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Biomedical subjects

Q H Wang

Publications and source records attributed to Q H Wang.

At least 19 recordsLinked to original sources
PubMed2004

Research on solid-state fermentation on rice chaff with a microbial consortium.

A microbial consortium of Trichoderma reesei AS3.3711, Aspergillus niger 3.316 and Saccharomyces cerevisiaes AS2.399 was constructed to decomposed rice chaff on the basis of the characters of each microorganism and the mechanism of cellulases. In this experiment, rice chaff was pretreated before fermentation with NaOH so that the lignin structure of rice chaff was degraded and hemicellulose was dissolved partly, which remove the protection of lignin and hemicellulose on cellulose and demolish its special crystal structure. After pretreatment, rice chaff can be degraded more easily with the microbial consortium. The optimal technical paths and technological methods were achieved for intenerating rice chaff with the microbial consortium perfectly through orthogonal experiment. According to the technological methods, some experiments were done at 30 degrees C with pH 4.5. It was found that the highest filter paper enzyme activity (FPA) was 5.64 U/g and the ratio of cellulose degradation (RCD) was 28.05%.

Aspergillus niger↗
PubMed2001

Staggered currents in the mixed state.

The current pattern in the mixed state of high-T(c) superconductors is studied in the U(1) mean-field theory of the t-J model. Assuming the absence of spin antiferromagnetism we find (1) at moderate doping staggered-current pattern exists in vortex cores and eventually percolates with increasing magnetic field. (2) The polarity of the staggered current is pinned by the magnetic field. (3) Vortex cores with (without) staggered current are slightly negatively (positively) charged. (4) Gutzwiller projection does not wash out the staggered current. We discuss the signature of staggered current in neutron scattering and scanning tunneling microscopy.

Journal Article↗
PubMed2001

Superfluid density in the d-density-wave scenario.

Recently Chakravarty, Laughlin, Morr, and Nayak [Phys. Rev. B 62, 4880 (2000)] made an interesting proposal that the cuprate superconductors possess a hidden " d-density-wave" (DDW) order. We study the implication of this proposal for the superfluid density rho(s). We find that it predicts a temperature gradient [d rho(s)/dT](T = 0) that is strongly doping dependent near the critical doping at which the superconducting gap vanishes. This demonstrates that the DDW scenario is inconsistent with existing well-established experimental data.

Journal Article↗
PubMed2001

Genetic progression and heterogeneity associated with the development of esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma is a common fatal cancer, and Shanxi province, a region in north-central China, has some of the highest esophageal cancer rates in the world. Chromosomal regions with frequent allelic loss may point to major susceptibility genes that will assist us in understanding the molecular events involved in esophageal carcinogenesis and may serve as the basis for the development of markers for genetic susceptibility and screening for early detection of this cancer. This study was designed to identify events in the molecular progression of precursor and invasive lesions of squamous esophageal cancer. Twelve marker loci identified during our previous studies as having some of the highest rates of loss of heterozygosity (LOH) in invasive esophageal cancer were evaluated in laser-microdissected DNA obtained from low- and high-grade dysplastic lesions and invasive tumor foci from 10 fully embedded esophageal resection specimens. Each resection specimen contained a spectrum of disease, from epithelium that appeared histologically normal to invasive cancer, including a single dominant tumor surrounded by a region of precursor lesions (low- and high-grade dysplasia) and occasional "remote," nonadjacent precancerous foci. Using the 12 polymorphic markers, LOH was found in all of the three stages of disease. The frequency of LOH for all of the markers together increased with increasing disease severity. Among the informative low-grade dysplasia samples, LOH was detected with markers D3S1766 (3p), D4S2632 (4p), D9S910 (9q), and D13S1493 (13q), suggesting that LOH at these loci may be associated with early stages of tumor initiation and/or progression. LOH was detected among the informative high-grade (but not low-grade) dysplasia samples for the other eight markers tested, suggesting that LOH at these loci may occur later in the neoplastic process. In addition to the association between disease progression and these genetic changes, considerable genetic heterogeneity was found in each fully embedded resection specimen both between and within geographically separate neoplastic lesions.

Adult↗
PubMed2001

Allelic loss on chromosome bands 13q11-q13 in esophageal squamous cell carcinoma.

Allelic loss on chromosome 13 occurs frequently in esophageal squamous cell carcinoma. However, studies of the two known tumor suppressor genes located on 13q, RB1 and BRCA2, have shown few mutations, suggesting that other genes are likely to be involved in the development of this tumor type. To identify a minimal deletion interval, we first analyzed 42 microsatellite markers spanning chromosome bands 13q11-q13 in 56 esophageal squamous cell carcinoma patients, including 34 with a family history of upper gastrointestinal cancer and 22 without a family history of cancer. Lifestyle risk factors and clinical/pathologic characteristics were also collected. Two commonly deleted regions were identified: one was located on band 13q12.11, between markers D13S787 and D13S221; the other was located on bands 13q12.3-q13.1 from markers D13S267 to D13S219. We observed higher allelic loss frequencies for eight of the microsatellite markers in those patients with a family history of upper gastrointestinal cancer compared to patients without such a history. This study suggests that one or more unidentified tumor suppressor genes are located on chromosome arm 13q that play a role in the development of esophageal squamous cell carcinoma.

Carcinoma, Squamous Cell↗
PubMed2001

Genetic analysis of the capsid region of astroviruses.

Eight serotypes of human astroviruses (HAstV-1 to HAstV-8) have been described. To date, the entire genomes of HAstV-1 and HAstV-2 as well as the ORF2 sequences of HAstV-1-6 and 8 have been reported. In this study, the ORF2 sequences of seventeen strains of HAstVs originating from different countries were determined, as well as the sequence ORF2 of one porcine astrovirus (PAstV) strain. Afterwards, comparison of the capsid protein precursors encoded by ORF2 of 46 strains of HAstVs, PAstV, and feline astrovirus (FAstV) was carried out. A phylogenetic tree showed eight genogroups of HAstVs that corresponded exactly to the serotypes. HAstV-3 and 7 were the most closely related, whereas HAstVs, FAstV, and PAstV segregated from each other. Compared to a PAstV, a FAstV is closer to HAstVs. Furthermore, the capsid protein precursors were divided into four regions (after amino acid residues 424, 688, and 776, respectively) based on sequence identity. Region I was the most conserved, and FAstV was very close in identity to HAstVs. Two amino acid motifs in region I were predicted to contain the common antigenic epitopes. Region II was relatively variable. Deletions and insertions were characteristic of region III, and region IV was relatively conserved. To our knowledge, this is the first comparative sequence analysis of the capsid protein precursors of eight serotypes of HAstVs as well as two animal astroviruses (FAstV and PAstV).

Amino Acid Motifs↗
PubMed2001

Enantiomer separation of mandelates and their analogs on cyclodextrin derivative chiral stationary phases by capillary GC.

Enantiomer separation of mandelates and their analogs, which are important intermediates in asymmetric synthetic and pharmaceutical chemistry, was investigated by capillary gas chromatography using different cyclodextrin derivative chiral stationary phases (CD CSPs). The used cyclodextrin derivatives included permethylated beta-CD (PMBCD), permethylated gamma-CD, heptakis(2,6-di-O-butyl-3-O-butyryl)-beta-CD, heptakis(2,6-di-O-pentyl-3-O-acetyl)-beta-CD and heptakis(2,6-di-O-nonyl-3-O-trifluoroacetyl)-beta-CD (DNTBCD), respectively. Among all the CSPs used, PMBCD and DNTBCD exhibited the broadest and best enantioselectivity for all the racemates investigated. Some thermodynamic parameters were evaluated and an enthalpy-entropy compensation effect was observed in enantiomer separation processes of mandelates and their analogs. Based on thermodynamic data and molecular mechanics calculations, the chiral recognition mechanism of mandelate derivatives on CD CSPs is discussed.

Chromatography, Gas↗
PubMed2001

Frequent inactivation of the TP53 gene in esophageal squamous cell carcinoma from a high-risk population in China.

Esophageal squamous cell carcinoma (ESCC) is one of the most common fatal cancers worldwide, and north central China has some of the highest rates in the world. Previous studies from tumors in this area of China have shown high frequencies of allelic loss on chromosome 17p13-11, which includes the region where the TP53 gene is found. We examined 56 ESCC patients using single-strand conformation polymorphism and DNA sequencing to assess the frequency and spectrum of TP53 mutation and the association between allelic loss at microsatellite marker TP53 and TP53 mutations. Ninety-six % of cases were found to have at least one genetic alteration, including TP53 mutation (77%), allelic loss within the TP53 gene (73%), and/or loss of heterozygosity at the TP53 microsatellite marker (80%); 75% had two or more such alterations, including 59% with both a point mutation and an intragenic allelic loss ("two hits"). The majority of mutations observed were in exon 5, where the most common type of nucleotide substitution was a G:C-->A:T or C:G-->T:A transition, including half that occurred at CpG sites. Allelic loss was most commonly found in exon 4 but was very common in exon 5 as well. Taken together, the multiple genetic alterations of TP53 in this population at high risk for ESCC indicate that there is a very high degree of genetic instability in these tumors, that TP53 is a primary target for inactivation, and that this tumor suppressor gene plays a critical role in the carcinogenesis process for ESCC.

Adult↗
PubMed2000

Loss of annexin 1 correlates with early onset of tumorigenesis in esophageal and prostate carcinoma.

Annexin I protein expression was evaluated in patient-matched longitudinal study sets of laser capture microdissected normal, premalignant, and invasive epithelium from human esophageal squamous cell cancer and prostatic adenocarcinoma. In 25 esophageal cases (20 by Western blot and 5 by immunohistochemistry) and 17 prostate cases (3 by Western blot and 14 by immunohistochemistry), both tumor types showed either complete loss or a dramatic reduction in the level of annexin I protein expression compared with patient-matched normal epithelium (P < or = 0.05). Moreover, by using Western blot analysis of laser capture microdissected, patient-matched longitudinal study sets of both tumor types, the loss of protein expression occurred in premalignant lesions. Concordance of this result with immunohistochemical analysis suggests that annexin I may be an essential component for maintenance of the normal epithelial phenotype. Additional studies investigating the mechanism(s) and functional consequences of annexin I protein loss in tumor cells are warranted.

Adenocarcinoma↗
PubMed2000

Identification of novel regions of allelic loss from a genomewide scan of esophageal squamous-cell carcinoma in a high-risk Chinese population.

Esophageal cancer is one of the most common fatal cancers worldwide. Deletions of genomic regions are thought to be important in esophageal carcinogenesis. We conducted a genomewide scan for regions of allelic loss using microdissected DNA from 11 esophageal squamous-cell carcinoma patients with a family history of upper gastrointestinal tract cancer from a high-risk region in north central China. Allelic patterns of 366 fluorescently labeled microsatellite markers distributed at 10-cM intervals over the 22 autosomal chromosomes were examined. We identified 14 regions with very high frequency (>/= 75%) loss of heterozygosity (LOH), including broad regions encompassing whole chromosome arms (on 3p, 5q, 9p, 9q, and 13q), regions of intermediate size (on 2q, 4p, 11p, and 15q), and more discrete regions identified by very high frequency LOH for a single marker (on 4q, 6q, 8p, 14q, and 17p). Among these 14 regions were 7 not previously described in esophageal squamous-cell carcinoma as having very high frequency LOH (on 2q, 4p, 4q, 6q, 8p, 14q, and 15q). The very high frequency LOH regions identified here may point to major susceptibility genes, including potential tumor suppressor genes and inherited gene loci, which will assist in understanding the molecular events involved in esophageal carcinogenesis and may help in the development of markers for genetic susceptibility testing and screening for the early detection of this cancer. Genes Chromosomes Cancer 27:217-228, 2000. Published 2000 Wiley-Liss, Inc.

Adult↗
PubMed2000

High frequency allelic loss on chromosome 17p13.3-p11.1 in esophageal squamous cell carcinomas from a high incidence area in northern China.

Allelic loss on chromosome 17p has been reported frequently in esophageal squamous cell carcinoma (ESCC) and generally encompasses the p53 locus at 17p13.1. However, a good correlation between allelic loss on 17p and mutation of p53 has not been found. This suggests the possibility that unknown tumor suppressor genes near p53 may be involved in the development of ESCC. To evaluate this possibility, we analyzed 30 microsatellite markers covering the entire short arm of chromosome 17 in 56 ESCC patients from a high risk population in northern China, including 34 with a family history of upper gastrointestinal (UGI) cancer and 22 without a family history of any cancer. Cancer lifestyle risk factors and clinical/pathological characteristics were also collected. We found frequent allelic loss (>/=65%) at 28 of the 30 markers evaluated in these ESCC patients. The highest frequencies of allelic loss (> or =80%) were found in three smaller regions: deletion region I located at 17p13.3-p13.2 (between D17S849 and D17S1828); deletion region II located at 17p13.2-p13.1 (between D13S938 and TP53); deletion region III located at 17p13.1-p12 (between D17S804 and D17S799). A number of genes have already been identified in these deleted regions, including: OVCA1, OVCA2 and HIC-1 in deletion region I; p53 in deletion region II; ZNF18, ZNF29, ALDH3 and ALDH10 in deletion region III. These results will help us direct future testing of candidate genes and narrow the search region for major new tumor suppressor genes that may play a role in the pathogenesis of ESCC.

Adult↗
PubMed2000

An approach to proteomic analysis of human tumors.

A strategy for proteomic analysis of microdissected cells derived from human tumor specimens is described and demonstrated by using esophageal cancer as an example. Normal squamous epithelium and corresponding tumor cells from two patients were procured by laser-capture microdissection and studied by two-dimensional polyacrylamide gel electrophoresis (2D-PAGE). Fifty thousand cells resolved approximately 675 distinct proteins (or isoforms) with molecular weights ranging between 10 and 200 kDa and isoelectric points of pH 3-10. Comparison of the microdissected protein profiles showed a high degree of similarity between the matched normal-tumor samples (98% identical). However, 17 proteins showed tumor-specific alterations, including 10 that were uniquely present in the tumors and seven that were observed only in the normal epithelium. Two of the altered proteins were characterized by mass spectrometry and immunoblot analysis and were identified as cytokeratin 1 and annexin I. Acquisition of 2D-PAGE protein profiles, visualization of disregulated proteins, and subsequent determination of the identity of selected proteins through high-sensitivity MS-MS microsequencing are possible from microdissected cell populations. These separation and analytical techniques are uniquely capable of detecting tumor-specific alterations. Continued refinement of techniques and methodologies to determine the abundance and status of proteins in vivo holds great promise for future study of normal cells and associated neoplasms. Mol.

Electrophoresis, Gel, Two-Dimensional↗
PubMed2000

Molecular epidemiology of astroviruses in Japan from 1995 to 1998 by reverse transcription-polymerase chain reaction with serotype-specific primers (1 to 8).

In addition to the serotype-specific primers described previously (1 to 7), a new serotype 8-specific primer has been designed, allowing detection of all astrovirus serotypes. A total of 1,382 diarrheal stool samples in 5 regions in Japan were examined by reverse transcription-polymerase chain reaction (RT-PCR). The incidence of astrovirus infection in all 5 regions was 5.9% (82 of 1,382 samples) and infection occurred mainly from November to April. Serotypes 1, 3, and 4 were detected in 66, 14, and 2 of the 82 positive samples, respectively. None of the other serotypes was detected. The highest detection rate was from 0 to 1 year old, 39.0%, and the next highest was from 1 to 2 years old, 34.1%. The primers provide a useful approach for study of the epidemiology of astroviruses.

Astroviridae Infections↗
PubMed2000

[Cloning and sequence analysis of a gene encoding amastin from Leishmania major].

OBJECTIVE: To clone a gene encoding surface protein from Leishmania major. METHODS: Using T. cruzi amastin DNA sequence as a reference, computer search was done on GenBank and dbEST databases by using BLAST path. A Leishmania major DNA library has been constructed and screened by in situ colony hybridization. RESULTS: A 309nt DNA fragment from Leishmania major was found in dbEST. Leishmania major DNA library was screened using specific primers synthesized according to 309 nt DNA sequence, and a full-length coding sequence for Leishmania major amastin was cloned. The coding sequence consisted of 552 nt, and translated into 183 amino acid residues. The homology is 23.5% at amino acid sequence level between Leishmania major and T. cruzi amastins. CONCLUSION: A full length amastin coding gene for Leishmania major has been cloned.

Amino Acid Sequence↗
PubMed1999

Allelic loss in esophageal squamous cell carcinoma patients with and without family history of upper gastrointestinal tract cancer.

Chromosomal regions with frequent allelic loss may point to major susceptibility genes that will assist in understanding molecular events involved in esophageal carcinogenesis. Esophageal squamous cell carcinoma samples and blood from 46 patients, including 23 patients with and 23 patients without a family history of upper gastrointestinal cancer, were screened using laser microdissected DNA and tested for loss of heterozygosity (LOH) at 18 marker loci representing 14 chromosomal regions (on 2q, 3p, 4p, 4p, 5q, 6q, 8p, 9p, 9q, 11p, 13q, 14q, 15q, and 17p) identified in an earlier genome-wide scan to have frequent LOH. Clinical/pathological and lifestyle risk factor data were also collected. For all 46 tumors combined, the lowest frequency LOH for any of the 18 markers was 37%, and 8 markers showed LOH in > or =75% of informative tumors. One marker (D13S894 on 13q) showed greater LOH in patients with a positive family history (93% versus 50%; P = 0.04), whereas two markers (D6S1027 on 6q and D9S910 on 9q) had significantly more LOH in patients with metastasis, and one marker (D4S2361 on 4p) showed significantly higher LOH in patients with a lower pathological tumor grade. No relation was seen between LOH and lifestyle risk factors. This study confirms the previously observed high frequency LOH for these 14 chromosomal regions, including a locus on 13q where LOH is more common in patients with a family history of upper gastrointestinal cancer than in those without such history, suggesting that a gene in this area may be involved in genetic susceptibility to esophageal cancer.

Adult↗
PubMed1999

N-acetylglucosaminyltransferase V activity in metastatic models of human hepatocellular carcinoma in nude mice.

N-linked beta 1-6 branched oligosaccharides may contribute directly to the malignant phenotype including metastatic potential of tumour cells. Increased beta 1-6 branching was associated with an increased level of N-acetylglucosaminyltransferase V (GnT V). In this report, the tissues from two metastatic models of human hepatocellular carcinoma (HCC) in nude mice were obtained. GnT V activity and mRNA level were determined. Results showed that GnT V activity in highly metastatic LCI-D20 models (Liver Cancer Institute, passage time: 20 days) (413.1+/-86.4U) was much higher than that in low metastatic LCI-D35 model (passage time 35 days) (155.3+/-31.9U). Northern blot showed that the mRNA level of GnT V in two models had no change. During the selection of a highly metastatic LCI-D20 model, GnT V activity increased from 301.6+/-57.3U to 413.1+/-86.4U while the highly metastatic LCI-D20 model acquired higher metastatic ability after selection. When highly metastatic LCI-D20 model tissues were implanted subcutaneously (s.c.), the GnT V activity decreased dramatically from 413.1+/-86.4U to 94.9U. This is the first report that GnT V activity increased in HCC during metastasis in vivo.

Animals↗
PubMed1999

Morphological changes of spermatozoa in proximal vas deferens after vasectomy.

AIM: To investigate the morphological changes of spermatozoa in the proximal vas deferens after vasectomy. METHODS: Proximal vas deferens fluids were collected from 79 fertile men (group A) and 64 vasectomized men (group B) during the operations of vasectomy or vasovasostomy. Sperm morphology in the proximal vas deferens was analyzed after staining with the modified Papanicolaou method. RESULTS: The percentage of spermatozoa with a normal oval head from group B (50. 7% +/- 21.7%) was significantly lower than that of group A (75.2% +/- 11.1%). The data in group A was similar to those of normal semen and therefore represents the physiological condition of the proximal vas deferens sperm of fertile men. There were no significant differences in the percentages of normal oval heads in group B with the time since vasectomy. CONCLUSION: After vasectomy, the spermatozoa in the proximal vas deferens and epididymis were continuously degenerating and being replenished by spermatozoa coming from testis. The obvious morphological degeneration occurred in the sperm tail and spermatozoa with a small oval head and amorphous heads were increased.

Adult↗