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Biomedical subjects

S Zhai

Publications and source records attributed to S Zhai.

At least 37 records · Page 2Linked to original sources

Simultaneous determination of theophylline, enoxacin and ciprofloxacin in human plasma and saliva by high-performance liquid chromatography.

A simple reversed-phase high-performance liquid chromatographic method has been developed for the simultaneous determination of theophylline, ciprofloxacin and enoxacin in plasma and saliva. The biological fluid samples were extracted with methylene chloride-isopropyl alcohol prior to isocratic chromatography on a Waters C18 mu Bondapak column. Ultraviolet detection was carried out at 268 nm. The assay is linear for ciprofloxacin and enoxacin (0.05-10 micrograms/ml), and theophylline (0.1-20 micrograms/ml). The assay can be used to investigate the interaction of these two fluoroquinolones with theophylline.

Anti-Infective Agents↗

[Analysis of antigenity of membranous labyrinth proteins of guinea pigs].

An electrophoretic dot immunobinding assay and a modified western blotting method were established. The components and antigenity of the membranous labyrinth proteins of guinea pigs were analysed. There are the same epitopes between some components of the antigen, between the antigen and extractives of acoustic nerve, cochlear nuclei, kidney and Klebsiella pneumoniae. The antigen distributes in stria vascularis, spiral ligament, spiral ganglion, the organ of Corti and Reissner's membrane etc.

Animals↗

[Effect of radix Ginseng-faeces Trogopterori combination on pharmacodynamics and effective chemical composition of radix Ginseng].

The experiments have shown that there is incompatibility on anti-stress because the action of Radix Ginseng alone is stronger than that of Radix Ginseng and Faeces Trogopterori combined, but there is little incompatibility on non-specific immune function when both are used. The analysis of chemical composition of Radix Ginseng has indicated that the acquired rate of total saponin from the semifinished products and Rg1 of Radix Ginseng is markedly increased when the two drugs are decocted together. The results suggest that the traditional theory is limited in holding that Radix ginseng and Faeces Trogopterori are incompatible with each other.

Animals↗

Brain mitochondrial citrate synthase and glutamate dehydrogenase: differential inhibition by fatty acyl coenzyme A derivatives.

Organic acidemia is found in several metabolic encephalopathies (e.g., hepatic and valproate encephalopathies, Reye's syndrome, and hereditary organic acidemias). Although fatty acids are known to be neurotoxic, the underlying mechanisms have not been fully elucidated. It has been hypothesized that one mechanism underlying fatty acid neurotoxicity is the selective inhibition of rate-limiting and/or regulated tricarboxylic acid (TCA) cycle and related enzymes by fatty acyl-coenzyme A (CoA) derivatives. To test the hypothesis, this study has examined the effects of several fatty acyl-CoAs on citrate synthase (CS) and glutamate dehydrogenase (GDH) in brain mitochondria. At levels higher than 100 microM, butyryl-CoA (BCoA; a short-chain acyl-CoA; IC50 approximately 640 microM), octanoyl-CoA (OCoA; a medium-chain acyl-CoA; IC50 approximately 380 microM), n-decanoyl-CoA (DCoA; a medium-chain acyl-CoA; IC50 approximately 436 microM), and palmitoyl-CoA (PCoA; a long-chain acyl-CoA; IC50 approximately 340 microM) inhibited brain mitochondrial CS activity in a concentration-related manner. However, these fatty acyl-CoAs were less effective inhibitors (IC50 values for OCoA, DCoA, and PCoA being approximately 1260, 420, and 720 microM, respectively) of brain mitochondrial GDH activity. Compared to the other three acyl-CoAs investigated, BCoA was a very poor inhibitor of GDH. These results demonstrate that fatty acyl-CoAs are inhibitors of brain mitochondrial CS and GDH activities only at pathological/toxicological levels. Thus, the fatty acyl-CoA inhibition of brain mitochondrial CS and GDH is unlikely to assume major pathophysiological and/or pathogenetic importance.(ABSTRACT TRUNCATED AT 250 WORDS)

Acyl Coenzyme A↗

The trk family of receptors mediates nerve growth factor and neurotrophin-3 effects in melanocytes.

We have recently shown that (a) human melanocytes express the p75 nerve growth factor (NGF) receptor in vitro; (b) that melanocyte dendricity and migration, among other behaviors, are regulated at least in part by NGF; and (c) that cultured human epidermal keratinocytes produce NGF. We now report that melanocyte stimulation with phorbol 12-tetra decanoate 13-acetate (TPA), previously reported to induce p75 NGF receptor, also induces trk in melanocytes, and TPA effect is further potentiated by the presence of keratinocytes in culture. Moreover, trk in melanocytes becomes phosphorylated within minutes after NGF stimulation. As well, cultures of dermal fibroblasts express neurotrophin-3 (NT-3) mRNA; NT-3 mRNA levels in cultured fibroblasts are modulated by mitogenic stimulation, UV irradiation, and exposure to melanocyte-conditioned medium. Moreover, melanocytes constitutively express low levels of trk-C, and its expression is downregulated after TPA stimulation. NT-3 supplementation to cultured melanocytes maintained in Medium 199 alone prevents cell death. These combined data suggest that melanocyte behavior in human skin may be influenced by neurotrophic factors, possibly of keratinocyte and fibroblast origin, which act through high affinity receptors.

Amino Acid Sequence↗

[Components of membranous labyrinth proteins of guinea pig and the detection of anti-68kD antibody in sensorineural hearing loss].

The membranous labyrinth proteins (MLP) of guinea pig were isolated with various methods. The isolations with SDS or Triton X-100 were efficient. Western blot was successfully established and used to detect the anti-MLP antibody. Among 42 cases of idiopathic sensorineural hearing loss, 16 are positive of anti-68kD antibody in their sera with increased IgG, IgM and IgA. Anti-68kD antibody was also found in some normal controls, though it had weaker reaction and less repetition.

Animals↗

Treatment of human melanocytes and S91 melanoma cells with the DNA repair enzyme T4 endonuclease V enhances melanogenesis after ultraviolet irradiation.

Tanning is a protective response of ultraviolet (UV)-irradiated skin that decreases damage from subsequent sun exposures by increasing the epidermal content of melanin, a brown-black pigment that absorbs light energy throughout the UV and visible portions of the electromagnetic spectrum. The melanin pigment is made by epidermal melanocytes and transferred to surrounding keratinocytes. The action spectrum, time course, and histologic features of tanning are well studied, but the initiating molecular events are unknown. Previous work has shown that T4 endonuclease V, a prokaryotic DNA repair enzyme that catalyzes the first and rate-limiting step in repair of UV-induced pyrimidine dimers, delivered in carrier liposomes (T4N5), enhances repair of UV-induced DNA damage in cultured human cells and protects against photocarcinogenesis in an animal model. We now report that T4N5 treatment enhances UV-induced melanogenesis, as measured by melanin content, tyrosinase activity, 14C-dopa incorporation, and visual assessment in both S91 murine melanoma cells and human melanocytes. T4N5 treatment also increases cell yields following UV irradiation. These data suggest that tanning can be stimulated through enhanced DNA repair.

Cell Division↗

Band 3 Memphis: a widespread polymorphism with abnormal electrophoretic mobility of erythrocyte band 3 protein caused by substitution AAG----GAG (Lys----Glu) in codon 56.

Band 3 Memphis (b3M) is a variant of the erythrocyte band 3 protein detected in individuals of virtually all ethnic groups and characterized by a reduced mobility of proteolytic fragments derived from the N-terminus of the cytoplasmic domain of band 3 (cdb3). We have sequenced band 3 cDNA corresponding to cdb3 in 12 heterozygotes for the b3M polymorphism including one white, one black, one Chinese, one Philippino, one Malay, and seven Melanesian subjects. In all individuals, we found a single-base substitution in codon 56 of one band 3 allele changing lysine to glutamic acid (AAG----GAG) which, in some of them, was linked with an additional mutation in cdb3. Since the change of codon 56 from AAG to GAG was the only mutation in the studied individuals found within the cDNA segment coding for the abnormally migrating fragment of cdb3, we conclude that it represents the underlying molecular basis of the b3M polymorphism. We further support this conclusion by showing that electrophoresis in the presence of 4 mol/L urea abolished the difference in migration between proteolytic products of b3M and normal band 3, and that a fusion protein prepared from cDNA coding for the b3M allele again exhibits reduced electrophoretic mobility compared with the normal fusion protein. Finally, since most of the previously cloned mouse, rat, and chicken band 3 and band 3-related proteins contain glutamic acid in the position corresponding to amino acid 56 in the human band 3, we propose that the Memphis variant is the evolutionarily older form of band 3.

Anion Exchange Protein 1, Erythrocyte↗

Temporal changes and rural-urban differences in cardiovascular disease risk factors and mortality in China.

We summarize several studies, from the last 10 years, of temporal changes and rural-urban differences in the risk factors of cardiovascular disease (CVD) in China to indicate the influences of economic modernization. Two national blood pressure surveys have shown that the prevalence of hypertension increased from 5.1% to 7.7% between 1958-1959 and 1979-1980. Throughout China hypertension is more prevalent in urban areas than in rural areas. Within the Shanghai region body mass index, blood pressure, and total serum cholesterol were higher in urban districts than in rural areas. Rural-urban differences in lipid levels were also found in the Beijing and Guangzhou regions. A related four-year followup study showed that total serum cholesterol and triglycerides increased markedly in both urban and rural areas of Guangzhou. In Shanghai part-time farmers who worked in factories had a higher age-adjusted prevalence of definite hypertension than farmers who worked full-time in the fields (5.0% versus 2.3%). In a prospective study in Wuhan a new productivity-based salary system was associated with increased serum cholesterol and blood pressure. Age-adjusted CVD mortality increased from 1973 to 1982 in a rapidly industrializing county in the Shanghai metropolitan region. The results from several studies indicate that China is undergoing the expected increase in modernization-related CVD risk factors and mortality, especially in urban metropolitan regions.

Adult↗

[Comparative studies of brain CT scan in schizophrenia].

CT Scan was undertook to 48 schizophrenics and 30 healthy volunteers. The results revealed that: the incidence rate of CT abnormalities was higher in schizophrenics than in normal control; the incidence rate of CT abnormalities in winter-born schizophrenics was higher than in non-winter-born patients; the incidence rate of abnormalities was higher in familial type schizophrenics than in sporadic type; the incidence rate in negative symptom schizophrenics was higher than in positive symptom patients.

Adolescent↗

Deletion in erythrocyte band 3 gene in malaria-resistant Southeast Asian ovalocytosis.

Southeast Asian ovalocytosis (SAO) is a hereditary condition that is widespread in parts of Southeast Asia. The ovalocytic erythrocytes are rigid and resistant to invasion by various malarial parasites. We have previously found that the underlying defect in SAO involves band 3 protein, the major transmembrane protein, which has abnormal structure and function. We now report two linked mutations in the erythrocyte band 3 gene in SAO: (i) a deletion of codons 400-408 and (ii) a substitution, A----G, in the first base of codon 56 leading to substitution of Lys-56 by Glu-56. The first defect leads to a deletion of nine amino acids in the boundary of cytoplasmic and membrane domains of band 3. This defect has been detected in all 30 ovalocytic subjects from Malaysia, the Philippines, and two unrelated coastal regions of Papua New Guinea, whereas it was absent in all 30 controls from Southeast Asia and 20 subjects of different ethnic origin from the United States. The Lys-56----Glu substitution has likewise been found in all SAO subjects. However, it has also been detected in 5 of the 50 control subjects, suggesting that it represents a linked polymorphism. We conclude that the deletion of codons 400-408 in the band 3 gene constitutes the underlying molecular defect in SAO.

Anion Exchange Protein 1, Erythrocyte↗

Uncoupling of the spectrin-based skeleton from the lipid bilayer in sickled red cells.

The distribution of spectrin and band 3 in deoxygenated reversibly sickled cells was visualized by immunofluorescence and immunoelectron microscopy. Antibodies against band 3, the major lipid-associated transmembrane protein, labeled the entire cell body, including the entire length of the long protruding spicule, whereas antibodies against spectrin labeled only the cell body and the base region of the spicules. The results suggest that the formation of long spicules during sickling is associated with a continuous polymerization of hemoglobin S polymers, presumably through gaps in the spectrin-actin meshwork, and a subsequent uncoupling of the lipid bilayer from the submembrane skeleton.

Anemia, Sickle Cell↗

[Effects of explosions on cortical response threshold and enzyme activities in inner ear of guinea pigs].

Effects of explosions of different intensities on cortical response threshold (CRT) and activities of succinic dehydrogenase (SDH) and acetylcholinesterase (AchE) in the inner ear were studied on 37 guinea pigs. The results revealed various degrees of cochlear damages due to different doses of explosions, and also a negative correlation between hearing loss and the enzyme activities in both TTS and PTS. The significance of the results is discussed.

Acetylcholinesterase↗

Molecular defect of the band 3 protein in southeast Asian ovalocytosis.

BACKGROUND: Southeast Asian ovalocytosis is a form of hereditary elliptocytosis in which the red cells are rigid and resistant to malaria invasion. The underlying molecular defect is unknown. METHODS AND RESULTS: We studied the red cells of 54 patients with ovalocytosis and 122 normal controls. We found that ovalocytes contain a structurally and functionally abnormal band 3 protein, the principal transmembrane protein of red cells. The structural lesion of ovalocyte band 3 was revealed by limited proteolytic cleavage of the protein, which produced fragments of abnormal size that were derived from the cytoplasmic domain of the protein. The structural lesion was present in all the subjects with ovalocytosis but none of the controls. This region of band 3 serves as the principal binding site for the membrane skeleton, a submembrane protein network composed of ankyrin, spectrin, actin, and protein 4.1. The structural defect is dominantly inherited, being tightly linked with the inheritance of ovalocytosis (the probability of linkage is in excess of 10 million to 1). Ovalocyte band 3 bound considerably more tightly than normal band 3 to ankyrin, which connects the membrane skeleton to the band 3 protein. This tight binding of ovalocyte band 3 to the underlying skeleton containing ankyrin was directly confirmed in intact cells by the finding that ovalocyte band 3 had markedly reduced lateral mobility in the membrane. CONCLUSIONS: The red cells in Southeast Asian ovalocytosis carry a structurally and functionally abnormal band 3 protein. This molecular defect may underlie the increased rigidity of the red cells and their resistance to invasion by malaria parasites.

Anion Exchange Protein 1, Erythrocyte↗

Detection of hemin release during hemoglobin S denaturation.

Sickle hemoglobin is relatively unstable upon oxidation or mechanical shaking. During denaturation, it generates oxygen radicals and hemichromes and ultimately precipitates in the form of micro-Heinz bodies. It is not clear, however, whether the degradation product hemin, which is a potent hemolytic agent and a potential perturbant to protein-protein interactions in the red cell membrane skeleton, is also generated during sickle hemoglobin denaturation. By specific absorption of hemin with Dowex AG 1-X8 anion-exchange resin at high-ionic strength conditions, we now separate hemin for quantitation from the bulk hemoglobin and its derivatives. We demonstrate that upon mechanical shaking oxyhemoglobin S denatures much faster than oxyhemoglobin A and that a considerably higher level of hemin is detected in the shaken hemoglobin S as compared with hemoglobin A. By using the same method to measure the hemin content in the hemolysate of fresh red cells from patients with sickle cell disease, we detect a three- to fivefold increase in the hemin content in these patients (0.4 to 0.75 mumol/L) as compared with normal individuals (0.1 to 0.15 mumol/L). These data suggest that the instability of sickle oxyhemoglobin leads to increased intracellular precipitation of hemoglobin and the release of hemin, which may play a role in the membrane lesion of sickle red cells.

Anemia, Sickle Cell↗

Hemin-mediated dissociation of erythrocyte membrane skeletal proteins.

Spectrin tetramers and oligomers in normal erythrocytes are cross-linked by actin and protein 4.1 to form a two-dimensional membrane skeletal network. In the present study, we find that hemin, a breakdown product of hemoglobin, progressively (a) alters the conformation of spectrin as revealed by electron microscope studies and by the decreased resistance of spectrin to proteolytic degradation, (b) alters the conformation of protein 4.1 as revealed by the increased mobility of protein 4.1 on nondenaturing gel electrophoresis, (c) weakens spectrin dimer alpha beta-dimer alpha beta, spectrin alpha-spectrin beta, as well as spectrin-protein 4.1 associations as analyzed by nondenaturing gel electrophoresis, and (d) diminishes the structural stability of erythrocyte membrane skeletons (i.e. Triton-insoluble ghost residues) subjected to mechanical shearing. Since hemin may be liberated from oxidized or unstable mutant hemoglobin under pathological conditions, these hemin-induced effects on spectrin, protein 4.1, and membrane skeletal stability may play a role in the membrane lesion of these erythrocytes.

Electrophoresis, Polyacrylamide Gel↗