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Biomedical subjects

Y Guo

Publications and source records attributed to Y Guo.

At least 595 records · Page 33Linked to original sources

[The influence of changing the Ca2+ concentration of the point quze (PC3) on the curative effect of puncturing neiguan (PC6) in experimental arrhythmic rabbits].

The experimental arrhythmic model was made with Aconitin in rabbits. The Neiguan (PC6) point was punctured to observe the influence on recovering time of arrhythmia. After the curative effect of puncturing Neiguan(P6) was confirmed, Ca2+ in the Quze (PC3) point of the Pericardium is chelated by EDTA solution to observe the influence on curative effect of arrhythmia by puncturing Neiguan. The result shows that the curative effect doesn't exist after the Ca2+ in Quze is chelated. It is probable that Ca2+ is one of the most important factors producing acupuncture effect. As a result, Ca2+ probably involves in the activities of channels and collaterals.

Aconitine↗

[Application of RFLP analysis to Duchenne and Becker muscular dystrophy in Shandong Province. I. Carrier detections in females at risk].

There were eight intragenic and two flanking bridge DNA polymorphic markers used in the RFLP analysis in 21 Duchenne and Becker muscular dystrophy selected from nine different districts in Shandong Province. A total number of 173 individuals of the families were accepted for gene tracking and carrier detection, as well as prenatal diagnosis. Based on the frequency of the probe polymorphism tested in our study of 53 unrelated individuals, one to three high polymorphic probes were sequentially used and all families presented the informativeness in RFLP analysis. Some more introgenio probes were supplied for assessment of mutated sites and carrier status with the help of gene phases, if recombinations were found. Our results presented a ratio of 85.45% of carrier detection at risk females with 95% or more reliability, including 17 carriers and 30 non-carriers. It was not able to ascertain the carrier status of 8 females because of DNA absence from key family members. Finally, we proposed a diagnostic procedure for the RFLP analysis to DMD/BMD families.

Female↗

Pharmacokinetics and relative bioavailability of tablet of micronized glibenclamide in 4 Chinese healthy men.

Pharmacokinetic characteristics and relative bioavailability of the regular preparation (RG) and micronized preparation (MG) of glibenclamide (Gli) were studied in 4 Chinese healthy men. Each volunteer entered 2 consecutive experiments at the same dose (10.5 mg) of RG and MG tablets given orally. Blood samples were drawn before and 0.5, 1, 2, 3, 4, 6, 8, 10, and 12 h after po. A selective HPLC method with a uv spectrophotometric detector (sensitivity: 16 ng.ml-1) was established for determining serum Gli concentration. Cmax for RG was 212 +/- 41 ng.ml-1, for MG 529 +/- 73 ng.ml-1. Tmax for RG and MG were 3.5 +/- 0.6 and 2.2 +/- 0.3 h, respectively. The relative oral bioavailability of MG was found to be 77%, increased approximately 1.7-fold that of RG. The other pharmacokinetic parameters (Vd, Cl, T1/2) were substantially the same after ingestion of GR and MG.

Adult↗

[The effect of high energy shock waves on growth and metastasis of implanted tumors of nude mice in vivo].

We observed the effect of high energy shock waves (HESW) on tumor growth, histological and ultrastructural variations, and metastasis to lymph nodes and viscera in nude mice with implanted tumors. HESW was cytotoxic to tumors in vivo, and acted on levels of cell membrane, cytoplasmic organelles, and nuclear chromatins. At definite working voltage, this effect was positively proportional to the impulse number. Histological examination showed no metastatic focci to lymph nodes and viscera of nude mice with implanted tumors. The possible mechanism of HESW in vivo may be direct mechanical damage and indirect inhibition of tumor growth due to damage to the blood supply. Other hypotheses were also discussed.

Animals↗

[Immunoglobulin deposition in skeletal muscle in polymyositis and dermatomyositis].

An immunohistochemical study was conducted using the biotin avidin technique in 22 muscle specimens from PM/DM patients and 19 control subjects. Deposition of IgG, IgM or C3 in the wall of capillaries and small vessels was demonstrated in 72.7% of PM/DM patients and in 31.6% of those with other neuromuscular disorders. This finding supports the contention that immunoglobulins and complement-mediated immunoreaction may play an important role in PM/DM pathogenesis.

Complement C3↗

Selection of COS cell mutants defective in the biosynthesis of heparan sulfate proteoglycan.

A simple procedure using human basic fibroblast growth factor (FGF) was utilized for the selection of COS cell mutants with defects in the biosynthesis or expression of heparan sulfate proteoglycan (HSPG). Our approach was based on the strong binding affinity exhibited by COS cells to human basic FGF that had been adsorbed to plastic dishes. Cell binding to basic FGF could be inhibited by heparin and heparan sulfate (HS), but not by chondroitin sulfate, dermatan sulfate, keratan sulfate, or hyaluronic acid, suggesting that the cell binding involved an interaction between basic FGF and cell surface heparin-like molecules. COS cells were treated with ethyl methanesulfonate and four stable mutants were subsequently isolated that did not bind strongly to basic FGF adsorbed to plastic. These mutants cell lines (CM-2, CM-8, CM-9, and CM-15) exhibited significantly reduced 35SO4 incorporation into HS (40-70% depending on the cellular pool analyzed). In one of these cell lines, CM-15, the incorporation of [6-3H]glucosamine into HS was unaltered, suggesting that the extent of oligosaccharide polymerization was equivalent to that observed for the wild-type cells. Structural analysis revealed that N-sulfated glucosamine residues were present much less frequently in HS derived from these cells as compared with that derived from wild-type cells. Furthermore, CM-15 was found to be three-fold deficient in HS N-sulfotransferase activity, but contained wild-type levels of HS O-sulfotransferase activities.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The neurotoxin 1-methyl-4-phenylpyridinium: a selective cytostatic agent in small-cell lung cancer cell lines with neuroendocrine properties.

BACKGROUND: Small-cell lung cancer (SCLC) is a common malignancy that is usually fatal, since it metastasizes and recurs even after aggressive chemotherapy. While the cellular origin of this cancer is not well established, the cells of certain tumors exhibit neuroendocrine markers, including L-dopa decarboxylase. PURPOSE: We designed in vitro and in vivo studies to investigate whether the neuroendocrine features in classic SCLC cell lines were sufficient to make them sensitive to 1-methyl-4-phenylpyridinium (MPP+), a known neurotoxin that destroys nigrostriatal dopaminergic neurons. METHODS: Both classic SCLC cell lines (NCI-H345, NCI-H510, NCI-H187, and NCI-H146) and variant SCLC cell lines (NCI-H417, NCI-H82, NCI-H446, and NCI-H524) were exposed to MPP+ (0-512 microM) for 3 days. Inhibition of DNA synthesis was determined by [3H]thymidine incorporation assays. In a related experiment, MPP+ was removed from the classic cell line culture, and the incorporation of [3H]thymidine was determined. In the in vivo study, male athymic nude mice received subcutaneous injections of 0.5 mL tumor cells with matrigel for 10 days to enhance tumor growth, followed by MPP+ at doses of 100-400 micrograms/d given intraperitoneally for 2 days. RESULTS: All four classic SCLC cell lines showed great sensitivity to MPP+, with detachment from laminin substrates and inhibition of DNA synthesis. MPP+ interfered with [3H]thymidine incorporation and, thus, with DNA synthesis in classic SCLC cell lines at low doses (median +/- SD, 12 +/- 4 microM), whereas much higher doses (median, > 512 microM) were required to inhibit [3H]thymidine incorporation in the variant lines. Treated cells excluded trypan blue dye, showing that inhibition of DNA synthesis was not due to cytotoxicity, and the cells incorporated [3H]thymidine when MPP+ was removed from the culture medium, demonstrating that the inhibition was reversible. MPP+ inhibited the growth of the classic NCI-H187 and variant NCI-H417 cell lines implanted in nude mice. CONCLUSIONS: These results suggest that MPP+ differentially interferes with DNA synthesis in SCLC cell lines in vitro; the selective inhibitory effect on classic cell lines suggests that the neuroendocrine properties expressed by classic SCLC cells may be responsible for the differential effect. IMPLICATIONS: MPP+ exerts a cytostatic effect on these cell lines, and the differential sensitivity observed in vitro is maintained in vivo, suggesting that MPP+ or other pyridinium compounds may be of therapeutic value in SCLC.

1-Methyl-4-phenylpyridinium↗

Structural analysis of periodate-oxidized heparin.

Treatment of heparin with HONO at pH 1.5 cleaves the polymer at N-sulfated, but not at N-acetylated GlcN residues, and yields di- and tetrasaccharides. The GlcNSO3 residues at the sites of cleavage are converted into anhydromannose (AMan) residues. Reduction of heparin cleavage products with NaB3H4 yields mixtures of di- and tetrasaccharides with reducing terminal [3H]anhydromannitol residues. The identification and quantification of these oligosaccharides by HPLC procedures have been described. These procedures have been used to determine the rates of periodate oxidation of the susceptible unsulfated GlcA and IdoA residues in heparin by measuring the disappearance of the di- and tetrasaccharides that contain GlcA and IdoA. Complete oxidation with IO4- results in the total loss of the unsulfated uronic acid-containing oligosaccharides, but kinetic studies reported here show that IdoA is oxidized much more rapidly than the major fraction of the GlcA under all reaction conditions. As the pH is lowered from 7 down to 3, the overall rate of the oxidation slows markedly, but the relative rates of GlcA and IdoA oxidation do not change. The slow rate of oxidation of GlcA residues at all pH's yields oxidation products early in the reaction progress in which all of the unsulfated IdoA residues are oxidized while 70-80% of the pH 1.5 nitrous acid-releasable GlcA----AMan(3,6-(SO4)2) are retained. The anticoagulant activity (APTT) of the partially oxidized product is reduced from 170 IU/mg to 38 IU/mg. Further studies show that the GlcA residue in the antithrombin III binding pentasaccharide is oxidized much more rapidly than the bulk of the GlcA residues in heparin. The results suggest that heparin contains GlcA----AMan(3,6-(SO4)2) sequences that lie outside of the antithrombin-binding pentasaccharide.

Antithrombin III↗

Medial edge epithelium fate traced by cell lineage analysis during epithelial-mesenchymal transformation in vivo.

Vital cell labeling techniques were used to trace the fate of the medial edge epithelial (MEE) cells during palatal fusion in vivo. Mouse palatal tissues were labeled in utero with DiI. The fetuses continued to develop in utero and tissues of the secondary palate were examined at several later stages of palatal ontogeny. The presence and distribution of DiI was correlated with the presence of cell phenotype-specific markers. During the initial stages of palatal fusion the DiI-labeled MEE were present in the midline position. These cells were attached to an intact laminin-containing basement membrane and contained keratin intermediate filaments. At later stages of palatogenesis the DiI-labeled MEE were not separated from the mesenchyme by an intact basement membrane and did not contain keratin. In late fetal development, DiI-labeled cells without an epithelial morphology were present in the mesenchyme. The transition of the DiI-labeled cells from an epithelial phenotype to a mesenchymal phenotype is consistent with a fate of epithelial-mesenchymal transformation rather than programmed cell death.

Animals↗

Characterization of a new avian-like influenza A virus from horses in China.

In March 1989 a severe outbreak of respiratory disease occurred in horses in the Jilin and Heilongjiang provinces of Northeast China that caused up to 20% mortality in some herds. An influenza virus of the H3N8 subtype was isolated from the infected animals and was antigenically and molecularly distinguishable from the equine 2 (H3N8) viruses currently circulating in the world. The reference strain A/Equine/Jilin/1/89 (H3N8) was most closely related to avian H3N8 influenza viruses. Sequence comparisons of the entire hemagglutinin (HA), nucleoprotein (NP), neuraminidase (NA), matrix (M), and NS genes along with partial sequences of the three polymerase (PB1, PB2, PA) genes suggest that six of the eight gene segments (PA, HA, NP, NA, M, NS) are closely related to avian influenza viruses. Since direct sequence analysis can only provide a crude measure of relationship, phylogenetic analysis was done on the sequence information. Phylogenetic analyses of the entire HA, NP, M, and NS genes and of partial sequences of PB1, PB2, and PA indicated that these genes are of recent avian origin. The NP gene segment is closely related to the gene segment found in the newly described H14 subtype isolated from ducks in the USSR. The A/Equine/Jilin/1/89 (H3N8) influenza virus failed to replicate in ducks, but did replicate and cause disease in mice on initial inoculation and on subsequent passaging caused 100% mortality. In ferrets, the virus caused severe influenza symptoms. A second outbreak of influenza in horses in Northeast China occurred in April 1990 in the Heilongjiang province with 48% morbidity and no mortality. The viruses isolated from this outbreak were antigenically indistinguishable from those in the 1989 outbreak and it is probable that the reduced mortality was due to the immune status of of the horses in the region. No influenza was detected in horses in Northern China in the spring, summer, or fall of 1991 and no influenza has been detected in horses in adjacent areas. Our analysis suggests that this new equine influenza virus in horses in Northeast China is the latest influenza virus in mammals to emerge from the avian gene pool in nature and that it may have spread to horses without reassortment. The appearance of this new equine virus in China emphasizes the potential for whole avian influenza viruses to successfully enter mammalian hosts and serves as a model and a warning for the appearance of new pandemic influenza viruses in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Specific chromosomal translocations and therapy-related leukemia induced by bimolane therapy for psoriasis.

This paper reports for the first time results of cytogenetic studies on 14 consecutive secondary acute non-lymphocytic leukemia (S-ANLL) induced by bimolane therapy. They included 10 males and 4 females with ages ranging from 17 to 54 years. They had all suffered from psoriasis and received bimolane treatment before the occurrence of their leukemia. The total dose of bimolane ranged from 40 to 400 g (mean dose 194 g). The interval between the initiation of bimolane therapy and the diagnosis of leukemia was 12-96 months (median 30 months). A preleukemic phase was only found in one case. No dysplastic features in the hemopoietic series were seen in any patient. Chromosome analysis of bone marrow cells using banding techniques revealed clonal karyotypic abnormalities in all cases: t(15;17) in 8 cases of M3, of which 75% had extra abnormalities, t(8;21) in 4 cases of M2, del(7q) only in one case of M4 and one case of M5. After antileukemic therapy, complete remission was obtained in 10 out of 12 cases with specific translocations and one out of 2 cases with 7q-anomaly, respectively. The former survived 4-58 months (median 12 months), while the latter 1 and 9 months, respectively. This study indicates that: (1) bimolane is a causative factor of leukemia in this series; (2) the leukemia in our series is therapy-related leukemia (TRL) rather than de novo ANLL; (3) there exists, in fact, a new subgroup of TRL characterized by specific rearrangements, whose clinical, hematological and prognostic features and pathogenetic mechanism may be different from classical TRL characterized by chromosome abnormalities involving absence or deletion of parts of chromosome 5 and/or 7.

Adolescent↗

Listeria monocytogenes activation of human peripheral blood lymphocytes: induction of non-major histocompatibility complex-restricted cytotoxic activity and cytokine production.

Gram-negative bacteria have been shown to activate human natural killer (NK) cells. In this report, we show that the gram-positive bacterium Listeria monocytogenes can also activate human NK cells with regard to non-major histocompatibility complex (MHC)-restricted killing and the production of cytokines. Overnight incubation of peripheral blood mononuclear (PBM) cells or enriched NK cell populations with live or Formalin-fixed L. monocytogenes resulted in high levels of non-MHC-restricted cytotoxic activity. Listeria-stimulated non-MHC-restricted cytotoxic activity could be achieved with pathogenic as well as nonpathogenic Listeria strains. PBM cells also produced tumor necrosis factor alpha and different interferons (IFNs) after incubation with Listeria strains. Optimal cytokine production appeared to be dependent on nylon wool- and plastic-adherent cells. Different IFNs were produced by Listeria-stimulated PBM cells obtained from different donors. IFN-gamma was always produced but was sometimes associated with IFN-alpha and/or IFN-beta. Interleukin-2 (IL-2) activity was never detected in culture supernatants obtained from Listeria-stimulated PBM cell cultures. However, IL-2 appeared to be produced by Listeria-stimulated PBM cells, since antibody to IL-2 inhibited Listeria-stimulated NK cell cytotoxic activity. Listeria activation of NK cell cytotoxic activity was also dependent on tumor necrosis factor alpha production. Antibody to IFN-gamma, IFN-beta, or IFN-alpha had no effect on Listeria-stimulated NK cell cytotoxic activity. These results demonstrate that NK cells can be activated by Listeria strains and add further evidence that NK cells may play an important role in host defense against bacterial infections.

Cytokines↗

Development and testing of a nonradioactive DNA oligonucleotide probe that is specific for Vibrio cholerae cholera toxin.

An alkaline phosphatase-labeled oligonucleotide DNA probe (CTAP) that was specific for the cholera toxin gene (ctxA) was identified. All cholera toxin-producing strains of Vibrio cholerae, regardless of serotype, hybridized with the CTAP probe, while nontoxigenic strains from either environmental sources or from deletion or substitution mutations did not hybridize. Unlike the whole-gene probes for either ctxA or for the heat-labile toxin or Escherichia coli (eltA), this 23-base sequence did not hybridize with E. coli or with vibrios other than V. cholerae that produce related toxins. By using CTAP to identify colonies grown on nonselective medium, V. cholerae was enumerated at concentrations of 10(3) to 10(7)/g from stool samples of volunteers who had ingested V. cholerae O1 strain 569B. CTAP provides a specific and sensitive tool for diagnosis and environmental monitoring of cholera toxin-producing V. cholerae.

Base Sequence↗

A simple, quantitative method for assessing angiogenesis and antiangiogenic agents using reconstituted basement membrane, heparin, and fibroblast growth factor.

BACKGROUND: Blood vessel growth is necessary for normal tissue homeostatis and contributes to solid tumor growth. Methods to quantitate neovascularization should be useful in testing biological factors and drugs that regulate angiogenesis or to induce a vascular supply to promote wound healing. EXPERIMENTAL DESIGN: An extract of basement membrane proteins (Matrigel) was found to reconstitute into a gel when injected subcutaneously into C57/BL mice and to support an intense vascular response when supplemented with angiogenic factors. RESULTS: New vessels and von Willebrand factor antigen staining were apparent in the gel 2-3 days after injection, reaching a maximum after 3-5 days. Hemoglobin content of the gels was found to parallel the increase in vessels in the gel allowing ready quantitation. Angiogenesis was obtained with both acidic and basic fibroblast growth factors and was enhanced by heparin. Several substances were tested for angiostatic activity in this assay by coinjection in Matrigel with fibroblast growth factor and heparin. Platelet-derived growth factor BB, interleukin 1-beta, interleukin-6, and transforming growth factor-beta were potent inhibitors of neovascularization induced by fibroblast growth factor. Tumor necrosis factor-alpha did not alter the response but was alone a potent inducer of neovascularization when coinjected with Matrigel and heparin. Consistent with the previously demonstrated importance of collagenase in mediating endothelial cell invasion, a tissue inhibitor of metalloproteinases that also inhibits collagenases was found to be a potent inhibitor of fibroblast growth factor-induced angiogenesis. CONCLUSIONS: Our assay allows the ready quantitative assessment of angiogenic and anti-angiogenic factors and should be useful in the isolation of endothelial cells from the capillaries that penetrate into the gel.

Angiogenesis Inducing Agents↗