Biomedical subjects

Y Peng

Publications and source records attributed to Y Peng.

At least 91 records · Page 5Linked to original sources

PubMed2000

[Pharyngeal plexus neurectomy for voice restoration of alaryngeal].

OBJECTIVE: To release the spasm of pharyngeal constrictor and raise the successful rate of voice rehabilitation in total laryngectomized patients wearing Blom-Singer prosthesis. METHODS: The main branch of the pharyngeal plexus nerves within the inferior contractor can be found at the posterior side of hyoid greater cornu, which is about 6.5 mm from the back of constrictor. The spasm of the inferior constrictor can be resolved by cut off the nerve. RESULTS: Voice restoration was achieved in 15 cases after pharyngeal plexus neurectomy, the successful rate was 93.75%. CONCLUSION: It is feasible to replace pharyngeal myotomy by nerve plexus neurectomy and raise the voice rehabilitation rate.

Aged↗

PubMed2000

[Vibrational spectroscopic investigation of a series of heterometallic cubane-like M'-Mo (W) cluster compounds].

By combining the results of IR spectroscopic experiments with the molecular structures, the main stretching vibrations of a series of the heterometallic tetranuclear cluster compounds with [M3YS3M'] cluster core (M = Mo, W; Y = O, S; M' = Cu, Sn, Pb, Sb, Bi) have been assigned. The characteristic features and the bonding situations of the five configuration types are discussed. It is shown from the IR and Raman spectra that when M' is a transition metal such as Cu, the nu M's frequency of the [M3YS3M'] core has a value comparable to that of corresponding M'-S covalent bond thus indicating a close combination of M' with [M3YS3]. Whereas when M' is a main group metal, the nu M'-s vibration is always observed in a lower region than of the M'-S covalent bond because of a loose combination of M' with[M3YS3]. However, remarkable enhancement of M-M band strength due to the addition of M' is demonstrated by Raman spectra. Some comments for the M-M vibration of various structures of these compounds are also described.

English Abstract↗

PubMed2000

[Study on the aggregation state of sulfonated phthalimidomethyl zinc phthalocyanine in CEL solution].

Sulfonated Phthalimidomethyl Zinc Phthalocyanine is a new photodynamic therapy reagent, it can be selectively attacked to cell, but how it attacks the target cell is still unknowable. The aggregation state of photosensitizer is significant to its mechanism proved in CEL solution. The aggregation of ZnPcS2P2 in CEL has been studied with absorption spectroscopy and fluorescence spectroscopy. The aggregation state is dimer through theory analysis, monomer molar absorption coefficient as well as equilibrium constant were estimated.

Antineoplastic Agents↗

PubMed1999

Opposite effects of FGF and BMP-4 on embryonic blood formation: roles of PV.1 and GATA-2.

In adult vertebrates, fibroblast growth factor (FGF) synergizes with many hematopoietic cytokines to stimulate the proliferation of hematopoietic progenitors. In vertebrate development, the FGF signaling pathway is important in the formation of some derivatives of ventroposterior mesoderm. However, the function of FGF in the specification of the embryonic erythropoietic lineage has remained unclear. Here we address the role of FGF in the specification of the erythropoietic lineage in the Xenopus embryo. We report that ventral injection of embryonic FGF (eFGF) mRNA at as little as 10 pg at the four-cell stage suppresses ventral blood island (VBI) formation, whereas expression of the dominant negative form of the FGF receptor in the lateral mesoderm, where physiologically no blood tissue is formed, results in a dramatic expansion of the VBI. Similar results were observed in isolated ventral marginal zones and animal caps. Bone morphogenetic protein-4 (BMP-4) is known to induce erythropoiesis in the Xenopus embryo. Therefore, we examined how the BMP-4 and FGF signaling pathways might interact in the decision of ventral mesoderm to form blood. We observed that eFGF inhibits BMP-4-induced erythropoiesis by differentially regulating expression of the BMP-4 downstream effectors GATA-2 and PV.1. GATA-2, which stimulates erythropoiesis, is suppressed by FGF. PV.1, which we demonstrate to inhibit blood development, is enhanced by FGF. Additionally, PV.1 and GATA-2 negatively regulate transcription of each other. Thus, BMP-4 induces two transcription factors which have opposing effects on blood development. The FGF and BMP-4 signaling pathways interact to regulate the specification of the erythropoietic lineage.

Animals↗

PubMed1999

Mitogenic up-regulation of the PRL-1 protein-tyrosine phosphatase gene by Egr-1. Egr-1 activation is an early event in liver regeneration.

The cellular signals that initiate cell growth are incompletely understood. Insight could be provided by understanding the signals regulating the transcriptional induction of immediate-early genes which occurs within minutes of the growth stimulus. The expression of the PRL-1 gene, which encodes a unique nuclear protein-tyrosine phosphatase, is rapidly induced in regenerating liver and mitogen-treated cells. Transcription of the PRL-1 gene increased in the rat liver remnant within a few minutes after partial hepatectomy and largely explained the increase in steady-state PRL-1 mRNA in the first few hours posthepatectomy. Egr-1 (early growth response factor) specifically bound a region of the proximal PRL-1 promoter P1 (-99). Egr-1 binding activity was more rapidly induced in regenerating liver than mitogen-treated H35 and NIH 3T3 cells, remained elevated through 4 h posthepatectomy, and appeared to be dependent not only on new Egr-1 protein synthesis but on post-translational regulation of Egr-1. Egr-1 efficiently transactivated a PRL-1 promoter reporter construct containing an intact not mutant Egr-1 site, and the Egr-1 site largely accounted for PRL-1 gene up-regulation in response to mitogen stimulation. These data predict that Egr-1 activation is an early event in liver regeneration and mitogen-activated cells that provides a regulatory stimulus for a subset of immediate-early genes.

3T3 Cells↗

PubMed1999

Beta-carotene produces sustained remissions in patients with oral leukoplakia: results of a multicenter prospective trial.

BACKGROUND: Beta-Carotene has been reported to produce regressions in patients with oral leukoplakia, a premalignant lesion. However, previous studies have all been of short duration, with clinical response as the end point. OBJECTIVE: To evaluate the duration of response and the need for maintenance therapy in subjects who respond to beta-carotene. METHODS: In this multicenter, double-blind, placebo-controlled trial, subjects were given beta-carotene, 60 mg/d, for 6 months. At 6 months, responders were randomized to continue beta-carotene or placebo therapy for 12 additional months. RESULTS: Fifty-four subjects were enrolled in the trial, with 50 being evaluable. At 6 months, 26 subjects (52%) had a clinical response. Twenty-three of the 26 responders completed the second, randomized phase. Only 2 (18%) of 11 in the beta-carotene arm and 2 (17%) of 12 in the placebo arm relapsed. Baseline biopsies were performed in all patients, with dysplasia being present in 19 (38%) of the 50 evaluable patients. A second biopsy was obtained at 6 months in 23 subjects who consented to this procedure. There was improvement of at least 1 grade of dysplasia in 9 (39%), with no change in 14 (61%). Nutritional intake was assessed using food frequency questionnaires. There was no change in carotenoid intake during the trial. Responders had a lower intake of dietary fiber, fruits, folate, and vitamin E supplements than did nonresponders. Beta-carotene levels were measured in plasma and oral cavity cells. Marked increases occurred during the 6-month induction. However, baseline levels were not restored in subjects taking placebo for 6 to 9 months after discontinuation of beta-carotene therapy. CONCLUSIONS: The activity of beta-carotene in patients with oral leukoplakia was confirmed. The responses produced were durable for 1 year.

Aged↗

PubMed1999

Dissociation of PTPase levels from their modulation of insulin receptor signal transduction.

Protein tyrosine phosphatases have been implicated in the regulation of receptor tyrosine kinase signalling pathways, including that of the insulin receptor. Here, cell density-dependent changes in PTPase expression have been exploited to investigate the relationship between cellular PTPase levels and the insulin receptor signal transduction pathway. Increasing cell density (20%, 50%, and >90%) in the rat McA-RH7777 hepatoma cell line resulted in increased protein expression of the receptor-like PTPase LAR (14-fold), and the nonreceptor PTPases PTP1B (11-fold) and SHP2 (10-fold). Each of these PTPases has previously been implicated in regulating insulin receptor signal transduction. Despite these marked increases, maximum insulin receptor autophosphorylation as well as receptor expression actually increased 2-fold. MAP kinase also increased approximately 2-fold as a function of cell density and paralleled increases in expression levels. Neither sensitivity nor maximum responsiveness to insulin were decreased at increasing cell densities as assessed by activation of PI 3-kinase. Duration of response was also unimpaired. These results suggest that expression levels of relevant PTPases are not the primary determinant in their modulation of insulin receptor kinase activity. Restricted accessibility at the molecular level or involvement of accessory proteins may be more critical parameters.

Animals↗

PubMed1999

Transcriptional regulatory signals define cytokine-dependent and -independent pathways in liver regeneration.

Partial hepatectomy and toxic liver damage induce signals in the liver that result in rapid changes in the transcriptional milieu, including activation of latent transcription factors NF-kappa B and STAT3, and induction of expression of early growth response genes. Several of these changes within hepatocytes, including STAT3 and NF-kappa B induction are dependent on the cytokines, TNF alpha and interleukin-6 (IL-6), that are presumably released from non-parenchymal liver cells within minutes of the hepatectomy. IL-6 is a critical factor in the mitogenic response during liver regeneration and is important for both cell cycle progression and protection from liver injury. However, it is not a complete factor in that it is responsible for only a subset of the gene expression changes that occur after hepatectomy and is insufficient alone to cause hepatic DNA synthesis. C/EBP beta, a leucine zipper transcription factor, acts in an IL-6 independent fashion to induce a separate set of genes and proteins and is also required for normal liver regeneration. Moreover, some early growth response genes such as PRL-1, which encodes a nuclear protein tyrosine phosphatase, are induced normally in the absence of C/EBP beta and IL-6 and highlight the role of other transcriptional complexes such as Egr-1 in the early phases of liver regeneration. Thus, cytokine-dependent and -independent pathways act cooperatively to control the complex series of events that result in liver regeneration. The requirement for multiple signals also protects the liver from undergoing hyperplasia in the absence of a compensatory need.

Animals↗

PubMed1999

An NMR study of the structural basis of the wide range of pharmacological functions of acetylsalicylic acid.

The interaction between acetylsalicylic acid (aspirin) and membrane was studied by NMR spectra. (1) NMR spectra showed acetylsalicylic acid did not insert into membrane; (2) 1H NMR spectrum recorded by spin-echo pulse sequence showed protons of the aromatic ring interacted with membrane; (3) the change of spin-lattice relaxation (T1) of 31P was ascribed to the association of acetylsalicylic acid to the polar head of lecithin; (4) the self-diffusion coefficient measured by pulsed field gradients NMR showed the mobility of acetylsalicylic acid was restricted by membrane and that acetylsalicylic acid changed membrane viscosity. Based on the results, the relationship between the interaction and the mechanism of the wide pharmacological functions of acetylsalicylic acid is discussed.

Aspirin↗

PubMed1999

Differential expressions of glycine transporter 1 and three glutamate transporter mRNA in the hippocampus of gerbils with transient forebrain ischemia.

The extracellular concentrations of glutamate and its co-agonist for the N-methyl-d-aspartate (NMDA) receptor, glycine, may be under the control of amino acid transporters in the ischemic brain. However, there is little information on changes in glycine and glutamate transporters in the hippocampal CA1 field of gerbils with transient forebrain ischemia. This study investigated the spatial and temporal expressions of glycine transporter 1 (GLYT1) and three glutamate transporter (excitatory amino acid carrier 1, EAAC1; glutamate/aspartate transporter, GLAST; glutamate transporter 1, GLT1) mRNA in the gerbil hippocampus after 3 minutes of ischemia. The GLYT1 mRNA was transiently upregulated by the second day after ischemia in astrocytelike cells in close vicinity to hippocampal CA1 pyramidal neurons, possibly to reduce glycine concentration in the local extracellular spaces. The EAAC1 mRNA was abundantly expressed in almost all pyramidal neurons and dentate granule cells in the control gerbil hippocampus, whereas the expression level in CA1 pyramidal neurons started to decrease by the fourth day after ischemia in synchrony with degeneration of the CA1 neurons. The GLAST and GLT1 mRNA were rather intensely expressed in the dentate gyrus and CA3 field of the control hippocampus, respectively, but they were weakly expressed in the CA1 field before and after ischemia. As GLAST and GLT1 play a major role in the control of extracellular glutamate concentration, the paucity of these transporters in the CA1 field may account for the vulnerability of CA1 neurons to ischemia, provided that the functional GLAST and GLT1 proteins are also less in the CA1 field than in the CA3 field. This study suggests that the amino acid transporters play pivotal roles in the process of delayed neuronal death in the hippocampal CA1 field.

ATP-Binding Cassette Transporters↗

PubMed1999

Inhibition of tumor necrosis factor alpha by an adenovirus-encoded soluble fusion protein extends transgene expression in the liver and lung.

The cellular and humoral immune responses to adenovirus (Ad) remain a major barrier to Ad-mediated gene therapy. We recently reported that mice deficient in tumor necrosis factor alpha (TNF-alpha) or Fas (APO-1, CD95) have prolonged expression of an Ad transgene expressing a foreign protein in the liver. To determine whether blockade of TNF-alpha or Fas would have the same effect in normal mice, we created transgenes that expressed soluble murine CD8 or CD8 fused to the extracellular regions of TNF receptor 1 (TNFR) or Fas and inserted into the left-end region of first-generation (E1/E3-) Ad vectors. Consistent with the results observed in TNF-deficient mice, expression of the TNFR-CD8 fusion protein was prolonged in vivo compared to that of control proteins. Not only did expression of TNFR-CD8 persist in the liver and the lung, but when coadministered with another first-generation vector, the protein provided "transprotection" for the companion vector and transgene. In addition, TNFR-CD8 attenuated the humoral immune response to the Ad. Together, these findings demonstrate that blockade of TNF-alpha is likely to be useful in extending the expression of an Ad-encoded transgene in a gene therapy application.

Adenoviridae↗

PubMed1999

ETB receptor activation leads to activation and phosphorylation of NHE3.

In OKP cells expressing ETB endothelin receptors, activation of Na+/H+ antiporter activity by endothelin-1 (ET-1) was resistant to low concentrations of ethylisopropyl amiloride, indicating regulation of Na+/H+ exchanger isoform 3 (NHE3). ET-1 increased NHE3 phosphorylation in cells expressing ETB receptors but not in cells expressing ETA receptors. Receptor specificity was not due to demonstrable differences in receptor-specific activation of tyrosine phosphorylation pathways or inhibition of adenylyl cyclase. Phosphorylation was associated with a decrease in mobility on SDS-PAGE, which was reversed by treating immunoprecipitated NHE3 with alkaline phosphatase. Phosphorylation was first seen at 5 min and was maximal at 15-30 min. Phosphorylation was maximal with 10(-9) M ET-1. Phosphorylation occurred on threonine and serine residues at multiple sites. In summary, ET-1 induces NHE3 phosphorylation in OKP cells on multiple threonine and serine residues. ETB receptor specificity, time course, and concentration dependence are all similar between ET-1-induced increases in NHE3 activity and phosphorylation, suggesting that phosphorylation plays a key role in activation.

Animals↗

PubMed1999

Glucocorticoids enhance acid activation of the Na+/H+ exchanger 3 (NHE3).

In the absence of exogenous glucocorticoids, decreasing media pH (from 7.4 to 6.8) for 24 hours increased the Na+/H+ exchanger 3 (NHE3) activity in opossum kidney (OKP) cells. 10(-7) M and 10(-8) M hydrocortisone increased NHE3 activity, and in their presence, acid incubation further increased NHE3 activity. Hydrocortisone (10(-9) M) had no effect on NHE3 activity, but in its presence, the effect of acid incubation on NHE3 activity increased twofold. Aldosterone (10(-8) M) had no effect. In the absence of hydrocortisone, acid incubation increased NHE3 protein abundance by 47%; in the presence of 10(-9) M hydrocortisone, acid incubation increased NHE3 protein abundance by 132%. The increase in NHE3 protein abundance was dependent on protein synthesis. However, 10(-9) M hydrocortisone did not modify the effect of acid incubation to cause a twofold increase in NHE3 mRNA abundance. In the absence of protein synthesis, 10(-9) M hydrocortisone did potentiate an effect of acid on NHE3 activity, which was due to trafficking of NHE3 to the apical membrane. These results suggest that glucocorticoids and acid interact synergistically at the level of NHE3 translation and trafficking.

Animals↗

PubMed1999

Proteasome inhibition leads to significant reduction of Bcr-Abl expression and subsequent induction of apoptosis in K562 human chronic myelogenous leukemia cells.

The chimeric oncogene bcr-abl is detected in virtually every case of chronic myelogenous leukemia. It has been shown that cells (such as K562) expressing Bcr-Abl/p210, a protein tyrosine kinase, not only undergo cellular transformation but also demonstrate multiple drug resistance. Recent studies also demonstrate that the proteasome is involved in the survival signaling pathway(s). In the current study, we tested the hypothesis that the proteasome might play a role in regulating Bcr-Abl function. We have demonstrated by using a variety of inhibitors that inhibition of the proteasome, but not of the cysteine protease, activity is able to activate the apoptotic cell death program in K562 cells. Proteasome inhibition-induced apoptosis is demonstrated by condensation and fragmentation of nuclei, appearance of an apoptotic population with sub-G1 DNA content, the internucleosomal fragmentation of DNA, and cleavage of poly(ADP-ribose) polymerase, and can be blocked by a specific caspase-3-like tetrapeptide inhibitor. Western blot analysis with specific antibodies to c-Abl and Bcr proteins show that treatment of K562 cells with a proteasome inhibitor results in significant reduction of Bcr-Abl protein expression, which occurs several hours before the onset of apoptotic execution. Levels of c-Abl/p145 and Bcr/p160 proteins, however, remain essentially unaltered at that time. Furthermore, reduced Bcr-Abl expression is reflected in significantly attenuated Bcr-Abl-mediated protein tyrosine phosphorylation. Taken together, these results indicate that proteasome inhibition is sufficient to inactivate Bcr-Abl function and subsequently activate the apoptotic death program in cells that are resistant to apoptosis induced by chemotherapy.

Apoptosis↗

PubMed1999

[Linkage analysis of chromosome 5 and asthma in a Chinese population].

OBJECTIVE: To investigate the linkage between asthma and 5q31-33 in a Chinese population. METHODS: The linkage between microsatellite markers in 5q and asthma and allergy was tested by lod score analysis. RESULTS: The linkage between asthma and 5q31-33 was not confirmed. CONCLUSION: The genes at 5q31-33 are not likely to contribute to inheritance of asthma in this Chinese population.

Asthma↗

PubMed1999

[Expression and its clinical significance of tissue factor pathway inhibitor and antithrombin-III in patients with hepatic inflammatory diseases].

OBJECTIVE: To investigate the change and clinical significance of tissue factor pathway inhibitor (TFPI) and antithrombin-III (AT-III) in the plasma of patients with hepatic inflammatory disease (HID). METHODS: The plasma levels and activation of TFPI and AT-III in patients with HID (Group I, n = 82) were compared to that in healthy people (Group II as control, n = 30). RESULTS: The plasma level of TFPI:Ag in Group I was higher (P < 0.05) and its activation was also increased dramatically (P < 0.01), the level of AT-III: A was lower in patients with chronic hepatitis B (P < 0.05) and no difference was found in other indices between the two groups. CONCLUSIONS: The elevation of TFPI:Ag and TFPI:A in hepatic inflammatory diseases is an indication of inflammation, and hepatic tissue injury in broad, the lower level of AT-III liver secretions.

Adult↗

PubMed1999

[Inhibition of gastric myoelectric activity and gastric motility by microinjection of substance P into dorsal vagal nucleus in rats].

The present investigation showed that microinjection of substance P (SP) into dorsal vagal nucleus inhibited gastric myoelectric fast wave and gastric motility. The effect could be blocked by SP antiserum or SP antagonist [Arg6, D-Trp7,9, N-Me-Phe8]-SP6-11 or vagotomy. Depletion of sympathetic transmitters by reserpine did not affect induction of the inhibition. The results indicate that both exogenous and endogenous SP of dorsal vagal nucleus decrease the gastric myoelectric fast wave and motility, which is mediated by vagus nerve.

Animals↗

PubMed1999

[Surveillance of primary resistance in 481 cases of pulmonary tuberculosis].

OBJECTIVE: To understand the primary resistance of Mycobacterium tuberculosis in Henan province, and to make scientific prophylactic and treatment strategies. METHODS: Drug resistance surveillance (DRS) was implemented in Henan province according to WHO/IUATLD Guidelines for Surveillance of Drug Resistance in Tuberculosis(1994), and proportional method was used to detect primary resistance in 481 new cases of bacillus-positive pulmonary tuberculosis without history of anti-tuberculosis drug use. RESULTS: The primary drug resistance(PDR) rates were 22.7%, 15.8%, 22.7% and 7.7% for INH, RFP, SM and EMB, respectively. The primary multi-drug resistance (MDR) rates were 2.3%, 5.0%, 0.4% and 5.4% for HR, HRS, HRE and HRSE, respectively. CONCLUSIONS: The results show that the problem of primary resistance of Mycobacterium tuberculosis is serious in Henan province, and uniform management of anti-tuberculosis drugs and implementation of DOTs are needed.

Drug Resistance, Bacterial↗