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Qian Li

Publications and source records attributed to Qian Li.

At least 73 records · Page 4Linked to original sources
PubMed2005

[The expression and clinical significance of early differentiation antigens in acute leukemia].

OBJECTIVE: To evaluate the expression and clinical significance of early differentiation antigens of hematopoietic cells CD(34), CD(90) and CD(133) in acute leukemia (AL). METHODS: The expression of CD(34), CD(90) and CD(133) on leukemic blasts in 76 AL patients was detected with three-color direct flow-cytometry and CD(133) mRNA was detected with hemi-quantitative reverse transcriptive polymerase chain reaction (RT-PCR). RESULTS: (1) CD(34) and CD(133) expression in AL patients was significantly higher than that in controls (46.37% vs 0.47%, 21.93% vs 0.29%, P < 0.01), but there was no obvious difference of CD(90) expression between them (0.51% vs 0.25%, P > 0.05). The expression of CD(133) antigen was highly correlated with CD(133) mRNA expression in both of the normal control donors and AL patients (r = 0.932, P < 0.01). (2) The positive rates of CD(34), CD(90) and CD(133) in all AL patients were 63.2%, 7.9% and 42.1%, respectively. The expression of CD(90) in ALL was higher than that in AML (P < 0.05). Positive expression of CD(133) in AML-M(4) was significantly higher than that in other AML subtypes (P < 0.01). The positive rate of CD(34) in B-ALL was much higher than that in T-ALL (P < 0.05). (3) CD(133) expression in AML was significantly correlated with the expression of CD(34) and HLA-DR (P < 0.01). (4) The expression of CD(34), CD(90) and CD(133) was not associated with the clinical prognostic factors such as cytogenetic or molecular aberrations, initial peripheral blood WBC counts, lactate dehydrogenase level, multiple drug resistant expression and age. (5) There was a trend toward lower completely remission (CR) rate and overall survival rate in CD(34), CD(90) and CD(133) positive cases, but only CD(34)(+)/CD(133)(+) cases had significant lower CR rate than negative ones (P < 0.05). CONCLUSIONS: It is indicated AL has significantly higher CD(34) and CD(133) expression as compared with the normal controls. CD(133)/CD(34) co-expression might provide adverse prognostic stratification of acute leukemia.

AC133 Antigen↗
PubMed2005

[Genomic abnormalities detected by panel fluorescence in situ hybridization in chronic lymphocytic leukaemia].

OBJECTIVE: To investigate the value of panel fluorescence in situ hybridization for detection of genomic aberrations in chronic lymphocytic leukemia(CLL). METHODS: Five types of fluorescein-labelled DNA probes including centromeric probes for chromosomes 3,12 and 18, and two sequence-specific probes D13S272 for 13q14.3 and ATM for 11q23 were used to perform fluorescence in situ hybridization (FISH) assays in 22 patients with CLL. Its results were compared with that of conventional cytogenetic (CC) examination in order to ascertain which method is more sensitive and reliable for the detection of chromosomal and genomic abnormalities in CLL. RESULTS: On CC examination, only 8 cases (36.3%) were found to have chromosomal abnormalities including sole trisomy 12 in 3 cases, simultaneous trisomies 3 and 12 in one case, simultaneous trisomies 3, 12 and 18 in one case, translocation between chromosomes 5 and 15 in one case, deletion of 13q14.3 in one case, 3q- and 18p+ in one case, 4q+ and 13q- in one case, whereas on panel FISH assay, 15 cases (68.1%) were found to have genomic aberrations including trisomy 3 in 4 cases, trisomy 12 in 6 cases, trisomy 18 in one case, deletion of 13q14.3 in 8 cases, deletion of 11q23 in 6 cases. CONCLUSION: Panel FISH is a useful method for detection of genomic aberration in CLL, if combined with CC, it can obviously enhance the detection rate of chromosomal abnormalities in CLL.

Adult↗
PubMed2004

Toll-like receptor 4 mutation impairs the macrophage TNFalpha response to peptidoglycan.

Macrophages produce TNFalpha when infected by bacteria, a response that follows recognition of microbial components by members of the Toll-like receptor (TLR) family. Cells that lack functional TLR4 are known to have markedly diminished responses to Gram-negative lipopolysaccharide. We demonstrate in the present work that peritoneal macrophages derived from strains of mice that carry a spontaneous, inactivating mutation in TLR4 also have impaired production of TNFalpha in response to peptidoglycan, a ligand for TLR2. This impairment is at a step of biosynthesis subsequent to the generation of mRNA. TLR4-activated signals act at this step to enhance peptidoglycan-induced TNFalpha production in wild-type mice. Based on these observations, we conclude that macrophages from wild-type mice are primed by chronically acting TLR4 signals, probably resulting from exposure to environmental lipopolysaccharide. These signals are required for optimal production of TNFalpha in response to TLR2 stimulation, and are absent in macrophages from TLR4 mutant animals.

Animals↗
PubMed2004

Medial hypothalamic 5-hydroxytryptamine (5-HT)1A receptors regulate neuroendocrine responses to stress and exploratory locomotor activity: application of recombinant adenovirus containing 5-HT1A sequences.

Our previous studies found that serotonin transporter (SERT) knock-out mice showed increased sensitivity to minor stress and increased anxiety-like behavior but reduced locomotor activity. These mice also showed decreased density of 5-hydroxytryptamine (5-HT1A) receptors in the hypothalamus, amygdala, and dorsal raphe. To evaluate the contribution of hypothalamic 5-HT1A receptors to these phenotypes of SERT knock-out mice, two studies were conducted. Recombinant adenoviruses containing 5-HT1A sense and antisense sequences (Ad-1AP-sense and Ad-1AP-antisense) were used to manipulate 5-HT1A receptors in the hypothalamus. The expression of the 5-HT1A genes is controlled by the 5-HT1A promoter, so that they are only expressed in 5-HT1A receptor-containing cells. (1) Injection of Ad-1AP-sense into the hypothalamus of SERT knock-out mice restored 5-HT1A receptors in the medial hypothalamus; this effect was accompanied by elimination of the exaggerated adrenocorticotropin responses to a saline injection (minor stress) and reduced locomotor activity but not by a change in increased exploratory anxiety-like behavior. (2) To further confirm the observation in SERT-/- mice, Ad-1AP-antisense was injected into the hypothalamus of normal mice. The density and the function of 5-HT1A receptors in the medial hypothalamus were significantly reduced in Ad-1AP-antisense-treated mice. Compared with the control group (injected with Ad-track), Ad-1A-antisense-treated mice showed a significant reduction in locomotor activity, but again no changes in exploratory anxiety-like behaviors, tested by elevated plus-maze and open-field tests. Thus, the present results demonstrate that medial hypothalamic 5-HT1A receptors regulate stress responses and locomotor activity but may not regulate exploratory anxiety-like behaviors.

Adenoviridae↗
PubMed2004

Tissue inhibitor of metalloproteinases-4 suppresses vascular smooth muscle cell migration and induces cell apoptosis.

In a previous study, we have demonstrated that overexpression of the tissue inhibitors of metalloproteinases-4 (TIMP-4) can inhibit the neointima formation in the rat carotid model. To define the functions of tissue inhibitor of metalloproteinases-4 (TIMP-4) in SMCs, we transduced human TIMP-4 cDNA into rat aortic SMCs by using adenoviral vector. Overexpression of TIMP-4 blocked the conversion of pro-MMP-2 to the active form and inhibited basic fibroblast growth factor-induced migration by 56.7% (p < 0.01). Overexpression of TIMP-4 markedly increased apoptotic cell death without changing their proliferation. Importantly, overexpression of human TIMP-4 in the wall of balloon-injured rat carotid artery also increased SMC apoptosis. The percentages of TUNEL-positive cells of total cells increased significantly in AdTIMP-4 infected group compared with AdGFP infected group. These findings demonstrate that TIMP-4 can inhibit SMCs migration and induce apoptosis in vitro and in vivo, which may generate new targets for prevention and treatment of vascular diseases.

Angioplasty, Balloon↗
PubMed2004

Alternative therapy of Alzheimer's disease via supplementation with choline acetyltransferase.

Much evidence indicates that the memory and cognitive deficits of patients with Alzheimer's disease are closely associated with dysfunction of central cholinergic system. The degree of reduction of choline acetyltransferase activity in cerebral cholinergic neurons is significantly correlated with the severity of dementia or cognitive impairments observed in Alzheimer's disease. Therefore, Alzheimer's disease may be slowed by supplementation of exogenous choline acetyltransferase. Here we show that choline acetyltransferase mediated by TAT protein transduction domain passes through the blood-brain barrier and enters the neurons in mice, increasing choline acetyltransferase and neurotransmitter acetylcholine contents. The recombination TAT-choline acetyltransferase fusion protein injected intravenously improves the memory and cognitive dysfunction in Alzheimer's disease model mice induced by amyloid-beta peptide. Our results imply a novel and potentially effective way for Alzheimer's disease therapy.

Alzheimer Disease↗
PubMed2004

Phenotypic assessment of galanin overexpressing and galanin receptor R1 knockout mice in the tail suspension test for depression-related behavior.

RATIONALE: Galanin and its receptors exert inhibitory neuromodulatory control over brain monoamines. Rat studies revealed that galanin expression is upregulated by exposure to stressors and that galanin manipulations modify neuroendocrine and behavioral responses to stress, leading to the hypothesis that galanin mediates depression-related behaviors. METHODS: In the present study, we examined the role of galanin in modulating antidepressant-related behavior in galanin overexpressing transgenic (GAL-tg) mice and galanin receptor R1 knockout (GAL-R1 KO) mice, using the tail suspension test (TST). Quantitative autoradiography for 5-HT(1A)-R and serotonin transporter binding density tested for changes in these two major regulatory components of the 5-HT system in galanin mutant mice. RESULTS: Baseline TST behavior was normal in GAL-tg and GAL-R1 KO mice, and intracerebroventricular administration of galanin failed to alter TST behavior in normal C57BL/6J mice. The TST anti-immobility effects of acute treatment with the serotonin reuptake inhibitor, fluoxetine (0-30 mg/kg), and the norepinephrine reuptake inhibitor, desipramine (0-30 mg/kg), were unaltered in galanin mutant mice. Hippocampal 5-HT(1A)-R density was significantly elevated in GAL-tg and GAL-R1 KO mice, while hippocampal 5-HTT density was reduced in GAL-R1 KO mice, relative to controls. CONCLUSION: Neither pharmacological nor molecular genetic manipulations of galanin altered depression-related profiles in the TST. Possible functional alterations in hippocampal 5-HT neurotransmission may have contributed to these negative results. These preliminary findings provide evidence against the hypothesis that galanin plays a central role in mouse depression-related behaviors. It remains possible that galanin modulates depression-related responses in other experimental paradigms and species.

Animals↗
PubMed2004

Dysregulation of HSG triggers vascular proliferative disorders.

Vascular proliferative disorders, such as atherosclerosis and restenosis, are the most common causes of severe cardiovascular diseases, but a common molecular mechanism remains elusive. Here, we identify and characterize a novel hyperplasia suppressor gene, named HSG (later re-named rat mitofusin-2). HSG expression was markedly reduced in hyper-proliferative vascular smooth muscle cells (VSMCs) from spontaneously hypertensive rat arteries, balloon-injured Wistar Kyoto rat arteries, or ApoE-knockout mouse atherosclerotic arteries. Overexpression of HSG overtly suppressed serum-evoked VSMC proliferation in culture, and blocked balloon injury induced neointimal VSMC proliferation and restenosis in rat carotid arteries. The HSG anti-proliferative effect was mediated by inhibition of ERK/MAPK signalling and subsequent cell-cycle arrest. Deletion of the p21(ras) signature motif, but not the mitochondrial targeting domain, abolished HSG-induced growth arrest, indicating that rHSG-induced anti-proliferation was independent of mitochondrial fusion. Thus, rHSG functions as a cell proliferation suppressor, whereas dysregulation of rHSG results in proliferative disorders.

Animals↗
PubMed2004

Salacia oblonga improves cardiac fibrosis and inhibits postprandial hyperglycemia in obese Zucker rats.

Diabetes has a markedly greater incidence of cardiovascular disease than the non-diabetic population. The heart shows a slowly developing increase in fibrosis in diabetes. Extended cardiac fibrosis results in increased myocardial stiffness, causing ventricular dysfunction and, ultimately, heart failure. Reversal of fibrosis may improve organ function survival. Postprandial hyperglycemia plays an important role in the development of type 2 diabetes and cardiovascular complications, and has been proposed as an independent risk factor for cardiovascular diseases. Salacia oblonga (S.O.) is traditionally used in the prevention and treatment of diabetes. We investigated the effects of its water extract on cardiac fibrosis and hyperglycemia in a genetic model of type 2 diabetes, the obese Zucker rat (OZR). Chronic administration of the extract markedly improved interstitial and perivascular fibrosis in the hearts of the OZR. It also reduced plasma glucose levels in non-fasted OZR, whereas it had little effect in the fasted animals, suggesting inhibition of postprandial hyperglycemia in type 2 diabetic animals, which might play a role in improvement of the cardiac complications of OZR. Furthermore, S.O. markedly suppressed the overexpression of mRNAs encoding transforming growth factor betas 1 and 3 in the OZR heart, which may be an important part of the overall molecular mechanisms. S.O. dose-dependently inhibited the increase of plasma glucose in sucrose-, but not in glucose-loaded mice. S.O. demonstrated a strong inhibition of alpha-glucosidase activity in vitro, which is suggested to contribute to the improvement of postprandial hyperglycemia.

Analysis of Variance↗
PubMed2004

[Adenovirus-mediated gene transfer of rHSG-1 inhibits proliferation of vascular smooth muscle cells from spontaneously hypertensive rats].

OBJECTIVE: To investigate the effect of rat hyperplasia suppressor gene-1(rHSG-1) on the proliferation of aortic vascular smooth muscle cells(VSMCs) from spontaneously hypertensive rats(SHR). METHODS: VSMCs were transfected with an adenoviral vector expressing rHSG-1(Ad5rHSG-1). The effect of rHSG-1 on the proliferation of VSMCs was investigated by cell counting, MTT assay and (3)H-thymidine incorporation. We also analyzed the cell-cycle using flow cytometry and detected the expression of p27(Kip1) and p21(Cip1) by Western Blot. RESULTS: The proliferation of VSMCs infected with Ad5rHSG-1 was inhibited a 40% reduction compared with the control group(P<0.01). The cell cycle was arrested in G(0)/G(1) phase and the expression of p27(Kip1) and p21(Cip1) was upregulated after the VSMCs transfection with Ad5rHSG-1. CONCLUSION: Adenovirus-mediated gene transfer of rHSG-1 inhibits the cell cycle progression and thus the proliferation of VSMCs from SHR.

Adenoviridae↗
PubMed2004

Electrophysiological effects of capsaicin on spontaneous activity of rabbit atrioventricular node cells.

To study the electrophysiological effects of capsaicin on spontaneous activity of rabbit atrioventricular (AV) node cells, parameters of action potential in AV node were recorded using intracellular microelectrode technique. Capsaicin (1-30 micromol/L) not only decreased the amplitude of action potential, maximal rate of depolarization (V(max)), velocity of diastolic (phase 4) depolarization, and rate of pacemaker firing, but also prolonged the duration of 90% repolarization of action potential (APD(90)) in a concentration-dependent manner. Both application of L-type Ca(2+) channel agonist Bay K8644 (0.5 micromol/L) and elevation of calcium concentration (5 mmol/L) in superfusate antagonized the effects of capsaicin on pacemaker cells. Pretreatment with ruthenium red (10 micromol/L), a capsaicin receptor blocker, did not affect the effects of capsaicin on AV node cells. Capsaicin exerted an inhibitory action on spontaneous activity of AV node cells in rabbits. These effects were likely due to reduction in calcium influx, but were not mediated by VR1.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2004

1H NMR relaxation investigation of acetylcholinesterase inhibitors from huperzine A and derivative.

The binding properties of huperzine A (1) with Torpediniforms Nacline acetylcholinesterase (TnAChE) were investigated by (1)H NMR methods. The noselective, selective and double-selective spin-lattice relaxation rates were acquired in absent and present of TnAChE at a ratio [ligand]/[protein]=1:0.005. The selective relaxation rates shown protons of 1 had dipole-dipole interaction with protein active site protons. The motional correlation time of bound ligand was calculated by double-selective relaxation rate at 1 tau(2,3)=40.5 ns at 298 K, which showed 1 had high affinity with TnAChE. The experiments give a possible method to use TnAChE to locate the new huperzine A derivatives as AChE inhibitors.

Alkaloids↗
PubMed2004

Cooperative interactions between flagellin and SopE2 in the epithelial interleukin-8 response to Salmonella enterica serovar typhimurium infection.

Flagellin is an important stimulus for epithelial interleukin-8 (IL-8) secretion because of its ability to activate Toll-like receptor 5 (TLR5). SopE2, a Salmonella guanine nucleotide exchange factor (GEF), is also involved in intestinal inflammation. To clarify the proinflammatory mechanisms of these proteins, we examined their effects on IL-8 secretion and intracellular signaling in T84 epithelial cells. A Salmonella strain lacking SopE2 (and its homolog SopE) induced lower levels of IL-8 than the wild type and exhibited reduced activation of mitogen-activated protein kinases (MAPKs). Overexpression of wild-type SopE2 in this strain restored MAPK activation and augmented IL-8 production, whereas a mutant lacking GEF activity failed to increase IL-8 expression. Additional effects on signaling were demonstrated in transient transfection experiments, in which SopE2 enhanced the ability of TRAF6, a signal transducer downstream of TLR5, to activate the NF-kappaB transcription factor in 293 cells. Flagellin was also found to be required for IL-8 induction in T84 cells. In its absence, the ability of SopE2 overexpression to increase IL-8 secretion was impaired. Part of this impairment was related to the decreased motility of the flagellin-deficient strain, but lack of flagellin also affected translocation of SopE2 into the infected cells. Our results indicate that flagellin and SopE2 interact functionally at multiple levels to increase IL-8 secretion by epithelial cells-flagellin facilitating the translocation of SopE2, and SopE2 enhancing signaling pathways activated by flagellin. These observations offer a mechanistic explanation for the involvement of these proteins in the pathogenesis of Salmonella-induced gastroenteritis.

Bacterial Proteins↗
PubMed2004

Life-long serotonin reuptake deficiency results in complex alterations in adrenomedullary responses to stress.

This study examined whether serotonin transporter (SERT) deficiency influences adrenal serotonin (5-HT), catecholamine and Angiotensin II (Ang II) systems, and the hormonal response to acute restraint stress. Control SERT mice (+/+) expressed high numbers of SERT binding sites in adrenal medulla. Fifteen minutes of restraint stress increased adrenal 5-HT, adrenomedullary tyrosine hydroxylase (TH) mRNA expression and plasma epinephrine (EPI), and norepinephrine levels without alterations in adrenal catecholamine content. In SERT+/+, these responses coincided with a significant increase in adrenomedullary Ang II AT(2) receptor expression. SERT-deficient mice did not express SERT binding sites; their adrenal 5-HT was significantly depleted and further reduced after stress. They had exaggerated stress-induced EPI release into plasma, the increase in TH transcription did not occur, adrenal catecholamine content was decreased compared with SERT+/+, and stress induced a reduction rather than increase in the number of adrenomedullary AT(2) receptors. SERT-/- mice also possessed decreased pituitary 5-HT. Their pituitary ACTH was reduced after stress, but stress-induced increases in plasma ACTH and corticosterone were not different from those of SERT+/+ mice. Our results indicate that SERT function not only restrains stress-induced EPI release but also is required for the increase in adrenal catecholamine synthesis and AT(2) receptor expression.

Adrenal Medulla↗