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Biomedical subjects

Z Zhou

Publications and source records attributed to Z Zhou.

At least 253 records · Page 14Linked to original sources
PubMed1999

Effects of Tryptergium Wilfordii Polyglyco-sidium on the tumour necrosis factor levels in aqueous humor after intraocular lens implantation.

PURPOSE: Effects of Tryptergium Wilfordii Polyglyco-sidium (TWP) on the Tumour Necrosis Factor (TNF) levels in aqueous humor after intraocular lens (IOL) implantation were studied in rabbits. METHODS: Twenty-seven pigmented rabbits were divided into three groups. In the first group, the IOL were placed in the capsular bag after lens extraction. In the second group, rabbits received TWP therapy after IOL implantation. And in the third group, rabbit received prednisone therapy after IOL implantation. Aqueous humor samples were aspirated on the 1st, 3rd, 7th, and 14th postoperative day. A modified double antibodies indirect sandwich ELISA was used to detect for the presence of TNF. The data were closely studied by means of analysis of variance with SAS software. RESULTS: It was found that TNF level in aqueous humor reached its maximum on the 7th postoperative day in the group with IOL implantation. It was also found that the TNF levels in aqueous humor on the 7th and 14th postoperative day were significantly lower (P < 0.05) in the TWP-treated group with IOL implantation than those in the non-treatment group and the steroid-treated group. CONCLUSIONS: The current study offers evidence that TWP is more effective than the steroid in reducing the TNF level in aqueous humor after IOL implantation.

Animals↗
PubMed1999

Expression of ICAM-1 and LFA-1 molecules in relation to renal allograft rejection in rats.

OBJECTIVE: The purpose of this study was to assess the renal graft expression of ICAM-1 (intercellular adhesion molecule-1) and LFA-1 (lymphocyte function-associated antigen-1) molecule with relation to graft rejection. METHODS: Rat kidney transplantation was performed according to the procedure of Kamada with some modification. Experimental rats were divided into 5 groups. The survival time of recipient rats and function of grafts after renal transplantation were observed. The sections of renal graft were stained for monoclonal antibody ICAM-1 and LFA-1, and then quantification of ICAM-1 and LFA-1 expression was accomplished by computer image analysis. RESULTS: ICAM-1 and LFA-1 increased significantly in the renal allograft rejection group as compared with the non-rejection groups (P<0.05). CONCLUSION: Both biopsy of renal graft and monitoring of ICAM-1 and LFA-1 are useful tools in diagnosing and treating acute rejection.

Animals↗
PubMed1999

[Photocurrent spectra of undoped LECSIGaAs].

Extrinsic photocurrent spectra of undoped LECSIGaAs have been measured to investigate the deep levels in this material. A broad photocurrent response band M1 ranging from 0.40 to 0.70 eV has been observed. M1 band reveals five peaks at 0.46, 0.49, 0.56, 0.65 and 0.69 eV, respectively. The onset thresholds for the 0.46, 0.49, 0.56 and 0.69 eV peaks are 0.44, 0.47, 0.51 and 0.67 eV, respectively. It is likely that M1 band is due to different deep levels and each of these deep levels has a concentration larger than 10(14) cm(-3). The origin of M1 band is discussed and possible associations of the 0.44, 0.47 and 0.51 eV thresholds with copper acceptor, EL3 and oxygen donor are presented. The relationship between M1 band and the photoresponse behavior of drain current of GaAs field effect transistor was also investigated.

English Abstract↗
PubMed1999

[Joint rotational analysis of twenty six bands of the H2(80) Se molecule].

This paper expressed the theory of Global fit model. Global fit of all known up today rotation-vibration energies of twenty four states of the H2(80) Se molecule had been made, and the corresponding set of 112 parameters, which reproduce the initial 3516 upper energies with the mean accuracy of 10.6 x 10(-3) cm(-1), were obtained. On this base fine rotational structures of the local-mode bands (500, A1) and (401, B2) were analyzed with 252 upper energies, which were analyzed in the normal-molde and local-mode also. In the end, with the results above, joint rotation-vibration energies of twenty six states of H2(80) Se molecule were made, and the corresponding set of 114 parameters obtained, which reproduce the initial 3768 upper energies with the mean accuracy of 9.62 x 10(-3) cm(-1).

English Abstract↗
PubMed1999

[Determination of trace amounts of zinc in nickel electrolyte by flow injection on-line enrichment].

A method for the determination of trace amount of zinc in nickel electrolyte utilizing the flow injection on-line enrichment technique is reported in this paper. Atomic absorption spectrometer was used as detector. Zinc was separated from large amounts of nickel andother components in the electrolyte by absorption its chlorocomplex on a mini-column packed with strongly basic anion exchangers. It was found that sodium chloride containing in the electrolyte offered a sufficient chloride concentration needed for the formation of the zinc chlorocomplex and thus no additional reagent was required for the determination. The throughput of the method is 30 determinations per hour. The detection limit of the method is 0.002 microg x mL(-1) and the precision is 1.9% (RSD). The proposed method is rapid and cost-effective. It has been used for almost three years in the quality control of the electrolyte in the factory with great success.

English Abstract↗
PubMed1999

[Determination of the content of aminopyrine in antongding injection by orthogonal function spectrophotometry].

Determination of the content of aminopyrine in the antongding injection by orthogonal function spectrophotometry was reported in this paper. The six wavelengths for the determination are 257, 261, 265, 269, 273 and 277 nm. The concentration of aminopyrine in the range of 5-25 microg x mL(-1) is in a good linear relation to P2, and the regression equation is P2 = + 0.018 - 0.032 9c, r = 0.999 9. The average recovery and relative standard deviation are 100.3% and 0.40%, respectively. On the basis of the data observed it is concluded that this method shows no obvious difference as compared with Hebei province pharmacy regulation.

Aminopyrine↗
PubMed1998

Identification of a site that modifies desensitization of P2X2 receptors.

The time course of desensitization of P2X2 receptors expressed in Xenopus oocytes and HEK 293 cells was examined. We found that there was virtually no desensitization in response to 5 microM ATP, but that responses to 50 microM ATP desensitized with a highly variable time course. The time constant of desensitization varied 250fold among oocytes (from 4 to over 1000 seconds) and 10 fold among HEK cells (from 4 to 40 seconds). Mutation of D349, which lies at the cytoplasmic end of the second transmembrane domain (to either A, N, or R), resulted in a dramatic acceleration of the median rate of desensitization, and eliminated variation in the rate of desensitization. In contrast, mutation of four other charged residues in putative transmembrane domains had no effect on desensitization. These results suggest that P2X2 receptor desensitization is strongly modulated by the intracellular environment, and that D349 is essential for this modulation.

Adenosine Triphosphate↗
PubMed1998

In search of the first flower: A jurassic angiosperm, archaefructus, from northeast china

Angiosperm fruiting axes were discovered from the Upper Jurassic of China. Angiosperms are defined by carpels enclosing ovules, a character demonstrated in this fossil. This feature is lacking in other fossils reported to be earliest angiosperms. The fruits are small follicles formed from conduplicate carpels helically arranged. Adaxial elongate stigmatic crests are conspicuous on each carpel. The basal one-third of the axes bore deciduous organs of uncertain affinities. No scars of subtending floral organs are present to define the individual fertile parts as floral units, but the leaf-like structures subtending each axis define them as flowers. These fruiting axes have primitive characters and characters not considered primitive.

Journal Article↗
PubMed1998

Up-regulation of human secreted frizzled homolog in apoptosis and its down-regulation in breast tumors.

In the screening of apoptosis-related genes, an elevated 4.5-kb transcript representing the full-length cDNA of human secreted frizzled-related protein (hsFRP) was cloned. To investigate its possible role in the regulation of cell proliferation, gene expression of hsFRP was examined in human immortalized breast epithelial cell line HBL-100 during growth arrest and apoptosis. Serum deprivation caused G arrest and induction of hsFRP. When serum was re-introduced into the cell culture, the expression of hsFRP declined. Adriamycin treatment induced accumulation of hsFRP mRNA and decrease of beta-catenin. This indicates that the regulation of hsFRP may be involved in the cell-cycle/apoptosis mechanism and possibly in the wnt signaling pathway. hsFRP transcripts were undetectable in cells derived from malignant breast carcinomas, but detectable in 3 immortalized non-malignant breast epithelial cell lines, indicating the involvement of hsFRP in the breast malignant transformation. When tumor and adjacent normal tissues from the same patients were examined, lower expression was found in 5/5 of breast tumors, 2/4 of ovary tumors and 3/5 of kidney tumors. These data suggest the possible involvement of hsFRP in regulation of cell proliferation and breast tumorigenesis.

Apoptosis↗
PubMed1998

The DNA replication and damage checkpoint pathways induce transcription by inhibition of the Crt1 repressor.

We have identified the yeast CRT1 gene as an effector of the DNA damage and replication checkpoint pathway. CRT1 encodes a DNA-binding protein that recruits the general repressors Ssn6 and Tup1 to the promoters of damage-inducible genes. Derepression of the Crt1 regulon suppresses the lethality of mec1 and rad53 null alleles and is essential for cell viability during replicative stress. In response to DNA damage and replication blocks, Crt1 becomes hyperphosphorylated and no longer binds DNA, resulting in transcriptional induction. CRT1 is autoregulated and is itself induced by DNA damage, indicating the existence of a negative feedback pathway that facilitates return to the repressed state after elimination of damage. The inhibition of an autoregulatory repressor in response to DNA damage is a strategy conserved throughout prokaryotic and eukaryotic evolution.

Animals↗
PubMed1998

Timing of dense-core vesicle exocytosis depends on the facilitation L-type Ca channel in adrenal chromaffin cells.

Secretion from dense-core vesicles is reputedly much slower than that from typical synaptic vesicles, possibly because of noncolocalization of Ca channels and release sites. We reinvestigated this question by measuring the kinetics of catecholamine release in chromaffin cells from calf and adult bovines. Amperometric recording from calf chromaffin cells stimulated by action potentials exhibited two latencies of secretion that depended on both the frequency of stimulation and the pathway of Ca entry. Short-latency responses (<25 msec delay; "strongly coupled") appeared at low (0.25 and 1 Hz) and high (7 Hz) frequencies and were entirely dependent on recruitment of "facilitation" L-type Ca channels as revealed by nisoldipine blockade. Long-latency responses (>25 msec delay; "weakly coupled") were more apparent at higher frequencies (7 Hz) and were substantially reduced by toxins that blocked N- and P-type Ca channels. Ca current recordings revealed that adult bovine chromaffin cells lack facilitation channels; virtually all secretion was weakly coupled in these cells. The mean delay of the strongly coupled signal was approximately 3 msec after the peak of the action potential (at 24 degreesC), indicating that dense-core vesicles can exhibit a rate of exocytosis approaching that occurring in neurons. Although other explanations are possible, these results are consistent with the idea that facilitation Ca channels are colocalized with release sites in calf chromaffin cells. Calculations based on a model incorporating this assumption suggest that these channels must be within 13 nm of secretory sites to account for such rapid exocytosis.

Action Potentials↗
PubMed1998

HERG channel dysfunction in human long QT syndrome. Intracellular transport and functional defects.

Mutations in HERG are associated with human chromosome 7-linked congenital long QT (LQT-2) syndrome. We used electrophysiological, biochemical, and immunohistochemical methods to study the molecular mechanisms of HERG channel dysfunction caused by LQT-2 mutations. Wild type HERG and LQT-2 mutations were studied by stable and transient expression in HEK 293 cells. We found that some mutations (Y611H and V822M) caused defects in biosynthetic processing of HERG channels with the protein retained in the endoplasmic reticulum. Other mutations (I593R and G628S) were processed similarly to wild type HERG protein, but these mutations did not produce functional channels. In contrast, the T474I mutation expressed HERG current but with altered gating properties. These findings suggest that the loss of HERG channel function in LQT-2 mutations is caused by multiple mechanisms including abnormal channel processing, the generation of nonfunctional channels, and altered channel gating.

Biological Transport↗
PubMed1998

Function of Escherichia coli MsbA, an essential ABC family transporter, in lipid A and phospholipid biosynthesis.

The Escherichia coli msbA gene, first identified as a multicopy suppressor of htrB mutations, has been proposed to transport nascent core-lipid A molecules across the inner membrane (Polissi, A., and Georgopoulos, C. (1996) Mol. Microbiol. 20, 1221-1233). msbA is an essential E. coli gene with high sequence similarity to mammalian Mdr proteins and certain types of bacterial ABC transporters. htrB is required for growth above 32 degreesC and encodes the lauroyltransferase that acts after Kdo addition during lipid A biosynthesis (Clementz, T., Bednarski, J., and Raetz, C. R. H. (1996) J. Biol. Chem. 271, 12095-12102). By using a quantitative new 32Pi labeling technique, we demonstrate that hexa-acylated species of lipid A predominate in the outer membranes of wild type E. coli labeled for several generations at 42 degreesC. In contrast, in htrB mutants shifted to 42 degreesC for 3 h, tetra-acylated lipid A species and glycerophospholipids accumulate in the inner membrane. Extra copies of the cloned msbA gene restore the ability of htrB mutants to grow at 42 degreesC, but they do not increase the extent of lipid A acylation. However, a significant fraction of the tetra-acylated lipid A species that accumulate in htrB mutants are transported to the outer membrane in the presence of extra copies of msbA. E. coli strains in which msbA synthesis is selectively shut off at 42 degreesC accumulate hexa-acylated lipid A and glycerophospholipids in their inner membranes. Our results support the view that MsbA plays a role in lipid A and possibly glycerophospholipid transport. The tetra-acylated lipid A precursors that accumulate in htrB mutants may not be transported as efficiently by MsbA as are penta- or hexa-acylated lipid A species.

ATP-Binding Cassette Transporters↗
PubMed1998

Oxygen-bridged dinuclear ruthenium amine complex specifically inhibits Ca2+ uptake into mitochondria in vitro and in situ in single cardiac myocytes.

Ruthenium red is a well known inhibitor of Ca2+ uptake into mitochondria in vitro. However, its utility as an inhibitor of Ca2+ uptake into mitochondria in vivo or in situ in intact cells is limited because of its inhibitory effects on sarcoplasmic reticulum Ca2+ release channel and other cellular processes. We have synthesized a ruthenium derivative and found it to be an oxygen-bridged dinuclear ruthenium amine complex. It has the same chemical structure as Ru360 reported previously (Emerson, J., Clarke, M. J., Ying, W-L., and Sanadi, D. R. (1993) J. Am. Chem. Soc. 115, 11799-11805). Ru360 has been shown to be a potent inhibitor of Ca2+-stimulated respiration of liver mitochondria in vitro. However, the specificity of Ru360 on Ca2+ uptake into mitochondria in vitro or in intact cells has not been determined. The present study reports in detail the potency, the effectiveness, and the mechanism of inhibition of mitochondrial Ca2+ uptake by Ru360 and its specificity in vitro in isolated mitochondria and in situ in isolated cardiac myocytes. Ru360 was more potent (IC50 = 0.184 nM) than ruthenium red (IC50 = 6.85 nM) in inhibiting Ca2+ uptake into mitochondria. 103Ru360 was found to bind to isolated mitochondria with high affinity (Kd = 0.34 nM, Bmax = 80 fmol/mg of mitochondrial protein). The IC50 of 103Ru360 for the inhibition of Ca2+ uptake into mitochondria was also 0.2 nM, indicating that saturation of a specific binding site is responsible for the inhibition of Ca2+ uptake. Ru360, as high as 10 microM, produced no effect on sarcoplasmic reticulum Ca2+ uptake or release, sarcolemmal Na+/Ca2+ exchange, actomyosin ATPase activity, L-type Ca2+ channel current, cytosolic Ca2+ transients, or cell shortening. 103Ru360 was taken up by isolated myocytes in a time-dependent biphasic manner. Ru360 (10 microM) applied outside intact voltage-clamped ventricular myocytes prevented Ca2+ uptake into mitochondria in situ where the cells were progressively loaded with Ca2+ via sarcolemmal Na+/Ca2+ exchange by depolarization to +110 mV. We conclude that Ru360 specifically blocks Ca2+ uptake into mitochondria and can be used in intact cells.

Animals↗
PubMed1998

Human homologs of yeast prp16 and prp17 reveal conservation of the mechanism for catalytic step II of pre-mRNA splicing.

Pre-mRNA splicing takes place in two catalytic steps. The second step is poorly understood, especially in mammals. In yeast, the splicing factors, Prps 16, 17, 18 and Slu7 function exclusively in step II. Here we report the isolation of cDNAs encoding human Prps 16 and 17 which are 41 and 36% identical to their yeast counterparts. The Prp16 gene is essential in yeast, and we show that a chimeric yeast-human Prp16 protein rescues a yeast Prp16 knockout strain. Immunodepletion of hPrp16 from splicing extracts specifically blocks step II, and the activity can be fully restored with recombinant hPrp16. Moreover, both hPrps 16 and 17 associate with the spliceosome late in the splicing pathway. Mutations at the 3' splice site that specifically block step II do not affect the association of hPrps 16 and 17 with the spliceosome, indicating that these factors may function at a stage of step II prior to recognition of the 3' splice site. Recently, the human homologs of Prp18 and Slu7 were identified. The observation that humans contain homologs of all four known step II proteins in yeast indicates that the mechanism for catalytic step II is highly conserved.

Adenosine Triphosphatases↗
PubMed1998

Prominent sex steroid metabolism in human lymphocytes.

Steroid metabolism was investigated in cultured human B-lymphoblastoid cells (B-LCL), and peripheral blood T and B cells. Gene expression was examined by reverse-transcription polymerase chain reaction amplification (RT-PCR). Appropriate sized transcripts were detected in both cultured and fresh peripheral lymphocytes for CYP11A, CYP17, HSD11L (11beta-hydroxysteroid dehydrogenase I), HSD17B1 (17beta-hydroxysteroid dehydrogenase type I) and SRD5A1 (5alpha-reductase I). B-LCL, but not T and B cells, expressed CYP11B. There was minimal expression of HSD3B1 and HSD3B2 (3beta-hydroxysteroid dehydrogenase I and II) in B-LCL and T cells. Transcripts for CYP19 and HSD11K were not detected. Corresponding enzymatic activity was detectable only for 17-hydroxysteroid dehydrogenase and 5alpha-reductase, respectively producing testosterone and 5alpha-dihydrotestosterone. Steroid identities were confirmed by gas chromatography/mass spectrometry (GC/MS). One metabolite thought to be deoxycorticosterone was identified by GC/MS as 6alpha-hydroxypregnanolone. It was concluded that sex hormone metabolism, including androgen synthesis, occurs in lymphocytes, and may modulate immune response.

Adult↗
PubMed1998

Genotoxicity of nitric oxide produced from sodium nitroprusside.

Induction of mutation and micronucleus (MN) formation by nitric oxide (NO) was investigated in mammalian cells using sodium nitroprusside (SNP) as a drug donor of NO. Results showed that the concentration of NO2- in the tested solution rose according to time- and concentration-exposure to SNP. The treatment of SNP (0.5-8 micromol/ml with S9 or 2-8 micromol/ml without S9) induced a concentration-dependent increase in the mutation frequency at the gpt gene locus in g12 cells and caused a 13- (-S9) to 25- (+S9) fold increase above the background level at the highest concentration. A statistically significant increase in the number of micronucleated binucleated cells (MNBN) was also observed in treated groups. MNBN per thousand, MN per thousand and the proportion of the multiple micronuleated cells increased in a concentration-dependent manner in the concentration range of SNP (0.5-4 micromol/ml with S9 or 2-8 micromol/ml without S9). Our results indicate that SNP, an NO releasing drug, is genotoxic in g12 cells.

Cell Line↗