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Biomedical subjects

Z Zhang

Publications and source records attributed to Z Zhang.

At least 73 records · Page 4Linked to original sources
PubMed2005

Investigation of the kinetics of a TiO2 photoelectrocatalytic reaction involving charge transfer and recombination through surface states by electrochemical impedance spectroscopy.

In this paper, the electrochemical impedance spectroscopy (EIS) mathematical model of TiO2 photoelectrocatalytic (PEC) reactions involving charge transfer and recombination through surface states was developed. The model was used to study the kinetics of photoelectrocatalytic decomposition of salicylic acid. The model simulation results show that the appearance of two distinguishable semicircles in the EIS response depends on the charging of surface state and light intensity. The experimental results demonstrated that similar phenomena to the theoretical simulation results. The model provides a way to obtain the rate constants for the photoelectrochemical reactions of surface states mediating charge transfer and recombination. The applied potential changes not only the recombination rate constant but also the charge-transfer rate constant. Moreover, the experimental EIS results here and those previous published on PEC degradation reactions can be explained by the present model satisfactorily. The relevance of surface states was discussed briefly. The results demonstrated that EIS is a powerful tool for studying the kinetics of PEC decomposition of organic pollutants on TiO2 electrodes.

Journal Article↗
PubMed2005

In vitro imaging of single living human umbilical vein endothelial cells with a clinical 3.0-T MRI scanner.

Iron oxide-labelled, single, living human umbilical vein endothelial cells (HUVECs) were imaged over time in vitro using a clinical 3.0-T magnetic resonance (MR) microscopy system. Labelling efficiency, toxicity, cell viability, proliferation and differentiation were assessed using flow cytometry, magnetic cell sorting and a phenanthroline assay. MR images were compared with normal light and fluorescence microscopy. Efficient uptake of iron oxide into HUVECs was shown, although with higher label uptake dose-dependent cytotoxic effects were observed, affecting cell viability. For MR imaging, a T2* weighted three-dimensional protocol was used with in-plane resolution of 39 x 48 microm2 and 100-microm slices with a scan time of 13 min. MRI could detect living cells in standard culture dishes at single-cell resolution, although label loss was observed that corresponded with the intracellular iron measurements. MR microscopy using iron oxide labels is a promising tool for studying HUVEC migration and cell biology in vitro and in vivo, but possible toxic effects of label uptake and loss of label over time should be taken into account.

Cell Proliferation↗
PubMed2005

Effects of 5-HT1A and 5-HT2A receptor stimulation on temporal differentiation performance in the fixed-interval peak procedure.

We examined the effects of the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) and 5-HT(2A/2C) receptor agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) on performance on the fixed-interval peak procedure, and the sensitivity of these effects to 5-HT1A and 5-HT2A receptor antagonists (N-[2-(4-[2-methoxyphenyl]-1-piperazinyl]ethyl]-N-2-pyridinylcyclohexanecarboxamide [WAY-100635] and ketanserin). Rats were trained to press a lever for food reinforcement in 50 min sessions consisting of 32 trials in which the lever was continuously available, separated by 10 s inter-trial intervals. In 16 trials, reinforcement was delivered following the first response after 30 s had elapsed since trial onset (fixed-interval 30 s). In 16 randomly interposed (peak/probe) trials, reinforcement was omitted, and the lever remained in the operant chamber for 120 s. Response rate in probe trials was plotted against time from trial onset. Time to peak response rate (t(peak)) and the Weber fraction were derived from modified Gaussian curves fitted to each rat's data. 8-OH-DPAT (0.05 mg kg(-1)) reduced t(peak) and increased the Weber fraction; the effect on t(peak) was antagonized by WAY-100635 (0.1 mg kg(-1)). DOI (0.25 mg kg(-1)) also reduced t(peak) and increased the Weber fraction; the reduction of t(peak) was antagonized by ketanserin (2 mg kg(-1)). Stimulation of 5-HT1A and 5-HT2A receptors alters temporal differentiation in qualitatively similar ways.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2005

Effects of operating conditions on the adhesive strength of Pseudomonas fluorescens biofilms in tubes.

Understanding the mechanical properties of biofilms, especially the force required to disrupt them and remove them from substrata is very important to development of antibiofouling strategies. In this work, a novel micromanipulation technique with a specially designed T-shaped probe has been developed to serve as an experimental means to measure directly the adhesive strength of biofouling deposits on the surface of a glass test stud. The basic principle of this novel technique is to pull away a whole biofilm accumulated on the surface of a glass test stud with T-shaped probe, and to measure simultaneously the force imposed on the biofilm. The adhesive strength between the biofilms and the surface to which they are attached, is defined as the work per unit area required to remove the biofilms from the surface. The biofouling experiments were performed on an elaborate design of a simulated heat exchanger system. A monoculture of Pseudomonas fluorescens was chosen as the fouling microorganism for the laboratory studies. Results indicate that the adhesive strength of the biofilm was affected by the conditions of operation, such as biofilm age, nutrient concentration, suspended cell concentration, pH, surface roughness of the substratum and fluid velocity. As noted, the effect of fluid velocity on the biofilm adhesive strength seemed to overwhelm other factors. At the same operating conditions, the biofilm adhesive strength increased as the fluid velocity increased within the range of 0.6-1.6m/s. In addition, the flow-related biofilm structures were observed that biofilms generally grew as a more compact pattern at the higher fluid velocity. Apparently, the fluid velocity can affect the biofilm structure, which in turn determines the biofilm adhesive strength. The knowledge of the biofilm adhesive strength with associated influences of the operating conditions may be used to define better cleaning procedures.

Bacterial Adhesion↗
PubMed2005

The effect of the amount of binder liquid on the granulation mechanisms and structure of microcrystalline cellulose granules prepared by high shear granulation.

The structure of granules changes during the high shear granulation process. The purpose of this research was to investigate the effect of the amount of binder liquid on the structure of the granules and the structural changes which occur during the granulation process, using microcrystalline cellulose (MCC) and water as the model system. The structure is the result of the granulation mechanism; therefore, conclusions can be drawn about the latter by studying the former. X-ray microtomography and scanning electron microscopy (SEM) were applied in order to visualise the densification process of granules, which were first freeze dried in order to preserve their structure. Variations in their porosity were quantified by applying image analysis to the tomography results. In order to link the granule mechanical properties to their structural differences, a micromanipulation technique was used to measure granule resistance to deformation. MCC granules granulated with 100% (w/w) water showed increased densification with time, as expected; detailed examination showed that densification is more pronounced in the core of the granule; whereas the outer part remained more porous. Increased densification reduces deformability, so that granules become more resistant to breakage. The lower deformability of the densified granules in the final stages of granulation might result in establishment of equilibrium between attrition and growth, without substantial gross breakage. On the other hand, when more water was used (125%, w/w), densification was hardly observed; the porosity of the granule core was still high even after prolonged granulation times. This may be explained by the fact that higher water content increases the ease of deformation of granules. This increased deformability led to significant granule breakage even during the final phases of the granulation process. Therefore, for these granules a final equilibrium between breakage and coalescence might be established. This also explains why more granules produced with 125% granulation liquid were composed of fragments of irregular shape. Our results establish the link between the granulation behaviour of MCC in the latter stages and the material structure of these granules, which is determined by their liquid content. The process conditions (amount of liquid) to be chosen depend largely on the final purpose for which the granular material is produced.

Cellulose↗
PubMed2005

Persistent shedding of viable SARS-CoV in urine and stool of SARS patients during the convalescent phase.

In order to further the present knowledge of the emerging severe acute respiratory syndrome-associated coronavirus (SARS-CoV), 486 different specimens from 54 patients with a clinical diagnosis of SARS were investigated for the presence of viral RNA, and 314 plasma specimens of 73 patients were examined for IgM and IgG antibodies specific against SARS-CoV using an indirect ELISA. Viral RNA was detectable in 28 of the 54 patients tested. Cumulative data showed that 67 of the 73 SARS patients demonstrated seroconversion by week 5 of illness. In contrast, only 1 of 278 healthy subjects enrolled in the study was found to be positive for the IgG antibody. Coexistence of viral RNA in plasma and specific antibodies was simultaneously observed over three consecutive weeks in two critical cases. In three convalescent patients in particular, cultivable SARS-CoV was detected in stool or urine specimens for longer than 4 weeks (29-36 days). These findings suggest that SARS-CoV may remain viable in the excretions of convalescent patients.

Adult↗
PubMed2005

Down-regulation of Bcl-2 enhances estrogen apoptotic action in long-term estradiol-depleted ER(+) breast cancer cells.

Postmenopausal women with estrogen receptor positive (ER(+)) breast cancer frequently respond paradoxically to estrogen administration with tumor regression. Using both LTED and E8CASS cells derived from MCF-7 breast cancer cells by long-term estrogen-deprivation, we previously reported that 17beta -estradiol (estradiol) is a powerful, pro-apoptotic hormone which kills the cancer cells through activation of the Fas/FasL death receptor pathway. We postulated that the mitochondrial interactive protein Bcl-2 might play a role in the regulation of estradiol-induced apoptosis in both LTED and E8CASS cells. In this study, we assessed estradiol effects on cell growth, proliferation and apoptosis. Additionally we investigated the effect of estradiol on caspase activation, NF-KB and Bcl-2 expression. The functional role of Bcl-2 in estradiol-induced apoptosis was further studied by knockdown or decrease of Bcl-2 with siRNA. Our results show that estradiol significantly inhibited cell growth primarily through a pro-apoptotic action involving caspase-7 and 9 activations (p < 0.01). Basal Bcl-2 and NF-KB levels were greatly elevated and estradiol decreased NF-KB, but not Bcl-2 expression. Knockdown of Bcl-2 expression with siRNA decreased the levels of this protein by 9 fold (p < 0.01). This reduction markedly sensitized both LTED and E8CASS cells to the pro-apoptotic action of estradiol, leading to a synergistic induction of apoptosis and a concomitant reduction in cell number (p < 0.01). Therefore, down-regulation of Bcl-2 synergistically enhanced estradiol-induced apoptosis in ER(+) postmenopausal breast cancer cells.

Apoptosis↗
PubMed2005

The relation between granule size, granule stickiness, and torque in the high-shear granulation process.

PURPOSE: To investigate the background of the observed relationship between measured torque and granule size in high-shear granulation processes. METHODS: Torque was measured during the granulation process; the behavior of individual wet granules during compaction was investigated using micromanipulation. Surface properties of wet granules were manipulated by coating them with talc. RESULTS: The torque-granule size relationship could not be explained by the rise in mass of the individual granules; it occurs rather through an increase in stickiness of the granules when the moisture content is increased. Obviously, the increased stickiness that causes the granules to grow also increases the torque. Increased stickiness was shown to be the result of an increased deformability of the granules at higher moisture contents, in combination with a change in surface properties. The elastic-plastic behavior (ratio of elastic to plastic deformation) was found to change at increasing moisture contents. CONCLUSIONS: Our results imply that changes in the stickiness of the granular material that may be caused by changes in composition shift the torque-size relationship. This may be of particular importance when, for example, granulation results from placebo batches are used to predict the granule size of drug-containing batches.

Particle Size↗
PubMed2005

Adaptive hypersensitivity to estrogen: mechanisms and clinical relevance to aromatase inhibitor therapy in breast cancer treatment.

Breast tumors in women can adapt to endocrine deprivation therapy by developing hypersensitivity to estradiol. For this reason, aromatase inhibitors can be effective in women relapsing after treatment with tamoxifen or following oophorectomy. To understand the mechanisms responsible, we examined estrogenic stimulation of cell proliferation in a model system and provided in vitro and in vivo evidence that long-term estradiol deprivation (LTED) causes "adaptive hypersensitivity". The primary mechanisms responsible involve up-regulation of ER alpha as well as the MAP kinase, PI-3 kinase, and mTOR growth factor pathways. ER alpha is 4-10-fold up-regulated and co-opts a classical growth factor pathway using Shc, Grb2, and Sos. This induces rapid non-genomic effects which are enhanced in LTED cells. Estradiol binds to cell membrane associated ER alpha, physically associates with the adaptor protein Shc, and induces its phosphorylation. In turn, Shc binds Grb2 and Sos which result in the rapid activation of MAP kinase. These non-genomic effects of estradiol produce biologic effects as evidenced by Elk activation and by morphologic changes in cell membranes. Additional effects include activation of PI-3 kinase and mTOR pathways through estradiol induced binding of ER alpha to the IGF-1 and EGF receptors. Further proof of the non-genomic effects of estradiol involved use of "designer" cells which selectively express ER alpha in nucleus, cytosol, and cell membrane. We have used a new downstream inhibitor of these pathways, farnesyl-thio-salicylic acid (FTS), to block proliferation in hypersensitive cells as a model for a potentially effective strategy for treatment of patients.

Animals↗
PubMed2005

Two genes encoding immune-regulatory molecules (LAG3 and IL7R) confer susceptibility to multiple sclerosis.

Multiple sclerosis (MS) is a T-cell-mediated disease of the central nervous system, characterized by damage to myelin and axons, resulting in progressive neurological disability. Genes may influence susceptibility to MS, but results of association studies are inconsistent, aside from the identification of HLA class II haplotypes. Whole-genome linkage screens in MS have both confirmed the importance of the HLA region and uncovered non-HLA loci that may harbor susceptibility genes. In this two-stage analysis, we determined genotypes, in up to 672 MS patients and 672 controls, for 123 single-nucleotide polymorphisms (SNPs) in 66 genes. Genes were chosen based on their chromosomal positions or biological functions. In stage one, 22 genes contained at least one SNP for which the carriage rate for one allele differed significantly (P<0.08) between patients and controls. After additional genotyping in stage two, two genes--each containing at least three significantly (P<0.05) associated SNPs--conferred susceptibility to MS: LAG3 on chromosome 12p13, and IL7R on 5p13. LAG3 inhibits activated T cells, while IL7R is necessary for the maturation of T and B cells. These results imply that germline allelic variation in genes involved in immune homeostasis--and, by extension, derangement of immune homeostasis--influence the risk of MS.

Antigens, CD↗
PubMed2005

Subtractive chromatography for purification and recovery of nano-bioproducts.

A novel polymer-coated adsorbent (subtractive adsorbent) has been manufactured and evaluated for the recovery of nanoparticle bioproducts. The core principle was to coat inert macroporous polymers (e.g. agarose) upon adsorbent beads of varied ligands. Here BSA nanoparticles, with an average nanoparticle diameter 95 nm, were fabricated and selected as feedstock for the demonstration of the principle. The adsorption of a mixture of fluorescently labelled BSA solution and BSA nanoparticles was investigated in a batch binding experiment upon polymer-coated Streamline DEAE and visualised by laser scanning confocal microscopy. The mechanistic design of such adsorbents and their basic application for the recovery of target nano-bioproducts from complex feedstock is strongly indicated.

Adsorption↗
PubMed2005

Pigpen is a cellular binding protein of therapeutic oligonucleotides.

BACKGROUND: Understanding the mechanism of oligonucleotide (ON) uptake and cellular distribution is important for rational design of ON-based therapeutic strategies. The aim of this study was to investigate the possible relationship between cellular distribution of ON and the protein pigpen. METHODS: In vitro interaction of ON with the protein pigpen was detected using mass spectrometry. Cellular distribution of pigpen and co-localization of pigpen with ON was studied by fluorescence microscopy in endothelial YPEN and microglial N9 cells. RESULTS: Pigpen had similar distribution patterns in endothelial YPEN and microglial N9 cells. Pigpen was localized to the cytoplasm of both cell types. In addition, pigpen distributed to nuclei, excluding the nucleoli, and concentrated along the nuclear membrane and plasma membrane. Intensely stained foci were only observed in the nucleus and cytoplasm of YPEN cells. Although co-localization of pigpen with phosphorothioate (PS) ON was not observed for the first hour after ON uptake, co-localization was observed 8 h later. DISCUSSION: These data suggest that pigpen binds therapeutic ON and thus might contribute to ON cellular distribution.

Animals↗
PubMed2005

Effects of quipazine and m-chlorophenylbiguanide (m-CPBG) on the discrimination of durations: evidence for the involvement of 5-HT2A but not 5-HT3 receptors.

The ability of rats to discriminate durations of exteroceptive stimuli is disrupted by 5-HT(1A) receptor agonists; it is not known whether temporal discrimination is sensitive to stimulation of other 5-HT receptor subtypes. We examined the effect of quipazine, a 5-HT receptor agonist with nanomolar affinity for 5-HT(3) receptors and micromolar affinity for 5-HT(2A) receptors, and m-chlorophenylbiguanide (m-CPBG), a selective 5-HT(3) receptor agonist, on temporal discrimination. Twenty-four rats pressed levers for sucrose reinforcement under a discrete-trials psychophysical procedure. In each 50-s trial, a light was presented for t s, following which two levers (A and B) were presented. A response on A was reinforced if t < 25 s, and a response on B if t > 25 s. Logistic psychometric functions were fitted to the data, and timing parameters estimated (T(50): value of t corresponding to %B = 50; Weber fraction: [T(75)-T(25)]/2T(50), where T(75) and T(25) are values of t corresponding to %B = 75 and %B = 25). Quipazine (0.5-2 mg/kg) displaced the psychometric curve to the right and reduced its slope, reflected in increases in T50 and the Weber fraction; m-CPBG (2.5-10 mg/kg) had no effect. The effects of quipazine were reversed by the 5-HT(2A) receptor antagonist ketanserin (2 mg/kg) but not by the 5-HT3 receptor antagonist topanyl 3,5-dichlorobenzoate (MDL-72222) (1 mg/kg). The results indicate that 5-HT(2A) but not 5-HT(3) receptor stimulation disrupts temporal discrimination.

Animals↗
PubMed2005

Acquired but reversible loss of erythrocyte complement receptor 1 (CR1, CD35) and its longitudinal alteration in patients with severe acute respiratory syndrome.

This longitudinal study investigates the change of erythrocyte complement receptor (E-CR1) expression in patients with severe acute respiratory syndrome (SARS). Circulating E-CR1 expression was semiquantified by flow cytometric analyses in 54 SARS patients and in 212 healthy individuals as a control. Since E-CR1 expression is influenced by the genetic polymorphisms in the CR1 gene, a major genetic polymorphism located within intron 27 of the CR1 gene was simultaneously analysed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). The results showed that the expression level of E-CR1 (referred to as net fluorescence intensity values, NFI) was statistically correlated with the relevant genetic genotypes among the Chinese population including the healthy individuals (NFI: 5.14 +/- 0.82, 3.57 +/- 0.66 and 2.67 +/- 0.32 for HH, HL and LL genotypes, respectively) and SARS patients (NFI: 3.52 +/- 0.91 and 2.63 +/- 0.70 for HH and HL genotypes, respectively). Interestingly, the expression density of E-CR1 was found to fall significantly during the initiation and progressive phases (weeks 1 and 2 after the disease onset) and gradually returned close to normal through their whole convalescent phase (beginning from weeks 2 or 3 to weeks 7 or 8) in SARS patients irrespective CR1 genotype. In conclusion, our findings, at least, suggest that E-CR1 is likely involved in immune pathogenesis of SARS disease.

Adolescent↗
PubMed2005

Production of recombinant protein Pap31 and its application for the diagnosis of Bartonella bacilliformis infection.

Tropical bartonellosis is a highly fatal epidemic and endemic infectious disease that occurs throughout the communities of the Andes Mountains in South America. The disease is caused by the facultative intracellular bacteria, Bartonella bacilliformis. The emergence of bartonellosis in new geographic areas and an increase in the number of reported cases suggest the need for a rapid test for epidemiologic study and investigation of the disease burden. The objective of this research is to develop a rapid serologic diagnostic test using recombinant antigens to overcome the limitations of the current standard IFA technique for laboratory diagnosis. Western blot analysis with patient sera of whole cell lysate separated on a 2D gel identified Pap31 as a dominant antigen. PCR primers were designed according to the sequence of ATCC strain 35685 to amplify the gene coding for Pap31 from a local isolate (HOSP 800-09, Peru). The amplicon was subsequently cloned into pET24a, adding the T7 tag, and expressed in E. coli. Patient sera with different IFA titers confirmed the diagnostic band of 31 kDa on a Western blot of SDS-PAGE. The performance of affinity-purified recombinant Pap31 (rPap31) was also evaluated in an ELISA format with 137 patient sera of known IFA titers. The range of ELISA reading from positive sera did not overlap with the range of those from negative sera, suggesting the potential application of rPap31 in both ELISA for high throughput regional hospital settings and in the construction of handheld rapid tests for rural clinical sites.

Antigens, Bacterial↗
PubMed2005

Long-term estradiol deprivation in breast cancer cells up-regulates growth factor signaling and enhances estrogen sensitivity.

Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby long-term estradiol deprivation (LTED) causes cells to adapt and develop hypersensitivity to estradiol. Several mechanisms are associated with this response, including up-regulation of estrogen receptor-alpha (ERalpha) and the MAP kinase, phosphoinositol 3 kinase (PI3-K) and mammalian target of rapamycin (mTOR) growth factor pathways. ERalpha is four- to tenfold up-regulated and co-opts a classical growth factor pathway using Shc, Grb-2 and Sos. This induces rapid non-genomic effects which are enhanced in LTED cells. The molecules involved in the non-genomic signaling process have been identified. Estradiol binds to cell membrane-associated ERalpha, which physically associates with the adaptor protein Shc, and induces its phosphorylation. In turn, Shc binds Grb-2 and Sos, which result in the rapid activation of MAP kinase. These non-genomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membranes. Additional effects include activation of the PI3-K and mTOR pathways through estradiol-induced binding of ERalpha to the IGF-I and epidermal growth factor receptors. A major question is how ERalpha locates in the plasma membrane since it does not contain an inherent membrane localization signal. We have provided evidence that the IGF-I receptor serves as an anchor for ERalpha in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, Shc and the IGF-I receptor itself. Shc, after binding to ERalpha, serves as the 'bus' which carries ERalpha to Shc-binding sites on the activated IGF-I receptors. Use of small inhibitor (si) RNA methodology to knockdown Shc allows the conclusion that Shc is needed for ERalpha to localize in the plasma membrane. In order to abrogate growth factor-induced hypersensitivity, we have utilized a drug, farnesylthiosalicylic acid, which blocks the binding of GTP-Ras to its membrane acceptor protein, galectin 1, and reduces the activation of MAP kinase. We have also shown that this drug is a potent inhibitor of mTOR as an additional mechanism of inhibition of cell proliferation. The concept of 'adaptive hypersensitivity' and the mechanisms responsible for this phenomenon have important clinical implications. The efficacy of aromatase inhibitors in patients relapsing on tamoxifen could be explained by this mechanism and inhibitors of growth factor pathways should reverse the hypersensitivity phenomenon and result in prolongation of the efficacy of hormonal therapy for breast cancer.

Adaptor Proteins, Signal Transducing↗