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Y Zhang

Publications and source records attributed to Y Zhang.

At least 145 records · Page 8Linked to original sources
PubMed2005

Electronic control of chemistry and catalysis at the surface of an individual tin oxide nanowire.

Tin oxide single nanowires configured as field effect transistors were shown to be operable and tunable alternately as gas sensors or as catalysts under a gaseous atmosphere that simulated realistic ambient conditions. The unusually large surface-to-volume ratio available with nanowires causes adsorption or desorption of donor or acceptor molecules on the nanowire's surface to greatly alter its bulk electron density at relatively small values of the gate voltage. This process can be sensitively monitored as changes in the nanowire's conductivity. The potentially radical change in carrier density can lead to significant changes in the nanowire's sensitivity as a sensor or reciprocally as a catalyst in reactions that involve charge exchange across the nanowire's surface. This leads to the prospect of tuning catalysis or other surface reactions entirely through electronic means.

Journal Article↗
PubMed2005

Comparison of blood counts in splenic, renal and mesenteric arterial and venous blood in post-pubertal rabbits.

OBJECTIVES: To compare blood counts between arterial and venous blood to and from visceral organs and indirectly look into the function of the organs. METHODS: Splenic, renal and superior mesenteric arterial and venous blood samples were obtained from the arteries and veins in 38 post-pubertal rabbits and blood profile, including complete and differential blood counts, haemoglobin concentration and haematocrit, were measured with an automatic haematology analyser. RESULTS AND CONCLUSIONS: The rabbit spleen released a large amount of leucocytes (both lymphocytes and granulocytes) into the splenic venous blood (a venous increase of 33% in total leucocyte count), and also received more leucocytes (36-58% more in terms of concentration) from the artery than the kidney or intestine. Significantly fewer red blood cells were present in the renal venous blood than in the arterial blood (a venous reduction of 5% in erythrocyte count), but it remains to be clarified why and how the reduction was induced. More than 3-4% of water might be taken into the mesenteric venous blood during microcirculation (a venous reduction of 3-4% in erythrocyte-related parameters) and a significant number of leucocytes (mainly large leucocytes) in the mesenteric blood capillaries might migrate into the surrounding intestinal tissue (a venous reduction of 13% in leucocyte count).

Animals↗
PubMed2005

Specificity and heregulin regulation of Ebp1 (ErbB3 binding protein 1) mediated repression of androgen receptor signalling.

Although ErbB receptors have been implicated in the progression of prostate cancer, little is known about proteins that may mediate their interactions with the androgen receptor (AR). Ebp1, a protein cloned via its association with the ErbB3 receptor, binds the AR and inhibits androgen-regulated transactivation of wild-type AR in COS cells. As the complement of coregulators in different cells are important for AR activity, we determined the effect of Ebp1 on AR function in prostate cancer cell lines. In addition, we examined the regulation of Ebp1 function by the ErbB3/4 ligand heregulin (HRG). In this study, we demonstrate, using several natural AR-regulated promoters, that Ebp1 repressed transcriptional activation of wild-type AR in prostate cancer cell lines. Downregulation of Ebp1 expression in LNCaP cells using siRNA resulted in activation of AR in the absence of androgen. Ebp1 associated with ErbB3 in LNCaP cells in the absence of HRG, but HRG induced the dissociation of Ebp1 from ErbB3. In contrast, HRG treatment enhanced both the association of Ebp1 with AR and also the ability of Ebp1 to repress AR transactivation. These studies suggest that Ebp1 is an AR corepressor whose biological activity can be regulated by the ErbB3 ligand, HRG.

Adenocarcinoma↗
PubMed2005

Influence of pulsed electromagnetic field with different pulse duty cycles on neurite outgrowth in PC12 rat pheochromocytoma cells.

The influence of low frequency (50 Hz repetition rate) pulsed electromagnetic field (EMF) on PC12 cell neurite outgrowth in vitro was investigated in this study. We studied the percentage of neurite bearing cells, average length of neurites, and directivity of neurite outgrowth in PC12 cells cultured for 96 h in the presence of nerve growth factor (NGF). PC12 cells were exposed in one incubator to pulsed EMF at 1.36 mT (peak value) generated by a pair of Helmholtz coils, and the control samples were placed in another identical incubator. We found that the pulse duty cycle had significant effect on neurite outgrowth. Low (10%) pulse on-time significantly inhibited the percentage of neurite bearing cells, but at the same time increased the average length of neurites, while 100% on-time (DC) had exactly the opposite effects. Furthermore, we found that neurites were prone to extend along the direction of pulsed EMF with 10% pulse on-time. Our studies show that neurite outgrowth in PC12 cells is sensitive to the pulse duty and this sensitivity was associated with NGF concentration.

Animals↗
PubMed2005

Medication refill logistics and refill adherence in HIV.

PURPOSE: Strict adherence to antiretroviral therapy is instrumental in viral suppression and treatment success. The relation between pharmacy-based factors and treatment adherence has been under-explored. We aimed to determine whether different medication refill mechanisms were associated with differences in antiretroviral refill adherence. METHODS: We conducted a retrospective cohort study of 110 HIV-infected subjects on standard antiretroviral regimens for >or=3 months cared for at the Philadelphia Veterans' Affairs Medical Center HIV clinic. The primary outcome was a pharmacy-based measure of antiretroviral refill adherence over the 3 months of treatment immediately prior to the study date. RESULTS: The group obtaining refills at the pharmacy had lower adherence [80% (interquartile range (IQR), 69-99%)] than the group obtaining refills via pill organizers dispensed by a pharmacist [99% (IQR, 97-100%), p=0.003] and the group obtaining refills via mail order [91% (IQR, 79-100%); p=0.04]. CONCLUSIONS: Mail ordering and pharmacists dispensing refills in pill organizers may each be effective strategies for improving medication adherence, although they target different barriers and differ in their degree of intensity. Each should be considered for adherence interventions in HIV and further studied in other disease and treatment settings.

Adult↗
PubMed2005

Role of macrophage apoptosis in the pathogenesis of Yersinia.

Yersinia species that are pathogenic for humans (Yersinia pestis, Yersinia pseudotuberculosis, and Yersinia enterocolitica) induce apoptosis in macrophages. Yersinia-induced apoptosis utilizes the mitochondrial pathway and is executed by activation of caspase cascades. The mechanism of Yersinia-induced apoptosis in macrophages has two essential components. One component is the innate immune response of macrophages to the pathogen, which leads to the activation of a survival response and a death response. Recognition of the bacterial cell envelope component lipopolysaccharide by Toll-like receptor 4 (TLR4) constitutes an important part of the innate immune response to the pathogen. The second essential component is YopJ, a protein secreted into Yersinia-infected macrophages via a bacterial type III secretion system, which selectively shuts down the survival pathway. In the absence of the survival pathway, the death pathway is executed, and Yersinia-infected macrophages undergo apoptosis. In this review, we introduce the basic features of Yersinia pathogenesis, summarize our current understanding of Yersinia-induced apoptosis, and discuss the role of apoptosis during Yersinia infection.

Apoptosis↗
PubMed2005

Molecular mechanisms of survival and apoptosis in RAW 264.7 macrophages under oxidative stress.

Organisms living in an aerobic environment are continuously exposed to reactive oxygen species (ROS). Apoptosis of cells can be induced by ROS and cells also develop negative feedback mechanisms to limit ROS induced cell death. In this study, RAW264.7 murine macrophage cells were treated with H(2)O(2) and cDNA microarray technique was used to produce gene expression profiles. We found that H(2)O(2) treatment caused up-regulation of stress, survival and apoptosis related genes, and down-regulation of growth and cell cycle promoting genes. Numerous genes of metabolism pathways showed special expression patterns under oxidative stress: glycolysis and lipid synthesis related genes were down-regulated whereas the genes of lipid catabolism and protein synthesis were up-regulated. We also identified several signaling molecules as ROS-responsive, including p53, Akt, NF-kappa B, ERK, JNK, p38, PKC and INF-gamma . They played important roles in the process of apoptosis or cell survival. Finally, an interactive pathway involved in cellular response to oxidative stress was proposed to provide some insight into the molecular events of apoptosis induced by ROS and the feedback mechanisms involved in cell survival.

Animals↗
PubMed2005

Effect of water-soluble fraction of cigarette smoke on human aortic endothelial cells--a proteomic approach.

Proteomic analysis is an important investigative tool used to systematically explore cellular proteins that are responsive to adverse environmental challenges. Tobacco smoking is the second major cause of death in the world. In this study, we utilized two-dimensional electrophoresis (2-DE) and mass spectrometry (MS) technologies to explore protein changes in human aortic endothelial cells (HAECs) in response to cigarette smoke extracts (CSE). Among 389 individual proteins resolved using 2-DE, 43 had a 2- to 3-fold change in levels as measured by spot intensity and 32 had more than a 3-fold change. Sixteen of the 32 spots with sufficient amount of proteins were excised for identification by performing matrix-assisted laser desorption/ionization (MALDI)-MS analysis. Using a peptide mass fingerprinting (PMF) to search the nrNCBI database, we identified all these 16 proteins, which were either increased (n = 9) or decreased (n = 7) after CSE treatment. All these proteins have known functions, however, none have been reported to be altered after CSE treatment. The findings from our study suggest that utilizing a systemic investigative tool, such as the proteomic approach using 2-DE, may play an important role in discovering novel molecular mechanisms for cigarette smoking-induced pathological changes. Further investigation following the systemic discoveries must be further examined as they may potentially lead to new therapeutic approaches to smoking-induced diseases - a health issue affecting everyone in the world.

Aorta↗
PubMed2005

The role of c-Jun in the AP-1 activation induced by naturally occurring isothiocyanates.

Despite strong evidence that isothiocyanates (ITCs) inhibit cancer development, there are also reports that some of them induce or promote carcinogenesis. The molecular basis of the latter is largely unknown. We report here that all three ITCs that caused urinary bladder cancer in rats, including allyl ITC, benzyl ITC, and phenethyl ITC, increased the transactivation of activator protein 1 (AP-1) and AP-1 DNA binding in human bladder cancer UM-UC-3 cells. Amongst all Fos and Jun family members examined, only were the levels of c-Jun and Fra-2 consistently elevated by the ITCs. However, whereas c-Jun was identified as the predominant component in the AP-1 DNA binding complex, Fra-2 was not detected, suggesting that c-Jun may be mainly responsible for ITC-induced AP-1 activation. c-Jun was also induced by the ITCs in other bladder cancer cell lines (both human and rat) and by their N-acetylcysteine derivatives--their main urinary metabolites. c-Jun induction by the ITCs appears to involve both transcriptional activation and protein phosphorylation; the latter resulted from activation of c-Jun N-terminal kinase by the ITCs. Because c-Jun has been implicated in cancer development, including human bladder cancer, our data suggest that c-Jun activation may play an important role in ITC-induced bladder carcinogenesis.

Anticarcinogenic Agents↗
PubMed2005

Magnesium and bupivacaine-induced convulsions in awake pregnant rats.

BACKGROUND: Magnesium sulfate (MgSO(4)) is widely used for the treatment and prevention of convulsions associated with preeclampsia. The aim of this study was to determine whether it alters the dose of bupivacaine required to produce convulsions in awake pregnant rats. METHOD: Twelve pregnant rats were pretreated with an intravenous infusion of either MgSO(4) or saline. Following 2 h of the pretreatment, bupivacaine was concomitantly infused in all animals until the onset of convulsions. Mean arterial pressure (MAP) and heart rate (HR) were monitored throughout. Serial arterial samples were obtained during the infusion. At the onset of convulsions, fetuses were delivered and maternal and fetal blood, as well as various tissue samples, were obtained. All samples were assayed for bupivacaine and magnesium concentrations. RESULTS: Maternal MAP and HR decreased significantly shortly after the initiation of MgSO(4), while saline did not affect these measurements. Baseline concentrations of magnesium in plasma were similar in both MgSO(4) and saline groups; magnesium increased significantly during the infusion of MgSO(4). The dose (mean+/-SD) of bupivacaine required to produce convulsions in the animals receiving MgSO(4) was significantly larger (10.2+/-1.9 mg/kg) than that in the saline group (5.9+/-1.0 mg/kg) (P<0.05). As a consequence, bupivacaine concentrations in the brain and liver at the onset of convulsions were greater in animals receiving MgSO(4) (16.0+/-8.4 and 18.2+/-4.3 microg/g wet weight, respectively) than in those given saline (12.1+/-2.2 and 9.9+/-2.0 microg/g wet weight, respectively). Fetal bupivacaine concentrations at the onset of convulsions in the MgSO(4) group were also higher than those in saline group. However, the rate of placental transfer of this drug was similar between MgSO(4) and saline animals. CONCLUSION: This study demonstrates that the clinically used concentration of magnesium sulfate increased the threshold of bupivacaine-induced convulsions in awake rats.

Anesthetics, Local↗
PubMed2005

A pilot study of fatty acid metabolism in oral squamous cell carcinoma.

This study was undertaken to determine the characteristics of fatty acid synthesis in squamous carcinoma cells and to assess the possibility of exploiting this synthesis pathway in anticancer therapy. Incorporation of [(3)H]acetate into total lipids of the TCA-83 squamous carcinoma cell line and normal gingival fibroblasts was measured. The effects of cerulenin, a specific, potent, noncompetitive inhibitor of fatty acid synthase (FAS), on growth of TCA-83 cells and normal gingival fibroblasts was determined by the MTT method, and the effect of cerulenin on apoptosis was determined by electrophoresis of cellular DNA. Incorporation of [(3)H]acetate into total lipids was significantly higher in TCA-83 cells (68 +/- 12.7 cpm per 2 x 10(5) cells) than in normal gingival fibroblasts (13 +/- 4.2 cpm per 2 x 10(5) cells; P = 0.011). Cerulenin inhibited TCA-83 cell growth in a dose-dependent manner, even at 2.5 microg/ml, a concentration at which normal gingival fibroblasts were not inhibited. After exposure to cerulenin, TCA-83 cells showed typical apoptotic DNA ladders. These results indicate that cerulenin exerts selective cytotoxic effects on squamous carcinoma cells and can induce their apoptosis. These findings suggest that targeting of fatty acid synthesis may be useful in the treatment of squamous cell carcinomas.

Apoptosis↗
PubMed2005

alpha2-adrenoceptors inhibit the intracellular Ca2+ response to electrical stimulation in normal and injured sensory neurons, with increased inhibition of calcitonin gene-related peptide expressing neurons after injury.

Nerve injury resulting in chronic pain is associated with novel excitatory effects of norepinephrine on injured peripheral nerve terminals and their cell bodies, due to actions on alpha2-adrenoceptors. Paradoxically, alpha2-adrenoceptor agonists administered near peripheral terminals or their cell bodies results in analgesia, not pain. This study tested, using intracellular Ca2+ response to stimulation, the effects of alpha2-adrenoceptor agonists on injured sensory neurons and classified their neuronal phenotype. Dorsal root ganglion cells from normal and spinal nerve-ligated rats were dissociated and activated twice with electrical field stimulation, while measuring Fura-2 fluorescence. Cells were perfused between stimulations with vehicle or alpha2-adrenoceptor agonists alone or with antagonists. Cells were considered inhibited if the ratio of their peak Ca2+ response to the second stimulus divided by the first was less than the 2.5th percentile for vehicle controls. alpha2-, But not alpha1-adrenoceptor agonists inhibited the Ca2+ response in a concentration related fashion, and this inhibition was blocked by alpha2-adrenoceptor antagonists. Clonidine inhibited a similar percentage of cells in the normal and spinal nerve-ligated group. In both groups, the large majority of clonidine-inhibited cells stained for isolectin B4. Spinal nerve ligation resulted in a 4-10-fold increase in the percentage of clonidine inhibited cells which immunostained for calcitonin gene-related peptide. These data are consistent with the known inhibition of Ca2+ currents by alpha2-adrenoceptors and suggest that, at the level of intracellular Ca2+, the key determinant of neurotransmitter release, alpha2-adrenoceptors are inhibitory after nerve injury, not excitatory. There is a shift in phenotype of sensory neurons which are inhibited by clonidine after nerve injury, which may explain clonidine's increased potency in the treatment of neuropathic compared with acute pain.

Animals↗
PubMed2005

Increase of delayed rectifier potassium currents in large aspiny neurons in the neostriatum following transient forebrain ischemia.

Large aspiny (LA) neurons in the neostriatum are resistant to cerebral ischemia whereas spiny neurons are highly vulnerable to the same insult. Excitotoxicity has been implicated as the major cause of neuronal damage after ischemia. Voltage-dependent potassium currents play important roles in controlling neuronal excitability and therefore influence the ischemic outcome. To reveal the ionic mechanisms underlying the ischemia-resistance, the delayed rectifier potassium currents (Ik) in LA neurons were studied before and at different intervals after transient forebrain ischemia using brain slices and acute dissociation preparations. The current density of Ik increased significantly 24 h after ischemia and returned to control levels 72 h following reperfusion. Among currents contributing to Ik, the margatoxin-sensitive currents increased 24 h after ischemia while the KCNQ/M current remained unchanged after ischemia. Activation of protein kinase A (PKA) down-regulated Ik in both control and ischemic LA neurons, whereas inhibition of PKA only up-regulated Ik and margatoxin-sensitive currents 72 h after ischemia, indicating an active PKA regulation on Ik at this time. Protein tyrosine kinases had a tonic inhibition on Ik to a similar extent before and after ischemia. Compared with that of control neurons, the spike width was significantly shortened 24 h after ischemia due to facilitated repolarization, which could be reversed by blocking margatoxin-sensitive currents. The increase of Ik in LA neurons might be one of the protective mechanisms against ischemic insult.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2005

Sildenafil citrate treatment for erectile dysfunction after kidney transplantation.

OBJECTIVE: Our goal was to analyze the morbidity of organic erectile dysfunction (ED) in kidney-transplant patients and to evaluate the efficacy and reliability of sildenafil citrate treatment. METHOD: Sixty-five ED patients with normal graft function for 3 to 12 months after kidney transplantation were involved in our study. Erectile dysfunction was diagnosed in all the patients by the International Index of Erectile Dysfunction (IIEF). Among them, 10 patients were in light degree; 32 patients in moderate degree, and 23 patients in severe degree according to IIEF score. All of the patients underwent medical history, physical and chemical examinations. In each patient, the IIEF score, blood urea nitrogen, creatinine, and trough concentrations of cyclosporine were compared before and after taking sildenafil citrate at an initial dose of 50 mg every night. RESULTS: Twenty-six patients without ED before transplantation suffered ED after the operation, and 32 patients with ED before transplantation noticed worsening. Taking sildenafil citrate was effective in 53 patients (81.54%). There were no statistical differences in blood urea nitrogen, creatinine, or trough concentrations of cyclosporine in patients before and after sildenafil treatment. CONCLUSIONS: The morbidity of organic erectile dysfunction increased after transplantation. Sildenafil citrate treatment for ED in kidney-transplant patients was effective and safe. Graft function and trough concentrations of cyclosporine were not affected by sildenafil citrate.

Blood Urea Nitrogen↗
PubMed2005

Clinical study of Lipo PGE1-inhibiting platelet activation in acute rejection after kidney transplantation.

To observe the efficacy of the platelet activation inhibitor Lipo PGE1 therapy in the recovery of graft function after an acute rejection episode after kidney transplantation. Forty patients with acute rejection after kidney transplantation were randomly assigned into groups treated with or without Lipo PGE1. The expression levels of CD61, CD63, and PAC-1 on platelet surfaces were assayed by flow cytometry. The recovery time for graft function and 1-year patient and graft survival rates were recorded. Compared with controls, the expression levels of CD61, CD63, and PAC-1 were lower among acute rejection patients who received Lipo PGE1 therapy. The recovery time for graft function was shorter and the 1-year patient and graft survival rates higher. Lipo PGE1 therapy in patients with acute rejection episodes may inhibit platelet activation thereby benefiting graft functional recovery. The 1-year survival rates of patients and grafts might be increased if the expression levels of CD61, CD63, and PAC-1 on the platelet surfaces was decreased by Lipo PGE1 therapy.

Adult↗