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Biomedical subjects

Q Zeng

Publications and source records attributed to Q Zeng.

At least 55 records · Page 3Linked to original sources
PubMed2001

[Diagnosis and surgical treatment of carotid body tumor].

OBJECTIVE: To promote the rate of diagnosis and successful rate of operation for carotid body tumor. METHOD: 26 cases of the 30 patients with carotid body tumor were performed by DSA and 5 cases of them, feeding arteries of tumor were embolized with gelfoam through superlective catheterization, preoperativelly. The tumor was resected under carotid adventitial plane in 12 cases, with extracervical artery in 8 cases and with tumor-carotid segment block in 10 cases. RESULT: Of the 30 cases, no one died from operation or cerebral vascular complications. DSA plays a significant role in diagnosis of the tumor. Intraoperative bleeding can be remarkably reduced if feeding arteries were embolized preoperativelly. The tumor fixed to segment of the carotid arteries block was resected and the reconstruction of vasculature was unnecessary as soon as candidates were certified to be qualified by carotid training and DSA or/and TCD tests. Follow up of these 30 patients revealed that 25 of them survived free from cerebrovascular complications and tumor recurrence for 5 months-10 years. 1 of them died from traffic accident 2 year after operation, 4 of them had lost communication. CONCLUSION: DSA is a most authritative approach for diagnosis of carotid body tumor, DSA and TCD tests play a key role to resect carotid artery without reconstruction. Successful operation based on a precise preoperative evaluation, choice of operative ways and proper procedure.

Adult↗
PubMed2001

[A comparative observation preoperatively and postoperatively of nasal mucosa in chronic sinusitis treated with endoscopic sinus surgery].

OBJECTIVES: To study morphologic and functional mucosal changes both preoperatively and postoperatively in chronic sinusitis (CS) treated with endoscopic sinus surgery (ESS). METHODS: 1. Saccharin test and light microscopic examination of nasal mucosa were taken preoperatively and postoperatively in 32 cases with CS and in 28 normal subjects as control. 2. Scanning and transmission electron microscopy were performed to exam preoperatively and postoperatively the nasal mucosa in 10 cases with CS and in 2 normal cases as control. RESULTS: 1. The preoperative saccharin test time (STT) in patients with CS was significantly longer than that in the controls (P < 0.001), and the postoperative STT became significantly shorter than that in preoperative one(P < 0.001). 2. The pathological changes of nasal mucosa, such as infiltration in inflammatory cells, edema, polypoid formations and pathologic glands were observed preoperatively. The infiltration in inflammatory cells, edema and polypoid formations were significantly released (P < 0.01) at four months after operation, and there was no significant difference comparing with the controls (P > 0.05). However, the pathologic glands were not reduced even after four months postoperatively. 3. The examination of electron microscopy demonstrated that the ultrastructure of nasal mucosa was impaired preoperatively and almost completely recovered at four months postoperatively. CONCLUSIONS: The normal structure and clearance function of nasal mucosa in patients with CS was impaired preoperatively, and the impaired structure and mucociliary clearing function of nasal mucosa were greatly improved after ESS and almost completely recovered at four months postoperatively. The pathologic glands and secretive function of nasal mucosa may need longer period for recovering.

Adolescent↗
PubMed2001

[Determination of cobalt in solidified resin promoter by successive extraction and FAAS].

A new method had been investigated for the analysis of micro-amount of cobalt in solidified resin promoter. Methyl isobutyl ketone (MIBK) was used in 1 mol.L-1 NH4SCN medium followed by 4 mol.L-1 nitric acid back extraction step, then analysis by flame atomic absorption spectrometry. The results indicated that the method was accurate and the interference with concomitant in solidified resin promoter was negligible. The method had a recovery of 96.2%-104.6%.

Carboxylic Acids↗
PubMed2000

Gustatory innervation and bax-dependent caspase-2: participants in the life and death pathways of mouse taste receptor cells.

In the adult mouse tongue, an average of 11% of the gustatory receptor cells are replaced each day. In investigating homeostatic cell death mechanisms in gustatory renewing epithelium, we observed that taste receptor cells were selectively immunopositive for the bcl-2 family death factor, Bax, and for the protease Caspase-2 (Nedd2/Ich1). We determined that 8-10% of the taste receptor cells of the vallate papilla were Bax positive and that 11% were Caspase-2 positive. Some of these immunopositive taste cells had apoptotic morphological defects. Within the subset of vallate taste cells immunopositive for either Caspase-2 or Bax, up to 79% coexpressed both death factors. Bax and Caspase-2 first appeared in occasional vallate taste receptor cells on the same postnatal day-the day after birth. bax null mutation markedly reduced gustatory Caspase-2 immunoexpression. These observations suggest that taste cell death pathways utilize p53, Bax, and Caspase-2 to dispose of aged receptor cells. Apart from reducing Caspase-2 expression, Bax deficiency also altered taste organ development. bax(-/-) mice had a more profusely innervated vallate papilla, which grew to be 25% longer and taller, with the mean taste bud containing more than twice the normal number of taste cells. This augmentation of taste organ development with increased innervation is complementary to the well-documented reduction in taste organ development with sparse innervation. We propose that additional taste neurons survived programmed cell death in Bax-deficient mice, thereby providing an inductive boost to vallate gustatory development.

Afferent Pathways↗
PubMed2000

Multi-epitope schistosome vaccine candidates tested for protective immunogenicity in mice.

The major challenge in the development of anti-schistosome vaccines is to use defined antigens to stimulate an appropriate immune response that leads to resistance. Several promising candidate vaccine antigens including the glycolytic enzyme triose-phosphate isomerase (SmTPI), a 28 kDa glutathione-S-transferase (Sm28), the myofibrilar protein paramyosin (Sm97), an integral membrane protein (Sm23) and calpain (Smcalpain) have been characterised and their primary sequences derived for Schistosoma mansoni. Furthermore, sequences are available for synthetic peptides mimicking epitopes on these molecules capable of inducing schistosome-specific T- and B-cell responses. These schistosome vaccine candidates have generally been tested with varying degrees of success as single components, with only one report of the use of a multivalent antigen or multi-epitope approach. We describe the assembly of multiple defined and different epitopes of S. mansoni into a variety of single covalent structures; these included a DNA vaccine encoding different epitopes in tandem, the polyprotein itself that is encoded by this DNA and branched synthetic peptide epitope-based polymers in which the individual epitopes are pendant from an inert backbone. Each of the vaccine constructs examined, with the exception of the DNA vaccine, generated antibodies that were capable of binding to a tandem sequence of the epitopes. Although these results were encouraging, none of the constructs protected animals from subsequent challenge infection, indicating that the immune responses elicited were inadequate or inappropriate for parasite killing in vivo.

Animals↗
PubMed2000

Prenylation-dependent association of protein-tyrosine phosphatases PRL-1, -2, and -3 with the plasma membrane and the early endosome.

PRL-1, -2, and -3 represent a novel class of protein-tyrosine phosphatase with a C-terminal prenylation motif. Although PRL-1 has been suggested to be associated with the nucleus, the presence of three highly homologous members and the existence of a prenylation motif call for a more detailed examination of their subcellular localization. In the present study, we first demonstrate that mouse PRL-1, -2, and -3 are indeed prenylated. Examination of N-terminal epitope-tagged PRL-1, -2, and -3 expressed in transiently transfected cells suggests that PRL-1, -2, and -3 are present on the plasma membrane and intracellular punctate structures. Stable Chinese hamster ovary cells expressing PRL-1 and -3 in an inducible manner were established. When cells were treated with brefeldin A, PRL-1 and -3 accumulated in a collapsed compact structure around the microtubule-organizing center. Furthermore, PRL-1 and -3 redistributed into swollen vacuole-like structures when cells were treated with wortmannin. These characteristics of PRL-1 and -3 are typical for endosomal proteins. Electron microscope immunogold labeling reveals that PRL-1 and -3 are indeed associated with the plasma membrane and the early endosomal compartment. Expression of PRL-3 is detected in the epithelial cells of the small intestine, where PRL-3 is present in punctate structures in the cytoplasm. When cells are treated with FTI-277, a selective farnesyltransferase inhibitor, PRL-1, -2, and -3 shifted into the nucleus. Furthermore, a mutant form of PRL-2 lacking the C-terminal prenylation signal is associated with the nucleus. These results establish that the primary association of PRL-1, -2, and -3 with the membrane of the cell surface and the early endosome is dependent on their prenylation and that nuclear localization of these proteins may be triggered by a regulatory event that inhibits their prenylation.

Alkyl and Aryl Transferases↗
PubMed2000

Phosphorylation of myosin light chain kinase by p21-activated kinase PAK2.

Phosphorylation of myosin II regulatory light chains (RLC) by Ca(2+)/calmodulin-dependent myosin light chain kinase (MLCK) is a critical step in the initiation of smooth muscle and non-muscle cell contraction. Post-translational modifications to MLCK down-regulate enzyme activity, suppressing RLC phosphorylation, myosin II activation, and tension development. Here we report that PAK2, a member of the Rho family of GTPase-dependent kinases, regulates isometric tension development and myosin II RLC phosphorylation in saponin permeabilized endothelial monolayers. PAK2 blunts tension development by 75% while inhibiting diphosphorylation of myosin II RLC. Cdc42-activated placenta and recombinant, constitutively active PAK2 phosphorylate MLCK in vitro with a stoichiometry of 1.71 +/- 0. 21 mol of PO(4)/mol of MLCK. This phosphorylation inhibits MLCK phosphorylation of myosin II RLC. PAK2 catalyzes MLCK phosphorylation on serine residues 439 and 991. Binding calmodulin to MLCK blocks phosphorylation of Ser-991 by PAK2. These results demonstrate that PAK2 can directly phosphorylate MLCK, inhibiting its activity and limiting the development of isometric tension.

Calcium↗
PubMed2000

Constitutive activation of Stat3 signaling abrogates apoptosis in squamous cell carcinogenesis in vivo.

Field cancerization predisposes the upper aerodigestive tract mucosa to the formation of multiple primary tumors, when exposed to environmental carcinogens. Up-regulation of epidermal growth factor receptor occurs early in squamous cell carcinogenesis and is critical for the loss of growth control in a variety of human cancers, including head and neck squamous cell carcinomas. In these tumor cells in culture, epidermal growth factor receptor stimulation initiates signaling via persistent activation of selective STAT proteins. To determine the timing of Stat3 activation in head and neck carcinogenesis, we studied the expression and constitutive activation of Stat3 in tumors and normal mucosa from patients with head and neck cancer compared with mucosa from controls without cancer. Stat3 was up-regulated and constitutively activated in both primary human head and neck tumors as well as in normal mucosa from these cancer patients compared with control normal mucosa from patients without cancer. In vivo liposome-mediated gene therapy with a Stat3 antisense plasmid efficiently inhibited Stat3 activation, increased tumor cell apoptosis, and decreased Bcl-x(L) expression in a head and neck xenograft model. These findings provide evidence that constitutively activated Stat3 is an early event in head and neck carcinogenesis that contributes to the loss of growth control by an anti-apoptotic mechanism.

Animals↗
PubMed2000

Regulation of tumor angiogenesis by p53-induced degradation of hypoxia-inducible factor 1alpha.

The switch to an angiogenic phenotype is a fundamental determinant of neoplastic growth and tumor progression. We demonstrate that homozygous deletion of the p53 tumor suppressor gene via homologous recombination in a human cancer cell line promotes the neovascularization and growth of tumor xenografts in nude mice. We find that p53 promotes Mdm2-mediated ubiquitination and proteasomal degradation of the HIF-1alpha subunit of hypoxia-inducible factor 1 (HIF-1), a heterodimeric transcription factor that regulates cellular energy metabolism and angiogenesis in response to oxygen deprivation. Loss of p53 in tumor cells enhances HIF-1alpha levels and augments HIF-1-dependent transcriptional activation of the vascular endothelial growth factor (VEGF) gene in response to hypoxia. Forced expression of HIF-1alpha in p53-expressing tumor cells increases hypoxia-induced VEGF expression and augments neovascularization and growth of tumor xenografts. These results indicate that amplification of normal HIF-1-dependent responses to hypoxia via loss of p53 function contributes to the angiogenic switch during tumorigenesis.

Adenocarcinoma↗
PubMed2000

Effects of L-THP on Ca2+ overload of cultured rat cardiomyocytes during hypoxia and reoxygenation.

The effects of L-tetrahydropalmatine (L-THP) on the cultured rat cardiomyocytes during hypoxia and reoxygenation and the mechanism of L-THP treating reperfusion-arrythmias were studied. The concentration of intracellular free calcium ([Ca2+]i) of single cultured ventricular myocyte was determined by using EPC-9 light-electricity measurement system. It was found that L-THP (100 mumol/L) could reduce the [Ca2+]i augmentation in single cultured ventricular myocyte during hypoxia and reoxygenation. Verapamil (10 mumol/L) had the similar effect. It was concluded that L-THP could inhibit the Ca2+ overload of cultured rat cardiomyocytes during hypoxia and reoxygenation.

Animals↗
PubMed2000

TGF-alpha antisense gene therapy inhibits head and neck squamous cell carcinoma growth in vivo.

Unlike normal mucosal squamous epithelial cells, head and neck squamous cell carcinomas (HNSCCs) overexpress TGF-alpha mRNA and protein which is required to sustain the proliferation of HNSCC cells in vitro. To determine whether TGF-alpha expression contributes to tumor growth in vivo, cationic liposome-mediated gene transfer was used to deliver an antisense expression construct targeting the human TGF-alpha gene into human head and neck tumor cells, grown as subcutaneous xenografts in nude mice. The TGF-alpha antisense gene was immediately detected in the cytoplasm of the tumor cells, translocated to the nucleus by 12 h and remained localized to the nucleus for up to 3 days. Direct inoculation of the TGF-alpha antisense (but not the corresponding sense) construct into established HNSCC tumors resulted in inhibition of tumor growth. Sustained antitumor effects were observed for up to 1 year after the treatments were discontinued. Down-modulation of TGF-alpha was accompanied by increased apoptosis in vivo. These experiments indicate that interference with the TGF-alpha/EGFR autocrine signaling pathway may be an effective therapeutic strategy for cancers which overexpress this ligand/receptor pair.

Animals↗
PubMed2000

Epidermal growth factor receptor--mediated stat3 signaling blocks apoptosis in head and neck cancer.

OBJECTIVES: Upregulation of epidermal growth factor receptor (EGFR) is critical for the loss of growth control in a variety of human cancers including squamous cell cancers of the head and neck (SCCHN). In these tumor cells in culture, EGFR stimulation initiates signaling via persistent activation of STAT proteins, particularly Stat3. The present study was conducted to study the association between EGFR stimulation and constitutive activation of Stat3 in SCCHN in vivo and to investigate the proliferative and apoptotic consequences of Stat3 downmodulation in SCCHN cells in vitro. METHODS: SCCHN tumor xenografts were analyzed using electrophoretic mobility shift assay. A dominant-negative mutant Stat3 expression construct or a Stat3 antisense plasmid was transfected into SCCHN cells using lipofectamine. Cell growth and apoptosis were determined by vital dye exclusion and flow cytometry, respectively. RESULTS: In vivo liposome-mediated gene therapy with an EGFR antisense plasmid efficiently inhibited Stat3 activation in a head and neck xenograft model. Downmodulation of Stat3 using a dominant-negative or antisense approach inhibited tumor cell growth and stimulated apoptosis. CONCLUSIONS: These findings provide evidence that constitutively activated Stat3 is linked to EGFR signaling in SCCHN in vivo, which contributes to the loss of growth control by an anti-apoptotic mechanism.

Animals↗
PubMed2000

Agouti-related protein-like immunoreactivity: characterization of release from hypothalamic tissue and presence in serum.

A novel RIA was used to examine the release of agouti-related protein-like immunoreactivity (AGRP-LI) from perfused rat hypothalamic tissue slices and to characterize AGRP-LI in rat serum. A continuous low level basal AGRP-LI release was observed from hypothalami of rats fed ad libitum before the rats were killed. Basal AGRP-LI release was 3-fold greater in rats fasted 48 h. In fasted animals leptin dose-dependently suppressed basal AGRP-LI release. In fed animals no change in basal AGRP-LI release was detected in response to 10(-6) M alpha-MSH, orexin B, melanin-concentrating hormone, or serotonin. HPLC analysis of AGRP-LI in rat serum identified a single peak that eluted in close proximity to synthetic AGRP (87-132) and mouse [Leu127Pro]AGRP and that was identical to the peak seen in hypothalamic and adrenal tissue extracts. The serum concentration of AGRP-LI in rats fed ad libitum was 0.865+/-0.323 nmol/liter (mean +/- SE). Food deprivation resulted in a slow, but statistically significant rise in serum immunoreactivity at 48 h [1.174+/-0.118 nmol/liter (mean +/- SE)]. Bilateral adrenalectomy did not change serum levels of AGRP-LI. These studies demonstrate that in the rat there are different levels of basal hypothalamic AGRP-LI release in fed and fasted states and that in the fasted rat this release can be profoundly suppressed by leptin. These studies also suggest that AGRP is present in the systemic circulation of rats.

Adrenal Glands↗
PubMed2000

RGS proteins inhibit Xwnt-8 signaling in Xenopus embryonic development.

RGS family members are GTPase activating proteins (GAPs) that antagonize signaling by heterotrimeric G proteins. Injection of Xenopus embryos with RNA encoding rat RGS4 (rRGS4), a GAP for G(i) and G(q), resulted in shortened trunks and decreased skeletal muscle. This phenotype is nearly identical to the effect of injection of either frzb or dominant negative Xwnt-8. Injection of human RGS2, which selectively deactivates G(q), had similar effects. rRGS4 inhibited the ability of early Xwnt-8 but not Xdsh misexpression to cause axis duplication. This effect is distinct from axin family members that contain RGS-like domains but act downstream of Xdsh. We identified two Xenopus RGS4 homologs, one of which, Xrgs4a, was expressed as a Spemann organizer component. Injection of Xenopus embryos with Xrgs4a also resulted in shortened trunks and decreased skeletal muscle. These results suggest that RGS proteins modulate Xwnt-8 signaling by attenuating the function of a G protein.

Adaptor Proteins, Signal Transducing↗
PubMed2000

Endothelial cell retraction is induced by PAK2 monophosphorylation of myosin II.

The p21-activated kinase (PAK) family includes several enzyme isoforms regulated by the GTPases Rac1 and Cdc42. PAK1, found in brain, muscle and spleen, has been implicated in triggering cytoskeletal rearrangements such as the dissolution of stress fibers and reorganization of focal complexes. The role of the more widely distributed PAK2 in controlling the cytoskeleton has been less well studied. Previous work has demonstrated that PAK2 can monophosphorylate the myosin II regulatory light chain and induce retraction of permeabilized endothelial cells. In this report we characterize PAK2's morphological and biochemical effect on intact endothelial cells utilizing microinjection of constitutively active PAK2. Under these conditions we observed a modification of the actin cytoskeleton with retraction of endothelial cell margins accompanied by an increase in monophosphorylation of myosin II. Selective inhibitors were used to analyze the mechanism of action of PAK2. Staurosporine, a direct inhibitor of PAK2, largely prevented the action of microinjected PAK2 in endothelial cells. Butanedione monoxime, a non-specific myosin ATPase inhibitor, also inhibited the effects of PAK2 implicating myosin in the changes in cytoskeletal reorganization. In contrast, KT5926, a specific inhibitor of myosin light chain kinase was ineffective in preventing the changes in morphology and the actin cytoskeleton. The additional finding that endogenous PAK2 associates with myosin II is consistent with the proposal that cell retraction and cytoskeletal rearrangements induced by microinjected PAK2 depend on the direct activation of myosin II by PAK2 monophosphorylation of the regulatory light chain.

Actins↗
PubMed2000

A cDNA encoding ribosomal protein RPL15 from the desiccation-tolerant bryophyte Tortula ruralis: mRNA transcripts are stably maintained in desiccated and rehydrated gametophytes.

A Tortula ruralis cDNA, Rpl15, encoding a predicted polypeptide with significant similarity to the large-subunit ribosomal protein L15 (RPL15) was isolated from a desiccated gametophyte cDNA library, and is the first L15 homologue identified from a bryophyte. The deduced 203 amino acid polypeptide is approximately 24.1 kDa, with a predicted pI of 11.1, and shares extensive identity with rat RPL15 deduced polypeptide (>57%). RNA blot hybridization using total RNA demonstrated that Rpl15 is constitutively expressed in moss gametophytes during a desiccation-rehydration cycle and that Rpl15 mRNA transcripts are maintained in desiccated gametophytes as conserved mRNAs.

Amino Acid Sequence↗
PubMed2000

Multi-step polymer-assisted solution-phase (PASP) library synthesis of functionalized diaminobenzamides.

A parallel solution-phase library synthesis of functionalized diaminobenzamides is described. The four-step library synthesis is accomplished using polymer-assisted solution-phase (PASP) synthesis techniques. This high-yielding, multi-step sequence utilizes sequestering resins for the removal of reactants, reactant by-products, and employs a resin capture/release strategy as a key library synthesis step. Step one of the sequence relies on the displacement of an activated fluoro-group from the aromatic ring of 1a, b with a variety of primary amines to introduce the first diversity position. Step two is hydrolysis of the benzoate ester to a benzoic acid which is subsequently captured on a polyamine resin, washed, and released to give 4a, b in pure form. Step three utilizes PASP resins to mediate the amide coupling of a benzoic acid with a variety of primary amines to give the aminonitrobenzamides 5a, b and introduces the second diversity position. Step four is the parallel reduction of the aminonitrobenzamides 5a, b to the functionalized diaminobenzamides 6a, b. This library synthesis proceeds with high overall purities which average 80 % over the 4-step sequence.

Amines↗