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W M Zhang

Publications and source records attributed to W M Zhang.

At least 19 recordsLinked to original sources

Modeling synergistic adsorption of phenol/aniline mixtures in the aqueous phase onto porous polymer adsorbents.

The adsorption equilibria of phenol and aniline on nonpolar polymer adsorbents (NDA-100, XAD-4, NDA-16 and NDA-1800) were investigated in single- and binary-solute adsorption systems at 313 K. The results showed that all the adsorption isotherms of phenol and aniline on these adsorbents can be well fitted by Freundlich and Langmuir equations, and the experimental uptake of phenol and aniline in all binary-component systems is obviously higher than predicted by the extended Langmuir model, arising presumably from the synergistic effect caused by the laterally acid-base interaction between the adsorbed phenol and aniline molecules. A new model (MELM) was developed to quantitatively describe the synergistic adsorption behavior of phenol/aniline equimolar mixtures in the binary-solute systems and showed a marked improvement in correlating the binary-solute adsorption of phenol and aniline by comparison with the widely used extended Langmuir model. The newly developed model confirms that the synergistic coefficient of one adsorbate is linearly correlated with the adsorbed amount of the other, and the larger average pore size of adsorbent results in the greater synergistic effect of phenol/aniline equimolar mixtures adsorption.

Journal Article↗

Application of an effective method in predicting breakthrough curves of fixed-bed adsorption onto resin adsorbent.

Removal of many organic pollutants including phenolic compounds from industrial wastewater can always be achieved by fixed-bed adsorption onto the polymeric resin adsorbent, and the relevant breakthrough curves would provide much valuable information to help to design a fixed-bed adsorption process in field application. In the present study, a model developed based on the constant-pattern wave approach theory and the Freundlich model was adopted to describe the breakthrough curves of phenol and p-nitrophenol adsorption onto a macroreticular resin adsorbent NDA-100 from aqueous solution. Column experiments were performed at different conditions to verify the model and the results proved that the model would describe the breakthrough curves well. Effect of the operation parameters on breakthrough curves was also discussed to get helpful information in choosing the adsorption process.

Adsorption↗

Adsorption of phenolic compounds from aqueous solution onto a macroporous polymer and its aminated derivative: isotherm analysis.

Adsorption of phenolic compounds from aqueous solution to a macroporous polymeric adsorbent (CHA-111), its animated derivative (MCH-111) and a reference weakly anion exchanger (ND-900) was studied. Experimental results indicated that amino functional groups on the polymeric matrix play an important role in phenol adsorption by MCH-111 and ND-900, which was attributed to the formation of hydrogen bonding between the phenol molecule and the amino group on the polymeric matrix. The semi-empirical Freundlich isotherm equation and its reduced form were employed to interpret the adsorption behavior. A site energy distribution model based on the Polanyi adsorption potential theory can elucidate the adsorption mechanism reasonably.

Adsorption↗

Effects of food deprivation on expression of growth hormone receptor and proximate composition in liver of black seabream Acanthopagrus schlegeli.

The effects of food deprivation on the hepatic level growth hormone receptor (GHR) were investigated in black seabream (Acanthopagrus schlegeli) both at the protein level (by radioreceptor assay) and at the mRNA level (by ribonuclease protection assay). Serum levels of growth hormone (GH) and triiodothyronine (T(3)) were also measured. Condition factor and hepatic proximate composition of the fish were also assessed. Significant decrease in hepatic GHR binding was recorded as early as on day 2 of starvation. On day 30 this decrease was even more pronounced, with the level in the starved fish reaching less than 20% the fed control level. A concomitant decrease in the hepatic GHR mRNA content was also noted during this period, with a progressive decrease from day 2 to day 30 of starvation. The extent of decrease in the mRNA content was less pronounced than the decrease in receptor binding, with the hepatic GHR mRNA content in the day 30 starved fish representing approximately 30% of the level in the fed control. In large contrast, serum GH level increased progressively during starvation. After 30 days of starvation, serum GH levels in the starved fish were more than three times the concentration found in the fed control. Serum T(3) levels, on the other hand, decreased during starvation, with the difference reaching significance on day 15 and day 30. After 30 days of starvation, serum T(3) levels in the starved fish were only approximately 40% the concentration found in the fed control. The hepatic lipid content exhibited an increasing trend during starvation. On day 30 the hepatic lipid content of the starved fish had doubled the level found in the fed control. However, the hepatic protein content did not exhibit much change during starvation. There was also a minor decrease in the moisture content of the liver during starvation, but the condition factor of the fish as a whole registered a gradual decrease during the course of food deprivation.

Animal Nutritional Physiological Phenomena↗

Quantification of prostate specific antigen mRNA levels in circulation after prostatic surgery and endocrine treatment by quantitative reverse transcription-polymerase chain reaction.

Various methods to detect prostatic cells in circulation have given conflicting results. This is probably because qualitative rather than quantitative methods have been used to detect mRNA from prostatic cells. A quantitative method has been developed based on reverse transcription-polymerase chain reaction (RT-PCR) for detection of prostate specific antigen (PSA) mRNA in peripheral blood. A competitive internal mRNA standard was used for quantification of absolute amounts of PSA mRNA. The detection limit of the assay was 7 copies of mRNA, and the highest level of circulating PSA mRNA in 88 control subjects was 25 copies per milliliter of blood. This method was used to study the influence of prostatic surgery and endocrine treatment on prostatic cells in the circulation of 56 patients undergoing biopsy, radical prostatectomy, transurethral resection of the prostate (TURP), orchiectomy, or androgen blockade. Blood samples were drawn before, during and up to 26 weeks after these procedures had been carried out. The highest level of PSA mRNA in controls was 25 copies per milliliter of blood. After RP, TURP or orchiectomy, PSA mRNA levels increased above this level in 27%, 29%, and 25% of the samples, respectively. After prostate biopsy, two out of 15 patients became positive. PSA mRNA levels that were elevated by surgery became undetectable within 1-3 days. No significant correlation was found between PCR positivity and the clinical characteristics of the patients. It is concluded that the level of PSA mRNA in peripheral blood increases after prostatic surgery, indicating temporary dissemination of prostatic cells. However, preoperative levels do not correlate with serum PSA, stage or grade.

Cell Line↗

Seabream growth hormone receptor: molecular cloning and functional studies of the full-length cDNA, and tissue expression of two alternatively spliced forms.

A full-length clone of the growth hormone receptor (GHR) was isolated from a cDNA library constructed from the liver of black seabream (Acanthopagrus schlegeli). The seabream GHR (sbGHR) cDNA sequence encodes a transmembrane protein of 640 amino acids (aa) possessing the characteristic motifs and architectural design of GHRs of other species. When compared to the other fish GHRs, it is most homologous to another marine fish species, the turbot, where the aa identity is 79.3%. But the sbGHR sequence is more remotely related to the goldfish GHR (51.6% aa identity) and the salmonid GHRs (approximately 46-48% aa identities). Phylogenetic comparison with other known GHRs indicates that the fish GHRs constitute a distinct group among the different vertebrate classes. The aa identities between sbGHR and other GHRs are low, being around 40% with mammalian GHRs, around 45% with avian and reptilian GHRs, and less than 35% with Xenopus GHR. CHO cells transfected with the sbGHR cDNA can be stimulated to proliferate by recombinant seabream growth hormone (sbGH). In addition, the transfected cells can transactivate a co-expressed mammalian serine protease inhibitor (Spi) 2.1 promoter upon stimulation by sbGH. These functional assays indicated that the fish receptor can interact with its homologous ligand to evoke the downstream post-receptor events. Reverse transcription-polymerase chain reaction (RT-PCR) and genomic PCR using a pair of gene-specific primers revealed the expression of two alternatively spliced forms of sbGHR in various tissues of the fish. A 93-bp intron, unique to the sbGHR gene and not found in any other known GHR genes, is alternatively spliced to give rise to two forms of receptor mRNA transcripts. The two forms of the receptor are differentially expressed among the different tissues of the fish.

Alternative Splicing↗

A founder mutation (R254X) of SLC22A5 (OCTN2) in Chinese primary carnitine deficiency patients.

Mutations in the SLC22A5 gene, which encodes for the plasma membrane carnitine transporter OCTN2, cause primary carnitine deficiency (PCD). After our first report of OCTN2 mutations in Chinese, three more Chinese PCD patients were identified. The parents of these families were non-consanguineous and these families were unrelated. Two novel truncating mutations were found: R254X, a single-base mutation at cDNA position 981 (c.981C>T); and Y387X (c.1382T>G). Two probands, one each from Taiwan and Macau, were homozygous for R254X. The other proband from Taiwan carried both R254X and Y387X. Two additional heterozygote carriers of R254X were also identified among 250 control samples, while none was detected for Y387X. The population carrier rate for R254X would be about 1 in 125. Haplotypes of R254X alleles were examined and patients homozygous for R254X were also homozygous for the same haplotype of intragenic and microsatellites markers. Analysis of population frequencies of haplotypes revealed that the chance of 4 chromosomes having arisen as independent events was 0.016. We conclude that R254X is probably a founder mutation in Chinese. Other previously reported mutations found in the Japanese population were also screening in 250 control samples but no carrier was identified, indicating that they were either very rare or not present in Southern Chinese.

Carnitine↗

Kappa-opioid receptor agonist inhibits the cholera toxin-sensitive G protein in the heart.

To explore the signaling mechanisms of the negative modulation of beta-adrenoceptors by kappa-Opioid receptors (kappa-OR) in the heart, the possibility of the interaction at the level of G protein and receptor was determined. Cholera toxin, an activator of the stimulatory G protein (Gs), elevated electrically induced intracellular Ca2+ ([Ca2+]i) transients and induced ribosylation of the alpha-subunit of Gs (Gsalpha) in rat ventricular myocytes. The effects were significantly attenuated by U50,488H, a specific agonist of kappa-OR, and were abolished by nor-binaltorphimine, a selective kappa-OR antagonist. The content of Gsalpha, however, was not affected by U50,488H. Receptor binding experiments showed that neither Bmax nor Kd of the binding of [3H]CGP-12177, a beta-adrenoceptor antagonist, was affected by U50,488H. The current study provides the first evidence that kappa-OR stimulation inhibits the ribosylation of the alpha-subunit of the Gs protein, thus inhibiting the action of cholera toxin on the protein.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

[Study of the antiosteoporosis effects of bushenqianggu capsule].

OBJECTIVE: To study the antiosteoporosis effects of Bushenqianggu capsule. METHOD: Observing the pharmacological effects of Bushenqianggu capsule with blank and positive control, and then analyzing the data with biological statistics. RESULT: The testis and uterus weight index of "the kidney assessed" model mice, weight of thighbone and blood concentration of Ca2+ increased significantly. Meanwhile, the thighbone mass density of castrated rats was improved and the incidence of the thighbone fracture in the osteoporosis model rats induced by retinoic acid was reduced. Besides, it had analgesia and anti-inflammatory effects. CONCLUSION: Bushenqianggu capsule has a good effect on osteoporosis, which provides evidence for clinical use.

Animals↗

Expression of stanniocalcin in the epithelium of human choroid plexus.

Stanniocalcin (STC) is a 28 kD glycoprotein hormone originally found in bony fish in which it regulates calcium/phosphate homeostasis and protects against hypercalcemia. The recently characterized mammalian STC shows about 70% homology with fish STC. The epithelial cells of proximal tubuli in human and rat kidney and brain neurons have been found to express STC. Here we show that the epithelium of the choroid plexus, already at 16 weeks of fetal age, and of plexus papillomas, synthesize and express STC. Our findings suggest that STC may be of importance for the distribution of calcium and phosphate between the cerebrospinal fluid and blood.

Adult↗

Determination of prostate-specific antigen complexed to alpha(2)-macroglobulin in serum increases the specificity of free to total PSA for prostate cancer.

OBJECTIVES: To determine whether prostate-specific antigen (PSA) complexed to alpha(2)-macroglobulin (A2M) increases the specificity of free PSA (fPSA) and total PSA (tPSA) for the diagnosis of prostate cancer (PCa). METHODS: In a series of 73 patients with PCa and 58 with benign prostatic hyperplasia (BPH), fPSA, tPSA, and PSA complexed with A2M (PSA-A2M) in serum were determined by specific immunoassays. The assay for PSA-A2M was based on the immunoadsorption of immunoreactive PSA in serum and the measurement of the PSA immunoreactivity released by denaturation of PSA-A2M at pH 11.4. RESULTS: The median proportion of PSA-A2M [ %PSA-A2M=PSA-A2M/(tPSA+PSA-A2M)] and that of fPSA ( %fPSA=fPSA/tPSA) were significantly lower in patients with PCa (8.2% and 12.4%, respectively) than in patients with BPH (11.6% and 22.5%, P = 0.0014 and P <0.0001, respectively). The median sum of %PSA-A2M and %fPSA was 22.4% in PCa and 38.2% in BPH (P <0.0001). When the sum of %PSA-A2M and %fPSA was used as a diagnostic test for PCa, 57% of patients with "falsely" elevated PSA concentrations (4 to 10 ng/mL) caused by BPH could be correctly identified without missing patients with PCa compared with 18% of the patients with BPH but not PCa using %fPSA alone. CONCLUSIONS: Measurement of the sum of %PSA-A2M and %fPSA in serum significantly improves the cancer specificity of the PSA test compared with the use of tPSA and %fPSA.

Aged↗

kappa -opioid receptor stimulation induces arrhythmia in the isolated rat heart via the protein kinase C/Na(+)-H(+)exchange pathway.

The present study attempted to determine whether the protein kinase C (PKC)/Na(+)-H(+)exchange (NHE) pathway would mediate the arrhythmogenic action of kappa -opioid receptor (OR) stimulation. We first determined the effects of U50,488H, a selective kappa -OR agonist, on PKC activity and cardiac rhythm in the isolated perfused rat heart, and intracellular pH (pH(i)), and Ca(2+)([Ca(2+)](i)) and Na(+)([Na(+)](i)) concentrations in the isolated ventricular myocyte. At 5-40 microm U50,488H concentration dependently increased the particulate PKC activity and pH(i), and induced arrhythmia. 40 microm U50,488H also increased [Na(+)](i)and [Ca(2+)](i). The arrhythmogenic effects of 40 microm U50,488H were abolished by nor-binaltorphimine, a selective kappa -OR antagonist. Blockade of PKC and NHE with respective blockers, 1 microm bisindolylmaleimide I or 0.5 microm calphostin C, and 1 microm 5-[N -methyl- N -isobutyl]amiloride or 1 microm 5-([N -ethyl- N -isopropopyl]amiloride, abolished and significantly attenuated, respectively, the effects of kappa -OR stimulation on pH(i), [Na(+)](i)and [Ca(2+)](i), and arrhythmia. To determine the role of pH(i), we observed U50,488H-induced arrhythmia at pH(i)6.8. At this pH(i), the pH(i)increased gradually both in the presence and absence of 40 microm U50,488H to a similar extent. While the increase in response to U50,488H was significantly less at pH(i)6.8 (from 0.09 to 0.10) than that at pH(i)7.1 (from 0.01 to 0.18), the arrhythmia induced by the agonist was the same at both high and low pHs. On the other hand, 5 microm monensin, a sodium ionophore, increased [Na(+)](i)and [Ca(2+)](i), and induced arrhythmia to similar extents as U50,488H. PKC and NHE inhibitors, that significantly attenuated the effects induced by U50,488H, had no effect on those induced by monensin. In conclusion, kappa -OR stimulation induces arrhythmia via PKC/NHE. [Na(+)](i)and [Ca(2+)](i), but not pH(i), may be directly responsible for arrhythmia induced by kappa -OR stimulation.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

Expression and characterization of trypsinogen produced in the human male genital tract.

Trypsinogen is a serine proteinase produced mainly by the pancreas, but it has recently been found to be expressed also in several cancers such as ovarian and colon cancer and in vascular endothelial cells. In this study, we found that trypsinogen-1 and -2 are present at high concentrations (median levels, 0.4 and 0.5 mg/L, respectively) in human seminal fluid and purified them to homogeneity by immunoaffinity and anion exchange chromatography. Purified trypsinogen isoenzymes displayed a M(r) of 25 to 28 kd in sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting. Most of the trypsinogen-1 purified from seminal fluid was enzymatically active whereas trypsinogen-2 occurred as the proform, which could be activated by enteropeptidase in vitro. Immunohistochemically, trypsinogen protein was detected in the human prostate, urethra, utriculus, ejaculatory duct, seminal vesicles, deferent duct, epididymal glands, and testis. Expression of trypsinogen mRNA in the same organs was demonstrated by in situ hybridization. Trypsinogen mRNA was also detected in the prostate and seminal vesicles by reverse transcriptase-polymerase chain reaction and Northern blotting. Isolated trypsin was shown to activate the proenzyme form of prostate-specific antigen. These results suggest that trypsinogen isoenzymes found in seminal fluid are produced locally in the male genital tract and that they may play a physiological role in the semen.

Blotting, Northern↗

Insulin-like growth factor I is not a useful marker of prostate cancer in men with elevated levels of prostate-specific antigen.

High serum levels of insulin-like growth factor I (IGF-I) and low levels of IGF-binding protein-3 (IGFBP-3) have been shown to correlate with increased prostate cancer risk. To evaluate this, IGF-I, IGFBP-3, and prostate-specific antigen (PSA) were measured in serum from 665 consecutive men (179 with prostate cancer), aged 55-67 yr, with elevated serum prostate-specific antigen (PSA; > or = 4 microg/L) in a screening trial. Men in the highest quartile of IGF-I levels had an odds ratio (OR) for prostate cancer of 0.50 [95% confidence interval (CI) 0.26-0.97] when adjusting for serum IGFBP-3. IGFBP-3 itself was not significantly associated with prostate cancer risk (OR, 1.24; 95% CI, 0.68-2.24). Prostate volume was larger in men without than in those with prostate cancer (P < 0.001), and after adjustment for prostate volume, the negative association between serum IGF-I and prostate cancer risk was no longer significant (OR, 0.57; 95% CI, 0.28-1.16). In screen-positive men with elevated serum PSA, serum IGF-I is not a useful diagnostic test for prostate cancer, but it may be associated with benign prostatic hyperplasia and enlargement.

Aged↗

The role of phosphodiesterase in mediating the effect of protein kinase C on cyclic AMP accumulation upon kappa-opioid receptor stimulation in the rat heart.

This study determined whether phosphodiesterase (PDE) was activated by protein kinase C (PKC) upon kappa-receptor stimulation, and if so, to identify the isozyme. We first studied the effects of trans-(+/-)-3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl] cyclohexyl) benzeneacetamide methanesulphonate (U50,488H), a selective kappa-opioid receptor (OR) agonist, and phorbol-12-myristate-13-acetate (PMA), a PKC activator, on cAMP accumulation and PDE activity in rat ventricular myocytes when PKC and PDE were inhibited by respective inhibitors. Like PMA, U50,488H decreased the forskolin-stimulated cAMP accumulation and dose-dependently stimulated the PDE activity, which were antagonized by 10(-6) M chelerythrine and bisindolylmaleimide I, selective PKC antagonists. In addition, 3-isobutyl-1-methylxanthine, a PDE inhibitor, dose-dependently attenuated the inhibition on forskolin-stimulated cAMP accumulation and abolished the stimulation on PDE activity by U50,488H and PMA. The observations suggest that PKC may enhance cAMP degradation through activating PDE upon kappa-OR stimulation. To identify the isozyme(s) mediating the effect of PKC upon kappa-OR stimulation, selective inhibitors were used. We found that 10(-5) M Ro-20-1724, a selective cAMP-specific PDE (PDE-IV) inhibitor, abolished the inhibitory effects of U50,488H and PMA, whereas 8-methoxymethyl-3-isobutyl-1-methylxanthine, erythro-9-(2-hydroxy-3-nonyl) adenine, cilostamide, and zaprinast, selective inhibitors of Ca(2+)/calmodulin-dependent PDE (PDE-I), cGMP-stimulated PDE (PDE-II), cGMP-inhibited PDE (PDE-III), and cGMP-specific PDE (PDE-V), respectively, had no effect. Moreover, rolipram, another selective PDE-IV inhibitor, also dose-dependently attenuated the inhibition on forskolin-stimulated cAMP accumulation and stimulation on PDE activity by U50,488H and PMA. In conclusion, this study has provided evidence for the first time that PKC and PDE-IV mediate the action of kappa-OR.

1-Methyl-3-isobutylxanthine↗

Use of the complex between prostate specific antigen and alpha 1-protease inhibitor for screening prostate cancer.

PURPOSE: We assess whether the complex between prostate specific antigen (PSA) and alpha1-protease inhibitor in serum can be used to reduce further the number of false-positive PSA screen results independent of total and free PSA. MATERIALS AND METHODS: Sera from 304 consecutive screen positive subjects, including 78 with and 226 without prostate cancer, and serum PSA of 4 to 10 microg./l. or higher in the Finnish, randomized, population based prostate cancer screening trial were analyzed for PSA-alpha-protease inhibitor, and total and free PSA. Main outcome measures were specificity, sensitivity and area under receiver operating characteristics curve for proportions of free PSA and PSA-alpha 1-protease inhibitor, and for a combination of these among screen positive cases. RESULTS: The proportion of serum PSA-alpha 1-protease inhibitor of total PSA was lower in cancer cases than in controls (0.9% versus 1.6%, p <0.001). Logistic regression analysis of total PSA, free PSA and PSA-alpha 1-protease inhibitor showed that PSA-alpha 1-protease inhibitor in serum was an independent variable for discrimination between subjects with and without prostate cancer (p = 0.006) in the PSA range of 4 to 10 microg./l. The proportion of PSA-alpha 1-protease inhibitor alone improved specificity less than the proportion of free PSA but when these were combined by logistic regression they performed better than the proportion of free PSA alone at sensitivities of 85% to 95% (p <0.001). CONCLUSIONS: Serum PSA-alpha 1-protease inhibitor improves the specificity of total and free PSA in a screening population with total PSA 4 to 10 microg./l.

Aged↗

Characterization and determination of the complex between prostate-specific antigen and alpha 1-protease inhibitor in benign and malignant prostatic diseases.

Prostate-specific antigen (PSA) is a tissue-specific serine protease which forms complexes with protease inhibitors such as alpha 1-antichymotrypsin and alpha 2-macroglobulin. We have studied the interaction between PSA and alpha 1-protease inhibitor (API) in vitro and found that 15% of the added PSA binds to API while the majority of API is cleaved between Met358 and Ser359 when PSA is incubated with a 5-fold excess of API at 37 degrees C for 7 days. The complex between PSA and API (PSA-API) formed in vitro displays the same chromatographic behavior, molecular size and immunoreactivity as endogenous PSA-API occurring in serum, indicating that they are identical. PSA-API can be detected in serum by a time-resolved immunofluorometric assay (IFMA), in which a monoclonal antibody to PSA is used as a catcher and a polyclonal antibody to API labeled with a Eu-chelate is used as a tracer. Purified PSA-API formed in vitro is used as a calibrator. PSA-API in serum represents 1.0-7.9% (median 2.4%) of total PSA (tPSA) in prostate cancer (PCa, n = 82) and 1.3-12.2% (median 3.6%, p < 0.01) in patients with benign prostatic hyperplasia (BPH, n = 66). The IFMA for PSA-API in serum is hampered by a variable background, which is caused by non-specific adsorption of the huge excess of API in serum to the solid phase. The background can be determined by an assay using the same tracer as in the IFMA for PSA-API but PSA-unrelated antibody on the solid phase. The background signal is subtracted from the PSA-API signal. The clinical utility of PSA-API in serum has been evaluated in PSA-positive subjects from the Finnish PCa screening trial. After subtraction of the background, the proportion of PSA-API in relation to tPSA is lower in PCa than in controls, 0.9% vs. 1.6%, respectively (p < 0.001). Logistic regression analysis showed that the concentration of PSA-API was independent of the proportion of free PSA as a diagnostic variable among subjects with a tPSA of 4-10 micrograms/l (p = 0.009). The probability of PCa calculated by logistic regression using the concentration of PSA-API and the proportion of free PSA in serum significantly improved cancer specificity at high sensitivity levels (85-95%) as compared to the proportion of free PSA alone.

Humans↗