531 results on '"Chen, Yan‐Hua"'
Search Results
202. Numerical Simulation of Interfacial Bonding Degradation of Composites under Two-Stage Loading
- Author
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Chen, Yan Hua, primary and Zhu, Qing Jie, additional
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- 2008
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203. WNK4 phosphorylates ser206of claudin-7 and promotes paracellular Cl−permeability
- Author
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Tatum, Rodney, primary, Zhang, Yuguo, additional, Lu, Qun, additional, Kim, Kwonseop, additional, Jeansonne, Beverly G., additional, and Chen, Yan-Hua, additional
- Published
- 2007
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204. The first extracellular domain of claudin-7 affects paracellular Cl− permeability
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Alexandre, Michele D., primary, Jeansonne, Beverly G., additional, Renegar, Randall H., additional, Tatum, Rodney, additional, and Chen, Yan-Hua, additional
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- 2007
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205. Characterizing Wheat Root Branching Using a Markov Chain Approach
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Chen, Yan Hua, primary, Zhang, Qian, additional, Li, Bao Guo, additional, and Zhang, Bao Gui, additional
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- 2006
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206. Increased expression of δ-catenin/neural plakophilin-related armadillo protein is associated with the down-regulation and redistribution of E-cadherin and p120ctn in human prostate cancer
- Author
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Lu, Qun, primary, Dobbs, Larry J., additional, Gregory, Christopher W., additional, Lanford, George W., additional, Revelo, Monica P., additional, Shappell, Scott, additional, and Chen, Yan-hua, additional
- Published
- 2005
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- View/download PDF
207. Overexpression of claudin-7 decreases the paracellular Cl– conductance and increases the paracellular Na+ conductance in LLC-PK1 cells
- Author
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Alexandre, Michele D., primary, Lu, Qun, additional, and Chen, Yan-Hua, additional
- Published
- 2005
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208. Dendrite-like Process Formation and Cytoskeletal Remodeling Regulated by δ-Catenin Expression
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Kim, Kwonseop, primary, Sirota, Anna, additional, Chen, Yan-hua, additional, Jones, Shiloh B., additional, Dudek, Ronald, additional, Lanford, George W., additional, Thakore, Chittam, additional, and Lu, Qun, additional
- Published
- 2002
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209. Occludin, a Constituent of Tight Junctions.
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Gonzalez-Mariscal, Lorenza, Chen, Yan-Hua, Goodenough, Daniel A., and Lu, Qun
- Abstract
Occludin was the first tight junction (TJ) integral membrane protein identified. This ∼65 kDa protein specifically localizes at TJs of epithelial and endothelial cells and is incorporated into the network of TJ strands. Occludin has a predicted tetraspan membrane topology with two extracellular loops and a large COOH-terminal cytoplasmic domain. Both extracellular domains are enriched with tyrosine residues, and in the first domain, more than half of the residues are tyrosines and glycines. Multiple domains of occludin are responsible for its localization and functions. Occludin interacts with many structural as well as signaling molecules and participates in the regulation of TJ functions. Although occludin-deficient mice show various phenotypes such as significant postnatal growth retardation, chronic inflammation, hyperplasia of the gastric epithelium, and calcification in the brain, the roles of occludin in vivo remain unclear since many epithelia in occludin null mice seem unaffected. [ABSTRACT FROM AUTHOR]
- Published
- 2006
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210. Nonreceptor Tyrosine Kinase c-Yes Interacts with Occludin during Tight Junction Formation in Canine Kidney Epithelial Cells
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Chen, Yan-Hua, primary, Lu, Qun, additional, Goodenough, Daniel A., additional, and Jeansonne, Beverly, additional
- Published
- 2002
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211. Association of Nonreceptor Tyrosine Kinase c-Yes with Tight Junction Protein Occludin by Coimmunoprecipitation Assay.
- Author
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Walker, John M., Terrian, David M., Chen, Yan-Hua, and Lu, Qun
- Abstract
Immunoprecipitation is one of the most commonly used techniques to study protein-protein interaction in vivo. There are three major steps involved in an immunoprecipitation procedure: 1) lysis of the cells to make the antigen of interest available; 2) formation of the antibody-antigen complex by adding specific antibody; 3) separation and detection of the immune complex by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting. Both polyclonal and monoclonal antibodies can be used to immunoprecipitate the antigen. Polyclonal antibodies usually bind to multiple sites on the antigen and, therefore, are more efficient than monoclonal antibodies. The advantage of using monoclonal antibodies for immunoprecipitations is the specificity of the antibody-antigen interaction because monoclonal antibodies bind to only one epitope of the antigen. If the antigen of interest is tyrosine phosphorylated, and this tyrosine phosphorylation is under investigation, each step has to be handled with extra care to ensure success of the procedure. The buffer used to lyse the cells depends on the nature of the antigen, with more stringent conditions required for integral membrane proteins than for soluble cytosolic proteins. In either case, it is very important to add the protease inhibitors to the lysis buffer in order to prevent degradation of the antigen. [ABSTRACT FROM AUTHOR]
- Published
- 2003
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212. Restoration of Tight Junction Structure and Barrier Function by Down-Regulation of the Mitogen-activated Protein Kinase Pathway in Ras-transformed Madin-Darby Canine Kidney Cells
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Chen, Yan-hua, primary, Lu, Qun, additional, Schneeberger, Eveline E., additional, and Goodenough, Daniel A., additional
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- 2000
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213. Small molecules targeting Rho GTPase signaling altered in Alzheimer's disease
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Lu, Qun, Friesland, Amy, Lee, Jonathan, and Chen, Yan-Hua
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- 2013
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214. Environmental Awareness Automation Monitoring System for Training Dog Kennel.
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chaisit, Sumalee, Kung, Hsu-Yang, Pan, Jian-Liang, and Chen, Yan-Hua
- Abstract
Environmental awareness is currently significant caring in all industrial sectors, particularly in the animal industries. Animals are directly affected by environmental conditions and climate changes. Working dog is costly production in time and money to be successful. Health and temperament are key factors to be successful in training dog program. Working training dog school, NPUST is located in mountainous areas. The weather has frequently extreme change in temperature and humidity. The changes cause the heat in in-house and humidity in the air that may cause the dog illness. Therefore, working training dog school has to provide an appropriate kennel environment for all dogs throughout the training program. In order to secure the dogs, the automatic environmental sensing should be deployed. Web sensors and radio frequency identification (RFID) technologies were integrated, and have been implemented that are the weather sensing system and in-out control system, combining with health care management. Web based monitoring systems have provided based on user-friendly interface along with real-time information. In addition, it is very attractive use when the system operating via more convenient for computer and mobile communication devices. [ABSTRACT FROM AUTHOR]
- Published
- 2013
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215. Fe3O4 nanoparticles with daunorubicin induce apoptosis through caspase 8-PARP pathway and inhibit K562 leukemia cell-induced tumor growth in vivo.
- Author
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Zhang, Gen, Lai, Bin Bin, Zhou, Yan Yan, Chen, Bao An, Wang, Xue Mei, Lu, Qun, and Chen, Yan-Hua
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IRON oxides ,NANOPARTICLES ,ANTINEOPLASTIC agents ,APOPTOSIS ,TUMOR growth ,LEUKEMIA ,DRUG delivery systems ,ENZYME inhibitors - Abstract
Abstract: Nanomaterials can enhance the delivery and treatment efficiency of anticancer drugs, but the mechanisms of the tumor-reducing activity of ferrous-ferric oxide (Fe
3 O4 ) nanoparticles (NPs) with daunorubicin (DNR) have not been established. Here we investigate the synergistic effects of Fe3 O4 NPs with DNR on the induction of apoptosis using K562 leukemia cells. Fe3 O4 NPs increased the ability of DNR to induce apoptosis in both adriamycin-sensitive and adriamycin-resistant K562 cells through the caspase 8-poly(ADP-ribose) polymerase pathway. Fe3 O4 NPs combined with DNR also effectively inhibited the tumor growth induced by the inoculation of K562 cells into nude mice. The increased cell apoptotic rate was closely correlated with the enhanced inhibition of tumor growth. Biodistribution studies in xenograft tumors indicated that Fe3 O4 NPs could be potentially excreted from the body via the gastrointestinal system. In conclusion, our study suggests that Fe3 O4 NPs combined with anticancer drugs could serve as a better alternative for targeted therapeutic approaches to cancer treatments.▪ From the Clinical Editor: In this paper, the synergistic effects on tumor growth of ferrous-ferric oxide nanoparticles with daunorubicin are investigated. The combined treatment was demonstrated to be superior in a leukemia cell line murine model in vivo. [Copyright &y& Elsevier]- Published
- 2011
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216. Hydroxycamptothecin-loaded Fe.
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Zhang, Gen, Ding, Lei, Renegar, Randall, Wang, Xuemei, Lu, Qun, Huo, Shouquan, and Chen, Yan-Hua
- Abstract
10-Hydroxycamptothecin (HCPT) elicits strong anti-cancer effects and is less toxic than camptothecin (CPT), making it widely used in recent clinical trials. However, its low solubility limits its application as an effective anti-cancer therapy. In the present study we investigate the hypothesis that the unique water dispersible oleic acid-Triton X-100-coated FeO nanoparticles loaded with HCPT disrupt epithelial cell-cell junctions and induce human lung cancer cell apoptosis through the caspase-8 pathway. We characterized the HCPT-loaded nanoparticles and determined their effects on lung cancer cell viability and apoptosis by using immunofluorescence light microscopy and SDS-PAGE/immunoblots. We found that HCPT-loaded nanoparticles elicited an anti-proliferative effect in a dose-dependent manner. HCPT-loaded nanoparticles reduced the expression of cell-cell junction protein claudins, E-cadherin and ZO-1, and transmission electron microcopy demonstrated a disrupted tight junction ultrastructure. Transepithelial electric resistance was also reduced, indicating the reduction of tight junction functions. The HCPT-loaded nanoparticles increased phosphorylation of p38 and SAPK/JNK while it showed no effects on p42/44 MAP kinase. Compared with void FeO nanoparticles or HCPT drug alone, HCPT drug-loaded nanoparticles evoked synergistic effects by increasing cell apoptosis with enhanced activation of the caspase-8 pathway. Therefore, our current study highlights the potential of HCPT drug-loaded nanoparticles as a chemotherapeutic agent for increasing anti-cancer drug efficacy. ( Cancer Sci 2011; 102: 1216-1222) [ABSTRACT FROM AUTHOR]
- Published
- 2011
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217. Extended Graphite Supported Flower-like MnO 2 as Bifunctional Materials for Supercapacitors and Glucose Sensing.
- Author
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Chang, Han-Wei, Dong, Chung-Li, Chen, Yan-Hua, Xu, Yuan-Zhang, Huang, Tzu-Chi, Chen, Song-Chi, Liu, Feng-Jiin, Lai, Yin-Hung, and Tsai, Yu-Chen
- Subjects
SUPERCAPACITORS ,GLUCOSE ,SUPERCAPACITOR electrodes ,ION transport (Biology) ,ELECTRIC conductivity ,GRAPHITE ,DETECTION limit - Abstract
A simple, efficient, and cost-effective extended graphite as a supporting platform further supported the MnO
2 growth for the construction of hierarchical flower-like MnO2 /extended graphite. MnO2 /extended graphite exhibited an increase in sp2 carbon bonds in comparison with that of extended graphite. It can be expected to display better electrical conductivity and further promote electron/ion transport kinetics for boosting the electrochemical performance in supercapacitors and glucose sensing. In supercapacitors, MnO2 /extended graphite delivered an areal capacitance value of 20.4 mF cm−2 at 0.25 mA cm−2 current densities and great cycling stability (capacitance retention of 83% after 1000 cycles). In glucose sensing, MnO2 /extended graphite exhibited a good linear relationship in glucose concentration up to about 5 mM, sensitivity of 43 μA mM−1 cm−2 , and the limit of detection of 0.081 mM. It is further concluded that MnO2 /extended graphite could be a good candidate for the future design of synergistic multifunctional materials in electrochemical techniques. [ABSTRACT FROM AUTHOR]- Published
- 2021
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218. WNK4 phosphorylates ser206 of claudin-7 and promotes paracellular Cl− permeability
- Author
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Tatum, Rodney, Zhang, Yuguo, Lu, Qun, Kim, Kwonseop, Jeansonne, Beverly G., and Chen, Yan-Hua
- Subjects
KIDNEY tubules ,GENETIC mutation ,PHOSPHORYLATION ,EPITHELIAL cells - Abstract
Abstract: Mutations in WNK4 have been linked to hypertension in PHAII. Paracellular ion transport has been reported to be involved in this disease process; however, the specific molecular target has not been identified. In this study, we found that TJ protein claudin-7 and WNK4 were partially co-localized in renal tubules of rat kidney and co-immunoprecipitated in kidney epithelial cells. The wild-type and PHAII-causing mutant, but not the kinase-dead mutant, phosphorylated claudin-7. We have identified ser
206 in the COOH-terminus of claudin-7 as a putative phosphorylation site for WNK4. More importantly, disease-causing mutant enhanced claudin-7 phosphorylation and significantly increased paracellular permeability to Cl− . [Copyright &y& Elsevier]- Published
- 2007
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219. Increased expression of δ-catenin/neural plakophilin-related armadillo protein is associated with the down-regulation and redistribution of E-cadherin and p120ctn in human prostate cancer.
- Author
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Lu, Qun, Dobbs, Larry J., Gregory, Christopher W., Lanford, George W., Revelo, Monica P., Shappell, Scott, and Chen, Yan-hua
- Subjects
PROSTATE cancer ,GENOMES ,HUMAN gene mapping ,NUCLEOTIDE sequence - Abstract
Summary: δ-Catenin, or neural plakophilin-related armadillo protein, is a unique armadillo domain-containing protein in that it is neural-specific and primarily expressed in the brain. However, our recent analysis of the human genome revealed a consistent association of δ-catenin messenger RNA sequences with malignant cells, although the significance of these findings was unclear. In this study, we report that a number of δ-catenin epitopes were expressed in human prostate cancer cells. Western blot and tissue microarray revealed a close association between increased δ-catenin expression and human primary prostatic adenocarcinomas. The analyses of 90 human prostate cancer and 90 benign prostate tissue samples demonstrated that an estimated 85% of prostatic adenocarcinomas showed enhanced δ-catenin immunoreactivity. δ-Catenin expression increased with prognostically significant increased Gleason scores. By analyzing the same tumor cell clusters using consecutive sections, we showed that an increased δ-catenin immunoreactivity was accompanied by the down-regulation and redistribution of E-cadherin and p120
ctn , major cell junction proteins whose inactivation is frequently associated with cancer progression. Furthermore, overexpression of δ-catenin in tumorigenic CWR-R1 cells that are derived from human prostate cancer xenograft resulted in reduced immunoreactivity for E-cadherin and p120ctn at the cell-cell junction. This is the first study comparing overexpression of δ-catenin with the E-cadherin/catenin system in cancer and shows that δ-catenin may be intimately involved in regulating E-cadherin/p120ctn cell-cell adhesion in prostate cancer progression. [Copyright &y& Elsevier]- Published
- 2005
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220. Development of Gap Junctions
- Author
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DEHAAN, ROBERT L., primary and CHEN, YAN-HUA, additional
- Published
- 1990
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221. Identification of a novel mutation in a Chinese family with Nance-Horan syndrome by whole exome sequencing
- Author
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Hong, Nan, Chen, Yan-hua, Xie, Chen, Xu, Bai-sheng, Huang, Hui, Li, Xin, Yang, Yue-qing, Huang, Ying-ping, Deng, Jian-lian, Qi, Ming, and Gu, Yang-shun
- Abstract
Nance-Horan syndrome (NHS) is a rare X-linked disorder characterized by congenital nuclear cataracts, dental anomalies, and craniofacial dysmorphisms. Mental retardation was present in about 30% of the reported cases. The purpose of this study was to investigate the genetic and clinical features of NHS in a Chinese family. Whole exome sequencing analysis was performed on DNA from an affected male to scan for candidate mutations on the X-chromosome. Sanger sequencing was used to verify these candidate mutations in the whole family. Clinical and ophthalmological examinations were performed on all members of the family. A combination of exome sequencing and Sanger sequencing revealed a nonsense mutation c.322G〉T (E108X) in exon 1 of NHSgene, co-segregating with the disease in the family. The nonsense mutation led to the conversion of glutamic acid to a stop codon (E108X), resulting in truncation of the NHS protein. Multiple sequence alignments showed that codon 108, where the mutation (c.322G〉T) occurred, was located within a phylogenetically conserved region. The clinical features in all affected males and female carriers are described in detail. We report a nonsense mutation c.322G〉T (E108X) in a Chinese family with NHS. Our findings broaden the spectrum of NHSmutations and provide molecular insight into future NHS clinical genetic diagnosis. 通过对一个中国Nance-Horan 综合征家系的临床表型及基因突变分析, 揭示本家系的致病遗传机制。 对该Nance-Horan 综合征家系的一个男性患者进行全外显子组测序, 结合此家系临床表型及遗传方式分析, 选定X 染色体上NHS基因上的一个无义突变 c.322G〉T (E108X) 为可疑致病突变。 通过聚合酶链式反应 (PCR) 和Sanger 测序, 对该家系内其他成员进行NHS基因突变分析, 同时对50 名健康对照者的NHS基因的突变检测结果进行对比。 另外, 将该突变的位点第108 位氨基酸残基进行多物种NHS 蛋白内序列比对。 最后, 对该家系成员眼部及全身的临床特点进行全面检查和分析。 全外显子组测序结合Sanger 测序发现 NHS基因第一个外显子上的 c.322G〉T (E108X) 突变为引起该家系临床病变的突变位点; 多物种 NHS 蛋白内序列比对发现该突变位点第108 位氨基酸残基位于高度保守区; 临床表型分析发现该家系内存在表型异质性。 此家系为国内首次报道的无义突变引起的Nance-Horan 综合征家系。
- Published
- 2014
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222. Electrochemical Organophosphorus Pesticide Detection Using Nanostructured Gold-Modified Electrodes.
- Author
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Chang, Han-Wei, Chen, Chien-Lin, Chen, Yan-Hua, Chang, Yu-Ming, Liu, Feng-Jiin, and Tsai, Yu-Chen
- Subjects
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METHYL parathion , *ORGANOPHOSPHORUS pesticides , *PESTICIDE residues in food , *X-ray photoelectron spectroscopy , *AGRICULTURAL wastes , *FARM produce , *BOK choy , *PESTICIDE pollution - Abstract
In this study, nanostructured gold was successfully prepared on a bare Au electrode using the electrochemical deposition method. Nanostructured gold provided more exposed active sites to facilitate the ion and electron transfer during the electrocatalytic reaction of organophosphorus pesticide (methyl parathion). The morphological and structural characterization of nanostructured gold was conducted using field-emission scanning electron microscopy (FESEM), X-ray photoelectron spectroscopy (XPS), and X-ray diffraction (XRD), which was further carried out to evaluate the electrocatalytic activity towards methyl parathion sensing. The electrochemical performance of nanostructured gold was investigated by electrochemical measurements (cyclic voltammetry (CV) and differential pulse voltammetry (DPV)). The proposed nanostructured gold-modified electrode exhibited prominent electrochemical methyl parathion sensing performance (including two linear concentration ranges from 0.01 to 0.5 ppm (R2 = 0.993) and from 0.5 to 4 ppm (R2 = 0.996), limit of detection of 5.9 ppb, excellent selectivity and stability), and excellent capability in determination of pesticide residue in real fruit and vegetable samples (bok choy and strawberry). The study demonstrated that the presented approach to fabricate a nanostructured gold-modified electrode could be practically applied to detect pesticide residue in agricultural products via integrating the electrochemical and gas chromatography coupled with mass spectrometry (GC/MS-MS) analysis. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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223. Nanoarchitecture and Molecular Interactions of Epithelial Cell Junction Proteins Revealed by Super‐Resolution Microscopy.
- Author
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Naser, Amna, Guiler, William, Lu, Qun, and Chen, Yan‐Hua
- Published
- 2021
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224. Cooh terminus of occludin is required for tight junction barrier function in early Xenopus.
- Author
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Chen, Yan-hua and Merzdorf, Christa
- Subjects
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CYTOLOGY - Abstract
Investigates the ability of mutant occludin molecules to assemble in tight injunctions during the biogenesis of an epithelium in an organism, focusing on cell biology. Methodology used in the investigation; Importance of occludin to cells; Results from the investigation; Provision of statistical information.
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- 1997
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225. Asymmetric voltage dependence of embryonic cardiac gap junction channels.
- Author
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CHEN, YAN-HUA and DEHAAN, ROBERT L.
- Published
- 1996
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226. Temperature dependence of embryonic cardiac gap junction conductance and channel kinetics.
- Author
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Chen, Yan-hua, DeHaan, Robert, Chen, Y H, and DeHaan, R L
- Subjects
HEART physiology ,CELL membranes ,ANIMAL experimentation ,COMPARATIVE studies ,DYNAMICS ,ELECTROPHYSIOLOGY ,HEART ,RESEARCH methodology ,MEDICAL cooperation ,MEMBRANE proteins ,RESEARCH ,RESEARCH funding ,TEMPERATURE ,EVALUATION research ,PHYSIOLOGY - Abstract
We have investigated the effects of temperature on the conductance and voltage-dependent kinetics of cardiac gap junction channels between pairs of seven-day embryonic chick ventricle myocytes over the range of 14-26 degrees C. Records of junctional conductance (Gj) and steady-state unit junctional channel activity were made using the whole-cell double patch-clamp technique while the bath temperature was steadily changed at a rate of about 4 degrees C/min. The decrease in Gj upon cooling was biphasic with a distinct break at 21 degrees C. In 12 cell pairs, Q10 was 2.2 from 26 to 21 degrees C, while between 21 and 14 degrees C it was 6.5. The mean Gj at 22 degrees C (Gj22) was 3.0 +/- 2.1 nS, ranging in different preparations from 0.24 to 6.4 nS. At room temperature, embryonic cardiac gap junctions contain channels with conductance states near 240, 200, 160, 120, 80 and 40 pS. In the present study, we demonstrate that cooling decreases the frequency of channel openings at all conductance levels, and at temperatures below 20 degrees C shifts the prevalence of openings from higher to lower conductance states: all 240 pS openings disappear below 20 degrees C; 200 pS openings are suppressed at 17 degrees C; below 16 degrees C 160 and 120 pS events disappear and only 80 and 40 pS states are seen. Temperature also affected the voltage-dependent kinetics of the channels. Application of a 6 sec, 80 mV voltage step across the junction (Vj80) caused a biexponential decay in junctional conductance. Decay was faster at lower temperatures, whereas the rate of recovery of Gj after returning to Vj0 was slowed. Cooling reduced the fast decay time constant, increased both recovery time constants, and decreased the magnitude of Gj decay, thus leaving a 10-16% larger residual conductance (Gss/Ginit, +/- 80 mV Vj) at 18 than at 22 degrees C. From these results we propose that embryonic chick cardiac gap junctions contain at least two classes of channels with different conductances and temperature sensitivities. [ABSTRACT FROM AUTHOR]
- Published
- 1993
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227. Multiple-channel conductance states and voltage regulation of embryonic chick cardiac gap junctions.
- Author
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Chen, Yan-hua and DeHaan, Robert
- Abstract
We used the double whole-cell voltage-clamp technique on ventricle cell pairs isolated from 7-day chick heart to measure the conductance of their gap junctions ( G) and junctional channels ( γ) with a steady-state voltage difference ( V) applied across the junction. Currents were recorded from single gap junction channels ( i) as symmetrical rectangular signals of equal size and opposite sign in the two cells, and γ was measured from i/ V. We observed channel openings at six reproducible conductance levels with means of 42.6, 80.7, 119.6, 157.7, 200.4 and 240.3 pS. More than half of all openings were to the 80-and 160-pS conductance levels. The probability that a high conductance event (e.g., 160 or 240 pS) results from the random simultaneous opening of several 40-pS channels is small, based on their frequency of occurrence and on the prevalence of shifts between small and large conductance states with no intervening 40-pS steps. Our results are consistent with three models of embryonic cardiac gap junction channel configuration: a homogeneous population of 40-pS channels that can open cooperatively in groups of up to six; a single population of large channels with a maximal conductance near 240 pS and five smaller substates; or several different channel types, each with its own conductance. G was determined from the junctional current ( I) elicited by rectangular pulses of applied transjunctional voltage as I/ V. It was highest near 0 V and was progressively reduced by application of V between 20 and 80 mV or −20 and −80 mV. In response to increases in V, G decayed in a voltage-and timedependent fashion. After a 6-sec holding period at 0 V, the initial conductance ( G) measured immediately after the onset of an 80-mV step in V was nearly the same as that measured by a 10-mV prepulse. However, during 6-sec pulses of V>±20 mV, G declined over several seconds from G to a steady-state value ( G). At potentials greater than ±20 mV the current decay could be fit with biexponential curves with the slow decay time constant ( τ) 5-20 times longer than τ. For the response to a step to 80 mV V, for example, τ=127 msec and τ=2.6 sec. The rate of current decay in response to smaller positive or negative steps in V was slower, the magnitude of the decline was smaller, and the ratio τ/ τ decreased. The relationship between G and V was approximately linear between 0 and 80 mV or −80 mV. whereas the relationship between G and V was nonlinear beyond ±20 mV. Upon returning to 0 V, G recovered with a biexponential time course, reaching its maximal value after several seconds; recovery time constants after a step in V from 80 to 0 mV were 225 msec and 1.9 sec. In the resting state, at low junctional voltage, high conductance channel activity (160-240 pS) is favored. Voltage-dependent decline of G results in part from a shift from high to lower conductance states. [ABSTRACT FROM AUTHOR]
- Published
- 1992
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228. Renal salt wasting and chronic dehydration in claudin-7-deficient mice
- Author
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Tatum, Rodney, Zhang, Yuguo, Salleng, Kenneth, Lu, Zhe, Lin, Jen-Jar, Lu, Qun, Jeansonne, Beverly G., Ding, Lei, and Chen, Yan-Hua
- Abstract
Claudin-7, a member of the claudin family, is highly expressed in distal nephrons of kidneys and has been reported to be involved in the regulation of paracellular Cl−permeability in cell cultures. To investigate the role of claudin-7 in vivo, we generated claudin-7 knockout mice (Cln7−/−) by the gene-targeting deletion method. Here we report that Cln7−/−mice were born viable, but died within 12 days after birth. Cln7−/−mice showed severe salt wasting, chronic dehydration, and growth retardation. We found that urine Na+, Cl−, and K+were significantly increased in Cln7−/−mice compared with that of Cln7+/+mice. Blood urea nitrogen and hematocrit were also significantly higher in Cln7−/−mice. The wrinkled skin was evident when Cln7−/−mice were ∼1 wk old, indicating that they suffered from chronic fluid loss. Transepidermal water loss measurements showed no difference between Cln7+/+and Cln7−/−skin, suggesting that there was no transepidermal water barrier defect in Cln7−/−mice. Claudin-7 deletion resulted in the dramatic increase of aldosterone synthase mRNA level as early as 2 days after birth. The significant increases of epithelial Na+channel α, Na+-Cl−cotransporter, and aquaporin 2 mRNA levels revealed a compensatory response to the loss of electrolytes and fluid in Cln7−/−mice. Na+-K+-ATPase α1expression level was also greatly increased in distal convoluted tubules and collecting ducts where claudin-7 is normally expressed. Our study demonstrates that claudin-7 is essential for NaCl homeostasis in distal nephrons, and the paracellular ion transport pathway plays indispensable roles in keeping ionic balance in kidneys.
- Published
- 2010
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229. The NGF Point-Injection for Treatment of the Sound-Perceiving Nerve Deafness and Tinnitus in 68 Cases
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ZHOU, Feng, WU, Ping, WANG, Li, WANG, Hai-tao, ZHANG, Shao-bin, LIN, Yi, ZHONG, Hui, and CHEN, Yan-hua
- Published
- 2009
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230. Using Lyapunov function to design optimal controller for AQM routers
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Zhang, Peng, Ye, Cheng-qing, Ma, Xue-ying, Chen, Yan-hua, and Li, Xin
- Abstract
It was shown that active queue management schemes implemented in the routers of communication networks supporting transmission control protocol (TCP) flows can be modelled as a feedback control system. In this paper based on Lyapunov function we developed an optimal controller to improve active queue management (AQM) router’s stability and response time, which are often in conflict with each other in system performance. Ns-2 simulations showed that optimal controller outperforms PI controller significantly.
- Published
- 2007
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231. The Combined Antenatal Corticosteroids and Vitamin K Therapy for Preventing Periventricular–Intraventricular Hemorrhage in Premature Newborns less than 35 weeks Gestation
- Author
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Liu, Jing, Wang, Qi, Zhao, Jin-hui, Chen, Yan-hua, and Qin, Gui-lian
- Abstract
We prospectively evaluated whether combined antenatal corticosteroid and vitamin K administration have any benefit, over and above that of corticosteroid or vitamin K used alone, in reducing the frequency and the degree of PIVH in premature newborns less than 35 weeks’ gestation. All of these 280 pregnant women were randomly allocated into five groups according to the in-patient sequence. Group A (vitamin K1 group) including 38 pregnant women (40 newborns) received antenatal intramuscular or intravenously injection of vitamin K1 10 mg per day for 2–7 days. Group B (single dose corticosteroid group) including 57 pregnant women (63 newborns) received antenatal intramuscular or intravenously injection of dexamethasone 10 mg per day for 1 day. Group C (two dose corticosteroid group) including 62 pregnant women (70 newborns) received antenatal intramuscular or intravenously injection of dexamethasone 10 mg per day for 2 days. Group D (combined using dexamethasone and vitamin K1) including 41 pregnant women (44 newborns) received dexamethasone 10 mg per day for 1 day and vitamin K110 mg per day for 2–7 days. Control group, including 82 pregnant women (87 newborns) were received neither dexamethasone nor vitamin K1 injection. The results showed PIVH was diagnosed in 17 of 40 (42.5%) in Group A, 34 of 63 (54.0%) in Group B, 36 of 70 (51.4%) in Group C, 14 of 44 (31.8%) in Group D, and 57 of 87 (65.2%) in control infants (p = 0.004). More infants in the control group had grade III or IV intracranial hemorrhage after birth (p = 0.049). After antenatal supplement of dexamethasone and vitamin K1, both the total incidence of PIVH and the frequency of severe PIVH decreased significantly. The total and severe incidence of PIVH in Group B (single doses dexamethasone) and Group C (two courses dexamethasone) there were no significant difference. It showed that after antenatal supplement of dexamethasone and vitamin K1, both the total incidence of PIVH and the frequency of severe PIVH decreased significantly, and combined antenatal corticosteroid and vitamin K administration have much benefit, over and above that of corticosteroid or vitamin K used alone.
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- 2006
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232. Formation of Functional Tight Junctions inXenopusEmbryos
- Author
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Merzdorf, Christa S., Chen, Yan-Hua, and Goodenough, Daniel A.
- Abstract
Formation of the blastocoel in earlyXenopusembryos was studied with a novel biotin-permeability assay and newly generated tight junction markers. The blastocoel forms at the first cleavage division since functional tight junctions which excluded biotin and established a segregated intraembryonic compartment were found at the 2-cell and all subsequent developmental stages. Unexpectedly, tight junctions before the 64-cell stage were not at their normal apical positions, but were found deep in the embryos, up to 200 μm from the apical surface. In these positions, the tight junctions left large areas of ion permeable lateral membranes exposed to the extraembryonic environment, explaining why electrophysiological experiments record a decrease in embryonic input resistances concomitant with early cleavage stages. Immunohistochemistry revealed that the recessed tight junctions did not influence the distribution of C-cadherin and Na+,K+ATPase. Both markers were present apical to recessed tight junctions, indicating that the maintenance of polarization of these basolateral markers does not require tight junctions. With further development, tight junctions assumed an increasingly apical location until, by the 2000-cell stage, they occupied their conventional positions between the blastomeres at the apical/lateral membrane boundaries.
- Published
- 1998
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233. Colonic crypt stem cell functions are controlled by tight junction protein claudin‐7 through Notch/Hippo signaling.
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Naser, Amna N., Xing, Tiaosi, Tatum, Rodney, Lu, Qun, Boyer, Philip J., and Chen, Yan‐Hua
- Subjects
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TIGHT junctions , *NOTCH genes , *HIPPO signaling pathway , *CELL physiology , *STEM cells , *NOTCH signaling pathway - Abstract
The tight junction protein claudin‐7 is essential for tight junction function and intestinal homeostasis. Cldn7 deletion in mice leads to an inflammatory bowel disease‐like phenotype exhibiting severe intestinal epithelial damage, weight loss, inflammation, mucosal ulcerations, and epithelial hyperplasia. Claudin‐7 has also been shown to be involved in cancer metastasis and invasion. Here, we test our hypothesis that claudin‐7 plays an important role in regulating colonic intestinal stem cell function. Conditional knockout of Cldn7 in the colon led to impaired epithelial cell differentiation, hyperproliferative epithelium, a decrease in active stem cells, and dramatically altered gene expression profiles. In 3D colonoid culture, claudin‐7–deficient crypts were unable to survive and form spheroids, emphasizing the importance of claudin‐7 in stem cell survival. Inhibition of the Hippo pathway or activation of Notch signaling partially rescued the defective stem cell behavior. Concurrent Notch activation and Hippo inhibition resulted in restored colonoid survival, growth, and differentiation to the level comparable to those of wild‐type derived crypts. In this study, we highlight the essential role of claudin‐7 in regulating Notch and Hippo signaling–dependent colonic stem cell functions, including survival, self‐renewal, and differentiation. These new findings may shed light on potential avenues to explore for drug development in colorectal cancer. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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234. Claudin-7 Modulates Cl− and Na+ Homeostasis and WNK4 Expression in Renal Collecting Duct Cells.
- Author
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Fan, Junming, Tatum, Rodney, Hoggard, John, and Chen, Yan-Hua
- Subjects
TRANSCYTOSIS ,CURRENT-voltage curves ,SODIUM channels ,CELLS ,HOMEOSTASIS ,CELL lines - Abstract
Claudin-7 knockout (CLDN7
−/− ) mice display renal salt wasting and dehydration phenotypes. To address the role of CLDN7 in kidneys, we established collecting duct (CD) cell lines from CLDN7+/+ and CLDN7−/− mouse kidneys. We found that deletion of CLDN7 increased the transepithelial resistance (TER) and decreased the paracellular permeability for Cl− and Na+ in CLDN7−/− CD cells. Inhibition of transcellular Cl− and Na+ channels has no significant effect on TER or dilution potentials. Current-voltage curves were linear in both CLDN7+/+ and CLDN7−/− CD cells, indicating that the ion flux was through the paracellular pathway. The impairment of Cl− and Na+ permeability phenotype can be rescued by CLDN7 re-expression. We also found that WNK4 (its mutations lead to hypertension) expression, but not WNK1, was significantly increased in CLDN7−/− CD cell lines as well as in primary CLDN7−/− CD cells, suggesting that the expression of WNK4 was modulated by CLDN7. In addition, deletion of CLDN7 upregulated the expression level of the apical epithelial sodium channel (ENaC), indicating a potential cross-talk between paracellular and transcellular transport systems. This study demonstrates that CLDN7 plays an important role in salt balance in renal CD cells and modulating WNK4 and ENaC expression levels that are vital in controlling salt-sensitive hypertension. [ABSTRACT FROM AUTHOR]- Published
- 2019
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235. Risk factors for Barrett's esophagus in young adults who underwent upper gastrointestinal endoscopy in a health examination center.
- Author
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Wu, Pin-Chieh, Chen, Yan-Hua, Wu, Fu-Zong, Lin, Kung-Hung, Hsu, Chiao-Lin, Chen, Chi-Shen, Chen, Yu-Hsun, Lin, Po-Hsiang, Mar, Guang-Yuan, and Yu, Hsien-Chung
- Subjects
- *
BARRETT'S esophagus , *GASTROESOPHAGEAL reflux , *YOUNG adults , *PERIODIC health examinations , *MEDICAL centers , *LOGISTIC regression analysis , *PRECANCEROUS conditions ,EXAMINATION of the gastrointestinal system - Abstract
Background: Barrett's esophagus (BE) is a premalignant condition with increased incidence worldwide both in old and young individuals. However, the role of certain potential risk factors remains unclear in young adults (< 50 years). We aimed to determine the risk factors of BE in young adults. Methods: A total of 4943 young adults who underwent upper gastrointestinal endoscopy at our health check-up center were enrolled. The diagnosis of BE was based on histological confirmation. We analyzed demographic factors, laboratory data, potential risk factors such as smoking, alcohol consumption, presence of gastroesophageal reflux disease (GERD) symptoms, and metabolic syndrome for the risk of BE by using binary logistic regression analysis. Results: The prevalence of BE was 1.8% (88/4943). Male sex, the presence of GERD symptoms, and smoking were three significant risk factors related to BE. Furthermore, participants who had smoked for 10 pack-years or more had increased risk of BE with dose-dependent phenomenon (p trend < 0.001). The proportion of BE in male participants with both GERD symptoms and a smoking history of 10 pack-years or more was as high as 10.3% (16/155). Conclusions: Significant risk factors of BE in young adults are male sex, the presence of GERD symptoms, and smoking. The risk also increases with an increase in cumulative exposure to smoking. [ABSTRACT FROM AUTHOR]
- Published
- 2019
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236. Role of Fatty Liver Index and Metabolic Factors in the Prediction of Nonalcoholic Fatty Liver Disease in a Lean Population Receiving Health Checkup.
- Author
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Hsu, Chiao-Lin, Wu, Fu-Zong, Lin, Kung-Hung, Chen, Yu-Hsun, Wu, Pin-Chieh, Chen, Yan-Hua, Chen, Chi-Shen, Wang, Wen-Hwa, Mar, Guang-Yuan, and Yu, Hsien-Chung
- Published
- 2019
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237. Necrotizing enterocolitis leads to disruption of tight junctions and increase in gut permeability in a mouse model.
- Author
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Ravisankar, Srikanth, Tatum, Rodney, Garg, Parvesh M., Herco, Maja, Shekhawat, Prem S., and Chen, Yan-Hua
- Subjects
NEONATAL necrotizing enterocolitis ,TIGHT junctions ,CLAUDINS ,SEPSIS ,EPITHELIAL cells ,ANIMAL experimentation ,BIOLOGICAL models ,CAPILLARY permeability ,CELL membranes ,INFLAMMATORY mediators ,INTESTINAL mucosa ,MEMBRANE proteins ,MICE ,RESEARCH funding - Abstract
Background: Necrotizing enterocolitis (NEC) is a leading cause of death in preterm infants. Neonates weighing <1500 grams are at the highest risk for acquiring NEC, with a prevalence of nearly 7-10%, mortality up to 30%, and several long-term complications among survivors. Despite advancements in neonatal medicine, this disease remains a challenge to treat. The aim of this study is to investigate the effect of NEC on gut epithelial tight junctions and its barrier function using a NEC mouse model.Methods: Three-day old C57BL/6 mouse pups were fed with Esbilac formula every 3 hours and then subjected to hypoxia twice daily followed by cold stress. Dam fed pups from the same litters served as controls. Pups were observed and sacrificed 96 hours after the treatments and intestines were removed for experiments. The successful induction of NEC was confirmed by histopathology. Changes in tight junction proteins in NEC intestines were studied by western blotting and immunofluorescent microscopy using specific protein markers. The gut leakage in NEC was visualized using biotin tracer molecules.Results: Our study results demonstrate that we induced NEC in >50% of experimental pups, pups lost nearly 40% of weight and their intestines showed gross changes and microscopic changes associated with NEC. There were inflammatory changes with loss of tight junction barrier function and disruption of tight junction claudin proteins in the intestines of NEC mouse model. We have demonstrated for the first time that NEC intestines develop increased leakiness as visualized by biotin tracer leakage.Conclusions: NEC leads to breakdown of epithelial barrier due to changes in tight junction proteins with increased leakiness which may explain the transmigration of microbes and microbial products from the gut lumen into the blood stream leading to sepsis like signs clinically witnessed. [ABSTRACT FROM AUTHOR]- Published
- 2018
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238. Claudin-7 modulates cell-matrix adhesion that controls cell migration, invasion and attachment of human HCC827 lung cancer cells.
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Kim, Do Hyung, Lu, Qun, and Chen, Yan-Hua
- Subjects
- *
CELL-matrix adhesions , *CELL migration , *CANCER cells , *TIGHT junctions , *LUNG cancer - Abstract
Claudins are a family of tight junction proteins, and serve important roles in epithelial barrier, selective ion transports and cancer metastasis. Although the exact role of claudin-7 in human lung cancer has not been completely elucidated, recent clinical studies have demonstrated that claudin-7 is associated with the survival of patients with lung cancer. Our previous studies have demonstrated that claudin-7 forms a protein complex with integrin β1 in human lung cancer cells. The knockdown (KD) of claudin-7 by short hairpin RNA (shRNA) reduced integrin β1 expression and increased the cell proliferative rate, whereas claudin-7 re-expression in the KD cells decreased the cell proliferation. It is unknown as to whether claudin-7 and integrin β1 regulate cell proliferation and invasion synergistically or independently. In the present study, it was observed that ectopic expression of integrin β1 in claudin-7 KD lung cancer cells did not reduce the cell proliferation. However, integrin β1-transfected cells migrated more effectively in wound healing and cell invasion assays and were more adhesive in a cell attachment assay when compared with those of claudin-7 KD cells. This indicates that claudin-7 controls cell proliferation, while cell attachment and motility were regulated partially through integrin β1. Additionally, claudin-7 overexpression in claudin-7 KD cells resulted in an improved ability to attach to the surface of cell culture plates and a higher expression of focal adhesion proteins when compared with claudin-7 non-KD control cells, which supports the role of claudin-7 in cell adhesion and motility. Taken together, these data suggest that claudin-7 regulates cell motility through integrin β1, providing additional insight into the roles of claudins in carcinogenesis and cancer cell metastasis. [ABSTRACT FROM AUTHOR]
- Published
- 2019
239. A novel surgical method for treating medial-end clavicle fractures.
- Author
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Xie, Wen-Peng, Zhang, Yong-Kui, Chen, Yan-Hua, Wang, Shi-Lu, Xu, Hong-Hao, and Bi, Rong-Xiu
- Subjects
- *
CLAVICLE injuries , *DISABILITIES , *ARM , *SHOULDER , *STANDARDIZATION - Abstract
The present study examined the effectiveness of the method of inversing the distal clavicle anatomic locking plate to treat medial-end clavicle fractures. This involved retrospectively analyzing six cases of medial-end clavicle fractures treated using the method of inversing the distal clavicle anatomic locking plate between September 2013 and December 2015. These cases included five men and one woman with an average age of 46.3±10.6 years old and a range of 24–66 years old. Among these cases, one was type A, two were type C, and three were type D, based on the Throckmorton type classification. All patients had fresh closed fractures, which were caused by direct injury. A regular postoperative follow-up was performed and the therapeutic efficacy was evaluated systematically with reference to the Rockwood and Disability of the Arm, Shoulder and Hand (DASH) score standards. All six cases had a follow-up visit, which was between 10 and 14 months with an average of 12.0±2.2 months. All patients exhibited osseous healing and functional recovery without incision infection, nerve vascular injury, chest injury, fracture nonunion, or other complications. According to the Rockwood and DASH score standards, evaluation of the curative effect showed that five cases were excellent and one case was good, and the associated rate for achieving good or excellent outcomes was 100%. All of the DASH scores were <10. These results indicated that the effect of the treatment of medial-end clavicle fractures by the method of inversing the distal clavicle anatomic locking plate was reliable, and the functional recovery of patients was good, making this method worthy of clinical promotion. [ABSTRACT FROM AUTHOR]
- Published
- 2018
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240. Erratum to: Identification of a novel mutation in a Chinese family with Nance-Horan syndrome by whole exome sequencing.
- Author
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Hong, Nan, Chen, Yan-hua, Xie, Chen, Xu, Bai-sheng, Huang, Hui, Li, Xin, Yang, Yue-qing, Huang, Ying-ping, Deng, Jian-lian, Qi, Ming, and Gu, Yang-shun
- Published
- 2014
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- View/download PDF
241. Nanoarchitecture and molecular interactions of epithelial cell junction proteins revealed by super‐resolution microscopy.
- Author
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Naser, Amna N., Guiler, William, Lu, Qun, and Chen, Yan‐Hua
- Subjects
- *
CELL junctions , *MOLECULAR interactions , *FOCAL adhesion kinase , *EPITHELIAL cells , *HOLLIDAY junctions , *CELL adhesion molecules , *TIGHT junctions , *INTEGRINS - Abstract
Epithelial cells are polarized with defined apical tight junctions (TJs), lateral adherens junctions (AJs), and basal integrin–matrix interactions. However, it is increasingly recognized that resident cell junction proteins can be found in varying locations and with previously unrecognized functions. Our study here presents the nanoarchitecture and nanocolocalization of cell junction proteins in culture and tissue by stochastic optical reconstruction microscopy (STORM). The Z‐axial view of noncancerous MDCK‐II and PZ‐HPV‐7 cell–cell junctions resolved β‐catenin and p120ctn localizations to TJs and AJs, with p120ctn apical to β‐catenin and colocalizing with TJ protein claudin‐7. More basally, p120ctn and β‐catenin become colocalized. This topography was lost in isogenic Ras‐transformed MDCK cells and cancerous PC3 cells, where p120ctn becomes basally localized in relation to β‐catenin. Claudin‐7 gene conditional knockout (cKO) in mice also have altered polarity of p120ctn relative to β‐catenin, like that seen in normal‐to‐cancer cell phenotypic transformation. Additionally, claudin‐7 cKO resulted in redistribution and relocalization of other cell junction proteins, including claudin‐1, zonula occludens‐1, integrin α2, epithelial cell adhesion molecule, and focal adhesion kinase (FAK); specifically, integrin α2 and FAK were observed at the apical–lateral compartment. Our data show that STORM reveals regional cellular junction nanoarchitecture previously uncharacterized, providing new insight into potential trans‐compartmental modulation of protein functions. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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242. Antioxidant and Antimicrobial Phenolic Compounds from Setaria viridis.
- Author
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Fan, Lu, Ma, Jie, Chen, Yan-Hua, and Chen, Xuan-Qin
- Subjects
- *
SETARIA , *GRASSES , *PHENOLS , *ANTIOXIDANTS , *RHAMNOSE - Abstract
A chemical study of the 80% aqueous acetone extract of aerial parts of Setaria viridis led to the isolation of three new naphthol rhamnosides, 8-O-α-L-rhamnosyl-β-sorigenin ( 1), 6-hydroxy-8-O-α-L-rhamnosyl-β-sorigenin ( 2), and 6-methoxy-8-O-α-L-rhamnosyl-β-sorigenin ( 3), together with nine ( 4-12) known compounds. Their structures were established on the basis of spectroscopic data, including IR, MS, 1D, and 2D NMR. All the 12 compounds were tested for their antioxidant activity against 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals, as well as antimicrobial activity. Compounds 1-3 exhibited strong antioxidant activity with IC values of 10.5, 13.8, and 15.3 μM, respectively, and modest activity against Staphylococcus aureus (ATCC 29213). [ABSTRACT FROM AUTHOR]
- Published
- 2014
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243. Cytotoxicity of cyclometalated platinum complexes based on tridentate NCN and CNN-coordinating ligands: Remarkable coordination dependence.
- Author
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Vezzu, Dileep A.K., Lu, Qun, Chen, Yan-Hua, and Huo, Shouquan
- Subjects
- *
CELL-mediated cytotoxicity , *PLATINUM , *COMPLEX compounds , *ANTINEOPLASTIC agents , *CANCER cell analysis , *DNA-binding proteins - Abstract
Abstract: A series of cyclometalated platinum complexes with diverse coordination patterns and geometries were screened for their anticancer activity. It was discovered that the N^C^N-coordinated platinum complex based on 1,3-di(pyridyl)benzene displayed much higher cytotoxicity against human lung cancer cells NCI-H522, HCC827, and NCI-H1299, and human prostate cancer cell RV1 than cisplatin. In a sharp contrast, the C^N^N-coordinated platinum complex based on 6-phenyl-2,2′-bipyridine was ineffective on these cancer cells. This remarkable difference in cytotoxicity displayed by N^C^N- and C^N^N-coordinated platinum complexes was related to the trans effect of the carbon donor in the cyclometalated platinum complexes, which played a crucial role in facilitating the dissociation of the chloride ligand to create an active binding site. The DNA binding was studied for the N^C^N-coordinated platinum complex using electrophoresis and emission titration. The cellular uptake observed by fluorescent microscope showed that the complex is largely concentrated in the cytoplasm. The possible pathways for the cell apoptosis were studied by western blot analysis and the activation of PARP via caspase 7 was observed. [Copyright &y& Elsevier]
- Published
- 2014
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244. Differential expression profile of MAGE family in non-small-cell lung cancer
- Author
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Tsai, Jong-Rung, Chong, Inn-Wen, Chen, Yan-Hua, Yang, Ming-Je, Sheu, Chau-Chyun, Chang, Huang-Chou, Hwang, Jhi-Jhu, Hung, Jen-Yu, and Lin, Shiu-Ru
- Subjects
- *
CANCER cells , *IMMUNOTHERAPY , *MAJOR histocompatibility complex , *GENE expression - Abstract
Summary: The expression of the melanoma-associated antigen (MAGE) genes consists of variables in all tumor types, such as lung cancer, which are relevant to be silent in all normal tissues except germ cells. They are considered as tumor-specific antigens, and are ideal targets for cancer immunotherapy. A complete MAGE genes differential expression profile analysis of lung cancer can provide this study not only various target genes for immunotherapy, but also valuable markers for further diagnosis and prognosis. This research has constructed a membrane array, which was consisted 32 MAGE genes, to detect whether the differential expression profile occurred in 52 pairs of non-small-cell lung cancer (NSCLC) samples. Nearly 32 MAGE genes have been differential expressed in NSCLC except MAGE-B1 and -E2. MAGE-B, -C, -D, and subgroup -B6, -D4 have showed prominences in lung adenocarcinoma. High-frequent expression of MAGE-D, and subgroup -A2, -D2 has also been discovered in non-metastasis group (p <0.05). However, there is no significant difference of MAGE genes differential expression shown among different primary tumor (T), nodal involvement (N) and overall stages. Several MAGE subgroup genes, such as MAGE-A5, -A7, -A8, -A9, -A11, -B3, -B4, -B10, -D2, -D3, -F1, -G1, -H1, and -L2, have been first discovered to show differential expression in NSCLC. Although the small size of the sample may limit the diagnostic and prognostic value of MAGE genes, the function of the membrane array can provide this study a high-throughput method to detect the whole MAGE genes differential expression profile. [Copyright &y& Elsevier]
- Published
- 2007
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245. Tetracycline‐levofloxacin versus amoxicillin‐levofloxacin quadruple therapies in the second‐line treatment of Helicobacter pylori infection.
- Author
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Hsu, Ping‐I, Tsay, Feng‐Woei, Kao, John Y., Peng, Nan‐Jing, Chen, Yan‐Hua, Tang, Sheng‐Yeh, Kuo, Chao‐Hung, Kao, Sung‐Shuo, Wang, Huay‐Min, Wu, I‐Ting, Shie, Chang‐Bih, Chuah, Seng‐Kee, and Wu, Deng‐Chyang
- Subjects
- *
HELICOBACTER pylori infections , *HELICOBACTER pylori - Abstract
Background: The Maastricht V/Florence Consensus Report recommends amoxicillin‐fluoroquinolone triple or quadruple therapy as a second‐line treatment for Helicobacter pylori infection. An important caveat of amoxicillin‐fluoroquinolone rescue therapy is poor eradication efficacy in the presence of fluoroquinolone resistance. The study aimed to investigate the efficacies of tetracycline‐levofloxacin (TL) quadruple therapy and amoxicillin‐levofloxacin (AL) quadruple therapy in the second‐line treatment of H. pylori infection. Methods: Consecutive H. pylori‐infected subjects after the failure of first‐line therapies were randomly allocated to receive either TL quadruple therapy (tetracycline 500 mg QID, levofloxacin 500 mg QD, esomeprazole 40 mg BID, and tripotassium dicitrato bismuthate 300 mg QID) or AL quadruple therapy (amoxicillin 500 mg QID, levofloxacin 500 mg QD, esomeprazole 40 mg BID, and tripotassium dicitrato bismuthate 300 mg QID) for 10 days. Post‐treatment H. pylori status was assessed 6 weeks after the end of therapy. Results: The study was early terminated after an interim analysis. In the TL quadruple group, 50 out of 56 patients (89.3%) had successful eradication of H. pylori infection. Cure of H. pylori infection was achieved only in 39 of 52 patients (69.6%) receiving AL quadruple therapy. Intention‐to‐treat analysis showed that TL quadruple therapy achieved a markedly higher eradication rate than AL quadruple therapy (95% confidence interval: 4.8% to 34.6%; p = 0.010). Further analysis revealed that TL quadruple therapy had a high eradication rate for both levofloxacin‐susceptible and resistant strains (100% and 88.9%). In contrast, AL quadruple therapy yielded a high eradication for levofloxacin‐susceptible strains (90.9%) but a poor eradication efficacy for levofloxacin‐resistant strains (50.0%). The two therapies exhibited comparable frequencies of adverse events (37.5% vs 21.4%) and drug adherence (98.2% vs 94.6%). Conclusions: Ten‐day TL quadruple therapy is more effective than AL quadruple therapy in the second‐line treatment of H. pylori infection in a population with high levofloxacin resistance. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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246. Hepatotoxicity evaluations of different surface charged carbon quantum dots in vivo and in vitro.
- Author
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Chen, Yi-Chun, Chen, Hung-Hsiang, Lin, Han-Jia, Huang, Chih-Ching, Chen, Ku-Fan, Peng, Yen-Ping, Tsang, Yiu Fai, Chen, Yan-Hua, Lin, Kun-Yi Andrew, and Lin, Chia-Hua
- Subjects
- *
SURFACE charges , *QUANTUM dots , *SURFACE charging , *HEPATOTOXICOLOGY , *CYTOTOXINS - Abstract
Recently, carbon quantum dots (CQDs) have become popular because of their simple synthesis and potential applications. Although CQDs have high biocompatibility, their biotoxicity must be verified to reduce the possible risks associated with large-scale application. In this study, the hepatotoxicity of three CQD types, namely diammonium citrate (AC)-based (CQDs-AC), spermidine trihydrochloride (Spd)-based (CQDs-Spd), and AC- and Spd-based CQDs (CQDs-AC/Spd), were evaluated in vivo and in vitro. It was observed in vivo that CQDs-Spd and CQDs-AC/Spd, but not CQDs-AC, caused histopathological damage, including liver steatosis and mild mixed inflammatory cell infiltration; however, reduced liver function was only observed in CQD-Spd–treated mice. The in vitro results revealed that only CQDs-Spd significantly decreased the number of viable HepG2 cells (NADH depletion) and induced oxidative stress (heme oxygenase-1 activation) after 24 h of exposure, which promoted inflammatory factor secretion (NF-κB activation). Additionally, decreasing zonula occludens-2 and α1-antitrypsin protein expression in HepG2 cells suggested that CQD-Spd exposure increases the risk of liver diseases. Our results revealed that CQDs-Spd had greater hepatotoxic potential than CQDs-AC and CQDs-AC/Spd, which might be attributable to their high positive surface charge. Overall, the risk of CQD-induced hepatotoxic risk must be considered when applying positively charged CQDs. [Display omitted] • CQDs-Spd can induce histopathological harm and impair liver function. • CQDs-Spd initiates pronounced oxidative cytotoxicity. • CQDs-Spd triggers heightened inflammatory responses. • CQDs-Spd may accelerate the initial stages of liver disease. • Exposure to positively charged surface CQDs can impact hepatic well-being. [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF
247. Equivalent efficacies of reverse hybrid and concomitant therapies in first‐line treatment of Helicobacter pylori infection.
- Author
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Hsu, Ping‐I, Tsay, Feng‐Woei, Kao, John Y, Peng, Nan‐Jing, Tsai, Kuo‐Wang, Tsai, Tzung‐Jiun, Kuo, Chao‐Hung, Kao, Sung‐Shuo, Wang, Huay‐Min, Chen, Yan‐Hua, Shie, Chang‐Bih, and Wu, Deng‐Chyang
- Subjects
- *
HELICOBACTER pylori infections , *HELICOBACTER pylori , *TREATMENT effectiveness , *DRUG resistance in bacteria - Abstract
Background and Aim: Concomitant therapy is a recommended first‐line treatment for Helicobacter pylori infection in most national or international consensuses. Reverse hybrid therapy is a modified 14‐day concomitant therapy without clarithromycin and metronidazole in the final 7 days. This study aims to test whether 14‐day reverse hybrid therapy is non‐inferior to 14‐day concomitant therapy in the first‐line treatment of H. pylori infection. Methods: Helicobacter pylori‐infected adult patients were randomly assigned to receive either reverse hybrid therapy (dexlansoprazole 60 mg o.d. plus amoxicillin 1 g b.d. for 14 days, and clarithromycin 500 mg plus metronidazole 500 mg b.d. for initial 7 days) or concomitant therapy (dexlansoprazole 60 mg once o.d. plus amoxicillin 1 g, clarithromycin 500 mg, and metronidazole 500 mg b.d. for 14 days). H. pylori status was assessed 6 weeks after the end of treatment. Results: Helicobacter pylori‐infected participants (n = 248) were randomized to receive either 14‐day reverse hybrid therapy (n = 124) or 14‐day concomitant therapy (n = 124). Intention‐to‐treat analysis demonstrated that the two therapies had comparable eradication rate (95.2% vs 93.5%; 95% confidence interval, −4.0% to 7.4%; P = 0.582). However, reverse hybrid therapy had a much lower frequency of adverse events than concomitant therapy (20.2% vs 38.7%, P = 0.001). The two therapies exhibited comparable drug adherence (93.5% vs 87.9%, P = 0.125). Conclusions: Fourteen‐day reverse hybrid therapy and 14‐day concomitant therapy are equivalent in efficacy for the first‐line treatment of H. pylori infection. However, reverse hybrid therapy has fewer adverse events compared with concomitant therapy. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
248. Kinetics of hepatitis B surface antigen and estimated glomerular filtration rate in telbivudine-treated hepatitis B patients with different rescue strategies.
- Author
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Yu, Hsien-Chung, Lin, Kung-Hung, Tsay, Feng-Woei, Tsai, Tzung-Jiun, Wu, Pin-Chieh, Chen, Yu-Hsun, and Chen, Yan-Hua
- Subjects
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HEPATITIS associated antigen , *CHRONIC hepatitis B , *GLOMERULAR filtration rate , *HEPATITIS B - Abstract
This study investigated the kinetics of estimated glomerular filtration rate (eGFR) and quantitative hepatitis B surface antigen (qHBsAg) in telbivudine (LdT)-treated chronic hepatitis B (CHB) patients whose treatment was subsequently adjusted with the adding on adefovir or by switching to tenofovir disoproxil fumarate (TDF) as rescue. Of 295 CHB patients initially treated with LdT, 102 of them who subsequently receiving either adding-on adefovir (group A, n = 58) or switching to TDF (group B, n = 44) for more than 24 months were enrolled. Serial eGFR and qHBsAg levels (3 to 6 monthly) in both LdT monotherapy and rescue therapy periods were analyzed retrospectively. Subsequent decline of qHBsAg especially in rescue therapy period were noted (p<0.001 and p = 0.068 in group A and B). However, patients in group B achieved a significant increase of eGFR (p = 0.010) in LdT monotherapy period but had a significant decline of eGFR (p<0.001) in rescue therapy period. In contrast, patients in group A maintained eGFR levels in both periods. Meanwhile, switch to TDF (hazard ratio: 3.036; 95% confidence interval: 1.040–8.861; p = 0.042) was the sole factor related to the decrease of eGFR>20% from baseline. Both rescue therapies achieved subsequent declines of qHBsAg over time but caused different changes in eGFR. LdT-based rescue therapy maintained eGFR but TDF switching therapy descended eGFR. Therefore, it is essential to monitor patient's renal function intensively when switching from LdT to TDF as a rescue strategy. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
249. The expression of glucose transporters and mitochondrial division and fusion proteins in rats exposed to hypoxic preconditioning to attenuate propofol neurotoxicity.
- Author
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Xiao, Fei, Lv, Jing, Liang, Yu Bing, Chen, Yan Hua, Tu, You Bing, Guan, Rui Cong, Li, Li, and Xie, Yu Bo
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GLUCOSE transporters , *CHIMERIC proteins , *HYPOXIA-inducible factor 1 , *NEUROTOXICOLOGY , *RATS , *TRANSMISSION electron microscopy - Abstract
Purpose: Evidence has shown that propofol may cause widespread apoptotic neurodegeneration. Hypoxic preconditioning has been demonstrated to provide neuroprotection and brain recovery from both acute and chronic neurodegeneration in several cellular and animal models. However, the mechanism has not been well elucidated. Therefore, the present study was designed to investigate the expression of glucose transporters (GLUT1 and GLUT3) and mitochondrial division and fusion (Drp1 and Mfn2) proteins in rats exposed to hypoxic preconditioning to attenuate propofol neurotoxicity. Methods: Propofol (100 mg/kg) was given to 7-day-old Sprague-Dawley rats; in some rats, hypoxic preconditioning was administered before intraperitoneal propofol injection by subjecting rats to five cycles of 10 min of hypoxia (8% O2) and 10 min of normoxia (21% O2). Then, the rats were allowed to breathe room air for 2 h. Neuronal mitochondrial morphology was observed by transmission electron microscopy. ATP content was detected using an ATP assay kit. The expression levels of GLUT1, GLUT3, pDrp1, Drp1 and Mfn2 were detected by Western blot, and the expression levels of GLUT1 and GLUT3 were further examined by immunohistochemistry. Results: Propofol damaged mitochondria, and decreased ATP content and GLUT3 and pDrp1 protein expression. However, our results suggested that hypoxic preconditioning could attenuate propofol neurotoxicity by reducing mitochondrial damage and increasing ATP content and pDrp1, GLUT1 and GLUT3 protein expression. Conclusion: Hypoxic preconditioning reduced propofol-induced damage in the hippocampus of neonatal rats by attenuating the increase in mitochondrial division and decrease in GLUT3 expression. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
250. Short‐term and long‐term impacts of Helicobacter pylori eradication with reverse hybrid therapy on the gut microbiota.
- Author
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Hsu, Ping‐I, Pan, Chao‐Yu, Kao, John Y, Tsay, Feng‐Woei, Peng, Nan‐Jing, Kao, Sung‐Shuo, Chen, Yan‐Hua, Tsai, Tzung‐Jiun, Wu, Deng‐Chyang, and Tsai, Kuo‐Wang
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HELICOBACTER pylori , *GUT microbiome , *PATHOGENIC bacteria , *POLYMERASE chain reaction - Abstract
Background and Aims: Anti‐Helicobacter pylori therapy may lead to the growth of pathogenic or antibiotic‐resistant bacteria in the gut. The study aimed to investigate the short‐term and long‐term impacts of H. pylori eradication with reverse hybrid therapy on the components and macrolide resistance of the gut microbiota. Methods: Helicobacter pylori‐related gastritis patients were administered a 14‐day reverse hybrid therapy. Fecal samples were collected before treatment and at the end of week 2, week 8, and week 48. The V3–V4 region of the bacterial 16S rRNA gene in fecal specimens was amplified by polymerase chain reaction and sequenced on Illumina MiSeq platform. Additionally, amplification of erm(B) gene (encoding erythromycin resistance methylase) was performed. Results: Reverse hybrid therapy resulted in decreased relative abundances of Firmicutes (from 62.0% to 30.7%; P < 0.001) and Actinobacteria (from 3.4% to 0.6%; 0.032) at the end of therapy. In contrast, the relative abundance of Proteobacteria increased from 10.2% to 49.1% (0.002). These microbiota alterations did not persist but returned to the initial levels at week 8 and week 48. The amount of erm(B) gene in fecal specimens was comparable with the pretreatment level at week 2 but increased at week 8 (0.025) and then returned to the pretreatment level by week 48. Conclusions: Helicobacter pylori eradication with reverse hybrid therapy can lead to short‐term gut dysbiosis. The amount of erm(B) gene in the stool increased transiently after treatment and returned to the pretreatment level at 1‐year post‐treatment. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
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