[A case clinic analysis of leukemoid reaction].
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Blood Cells↗
Biomedical subjects
Hui Chen
Publications and source records attributed to Hui Chen.
[Ginkgo biloba extract protection in acute paraquat poisoning of rat lung tissue ].
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Acute Disease↗
[Determination of daurisoline in rabbit plasma and study on its pharmacokinetics].
AIM: To establish an HPLC method for the determination of daurisoline (DS) in rabbit plasma and investigate its pharmacokinetic characteristics after intravenous administration. METHODS: Dauricine was used as internal standard. The plasma samples were deproteinated with acetonitrile and extracted with two-step dichloromethane. Acetonitrile-water-triethylamine (18:82:0.28, pH 3) was used as mobile phase at a flow rate of 1.0 mL.min-1. The UV-detector was set at 284 nm. RESULTS: The linear range was 0.05-20.00 micrograms.h.mL-1 with correlation coefficients 0.9996. The limit of quantitation (LOQ) was 0.05 mg.L-1 of plasma. The absolute and relative recoveries were above 80% and (101 +/- 5)%, respectively. The intra- and inter-assay coefficient of variation were 1.9%-5.6% and 3.5%-6.5%, respectively. The plasma concentration-time profiles were adequately described by a two-compartment open model. CONCLUSION: A sensitive, precise and accurate method for the determination of DS in plasma was described, which can be used in its pharmacokinetic studies.
Animals↗
[Role of cytomegalovirus infection in the pathogenesis of type 2 diabetes mellitus].
OBJECTIVE: To further study the role of human cytomegalovirus (HCMV) infection in the pathogenesis of the type 2 diabetes mellitus. METHODS: HCMV DNA levels in sera from 29 type 2 diabetic patients and 23 controls were measured by quantitative polymerase chain reaction (PCR), and comparative analyses was made between HCMV DNA and T cell subsets, blood glucose (BG), insulin (Ins) and C peptide (C-P). RESULTS: The levels of HCMV DNA were (1.81+/-1.67) x 10(8) copies/ml for type 2 diabetic patients, a level significantly higher than that (5.50+/-4.30) x 10(7) copies/ml of controls. The percentage of CD8 for type 2 diabetic patients with positive HCMV DNA was 29.53%+/-2.00%, being much higher than that for controls (27.13%+/-4.12%), while the ratio of CD4/CD8 1.24+/-0.05 was significantly lower than that 1.41+/-0.10 of controls. Fasting C-P of type 2 diabetic patients with positive HCMV DNA was far lower than that of those with negative HCMV DNA, but the differences of BG and Ins between the two groups were not significant. CONCLUSION: Active HCMV infection of type 2 diabetic patients may suppress cellular immunity and its influence on the pathogenesis of the type 2 diabetes mellitus should be further studied.
Adult↗
End-group analysis of blue light-emitting polymers using matrix-assisted laser desorption/ ionization time-of-flight mass spectrometry.
An analytical method based on matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) has been applied to provide information on the structure of a copolymer, e.g., repeat unit and end group. Seven conjugated polymers, which have been demonstrated as the active component in blue light-emitting diodes, were synthesized through Suzuki polycondensation reaction in the presence of Pd(PPh3)4 catalyst. Their molecular weights were obtained using gel permeation chromatography analysis. MALDI-TOF MS was used to investigate the structure information in detail. The proposed end-group structures were confirmed by the identity between the observed and the simulated isotopic distribution of each polymer. The results demonstrate that these synthetic polymers possess various end groups and even contain macrocycles. The catalyst Pd(PPh3)4 was found to introduce phenyl end groups via aryl-aryl exchange between the catalytic palladium intermediate and the triphenylphosphine ligand. All these results are based on the analysis of the mass spectrum data, which suggests that MALDI-TOF MS is an extraordinarily strong tool in synthetic polymer structure analysis.
Journal Article↗
Secretion of Annexin II via activation of insulin receptor and insulin-like growth factor receptor.
Annexin II is secreted into the extracellular environment, where, via interactions with specific proteases and extracellular matrix proteins, it participates in plasminogen activation, cell adhesion, and tumor metastasis and invasion. However, mechanisms regulating annexin II transport across the cellular membrane are unknown. In this study, we used coimmunoprecipitation to show that Annexin-II was bound to insulin and insulin-like growth factor-1 (IGF-1) receptors in PC12 cells and NIH-3T3 cells overexpressing insulin (NIH-3T3(IR)) or IGF-1 receptor (NIH-3T3(IGF-1R)). Stimulation of insulin and IGF-1 receptors by insulin caused a temporary dissociation of annexin II from these receptors, which was accompanied by an increased amount of extracellular annexin II detected in the media of PC12, NIH-3T3(IR), and NIH-3T3(IGF-1R) cells but not in that of untransfected NIH-3T3 cells. Activation of a different growth factor receptor, the platelet-derived growth factor receptor, did not produce such results. Tyrphostin AG1024, a tyrosine kinase inhibitor of insulin and IGF-1 receptor, was shown to inhibit annexin II secretion along with reduced receptor phosphorylation. Inhibitors of a few downstream signaling enzymes including phosphatidylinositol 3-kinase, pp60c-Src, and protein kinase C had no effect on insulin-induced annexin II secretion, suggesting a possible direct link between receptor activation and annexin II secretion. Immunocytochemistry revealed that insulin also induced transport of the membrane-bound form of annexin II to the outside layer of the cell membrane and appeared to promote cell aggregation. These results suggest that the insulin receptor and its signaling pathways may participate in molecular mechanisms mediating annexin II secretion.
3T3 Cells↗
Attenuating toluene mobility in loess soil modified with anion-cation surfactants.
Soils, subsoils, and aquifer materials can be modified with hydrophobic cationic surfactants to increase their sorption capabilities for organic contaminants. The objective of this study was to examine in detail the sorptive characteristics of the natural loess soil and the resultant organo-modified soils for aqueous-phase neutral organic compounds (NOCs) in an attempt to define the operative sorptive mechanisms. Under the laboratory conditions, a series of modified loess soils in this study were prepared by replacing the cations of loess soil with both cationic surfactant hexadecyltrimethylammonium bromide (HDTMA-Br) and anionic surfactant sodium dodethylbenzene sulfonate (SDBS). Toluene was selected as an indicator to study the sorption behavior of the NOCs in loess soils. The sorption isotherms of toluene in soil samples obtained using the batch equilibration method. The results indicated that natural loess had a poor sorption capability for NOCs, and sorption isotherms of toluene appeared likely nonlinear and fit the Freundlich equation very well. When the soils were coated with large alkyl surfactants such as HDTMA-Br, sorption isotherms correspondingly became linear and the sorptive capability was prominently dependent on the quantity of hexadecyltrimethylammonium (HDTMA) and SDBS added into the soils. The study could provide an essential basis on attenuation of organic contaminants in the subsurface environment.
Adsorption↗
Structural elements of antizymes 1 and 2 are required for proteasomal degradation of ornithine decarboxylase.
The antizymes constitute a conserved gene family with at least three mammalian orthologs. As described previously, in a degradation system utilizing rabbit reticulocyte lysate, antizyme 1 (AZ1) accelerates proteasomal ornithine decarboxylase (ODC) degradation, but antizyme 2 (AZ2) does not. To examine the relationship between antizyme structure and function, we further characterized the properties of AZ1 and AZ2 and protein chimeras composed of elements of the two. AZ1 binds to ODC with about a 3-fold higher potency than AZ2, but this cannot account for their distinct degradative activities. The dissimilar degradative capacity of AZ1 and AZ2 is also observed using purified proteasomes. A series of reciprocal AZ1/AZ2 chimeras was used to determine the sequence elements needed to direct ODC degradation. An element contained within amino acids 130-145 of AZ1 is essential for this function. Constructs in which amino acids 130-145 were exchanged between the antizymes confirmed the critical nature of this region. Within this region, amino acids 131 and 145 proved responsible for the functional difference between the two forms of AZ.
Amino Acid Sequence↗
Molecular and biochemical characterization of a novel two-component signal transduction system, amrA- amkA, involved in rifamycin SV production in Amycolatopsis mediterranei U32.
Two-component and phosphorelay signal transduction systems are the major means by which bacteria recognize and respond to a variety of environmental stimuli. Although several model systems, including sporulation in Bacillus subtilis and chemotaxis in Escherichia coli, have been extensively studied, the two-component signal transduction systems in industrially important actinomycetes are not well studied. We report the molecular and biochemical characterization of a novel two-component signal system, amrA-amkA,from the rifamycin-SV-producing Amycolatopsis mediterranei U32. The deduced sequences of amkAand amrA contain all the structural features that are highly conserved in the typical bacterial histidine kinases and response regulators, respectively. BLAST analyses showed that AmrA and AmkA displayed high similarities to AfsQ1/AfsQ2 of Streptomyces coelicolor and MtrA/MtrB of Mycobacterium tuberculosis. The amrAand amkA genes were over-expressed and the gene products were purified from E. coli. Biochemical studies showed that AmkA is able to autophosphorylate, supporting its functional assignment as a histidine kinase. That AmrA functions as the cognate response regulator for histidine kinase AmkA was demonstrated by in vitro phosphotransfer from [gamma-(32)P]ATP-labeled AmkA to AmrA. Rifamycin SV production was also decreased by 10-20% in amrAor amkA gene disruption mutants under the tested condition. Although the detailed regulatory mechanism is still unknown, this is the first report regarding the involvement of two-component signal systems in rifamycin biosynthesis in the genus Amycolatopsis.
Actinomycetales↗
Rational design of 4,5-disubstituted-5,7-dihydro-pyrrolo[2,3-d]pyrimidin-6-ones as a novel class of inhibitors of epidermal growth factor receptor (EGF-R) and Her2(p185(erbB)) tyrosine kinases.
A novel class of 4,5-disubstituted-5,7-dihydro-pyrrolo[2,3-d]pyrimidin-6-ones has been discovered as potent and selective inhibitors of the EGF-R tyrosine kinase family. These compounds selectively inhibit EGF-R kinase activity at low nanomolar concentration and tyrosine autophosphorylation in cells expressing EGF-R or Her2 (p185(erbB)). Structure-activity relationships (SARs) for this class of compounds are presented.
Drug Design↗
Xenopus actin-interacting protein 1 (XAip1) enhances cofilin fragmentation of filaments by capping filament ends.
Xenopus actin-interacting protein 1 (XAip1) is thought to promote fragmentation of actin filaments by cofilin. To examine the mechanism of XAip1, we measured polymer lengths by fluorescence microscopy and the concentration of filament ends with an elongation assay. Cofilin creates ends by severing actin filaments. XAip1 alone does not sever actin filaments or prevent annealing/redistribution of mechanically severed filaments and has no effect on the concentration of ends available for subunit addition. In the presence of XAip1, the apparent filament fragmentation by cofilin is enhanced, but XAip1 reduces rather than increases the concentration of ends capable of adding subunits. Electron microscopy with gold-labeled antibodies showed that a low concentration of XAip1 bound preferentially to one end of the filament. A high concentration of XAip1 bound along the length of the filament. In the presence of gelsolin-actin to cap filament barbed ends, XAip1 does not enhance cofilin activity. We conclude that XAip1 caps the barbed end of filaments severed by cofilin. This capping blocks annealing and depolymerization and allows more extensive severing by cofilin.
Actin Depolymerizing Factors↗
Application of LC/MS/MS in the quantitation of SU101 and SU0020 uptake by 3T3/PDGFr cells.
SU101 or leflunomide, has been studied extensively because of its anti-cancer and immunomodulating properties. The parent isoxazole compound is converted in vitro and metabolized in vivo to an open ring isomeric form, SU0020. Several pharmacological activities have been reported for the parent and metabolite compounds including inhibition of platelet-derived growth factor (PDGF)-mediated signaling for the parent compound and inhibition of de novo pyrimidine biosynthesis for the metabolite. The inhibition of PDGF-mediated signaling and the anti-tumor properties have been ascribed to the parent compound. In spite of its short plasma half-life of the parent molecule, SU101 can be administered intermittently in animal tumor models and retain efficacy. Therefore, the relationship between plasma levels of SU101 and its efficacy in tumor-implanted immuno-compromised mice is not well established. This study was conducted to assess the concentration of SU101 in 3T3/PDGFr alpha and beta cells (NIH3T3 mouse fibroblasts engineered to overexpress human PDGFr alpha or beta) to better understand the cellular levels of SU101 and SU0020. Two strains of 3T3/PDGFr cells (alpha and beta) were incubated with 1, 25, and 100 microM concentrations of SU101 for 1, 6, 24, and 48 hours. Quantitation of SU101 and SU0020 in these cell lines was achieved by a specific and sensitive liquid chromatography-tandem mass spectrometry (LC/MS/MS) method. Interestingly, in both alpha and beta cell lysates SU101 was much more concentrated than SU0020. The greater concentration of SU101 versus SU0020 that was observed may be due to the preferential partitioning of SU101 into the cells and this shows that significant levels of the parent drug can reach the pharmacological site of action for inhibition of PDGF receptors. The data suggest that the conversion of SU101 to SU0020 is much slower in these cells than in the incubation media.
3T3 Cells↗
Substitution of the autophosphorylation site Thr516 with a negatively charged residue confers constitutive activity to mouse 3-phosphoinositide-dependent protein kinase-1 in cells.
3-Phosphoinositide-dependent protein kinase-1 (PDK-1)is a serine/threonine kinase that has been found to phosphorylate and activate several members of the AGC protein kinase family including protein kinase B (Akt), p70 S6 kinase, and protein kinase Czeta. However, the mechanism(s) by which PDK-1 is regulated remains unclear. Here we show that mouse PDK-1 (mPDK-1) undergoes autophosphorylation in vitro on both serine and threonine residues. In addition, we have identified Ser(399) and Thr(516) as the major mPDK-1 autophosphorylation sites in vitro. Furthermore, we have found that these two residues, as well as Ser(244) in the activation loop, are phosphorylated in cells and demonstrated that Ser(244) is a major in vivo phosphorylation site. Abolishment of phosphorylation at Ser(244), but not at Ser(399) or Thr(516), led to a significant decrease of mPDK-1 autophosphorylation and kinase activity in vitro, indicating that autophosphorylation at Ser(399) or Thr(516) is not essential for mPDK-1 autokinase activity. However, overexpression of mPDK-1(T516E), but not of mPDK-1(S244E) or mPDK-1(S399D), in Chinese hamster ovary and HEK293 cells was sufficient to induce Akt phosphorylation at Thr(308) to a level similar to that of insulin stimulation. Furthermore, this increase in phosphorylation was independent of the Pleckstrin homology domain of Akt. Taken together, our results suggest that mPDK-1 undergoes autophosphorylation at multiple sites and that this phosphorylation may be essential for PDK-1 to interact with and phosphorylate its downstream substrates in vivo.
3-Phosphoinositide-Dependent Protein Kinases↗
NKX-3.1 interacts with prostate-derived Ets factor and regulates the activity of the PSA promoter.
The NKX-3.1 homeobox gene maps to human chromosome 8p21, a region that undergoes frequent loss of heterozygosity in prostate tumors. Loss of Nkx-3.1 function in mice leads to epithelial overgrowth. To further elucidate the molecular basis of NKX-3.1 function, a genetic screen for proteins that interact with NKX-3.1 was performed. Prostate-derived Ets factor (PDEF) was identified as a potential partner of NKX-3.1. Coimmunoprecipitation analyses demonstrated that NKX-3.1 and PDEF are physically associated in prostate epithelial cells. Cotransfection analyses demonstrated that NKX-3.1 can abolish the transcriptional activation function of PDEF on the prostate-specific antigen (PSA) promoter. These data identify PSA as a target gene for NKX-3.1 and provide new insights into the function of this candidate tumor suppressor.
Epithelial Cells↗
Study on the pharmacokinetics and relative bioavailability of irbesartan capsules in healthy volunteers.
The pharmacokinetics and relative bioavailability were studied in 18 healthy volunteers. A single oral dose of 150 mg irbesartan capsule (test) or tablet (reference) was given to each volunteer according to a randomized 2-way crossover study. The concentrations in plasma were determined by HPLC-UV method. The main parameters of irbesartan capsules were: Cmax: 1.502 +/- 0.295 micrograms/ml, tmax: 1.44 +/- 0.34 h, t 1/2: 20.21 +/- 14.71 h, AUC0-t: 11.087 +/- 3.443 micrograms/ml-1.h. The relative bioavailability of capsule to tablet was (101.4 +/- 28.9)%. The results of statistical analysis showed that two formulations were bioequivalent.
Adult↗
X-ray diagnosis of salpingian diverticulum--a report of 7 cases.
Seven cases of typical salpingian diverticulum were identified by hysterosalpinography (HSG). The differentiation diagnosis of the disease was discussed. HSG is believed to be the method of choice for the diagnosis of this disease.
Adnexal Diseases↗
Possible relationship between deficiency of interstitial cells of Cajal and colonic inertia in a patient with colon malfixation.
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Colon↗
Photocatalytic oxidative degradation of acridine orange in aqueous solution with polymeric metalloporphyrins.
In the presence of polymeric M [meso-tetra (4,4'-biphenybisulfony) phenylporphyrin] (PMTBPBSOPP, M = Co, Mn, Cu, Zn, Fe), the photocatalytic oxidative degradation of acridine orange (AO) was investigated under conditions of irradiation with high-pressure mercury lamp (HPML), iodine tungsten lamp (ITL) and natural sunlight (NSL), respectively. The results indicated that PCoTBPBSOPP had remarkable effects on photodegradation of AO under NSL irradiation. The experiments also proved that the photocatalytic degradation of AO in aqueous solutions could be enhanced when hydrogen peroxide 0.4 g/L was added. When the initial concentration of AO was 43.8 mg/L, the degradation and the decolorization rates of AO under HPML irradiation were up to 98% and 97%, respectively. A number of factors affecting photocatalytic degradation effects, such as the initial concentration of AO, light sources, pH etc., were studied in detail. The experimental results confirmed that polymeric metalloporphyrins could fully decompose AO by using artificial light source such as HPML and ITL, moreover could degrade AO rapidly under NSL in 3 h. Definitely, polymer of metalloporphyrins in the heterogeneous photocatalysis phase had a potential application
Acridine Orange↗