Search PubMed⌕ Search

Biomedical subjects

S Zheng

Publications and source records attributed to S Zheng.

At least 37 records · Page 2Linked to original sources
PubMed2002

Endoscopic screening and determination of p53 and proliferating cell nuclear antigen in esophageal multistage carcinogenesis: a comparative study between high- and low-risk populations in Henan, northern China.

The objective of this study was to characterize the histologic changes from endoscopic screening for early esophageal cancer (EC) on subjects at high-incidence area (HIA) and low-incidence area (LIA) in Henan, China, and to further compare the changes in p53 and proliferating cell nuclear antigen (PCNA) in the multistage of human esophageal carcinogenesis from these two populations. The detection rate of basal cell hyperplasia (BCH) and dysplasia (DYS) was higher in the subjects from HIA than in those from LIA. Out of the 1568 symptom-free subjects examined at HIA, 10 (0.6%) cases with early squamous cell carcinoma (SCC) were identified. Immunoreactivity of p53 and PCNA was observed in cell nuclei of esophageal biopsies and surgically resected esophageal cancer specimens both in HIA and LIA. With the lesions progressed from normal epithelium to BCH to DYS to SCC, the positive-immunostaining cells expanded from basal layer to superficial layer, and the number of positive cells/mm2 for p53 and PCNA increased, and was significantly higher in HIA than in LIA among the similar morphological lesions (P < 0.01). The number of p53 positive cells/mm2 in SCC from HIA was almost fivefold higher than SCC from LIA (P < 0.01). The remarkable difference was also observed between HIA and LIA in DYS and BCH. The present results indicate that p53 protein accumulation is an important early biomarker for identifying high-risk subjects for EC.

Adult↗
PubMed2001

Differential expression of manganese superoxide dismutase and catalase in lung cancer.

Reactive oxygen species (ROS) are important in the initiation and promotion of cells to neoplastic growth. In this context, cigarette smoke exposure, the primary risk factor in lung cancer development, leads to high levels of ROS within the human airway. Although well-equipped with an integrated antioxidant defense system consisting of low-molecular weight antioxidants such as glutathione and intracellular enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase, the lungs are vulnerable to increased endogenous and exogenous oxidative insults. Antioxidants increase in response to oxidative stress and minimize ROS-induced injury in experimental systems, indicating that antioxidant levels may determine whether ROS can initiate lung carcinogenesis. On this basis, we hypothesized that antioxidants would be decreased in lung carcinoma cells as compared with tumor-free adjacent lung tissues. Antioxidant expression was evaluated in 16 lung tumor and 21 tumor-free lung tissues collected between the years 1993 and 2001 from 24 individuals with surgically resectable non-small cell lung cancer, i.e., adenocarcinoma and squamous cell carcinoma. Total SOD activity was increased (P = 0.035), catalase activity decreased (P = 0.002), and glutathione and glutathione peroxidase were similar in tumors compared with tumor-free lung tissues. Alterations in antioxidant activities were attributable to increased manganese SOD and decreased catalase protein and mRNA expression in tumors. Immunohistochemical localization of catalase in the lung revealed decreased or no expression in the tumor cells, although healthy adjacent airway epithelial cells were strongly positive for catalase. Parallel changes in antioxidant activities, protein, and mRNA expression were noted in A549 lung carcinoma cell lines exposed to cytokines (tumor necrosis factor-alpha, interleukin 1beta, and IFN-gamma). Thus, inflammation in the lung may contribute to high levels of manganese SOD and decreased catalase, which together may lead to increased hydrogen peroxide intracellularly and create an intracellular environment favorable to DNA damage and the promotion of cancer.

Aged↗
PubMed2001

[A further study on potential of microsatellite analysis of urine in diagnosis of bladder cancer].

OBJECTIVES: To investigate the application value of microsatellite analysis of voided urine in diagnosis of bladder cancer and compare the advantages and disadvantages of this method and urine cytology. METHODS: Thirteen microsatellite markers, including the nine markers used in the authors' previous study and another four new markers, were tested on urine DNA from 143 individuals with or without bladder lesions in a blinded fashion. Urine cytology was applied at the same time. RESULTS: The urine DNA from 89% (97/109) of the patients with bladder cancer, 86% (6/7) of the patients with inverted papilloma of the bladder, 3 out of 7 patients with cystitis and one patient with hematuria of unknown cause showed alterations, at least, in one of the 13 microsatellite markers, while the 19 individuals without bladder lesion had no change at any of these loci. Nucleic atypia or suspicious cancer cells were detected by routine cytology in the urine of the 3 patients with cystitis and one patient with hematuria of unknown cause who showed alterations of microsatellite in their urine sediments. Among the 81 cases of bladder cancer whose urine was examined by both microsatellite analysis and routine cytology, 73 cases (90%), of various stage or grade, were identified by microsatellite analysis, while only 41 cases (51%), mainly at advanced stage, were detected by cytology. Cancer cells were detected in the urine sediments of 4 of the 12 cases that were not identified by microsatellite analysis. CONCLUSION: Microsatellite analysis of urine is useful for detection of bladder cancer. Microsatellite analysis and urine cytology could be complementary to each other.

Female↗
PubMed2001

A comparison between microsatellite analysis and cytology of urine for the detection of bladder cancer.

We have studied, in a blinded fashion, cytology and microsatellite analysis on urine sediments of 143 Chinese with or without bladder lesions. Microsatellite analysis succeeded in all 143 individuals, while cytology could not be performed on 42 subjects due to insufficient urine samples. Both microsatellite analysis and routine urine cytology succeeded in 81 bladder cancer patients. Seventy-three patients (90%) were identified by microsatellite analysis, while only 41 patients (51%) were identified by cytology. However, four patients were identified by routine cytology but not by microsatellite analysis. Our results proved that microsatellite analysis is more sensitive than routine cytology but the two methods are complementary to each other.

Adult↗
PubMed2001

Requirement of tissue-selective TBP-associated factor TAFII105 in ovarian development.

Transcription factor TFIID, composed of TBP and TAFII subunits, is a central component of the RNA polymerase II machinery. Here, we report that the tissue-selective TAFII105 subunit of TFIID is essential for proper development and function of the mouse ovary. Female mice lacking TAFII105 are viable but infertile because of a defect in folliculogenesis correlating with restricted expression of TAFII105 in the granulosa cells of the ovarian follicle. Gene expression profiling has uncovered a defective inhibin-activin signaling pathway in TAFII105-deficient ovaries. Together, these studies suggest that TAFII105 mediates the transcription of a subset of genes required for proper folliculogenesis in the ovary and establishes TAFII105 as a cell type-specific component of the mammalian transcriptional machinery.

Animals↗
PubMed2001

[N-actyltransferase2 polymorphism in recurrence of colorectal polyps and adenomas].

OBJECTIVE: To observe the polymorphism of metabolizing enzyme N-actyltransferase 2 gene in populations with history of colorectal adenoma and polyp and to explore the relationship between NAT2 gene phenotype and colorectal cancer genetic susceptibility. METHODS: A cohort of 4,076 patients with history of colorectal adenoma or polyp was established Fifty-two cases were randomly selected from those with recurrence more than 2 times during the twenty years' follow-up. Fifty-two without recurrence were randomly selected as controls. DNA was isolated from the lymphocytes of peripheral blood of these 104 subjects. NAT2 polymorphism was detected by PCR-RFLP. RESULTS: The frequency of wild-type NAT2 (Wt/Wt) was significantly higher in control group (17/52, 32.7%) than in recurrence group (8/52, 15.4%) (P < 0.05). The frequency of heterogeneity type of NAT2 was significantly higher in recurrence group (40/52, 76.9%) than in control group (30/52, 57.7%) (P < 0.05). If OR of wild-type NAT2 (Wt/Wt) was 1, OR of Wt/M* genotype was 2.96 (95% CI: 1.091-8.009), and OR of M*/M* genotype was 2.125 (95% CI: 0.666-6.781). There was no difference of distribution between rapid enzyme type and slow enzyme type in the two groups. CONCLUSION: The frequency of wild-type NAT2 gene (Wt/Wt) is significantly higher in patients without recurrence of adenoma or polyp than in patients with recurrence. The frequency of heterogeneity genotype of NAT2 is significantly higher in patients with recurrence of adenoma or polyp than in those without recurrence. Wild-genotype (Wt/Wt) may be a protection factor in recurrence of colorectal adenomas. No difference can be seen between the distribution of rapid and slow enzyme types in these two groups.

Adenomatous Polyposis Coli↗
PubMed2001

First experimental observation on different ionic states of the tert-butoxy [(CH3)3CO*] radical.

A continuous tert-butoxy (CH3)+CO* radical beam is produced in situ by respective pyrolysis of both (CH3)3CONO at 115(+/-0.5) degrees C and (CH3)3COOC(CH3)3 at 87(+/- 0.5) degrees C. By combining the HeI photoelectron (PE) spectrum with the improved density function theory (DFT) calculations, we have concluded that the (CH3)3CO* radical has C3V symmetry and X2E ground state. The study does not only provide the ionization energies of different ionic states of the (CH3)3CO* radical for the first time, but also the first example in which there have been similar vibrational structures in different ionic states caused by removal of the electron on an orbital. It is also pointed out that (CH3)3CONO is a good source for obtaining the (CH3)3CO* radical beam, and that NO is a stable regent for the active radical. The results will promote the studies in electron spin resonance (ESR) research on the mechanisms of both the initiation of the formation of a new radical and the radical-chain polymerization in which the (CH3)3CO* radical participates.

Journal Article↗
PubMed2001

Platelets from patients with the Quebec platelet disorder contain and secrete abnormal amounts of urokinase-type plasminogen activator.

The Quebec platelet disorder (QPD) is an autosomal dominant platelet disorder associated with delayed bleeding and alpha-granule protein degradation. The degradation of alpha-granule, but not plasma, fibrinogen in patients with the QPD led to the investigation of their platelets for a protease defect. Unlike normal platelets, QPD platelets contained large amounts of fibrinolytic serine proteases that had properties of plasminogen activators. Western blot analysis, zymography, and immunodepletion experiments indicated this was because QPD platelets contained large amounts of urokinase-type plasminogen activator (u-PA) within a secretory compartment. u-PA antigen was not increased in all QPD plasmas, whereas it was increased more than 100-fold in QPD platelets (P <.00009), which contained increased u-PA messenger RNA. Although QPD platelets contained 2-fold more plasminogen activator inhibitor 1 (PAI-1) (P <.0008) and 100-fold greater u-PA-PAI-1 complexes (P <.0002) than normal platelets, they contained excess u-PA activity, predominantly in the form of two chain (tcu-PA), which required additional PAI-1 for full inhibition. There was associated proteolysis of plasminogen in QPD platelets, to forms that comigrated with plasmin. When similar amounts of tcu-PA were incubated with normal platelet secretory proteins, many alpha-granule proteins were proteolyzed to forms that resembled degraded QPD platelet proteins. These data implicate u-PA in the pathogenesis of alpha-granule protein degradation in the QPD. Although patients with the QPD have normal to increased u-PA levels in their plasma, without evidence of systemic fibrinogenolysis, their increased platelet u-PA could contribute to bleeding by accelerating fibrinolysis within the hemostatic plug. QPD is the only inherited bleeding disorder in humans known to be associated with increased u-PA.

Blood Platelet Disorders↗
PubMed2001

[Structure and expression of colorectal cancer related Immunoglobulin novel gene SNC73].

OBJECTIVE: To study the structure and function of a colorectal cancer-associated gene SNC73 obtained by subtractive hybridization technique. METHODS: Direct sequencing was performed on cDNA of SNC73 gene. In situ-max fluorescence in situ hybridization was used in chromosome mapping of SNC73. Expression of SNC73 in various cancer cell lines and differential expression between normal mucosa and colorectal cancer tissue were examined by Northern blotting and RT-PCR. Expression of SNC73 in colorectal epithelium was detected by in situ hybridization and in situ PCR. RESULTS: Open reading frame prediction showed that SNC73 encodes a peptide identical to the constant region of an IgA molecule in the carboxyl-terminus. The gene was mapped to human chromosome 14q32. The expression of SNC73 in colorectal cancer tissue and that in normal mucosa was different (P < 0.05). SNC73 was lowly expressed in colorectal epithelium. CONCLUSION: Decrease in SNC73 expression may be a potential genetic marker for the development of colorectal cancer. An immunoglobulin alpha-1 gene can be expressed in non-lymphoid cells.

Blotting, Northern↗
PubMed2001

p16(INK4a) and histology-specific methylation of CpG islands by exposure to tobacco smoke in non-small cell lung cancer.

The p16(INK4a) protein inhibits cyclin-dependent kinase 4, a key regulator of progression through the G(1) phase of the cell cycle. Methylation of CpG islands in the promoter region is an important avenue for inactivation of p16. The mechanism of methylation of the p16 promoter region, however, has not been elucidated. Recent reports investigating p16 methylation in non-small cell lung cancer (NSCLC) suggest that carcinogens in tobacco smoke induce the DNA methylation process. We investigated the association between methylation of the p16 promoter region and exposure to tobacco smoke in 185 primary NSCLCS: We also studied the relationship of p16 methylation with mutation of the K-ras and p53 genes, as well as with methylation at the DAP-kinase and p14(ARF) loci. Finally, we evaluated the prognostic significance of p16 methylation in NSCLC. The prevalence of p16 methylation was greater in squamous cell carcinoma (41%) compared with adenocarcinoma (22%; P = 0.03; Fisher's exact test). Methylation of p16 was significantly associated with pack-years smoked (P = 0.007; Wilcoxon rank sum test), duration of smoking (P = 0.0009; Wilcoxon rank sum test), and negatively with the time since quitting smoking (P = 0.03; Wilcoxon rank sum test). No methylation of the nearby p14(ARF) locus was detected, and methylation of the DAP-kinase locus was not associated with either p16 methylation or with exposure to tobacco smoke. In patients with stage 1 adenocarcinoma, p16 methylation was an independent risk factor predicting significantly shorter postsurgery survival (P = 0.03), controlling for the significant effects of other factors, including K-ras mutation. These findings suggest that methylation of CpG islands in tobacco-associated cancers occurs in a gene- and tissue-specific manner and is induced directly or indirectly by exposure to tobacco smoke in NSCLC.

Aged↗
PubMed2001

Positional order and thermal expansion of surface crystalline N-alkane monolayers.

We report a high-resolution synchrotron grazing incidence x-ray diffraction measurement of a surface crystalline monolayer at the liquid-vapor interface of the n-alkane eicosane (C20H42) just above its melting temperature. The peak width of the surface monolayer rotator phase is shown to be resolution limited and implies positional correlations of at least approximately 1 microm. The high resolution allowed determination of the temperature dependence of the peak position over the narrow (3 degrees C) temperature range of the surface crystal phase. The two-dimensional thermal expansion was determined to be (dA/dT)/A=1.8(+/-0.1)x10(-3) degrees C-1, which is comparable to the expansion in similar chain length bulk n-alkane rotator phases. Our data are consistent with the power-law shaped scattering tails expected from quasi-long-range order in two dimensions.

Journal Article↗
PubMed2001

Developmental expression and stress induction of glutathione S-transferase in the spruce budworm, Choristoneura fumiferana.

Developmental and stress-induced expression of Choristoneura fumiferana glutathione S-transferase (CfGST) mRNA and protein were examined using Northern blots and Western blots. High levels of CfGST mRNA and protein were detected in 1st instar larvae and diapausing 2nd instar larvae. Expression of CfGST gradually decreased during larval development from 3rd to 5th instar, after which the expression increased once again, reaching peak levels in 6th instar larvae. CfGST mRNA and protein were undetectable in the pupal stage. Exposure to low temperature did not induce an increase in CfGST expression. Feeding on balsam fir foliage resulted in an increase in the expression of CfGST as compared to larvae that fed on artificial diet. The bacterial insecticide, Bacillus thuringiensis delta-endotoxin (Bt), the non-steroidal ecdysone analog, tebufenozide, and the synthetic pyrethroid, permethrin, induced the expression of CfGST mRNA in 5th instar larvae, whereas the chitin synthesis inhibitor, diflubenzuron, did not have any such effect. These results suggest that CfGST plays an important role in detoxifying various allelochemicals and insecticides in the spruce budworm. The developmental expression pattern strongly suggests that in addition to detoxification, CfGST might be involved in other functions.

Journal Article↗
PubMed2001

Platelet factor V New York: a defect in factor V distinct from that in factor V Quebec resulting in impaired prothrombinase generation.

Studies were performed on a patient with a longstanding bleeding disorder whose major defects were impaired platelet prothrombinase activity in the absence of added factor Va, and a platelet factor V value that was either decreased or at the lower limit of normal when assayed on multiple occasions. In contrast, plasma factor V values were consistently normal. Unlike Scott Syndrome, in which platelet prothrombinase activity is decreased in both the presence and absence of added factor V, her platelets appeared to utilize added factor Va normally in supporting the generation of prothrombinase activity. These findings suggest an intrinsic defect in platelet factor V as the basis of her platelet prothrombinase defect. This defect appears to be different than that described in the Quebec platelet disorder (factor V Quebec). Immunoblot analyses of washed platelet lysates demonstrated a pattern of variably sized factor V molecules that was entirely similar to that observed in normal platelets, and both the heavy and light chains of her factor V after thrombin cleavage were of the same size as that observed in normal platelets. In addition, her platelet multimerin was normal and immunoblot analysis excluded the type of generalized granular protein defect and pathological proteolysis that has been suggested to explain the factor V defect in the Quebec platelet disorder. The findings in this patient thus suggest a new type of platelet factor V defect as the basis for the impaired capacity of her activated platelets to support prothrombinase generation. The findings further support an important role for platelet factor V in hemostasis.

Blood Coagulation Factors↗
PubMed2001

Multi-residue determination of 41 insecticides in garlic by gas chromatography and ion trap mass spectrometry using the selective ion storage technique.

A method is described for determining 41 insecticide residues in garlic (Allium sativum L.), including organophosphorus, organochlorine, carbamate, and synthetic pyrethroid insecticides. These insecticides were extracted from samples with acetone and dichloromethane, and co-extractives removed using a charcoal/Celite/alumina column. Analysis was performed by gas chromatography with ion trap mass spectrometry in selective ion storage (SIS) mode. Retention times and specific ions (m/z values) were used to confirm insecticides. Recoveries for most insecticides (blank samples spiked at 0.05, 0.2 and 1 microg mL(-1) levels) ranged from 70% to 110%, the coefficient of variation (CV) of the method was <20% for every case, and the limit of detection (LOD), defined in terms of 3 times baseline noise, varied between 0.01 and 0.16 mg kg(-1), depending on the compound.

Food Contamination↗
PubMed2001

The CH3 N Diradical: Experimental and Theoretical Determinations of the Ionization Energies.

Pyrolysis of CH3 N3 under the protection of NO generates a continuous methylnitrene CH3 N diradical beam that enables the ionization energies of different ionic states of the CH3 N diradical to be determined by HeI photoelectron spectroscopy (PES; see spectrum) and both ab initio and density functional theory (DFT) calculations. The ab initio and DFT results are in excellent agreement with the PES experiment and show that the CH3 N diradical has C3v symmetry and the ground state of the CH3 N radical cation is the (2) E state.

ab initio calculations↗
PubMed2001

Structural studies of the HIV-1 accessory protein Vpu in langmuir monolayers: synchrotron X-ray reflectivity.

Vpu is an 81 amino acid integral membrane protein encoded by the HIV-1 genome with a N-terminal hydrophobic domain and a C-terminal hydrophilic domain. It enhances the release of virus from the infected cell and triggers degradation of the virus receptor CD4. Langmuir monolayers of mixtures of Vpu and the phospholipid 1,2-dilignoceroyl-sn-glycero-3-phosphocholine (DLgPC) at the water-air interface were studied by synchrotron radiation-based x-ray reflectivity over a range of mole ratios at constant surface pressure and for several surface pressures at a maximal mole ratio of Vpu/DLgPC. Analysis of the x-ray reflectivity data by both slab model-refinement and model-independent box-refinement methods firmly establish the monolayer electron density profiles. The electron density profiles as a function of increasing Vpu/DLgPC mole ratio at a constant, relatively high surface pressure indicated that the amphipathic helices of the cytoplasmic domain lie on the surface of the phospholipid headgroups and the hydrophobic transmembrane helix is oriented approximately normal to the plane of monolayer within the phospholipid hydrocarbon chain layer. At maximal Vpu/DLgPC mole ratio, the tilt of the transmembrane helix with respect to the monolayer normal decreases with increasing surface pressure and the conformation of the cytoplasmic domain varies substantially with surface pressure.

Amino Acid Sequence↗
PubMed2001

The storage defects in grey platelet syndrome and alphadelta-storage pool deficiency affect alpha-granule factor V and multimerin storage without altering their proteolytic processing.

Among proteins stored in alpha-granules, multimerin and factor V share unusual features: they bind to each other, are proteolysed to unique forms and are stored eccentrically in alpha-granules. These unique features of their processing led us to study these proteins in alpha delta storage pool deficiency (alphadelta-SPD) and grey platelet syndrome (GPS, alpha-SPD), two conditions known to impair alpha-granule protein storage. Platelet factor V and multimerin were severely reduced in GPS, whereas they ranged from reduced to normal in alphadelta-SPD. The platelet levels of factor V and multimerin in these disorders indicated multimerin deficiency was not predictive of platelet factor V deficiency, although it reduced the amount of multimerin associated with platelet factor V. In GPS only, the defect in storing proteins was associated with increased multimerin and multimerin-factor V complexes in plasma. Like normal platelets, GPS and alphadelta-SPD platelets contained factor V mainly in granules. Platelet factor V and multimerin were proteolysed to normal platelet forms in GPS and alphadelta-SPD platelets, indicating that these conditions preserve some aspects of normal alpha-granule protein processing. Although we found factor V can be stored in platelets deficient in multimerin, our data indicate that multimerin storage influences the point at which multimerin binds factor V.

Blood Platelets↗