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Biomedical subjects

H Wang

Publications and source records attributed to H Wang.

At least 865 records · Page 48Linked to original sources

Common trisomy mosaicism diagnosed in amniocytes involving chromosomes 13, 18, 20 and 21: karyotype-phenotype correlations.

Karyotype-phenotype correlations of common trisomy mosaicism prenatally diagnosed via amniocentesis was reviewed in 305 new cases from a collaboration of North American cytogenetic laboratories. Abnormal outcome was noted in 10/25 (40%) cases of 47,+13/46, 17/31 (54%) cases of 47,+18/46, 10/152 (6.5%) cases of 47,+20/46, and in 49/97 (50%) cases of 47,+21/46 mosaicism. Risk of abnormal outcome in pregnancies with less than 50% trisomic cells and greater than 50% trisomic cells were: 26% (4/15) versus 60% (6/10) for 47,+13/46, 52% (11/21) versus 75% (6/8) for 47,+18/46, 4.5% (6/132) versus 20% (4/20) 47,+20/46, and 45% (27/60) versus 59% (22/37) for 47,+21/46. Phenotypically normal liveborns were observed with mean trisomic cell lines of 9.3% for 47,+13/46, 8.6% for 47,+18/46, 27% for 47, +20/46, and 17% for 47,+21/46. Cytogenetic confirmation rates were 46% (6/13 cases) for 47,+13/46 mosaicism, 66% (8/12 cases) for 47, +18/46, 10% (10/97 cases) for 47,+20/46, and 44% (24/54 cases) for 47,+21/46. There were higher confirmation rates in pregnancies with abnormal versus normal outcome: 50% versus 44% for 47,+13/46 mosaicism, 100% versus 33% for 47,+18/46, 66% versus 7% for 47, +20/46, and 55% versus 40% for 47,+21/46. Repeat amniocentesis is not helpful in predicting clinical outcome. It may be considered when there is insufficient number of cells or cultures to establish a diagnosis. Fetal blood sampling may have a role in mosaic trisomy 13, 18, and 21 as the risk for abnormal outcome increases with positive confirmation: 1/5 (20%) normal cases versus 5/8 (62%) abnormal cases. High resolution ultrasound examination(s) is recommended for clinical correlation and to facilitate genetic counselling.

Abnormalities, Multiple↗

Expression of Jun family members in human colorectal adenocarcinoma.

The products of the Jun family genes, c-Jun, JunB and JunD, are essential components of the activating protein-1 transcription factor complexes that are critically important in the control of cell growth, differentiation and neoplastic transformation. Although increased c-Jun expression has been reported in human colorectal tumors, expression of JunB and JunD in these tumors has not previously been characterized. In the current study, we examined 24 cases of human colorectal adenocarcinoma by western immunoblotting analysis and immunohistochemical staining for the expression of c-Jun, JunB and JunD proteins. Normal-appearing colonic mucosa distant from the tumors in the same colectomy specimens were used as a reference for comparison. The results showed that both c-Jun and JunB proteins were undetectable or barely detectable in normal mucosa but their expression levels were significantly increased in human colorectal adenocarcinomas. In contrast, JunD protein was present at high levels in normal mucosa and only showed a minimal increase in adenocarcinomas. These observations suggest that different Jun proteins may serve different roles in regulating colonic epithelial cell growth and in colorectal tumorigenesis.

Adenocarcinoma↗

A distinct mutational spectrum of p53 and K-ras genes in lung cancer of workers with silicosis.

Crystalline silica was recently classified as a human carcinogen by the International Agency for Research on Cancer (IARC). However, the direct genotoxic effect of silica in humans remains unclear. We examined the p53 and K-ras gene mutations in lung cancer in workers with silicosis (LCWS). DNA was extracted from paraffin-embedded tissues and examined by PCR-RFLP, PCR-SSCP, and DNA sequencing. The mutation frequencies of p53 gene were high, but the mutation distributions in exons and among the histological types of LCWS differed from those of common (i.e., not silicosis-related) lung cancer. Furthermore, no mutations in codon 12 of K-ras gene (predominant in common lung cancer) were found in LCWS. These findings in the mutational spectrum support a carcinogenic effect of silica dust at the DNA molecular level.

DNA Mutational Analysis↗

DNA damage and activation of c-ras in human embryo lung cells exposed to chrysotile and cigarette smoking solution.

Epidemiological studies and animal experiments showed that asbestos and cigarette smoking can act synergistically in the development of lung cancer. The mechanism of this synergism is largely unknown. It is well documented that DNA damage and activation of oncogenes play important roles in the development of cancer. The aim of our study was to find out if DNA damage could be increased and c-ras oncogene could be activated when human embryo lung cells were treated with chrysotile (CH) and cigarette smoking solution (CSS) separately or simultaneously. Human embryo lung (HEL) cells were treated with different doses of CH and CSS separately or simultaneously, then DNA strand breaks were detected with single-cell gel electrophoresis assay and the expression of p21 was detected by flow cytometry. Factorial analysis was used to evaluate the combined effect of chrysotile and cigarette smoking solution. The results showed that DNA strand breaks could be increased significantly when HEL cells were exposed to CH and CSS separately for 1 hour and increased in a dose-dependent relationship when cells were exposed to CH and CSS simultaneously for 1 hour. The expression of p21 increased significantly when cells were exposed to CH for 24 hours, but there was no significant increase when cells were exposed to CSS for 24 hours. However, there was an additive effect on the expression of p21 when cells were exposed to CH and CSS simultaneously for 24 hours. When cells were exposed to CH and CSS simultaneously three times (24 hours each time), then passaged for 1 month, the expression of p21 increased synergistically. In conclusion, DNA damage and activation of c-ras may be involved in the process of combined carcinogenesis of CH and CSS.

Asbestos, Serpentine↗

The fumonisin B1 content in corn from North China, a high-risk area of esophageal cancer.

Fusarium moniliforme is the primary fungus contaminating corn throughout the world. Fumonisin B1 (FB1) is the major metabolite of F. moniliforme. It has been shown that FB1 is the promoter and initiator of liver cancer in rat. The corn of Cixian, in Hebei Province, the high-risk area for esophageal cancer in China, is often contaminated by this fungus. A total of 21 corn samples were collected from households in the Cixian County. High levels of FB1 (88.90+/-13.1 microg/g) were found in 10 moldy samples, and low levels (1.40+/-0.50 microg/g) of FB1 were found in 11 apparently healthy corn samples. The positive detection rates of FB1 in moldy and normal samples were 100 and 90.9%, respectively. The frequency of FB1 contamination in the high-risk area is about twice that in the low-risk areas, and the average content of FB1 in samples from high-risk areas was approximately three times that from low-risk areas. Our data indicate that FB1-contaminated corn may be involved in the carcinogenesis of esophageal cancer in high-risk areas of North China.

Carboxylic Acids↗

[The application of fluorescence in situ hybridization performed on the decolorized G-banding chromosomes in detecting the marker chromosomes of gastric cancer].

OBJECTIVE: Using a rapid, accurate method that detects the marker chromosomes of gastric cancer and enhancing the ability of discriminating complicated chromosome rearrangements of gastric cancer. METHODS: The improved method of fluorescence in situ hybridization(FISH) performed on the decolorized G-banding chromosome was used. RESULTS: The changes of two marker chromosomes (M1, M2) of the cell line(SGC-7901) of gastric cancer and one marker chromosomes(M3) of one primary gastric cancer were respectively analyzed by this method. The M1, M2 and M3 had complicated structural chromosome aberrations: del(7)(p15)/del(7)(q22), t(1;3)(p11;q11) and del(7)(q32). CONCLUSION: This method showed strong signals, low backgrounds and well-repetitions. It may play an important part in exploring the chromosome rearrangements in the process of pathogenesis and development of gastric cancer.

Chromosome Aberrations↗

Transport of N-acetylaspartate by the Na(+)-dependent high-affinity dicarboxylate transporter NaDC3 and its relevance to the expression of the transporter in the brain.

N-Acetylaspartate is a highly specific marker for neurons and is present at high concentrations in the central nervous system. It is not present at detectable levels anywhere else in the body other than brain. Glial cells express a high-affinity transporter for N-acetylaspartate, but the molecular identity of the transporter has not been established. The transport of N-acetylaspartate into glial cells is obligatory for its intracellular hydrolysis, a process intimately involved in myelination. N-Acetylaspartate is a dicarboxylate structurally related to succinate. We investigated in the present study the ability of NaDC3, a Na(+)-coupled high-affinity dicarboxylate transporter, to transport N-acetylaspartate. The cloned rat and human NaDC3s were found to transport N-acetylaspartate in a Na(+)-coupled manner in two different heterologous expression systems. The Michaelis-Menten constant for N-acetylaspartate was approximately 60 microM for rat NaDC3 and approximately 250 microM for human NaDC3. The transport process was electrogenic and the Na(+):N-acetylaspartate stoichiometry was 3:1. The functional expression of NaDC3 in the brain was demonstrated by in situ hybridization and reverse transcription-polymerase chain reaction as well as by isolation of a full-length functional NaDC3 from a rat brain cDNA library. In addition, the expression of a Na(+)-coupled high-affinity dicarboxylate transporter and the interaction of the transporter with N-acetylaspartate were demonstrable in rat primary astrocyte cultures. These studies establish NaDC3 as the transporter responsible for the Na(+)-coupled transport of N-acetylaspartate in the brain. This transporter is likely to be an essential component in the metabolic role of N-acetylaspartate in the process of myelination.

Animals↗

Intermediate and late rheumatoid arthritis treated by tonifying the kidney, resolving phlegm and removing blood stasis.

Eighty-seven cases of intermediate and late rheumatoid arthritis were treated with Instant Shu Guan Wen Jing Granules ([symbol: see text] Relaxing Joints by Warming Channels) and Instant Shu Guan Qing Luo Granules ([symbol: see text] Relaxing Joints by Removing Heat from the Lung Channel) to tonify the kidney, resolve phlegm and remove blood stasis, and compared with 41 cases treated with Instant Wang Bi Granules ([symbol: see text] Prescription for Arthralgia-syndrome). The treatment produced a clinical cure rate of 54.0% and a total effective rate of 90.8% as in against 29.3% and 73.2% respectively in the control group. The difference was significant (P < 0.01). Improvement in main symptoms and laboratory findings in the treatment group was all more marked than that in the control group (P < 0.05 or P < 0.01), with no side effects observed.

Adult↗

Chronic intragastric infusion of ethanol-containing diets induces CYP3A9 while decreasing CYP3A2 in male rats.

The CYP3A subfamily is the most abundant of the human hepatic cytochrome P450 enzymes. They mediate the biotransformation of many drugs, including a number of psychotropic, cardiac, analgesic, hormonal, immunosuppressant, antineoplastic, and antihistaminic agents. We studied diet/ethanol interactions using total enteral nutrition in adult male Sprague-Dawley rats with diets containing 16% protein, ethanol (13 g/kg), corn oil (fat; 25-45%), and carbohydrate (CHO; 1-21%). Using this model, chronic ethanol feeding decreased CYP3A activity (testosterone 6 beta-hydroxylation) and apoprotein levels (Western blot) (P <.05) and these effects were independent of the dietary CHO/fat ratio. The CYP3A2 mRNA levels decreased (P <.05) in the rats fed ethanol-containing diets by 73 to 83% compared with rats fed control diets, regardless of the CHO/fat ratio. In contrast, ethanol induced CYP3A9 mRNA levels (P <.05) and this effect was greater (P <.05) in the high-CHO/low-fat group (11.3-fold) than in the low-CHO/high-fat group (2.6-fold). Purified recombinant rat P450 3A9 had a chlorzoxazone 6-hydroxylase activity with a turnover number 1.3 nmol/min/nmol of P450. These results indicate that 1) ethanol differentially affects the expression of CYP3A gene family and this regulation appears to be modulated by dietary CHO/fat ratio; 2) the decrease in testosterone 6 beta-hydroxylase activity and CYP3A apoprotein levels are most likely due to the ethanol-induced decrease in CYP3A2 mRNA levels; and 3) CYP3A9 is induced by ethanol and is a low-affinity, high-K(m) chlorzoxazone hydroxylase.

Animals↗

Studies on the resuscitative efficacy of polymerized bovine hemoglobin.

The paper described modified hemoglobin (Hb) with glycolaldehyde for the efficacy on resuscitation of severe hemorrhagic shock. Our objective was to compare the effect on resuscitation of severe hemorrhagic shock with different experimental groups. Results showed early resuscitation with modified bovine Hb is superior to lactated Ringer's solution group in improving hemodynamic and acidosis, but the effect of polymerized Hb with glycolaldehyde were similar to fresh whole blood in this rat model.

Acetaldehyde↗

Vector-host interactions in disease transmission.

Tick-borne spirochetes include borreliae that cause Lyme disease and relapsing fever in humans. They survive in a triangle of parasitic interactions between the spirochete and its vertebrate host, the spirochete and its tick vector, and the host and the tick. Until recently, the significance of vector-host interactions in the transmission of arthropod-borne disease agents has been overlooked. However, there is now compelling evidence that the pharmacological activity of tick saliva can have a profound effect on pathogen transmission both from infected tick to uninfected host, and from infected host to uninfected tick. The salivary glands of ticks provide a pharmacopoeia of anti-inflammatory, anti-haemostatic and anti-immune molecules. These include bioactive proteins that control histamine, bind immunoglobulins, and inhibit the alternative complement cascade. The effect of these molecules is to provide a privileged site at the tick-host interface in which borreliae and other tick-borne pathogens are sheltered from the normal innate and acquired host immune mechanisms that combat infections. Understanding the key events at the tick vector-host interface, that promote spirochete infection and transmission, will provide a better understanding of the epidemiology and ecology of these important human pathogens.

Animals↗

[Changes of genomic density polymorphism and quantitative expression of complement receptor type 1 in patients with liver diseases].

OBJECTIVE: To study the changes of genomic density polymorphism and quantitative expression of complement receptor type 1 (CR1) on erythrocytes in patients with liver diseases. METHODS: Polymerase chain reaction (PCR) and Hind III restriction enzyme digestion and the quantitative assay of erythrocytic CR1 were used. RESULTS: The spot mutation rate (25.0% approximately 30.3%) of erythrocyte CR1 density gene in patients with liver diseases was not significantly different with that of healthy individuals (28.0%). The amount of erythrocytic CR1 in patients with liver diseases, except for those with normal liver function, was significantly lower than that of healthy individuals (t=10.44, P<0.0001). The quantitative expression of erythrocytic CR1 in decompensated cirrhosis was obviously lower than that of compensated cirrhosis (t=2.21, P<0.05). CONCLUSION: Defective expression of CR1 in liver diseases is acquired through central and/or peripheral mechanisms. It is very important to study the quantitative expression in the evaluation of the development of liver diseases.

Erythrocytes↗

[Predicting mortality for 205 cirrhotic patients by APARCHEIII score system].

OBJECTIVE: To evaluate the prognostic value of APARCHEIII (acute physiology, age and chronic health evaluation) score system for cirrhosis patients. METHODS: The clinic data of 205 cirrhotic patients were prospectively collected, APARCHEIII and Child-Pugh scores for each patient were recorded on admission day. Using discrimination analysis, the predictive accuracy of the two systems was investigated. RESULTS: The complication included GI bleeding (15.6%), encephalopathy (10.6%), hepatorenal syndrome (8.8%), primary liver carcinoma (8.8%), and spontaneous bacterial peritonitis (4.8%). Fifty patients (24%) died. The major cause of death was GI bleeding (40%), hepatorenal syndrome (34%), hepatic failure (20%) and spontaneous bacterial peritonitis (6%). APARCHEIII and Child score for survivors was 19.3+/-8.6 and 7.4+/-1.8, significantly lower than those for nonsurvivors (47.9+/-20.1 and 10.6+/-2.4). APARCHEIII score system correctly predicted 82.3% of death cases vs 72.7% for Child system. When combined with the information of ascites and prothrombin prolongation time, 88.2% cases could be correctly identified in advance. CONCLUSION: The APARCHEIII score system is a more efficient and accurate predictive system than Child for prognosticating short-term survival of cirrhotic patients and worth use in clinic.

APACHE↗

Combined effect of docetaxel and cisplatin for non-small cell lung cancer cell lines in vitro.

Docetaxel (DOC) plus cisplatin (CDDP) is a novel combination chemotherapy for the treatment of advanced non-small-cell lung cancer (NSCLC). We investigated the combined effect of DOC with CDDP in sequence and the reverse schedule for NSCLC cell lines EBC-1 (squamous cell carcinoma) and RERF-LC-MS (adenocarcinoma) using an MTT assay and an improved isobologram method. The results showed that the combination of DOC and CDDP in human lung cancer cell lines was antagonistic. To investigate the possible mechanism of the antagonistic effect, we focused on the cell cycle perturbation and the inhibition of apoptosis fractions induced by chemotherapeutic agents. Pretreatment of CDDP significantly blocked the following DOC-induced apoptosis fraction. Therefore we consider that the suppression of apoptosis could be one of the mechanisms for antagonistic effects of combination chemotherapy of DOC and CDDP.

Adenocarcinoma↗