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Biomedical subjects

X Cheng

Publications and source records attributed to X Cheng.

At least 109 records · Page 6Linked to original sources
PubMed1999

Antithrombotic effects of low-molecular-weight heparin calcium (LMWH-Ca) in experimental models.

The antithrombotic activity of low-molecular-weight heparin calcium (LMWH-Ca) was studied in venous and arterial thrombosis models, arterial thrombosis model in rats, arterio-venous shunt model and venous thrombosis model in rabbits. The data showed that LMWH-Ca reduced thrombus formation in a dose-dependent manner. It suggests that LMWH-Ca is a potent antithrombotic agent for venous thrombosis, and also may be a beneficial therapeutic agent in arterial thrombosis.

Animals↗
PubMed1999

Local tumor recurrence or emergence of a new primary lesion? A molecular analysis.

The distinction between a new primary oral tumor and recurrence may bear significant prognostic implications. Currently, this differentiation relies mainly on tumor location: when both lesions are at or near the same site, the new one is regarded as a recurrence; when the two are at different sites, the second lesion is regarded as a new primary. Recent investigations using molecular analysis have demonstrated that some oral squamous cell carcinomas (SCC) arising from different sites show the same clonogenical changes. In this case report, we studied the clonality of three SCC (one primary, two apparent recurrences) from the right lateral tongue of a young, non-smoking woman by using microsatellite analysis for loss of heterozygosity. The results showed that while the first two tumors were clonogenically similar, the third tumor was clonogenically different and was consistent with the development of a new primary. This result indicates that location of tumors alone is not always reliable in determining whether a new tumor is a recurrence or a new primary lesion.

Adult↗
PubMed1999

Construction of La-tPA vector and expression in the mammary gland of transgenic mice.

Expression vectors of long acting human tissue plasminogen activator (La-tPa) in the mammary gland was constructed using the promoters of sheep beta-lactoglobulin gene (BLG, 5 kb) containing the first and the second introns obtained by PCR. Transgenic mice were established by microinjection. 540 fertilized eggs were injected and 6 transgenic mice were screened out from the offspring by PCR and Southern Blot analysis. The foreign gene integrating rate was 32%. The expression of La-tPA in mammary glands of transgenic mice was confirmed by milk assay and Northern blot analysis. Expression level of La-tPA reached 6 ug/ml in milk of transgenic mice.

Animals↗
PubMed1999

[Allotransplantation of cryopreserved fetal cartilage in plastic surgery].

OBJECTIVE: To study the applicability of homologous fetal cartilage in plastic surgery. METHODS: Limb and costal cartilage were taken from the dead fetus. The fetal cartilage was then frozen at -80 degrees C and preserved in -196 degrees C liquid nitrogen with a cryoprotective agent. A total of 38 patients received fetal cartilage transplantation. Of them there were 24 saddle nose, 4 auricle defects, 6 secondary deformities of cheiloschisis, 4 mandible deformities. RESULTS: Through follow-up of three and a half years, it was found that none of the transplanted cartilage was absorbed, deformed or rejected due to immunological reaction. The contours were satisfactory except 2 cases with auricle reconstruction. CONCLUSION: The clinical application of homologous fetal cartilages is of value in plastic surgery.

Adolescent↗
PubMed1999

[The relationship between smoking and the incidence of COPD].

OBJECTIVE: To study the relationship between smoking index and the incidence of COPD to persuade smokers quit smoking. METHODS: COPD was diagnosed based on family inquiring, questionnaire and pulmonary function test. The smoking index was calculated by the average cigarettes a day times the years of smoking. RESULTS: 822 cases(account for 24.6% of investigated subjects) of COPD due to smoking were identified, and 624 cases were found (account for 40.4% of investegated subjects) to have a history of both smoking and chronic airway inflammation. The higher the smoking index, the higher the incidence of COPD (above 40%), and the more severe their lung function imparement. The smoking was 71.6% of the cause in COPD patients. CONCLUSIONS: The incidence of COPD associated with smoking is higher in China than that in the Western countries. The incidence of COPD in population with long smoking history is not invariable, while it is gradually rising with increasing smoking index.

Adolescent↗
PubMed1999

[Study on susceptible risk factors for COPD in smokers].

OBJECTIVE: To explore the susceptible risk factors for COPD in smokers. METHODS: 154 patients with COPD (FEV1/FVC < 70%) were recruited as the case group whose smoking index (average cigarettes a day times smoking years) was > or = 300 and there was no complaint of chronic respiratory symptoms. The control group included 154 smokers pair-matched in age(+/- 3 years) gender, residence, absence of COPD (FEV1/FVC > or = 75%) and respiratory symptoms. 23 never-smoking subjects with FEV1/FVC > or = 75% and no respiratory symptoms served as healthy control. The following parameters were evaluated: questionaire, physical examination, ECG, chest X-ray, lung function test, methacholine provocation test of bronchial responsiveness and serum levels of elastase activity, alpha 1-AT activity, MDA, PIIIP, IgE and IgG. RESULTS: The positive rate of bronchial hyperresponsiveness was 78% in the case group, PC20 = (1.4 +/- 1.6) g/L; but 28% in the matched group were positive, PC20 = (2.7 +/- 2.3) g/L, (P < 0.001). No one was found hyperresponsive in the healthy control group. There were no differences in serum PIIIP and IgE between the case and the control groups, but they were markedly higher than those in the healthy control. Serum alpha 1-AT activity, room condition, occupational exposure, smoking habit (deep inhalation), cigarettes with or without filter tip, parents with bronchitis and(or) emphysema history, brothers or sisters with bronchitis history were correlated with COPD, OR being 2.33, 2.00, 1.64, 1.88, 1.76 and 3.67, respectively. Logistic regression revealed that alpha 1-AT activity, bronchial hyperresponsiveness, room condition and occupational exposure, smoking habit and respiratory disease history in family were related to COPD. CONCLUSIONS: alpha 1-AT deficiency may be a risk factor for COPD susceptible smokers. There may be relationship between bronchial hyperresponsiveness and developing COPD, but whether it is the cause or result of COPD needs further study. Smoking may induce elevation of serum PIIIP and IgE, but both of them are not directly related to COPD. Room condition, occupational exposure, smoking habit, and respiratory disease history in family may be associated with COPD in smokers.

China↗
PubMed1999

[Changes of serum elastase, alpha 1-antitrypsin, procollagen III peptide and malonaldehyde in smokers with and without chronic obstructive pulmonary diseases].

OBJECTIVE: Serum elastase, alpha(1)-antitrypsin (alpha(1)-AT), procollagen III peptide (PIIIP) and malonaldehyde (MDA) were studied in smokers with and without chronic obstructive pulmonary disease (COPD) to explore the roles of these factors in COPD induced by smoking. METHODS: A design of 154-pair case-control study was used. alpha(1)-AT, MDA and PIIIP were determined with colorimetric method, fluo-spectrophotometric method and radio-immunological assay, respectively, in non-smoker control and smokers with and without COPD. RESULTS: Serum PIIIP content was increased in smokers and alpha(1)-AT decreased significantly in patients with COPD. CONCLUSION: Decreased alpha(1)-AT may be a susceptible factor in the development of COPD caused by smoking.

Adult↗
PubMed1999

[Strain screening and fermentation conditions of a novel heparinase-producing strain].

The novel heparinase-producing bacterial strain Corynebacterium sp. was screened and isolated from soil. The optimum medium composition is (g/L): Trypticase 20, NaCl 1, K2HPO4 2.5, MgSO4 0.5, Heparin 2, maltose 20, pH 6.5. The optimum growth temperature was 27 degrees C while, maximum enzyme production was achieved at temperature 31 degrees C. When cultured at a rotating shaker at 30 degrees C for 24 hours, 200 r/min, 40 mL medium in 500 mL flask, the Production of heparinase reached 1700 u/L.

Corynebacterium↗
PubMed1999

[Nucleotide sequence at position -155 to +25 of the 5' flanking region of the angiotensinogen gene of Han people].

OBJECTIVE: To study the polymorphism of 5'-flanking region of angiotensinogen gene and relations to essential hyperfension. METHODS: The nucleotide sequence at position -155 to +25 of the 5'-flanking region in angiotensinogen gene of Han people in Chinese population was identified by applying PCR-single stranded conformational polymorphism(SSCP) and PCR-directed sequencing. RESULTS: (1) The Han people carry an adenylate(A), instead of a cytidylate(C) at position -20 of the 5'-flanking region of AGT gene; (2) A new mutation T-->A at position -46 was detected and A-allele frequencies was similar in both hypertensives and normotensive controls. CONCLUSIONS: The variant T-->A at position -46 of AGT gene was not associated with hypertension, but an adenylate (A) at position -20 of the 5'-flanking region of AGT gene. might be an genetic marker for Hans people.

5' Flanking Region↗
PubMed1999

[Characterization of HA1 genes of influenza A (H1N1) viruses isolated in Shenzhen City].

OBJECTIVE: To understand the molecular bases of intention of influenza virus activity and emergence of "O" phase of influenza A(H1N1) strains in human population in Shenzhen in recently years, and also the evolutionary characterization of influenza A(H1N1) HA1 gene. METHODS: Virion RNA was transcribed into cDNA by reverse transcriptase, cDNA was amplified by PCR, the products of PCR were purified. Afterward, RNA sequence analysis was performed by the dideoxynucleotide chain termination method using synthetic oligodeoxynucleotide primers. Finally, phylogenetic analysis of the sequencing data was performed with MegAlign (version 1.03) and Editseq (version 3.69) softwares. RESULTS: Since 1995, there were three different genetic lineages of influenza A(H1N1) virus HA1 gene cocirculating in men in Shenzhen city. Adding one and deleting one of potential glycosylation sites at 54 and 155 positions of amino acid sequences on HA1 protein domain of H1N1 viruses isolated recently was found as compared with those of A/Singapore/6/86(H1N1) virus. Meanwhile, there were some differences of amino acid sequences on HA1 protein molecules among H1N1 viruses tested and A/Singapore/6/86 (H1N1) virus. CONCLUSION: The intention of influenza A(H1N1) virus activity occurred since 1995 was due to emergence of substitution in amino acid sequences, especially the appearance of one addition and one deletion of potential glycosylation sites on their HA1 protein domains, and also was due to occurrence of influenza A(H1N1) virus with feature of "O" phase.

Amino Acid Sequence↗
PubMed1998

Asp34 of PvuII endonuclease is directly involved in DNA minor groove recognition and indirectly involved in catalysis.

The PvuII restriction endonuclease is a homodimer that recognizes and cleaves the DNA sequence 5'-CAGCTG-3' in double-stranded DNA, and the structure of this enzyme has been reported. In the wild-type enzyme, Asp34 interacts with the internal guanine of the recognition sequence on the minor groove side. The Asp34 codon was altered to specify Gly (D34G), and in vitro studies have revealed that the D34G protein has lost binding specificity for the central G.C base-pairs, and that it cuts the canonical sequence with 10(-4)-fold reduced activity as compared to the wild-type enzyme. We have now determined the structure at 1.59 A resolution of the D34G PvuII endonuclease complexed with a 12 bp duplex deoxyoligonucleotide containing the cognate sequence. The D34G alteration results in several structural changes relative to wild-type protein/DNA complexes. First, the sugar moiety of the internal guanine changes from a C2'-endo to C3'-endo pucker while that of the 3' guanine changes from C3'-endo to C2'-endo pucker. Second, the axial rise between the internal G.C base-pairs is reduced while that between the G.C and flanking base-pairs is expanded. Third, two distinct monomeric active sites are observed that we refer to as being "primed" and "unprimed" for phosphodiester bond cleavage. The primed and unprimed sites differ in the conformation of the Asp58 side-chain, and in the absence from unprimed sites of four networked water molecules. These water molecules, present in the primed site, have been implicated in the catalytic mechanism of this and other endonucleases; some of them can be replaced by the Mg2+ necessary for cleavage. Taken together, these structural changes imply that the Asp34 side-chains from the two subunits maintain a distinct conformation of its DNA substrate, properly situating the target backbone phosphates and indirectly manipulating the active sites. This provides some insight into how recognition of the specific DNA sequence is linked to catalysis by the highly specific restriction endonucleases, and reveals one way in which the structural conformation of the DNA is modulated coordinately with that of the PvuII protein.

Aspartic Acid↗
PubMed1998

Recombinant human respiratory syncytial virus (RSV) from cDNA and construction of subgroup A and B chimeric RSV.

Infectious human respiratory syncytial virus (RSV) was produced from a cDNA clone that contains 15,222 nucleotides of RSV genome derived from the A2 strain of subgroup A. Recovery of infectious RSV from cDNA required cotransfection of only three expression plasmids encoding the nucleoprotein (N), the phosphoprotein (P), and the major polymerase protein (L). Inclusion of the M2-1 plasmid was not required in the transfection reaction and if included did not significantly increase the rescue efficiency. However, a single nucleotide substitution in the RSV leader region (C to G at position 4 in the antigenomic sense), greatly increased the amount of infectious virus recovered from cDNA. A recombinant RSVA2 virus that expresses an additional structural G protein derived from a subgroup B RSV was also obtained. Both A2 and B strain G glycoproteins were expressed in cells infected with the chimeric RSV. A chimeric RSV that expresses a heterologous subgroup antigen in a live attenuated vaccine candidate may be important for prevention of diseases associated with both RSV subgroup A and subgroup B infection.

Animals↗
PubMed1998

Molecular events after antisense inhibition of hMSH2 in a HeLa cell line.

To establish a cause-effect relationship between the human mismatch repair pathway deficiency and the observed phenotypes, a hMSH2 deficient HeLa cell line (HeLa-MSH2-) was established by transfecting the HeLa cells with an antisense RNA expression plasmid. The expression plasmid was constructed by inserting an 851 bp fragment of hMSH2 cDNA into the polyclonal site of the vector pREP9 in a reversed orientation. The production of the mismatch binding protein, hMSH2, was inhibited in HeLa-MSH2- cells, as demonstrated by Western blotting and band shift assay of its whole cell extract. The growth rate of this cell line was not different from the parental HeLa cells soon after transfection. However, the rate was faster after 10 subcultures. The spontaneous mutation frequency at the hypoxanthine phosphoribosyltransferase (HPRT) locus increased markedly, but no N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) tolerance appeared in this cell line. Our results clearly demonstrated several molecular events happened after the inhibition of a major mismatch recognition protein, hMSH2, in the mismatch repair pathway, mimicking carcinogenesis processes.

Base Pair Mismatch↗
PubMed1998

Mapping substrate-induced conformational changes in cAMP-dependent protein kinase by protein footprinting.

Upon binding of substrates the catalytic subunit (C) of cAMP-dependent protein kinase (cAPK) undergoes significant induced conformational changes that lead to catalysis. For the free apoenzyme equilibrium favors a more open and malleable conformation while the ternary complex of C, MgATP, and a 20-residue inhibitor peptide [PKI (5-24)] adopts a tight and closed conformation [Zheng, J., et al. (1993) Protein Sci. 2, 1559]. It is not clear that binding of either ligand alone is responsible for this conformational switch or whether both are required. In addition, the catalytic subunit binds MgATP and inhibitor peptide synergistically. The structural basis for this synergism is also not defined at present. Using an Fe-EDTA-mediated protein footprinting technique, the conformational changes associated with the binding of MgATP and the heat stable protein kinase inhibitor (PKI) were probed by mapping the solvent-accessible surface and structural dynamics of C. The conformation of the free enzyme was clearly distinguished from the ternary complex. Furthermore, binding of MgATP alone induced extensive conformational changes, both local and global, that include the glycine-rich loop, the linker connecting the small and large lobes, the catalytic loop, the Mg2+ positioning loop, the activation loop, and the F helix. These changes, similar to those seen in the ternary complex, are consistent with a transition from an open to a more closed conformation and likely reflect the motions that are associated with catalysis and product release. In contrast, the footprinting pattern of C.PKI resembled free C, indicating minimal conformational changes. Binding of MgATP, by shifting the equilibrium to a more closed conformation, "primes" the enzyme so that it is poised for the docking of PKI and provides an explanation for synergism between MgATP and PKI.

Adenosine Triphosphate↗
PubMed1998

Calculation of concentrations of equilibrium components in an in vitro activity test of vancomycin antibiotics and the possible mode of action.

The vancomycin group of antibiotics is considered to act by binding the bacterial cell wall mucopeptide precursor terminating in -L-Lys-D-Ala-D-Ala. The dimerization of these antibiotics is also believed to play a role in the action. In this paper, we analyzed the equilibria in the in vitro antibacterial activity test of the vancomycin antibiotics both with and without the cell wall precursor analogue di-acetyl-L-Lys-D-Ala-D-Ala (DALAA). Based on the equilibria and concentration balance, we obtained 10 equations (seven quadratic equations and three linear equations) containing 10 equilibrium concentrations which relate to the antibiotic, cell wall precursor and DALAA. A computer program was written to solve these equations from known dimerization constant and the binding constants (both monomer and dimer) with DALAA of the antibiotic. The concentrations in the test for vancomycin and eremomycin were obtained. The antibiotic activity of these antibiotics may be quantitatively correlated with their dimerization constants and the binding constants through the calculation. By analyzing the calculated results, we concluded that the cell wall-bound dimer may be the major contributor to the antibiotic activity in the case of eremomycin, while the cell wall-bound monomer is possibly the determinant for the activity of vancomycin.

Anti-Bacterial Agents↗
PubMed1998

Phosphorylation and activation of cAMP-dependent protein kinase by phosphoinositide-dependent protein kinase.

Although phosphorylation of Thr-197 in the activation loop of the catalytic subunit of cAMP-dependent protein kinase (PKA) is an essential step for its proper biological function, the kinase responsible for this reaction in vivo has remained elusive. Using nonphosphorylated recombinant catalytic subunit as a substrate, we have shown that the phosphoinositide-dependent protein kinase, PDK1, expressed in 293 cells, phosphorylates and activates the catalytic subunit of PKA. The phosphorylation of PKA by PDK1 is rapid and is insensitive to PKI, the highly specific heat-stable protein kinase inhibitor. A mutant form of the catalytic subunit where Thr-197 was replaced with Asp was not a substrate for PDK1. In addition, phosphorylation of the catalytic subunit can be monitored immunochemically by using antibodies that recognize Thr-197 phosphorylated enzyme but not unphosphorylated enzyme or the Thr197Asp mutant. PDK1, or one of its homologs, is thus a likely candidate for the in vivo PKA kinase that phosphorylates Thr-197. This finding opens a new dimension in our thinking about this ubiquitous protein kinase and how it is regulated in the cell.

3-Phosphoinositide-Dependent Protein Kinases↗
PubMed1998

Role of nitric oxide and peroxynitrite in the cytokine-induced sustained myocardial dysfunction in dogs in vivo.

Studies in vitro suggested that inflammatory cytokines could cause myocardial dysfunction. However, the detailed mechanism for the cytokine-induced myocardial dysfunction in vivo remains to be examined. We thus examined this point in our new canine model in vivo, in which microspheres with and without IL-1beta were injected into the left main coronary artery. Left ventricular ejection fraction (LVEF) was evaluated by echocardiography for 1 wk. Immediately after the microsphere injection, LVEF decreased to approximately 30% in both groups. While LVEF rapidly normalized in 2 d in the control group, it was markedly impaired in the IL-1beta group even at day 7. Pretreatment with dexamethasone or with aminoguanidine, an inhibitor of inducible nitric oxide synthase, prevented the IL-1beta-induced myocardial dysfunction. Nitrotyrosine concentration, an in vivo marker of the peroxynitrite production by nitric oxide and superoxide anion, was significantly higher in the myocardium of the IL-1beta group than in that of the control group or the group cotreated with dexamethasone or aminoguanidine. There was an inverse linear relationship between myocardial nitrotyrosine concentrations and LVEF. These results indicate that IL-1beta induces sustained myocardial dysfunction in vivo and that nitric oxide produced by inducible nitric oxide synthase and the resultant formation of peroxynitrite are substantially involved in the pathogenesis of the cytokine-induced sustained myocardial dysfunction in vivo.

Animals↗