Over-head extension--one of the methods of early treatment of CDH.
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Exercise Therapy↗
Biomedical subjects
J Ostrowski
Publications and source records attributed to J Ostrowski.
[Comparison of the value of serum caffeine and bile acid concentrations as indicators of liver injury].
In 56 patients with various liver diseases and in 15 healthy controls fasting serum concentrations of caffeine (HPLC method) and total endogenous bile acids (enzymatic-spectrophotometric assay) were determined. Serum caffeine concentrations were significantly higher in patients with chronic hepatitis or liver cirrhosis than in controls but no differences was found between patients with obstructive jaundice and controls. Contrary to caffeine, fasting serum bile acids concentrations were higher in all patients groups than in controls. In all studied groups there was no correlation between caffeine and serum bile acids estimations. In patients with liver cirrhosis there was correlation between caffeine test and the Child's classification score. However, no correlation existed between the Child's classification and the serum bile acids concentration. Our data suggest that fasting serum caffeine concentration is more usefull indicator of liver injury than determination of total endogenous serum bile acids.
Adult↗
Characterization of the flavoprotein moieties of NADPH-sulfite reductase from Salmonella typhimurium and Escherichia coli. Physicochemical and catalytic properties, amino acid sequence deduced from DNA sequence of cysJ, and comparison with NADPH-cytochrome P-450 reductase.
NADPH-sulfite reductase flavoprotein (SiR-FP) was purified from a Salmonella typhimurium cysG strain that does not synthesize the hemoprotein component of the sulfite reductase holoenzyme. cysJ, which codes for SiR-FP, was cloned from S. typhimurium LT7 and Escherichia coli B, and both genes were sequenced. Physicochemical analyses and deduced amino acid sequences indicate that SiR-FP is an octamer of identical 66-kDa peptides and contains 4 FAD and 4 FMN per octamer. Potentiometric titrations of SiR holoenzyme, SiR-FP, and FMN-depleted SiR-FP yielded the following redox potentials for the prosthetic groups at pH 7.7: E'1 (FMNH./FMN) = -152 mV; E'2 (FMNH2/FMNH.) = -327 mV; E'3 (FADH./FAD) = -382 mV; E'4 (FADH2/FADH.) = -322 mV. Microcoulometric titration of SiR-FP at 25 degrees C yielded data which were in full agreement with these potentials. Spectroscopic and catalytic studies of native SiR-FP and of SiR-FP depleted of FMN support the following electron flow sequence: NADPH----FAD----FMN. FMN can then contribute electrons to the hemoprotein component of sulfite reductase, as well as to cytochrome c and various diaphorase acceptors. The FMN is postulated to cycle between the FMNH2 and FMNH. oxidation states during catalysis; in this sense SiR-FP shares a catalytic mechanism with NADPH-cytochrome P-450 oxidoreductase. SiR-FP domains involved in binding FMN, FAD, and NADPH are proposed from amino acid sequence homologies with Desulfovibrio vulgaris flavodoxin (Dubourdieu, M., and Fox, J.L. (1977) J. Biol. Chem. 252, 1453-1463) and spinach ferredoxin-NADP+ oxidoreductase (Karplus, P.A., Walsh, K.A., and Herriott, J. R. (1984) Biochemistry 23, 6576-6583). Comparison of the deduced amino acid sequences of SiR-FP and NADPH-cytochrome P-450 oxidoreductase (Porter, T. D., and Kasper, C.B. (1985) Proc. Natl. Acad. Sci. U. S.A. 82, 973-977) also showed identities that suggest these two proteins are descended from a common precursor, which contained binding regions for both FMN and FAD.
Amino Acid Sequence↗
Characterization of the cysJIH regions of Salmonella typhimurium and Escherichia coli B. DNA sequences of cysI and cysH and a model for the siroheme-Fe4S4 active center of sulfite reductase hemoprotein based on amino acid homology with spinach nitrite reductase.
The hemoprotein component of Salmonella typhimurium sulfite reductase (NADPH) (EC 1.8.1.2) was purified to homogeneity from cysJ266, a mutant strain lacking sulfite reductase flavoprotein. The siroheme- and Fe4S4-containing enzyme was isolated as a monomeric 63-kDa polypeptide and consisted of a mixture of unligated enzyme and a complex with sulfite. Following reduction with 5'-deazaflavin-EDTA and reoxidation, the complex was converted to the uncomplexed, high spin ferri-siroheme state seen previously with Escherichia coli sulfite reductase hemoprotein preparations. The S. typhimurium hemoprotein exhibited catalytic and physical properties identical to the hemoprotein prepared by urea dissociation of E. coli sulfite reductase holoenzyme and was fully competent in reconstituting NADPH-sulfite reductase activity when combined with excess purified sulfite reductase flavoprotein. The DNA sequences of cysI and cysH from S. typhimurium and E. coli B were determined and, together with previously reported data, confirmed the organization of this region as promoter-cysJ-cysI-cysH with all three genes oriented in the same direction from the promoter. Molecular weights deduced for the cysI-encoded sulfite reductase hemoprotein and for the cysH-encoded 3'-phosphoadenosine 5'-phosphosulfate sulfotransferase were approximately 64,000 and 28,000, respectively. Comparison of the deduced amino acid sequence of sulfite reductase hemoprotein with that of spinach nitrite reductase (Back, E., Burkhart, W., Moyer, M., Privalle, L., and Rothstein, S. (1988) Mol. Gen. Genet. 212, 20-26), which also contains siroheme and an Fe4S4 cluster, showed two groups of cysteine-containing sequences with the structures Cys-(X)3-Cys and Cys-(X)5-Cys, which are homologous in the two enzymes and are postulated to provide the ligands of the Fe4S4 cluster in both proteins. From these sequences and from crystallographic (McRee, D. E., Richardson, D. C., Richardson, J. S., and Siegel, L. M. (1986) J. Biol. Chem. 261, 10277-10281) and spectroscopic data in the literature, a model is proposed for the structure of the active center of these two enzymes.
Amino Acid Sequence↗
Molecular characterization of the cysJIH promoters of Salmonella typhimurium and Escherichia coli: regulation by cysB protein and N-acetyl-L-serine.
The cysJIH promoter regions from Salmonella typhimurium LT7 and Escherichia coli B were cloned and sequenced. Primer extension analyses showed that the major in vivo transcription initiation site in S. typhimurium is located 171 nucleotides upstream of the cysJ start codon. Minor start sites were found 8 and 9 nucleotides downstream of the major site. In vivo transcription initiation in E. coli was found to occur at a single site 66 nucleotides upstream of the cysJ start codon. Primer extension studies also indicated that chromosomal cysJIH transcription is stimulated by sulfur limitation and repressed by growth on L-cystine. Paradoxically, in strains carrying plasmids containing the S. typhimurium cysJIH region, the highest levels of primer extension products were found with RNA from cells grown on L-cystine, even though levels of the proteins encoded by cysJ and cysI were normally repressed. In vitro transcription runoff studies with DNA template from the S. typhimurium cysJIH promoter region showed synthesis of a product originating at the major in vivo start site, which was dependent on the presence of purified cysB protein and either O-acetyl-L-serine or N-acetyl-L-serine. N-Acetyl-L-serine was 10- to 30-fold more active than O-acetyl-L-serine as an in vitro inducer of cysJIH transcription.
Acetylcysteine↗
Interaction of signal transduction pathways in mediating acid secretion by rat parietal cells.
To examine the role of protein kinase C (PKC) on the acid secretory activity of isolated rat parietal cells, histamine-and dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP)-stimulated [14C]aminopyrine accumulation was determined in the presence of agents that redistribute PKC activity to plasma membranes. Phorbol 12-myristate 13-acetate (PMA), 1-oleoyl-2-acetylglycerol (OAG), and phospholipase C inhibited, in a dose-dependent fashion, histamine- and DBcAMP-stimulated [14C]aminopyrine accumulation. Because PKC inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) reversed the effect, the results suggest that inhibition of histamine- or DBcAMP-stimulated [14C]aminopyrine accumulation induced by PMA, OAG, or phospholipase C was caused by increased activity of PKC in plasma membrane. To determine where in the cascade of events PKC inhibits acid secretion, histamine-, cholera toxin-, and forskolin-stimulated [14C]aminopyrine accumulation was measured with or without PMA. Because the percent of inhibition by PMA of [14C]aminopyrine accumulation was similar with the three secretagogues, the results suggest that PKC inhibits acid secretion at a point beyond adenosine 3',5'-cyclic monophosphate (cAMP) production. This was supported by the fact that PMA had no effect on histamine-stimulated production of cAMP and by the finding that activation of PKC had the same effect on histamine- or DBcAMP-stimulated [14C]aminopyrine accumulation. Histamine and DBcAMP inhibited PKC activity, suggesting a reciprocal interaction between PKC and histamine-triggered signal transduction pathway.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
Local anesthetics (benzyl alcohol, lidocaine, procainamide) inhibit aminopyrine accumulation in isolated rat parietal cells.
The present studies were designed to examine the effect of local anesthetics (benzyl alcohol, lidocaine, and procainamide) on the secretory response of parietal cells to histamine, dbcAMP, and carbachol. Studies were performed in vitro using isolated cells from rat stomachs, and acid production was determined by 14C-aminopyrine accumulation. In addition, the (H(+)-K+)-ATPase activity of microsomal vesicles isolated from parietal cells was determined. Lower concentrations of the drugs studied increased the basal aminopyrine accumulation and potentiated the secretory response of parietal cells to histamine and dbcAMP. At higher concentrations local anesthetics progressively inhibited both the basal 14C-aminopyrine accumulation and that stimulated by histamine, dbcAMP or carbachol. While a low concentration of local anesthetics increased gastric microsomal (H(+)-K+)-ATPase activity, higher concentrations inhibited enzyme activity to about 80% of those activities found in resting parietal cells. We conclude that increased aminopyrine accumulation may reflect the activation of membrane-bound enzyme(s) involved in the cAMP-dependent signal transduction pathway mediating acid secretion by parietal cells. In turn, it is possible that the inhibition of aminopyrine accumulation by local anesthetics at higher concentrations can relate to two different mechanisms: (1) the nonspecific effect of local anesthetics that causes simple proton neutralization (as weak bases), and (2) to a minor extent their inhibitory effect on proton pump activity.
Adenosine Triphosphatases↗
On the mechanism of NO release from sydnonimines.
The vasodilator and antiaggregatory properties of sydnonimines like SIN-1 are thought to be due to their marked stimulatory action on soluble guanylate cyclase. Enzyme activation and consecutive cyclic GMP accumulation is mediated by the liberation of nitric oxide (NO) from the open-ring A forms of sydnonimines. The purpose of the present study was to investigate the mechanism of NO release from sydnonimines in direct comparison to their stimulatory effect at the target enzyme, soluble guanylate cyclase. All sydnonimines tested were found to spontaneously liberate NO, the rate of which closely correlated with the extent of enzyme activation. NO release occurred nonlinearly with time and became maximal at high sydnonimine concentration. The in vitro stability of the A forms neither correlated with the measured rate of NO release nor with enzyme activation, indicating that a direct stimulation of guanylate cyclase by the A forms is rather unlikely. Besides NO, all sydnonimines generated NO2- and NO3- at a nearly equimolar rate. The addition of cysteine induced a marked shift from NO3- to NO2- with a small reduction in NO release, which is paralleled by a weak rightward shift of the EC50 at the guanylate cyclase. All tested sydnonimines were found to consume molecular oxygen at rates that closely corresponded to the measured rates of NO formation. By a molar comparison, the amounts of consumed oxygen are clearly higher, as would be expected for the oxidative conversion of NO to NO2- and NO3-. Oxygen seems to be additionally involved in the induction of NO formation while being converted to superoxide (O2-). In accordance with an autocatalytic process, O2- further enhances sydnonimine decomposition, since in the presence of superoxide dismutase (SOD) the rate of SIN-1C and NO2-/NO3- formation from SIN-1A was reduced, whereas the rate of NO liberation seemingly increased. O2- has, however, no influence on the rate of hydrolysis of SIN-1 to SIN-1A. At the level of guanylate cyclase, the presence of SOD induced a leftward shift of the concentration-response curve to SIN-1, in agreement with an enhancement of efficacy of NO by blocking the NO-scavenging effect of O2-. An additional O2- generation markedly enhanced SIN-1A decomposition to NO2-/NO3- and reduced the apparent rate of NO formation. We conclude from our results that oxygen plays a key role in the decomposition of sydnonimines and thus in the formation of NO as their pharmacodynamically active principle. Oxygen attack most probably occurs by one-electron abstraction from the A form of the respective sydnonimine compound.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
[A rare case of congenital dentin dysplasia in a child aged 8 years].
In the reported case the authors observed a considerable mobility of all milk teeth and permanent teeth. The degree of this mobility varied. The crowns of milk and permanent teeth had a normal size, shape and colour. All teeth were unresponsive to thermal and electric stimulation. Radiological examination showed a nearly complete lack of roots and complete absence of pulp chambers and root canals. This was confirmed by histological examinations demonstrating that the inner part of the teeth in the crown and root was filled with hard masses which in light microscopy resembled newly forming compact bone with Haversian structures. The absence of resorption sinuses in the rudimentary roots was noted. Paediatric examination failed to demonstrate any abnormalities.
Child↗
[2 cases of nodular pneumonia].
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Anti-Bacterial Agents↗
Liver vitamin A concentration in patients who died of cancer.
The concentrations of vitamin A in liver samples obtained at autopsy of patients who died of cancer was investigated. It was found that liver vitamin A levels in cancer patients were significantly lower than in controls. Although our recent results have suggested that the decreased serum retinol level in cancer patients reflects rather a functional impairment of vitamin A release from the liver, the results of this study suggest that this phenomenon can also indicate a true vitamin A deficiency in patients with neoplastic process.
Adult↗
Interferon-gamma and interleukin-1 alpha induce transient translocation of protein kinase C activity to membranes in a B lymphoid cell line. Evidence for a protein kinase C-independent pathway in lymphokine-induced cytoplasmic alkalinization.
We have previously shown that recombinant murine interferon-gamma, rIFN-gamma, and recombinant human interleukin-1 alpha, rIL-1 alpha, induce differentiation of murine pre-B-like cell line 70Z/3, a finding associated with stimulation of Na+/H+ exchange across the plasma membrane. The present study was designed to test whether the enhanced Na+/H+ exchange is mediated by Ca2+/phospholipid-dependent protein kinase C. The results show that two structurally different peptides, rIFN-gamma and rIL-1 alpha, induce identical patterns of transient translocation of protein kinase C from the cytosol to the membranes. The increase in membrane-associated protein kinase C activity was first detected 20 min after exposure to the lymphokines. This activity peaked at 30 min and was back to baseline by 2 h. At each time point, the increase in membrane-associated protein kinase C activity corresponded to a decrease in the activity of protein kinase C in the cytoplasmic fraction. The total cellular activity (cytosol + membrane) remained the same. Two series of experiments were carried out to test the role of protein kinase C in mediating the lymphokine-stimulated Na+/H+ exchange. In the first, the effects of rIFN-gamma and rIL-1 alpha on cytoplasmic pH were measured in the presence of a protein kinase C inhibitor 1-(5-isoquinolinesulfonyl)-2-methylpiperazine, H-7. In the second, rIFN-gamma- and rIL-1 alpha-induced cytoplasmic alkalinization was determined in cells containing decreased protein kinase C activity. Under both experimental conditions, lymphokine-induced cytoplasmic alkalinization was not attenuated. These results indicate that, although both rIFN-gamma and rIL-1 alpha cause association of protein kinase C with membranes, activation of protein kinase C is not required for rIFN-gamma or rIL-1 alpha to stimulate Na+/H+ exchange across the plasma membrane.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
Protective effect of 13-cis-retinoic acid on hematoporphyrin derivative-induced cell photosensitivity in vitro.
The influence of 13-cis-retinoic acid on the light-caused injury of hematoporphyrin-pretreated nontransformed 10 T1/2 fibroblasts and N2a neuroblastoma cells was investigated. Retinoid reduced the percentage of damaged cells as assessed by the plating efficiency assay. N2a neuroblastoma cells were found to be better protected than 10 T1/2 cells by 13-cis-retinoic acid on hematoporphyrin light-induced injury.
Animals↗
[Mandible magnitude in Crouzon syndrome].
The authors describe Crouzon syndrome in 5 patients aged 9, 10, 13, 40 and 43 years. Typical image of Crouzon syndrome has been found in the woman and three children and its abortive form--in the man. The authors present their own studies on branch height, length of the body of the mandible and the angle value of the mandible according to the Costaras-Volarich and Pruzancky method in their paper. The ratio of the branch to the body is 1:1 in all patients under examination and it is not equal to the normal ratio of 2:3. The angle of the mandible is also greater than the normal value. The authors put forward a hypothesis that pseudomesioclusion in the sick with Crouzon syndrome can be conditioned not only by maxilla dysplasia but also by excessive height of the branch and increased angle value of the mandible basing on their own observations. This hypothesis, however, exact further radiocephalometric studies and close cooperation of obstetricians, paediatricians and orthodontists.
Adolescent↗
Serum vitamin A and E after their oral administration in cancer patients.
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Aged↗
DNA sequences of the cysB regions of Salmonella typhimurium and Escherichia coli.
Nucleotide sequences of the cysB region of Salmonella typhimurium and Escherichia coli have been determined and compared. A total of 1759 nucleotides were sequenced in S. typhimurium and 1840 in E. coli. Both contain a 972-nucleotide open reading frame identified as the coding region for the cysB regulatory protein on the basis of sequence homology and by comparison of the deduced amino acid sequences with known physicochemical properties of this protein. The DNA sequence identity for the cysB coding region in the two species is 80.5%. The deduced amino acid sequences are 95% identical. The predicted cysB polypeptide molecular weights are 36,013 for S. typhimurium and 36,150 for E. coli. For both proteins a helix-turn-helix region similar to that found in other DNA-binding proteins is predicted from the deduced amino acid sequence. Sequences upstream to cysB contain open reading frames which represent the carboxyl-terminal end of the topA gene product, DNA topoisomerase I. A pattern of highly conserved nucleotide sequences in the 151 nucleotides immediately preceding the cysB initiator codon in both species suggests that this region may contain multiple signals for the regulation of cysB expression.
Amino Acid Sequence↗
[A case of leiomyoma of the small intestine with intussusception].
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Diagnosis, Differential↗
Erythrocyte porphobilinogen deaminase activity in liver disease.
The activities of erythrocyte porphobilinogen deaminase were studied in patients with various liver diseases and in control groups. The lowest enzyme activities were found in patients with acute intermittent porphyria, and the highest ones in those with increased hemopoietic activity. Patients with liver cirrhosis or chronic active hepatitis had porphobilinogen deaminase activities that were significantly higher than in normal subjects and did not depend on disease activity. In patients with acute hepatitis, porphobilinogen deaminase activities varied depending on the phase of disease, being normal at onset and after 3-4 mo, and elevated to the values observed in chronic liver disease between 2 and 4 wk of hospitalization. The differences in porphobilinogen deaminase activities between patients with liver disease and controls did not relate to red cell age as determined by density gradient centrifugation. Therefore, although the mechanism responsible for the increase in porphobilinogen deaminase activities in liver disease is not clear, the results of this study suggest that it is independent of the presence of immature red cells in the circulation.
Adolescent↗