Biomedical subjects

Yu Yang

Publications and source records attributed to Yu Yang.

At least 73 records · Page 4Linked to original sources

PubMed2004

Self-assembled electrooptic thin films with remarkably blue-shifted optical absorption based on an X-shaped chromophore.

An "X-shaped" two-dimensional electrooptic (EO) chromophore with extended orthogonal conjugation was designed and synthesized. Self-assembled thin films of this chromophore were fabricated via layer-by-layer chemisorptive siloxane-based self-assembly. The films exhibit a dramatically blue-shifted optical maximum (325 nm) while maintaining a large EO response (chi33(2) approximately 232 pm/V at 1064 nm; r33 approximately 43 pm/V at 1550 nm).

Journal Article↗

PubMed2004

Cerebral vasculitis and intracerebral hemorrhage in Henoch-Schönlein purpura treated with plasmapheresis.

Severe neurological complications in Henoch-Schonlein purpura (HSP) are rare. We report a 13-year-old girl with HSP receiving oral steroid therapy for HSP nephritis who presented with acute onset of headache, confusion, and loss of bilateral vision. However, immediate cranial computed tomography showed merely a small intracranial hematoma in the left occipital area, which was not consistent with her clinical manifestations. The subsequent magnetic resonance imaging of the brain demonstrated bilateral, multifocal abnormalities with features consistent with cerebral vasculitis. Therapeutic plasmapheresis was performed immediately and there was rapid clinical improvement. In conclusion, we propose that plasmapheresis is a reliable and effective therapy and may be considered as the first-line treatment in this critical condition to prevent massive intracerebral hemorrhagic complication of this immune complex-mediated cerebral vasculitis leading to irreversible neurological sequelae or mortality.

Adolescent↗

PubMed2004

Altered regulation of Src upon cell detachment protects human lung adenocarcinoma cells from anoikis.

Src plays an important role in cell proliferation, differentiation, adhesion, and migration. Altered Src activity has been strongly implicated in the development, growth, progression, and metastasis of human cancers. We have analysed the change and regulation of Src upon cell detachment in anoikis-resistant human lung adenocarcinoma cells and compared with that of relatively normal and anoikis-sensitive epithelial cells. We found that Src activity was increased in the anoikis-resistant lung tumor cells when they were detached and cultured in suspension. The detachment-induced Src activation in the tumor cells compensates for the loss of cell survival signals caused by disruption of cell--matrix interactions and contributes to anoikis resistance of the tumor cells. Pyk2, rather than PI 3K/Akt or Erk, appears to be the key downstream effecter of Src in mediating the cell survival signals. The increased Src activity is mainly due to the phosphorylation of Tyr-419, rather than the dephosphorylation of Tyr-530 of Src protein. PDGFR, not FAK or EGFR, appears to be the upstream protein tyrosine kinase responsible for the detachment-induced Src activation in the lung tumor cells. The increased Src activity upon cell detachment may contribute to the metastasis potential of malignant tumors.

Adenocarcinoma↗

PubMed2004

Sodium 4-phenylbutyrate induces apoptosis of human lung carcinoma cells through activating JNK pathway.

Sodium 4-phenylbutyrate (PB) has been used in the therapy of urea cycle defects for many years. Recently, it has been shown to cause cellular differentiation, growth arrest, and apoptosis in certain malignancies. We have analyzed the effects of PB on human lung carcinoma cells. PB has distinct patterns of effects on different lung carcinoma cells, inducing apoptosis in NCI-H460 and NCI-H1792 cells, causing G1 arrest in A549 and SK-LU-1 cells, but having no effect on a non-transformed bronchial epithelial cell line HBE4-E6/E7. We investigated the role of MAP kinase family members, extracellular signal-regulated kinase (ERK), JNK, and p38 mitogen-activated protein kinase (MAPK), as well as other important cell survival signaling molecules in PB-induced apoptosis. We observed activation of JNK and ERK by PB in the lung cancer cells. JNK was activated only in the two apoptotic cells, whereas ERK was activated in both the apoptotic and the growth-arrested cells, demonstrating a correlation between apoptosis and activation of JNK in response to PB. Both JNK inhibitor and JNK RNA interference (RNAi) inhibited PB-induced apoptosis, whereas MEK inhibitor did not, supporting that apoptosis induced by PB is through activation of JNK. De novo protein synthesis is required for the PB-induced JNK activation and induction of apoptosis. However, the production of known upstream activators of JNK, namely Fas/Fas ligand, tumor necrosis factor (TNF)-alpha, TNF-beta, and TRAIL, are not altered by PB treatment. Therefore, PB activates JNK through an unidentified and cell type-specific mechanism. Understanding of this mechanism is of therapeutic value in treating cancer patients with PB.

Adenocarcinoma↗

PubMed2004

Bienzymatic amperometric biosensor for choline based on mediator thionine in situ electropolymerized within a carbon paste electrode.

An amperometric enzyme biosensor for the determination of choline utilizing two enzymes, choline oxidase (CHOD) and horseradish peroxidase (HRP), is described. The biosensor consisted of CHOD cross-linked onto a HRP-immobilized carbon paste electrode. The biosensor was prepared by in situ electropolymerization of poly(thionine) within a carbon paste containing the enzyme HRP and thionine monomer and then CHOD was immobilized by using chitosan film through cross-linking with glutaraldehyde. The in situ electrogenerated poly(thionine) displays excellent electron transform efficiency between the enzyme HRP and the electrode surface, and the polymer enables improvement in enzyme immobilization within the paste. Several parameters such as the amount of thionine and enzyme, the applied potential, the pH, etc. have been studied. Amperometric detection of choline was realized at an applied potential of -0.2V vs saturated calomel electrode in 1/15M phosphate buffer solution (pH 7.4) with a linear response range between 5.0 x 10(-6) and 6.0 x 10(-4)M choline and a response time of 15s. When applied to the analysis of phosphatidylcholine in serum samples, a 0.997 correlation was obtained between the biosensor results and those obtained by a hospital method.

Alcohol Oxidoreductases↗

PubMed2004

Dopant ion size and electronic structure effects on transparent conducting oxides. Sc-doped CdO thin films grown by MOCVD.

A series of Sc-doped CdO (CSO) thin films have been grown on both amorphous glass and single-crystal MgO(100) substrates at 400 degrees C by MOCVD. Both the experimental data and theoretical calculations indicate that Sc3+ doping shrinks the CdO lattice parameters due to its relatively small six-coordinate ionic radius, 0.89 angstroms, vs 1.09 angstroms for Cd2+. Conductivities as high as 18100 S/cm are achieved for CSO films grown on MgO(100) at a Sc doping level of 1.8 atom %. The CSO thin films exhibit an average transmittance >80% in the visible range. Sc3+ doping widens the optical band gap from 2.7 to 3.4 eV via a Burstein-Moss energy level shift, in agreement with the results of band structure calculations within the sX-LDA (screened-exchange local density approximation) formalism. Epitaxial CSO films on single-crystal MgO(100) exhibit significantly higher mobilities (up to 217 cm2/(V x s)) and carrier concentrations than films on glass, arguing that the epitaxial CSO films possess fewer scattering centers and higher doping efficiencies due to the highly textured microstructure. Finally, the band structure calculations provide a microscopic explanation for the observed dopant size effects on the structural, electronic, and optical properties of CSO.

Journal Article↗

PubMed2004

Analysis of interfacial phenomena of aqueous solutions of polyethylene oxide and polyethylene glycol flowing in hydrophilic and hydrophobic capillary viscometers.

Viscosities of aqueous solutions of five polyethylene oxide (PEO) samples with molar masses from 1.5 x 10(5) to 1.0 x 10(6) were carefully measured in a polytetrafluoroethylene (PTFE) capillary Ubbelohde viscometer in the concentration range from dilute down to extremely dilute concentration regions and compared with those of the same sample obtained from a glass capillary viscometer. At the same time, viscosities of aqueous solutions of three PEG samples in glass and paraffin-coated capillary viscosity were measured. The wall effects occurred in viscosity measurements for PEO and PEG aqueous solutions in different capillary viscometers were theoretically analyzed and discussed. It was found that different interfacial behaviors occurred in both hydrophobic and hydrophilic capillary viscometers respectively and the interfacial behaviors also exhibit molar mass dependence.

Journal Article↗

PubMed2004

Transparent conducting oxides: texture and microstructure effects on charge carrier mobility in MOCVD-derived CdO thin films grown with a thermally stable, low-melting precursor.

A series of low-melting, thermally stable cadmium metal-organic chemical vapor deposition (MOCVD) precursors have been synthesized, structurally and spectroscopically characterized, and implemented in growth of highly conductive and transparent CdO thin films. One member of the series, bis(1,1,1,5,5,5-hexafluoro-2,4-pentanedionato)(N,N-diethyl-N',N'-dimethyl-ethylenediamine)cadmium(II), Cd(hfa)(2)()(N,N-DE-N',N'-DMEDA), represents a particularly significant improvement over previously available Cd precursors, owing to the low melting point and robust thermal stability. High-quality CdO films were grown by MOCVD on glass and single-crystal MgO(100) between 300 and 412 degrees C. Film growth parameters and substrate surface have large effects on microstructure and electron carrier transport properties. Enhanced mobilities observed for highly biaxially textured films grown on MgO(100) vs glass are attributed, on the basis of DC charge transport and microstructure analysis, to a reduction in neutral impurity scattering and/or to a more densely packed grain microstructure. Although single-grained films grown on MgO(100) exhibit greater mobilities than analogues with discrete approximately 100 nm grains and similar texture, this effect is attributed, on the basis of charge transport and Hall effect measurements as well as optical reflectivity analysis, to differences in carrier concentration rather than to reduced grain boundary scattering. Unprecedented conductivities and mobilities as high as 11,000 S/cm and 307 cm(2)/V.s, respectively, are obtained for epitaxial single-grained films (X-ray diffraction parameters: fwhm(omega) = 0.30 degrees, fwhm(phi) = 0.27 degrees ) grown in situ on MgO(100) at a relatively low temperature (400 degrees C).

Journal Article↗

PubMed2004

Distinctive regulation and function of PI 3K/Akt and MAPKs in doxorubicin-induced apoptosis of human lung adenocarcinoma cells.

Regulation and function of PI 3K/Akt and mitogen-activated protein kinases (MAPKs) in doxorubicin-induced cell death were investigated in human lung adenocarcinoma cells. Doxorubicin induced dose-dependent apoptosis of human lung adenocarcinoma NCI-H522 cells. Prior to cell death, both Akt and the MAPK family members (MAPKs: ERK1/2, JNK, and p38) were activated in response to the drug treatment. The kinetics of the inductions for Akt and MAPKs are, however, distinct. The activation of Akt was rapid and transient, activated within 30 min of drug addition, then declined after 3 h, whereas the activations of three MAPKs occurred later, 4 h after addition of the drug and sustained until cell death occurred. Inhibition of PI 3K/Akt activation had no effect on MAPKs' activation, suggesting that the two pathways are independently activated in response to the drug treatment. Inhibition of PI 3K/Akt and p38 accelerated and enhanced doxorubicin-induced cell death. On the contrary, inhibition of ERK1/2 or JNK had no apparent effect on the cell death. Taken together, these results suggest that PI 3K/Akt and MAPKs signaling pathways are all activated, but with distinct mechanisms, in response to doxorubicin treatment. Activation of PI 3K/Akt and p38 modulates apoptotic signal pathways and inhibits doxorubicin-induced cell death. These responses of tumor cells to cancer drug treatment may contribute to their drug resistance. Understanding of the mechanism and function of the responses will be beneficial for the development of novel therapeutic approaches for improvement of drug efficacy and circumvention of drug resistance.

Adenocarcinoma↗

PubMed2004

Cleavage of p130Cas in anoikis.

p130Cas is a multifunctional signaling adaptor protein. It integrates and relays signals generated from a variety of extracellular stimuli and regulates a number of cellular activities including cell death. In this study, we analyzed the regulation and function of p130Cas in anoikis, a type of apoptosis caused by disruption of cell-matrix interactions. We found that p130Cas was specifically cleaved during anoikis in anoikis-sensitive epithelial cells, but not in anoikis-resistant tumor cells. There is a close correlation between p130Cas cleavage and anoikis. Furthermore, we found that the cleavage of p130Cas, as well as another focal adhesion component FAK, is different from that of caspase substrate PARP and spectrin. Although caspases and calpain were found to be involved in the cleavage of p130Cas, there appear to be other unidentified proteases that are mainly responsible for the cleavage of p130Cas, particularly at the early stage of anoikis. Overexpression of the p130Cas cleavage product induced apoptosis. Taken together, these data suggest that there are novel proteases involved in the cleavage of p130Cas during anoikis, which may be functionally involved in the onset of anoikis. p130Cas may have a dual role in the regulation of anoikis. On one hand, it mediates a survival signal from cell-matrix interactions when cells are attached to the extracellular matrix. On the other hand, it participates in executing cell death when cell-matrix interactions are disrupted. These observations provide new insights into the understanding of the function of p130Cas and the molecular mechanism of anoikis.

Animals↗

PubMed2004

A novel mechanism of alternative promoter and splicing regulates the epitope generation of tumor antigen CML66-L.

This report describes the difference in the epitope generation of two isoforms of self-tumor Ag CML66 and the regulation mechanism. We identified a new CML66 short isoform, termed CML66-S. The previously identified long CML66 is referred to as CML66-L. CML66-S shares the C terminus with CML66-L but has its unique N terminus. CML66-S is predominantly expressed in testis, but is also expressed in very low levels in tumor cells, whereas CML66-L is expressed in tumor cells and testis. Differential expression of CML66-L and CML66-S in tumor cells resulted from regulation at transcription, although alternative splicing also participated in the generation of the isoforms. In addition, Ab titers to a CML66-L peptide were significantly higher than that to CML66-S peptide in the sera from patients with tumors. Finally, the Abs to full-length CML66-L in the sera from patients with tumors were correlated with the Abs in the sera from these patients to CML66-L-38, which is a fusion protein with a CML66-L-specific N terminus. This suggests that the CML66-L isoform is mainly responsible for the epitope generation. Our studies have identified the alternative promoter in combination with alternative splicing as a novel mechanism for regulation of the epitope generation of a self-tumor Ag.

Alternative Splicing↗

PubMed2004

Pharmacokinetics of the enantiomers of trans-tramadol and its active metabolite, trans-O-demethyltramadol, in healthy male and female chinese volunteers.

By using a high-performance capillary electrophoresis method, the pharmacokinetics of the enantiomers of trans-tramadol (trans-T) and its active metabolite, trans-O-demethyltramadol (M1), was studied in healthy male and female Chinese volunteers after oral administration of 100 mg trans-T hydrochloride. The values of Cmax for the enantiomers of trans-T and M1, and AUC0- infinity for (-)-trans T, (+)-M1, and (-)-M1 were higher in females than in males. The values of V(d)/F for the enantiomers of trans-T and CLr for (+)-M1 were lower in females than in males. The value of t(1/2) for (-)-M1 was longer in females than in males. There were significant differences in pharmacokinetic parameters of the two enantiomers of trans-T or M1 both in males and in females. The (+)/(-)-enantiomeric ratios of t(max), V(d)/F for trans-T in males were significantly different from those in females and the (+)/(-)-enantiomeric ratios of pharmacokinetic parameters for M1 in males were similar to those in females. There are gender-related differences in the pharmacokinetics of the enantiomers of trans-T and M1 which may be due to the greater body weights for men and/or the higher CYP2D6 activity in women. The pharmacokinetics of trans-T and M1 is stereoselective in men and women. There is a gender-related difference in the stereoselectivity in pharmacokinetics of trans-T in human and the stereoselectivity in pharmacokinetics of M1 in men is similar to that in women. Chirality 16:112-118, 2004.

Adolescent↗

PubMed2004

The relationship of expression of bcl-2, p53, and proliferating cell nuclear antigen (PCNA) to cell proliferation and apoptosis in renal cell carcinoma.

To investigate the relationship of bcl-2, p53, proliferating cell nuclear antigen (PCNA) to cell proliferation, apoptosis and pathological parameters, the patterns of cell growth and turnover in renal cell carcinoma (RCC), formalin-fixed and paraffin-embedded tissue blocks from 34 patients with RCC were examined. Cell proliferation activity was detected by PCNA immunostaining and the proliferation index (PI) was expressed as a percentage of the PCNA-positive cells in the tumor cells. Apoptosis was detected by terminal deoxy- nucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), and the apoptotic index (AI) was expressed as a percentage of the TUNEL-positive cells in the tumor cells. Expressions of bcl-2 and p53 were assessed immunohistochemically. Our results showed that the PI ranged from 6.0% to 24.0% (median 12.3%) and the AI from 2.0% to 8.0% (median 5.4%) in RCC. The expression of the bcl-2 protein was demonstrated in 15 cases (44.1%); the expression of the p53 protein, however, was seen in only 3 case. bcl-2 positivity was not associated with PI or AI or any pathological parameters. There were close associations between PI and tumor grade and stage, and a significant relationship between AI and the tumor grade of RCC, Our study suggests that bcl-2 positivity was not associated with PI or AI or any pathological parameters. There are close associations between PI and AI and tumor grade and stage of RCC. Active cell proliferation may be accompanied by frequent apoptosis in RCC.

Adult↗

PubMed2004

Increased noncanonical splicing of autoantigen transcripts provides the structural basis for expression of untolerized epitopes.

BACKGROUND: Alternative splicing is important for increasing the complexity of the human proteome from a limited genome. Previous studies have shown that for some autoantigens, there is differential immunogenicity among alternatively spliced isoforms. OBJECTIVES: Herein, we tested the hypothesis that alternative splicing is a common feature for transcripts of autologous proteins that are autoantigens. The corollary hypothesis tested was that nonautoantigen transcripts have a lower frequency of alternative splicing. METHODS: The extent of alternative splicing within 45 randomly selected self-proteins associated with autoimmune diseases was compared with 9554 randomly selected proteins in the human genome by using bioinformatics analyses. Isoform-specific regions that resulted from alternative splicing were studied for their potential to be epitopes for antibodies or T-cell receptors. RESULTS: Alternative splicing occurred in 100% of the autoantigen transcripts. This was significantly higher than the approximately 42% rate of alternative splicing observed in the 9554 randomly selected human gene transcripts ( P < .001). Within the isoform-specific regions of the autoantigens, 92% and 88% encoded MHC class I and class II-restricted T-cell antigen epitopes, respectively, and 70% encoded antibody binding domains. Furthermore, 80% of the autoantigen transcripts underwent noncanonical alternative splicing, which is also significantly higher than the less than 1% rate in randomly selected gene transcripts ( P < .001). CONCLUSION: These studies suggest that noncanonical alternative splicing may be an important mechanism for the generation of untolerized epitopes that may lead to autoimmunity. Furthermore, the product of a transcript that does not undergo alternative splicing is unlikely to be a target antigen in autoimmunity.

Alternative Splicing↗

PubMed2004

Surfactant-assisted synthesis of Keggin-type polyoxometalates nanorods.

It was demonstrated that Keggin-type polyoxometalates nanorods (POMs-nanorods) were prepared from a solution containing a surfactant polyethylene glycol (PEG), when heteropolyanions [X(n+)M12O40](-(8-n)) (X(n+) = P5+ and Si4+; M = W and Mo) were precipitated by ammonia ion obtained by hydrolysis of urea at 373 K. In this method, PEG was used as a template and ammonia ion (NH4+) was a counterion. In an oil bath kept at 373 K without stirring, three kinds of ammonium salts of POMs, i.e., (NH4)3PW12O40, (NH4)4SiW12O40, and (NH4)3PMo12O40 nanorods were obtained. The POMs-nanorods were characterized by transmission electron microscopy (TEM), selected area electron diffraction (SAED), infrared spectra (IR), inductively coupled plasma atomic emission spectrometry (ICP-AES) and X-ray powder diffraction (XRD). TEM showed that nanorods were 0.5-1.5 microm in length, and 50-150 nm in diameter. The results of IR, ICP-AES and XRD proved the existence of Keggin structure. The formation process of POMs-nanorods, (NH4)(8-n) [X(n+)M12O40](-(8-n)) (X(n+) = P5+ and Si4+; M = W and Mo) in a H2O/PEG system was discussed.

Electrons↗

PubMed2004

Effect of continuous positive airway pressure treatment on vascular endothelial function in patients with obstructive sleep apnea hypopnea syndrome and coronary artery disease.

BACKGROUND: Continuous positive airway pressure (CPAP) treatment has been proven to be effective in improving the symptoms of coexisting coronary heart disease (CHD) in patients with obstructive sleep apnea hypopnea syndrome (OSAHS). However, it is still unclear whether such improvements are linked to changes in vascular endothelial function. This research was carried out to investigate the effects of CPAP treatment on vascular endothelial function in patients with OSAHS and CHD. METHODS: Thirty-six patients with moderate or severe OSAHS and CHD undergoing three months of CPAP treatment were recruited for this study. The changes in their morning plasma nitric oxide (NO) and endothelin (ET) levels, NO/ET ratio, total ischemic burden (TIB) of the myocardium, apnea hypopnea index (AHI), and minimal and mean pulse oxygen saturation (SpO2) were compared and analyzed before and during CPAP treatment. RESULTS: Compared with the plasma levels of ET [(51.39 +/- 11.69) ng/L] and NO [(36.67 +/- 11.86) micromol/L], NO/ET (0.71 +/- 0.14), AHI (32.4 +/- 7.9), minimal SpO2 [(68.9 +/- 11.4)%], and myocardial TIB [(66.29 +/- 16.37) mm.min] before treatment, there were significant decreases in ET [(33.41 +/- 10.03) ng/L] (P < 0.05), increases in NO [(59.89 +/- 10.26) micromol/L] and NO/ET (1.79 +/- 0.38) (P < 0.01), decreases in AHI (1.9 +/- 0.5), and increases in minimal SpO2 [(90.6 +/- 1.8)%] (all P < 0.01) and myocardial TIB [(36.42 +/- 10.87) mm.min] (P < 0.05) after three months of CPAP treatment. CONCLUSION: CPAP treatment may play an important role in the improvement and protection of vascular endothelial dysfunction and myocardial ischemia in OSAHS patients with CHD.

Adult↗

PubMed2004

[Risk analysis of naphthalene pollution in soils of Tianjin].

Three approaches were applied and evaluated for probabilistic risk assessment of naphthalene in soils of Tianjin, China, based on the observed naphthalene concentration of 188 top soil samples from the area and LC50 of naphthalene to ten typical soil fauna species from the literature. It was found that the overlapping area of the two probability density functions of concentration and LC50 was 6.4%, the joint probability curve bend towards and very close to the bottom and left axis, and the calculated probability that exposure concentration exceeds LC50 of various species was as low as 1.67%, all indicating a very much acceptable risk of naphthalene to the soil fauna ecosystem and only some of very sensitive species or individual animals are threaten by localized extremely high concentration. The three approaches revealed similar results from different viewpoints.

Animals↗

PubMed2004

Glutathione S-transferase T1 deletion is a risk factor for developing end-stage renal disease in diabetic patients.

Reactive oxygen metabolites may contribute to the development of end-stage renal disease (ESRD) in diabetic and hypertensive patients. In this study, we used multiplex polymerase chain reaction (PCR) to analyze polymorphisms of two endogenous antioxidant genes, glutathione S-transferase M1 (GSTM1) and glutathione S-transferase T1 (GSTT1), and to determine their role in the development of ESRD in diabetic and hypertensive patients. Our results showed that homozygous deletion of the GSTT1 gene is a risk factor for developing ESRD in diabetic patients (p=0.004, OR=2.18, 95% confidence interval (CI) =1.29-3.70), but not in hypertensive patients. No association between homozygous deletion of GSTM1 and the development of ESRD was found in either diabetic patients or hypertensive patients. These results indicate that genetic variations in enzymes involved in free radical metabolism are associated with the development of ESRD in diabetes mellitus (DM) patients, and may permit the targeting of preventive and early intervention strategies to high-risk individuals.

Diabetes Mellitus, Type 1↗