoglycerate mutase is practically completely inhibited below pH value increases in long-term experiments with lower 2,3-bisphosphoglycerate levels. The formation of pyruvate corresponds to the breakdown of 2,3-bisphosphoglycerate afterconsumption of an unknown reducing substance.

Adenosine Diphosphate↗

Chromosome structure of Escherichia coli mutants temperature sensitive for deoxyribonucleic acid replication.

Folded chromosomes were isolated from Eschericia coli thermosensitive dnaA initiation mutants incubated at the nonpermissive temperature and were analyzed by neutral sucrose density gradient centrifugation. A chromosomal structure that sedimented at approximately 1,500S accumulated when the dnaA gene product was inactive. When the cells were returned to a permissive temperature, the folded chromosomes exhibited a decrease in sedimentation velocity to 1,300S but still retained their uniform structure. Very little deoxyribonucleic acid synthesis occurred during the period in which the chromosomes exhibited the reduction in sedimentation velocity. A dnaG elongation mutant showed no unique chromosome structure when the dnaG gene product was inactive.

Centrifugation, Density Gradient↗

pH-dependent changes of 2,3-bisphosphoglycerate.

A systematic study of the pH dependent changes in the range 6.6--7.4 of 2,3 bisphosphoglycerate (2,3-DPG) was performed in the presence and absence of glucose during transitional and steady states. The results indicate that 2,3-DPGase breaks down 2,3-DPG nealy independent of pH at a rate of 480 mu moles 2,3-DPG/1 cells.h. The 2,3-DPG mutase is practically completely inhibited below pH 6.9. The 2,3-DPG level in the presence of glucose reaches a pH dependent steady state after about 18 h. The share of the 2,3-DPG bypass in the steady state decreases from 24% at pH 7.4 to 12% at pH 7.0. The formation of pyruvate corresponds to the beadkdown of 2,3-DPG after consumption of an unknown reducing substance.

Adenosine Triphosphate↗

[Complete parenteral nutrition in childhood].

Complete parenteral nutrition by means of continuous intravenous drip into large veins, over a long period, has already shown itself to be of therapeutic use in the field of pediatrics. While the nutritional-physiological aspect of this therapeutic method is clear -- it depends on an accurate and sufficient supply of water, salts, glucose, amino-acids, triglycerides and essential fatty acids, vitamins and trace elements -- in practice it presents difficulties which though often serious are not insurmountable. Especially are to cite the septic complications, which are nearly imperceptible during their development. They are only to accept in view of the often almost hopeless condition of the child, who would be lost without complete parenteral feeding. Similar problems arise through metabolic complications which are caused non rarely only by insufficient dosages and lack of careful supervision but it is generally possible to correct these at an early stage. Complete parenteral nutrition must be exactly indicated. It is indeed a great therapeutic help, particularly when over a longer period -- at least a week or longer -- oral nutrition is impossible or insufficient. Practicall experiences will be reported. A retrospective assessment of 50 cases has shown the tendency (through taking too much care?) to hold the quantity of liquids and supply of calories too short and to administer too much carbohydrates and too little fat.

Adolescent↗

[Experiments on the biosynthesis of UDP-Glucuronyltransferase and UDP-Glucosyltransferase under the influence of eucalyptol (author's transl)].

To elucidate the reaction mechanism of the increased elimination rate of bilirubin in the blood of newborns under the influence of Eucalyptol, we performed a study on young mice. The following results were obtained: UDPGA-T activity is increased 33%, if measured with 4-MU as substrate after a single injection (i.p.) of Eucalyptol (0.3 mg/g body weight), with bilirubin as substrate the increase is 112%. UDPG-T activity increases 29%. The enhancement of enzyme activities can be inhibited by Actinomycin D (1 MUg/g body weight) 30% (bilirubin), 48% (4-MU) respectively in the case of UDPGA-T. Under cycloheximide (2 mug/g body weight) the increase of the activity of UDPGA-T is suppressed by 59% (bilirubin) or 99% (4-MU) as compared to the corresponding controls. No significant difference in the activity of UDPG-T by actinomycin or cycloheximide can be observed between the controls and the Eucalyptol-treated group. We conclude that the increase of enzyme activity of UDPGA-T is mainly due to enzyme induction, while in the case of UDPG-T activation of enzyme molecules might be the underlying mechanism. The effect of Eucalyptol on the bilirubin level in the blood of newborns is comparable to the effect of phenobarbital.

Animals↗

[Mycoplasma pneumonias in childhood (author's transl)].

During the winter months 1974/75 we were able to observe a number of unusual respiratory tract infections particularly in children over 6 years of age which appeared as pneumonias. Characteristic clinical findings included a dry, hacky cough, refractive to the usual antitussives, starting 1--2 weeks prior to admission, fever up to 104, malaise, headache, anorexia, shortness of breath and cyanosis. Several Pts were treated prior to admission with a number of antibiotics and failed to respond. Laboratory findings showed a peripheral polymorphonuclear leucocytosis with toxic granulations of neutrophiles. A sedimentation rate above 40 in the first hour occurred in most Pts. X Ray of the lung revealed a characteristic mottled appearance with patchy infiltrations, atelectasis and nodular densities. Frequently a shift of the mediastinum towards the infiltrate was seen. One of the hallmarks on physical examination was the discrepancy between the severity of the clinical illness and the paucity of physical findings. Decreased breath sounds over affected lung areas were often the only findings on auscultation; find rales, rhonchi or dullness on percussion were less often heard. The combination of a typical history, physical examination, laboratory tests and X Ray findings enabled us to make a presumptive clinical diagnosis of Mycoplasma pneumonia before serologic test results were available and to start with the appropriate antibiotic (Erythromycin, Tetracycline) early in the course of the disease. Complement fixation tests with a titer of 1 : 20 and a fourfold rise over the next two weeks or an initial titer of 1 : 80 and above were considered significant for acute disease.

Adolescent↗

Response of the glycolysis of human erythrocytes to the transition from the oxygenated to the deoxygenated state at constant intracellular pH.

The time course of the rate of the glycolysis of human erythrocytes and of some metabolites were determined before and after rapid deoxygenation at constant intracellular pH. For this purpose stripped deoxygenated haemoglobin was used as a rapid oxygen acceptor. Deoxygenation causes an increase of the glycolytic rate by 26%. Glucose 6-phosphate is decreased while the adenine nucleotides and 2,3-bisphosphoglycerate remain constant. Fructose 1,6-bisphosphate and the triose phosphates decrease transiently before rising. The data can be explained by increased binding of phosphocompounds to deoxygenated as compared with oxygenated haemoglobin. Thereby the control enzymes hexokinase and phosphofructokinase are influenced. It is concluded that under physiological conditions changes in the oxygenation state of haemoglobin per se alter the glycolytic rate.

Erythrocytes↗

Action of phospholipases on the cytoplasmic membrane of Escherichia coli. Stimulation by melittin.

The emission maximum of the single tryptophan residue of melittin was measured in the presence of phosphatidylethanolamine liposomes and Escherichia coli cytoplasmic membranes. In both cases, the fluorescence maximum was shifted to shorter wavelengths indicating a transfer of the indole ring to an apolar environment. E. coli membranes were labelled in position 2 of their phospholids with [14C]oleic acid. These membranes were used for measuring the activity of an endogenous phospholipase A2. A slow hydrolysis is observed, which can be accelerated by adding melittin. The extent of the stimulation depends on the molar ratio of melittin to membrane phospholipid. Under suitable conditions, the initial rate of hydrolysis is six to seven times higher in the presence than in the absence of melittin. The action of the phospholipase A2 from bee venom is also stimulated by melittin. An identical stimulation was observed with either E. coli membranes or pure phosphatidylethanolamine liposomes as substrate.

Cell Membrane↗

Vitamin B6 nutriture of children with acute celiac disease, celiac disease in remission, and of children with normal duodenal mucosa.

Patients with adult celiac disease excrete abnormal amounts of tryptophan metabolites after loading with this amino acid, suggesting vitamin B6 deficienty in these patients, In fact, the excretion of tryptophan metabolites returns to normal after administration of vitamin B6. The vitamin B6 nutriture was measured by means of determination of pyridoxal phosphate and activity of pyridoxalkinase in serum and in duodenal mucosa of 14 children with acute celiac disease and of six children with celiac disease in clinical and biochemical remission. Ten children with normal duodenal mucosa were studied as controls. Children with celiac disease had significantly decreased pyridoxal phosphate in serum and in duodenal mucosa when compared both with children in remission and controls. Activity of pyridoxalkinase, however, was significantly increased in serum and in duodenal mucosa when compared with controls but not when compared with children in remission. These children had the same increase in pyridoxalkinase activity as children with acute celiac disease. These data provide a strong evidence for the occurrence of vitamin B6 deficienty in children with acute celiac disease. The children with celiac disease in remission still had an increased activity of pyridoxalkinase which seems to be a compensating mechanism in consequence of vitamin B6 deficiency prior to the gluten-free diet.

Celiac Disease↗