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Hongwei Li

Publications and source records attributed to Hongwei Li.

At least 37 records · Page 2Linked to original sources
PubMed2005

Long-term tracing of adenoviral expression in rat and rabbit using luciferase imaging.

BACKGROUND: Luciferase optical imaging provides a novel method to monitor transgene expression in small living animals. As the genetic and immunological heritages of particular animals significantly affect the expression of adenovirus-delivered transgenes, it is essential to know the expression patterns specific to athymic nude and Sprague-Dawley rats, two strains commonly used in rodent models. In this study we set out to determine these patterns. At the same time, we tested luciferase optical imaging in a larger animal, the rabbit. METHODS: A recombinant luciferase adenoviral vector was injected subcutaneously or intramuscularly into athymic nude rats, Sprague-Dawley rats, and Dutch Belted rabbits. The luciferase expression was assessed using a cooled charge-coupled device. RESULTS: The luminescent signal was capable of passing through at least 1.3 cm of muscle tissue and proved to be much stronger when luciferin was delivered via a local injection than by an intraperitoneal injection. Although the types of immune cells differed between immunodeficient and immunocompetent rats, similar amounts and patterns of luciferase expression were observed in the musculature in two rat strains during the 1st month after a viral intramuscular injection. The duration of luciferase expression was longer than 15 months in athymic nude rats, 9 months in Sprague-Dawley rats, and 6 months in rabbits following a direct viral injection. CONCLUSIONS: Luciferase expression after adenoviral gene delivery can persist for longer than 6 months, even in immunocompetent animals. Live imaging of luciferase expression can be performed not only in small animals, but also in larger animals such as rabbits.

Adenoviridae↗
PubMed2005

stx2vha is the dominant genotype of Shiga toxin-producing Escherichia coli O157:H7 isolated from patients and domestic animals in three regions of China.

Shiga toxin-producing Escherichia coli(STEC) O157: H7 strains were isolated from domestic animals and patients from Xuzhou City, Jiangsu Province, China and the bordering Anhui and Henan Provinces and were examined for the stx genotype. Of 390 strains, 277 were identified as genotype stx2vha ; 41, stx2 ; 51, stx2-stx1 ; 1, stx2-stx2vha-stx1 ; 5, stx2-stx2vha ; and 15 were un-typeable. Of the 277 stx2vha-bearing isolates, 116 were isolated from goats; 42, cattle; 38, hens, and 35 from pigs. The study shows stx2vha is the dominant genotype and goats are an important reservoir.

Animals↗
PubMed2005

Serum C-reactive protein and circulating endothelial cells in patients with acute myocardial infarction.

As an in vivo indicator of vascular injuries, circulating endothelial cells (CECs) have been used as a marker of endothelial damage in a variety of vascular disorders. C-reactive protein (CRP) is a sensitive indicator of inflammation. To investigate the presence of CECs in patients with acute myocardial infarction (AMI) and to evaluate their clinical associations and possible relationship with infection, CECs from peripheral blood were isolated by using immunomagnetic beads coated with antibodies against CD146. Their endothelial origin was confirmed by the positive labeling of von Willebrand Factor (vWF), CD31 and electron microscope. Results showed that CECs number and CRP level were 52 (28-81.5) cell/ml, 7.98+/-2.25 mg/l and 10.5 (6-16.5) cell/ml, 1.41+/-2.05 mg/l in AMI patients (n=37) and health controls (n=42) respectively (p<0.001). The apoptosis rate and necrotic rate of CECs in AMI were 25% and 19%, respectively. Correlation analysis revealed a significant positive correlation between CECs and CRP (r=0.505, p=0.001). CECs numbers did not correlate with age, gender, serum cholesterol, hypertension, obesity, history of cardiovascular disease, or smoking. These results suggest a strong correlation between level of CRP and counts of CECs in patients with AMI. The number of CECs and CRP may be combined to reflecting the endothelial cell injury.

Antigens, CD↗
PubMed2005

Soluble angiopoietin receptor Tie-2 in patients with acute myocardial infarction and its effects on angiogenesis.

Tie-2 receptor has been shown to play a role in the neovascularization of tumors, but little is known about the role it may play in acute myocardial infarction (AMI). The aims of this research are (1) To study the variety of soluble Tie-2 (sTie-2) in patients with AMI. (2) To study the effects of recombinant soluble Tie-2/Fc on HUVECs viability and tube formation in vitro. Serum levels of sTie-2 in 27 patients with AMI were measured on admission (day 1), day 2, day 3 and day 7 after onset of chest pain and 28 healthy controls by ELISA. In addition, the viability of HUVECs and tube formation area were measured after stimulated with recombinant Tie-2/Fc chimera. Median level of sTie-2 increased significantly in the AMI patients when compared with the controls and the maximum level appeared at day 2 after onset of AMI. Tie-2/Fc induced EC apoptosis and inhibited HUVEC tube formation in vitro. Results of this study showed that the level of sTie-2 increased in AMI. The effects of Tie-2/Fc on EC viability and tube formation indicated that angiogenesis might be inhibited in the acute phase of AMI.

Aged↗
PubMed2005

[Landscape ecological planning of Jiaozuo city].

With the application of the principles of landscape ecology and the techniques of geographic information systems, the landscape of Jiaozuo city was divided into six types, i. e., farmland, garden plot, woodland, residential and industrial area, waters, and others. The landscape diversity, dominance, fragmentation, and isolation indexes were calculated by models and GIS to analyze the spatial patterns of these landscape types. Based on the optimization of landscape spatial patterns, a pattern for developing a rational and natural ecosystem in Jiaozuo city was proposed, i. e., keeping four or five large natural patches, planning small artificial green patches, linking the large and small patches by various corridors to ensure the ecosystem inside the city to circulate well, combining residential areas properly to form a urban troop with Jiaozuo town as the center and with seven surrounding towns joined through highways to form a network city pattern. After doing these, urban built-up areas could be linked each other, and inlayed in a natural ecological matrix. This pattern could strengthen the ecological connection, raise the stability of the ecosystem, and maintain the balance of urban ecological system.

China↗
PubMed2004

Macrophage migration inhibitory factor: an intracellular inhibitor of angiotensin II-induced increases in neuronal activity.

Angiotensin II (Ang II) elicits Ang II type 1 receptor (AT1-R)-mediated increases in neuronal firing within the hypothalamus and brainstem that are ultimately responsible for physiological actions such as increased blood pressure and fluid intake. Although there is a growing literature on the intracellular mechanisms that mediate the actions of Ang II via AT1-R in neurons, little is known about the mechanisms that diminish or "switch-off" the neuronal chronotropic action of Ang II. In the present study, we identified macrophage migration inhibitory factor (MIF) as an intracellular inhibitor of the actions of Ang II in neurons. The evidence is as follows. First, Ang II, acting via AT1-R, increases the intracellular levels of MIF in neurons cultured from rat hypothalamus and brainstem. Second, elevation of intracellular MIF by Ang II prevents further chronotropic actions of this peptide. Third, intracellular application of exogenous recombinant MIF abolishes the Ang II-induced chronotropic action in neurons. Finally, intracellular application of the MIF peptide fragment MIF-(50-65), which harbors the thiol oxidoreductase property of the MIF molecule, mimics the inhibitory actions of MIF on Ang II-stimulated neuronal firing. Thus, this study is the first to demonstrate the existence of an intracellular negative regulator of Ang II-induced actions in neurons and indicates that MIF may act as a physiological brake for the chronotropic effects of Ang II in rat neurons.

Action Potentials↗
PubMed2004

RNA silencing: a conserved antiviral immunity of plants and animals.

RNA silencing is a novel RNA-guided gene regulatory mechanism operational in a wide range of eukaryotic organisms from fission yeast, plants, to mammals. This article reviews the recent progress on aspects of RNA silencing that are related to its biological function as a conserved antiviral immunity of plants and animals, and highlights features of this novel antiviral response in invertebrate animals as compared to the known innate and adaptive immunities. Finally, we discuss evidence that suggests a natural antiviral role for RNA silencing in vertebrates as well as experimental approaches that may facilitate the identification of first mammalian viral suppressors of RNA silencing.

Animals↗
PubMed2004

Interferon antagonist proteins of influenza and vaccinia viruses are suppressors of RNA silencing.

Homology-dependent RNA silencing occurs in many eukaryotic cells. We reported recently that nodaviral infection triggers an RNA silencing-based antiviral response (RSAR) in Drosophila, which is capable of a rapid virus clearance in the absence of expression of a virus-encoded suppressor. Here, we present further evidence to show that the Drosophila RSAR is mediated by the RNA interference (RNAi) pathway, as the viral suppressor of RSAR inhibits experimental RNAi initiated by exogenous double-stranded RNA and RSAR requires the RNAi machinery. We demonstrate that RNAi also functions as a natural antiviral immunity in mosquito cells. We further show that vaccinia virus and human influenza A, B, and C viruses each encode an essential protein that suppresses RSAR in Drosophila. The vaccinia and influenza viral suppressors, E3L and NS1, are distinct double-stranded RNA-binding proteins and essential for pathogenesis by inhibiting the mammalian IFN-regulated innate antiviral response. We found that the double-stranded RNA-binding domain of NS1, implicated in innate immunity suppression, is both essential and sufficient for RSAR suppression. These findings provide evidence that mammalian virus proteins can inhibit RNA silencing, implicating this mechanism as a nucleic acid-based antiviral immunity in mammalian cells.

Animals↗
PubMed2004

Nitration and functional loss of voltage-gated K+ channels in rat coronary microvessels exposed to high glucose.

Coronary microvessels generate reactive oxygen species in response to high glucose (HG), resulting in vasodilator defects involving an impaired function of vascular K(+) channels. Inhibition of voltage-gated K(+) (K(v)) channels by peroxynitrite (ONOO(-)), formed by the interaction of superoxide and nitric oxide, may contribute to impaired dilation. The present study investigated whether HG induces ONOO(-) formation to mediate nitration and impairment of K(v) channels in rat small coronary arteries (RSCAs). Exposure to ONOO(-) reduced the dilator influence of K(v) channels in RSCAs. Patch-clamp studies revealed that ONOO(-) diminished whole-cell and unitary K(v) currents attributable to the K(v)1 gene family in smooth muscle cells. Subsequently, immunohistochemically detected enhancement of nitrotyrosine residues in RSCAs that were cultured in HG (23 mmol/l) compared with normal glucose (5.5 mmol/l) for 24 h correlated with the nitration of K(v)1.2 channel alpha-subunits. HG-induced nitrotyrosine formation was partially reversed by scavenging ONOO(-). Finally, RSCAs that were exposed to HG for 24 h showed a loss of K(v) channel dilator influence that also was partially restored by the ONOO(-) scavengers urate and ebselen. We conclude that ONOO(-) generated by HG impairs K(v) channel function in coronary microvessels, possibly by nitrating tyrosine residues in the pore-forming region of the K(v) channel protein.

Animals↗
PubMed2004

[Structural basis of alpha-tocopherol succinate as an antineoplastic agent].

Alpha-tocopherol succinate is a redox-silent analog of alpha-tocopherol which is the major component of vitamin E. Recently, the research findings showed that, as a kind of pro-vitamin E, alpha-tocopherol succinate possesses antineoplastic activity which alpha-tocopherol lacks of. In this review paper, the link between the structure and antineoplastic activity of alpha-tocopherol succinate was focused.

Antineoplastic Agents↗
PubMed2003

Synergistic effects of coactivators GRIP1 and beta-catenin on gene activation: cross-talk between androgen receptor and Wnt signaling pathways.

The p160 coactivators, such as GRIP1, bind nuclear receptors and help to mediate transcriptional activation. beta-Catenin binds to and serves as a coactivator for the nuclear receptor, androgen receptor (AR), and the Lymphoid Enhancer Factor/T Cell Factor family member, Lef1. Here we report that GRIP1 and beta-catenin can bind strongly to each other through the AD2 domain of GRIP1. Furthermore, GRIP1 and beta-catenin can synergistically enhance the activity of both AR and Lef1, and both coactivators are recruited specifically to AR-driven and Lef1-driven promoters. However, the mechanism of beta-catenin-GRIP1 coactivator function and synergy is different with AR and Lef1. While beta-catenin can bind directly to both AR and Lef1, GRIP1 can only bind directly to AR; the ability of GRIP1 to associate with and function as a coactivator for Lef1 is entirely dependent on the presence of beta-catenin. Thus, whereas GRIP1 coactivator function involves direct binding to nuclear receptors and most other classes of DNA-binding transcriptional activator proteins, the coactivator function of GRIP1 with Lef1 follows a novel paradigm where GRIP1 is recruited indirectly to Lef1 through their mutual association with beta-catenin. The beta-catenin-GRIP1 interaction represents another potential point of cross-talk between the AR and Wnt signaling pathways.

Animals↗
PubMed2003

Mitochondrial sources of H2O2 generation play a key role in flow-mediated dilation in human coronary resistance arteries.

We previously showed that hydrogen peroxide (H2O2) contributes to flow-induced dilation in human coronary resistance arteries (HCRAs); however, the source of this H2O2 is not known. We hypothesized that the H2O2 is derived from superoxide (O2*-) generated by mitochondrial respiration. HCRAs were dissected from right atrial appendages obtained from patients during cardiac surgery and cannulated with micropipettes. H2O2-derived radicals and O2*- were detected by electron spin resonance (ESR) using BMPO as the spin trap and by histofluorescence using hydroethidine (HE, 5 micromol/L) and dichlorodihydrofluorescein (DCFH, 5 micromol/L). Diameter changes to increases in pressure gradients (20 and 100 cm H2O) were examined in the absence and the presence of rotenone (1 micromol/L), myxothiazol (100 nmol/L), cyanide (1 micromol/L), mitochondrial complex I, III, and IV inhibitors, respectively, and apocynin (3 mmol/L), a NADPH oxidase inhibitor. At a pressure gradient of 100 cm H2O, ubisemiquinone and hydroxyl radicals were detected from effluents of vessels. Including superoxide dismutase and catalase in the perfusate reduced the ESR signals. Relative ethidium and DCFH fluorescence intensities in HCRAs exposed to flow were enhanced (1.45+/-0.15 and 1.57+/-0.12, respectively compared with no-flow) and were inhibited by rotenone (0.87+/-0.17 and 0.95+/-0.07). Videomicroscopic studies showed that rotenone and myxothiazol blocked flow-induced dilation (% max. dilation at 100 cm H2O: rotenone, 74+/-3% versus 3+/-13%; myxothiazol, 67+/-3% versus 28+/-4%; P<0.05). Neither cyanide nor apocynin altered flow-induced dilation. These results suggest that shear stress induced H2O2 formation, and flow-induced dilation is derived from O2*- originating from mitochondrial respiration.

Coronary Circulation↗
PubMed2003

Elevated glucose impairs cAMP-mediated dilation by reducing Kv channel activity in rat small coronary smooth muscle cells.

Hyperglycemia impairs endothelium-dependent vasodilation. In this study, we examined the effect of high glucose (HG) on vascular smooth muscle function. Rat small coronary arteries were freshly isolated or incubated for 24 h with normal glucose (NG; 5.5 mmol/l) or HG (23 mmol/l). In freshly isolated arteries, dilation to isoproterenol (Iso) was reduced by 3 mmol/l 4-aminopyridine (4-AP; 44 +/- 10% vs. 77 +/- 4%; P < 0.05) and further reduced by 4-AP + iberiotoxin (IbTX; 100 nmol/l; 17 +/- 2%). Dilation to forskolin was abolished by 4-AP (-3 +/- 17 vs. 73 +/- 9%). cAMP production was similar in NG and HG vessels. Dilations to Iso and forskolin were significantly reduced in HG arteries (Iso, 41 +/- 5% vs. 70 +/- 6%; forskolin, 40 +/- 4% vs. 75 +/- 4%) compared with NG arteries. A similar reduction was also observed to the dilation to papaverine. Endothelial denudation had no effect on Iso-induced dilation. In HG vessels, the reduced 4-AP-sensitive component of Iso-induced dilation was greater compared with the IbTX-sensitive component. Iso increased whole cell K+ current in NG cells but had little effect in HG cells. Similarly, 4-AP-, but not IbTX-sensitive, K+ currents were reduced in HG cells. These results suggest that HG impairs cAMP-mediated dilation primarily by reducing Kv channel function. We speculate that in addition to the endothelial dysfunction, altered smooth muscle function may also contribute to the reduced coronary vasodilation in diabetes.

4-Aminopyridine↗
PubMed2003

[Study on drug release after arterial embolism with cisplain-loaded albumin microspheres in treating carcinoma of tongue].

OBJECTIVE: The purpose of this study was to investigate the cisplatin release in peripheral blood and tumor tissue after cisplatin-loaded albumin microspheres (CDDP-AMS) were infused through lingual artery for treating carcinoma of tongue. METHODS: Anticancer agent cisplatin was encapsulated with biodegradable and non-antigenic albumin. The cisplatin-loaded albumin microspheres, which were 56.3 microns in diameter, were used for treating 7 patients with squamous carcinoma of tongue by infusing through lingual artery. The cisplatin in peripheral venous blood and carcinoma tissue were measured for analyzing the drug release in vivo. RESULTS: Concentration of the drug in peripheral venous blood increased to the highest level in 90 minutes after CDDP-AMS was infused through lingual arterial and still could be detected until 10th day. The cisplatin concentration in tumor tissue kept considerably stable and could be detected until 17 days. CONCLUSION: CDDP-AMS had the effect of controlled release in vive. Effective and steady local drug concentration played the role of killing tumor cells, the low concentration in peripheral blood reduced the side effects of cisplatin to minimum as well. It is concluded that CDDP-AMS is a useful and recommendable method for treating the carcinoma of tongue.

Adult↗
PubMed2003

Osteogenesis in rats induced by a novel recombinant helper-dependent bone morphogenetic protein-9 (BMP-9) adenovirus.

BACKGROUND: Although recombinant first-generation BMP adenoviruses can induce ectopic bone formation in immune deficient animals, the osteoinductive activity of these BMP vectors is reduced in immune competent animals. Helper-dependent adenoviral vectors have been developed to decrease the immune response and, therefore, increase gene expression in immune competent animals compared with first-generation vectors. In the present study, the osteoinductive activity of a helper-dependent GFP and BMP-9 adenoviral vector (ADGBMP9) was evaluated in vitro and in vivo. METHODS: Initially, purified ADGBMP9 was used to transduce human mesenchymal stem cells (hMSCs) and the alkaline phosphatase activity was determined as a measure of osteogenic activity. The vector was then injected into the thigh muscle of athymic nude and Sprague-Dawley rats, and CT scans and histology were subsequently used to assess bone formation. RESULTS: In vitro, ADGBMP9 was capable of inducing alkaline phosphatase expression in hMSCs. In vivo in athymic nude and Sprague Dawley rats, ADGBMP9 initiated the process of bone formation 3 days after percutaneous injection into the thigh musculature. The rats demonstrated intramuscular ectopic ossification in CT scans as early as day 9 post viral injection and ultimately formed significant amounts of ectopic bone. Histologically, the induced bone was formed via normal endochondral mechanisms. CONCLUSIONS: A helper-dependent adenoviral vector containing the BMP-9 and GFP genes has significant osteoinductive activity in both athymic nude and immune competent rats. Additional direct and ex vivo BMP gene therapy studies are required to assess the vector's activity in more animal models.

Adenoviridae↗
PubMed2003

Rat strain differences in the ectopic osteogenic potential of recombinant human BMP adenoviruses.

Different animal strains have different genetic backgrounds that influence their physiological function and pathological process. The differences in genetic background may affect the efficiency of adenoviral infection and target gene expression and further cause different gene therapy results when target genes are delivered with adenoviral vectors. In this study, ectopic bone was not seen in ADCMVBMP4 injection sites, but was formed in ADCMVBMP9 injection sites in all rat strains. The mean volumes of bone induced with ADCMVBMP9 were 0.87 +/- 0.2 cm3 in Wistar, 0.26 +/- 0.1 cm3 in Long-Evans, 0.34 +/- 0.2 cm3 in Sprague-Dawley, 0.44 +/- 0.1 cm3 in ACI, 0.66 +/- 0.2 cm3 in PVG, and 0.58 +/- 0.1 cm3 in Fischer 344 rats. This indicates that ADCMVBMP9 has different bone formation potentials in different immunocompetent rat strains (P = 0.02). The basic levels of CD4+ and CD8+ T cells in blood before viral infection and titers of adenoviral neutralizing antibodies 30 days post-viral infection were significantly different among rat strains (P < 0.01). The efficiencies of target gene expression delivered with adenovirus were also significantly different in primary muscle cell cultures from different rat strains (P < 0.01). The different osteogenic potentials of ADCMVBMP9 among rat strains may be, in part, due to the differences in immune factors and target gene expression efficiency in muscle tissue.

Adenoviridae↗
PubMed2003

CoCoA, a nuclear receptor coactivator which acts through an N-terminal activation domain of p160 coactivators.

The p160 coactivators bind to and potentiate transcriptional activation by nuclear receptors by recruiting secondary coactivators such as the histone acetyltransferases p300 and CBP and the protein methyltransferase CARM1. The function of the highly conserved N-terminal basic-helix-loop-helix/Per-Arnt-Sim (bHLH-PAS) domain of p160 coactivators is unknown. This region is required for coactivator synergy among p160, p300, and CARM1 coactivators. We identified a coactivator, coiled-coil coactivator (CoCoA), which binds to this domain and thereby enhances transcriptional activation by the estrogen receptor and other nuclear receptors. Endogenous CoCoA was found simultaneously with p160 coactivators on the promoter of an endogenous estrogen-responsive gene. Reduction of endogenous cellular CoCoA levels inhibited the estrogen-stimulated expression of transiently transfected and endogenous genes. Moreover, CoCoA cooperated synergistically with GRIP1, CARM1, and p300 to enhance ER-mediated transcription. Thus, the N-terminal region of p160 coactivators contains an additional activation domain which contributes to coactivator function by recruitment of CoCoA.

Amino Acid Sequence↗