Biomedical subjects

Q Jiang

Publications and source records attributed to Q Jiang.

At least 55 records · Page 3Linked to original sources

PubMed2001

Genomic organization and refined mapping of the human nuclear corepressor 2 (NCOR2)/ silencing mediator of retinoid and thyroid hormone receptor (SMRT) gene on chromosome 12q24.3.

The human nuclear co-repressor 2 (N-CoR2) gene (NCOR2, previously called silencing mediator for retinoid and thyroid hormone receptor SMRT) is recruited to nuclear and non-nuclear receptors in a large repressing complex containing also N-CoR1, mSin3 and HDACs. This large complex represses transcription in absence of ligand. Herein we report the high- resolution and refined mapping of NCOR2 at the boundary of sub-bands 12q24.23 and 12q24.31, and its intron/exon structure. The gene contains 45 exons. This information should allow further study of potential NCOR2 genomic alteration in some subsets of malignancies.

Chromosome Banding↗

PubMed2001

[Classification study on the marshland in endemic areas of Schistosoma japonicum using satellite TM image data].

OBJECTIVE: To create a land cover map of the marshland region of Schistosoma Japonicum using satellite TM data from Chayegang, Jiangxi Province. METHODS: Satellite data of three TM bands, namely TM3, TM4 and TM5, were selected to be used in classification study with Principal Components Analysis. Then TM satellite images were applied to false color composite and unsupervised classification with computer software to manage the TM data. Finally the resulting clusters were identified by undertaking site visits and a systematic sampling snail survey was also carried out in the study area in April, 2000. RESULTS: Three land cover classes were generated, including class 1, the carex zone that is both the dominant vegetation and main snail habitats of the study area. Based on the snail survey in the spring of 2000, the live snail density and infectious snail density of the carex zone were 2.51/0.11 m2 and 0.006 9/0.11 m2, respectively. The infection rate of the snail was 0.28%. No snail was found in land cover class 3, the mixed vegetation, because the altitude of this area is either above 17 m or under 14 m and therefore the vegetation in this area is unsuitable for snails to survive. CONCLUSION: Remote sensing can contribute the study on the distribution of snail habitats and become a promising epidemiological study method for schistosomiasis and other ecological diseases.

Animals↗

PubMed2001

Activation of NF-kappa B in bronchial epithelial cells from children with asthma.

OBJECTIVES: To determine whether nuclear factor-kappa B (NF-kappa B) is activated in epithelial cells from children with asthma and to understand the role of NF-kappa B in airway inflammation in asthma. METHODS: Bronchial mucosa specimens were obtained from 9 children with asthma and 6 control subjects. NF-kappa B expression in epithelial cells were detected by immunohistochemical examination, and NF-kappa B-DNA binding was measured by electrophoretic mobility shift assay (EMSA). RESULTS: Nuclear expression of NF-kappa B in epithelial cells was observed in the 9 asthmatic children. NF-kappa B-DNA binding was found in 4 asthmatic children (EMSA was performed in 6 asthmatic children). In contrast, both nuclear expression and NF-kappa B-DNA binding were absent in the 6 control subjects. CONCLUSION: These results indicated that NF-kappa B is activated in epithelial cells from asthmatic children and the NF-kappa B activation may be the basis for the increased expression of many inflammatory genes and for airway inflammation in asthma.

Asthma↗

PubMed2001

[Experimental study of interleukin-12 gene vaccines in the treatment of low-load malignant lymphoma (EL4)].

OBJECTIVE: Two kinds of murine interleukin-12 (mIL-12) fusion gene vaccines were used to treat the murine low-load malignant T cell lymphoma EL4 as minimal residual disease (MRD) model. METHODS: C57BL/6 synergistical mice were subcutaneously inoculated with 1 x 10(6) wild-type (wt) EL4 tumor cells as low-load lymphoma model treated with two mIL-12 gene vaccines. Package cell line PA317/12 producing mIL-12 retrovirus (RV) was used as in vivo vaccine and EL4 tumor cells transferred with mIL-12 gene as ex vivo vaccine. RESULTS: In both mIL-12 gene vaccine-treated groups, there was no tumor growth in 50% mice 60 days after inoculation. Nine of these no tumor growth mice were re-challenged with 5 x 10(5) wt EL4 cells, and 5 of them survived without tumors in another 60 days. All control mice died with tumors within one month after inoculation. Among those developed tumors in both vaccine-treated groups, the development of tumors was delayed, the survival period prolonged (P < 0.01), and the tumors size at death smaller (P < 0.05) as compared with the controls. In the long-survived vaccine-treated mice, no residual tumor cells were found by morphological examination. CONCLUSION: Both IL-12 gene vaccines can efficiently eliminate wt EL4 MRD in C57BL/6 mice.

Animals↗

PubMed2001

[Cluster analysis study on the marshland of Schistosoma Japonicum using satellite TM image data in Peng Lake, Jiangxi province].

OBJECTIVE: To create a category land cover map of the marshland region of Schistosoma Japonicum using satellite TM data. METHODS: TM satellite images from Peng Lake of Jiangxi province were applied to the Cluster analysis. Then the resulting clusters were identified and reclassified by undertaking site visits. RESULTS: Eight land cover classes were generated, including Carexspp Zone that was the snail habitat place. CONCLUSION: Cluster analysis, which is a technique for the interpretation of remotely sensed imagery, could contribute to the study on the distribution of snail habitats and become a new tool for the epidemiological ecology study.

Animals↗

PubMed2001

[Epidemiological effects of live attenuated hepatitis A vaccine (H(2)-strain): results of A 10-year observation].

OBJECTIVE: To assess the long-term epidemiological effects after a mass vaccination program, using live attenuated hepatitis A vaccine (H(2)-strain). METHODS: Shengsi county and Jiaojiang city in Zhejiang province were chosen where high incidence rate of hepatitis A was observed. Mass vaccination program of H(2)-strain vaccine was carried out on 1 - 15 year olds. Cohort studies included two groups were carried out in Shengsi. Cases reported program on hepatitis A was under the national standard on clinical diagnosis and partly through laboratory monitor of anti-HAV IgM and IgG, ELISA and Abbott EIA. Population size was estimated by the yearly reports of census bureau of the county and the city. Serum tests including neutralization test, immune-recall responses, and anti-HAV IgG were performed 10 years after the initial immunization. RESULTS: The morbidity of hepatitis A was significantly different between vaccinated groups and non-vaccinated groups (P < 0.01) in the cohort study. The protective efficacy in the site was 100 percent. There was a significantly negative correlation of regression between vaccine coverage and hepatitis A morbidity. In both sites, hepatitis A incidence rate showed decrease of 94.5% and 90.3% in whole population, with 96.9% and 97.9% in 1 - 15 year olds respectively. Neutralization test showed that 63.8% of the serum negative to ELISA after vaccination could still neutralize certain HAV. Immune-recall response after the booster was seen in vaccine group with 80.2% positive rate of anti HAV-IgG, 10 years after immunization among vaccinees in both sites. Not a single hepatitis A case was identified. CONCLUSION: Live attenuated hepatitis A vaccine seemed to have obviously long-term epidemiological effects.

Adolescent↗

PubMed2001

Cartilage-like phenomenon in the anterior cruciate ligamenta.

OBJECTIVE: To detect histological characteristic of anterior cruciate ligament (ACL) and medial collateral ligament (MCL). METHODS: In each of 20 skeletally mature male mongrels and 4 men, the ACL and MCL were examined by standard hematoxylin-eosin procedure and toluidine blue staining for histologic observation. RESULTS: The fibroblasts in medial collateral are elongated to spindle shape and aligned in a row between the bundles of collagenous fibers. Toluidine blue staining is negative. The anterior cruciate ligament demonstrated more heterogenous cell types and arrangement. It had three major cell forms: spindle, round and ovoid type, which were shorter but greater than the cells in medial collateral ligament. Toluidine blue staining was positive in anterior cruciate ligament. Most cells in anterior cruciate ligament were enclosed within lacunae. CONCLUSION: This study suggests that the ACL has different histological characteristics from MCL, and is more cartilage-like in nature.

Animals↗

PubMed2000

N-methyl-D-aspartate receptor activation results in regulation of extracellular signal-regulated kinases by protein kinases and phosphatases in glutamate-induced neuronal apototic-like death.

Extracellular signal-regulated kinases (ERK1/ERK2) have been shown transiently activated and involved in excitotoxicity. We searched for upstream molecules responsible for the regulation of glutamate-induced ERK1/ERK2 activation and ERK1/ERK2-mediated apototic-like death in cultured rat cortical neurons. ERK1/ERK2 activation (monitored by anti-active ERK1/ERK2 antibody) was almost completely prevented by blockage of NMDA receptor (NMDA-R) or elimination of extracellular Ca(2+), but not any other glutamate receptor or L-type voltage-gated Ca(2+) channel. It was prevented largely by inhibition of protein kinase C (PKC), protein-tyrosine kinases (PTK), respectively, but mildly by that of CaM kinase II. Combined inhibition of CaM kinase II (but not PTK) and PKC had an additive effect. Reversion of ERK1/ERK2 activation was largely prevented by inhibition of protein phosphatase (PP) 1 or protein tyrosine phosphatase (PTP). Combined inhibition of PP 1 and PTP had no additive effect. Glutamate-induced apoptotic-like death (determined by DAPI staining) was largely prevented by inhibition of NMDA-R, PKC, CaM kinase II, PTK and MEK1/MEK2 (ERK1/ERK2 kinase), respectively. Combined inhibition of CaM kinase II (but not PKC or PTK) and MEK1/MEK2 had an additive effect. Glutamate-induced apoptotic-like death was promoted by inhibition of PP1 and PTP, respectively. The above results suggested that in glutamate-induced cortical neurotoxicity ERK1/ERK2 activation be mainly mediated by NMDA-R. Subsequently, a pathway dependent on both PKC and PTK was mainly involved, which was also mainly responsible for ERK1/ERK2-mediated apoptotic-like death, and a CaM kinase II-dependent pathway was relatively mildly involved. Reversion of ERK1/ERK2 activation was mainly mediated by a pathway dependent on both PP1 and PTP, which might be involved in the restrain of glutamate-induced neurotoxicity.

Animals↗

PubMed2000

Total synthesis of (+)-quassin.

A total synthesis of (+)-quassin from naturally occurring (S)-(+)-carvone is described. The total number of steps was 28, and the overall yield was about 2.6%. The synthetic strategy for the construction of the tetracyclic carbon framework was based on a C-->ABC-->ABCD ring annulation sequence, involving an aldol reaction, an intramolecular Diels-Alder reaction, and an intramolecular acylation as the key steps. Subsequent functionalization of ring A and ring C then afforded the target (+)-quassin.

Antineoplastic Agents, Phytogenic↗

PubMed2000

gamma-tocopherol and its major metabolite, in contrast to alpha-tocopherol, inhibit cyclooxygenase activity in macrophages and epithelial cells.

Cyclooxygenase-2 (COX-2)-catalyzed synthesis of prostaglandin E(2) (PGE(2)) plays a key role in inflammation and its associated diseases, such as cancer and vascular heart disease. Here we report that gamma-tocopherol (gammaT) reduced PGE(2) synthesis in both lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and IL-1beta-treated A549 human epithelial cells with an apparent IC(50) of 7.5 and 4 microM, respectively. The major metabolite of dietary gammaT, 2,7,8-trimethyl-2-(beta-carboxyethyl)-6-hydroxychroman (gamma-CEHC), also exhibited an inhibitory effect, with an IC(50) of approximately 30 microM in these cells. In contrast, alpha-tocopherol at 50 microM slightly reduced (25%) PGE(2) formation in macrophages, but had no effect in epithelial cells. The inhibitory effects of gammaT and gamma-CEHC stemmed from their inhibition of COX-2 activity, rather than affecting protein expression or substrate availability, and appeared to be independent of antioxidant activity. gamma-CEHC also inhibited PGE(2) synthesis when exposed for 1 h to COX-2-preinduced cells followed by the addition of arachidonic acid (AA), whereas under similar conditions, gammaT required an 8- to 24-h incubation period to cause the inhibition. The inhibitory potency of gammaT and gamma-CEHC was diminished by an increase in AA concentration, suggesting that they might compete with AA at the active site of COX-2. We also observed a moderate reduction of nitrite accumulation and suppression of inducible nitric oxide synthase expression by gammaT in lipopolysaccharide-treated macrophages. These findings indicate that gammaT and its major metabolite possess anti-inflammatory activity and that gammaT at physiological concentrations may be important in human disease prevention.

Arachidonic Acids↗

PubMed2000

Lipopolysaccharide induces physical proximity between CD14 and toll-like receptor 4 (TLR4) prior to nuclear translocation of NF-kappa B.

CD14, a GPI-linked protein, plays a pivotal role in LPS-mediated signaling by potentiating leukocyte adherence, activation, and cytokine production. Recent studies have identified the Toll-like receptor 4 (TLR4) as a membrane cofactor in LPS-mediated transmembrane signaling in cytokine induction, although the mechanism responsible for this cooperation is unknown. Using fluorescence resonance energy transfer (RET) techniques, we demonstrate that LPS triggers a physical association between CD14 and TLR4. Because LPS stimulation upregulates CD14 and TLR4 expression, it was necessary to control for the possibility that these newly expressed molecules were associated with one another independent of LPS stimulation. Although the calcium ionophore A23187 increased the expression of CD14 and TLR4, they did not exhibit energy transfer. However, following A23187 treatment, LPS promoted physical proximity between CD14 and TLR4. Therefore, we suggest that a close interaction between CD14 and TLR4 participates in LPS signaling, leading to nuclear translocation of NF-kappaB.

Biological Transport↗

PubMed2000

Postischemic intracarotid treatment with TNK-tPA reduces infarct volume and improves neurological deficits in embolic stroke in the unanesthetized rat.

BACKGROUND AND PURPOSE: To simulate human stroke, we developed a model of focal cerebral embolic ischemia in the unanesthetized rat. Using this model, we tested the hypothesis that intra-arterial administration of TNK-tPA, a fibrin specific second generation thrombolytic agent, is effective in reducing ischemic volume without increasing intra-cerebral hemorrhage. METHODS: Under anesthesia, a catheter was inserted to the origin of the MCA of male Wistar rats. Forty-five minutes after recovery from anesthesia, the MCA was occluded in the awake rat by a single fibrin rich clot placed via the catheter. TNK-tPA (1.5 mg/kg) was administered intraarterially via the catheter at either 2 h or 4 h after stroke. All rats were sacrificed at 48 h after ischemia. Neurological deficits, gross hemorrhage and ischemic lesion volume were measured. RESULTS: A clot was detected at the origin of the MCA 4 h after MCA occlusion in the awake rats (n=4). Rats (n=12) subjected to MCA occlusion showed immediate neurological deficits which persisted for 48 h of ischemia. Ischemic rats had a lesion volume of 38.2+/-3.8% and 25% of rats exhibited gross hemorrhage. Ischemic rats (n=10) treated with TNK-tPA at 2 h showed a significant (P<0.05) reduction of neurological deficits, body weight loss and infarct volume (22.8+/-2.1%) without an increase in gross hemorrhage (10%) compared with the non treated ischemic rats (25%). Although treatment with TNK-tPA of ischemic rats (n=12) at 4 h did not significantly (P=0.06) reduce infarct volume (28.6+/-3.0%), it also did not increase gross hemorrhage (25%) compared with the control group (25%). CONCLUSIONS: This study demonstrates that intraarterial administration of TNK-tPA at 2 h of ischemia in the unanesthesthetized rat is effective in reducing neurological deficits and ischemic lesion volume without increasing hemorrhagic transformation and that administration of TNK-tPA at 4 h of ischemia does not increase the incidence of hemorrhagic transformation.

Animals↗

PubMed2000

Site-directed mutagenesis studies of human A(2A) adenosine receptors: involvement of glu(13) and his(278) in ligand binding and sodium modulation.

To provide insights into interactions between ligands and A(2A) adenosine receptors, site-directed mutagenesis was used to test the roles of a glutamic acid residue in the first transmembrane domain (Glu13) and a histidine residue in the seventh transmembrane domain (His278). The two residues, which have been suggested to be closely linked in molecular modeling studies, were mutated to glutamine (E13Q) and tyrosine (H278Y), respectively. Saturation experiments revealed that [(3)H]ZM241385 (4-2-[7-amino-2-(2-furyl)-1,2, 4-triazolo[1,5-a][1,3,5]triazin-5-yl-amino]ethylphenol) bound wild-type and mutant receptors in membranes from COS-7 cells expressing human A(2A) adenosine receptors with high affinity and low non-specific binding. It was found from the competition experiments that the affinity of the A(2A) adenosine receptor agonists for the mutant receptors was 3- to 200-fold lower than for the wild-type receptor. Among antagonist competitors of binding at E13Q and H278Y mutant receptors, there was variation in the affinity depending on their different structures, although changes were relatively minor (<3-fold) except in the case of theophylline, whose affinity was decreased approximately 20 times on the H278Y mutant. The possible involvement of the two residues in sodium ion regulation was also tested. The agonist competition curves for [(3)H]ZM241385 were shifted to the right in both wild-type and mutant receptors in the presence of 1 M sodium ions, but the extent of shift (2- to 27-fold) in wild-type receptor was generally larger than for the mutant receptors. Sodium ions also decreased [(3)H]ZM241385 dissociation from both wild-type and mutant receptors, being more influential on the former than the latter. The results suggest that the two closely linked residues Glu13 and His278 in A(2A) adenosine receptor are most important for agonist recognition and are partly responsible for the allosteric regulation by sodium ions.

Animals↗

PubMed2000

Formation of the catecholamine release-inhibitory peptide catestatin from chromogranin A. Determination of proteolytic cleavage sites in hormone storage granules.

The catestatin fragment of chromogranin A is an inhibitor of catecholamine release, but its occurrence in vivo has not yet been verified, nor have its precise cleavage sites been established. Here we found extensive processing of catestatin in chromogranin A, as judged by catestatin radioimmunoassay of size-fractionated chromaffin granules. On mass spectrometry, a major catestatin form was bovine chromogranin A(332-364); identity of the peptide was confirmed by diagnostic Met(346) oxidation. Further analysis revealed two additional forms: bovine chromogranin A(333-364) and A(343-362). Synthetic longer (chromogranin A(332-364)) and shorter (chromogranin A(344-364)) versions of catestatin each inhibited catecholamine release from chromaffin cells, with superior potency for the shorter version (IC(50) approximately 2.01 versus approximately 0.35 microm). Radioimmunoassay demonstrated catestatin release from the regulated secretory pathway in chromaffin cells. Human catestatin was cleaved in pheochromocytoma chromaffin granules, with the major form, human chromogranin A(340-372), bounded by dibasic sites. We conclude that catestatin is cleaved extensively in vivo, and the peptide is released by exocytosis. In chromaffin granules, the major form of catestatin is cleaved at dibasic sites, while smaller carboxyl-terminal forms also occur. Knowledge of cleavage sites of catestatin from chromogranin A may provide a useful starting point in analysis of the relationship between structure and function for this peptide.

Adrenal Medulla↗

PubMed2000

Identification of receptors for neuromedin U and its role in feeding.

Neuromedin U (NMU) is a neuropeptide with potent activity on smooth muscle which was isolated first from porcine spinal cord and later from other species. It is widely distributed in the gut and central nervous system. Peripheral activities of NMU include stimulation of smooth muscle, increase of blood pressure, alteration of ion transport in the gut, control of local blood flow and regulation of adrenocortical function. An NMU receptor has not been molecularly identified. Here we show that the previously described orphan G-protein-coupled receptor FM-3 (ref. 15) and a newly discovered one (FM-4) are cognate receptors for NMU. FM-3, designated NMU1R, is abundantly expressed in peripheral tissues whereas FM-4, designated NMU2R, is expressed in specific regions of the brain. NMU is expressed in the ventromedial hypothalamus in the rat brain, and its level is significantly reduced following fasting. Intracerebroventricular administration of NMU markedly suppresses food intake in rats. These findings provide a molecular basis for the biochemical activities of NMU and may indicate that NMU is involved in the central control of feeding.

Amino Acid Sequence↗

PubMed2000

Epithelial sodium channels regulate cystic fibrosis transmembrane conductance regulator chloride channels in Xenopus oocytes.

The cystic fibrosis transmembrane conductance regulator (CFTR), in addition to its well defined Cl(-) channel properties, regulates other ion channels. CFTR inhibits epithelial Na(+) channel (ENaC) currents in many epithelial and nonepithelial cells. Because modulation of net NaCl reabsorption has important implications in extracellular fluid volume homeostasis and airway fluid volume and composition, we investigated whether this regulation was reciprocal by examining whether ENaC regulates CFTR. Co-expression of human (h) CFTR and mouse (m) alphabetagammaENaC in Xenopus oocytes resulted in a significant, 3.7-fold increase in whole-cell hCFTR Cl(-) conductance compared with oocytes expressing hCFTR alone. The forskolin/3-isobutyl-1-methylxanthine-stimulated whole-cell conductance in hCFTR-mENaC co-injected oocytes was amiloride-insensitive, indicating an inhibition of mENaC following hCFTR activation, and it was blocked by DPC (diphenylamine-2-carboxylic acid) and was DIDS (4, 4'-diisothiocyanatostilbene-2,2'-disulfonic acid)-insensitive. Enhanced hCFTR Cl(-) conductance was also observed when either the alpha- or beta-subunit of mENaC was co-expressed with hCFTR, but this was not seen when CFTR was co-expressed with the gamma-subunit of mENaC. Single Cl(-) channel analyses showed that both CFTR Cl(-) channel open probability and the number of CFTR Cl(-) channels detected per patch increased when hCFTR was co-expressed with alphabetagammamENaC. We conclude that in addition to acting as a regulator of ENaC, CFTR activity is regulated by ENaC.

Animals↗

PubMed2000

Diphosphorylation of extracellular signal-regulated kinases and c-Jun N-terminal protein kinases in brain ischemic tolerance in rat.

Extracellular signal-regulated kinases (ERKs) and c-Jun N-terminal protein kinases (JNKs) activation in brain ischemic tolerance were examined by Western immunoblot. ERK but not JNK diphosphorylation (activation) were increased after preconditioning ischemia. The increased JNK1 but not ERK diphosphorylation after lethal ischemia was eliminated by pretreatment with preconditioning ischemia. The results suggest that the elimination of JNK1 activation after lethal ischemia by preconditioning ischemia may be one of the important protective mechanisms in ischemic tolerance, and ERKs activation may be involved in the induction of the protective responses.

Animals↗

PubMed2000

Diphosphorylation and involvement of extracellular signal-regulated kinases (ERK1/2) in glutamate-induced apoptotic-like death in cultured rat cortical neurons.

Glutamate-induced excitotoxicity, with certain characteristics of apoptosis, has been implicated in a variety of neuronal degenerative disorders. In some physiological cases, extracellular signal-regulated kinases (ERK1/2) are activated by stimulation of glutamate receptors. In the present study, the activation (diphosphorylation) and role of ERK1/2 in glutamate-induced apoptotic-like death in cultured cortical neurons were investigated. Protein levels and activation (diphosphorylation) levels of ERK1/2 were examined by Western immunoblot, probed with anti-ERK1/2 and anti-active (diphosphorylated) ERK1/2 antibodies, respectively. Apoptotic-like death was determined by DAPI staining. Before a remarkable increase of apoptotic-like cell death was observed at 9-18 h after 15 min exposure to 50 microM glutamate, diphosphorylation levels of ERK1/2 were rapidly increased, peaked at 5-15 min of the exposure, and reverted to sham control level 3 h after the exposure, while the protein levels of ERK1/2 were unaffected. The glutamate concentration effective for inducing apoptotic-like cell death was correlated with that for inducing ERK1/2 diphosphorylation. Both ERK1/2 diphosphorylation and the apoptotic-like cell death were largely prevented by MK-801, a specific NMDA receptor (a subtype receptor of glutamate) antagonist, or the elimination of extracellular Ca(2+) with EGTA. PD98059, a specific inhibitor of ERK1/2 kinase, completely inhibited ERK1/2 diphosphorylation and partially inhibited the apoptotic-like cell death. These results suggest that largely via NMDA receptor-mediated influx of extracellular Ca(2+), ERK1/2 were rapidly and transiently activated and were involved in glutamate-induced apoptotic-like death in cultured rat cortical neurons.

Animals↗