ObjectiveTo summarize the recent therapeutic effects of mesh-plug tension-free hernioplasty in elderly inguinal hernia. MethodsAll cases were performed with mesh-plug case-hardened products, which are manufactured by American Bard Company. ResultsAll the operative procedures were performed smoothly. Postoperative complications were:6 cases of urinary retention,4 scrotal hydroceles,2 persistent wound pain,2 local lightly projections with foreign body sensation,2 hypoincisional haematoma. 1～24 months of follow-up were taken,2 recent recurrences were reported. ConclusionMesh-plug tension-free hernioplasty is a perfect surgical operation. Its main characteristics are:simple performance, less trauma, tension-free, time-saving, good recent therapeutic effect, and fewer recent recurrence. It is especially suitable to the elderly patients and/or Patients with other diseases.

OBJECTIVETo study the alterations of alpha-7 nicotinic receptor (nAChR) status in human brain tissues with Alzheimer's disease (AD) and mouse brain tissues with Swedish APP670/671 gene mutation, and to study the effect of beta-amyloid peptides (A-beta) on alpha-7 nAChR status in cultured astrocytes and neurons.

METHODSPostmortem brain tissues from patients with AD and mouse brain tissues with Swedish APP mutation were collected. The expression of alpha-7 nAChR on astrocytes and neurons was detected by immunohistochemistry (ABC method). The alpha-7 nAChR protein level was measured by Western blotting. On the other hand, cultured astrocytes and neurons were treated with different concentrations of A-beta 25 - 35. The alpha-7 nAChR protein level was then measured.

RESULTSIncreased number of astrocytes surrounding senile plaques was observed in AD brain tissues. In AD brain tissues, as compared to age-matched controls, alpha-7 nAChR protein level was increased in astrocytes, but decreased in neurons. High level of alpha-7 nAChR protein was also observed in mouse brain tissues with APP mutation. Exposure to A-beta 25 - 35 induced an increase (up to 38%) in alpha-7 nAChR protein level in astrocytes but a decrease (up to 32%) in neurons.

CONCLUSIONSDecrease in alpha-7 nAChR level in neurons may be related to the pathogenesis of AD, whereas an increased level of alpha-7 nAChR in astrocytes, as induced by excessive A-beta, may represent a compensatory neuroprotective response.

Aged ; Aged, 80 and over ; Alzheimer Disease ; genetics ; metabolism ; pathology ; Amyloid beta-Peptides ; chemistry ; genetics ; metabolism ; Animals ; Astrocytes ; cytology ; drug effects ; metabolism ; Brain ; metabolism ; pathology ; Cell Line, Tumor ; Cells, Cultured ; Glial Fibrillary Acidic Protein ; analysis ; Humans ; Immunoblotting ; Immunohistochemistry ; Male ; Mice ; Mutation ; Neurons ; cytology ; drug effects ; metabolism ; Peptide Fragments ; pharmacology ; Receptors, Nicotinic ; biosynthesis

OBJECTIVE: To investigate the inhibition effects of Tianshen Yizhi Recipe (TSYZR), a compound traditional Chinese herbal medicine, on decreased expression of nicotinic acetylcholine receptor (nAChR) and the neurotoxicity as well as lipid peroxidation induced by beta-amyloid peptide (Abeta) in human SH-SY5Y neuroblastoma cells. METHODS: The SH-SY5Y cells were treated by a certain concentration of TSYZR, and then exposed to Abeta(25-35). Methyl thiazolyl tetrazolium reduction assay was carried out to understand the influences of the drugs on cellular viability. Expressions of nAChR subunits (alpha3 and alpha7) at protein and mRNA levels were detected by Western-blotting and reverse transcription polymerase chain reaction, respectively. Lipid peroxidation was measured by thiobarbituric acid to observe the capacity of antioxidant of the drugs. RESULTS: TSYZR at a safe concentration could increase alpha7 protein in the cells, inhibit decreased expressions of alpha3 and alpha7 nAChR subunit proteins, prevent lower expression of alpha7 mRNA in SH-SY5Y cells induced by Abeta, reduce the neurotoxicity and lipid peroxidation resulting from Abeta, but had no significant effect on the lower expression of alpha3 mRNA. CONCLUSIONS: TSYZR can up-regulate the expression of alpha7 nAChR subunit protein and prevent decreased expressions of nAChRs and neurotoxicity as well as lipid peroxidation induced by Abeta. This drug may play an important therapeutic role in treatment of Alzheimer disease.

Objective:To investigate the association between polymorphisms of FGFR2 and the susceptibility of breast cancer in Han population in Guizhou province.Methods:Genotyping was performed using PCR-sequence-specific primers(PCR-SSP)in 106 histologically confirmed breast cancer cases and 116 cancer-free controls.Results:The genotype frequencies of rs1219648 TT,TC,and CC were 50%,25.47%.and 24.53% in breast cancer cases and 29.31%,48.28%,and 22.41% in the controls.The gene frequencies of T in breast cancer cases and the controls were 62.74% and 53.45%.respectively.The gene frequencies of C were 37.26% and 46.55%.respectively.The distribution of allele and genotype frequencies of FGFR2 rs1219648 was statistically different between breast cancer cases and the controls(P<0.05).Conclusion:FGFR2 rs1219648 polymorphism influences the susceptibility of breast cancer.TT genotype might serve as a risk factor for breast cancer.

The goal of this study is to investigate the population pharmacokinetics of oral tacrolimus in Chinese renal transplant patients and to identify possible relationship between covariates and population parameters. Details of drug dosage history, sampling time and concentration of 802 data points in 58 patients were collected retrospectively. Before analysis, the 58 patients were randomly allocated to either the model building group (n=41) or the validation group (n=17). Population pharmacokinetic data analysis was performed using the nonlinear mixed-effects model (NONMEM) program on the model building group. The pharmacokinetics of tacrolimus was best described by a one compartment model with first-order absorption and elimination. Typical values of apparent clearance (CL/F), apparent volume of distribution (V/F) were estimated. A number of covariates including demographic index, clinical index and coadministration of other drugs were evaluated statistically for their influence on these parameters. The final population model related clearance with POD (post operative days), HCT (haematocrit), AST (aspartate aminotransferase) and coadministration of nicardipine and diltiazem. Predictive performance of the final model evaluated with the validation group showed insignificant bias between observed and model predicted concentrations. Typical value of CL/F and V/F was 21.7 L x h(-1) and 241 L, inter-patient variability (RSD) in CL/F and V/F was 41.6% and 49.7%, respectively. The residual variability (SD) between observed and model-predicted concentrations was 2.19 microg x L(-1). The population pharmacokinetic model of tacrolimus in Chinese renal transplant patients was established and significant covariates on the tacrolimus model were identified.
Administration, Oral ; Adolescent ; Adult ; Aged ; Asian Continental Ancestry Group ; Female ; Humans ; Immunosuppressive Agents ; administration & dosage ; blood ; pharmacokinetics ; Kidney Transplantation ; Male ; Metabolic Clearance Rate ; Middle Aged ; Models, Statistical ; Nonlinear Dynamics ; Retrospective Studies ; Tacrolimus ; administration & dosage ; blood ; pharmacokinetics ; Young Adult

OBJECTIVESTo investigate the neuroprotective function of alpha 3 nicotinic acetylcholine receptor (nAChR) by inhibiting the gene expression in human neuroblastoma (SH-SY5Y) cells using small interference RNA (siRNA).

METHODSThe siRNA coding oligonucleotide sequences targeting alpha 3 nAChR were designed and synthesized. The annealed product was cloned into pSilencer 3.1-H1 neo vector. The recombinant alpha 3 nAChR pSilencer 3.1-H1 neo vector was transfected into the SH-SY5Y cells. The stable clones were screened by G418 medium, and the levels of alpha 3 nAChR mRNA and protein were monitored by using real-time PCR and Western blotting, respectively. After the SH-SY5Y cells with siRNA treatment were exposed to 1 micromol/L Abeta(1-42), MTT [3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide], SOD, GSH-px and the lipid peroxidation were measured by spectrophotometry.

RESULTSCompared with the controls, the expression levels of mRNA and protein in the stable SH-SY5Y clone cells transfected with the recombinant alpha 3 nAChR pSilencer 3.1-H1 neo vector were decreased with inhibitory efficiency of 98% and 66%, respectively, the MTT reduction decreased; the product of lipid peroxidation was increased and the activities of SOD and GSH-px were decreased. Biologically, the gene expression inhibition of alpha 3 nAChR enhanced the toxicity induced by Abeta in SH-SY5Y cells.

CONCLUSIONSThe expression inhibition of alpha 3 nAChR as a result of recombinant alpha 3 nAChR siRNA can induce oxidative stress and improve the toxicity of Abeta on SH-SY5Y cells, indicating that alpha 3 nAChR may play a significant neuroprotective role in the pathogenesis of Alzheimer disease.

Amyloid beta-Peptides ; pharmacology ; Cell Line, Tumor ; Cell Membrane ; drug effects ; Gene Expression Regulation ; drug effects ; Humans ; Neuroblastoma ; pathology ; Oxidation-Reduction ; drug effects ; Peptide Fragments ; pharmacology ; RNA Interference ; immunology ; RNA, Small Interfering ; pharmacology ; Receptors, Nicotinic ; drug effects ; genetics ; metabolism ; Superoxide Dismutase ; antagonists & inhibitors ; genetics ; metabolism

OBJECTIVETo study the effects of beta-amyloid peptide (Abeta) on cell membrane lipids and cholinergic receptors of human neuroblastoma cells.

METHODSHuman SH-SY5Y neuroblastoma cells were treated with different concentrations of Abeta(1-42) with and without pretreatment of vitamin E. MTT [3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide] reduction, lipid peroxidation, protein oxidation and phospholipids were measured by spectrophotometry. Levels of cholesterol and unbiquinone were determined by high-performance liquid chromatography (HPLC). The numbers of cholinergic receptor binding sites were determined by receptor binding assay and the protein levels of nicotinic receptor alpha3 and alpha7 subunits were studied by Western blotting.

RESULTSSH-SY5Y cells showed decreased reduction rates of MMT and phospholipids, and increased lipid peroxidation and protein oxidation after exposure to Abeta (0.1 micromol/L) as compared to the control. The number of cholinergic receptor binding sites, the protein level of nicotinic receptor alpha3 and alpha7 subunits and the content of ubiquinone decreased in cells treated with high dose of Abeta (1 micromol/L). Although the level of cholesterol was not changed in any way, vitamin E partially prevented the neurotoxic effects of Abeta.

CONCLUSIONbeta-amyloid peptide reduces the level of cell membrane lipids and cholinergic receptors in human SH-SY5Y neuroblastoma cells, likely through the induction of an enhanced oxidative stress.

Amyloid beta-Peptides ; administration & dosage ; metabolism ; toxicity ; Cell Line, Tumor ; Cell Membrane ; metabolism ; Cholesterol ; metabolism ; Dose-Response Relationship, Drug ; Humans ; Lipid Peroxidation ; drug effects ; Malondialdehyde ; metabolism ; Membrane Lipids ; metabolism ; Neuroblastoma ; metabolism ; pathology ; Oxidative Stress ; drug effects ; Peptide Fragments ; administration & dosage ; metabolism ; toxicity ; Phospholipids ; metabolism ; Receptors, Nicotinic ; metabolism ; Ubiquinone ; metabolism ; Vitamin E ; metabolism ; pharmacology

OBJECTIVETo investigate the influence of APP(SWE) on the expression of neuronal acetylcholine receptors (nAChRs) and its relationship with Alzheimer's disease (AD).

METHODSAPP(SWE), carried the Swedish family AD double mutants, were transfected into SH-SY5Y cells and primary cultured neurons from rat brains to build a cellular model of AD. The mRNA levels of APP and nAChRs, and the protein levels of total APP, αAPPs and nAChRs in the cultured cells were measured using real-time PCR and Western blot, respectively. The numbers of α3 nAChR were determined by receptor-[³H]epibatidine binding assay.

RESULTSIncreased expressions of Swedish 670/671 APP at mRNA and protein levels, and down-regulation of αAPPs were observed in both of the cultured neuronal cells transfected with APP(SWE). A significant increase of α7 nAChR expression at protein and mRNA levels was detected in the APP(SWE) transfected SH-SY5Y cells. On the other hand, after transfection with APP(SWE), the expressions of α3 nAChR at protein and mRNA levels in SH-SY5Y cells, and α4 nAChR at mRNA level in primary cultured neurons were inhibited. In addition, the numbers of receptor binding sites were deceased in SH-SY5Y cells overexpressing with APP(SWE).

CONCLUSIONOverexpression of APP(SWE) can decrease αAPPs and modify nAChRs by increasing expression of α7 nAChR and decreasing α3 and α4 nAChRs, which might play an important role in the pathogenesis of AD.

Alzheimer Disease ; genetics ; Amyloid Precursor Protein Secretases ; secretion ; Amyloid beta-Protein Precursor ; genetics ; metabolism ; physiology ; Animals ; Brain Neoplasms ; metabolism ; pathology ; Cell Line, Tumor ; Cells, Cultured ; Cerebral Cortex ; cytology ; metabolism ; Down-Regulation ; Humans ; Neuroblastoma ; metabolism ; pathology ; Neurons ; cytology ; metabolism ; Plasmids ; RNA, Messenger ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Nicotinic ; genetics ; metabolism ; Transfection ; alpha7 Nicotinic Acetylcholine Receptor

The aim of this study was to investigate the gene expression profiles of acute promyelocytic leukemia (APL) cell line NB4 treated with arsenic trioxide (As2O3) by using cDNA microarray. cDNA probes were prepared through reverse transcription from mRNA of NB4 cells treated with or without arsenic trioxide. The probes were labeled with Cy3 and Cy5 fluorescence dyes individually, hybridized with cDNA microarray representing 201 different human genes, and their fluorescent intensities were scanned. The genes were screened through the analysis of the difference in the gene expression profile. The results showed that after the treatment of arsenic trioxide (2 micromol/L), 6 genes were up-regulated, and 12 genes related to apoptosis and signal transduction were down-regulated. The p21, survivin, cdc2 and Wee1Hu genes may be related to the differentiation and/or apoptosis of NB4 cells induced by As2O3. It is concluded that p21, survivin, cdc2 and Wee1Hu may play an important role in the mechanism underling arsenic trioxide-mediated NB4 cell apoptosis.
Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; genetics ; Arsenicals ; pharmacology ; CDC2 Protein Kinase ; Cell Line, Tumor ; Cyclin B ; metabolism ; Cyclin-Dependent Kinase Inhibitor p21 ; metabolism ; Cyclin-Dependent Kinases ; Gene Expression Regulation, Neoplastic ; Humans ; Inhibitor of Apoptosis Proteins ; Leukemia, Promyelocytic, Acute ; pathology ; Microtubule-Associated Proteins ; metabolism ; Oxides ; pharmacology

OBJECTIVETo identify differential genes between normal ovarian epithelium tissue and ovarian epithelial cancer using representational difference analysis of cDNA (cDNA-RDA).

METHODScDNA-RDA was performed to identify the differentially expressed sequences between cDNAs from cancer tissue and cDNAs from normal ovarian tissue in the same patient who was in the early stage of ovarian serous cystadenocarcinoma. These differentially expressed fragments were cloned and analyzed, then sequenced and compared with known genes.

RESULTSThree differentially expressed cDNA fragments were isolated using cDNA from normal ovarian tissue as tester and cDNA from cancer tissue as driver amplicon by cDNA-RDA. DP III-1 and DP III-2 cDNA clone showed significant homology to the cDNA of alpha actin gene; DP III-3 cDNA clone showed significant homology to the cDNA of transgelin gene.

CONCLUSIONcDNA-RDA can be used to sensitively identify the differentially expressed genes in ovarian serous cystadenocarcinoma. Ovarian serous cystadenocarcinoma involves alteration of multiple genes.

Actins ; analysis ; genetics ; Base Sequence ; Cystadenocarcinoma, Serous ; genetics ; DNA, Complementary ; genetics ; DNA, Neoplasm ; genetics ; Female ; Gene Expression Profiling ; Genes, Tumor Suppressor ; Humans ; Microfilament Proteins ; analysis ; genetics ; Molecular Sequence Data ; Muscle Proteins ; analysis ; genetics ; Ovarian Neoplasms ; genetics ; Ovary ; chemistry ; Sequence Analysis, DNA ; Sequence Homology, Nucleic Acid