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Biomedical subjects

J Dong

Publications and source records attributed to J Dong.

At least 163 records · Page 9Linked to original sources
PubMed1998

[Studies on the basis of molecular biology of the phase change of influenza A(H3N2) viruses].

The analysis of nucleotide sequences on HA1 domain of 35 strains of influenza A(H3N2) virus showed that their HA1 genes all were 984 nucleotides in length coding for a HA1 protein with 328 amino acids and there was not any occurrence of insertion or deletion of nucleotides on HA1 genes among them. The appearance of "O" phase strain of influenza A (H3N2) virus was closely related with substitution at 226 position of amino acid on HA1 protein molecule and the three-dimensional structural change of HA protein. The results in this paper indicated that the positions with multiple changes on HA1 protein molecule located at the top of HA protein, especially at antigenic determinant B site or receptor binding site. These further demonstrated that the substitution of amino acid on HA1 protein molecule was caused mainly by suppress of herd immunity. This study also showed that the position of the cysteine and proline residues on the HA1 protein molecule were conservative and that the glycosylation sites located at N and C terminals, especially at N terminal of the HA1 protein The significance of such a distribute delta of glycosylation sites in the evolution of viral genes and epidemiology still remain unknown.

Amino Acid Sequence↗
PubMed1998

Novel somatostatin analogs for the treatment of acromegaly and cancer exhibit improved in vivo stability and distribution.

The biodistribution of several radiolabeled somatostatin (SRIF) analogs was determined in the rat. Newly developed analogs BIM-23190 and BIM-23197 attained higher plasma levels and much greater target tissue concentrations than the clinically used BIM-23014 analog. Highest tissue concentrations of BIM-23190 and BIM-23197 were found in adrenal, kidney, pituitary and pancreas, tissues that are known to be abundant in mRNA for the somatostatin subtype 2 receptor. BIM-23190 and BIM-23197 associated radioactivity in these tissues was prolonged compared with that of BIM-23014, especially in the SRIF-receptor-rich pituitary. BIM-23190 and BIM-23197 were more stable in vivo and much less subject to biliary excretion than BIM-23014. These properties account for the elevated plasma and target tissue concentrations of these new SRIF analogs. Based on higher plasma levels, greater distribution to target tissues and longer in vivo stability, BIM-23190 and BIM-23197 may prove to be superior to BIM-23014 for the treatment of acromegaly and some types of cancer.

Acromegaly↗
PubMed1998

Full agonistic properties of BAY x 3702 on presynaptic and postsynaptic 5-HT1A receptors electrophysiological studies in the rat hippocampus and dorsal raphe.

The present studies evaluated the effects of acute and long-term administration of the 5-HT1A agonist BAY x 3702 on the responsiveness of dorsal raphe 5-HT neurons and of dorsal hippocampus CA3 pyramidal neurons. BAY x 3702 potently reduced the firing activity of 5-HT neurons and of CA3 pyramidal neurons when applied by microiontophoresis and this inhibitory effect of BAY x 3702 was fully antagonized by low intravenous doses of the 5-HT1A antagonist WAY 100635. Concurrent microiontophoretic application of BAY x 3702 did not antagonize the suppressant effect of 5-HT on firing activity of 5-HT and CA3 pyramidal neurons. Sustained administration of BAY x 3702 for 2 days (1 and 1.25 mg/kg/day using osmotic minipumps implanted subcutaneously) markedly decreased the firing rate of dorsal raphe 5-HT neurons. This was followed by a full recovery to normal after only 7 days of treatment. The postsynaptic 5-HT1A receptors in the hippocampus, contrary to the presynaptic 5-HT1A receptors, were not desensitized after a 14-day treatment. In conclusion, BAY x 3702 acted as a full and potent agonist both at somatodendritic 5-HT1A autoreceptors and at postsynaptic 5-HT1A receptors. Long-term administration of BAY x 3702 resulted in a desensitization of the somatodendritic 5-HT1A autoreceptors, but in an unaltered responsiveness of 5-HT1A receptors on pyramidal neurons. These results suggest that sustained administration of BAY x 3702 enhances neurotransmission at postsynaptic 5-HT1A receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1997

Preparation and Characterization of Surface-Covered Nanometer-Sized Catalyst by Carboxylate Phase Transfer

Surface-covered nanometer-sized CuO/Al2O3, CuO-ZnO/Al2O3, and CuO/ZnO catalysts were prepared by phase transfer with carboxylate. The surface-covered structure was studied using XPS, XRD, TEM, and high-resolution electron microscope. The results indicated that amorphous CuO and ZnO were dispersed on the surface of nanometer-sized Al2O3 particles in catalysts CuO-ZnO/Al2O3 and CuO/Al2O3, respectively. The thickness of its surface layer is about several angstroms. No spinel structure was found in the catalyst. The particle size of the surface-covered CuO/Al2O3 catalyst was about 2-3 nm. Al2O3 in the catalyst was amorphous. Surface-covered material CuO in the catalyst with low CuO content was also armophous. A large amount of copper carboxylate resulted in crystalline CuO and Cu2O. The protective ability of carboxylate to sol particles differs from the metal element of carboxylate. Copyright 1997 Academic Press. Copyright 1997Academic Press

Journal Article↗
PubMed1997

Biophysical and mutagenic analysis of Thermoanaerobacter ethanolicus secondary-alcohol dehydrogenase activity and specificity.

The Thermoanaerobacter ethanolicus 39E adhB gene encoding the secondary-alcohol dehydrogenase (secondary ADH) was overexpressed in Escherichia coli at more than 10% of total protein. The recombinant enzyme was purified in high yield (67%) by heat-treatment at 85 degrees C and (NH4)2SO4 precipitation. Site-directed mutants (C37S, H59N, D150N, D150Eand D150C were analysed to test the peptide sequence comparison-based predictions of amino acids responsible for putative catalytic Zn binding. X-ray absorption spectroscopy confirmed the presence of a protein-bound Zn atom with ZnS1(imid)1(N,O)3 co-ordination sphere. Inductively coupled plasma atomic emission spectrometry measured 0.48 Zn atoms per wild-type secondary ADH subunit. The C37S, H59N and D150N mutant enzymes bound only 0.11, 0.13 and 0.33 Zn per subunit respectively,suggesting that these residues are involved in Zn liganding. The D150E and D150C mutants retained 0.47 and 1.2 Zn atoms per subunit, indicating that an anionic side-chain moiety at this position preserves the bound Zn. All five mutant enzymes had </= 3% of wild-type catalytic activity, suggesting that the T. ethanolicus secondary ADH requires a properly co-ordinated catalytic Zn atom. The His-59 and Asp-150 mutations also altered secondary ADH affinity for propan-2-ol over a 140-fold range, whereas the overall change in affinity for ethanol spanned a range of only 7-fold, supporting the importance of the metal in secondary ADH substrate binding. The lack of significant changes in cofactor affinity as a result of these catalytic Zn ligand mutations suggested that secondary ADH substrate-and cofactor-binding sites are structurally distinct. Altering Gly198 to Asp reduced the enzyme specific activity 2.7-fold, increased the Km(app) for NADP+ 225-fold, and decreased the Km(app) for NAD+ 3-fold, supporting the prediction that the enzyme binds nicotinamide cofactor in a Rossmann fold. Our data indicate therefore that, unlike the liver primary ADH,the Rossmann-fold-containing T. ethanolicus secondary ADH binds its catalytic Zn atom using a sorbitol dehydrogenase-like Cys-His-Asp motif and does not bind a structural Zn atom.

Alcohol Dehydrogenase↗
PubMed1997

Glucose represses the lactose-galactose regulon in Kluyveromyces lactis through a SNF1 and MIG1- dependent pathway that modulates galactokinase (GAL1) gene expression.

Expression of the lactose-galactose regulon in Kluyveromyces lactis is induced by lactose or galactose and repressed by glucose. Some components of the induction and glucose repression pathways have been identified but many remain unknown. We examined the role of the SNF1 (KlSNF1) and MIG1 (KlMIG1) genes in the induction and repression pathways. Our data show that full induction of the regulon requires SNF1; partial induction occurs in a Klsnf1 -deleted strain, indicating that a KlSNF1 -independent pathway(s) also regulates induction. MIG1 is required for full glucose repression of the regulon, but there must be a KlMIG1 -independent repression pathway also. The KlMig1 protein appears to act downstream of the KlSnf1 protein in the glucose repression pathway. Most importantly, the KlSnf1-KIMig repression pathway operates by modulating KlGAL1 expression. Regulating KlGAL1 expression in this manner enables the cell to switch the regulon off in the presence of glucose. Overall, our data show that, while the Snf1 and Mig1 proteins play similar roles in regulating the galactose regulon in Saccharomyces cerevisiae and K.lactis , the way in which these proteins are integrated into the regulatory circuits are unique to each regulon, as is the degree to which each regulon is controlled by the two proteins.

Base Sequence↗
PubMed1997

c-Myc plays a role in cellular susceptibility to death receptor-mediated and chemotherapy-induced apoptosis in human monocytic leukemia U937 cells.

Human monocytic leukemia U937 cells readily undergo apoptosis when they are treated with TNF-alpha, anti-Fas antibody and anticancer drugs such as etoposide and Ara-C. To study the mechanism of apoptosis, we developed a novel apoptosis-resistant variant, UC, from U937 cells. The UC cells showed resistance to apoptosis induced by TNF-alpha, anti-Fas antibody, etoposide and Ara-C. Somatic cell hybridization between U937 and UC showed that apoptosis-resistance to TNF-alpha in UC was genetically recessive and resistance to etoposide was dominant, suggesting that UC has at least two different mutations functionally involved in apoptosis. Mechanistic analysis revealed that UC cells expressed reduced amounts of c-Myc. Transfection of the c-myc gene into UC cells restored the sensitivity of the cells to undergo apoptosis induced by TNF-alpha and anti-Fas, which attributes apoptosis-resistance in this circumstance to the reduced expression of c-Myc. On the other hand, c-myc transfection into UC cells could not restore their sensitivity to etoposide- and Ara-C-induced apoptosis, arguing against the role of c-myc in chemotherapy-induced apoptosis. However, treating the parental U937 cells with antisense oligonucleotides designed to reduce c-Myc expression rendered the cells resistant to etoposide-induced as well as to TNF-alpha-induced apoptosis. These results indicate that the reduced expression of c-Myc in UC is strongly associated with the resistance to etoposide-induced apoptosis. Our finding that c-myc transfection into UC could not restore the sensitivity to etoposide-induced apoptosis, suggests UC could have a second mutation that confers resistance to etoposide-induced apoptosis in a genetically dominant manner. Taken together, our present results indicate that c-Myc plays a role in cellular susceptibility to death receptor-mediated and chemotherapy-induced apoptosis.

Antibodies↗
PubMed1997

Mechanism of anti-beta-adrenoceptor antibody mediated myocardial damage in dilated cardiomyopathy.

Antibodies against beta(1)-adrenoceptor can be detected in serum of patients with dilated cardiomyopathy (DCM), which have beta-agonist-like activity, and induce a positive chronotropic effect on cardiac myocytes by its persistence at full strength. Effects of the antibodies against beta-adrenoceptor from sera of patients with DCM on myocardial cytotoxicity and cytoplasmic free Ca(2+)-concentration ([Ca2+]i) were observed in the cultured single layer SD rat ventricular cells by using the cytotoxicity assay and fluorescent Ca(2+)-indicator fura-2/AM. The positive sera of the anti-beta-adrenoceptor antibodies from patients with DCM markedly enhanced myocardial [Ca2+]i. Betaloc, a beta(1)-receptor blocker, might inhibit the increase of the antibody-mediated myocardial [Ca2+]i, and the sera from healthy donors had no effect on myocardial [Ca2+]i. Our results suggest that the anti-beta-adrenoceptor antibody might increase myocardial [Ca2+]i and result in myocardial damage. The antibodies might activate receptor-gating Ca(2+)-channel, thereby causing myocardial [Ca2+]i rise and calcium overload. Early use of betaloc is recommended in the treatment of dilated cardiomyopathy.

Adult↗
PubMed1997

Effect of acute and repeated versus sustained administration of the 5-HT1A receptor agonist ipsapirone: electrophysiological studies in the rat hippocampus and dorsal raphe.

The present study was aimed at examining the adaptation of presynaptic 5-HT1A autoreceptors in the dorsal raphe and of postsynaptic 5-HT1A receptors in the dorsal hippocampus during long-term administration of the 5-HT1A receptor agonist ipsapirone given either repeatedly or in a sustained fashion. Concurrent microiontophoretic application of ipsapirone did not attentuate the suppressant effect of 5-hydroxytyptamine (5-HT) on 5-HT neurons, but markedly decreased it when co-applied on CA3 pyramidal neurons in the dorsal hippocampus. Thus, ipsapirone acted as a full agonist in the dorsal raphe and as a partial agonist in the dorsal hippocampus. Ipsapirone (15 mg/kg/day, s.c. x 2 days) delivered by osmotic minipumps markedly decreased the firing activity of the dorsal raphe 5-HT neurons. After 14 days of treatment, there was a complete recovery of their firing activity and a desensitization of their somatodendritic 5-HT1A autoreceptors, as assessed using microiontophoretic applications of 5-HT and 8-hydroxy-2(di-n-propylamino)tetraline (8-OH-DPAT) onto 5-HT neurons. The same degree of desensitization was obtained when ipsapirone was administered with repeated injections (7.5 mg/kg b.i.d., s.c. x 14 days). In contrast, the two modalities of ipsapirone adminsitration left unaltered the responsiveness of CA3 pyramidal neurons to microiontophoretic applications of 5-HT and 8-OH-DPAT. In conclusion, long-term administration of ipsapirone most likely increases 5-HT neurotransmission by enhancing the tonic activation of postsynaptic 5-HT1A receptors. Therefore, the use of sustained release preparation of 5-HT1A receptor agonists should not alter their therapeutic effectiveness in anxiety and affective disorders since the same effects on 5-HT1A receptor functions were produced in this rat model by the sustained and the repeated modes of administration of ipsapirone.

Animals↗
PubMed1997

Studies of cation binding in ZnCl2-regenerated bacteriorhodopsin by x-ray absorption fine structures: effects of removing water molecules and adding Cl- ions.

The binding of Zn2+ in Zn2+-regenerated bacteriorhodopsin (bR) was studied under various conditions by x-ray absorption fine structures (XAFS). The 0.9:1 and 2:1 Zn2+:bR samples gave similar XAFS spectra, suggesting that Zn2+ might have only one strong binding site in bR. It was found that in aqueous bR solution, Zn2+ has an average of six oxygen or nitrogen ligands. Upon drying, two ligands are lost, suggesting the existence of two weakly bound water ligands near the cation-binding site in bacteriorhodopsin. When excess Cl- ions were present before drying in the Zn2+-regenerated bR samples, it was found that two of the ligands were replaced by Cl- ions in the dried film, whereas two remain unchanged. The above observations suggest that Zn2+ has three types of ligands in regenerated bR (referred to as types I, II, and III). Type I ligands are strongly bound. These ligands cannot be removed by drying or by exchanging with Cl- ions. Type II ligands cannot be removed by drying, but can be replaced by Cl- ligands. Type III ligands are weakly bound to the metal cation and are most likely water molecules that can be removed by evaporation under vacuum or by drying with anhydrous CaSO4. The results are discussed in terms of the possible structure of the strongly binding site of Zn2+ in bR.

Bacteriorhodopsins↗
PubMed1997

New spirostanol glycosides from Anemarrhena asphodeloides.

Two new spirostanol saponins, named anemarsaponin F (2b) and G (4b), along with six known spirostanol saponins were obtained from the rhizomes of Anemarrhena asphodeloides Bunge. On the basis of spectral analyses and chemical evidence, the structures of 2b and 4b were established as neogitogenin 3-O-beta-glucopyranosyl-(1-->2) [beta-xylopyranosyl-(1-->3)]-beta-glucopyranosyl (1-->4)-beta-galactopyranoside) and lilagenin 3-O-beta-glucopyranosyl-(1-->2)-[beta-xylopyranosyl-(1-->3)]-beta- glucopyranosyl-(1-->4)-beta-galactopyranoside, respectively.

Carbohydrate Conformation↗
PubMed1997

Severe myopia as a risk factor for progressive visual field loss in primary open-angle glaucoma.

The optic nerve head in severely myopic eyes may be particularly vulnerable to glaucomatous damage. To study this hypothesis, we examined 122 primary open-angle glaucoma eyes with fair to good control of the intraocular pressure and a sign of baseline optic nerve damage. Then, parameters for the progression of the visual field defects were evaluated by multivariate analysis. A high mean intraocular pressure (p = 0.007) and a large refractive error (p = 0.023) were significant risk factors for subsequent visual field loss. A high baseline cup-to-disk ratio (p = 0.100) was a marginal risk factor. Nonsignificant parameters included patient age (p = 0.692), the use of beta-adrenergic antagonists (p = 0.384), gender (p = 0.831) and left versus right side (p = 0.977). When the refractive error was used to subclassify patients into severely myopic (< or = -4 dpt), mildly myopic (-0.25 to -4 dpt), or emmetropic and hyperopic (> or = 0 dpt), only severe myopia was a significant risk factor for progressive visual field loss. Severe myopia, but not mild myopia, is a significant risk factor for subsequent visual field loss in patients with primary open-angle glaucoma.

Adolescent↗
PubMed1997

[Effect of B16 cells transfected with IL-2 gene on mouse immunity].

IL-2 was introduced into mice B16 melanoma cell line by using retrovirus infection method. Both B16 and B16-IL-2 cells were treated with Mit C beforehand and were then inoculated intraperitoneally as vaccines in mice respectively. Hanks solution was used instead of the vaccine in the control group. The data showed that the tumor incidence rate was zero in the group receiving B16-IL-2 vaccine followed by B16 inoculation. However, incidence rate was 100% in both the B16 vaccine immunization group and in the control groups. Experiments also indicated that the proliferation of splenic lymphocytes induced by MLTR, the specific cytotoxicity of CTL against B16 cells, the activities of splenic NK, LAK, and the level of IL-2 secretion in mice immunized by B16-IL-2 were much higher than those in the mice immunized only with B16 cells as well as the controls. These data indicated that secretion of IL-2 in mice promoted specific and nonspecific anti-tumor immunity of mice. The theoretic basis was provided for IL-2-secreting tumor vaccine.

Animals↗
PubMed1997

[Human papillomavirus type 16 E6 oncogene and expression of P53, RB and PCNA in human cervical carcinoma].

The aim of this study was to get some insights into the relationship between human papillomavirus type 16 E6 transforming gene and the expressed products of tumor suppressor gene, the P53, RB and proliferation cell nuclear antigen (PCNA) in human cervical carcinoma. 44 formalin-fixed paraffin-embedded cervical carcinoma sections were screened for P53, RB and PCNA by immunohistochemical assay with their monoclonal antibodies, and for the presence of HPV16 E6 ORF by in situ hybridization with HPV16 E6 DNA probe we have successfully labeled. The presence of HPV16 E6 gene was detected in 27 of 44 specimens (61.3%), including 8 of P53 protein positive (29.63%), 14 of RB protein positive (52.85%), and 20 of PCNA positive (74.07%). Of 17 HPV16 E6 negative cases, there were 7 of P53 protein positive (41.17%), 9 of RB protein positive (52.94%), 12 of PCNA positive (70.58%). There were no HPV16 E6 gene in control group. In positive cases PCNA only expressed in base cells. Our date indicated that HPV16 E6 ORF and PCNA had significantly related to cervical carcinoma. We could not find the relationship between HPV16 E6 ORF and P53, RB, PCNA in cervical carcinoma. There were some HPV16 E6-positive cases, obviously with strong P53, RB immunostaining in cytoplasm but not in nuclei, PCNA immunostaining was strong at the edge of the cervical carcinoma cells than in nuclear of them.

Carcinoma↗
PubMed1997

[Discovery of a novel reassortant H1N2 influenza virus].

Three strains of influenza A virus were isolated from patients suffering from influenza like disease in Railway Hygiene and Anti-epidemic Station of Taiyuan in January 1996. The identification results by serological method indicated that the isolates were different from H1N2 subtype of influenza A virus isolated from men in 1989 and 1992 and that their HA antigenicity was similar to that of A/RP/8/34 (H1N1) virus, but distinguishable from that of influenza A (H1N1) virus circulating in mans recently. The comparison of migration patterns of the RNA among the isolates, the A/PR//34 (H1N1) and the A/Wuhan/359/95 (H3N2) viruses revealed that the migration patterns of RNA 1-4 segments of the isolates were similar to those of A/PR/8/34 (H1N1) virus, but those of RNA 5-6 segments were indistinguishable from those of A/Wuhan/359/95 (H3N2) strain. However, the migration patterns of RNA 7-8 segments of the isolates were not only different from those of A/PR/8/34 (H1N1) virus, but also distingrasgable from those of A/Wuhan/359/95 (H3N2) strain. Therefore, it could be considered that the isolates were a novel reassortant H1N2 influenza A virus.

Adolescent↗
PubMed1997

[Detection of human papillomavirus DNA sequence in esophageal carcinoma using polymerase chain reaction].

Human Papillomavirus (HPV) DNA sequence in 68 paraffin-embedded specimens of esophageal carcinoma collected from high-risk Shantou City was detected and typed by polymerase chain reaction (PCR) technique. The results showed a 66.18% (45/68) positive rate of HPV DNA. Among these esophageal carcinoma specimens, 44 out of the 45 positive specimens were squamous cell carcinoma and one was adenosquamous carcinoma. The HPV DNA types detected were mostly HPV-6, -11, and -16. HPV-6 DNA was found in 19 (27.94%) of the 68 specimens, HPV-11 DNA in 25 (36.76%) and HPV-16 in 19 (27.94%) specimens. Among these three types, the difference gave no statistical significance (P > 0.05). But HPV-18 DNA was detected in only 6 (8.82%) specimens and the HPV in other 6 specimens was unidentified. It should be noted that as many as 24 (53.33%) of the 45 positive cases had multi-infection (coinfection of 2 or 3 types). Our results suggested that a higher detectable rate of HPV DNA was found in Shantou City as a high-risk region and that HPVs might be closely associated with the pathogenesis of the esophageal carcinoma.

Adult↗
PubMed1997

Establishment of doxorubicin-resistant human bladder cancer cell line (BUI-87/ADMR) and its mechanism of multidrug resistance.

OBJECTIVE: To establish a doxorubicin-resistant human bladder cancer cell line, BIU-87/ADMR, and to study its biological characteristics and mechanism of drug resistance. METHODS: A human bladder cancer cell line resistant to doxorubicin, BIU-87/ADMR, has been established in vitro by exposing BIU-87 parent cells to progressively increasing concentrations of the drug over a period of 8 months. The cell line has been characterized in terms of growth kinetics, morphology, cross-resistance to other anticancerous agents, pharmacokinetics of daunorubicin and expression of P-glycoprotein (P-gp) which is closely related to the MDR phenotype. RESULTS: The BIU-87/ADMR cell line was 6.3 times more resistant to doxorubicin than the parent BIU-87. It exhibited cross-resistance to doxorubicin derivatives (epirubicin, daunorubicin), vincristine and etoposide, but not to cisplatin and mitomycin C. Compared to the parent cells, the resistant cells have a slower growth rate and lower confluent density. Unlike the parent BIU-87, about 75% of the BIU-87/ADMR cells showed a positive reaction with monoclonal antibody against P-gp, JSB-1. Intracellular drug accumulation studies with fluorescence spectrometry indicated that the resistance exhibited by the BIU-87/ ADMR line was mainly caused by an increased active efflux. CONCLUSIONS: The results suggest that MDR is an important phenomenon in bladder cancer and that more than one pathway of MDR may be present in human bladder cancer cell lines. BIU-87/ADMR may be a useful model for the development of new chemotherapeutic strategies in overcoming drug-resistance in the treatment of bladder cancer.

ATP Binding Cassette Transporter, Subfamily B, Mem↗