Search PubMed⌕ Search

Biomedical subjects

S Xiong

Publications and source records attributed to S Xiong.

At least 73 records · Page 4Linked to original sources
PubMed1997

[Mutations and their significance in the corepromoter region of hepatitis B virus].

OBJECTIVE: To study the mutations in the core promoter (CP) region of hepatitis B virus (HBV) in Chinese viral hepatits B patients. METHODS: CP regions of 48 HBV strains were analysed by polymerase chain reaction (PCR) direct sequencing approach. RESULTS: 67% of the samples were detected to have point mutations in the CP region. The hot spots located in nt 1754-1766 and nt 1801-1811 while nucleotides in nt 1777-1800 and nt 1812-1836 were highly conserved. nt. 1764 mutation was present in HBeAg negative patients. There were 16 point mutations in region overlapping X gene, 9 of which lead to amino acid change. CONCLUSION: Though mutations in CP region of HBV appear frequently, the sequences associated with viral transcription are rarely changed. Point mutation at nt 1764 is related to HBeAg negative phenotype, but it is not the specific mutation of fulminant hepatitis. The importance of mutations in the X gene overlapping region needs to be further investigated.

Genetic Variation↗
PubMed1997

[Effect of Ganoderma japonicum (Fr.) Lloyd mixture on experimental thrombosis].

The therapeutic effect of Ganoderma japonicum(Fr.) Lloyd mixture on thrombosis and its mechanism were studied. The results showed that Ganoderma japonicum(Fr.) Lloyd mixture inhibited thrombus formation in vitro and in vivo, the thrombus weight and length formed in the rabbit common carotid artery and external jugular vein were significantly decreased in the experimental group compared with the control (P < 0.01). The results suggest that Ganoderma japonicum(Fr.) Lloyed mixture has anti-thrombotic effect, blood coagulation and platelet activation were inhibited, and the ability of vascular endothelial cells against the process of thrombosis was enhanced.

Animals↗
PubMed1997

[Pre- and post-operative changes in serum levels of glycocholic acid and 3,5,3'-triiodothyronine and their clinical significance in patients with cholelithiasis].

Pre- and post-operative changes of serum glycine-conjugated cholic acid (CG) and 3,5,3'-triiodothyronine (T3) levels were observed in twenty-two patients with cholelithiasis. The increase of the levels of serum CG varied with the patients; the highest levels were seen in patients with cirrhosis. After operation, the levels of serum CG and T3 were decreased significantly in patients without cirrhosis. There was positive correlation between serum CG and T3 (r = 0.4667, P < 0.01). It is indicated that the lowering of serum CG after operation may be related to the lowering of serum T3; the significant increase of serum CG level is useful to the diagnosis of liver cirrhosis, which is more sensitive than Type B ultrasonography or routine examination of liver function.

Adult↗
PubMed1997

[Effects of aprotinin on heparinized whole blood activated clotting time and whole blood prothrombin time].

When aprotinin is used during cardiopulmonary bypass, there is a prolongation of the activated clotting time (ACT), which is used to monitor heparinization. The aim of this study was to observe the effects of aprotinin and heparin on whole blood ACT and whole blood prothrombin time (BPT). The results showed that when kaolin was used as the contact activator, the intrinsic clotting system was also inhibited by aprotinin, the observed ACTs with various dose aprotinin and concomitant heparin were significantly prolonged (Q = 0.757, P < 0.01). There was a dose-dependent prolongation of BPT by heparin (r = 0.985, P < 0.01). However, the heparin-mediated prolongation of BPT was not enhanced by aprotinin. The authors conclude that aprotinin prolongs heparinized whole blood activated clotting time but was not whole blood prothrombin time.

Adult↗
PubMed1996

Analysis of hepatitis B virus genotypes and pre-core region variability during interferon treatment of HBe antigen negative chronic hepatitis B.

The clinical importance of hepatitis B virus (HBV) genome variability has been reported recently. One example is the occurrence of hepatitis B virus pre-core mutants, which arise during spontaneous or interferon-induced seroconversion from HBeAg to anti-HBe and are thought to be selected by immune pressure. A survey of HBV pre-core mutants and viral genotypes in 35 HBeAg negative patients during interferon therapy was carried out to understand viral pathogenesis in this form of chronic hepatitis B. Seventeen patients responded to interferon therapy as assessed by the sustained normalization of serum ALT levels and the significant decrease of viremia levels. The response rate to interferon was independent of both initial serum viral DNA level and interferon doses. During interferon therapy, a significant decrease of M0 (wild-type pre-core sequence at pos. 1887-1908), M1 (TGG to TAG at pos. 1896) or M2 (TGG to TAG at pos. 1896, and GGC to GAC at pos. 1899) positive viral genomes was found in 48%, 42%, and 33% of patients, respectively. A higher response rate to interferon therapy was observed in patients infected with HBV genotype A (70%) or M0 positive strains (75%) as compared to patients infected with genotype D/E (40%) or M1/M2 positive strains (44%). The data support the hypothesis that pre-core defective HBV represent viral mutants with an increased capacity to resist exogenous alpha interferon. These findings emphasize that characterization of HBV genome variability prior to interferon therapy may help to predict antiviral response in HBeAg negative patients.

Adult↗
PubMed1996

Effects of malathion on humoral immunity and macrophage function in mast cell-deficient mice.

Malathion, when administered at noncholinergic doses, was previously shown to enhance the humoral immune response to a T-dependent antigen, sheep red blood cells (SRBC), and macrophage function. In addition, malathion was shown to cause mast cell degranulation. The hypothesis that mast cells contribute to the observed alterations in humoral immunity and macrophage function was determined by examination of the effects of acute administration of malathion to mast cell-deficient mice on macrophage function and the generation of a humoral immune response to SRBC. Initial studies in two strains of mast cell-deficient mice (6-7 weeks old) indicated that oral administration of malathion reduced macrophage function in these mice, but enhanced macrophage function in the wild-type strain. Because both strains reacted in a similar fashion and the defect in the WBB6F1-W/WV strain allowed reconstitution, further studies were conducted with this strain. Exposure of either wild-type mice or mast cell-deficient mice with reconstituted with bone marrow-derived mast cells (BMMC) from the wild-type mice to malathion enhanced macrophage function and the production of circulating IgM, but not IgG, antibodies to SRBC on Days 3 and 5 after immunization. In contrast, administration of malathion to older mast cell-deficient mice suppressed the generation of IgM and IgG antibodies to SRBC on Days 3 and 5 after immunization, but did not affect macrophage function. In summary, the results presented indicate that the presence of mast cells was necessary for the increases in macrophage function and humoral immunity observed after acute oral administration of malathion to mice.

Animals↗
PubMed1996

Contribution of mast cell mediators to alterations in macrophage function after malathion administration.

Previous studies showed that acute administration of noncholinergic doses of malathion increased macrophage function and the generation of a primary humoral immune response to a T-dependent antigen and caused mast cell degranulation. Recent studies using mast cell-deficient mice showed that the presence of mast cells was necessary for the increase in macrophage function observed after oral administration of malathion, and reconstitution with bone marrow-derived mast cells restored the ability of malathion to increase macrophage function. In the present study, the contribution of mast cell mediators to alterations in macrophage function after oral administration of malathion was examined. Controls in this study included the effect of the agent to be examined on resident peritoneal macrophages and macrophages elicited with pristane, an agent that can stimulate macrophages in the absence of mast cells. Coadministration of intraperitoneal cromolyn, a stabilizer of mast cell membranes, with oral malathion blocked the ability of malathion to increase macrophage function as measured by the generation of respiratory burst activity, the phagocytosis of opsonized yeast, and the production of cathepsin D. On the other hand, administration of cromolyn to mice whose macrophage function was stimulated with pristane did not affect the observed increases in macrophage function. As oral administration of malathion caused histamine release, the ability of a histamine receptor antagonist, pyrilamine, to alter the response of peritoneal macrophages to oral administration of malathion was also examined. Intraperitoneal administration of pyrilamine partially blocked the effects of oral administration of malathion on peritoneal macrophage function, but did not affect the function of resident or pristane-elicited peritoneal macrophages. These data suggest that mediators from mast cells contribute to the elevation in macrophage function observed after oral malathion administration.

Administration, Oral↗
PubMed1996

[Autocrine transforming growth factor-beta stimulates human ovarian cancer cell growth in vitro and in vivo].

OBJECTIVES: Our previous studies have shown that human ovarian cancer cell lines COC1 and COC2 secrete transforming growth factor-beta (TGF-beta) like substance in serum-free culture. In this study the effect of COC1 and COC2-produced TGF-beta like substance on COC1 and COC2 cell growth was investigated. METHODS: The COC1 and COC2 RPMI 1640 serum-free conditioned media SFCM (SFCM1 from COC1, SFCM2 from COC2) were prepared, and their activities were investigated on COC1 and COC2 cell growth (SFCM1 on COC1, SFCM2 on COC2) in vitro and in vivo, and compared with that of TGF-beta. RESULTS: SFCM1 and SFCM2 could separately promote COC1 and COC2 cell proliferation in culture with dose-dependent response, SFCM2 significantly promoted COC2 cell growth in BABL/C nude mice. Radioreceptor assay showed that both COC1 and COC2 expressed TGF-beta receptor (or binding site). The above mentioned SFCM growth-stimulating effects can be partially blocked by anti-TGF-beta antibody. CONCLUSION: The results suggest that there may be TGF-beta autocrine loop in the two ovarian cancer cell lines, which is associated with autonomous proliferation of COC1 and COC2 cells.

Adenocarcinoma↗
PubMed1996

[Simultaneous rhinoplasty and blepharoplasty].

Simultaneous rhinoplasty and blepharoplasty are the commonest facial cosmetic operation. The paper presents 73 cases who underwent this procedure with satisfactory results from Jan. 1989 to Nov. 1993. The authors described operation steps, e.g., making lacuna in the dorsum, lengthening nasal columella, nasal tip plasty. It was emphasized that the pretarsal flap should contain complete network of the superficial fascia, and the soft tissue underneath be trimmed. All the dissection should be kept in the same cleavage, which would reduce intraoperative bleeding and postoperative edema.

Adolescent↗
PubMed1995

ATP-sensitive binding of a 70-kDa cytosolic protein to the glucose transporter in rat adipocytes.

We have identified a 70-kDa cytosolic protein (GTBP70) in rat adipocytes that binds to glutathione S-transferase fusion proteins corresponding to the cytoplasmic domains of the facilitative glucose transporter isoforms Glut1, Glut2, and Glut4. GTBP70 did not bind to irrelevant fusion proteins, indicating that the binding is specific to the glucose transporter. GTBP70 binding to the glucose transporter showed little isoform specificity but was significantly subdomain-specific; it bound to the C-terminal domain and the central loop, but not to the N-terminal domain of Glut4. The GTBP70 binding to Glut4 was not affected by the presence of 2 mM EDTA, 2.4 mM Ca2+, or 150 mM K+. The binding was inhibited by ATP in a dose-dependent manner, with 50% inhibition at 10 mM ATP. This inhibition was specific to ATP, as ADP and AMP-PCP (adenosine 5'-(beta, gamma-methylenetriphosphate)) were without effect. GTBP70 did not react with antibodies against phosphotyrosine, phosphothreonine, or phosphoserine, suggesting that it is not a phosphoprotein. The binding of GTBP70 to Glut4 was not affected by the pretreatment of adipocytes with insulin. When these experiments were repeated using rat hepatocyte cytosols, no ATP-sensitive 70-kDa protein binding to the glucose transporter fusion proteins was evident, suggesting that either GTBP70 expression or its function is cell-specific. These findings strongly suggest the possibility that GTBP70 may play a key role in glucose transporter regulation in insulin target cells such as adipocytes.

Adenosine Triphosphate↗
PubMed1995

[Effects of interferon treatment on mutation of hepatitis B virus precore genome].

Effects of interferon (IFN) treatment on mutation of hepatitis B virus (HBV) precore were studied with a rapid polymerase chain reaction method to investigate the stop codon in the distal precore region during HBV precore mutation. 6 cases of chronic hepatitis B were treated with recombinant IFN alpha 1 3 x 10(6) U/day for 14 weeks. In 4 of them HBV DNA was undetectable after treatment. Precore mutant was detected in the remaining 2 cases whose HBV DNA was still positive. In a group of 11 cases not treated with IFN, mutants were detected in 3. HBV e antigen (HBeAg) became negative after IFN treatment in one case, the original wild strain was replaced by a status of co-existence of mutant and wild strain. These results suggest that HBeAg negative seroconversion after IFN treatment does not necessarily implicate a complete clearance of HBV and the possibility of mutation of precore still exists.

Adult↗
PubMed1995

[A study on the relationship between morphology and gene heterogeneity in acute promyelocytic leukemia].

Aucte promyelocytic leukemia (APL) can be treated by all-trans retinoic acid (ATRA) with high complete remission rate. 50 cases of APL diagnosed morphologically were studied on their cytogenetics, molecular biology and response to treatment with ATRA. Forty-five cases showed chromosomal translocation t(15; 17) and PML/RAR alpha fusion gene (PML + RAR alpha + APL). They had typical morphologic change, in which hypergranular cells appeared more frequently in L type of PML/RAR alpha and microgranular cells in S type of PML/RAR alpha. Among the 45 PML + RAR alpha + APL patients 8 died early and 37 had complete remission with ATRA. In the remainging 5 patients, three had typical APL morphologic features in cytology, but one of them displayed t (11; 17) with PLZF+RARA alpha +, the second showed RAR alpha + PML - (PML - RAR alpha + APL) and the third PML - RAR alpha -(PML - RAR alpha - APL). They did not respond to ATRA treatment. These data indicate that APL is not a homogeneous disease. The other a patients had neither chromosomal translocation nor rearrangements of the two genes. On careful morphological reexamination, these two cases were not APL, but one of them responded well to ATRA. It is shown that morphology is the important diagnostic basis of APL, but in a few APL cases diagnosis should be made with the help of cytogenetics and molecular biology. Response of ATRA treatment may be of diagnostic value of APL, but is not a specific criterion.

Adolescent↗
PubMed1995

[Effect of ovarian cancer produced-transforming growth factor-beta on phytohemagglutinin and interleukin-2-inducing proliferation of peripheral blood mononuclear cells].

OBJECTIVES: Our previous observation has demonstrated that human ovarian cell lines COC1 and COC2 are able to secrete transforming growth factor-beta (TGF-beta) in serum-free culture. The effect of ovarian cancer produced-TGF-beta was observed on phytohemagglutinin and interleukin-2-inducing proliferation of peripheral blood mononuclear cells. METHODS: The effects of COC1 and COC2 from patients' ascitic fluid (AS1, AS2), the serum-free conditioned medium (SFCM1, SFCM2), and COC1- and COC2- bearing nude mice sera (NS1, NS2) on phytohemagglutinin (PHA) and interleukin-2 (IL-2)-inducing peripheral blood mononuclear cell (PBMC) proliferation and their correlation with TGF-beta were observed and compared. RESULTS: It was shown that AS, SFCM and NS possessed inhibitory effects on PBMC proliferation. But in very low concentrations, PHA-induced by SFCM2 and IL-2-induced by SFCM1 as well as by NS1 and NS2 exerted promotive effects on PBMC proliferation. The above-mentioned SFCM effects similar to that of TGF-beta, might be partially blocked by anti-TGF-beta antibody. CONCLUSIONS: The present results suggest that ovarian cancer cells may inhibit the host anti-tumor immunity through secreting TGF-beta, which may be associated with the highly malignant biological behavior of ovarian cancer and the threatening progressiveness of its clinical course.

Animals↗