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Biomedical subjects

S M Chen

Publications and source records attributed to S M Chen.

At least 109 records · Page 6Linked to original sources

Renal excretion of oxalate in patients with chronic renal failure or nephrolithiasis.

This study was carried out in order to investigate renal oxalate excretion in a group of normal subjects (n = 40), a group of patients with uremia (n = 52) and a group with nephrolithiasis (n = 34). We found that the mean concentrations of oxalate in the 24-hour urine specimens of both patient groups were below the normal range. Although the renal creatinine clearance (CCR) was significantly decreased in some stone patients (n = 14), decreased renal oxalate clearance was noted only in those patients with severe renal failure. Thus, plasma oxalate was found to be elevated only in patients with chronic renal failure (mean +/- SD, 49.7 +/- 12.4 mumol/l), while the normal value was 17.0 +/- 6.7 mumol/l. The mean tubular excretion fraction of oxalate was also found to increase markedly in uremia with a mean of 26.3 +/- 17.3% (in normal subjects, 11.7 +/- 7.5%), but their mean daily urinary excretion of oxalate decreased to 63.2 mumol/day (mean value of 232.6 mumol/day in normal subjects). A positive correlation was observed between oxalate and creatinine, and between oxalate and calcium excretion, which was not found in normal subjects or patients with kidney stones. In nephrolithiasic patients, the daily excretion of oxalate, calcium and phosphate had no discernible increment and the mean excretory ratio of oxalate, calcium or phosphate to creatinine was all within normal limits. But when the CCR of stone patients was below 80 ml/min, their daily excretion of oxalate and calcium decreased significantly (p less than 0.01) and the excretory ratio of phosphate to creatinine markedly increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Clinical correlation of anti-receptor antibody titer, sensitivity to curare and electromyographic changes in experimental autoimmune myasthenia gravis].

Experimental autoimmune myasthenia gravis (EAMG) was studied in 39 rabbits which were repeatedly immunized with purified membrane-bound Torpedo (Nacine timilei) acetylcholine receptor (N-AchR). These rabbits invariably formed anti-AChR antibodies and some of them developed muscular weakness or flaccid paralysis. Pharmacological, physiological and ultrastructural studies showed that the pathological features of EAMG in rabbits closely resembled those of human myasthenia gravis. Antibody titer to AChR of the rabbit sera was determined with ELISA. In some of the rabbits, a rise in antibody Level occurred without appearance of weakness, while it is still likely that AChR antibody could be necessary for the induction of neuromuscular blockage. The sensitivity to curare was found to correlates closely with the severity of the disease. Typical electromyographic changes were found only in some of the EAMG rabbits with these studies. It was considered that anti-AChR concentration would not be the single pathological factor in EAMG.

Animals↗

Autoregulation of RNase III operon by mRNA processing.

RNase III has been implicated in the control of gene expression by the processing of mRNA. We have found that the rnc operon is autoregulated; rnc- mutant strains oversynthesize the operon's mRNA and protein products. A site in the 5'-noncoding region of the operon's message is cleaved by RNase III. This site-specific cleavage appears to be the initial step in the functional inactivation of the message, since the half-life of the cut message is dramatically shorter than that of the uncut message.

Base Sequence↗

Effects of zinc and cholesterol/choleate on serum lipoproteins and the liver in rats.

The effects of short-term treatment with orally-administered zinc sulphate and/or a mixture of cholesterol/choleate on serum lipoprotein and hepatic enzyme levels were studied. Administration of graded doses of zinc sulphate (20 or 40 mg/kg, as zinc ion) for 5 days, dose-dependently increased serum and hepatic zinc levels but depressed the serum high-density lipoprotein-cholesterol (HDL-C) concentration and liver cytochrome P-450 activity. However, it did not affect hepatic concentrations of malondialdehyde and free beta-glucuronidase. Cholesterol/choleate treatment for 5 days markedly damaged the liver, as reflected by elevations of hepatic concentrations of malondialdehyde (both in the mitochondrial and microsomal fractions) and of free beta-glucuronidase; total cholesterol and low-density lipoprotein-cholesterol in the blood were increased, whereas HDL-C was decreased significantly. Concomitant administration of zinc sulphate with cholesterol/choleate further lowered HDL-C levels, but reversed the high hepatic concentrations of both malondialdehyde and free beta-glucuronidase. The present study indicates that both zinc ions and cholesterol can decrease circulatory HDL-C levels and that zinc protects against cholesterol-induced hepatic damage by reducing lysosomal enzyme release and preventing lipid peroxidation in the liver.

Animals↗

Genetic analysis of the rnc operon of Escherichia coli.

RNase III, an Escherichia coli double-stranded endoribonuclease, is known to be involved in maturation of rRNA and regulation of several bacteriophage and Escherichia coli genes. Clones of the region of the E. coli chromosome containing the gene for RNase III (rnc) were obtained by screening genomic libraries in lambda with DNA known to map near rnc. A phage clone with the rnc region was randomly mutagenized with a delta Tn10 element, and the insertions were recombined onto the chromosome, generating a series of strains with delta Tn10 insertions in the rnc region. Two insertions that had Rnc- phenotypes were located. One of them lay in the rnc gene, and one was in the rnc leader sequence. Polarity studies showed that rnc is in an operon with two other genes, era and recO. The sequence of the recO gene beyond era indicated it could encode a protein of approximately 26 kilodaltons and, like rnc and era, had codon usage consistent with a low level of expression. Experiments using antibiotic cassettes to disrupt the genes rnc, era, and recO showed that era is essential for E. coli growth but that rnc and recO are dispensable.

Bacterial Proteins↗

Temperature-sensitive lethal mutant of era, a G protein in Escherichia coli.

The era gene of Escherichia coli encodes a GTP-binding protein which has similarities to elongation factor Tu and the Saccharomyces cerevisiae RAS protein. To investigate its function, mutations affecting era were isolated. A mini-Tn10 insertion, which truncated 22 amino acids from the COOH end of Era, did not affect cell growth. By using this mini-Tn10 insert as a coselectable marker, a temperature-sensitive lethal era mutant was isolated by localized mutagenesis using P1 phage transduction. A single-base G to A change was found at position 23, causing a tyrosine residue to be substituted for the cysteine residue at position 8 (era-770), in addition to the COOH-terminal mini-Tn10 disruption. Both alterations were necessary for the temperature-sensitive phenotype. Purified Era-770 mutant protein exhibited reduced binding to GTP compared with that of the wild-type Era protein.

Amino Acid Sequence↗

Proton nuclear magnetic resonance studies of plasma to determine metabolic status of patients with adult respiratory distress syndrome.

Adult respiratory distress syndrome (ARDS) is a non-cardiogenic pulmonary edema of various etiologies. Here we report the first application of proton nuclear magnetic resonance (NMR) for the detection of abnormal metabolites in plasma from patients with ARDS. By comparing plasma obtained from the systemic artery with that obtained from the pulmonary artery, we could study the metabolic status of the lung in patients with ARDS. Although their concentrations may vary, the peaks for acetate, acetoacetate, beta-hydroxybutyrate, phenylalanine, and other unidentified compounds in water-suppressed NMR of these patients' plasma were higher than in the normal controls. The proton NMR resonance at a chemical shift of about 7.4 ppm (relative to sodium tetradeutero-3-trimethyl-silylpropionate), presumably caused by phenylalanine and its related metabolites produced by a disordered amino acid metabolism, is detected in greater than 65% of the samples from ARDS patients. We discuss the detection of abnormal metabolites in terms of possible deranged metabolism of carbohydrates, lipids, or amino acids in this syndrome.

3-Hydroxybutyric Acid↗

On the biomechanics of human hip complex in vivo--I. Kinematics for determination of the maximal voluntary hip complex sinus.

In recent years, multisegmented mathematical models of the total human body have gained increasing attention in view of the high cost of experiments with human cadavers and/or anthropometric dummies. While these models can simulate very complicated load-motion situations, their effectiveness depends heavily on the proper biomechanical description and modeling of the major articulating joints of the human body. In a research effort to obtain the in vivo biomechanical joint property data suitable for incorporation into these models, the senior author and his associates recently developed a new kinematic and force data collection methodology by means of sonic emitters. By applying and extending this data collection methodology, this paper in Part I presents kinematics for determination of the maximal voluntary hip complex sinus. An overdeterminate number of sonic emitters is utilized and the 'most accurate' three-dimensional kinematic data set is selected by first establishing a selection criterion. Quantitative results obtained from three male subjects are presented in a functional expansion form relative to a locally-defined joint axis system as well as in the form of globographic representation relative to the torso-fixed axis system.

Biomechanical Phenomena↗

On the biomechanics of human hip complex in vivo--II. Passive resistive properties beyond the hip complex sinus.

In multisegmented mathematical models of the total human body, the resistive force properties of the major articulating joints play a direct and significant role in determining the relative motion between two body segments and in the understanding of injury mechanisms. This paper presents three-dimensional passive resistive properties beyond the maximal voluntary hip complex sinus by applying the kinematic data collection methodology developed in Part I together with a recently developed force data collection technique with sonic emitters (previously reported elsewhere by the senior author and his associates). The same three male subjects as in Part I of this paper were tested. Quantitative results were displayed by establishing the constant resistive force (moment) contours on a modified local joint axis system.

Biomechanical Phenomena↗

Reversals of the neostigmine-induced tetanic fade and endplate potential run-down with respect to the autoregulation of transmitter release.

1. In order to shed more light on the role of presynaptic cholinoceptors in the modulation of transmitter release, the effects of tubocurarine, choline and hexamethonium on neostigmine-induced tetanic fade and run-down of endplate potentials (e.p.ps) in response to indirect stimulation with trains of pulses were studied in the intact and cut isolated phrenic nerve-diaphragm preparation of the mouse, respectively. 2. Tubocurarine, choline and hexamethonium reduced both the tetanic fade and e.p.p. run-down caused by neostigmine, despite the fact that they themselves also induced these two effects. 3. At a given degree of postsynaptic inhibition, choline and hexamethonium caused less e.p.p. run-down and reversed the neostigmine-induced tetanic fade and e.p.p. run-down better than tubocurarine. Moreover, the e.p.p. run-down caused by choline or hexamethonium, but not that induced by tubocurarine, was reciprocally reversed by neostigmine. 4. Tubocurarine, choline and hexamethonium significantly decreased the endplate depolarization induced by repetitive nerve stimulation in the presence of neostigmine. The remaining depolarization continued to grow during repetitive stimulation in the presence of choline or hexamethonium, but not, however, in the presence of tubocurarine; a finding which suggests that choline and hexamethonium but not tubocurarine may be displaced from the receptor by the accumulated acetylcholine. 5. The mutual reversal by neostigmine and cholinoceptor antagonists of e.p.p. run-down may implicate the presence of a positive (physiological) and a negative (pharmacological) feedback regulation for evoked transmitter release via nicotinic cholinoceptors in the mammalian motor nerve, depending on the concentration of acetylcholine within the synaptic cleft.

Animals↗

An improved method for the detection of malignancy by proton NMR spectroscopy of plasma.

The ratio of intensity (RI) of the plasma lipid methyl proton NMR resonance from two Carr-Purcell-Meiboom-Gill spectra acquired with a short (2.4 msec) and long (120 msec) pulse delay time is proposed to provide a potentially more sensitive and less variable marker of human malignancy than the linewidth parameter previously suggested (E.T. Fossel, J.M. Carr, and J. McDonagh (1986) N. Engl. J. Med. 315, 1369-1376). Linewidth and transverse (T2) relaxation data are presented which demonstrate that the observed correlation between methyl and methylene lipid linewidth and the methyl RI parameter arises from a combination of T2 differences and the relative amounts that fast- and slow-relaxing components contribute to the composite methyl resonance.

Humans↗

Activated c-Ha-ras oncogene with a guanine to thymine transversion at the twelfth codon in a human stomach cancer cell line.

The rat fibroblast cell line Rat 1 was transfected with total DNA of a gastrocarcinoma cell line, BGC-823. The transforming gene was cloned from the genomic library of the secondary transformants using in situ hybridization with a probe of the human Alu repeat sequence. This cloned gene is homologous to the protooncogene c-Ha-ras. The activation lesion of the transforming gene was identified by sequence analysis as a single nucleotide substitution of thymine for guanine in the 12th codon. This results in the substitution of valine for glycine at the 12th amino acid of the Mr 21,000 protein.

Adenocarcinoma↗

Improved purification and some molecular and kinetic properties of sn-glycerol-3-phosphate dehydrogenase from Saccharomyces cerevisiae.

The purification procedure for isolating sn-glycerol-3-phosphate dehydrogenase (EC 1.1.1.8) from Saccharomyces cerevisiae was improved by the introduction of an ion-exchange step. Enzyme yields were doubled and the specific activity was increased as compared to the original procedure. A new value of 42,000 was obtained for the molecular weight by several denaturing methods. By native gel chromatography the molecular weight appears to be 31,000 as reported earlier. Michaelis constants were found to be 0.37 mM with dihydroxyacetone phosphate as the variable substrate and 0.018 mM for NADH as the variable substrate.

Chemical Precipitation↗

GAL1-GAL10 divergent promoter region of Saccharomyces cerevisiae contains negative control elements in addition to functionally separate and possibly overlapping upstream activating sequences.

The upstream activating sequence (UASG) of the adjacent and divergently transcribed GAL1 and GAL10 promoters of Saccharomyces cerevisiae regulates the induction of the corresponding genes in response to the presence of galactose. We constructed chimeric yeast promoters in which a different UAS, UASC from the iso-1-cytochrome c (CYC1) gene of S. cerevisiae, was fused at different locations upstream of GAL1 (UASC-GAL1 promoters) or GAL10 (UASC-GAL10 promoters) and used to monitor the activity of UASG in cells grown in the presence or absence of galactose. Though the CYC1 promoter is fully induced in yeast grown in glycerol medium, UASC-GAL chimeric promoters containing UASG were repressed as much as 400-fold (UASC-GAL1) or 1350-fold (UASC-GAL10) in this growth medium. Several distinct portions of the GAL1-GAL10 divergent promoter region blocked the UASC-induced expression of the GAL1 and GAL10 promoters, whereas others did not, suggesting that several distinct negative control elements are present that may repress transcription of GAL1 and GAL10 in the absence of galactose. The approximate locations of these negative control elements were delimited to sites adjacent to or possibly overlapping the sites at which the positive control protein GAL4 binds in UASG. Deletion derivatives of GAL4 that fail to induce transcription from the wild-type GAL promoters but retain the DNA binding domain significantly derepressed the expression of the UASC-GAL chimeric promoters. These results, combined with those of earlier studies, suggest the possibility that GAL4 normally induces transcription of GAL1 and GAL10 by blocking the activity of these negative control elements, in addition to stimulating transcription by a mechanism of positive control.

Chromosome Mapping↗

Kinematic and passive resistive properties of human elbow complex.

In recent years, owing to their versatility and reduced cost of operation, multisegmented mathematical models of the total human body have gained increased attention in gross biodynamic motion studies. This, in turn, has stimulated the need for a proper biomechanical data base for the major human articulating joints. The lack of such a database for the humero-elbow complex is the impetus for this study. The total angular range of motion permitted by the complex and the passive resistive properties beyond the full elbow extension were studied. Results obtained on ten normal male subjects were utilized to establish a statistical data base for the humero-elbow complex. Results are also expressed in functional expansion form suitable for incorporation into the existing multisegmented models.

Biomechanical Phenomena↗