Hong Li

Publications (54)125.12 Total impact

• Article: [Identification of human small supernumerary marker chromosomes and discussion of its research value].

  Jian Ou, Wei Wang, Chengying Duan, Wenyu Fu, Yilin Liu, Jian Sun, Hongling Zhong, Hong Li
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  ABSTRACT: To identify the origin of human small supernumerary marker chromosomes (sSMCs) using fluorescent in situ hybridization (FISH) combined with G-banding karyotype analysis, and to discuss their mechanisms of formation and research value. Cep-FISH and SubcenM-FISH were used to analyze sSMCs in 3 patients for whom the result of G-banding was 47,XN,+mar. The FISH result of case 1 was 47,XY,+mar.ish inv dup(22)(q11.1)(D22Z4++,D14/22Z1+, RP11-172D7-). The marker has formed exclusively by heterochromatin. A boy was delivered later with no apparent clinical abnormalities. The FISH result of case 2 was 47,XX,+mar.ish r(10)(p11.2q11.2) (cep10+, RP11-232C13+, RP11-178A10+)[25]/46,XX[10]. The marker has formed by heterochromatin and nearby centromere. A girl was delivered later with no clinical abnormalities. The FISH result of case 3 was 47,XY,+mar.ish inv dup(22)(q11.1)(D22Z4+,D14/22Z1+). The marker has also formed exclusively by euchromatin. Fetal abnormalities were detected by type B ultrasonography, but were not necessarily related with the marker. The diversity of sSMCs has posed a great challenge for prenatal diagnosis. Identification of sSMCs will require combined karyotype analysis and FISH or other molecular techniques such as microarray based comparative genomic hybridization or sequencing. For its specific structure, the sSMCs may also provide a valuable tool for gene mapping, heterochromatin research and gene therapy.
  Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 02/2013; 30(1):91-4.
• Article: Are rabbits a suitable model to study sheep-associated malignant catarrhal fever in susceptible hosts?

  Cristina W Cunha, Donal O'Toole, Naomi S Taus, Donald P Knowles, Hong Li
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  ABSTRACT: Sheep-associated malignant catarrhal fever (SA-MCF), caused by ovine herpesvirus 2 (OvHV-2), is an often fatal syndrome affecting mainly ruminants. SA-MCF pathogenesis and vaccine studies rely solely on live animals, since OvHV-2 has not been successfully propagated in vitro. Thus, the identification of a laboratory animal model is desirable and necessary to accelerate the identification of virus-host interactions that lead to disease. Rabbits are susceptible to infection with OvHV-2 and the disease can be reliably induced experimentally; however, the viral dynamics and host immune responses in the context of SA-MCF development in rabbits have not yet been evaluated. We addressed these knowledge gaps by experimentally infecting rabbits with OvHV-2 and monitoring viral and host infection parameters. Following intranasal nebulization of OvHV-2 in rabbits, the virus transiently replicates in the lungs inducing only subtle local inflammatory responses; the virus then disseminates systemically and increased levels of viral DNA and transcripts can be detected in multiple tissues as disease develops. The severity of lesions was shown to increase with both viral DNA copy number and expression levels of ORF25, ORF50 and ORF73. The events observed in rabbits following OvHV-2 infection occurred in the same fashion previously reported in bison, a natural clinically susceptible host. The results of this study in conjunction with previous reports demonstrate that rabbits are a valuable model for SA-MCF pathogenesis and vaccine studies.
  Veterinary Microbiology 01/2013; · 3.33 Impact Factor
• Article: Development of an in vivo system to measure antibody-blocking of ovine herpesvirus 2 entry.

  Hong Li, Cristina W Cunha, Donal O'Toole, Anthony V Nicola, Donald P Knowles, Naomi S Taus
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  ABSTRACT: Ovine herpesvirus 2 (OvHV-2), the causative agent of sheep-associated malignant catarrhal fever (SA-MCF), has never been propagated in vitro. Thus, an alternative to in vitro virus neutralization is needed to assess neutralizing antibody activity to OvHV-2 in SA-MCF vaccine development. An in vivo system in sheep and rabbits was evaluated to determine whether it could be used to assess the ability of antibodies to block OvHV-2 at the entry site by mixing virus and anti-OvHV-2 serum before challenge by intranasal nebulization. A dose of OvHV-2 (10(6) viral DNA copies) incubated with sheep sera (1:4 final dilution) at 37°C for 1 hr was delivered by intranasal nebulization to sheep and rabbits. All sheep became infected, but the positive serum reduced viral infectivity by approximately 1,000 fold based on delayed detection of viral DNA and seroconversion as compared to the negative control group, which received virus treated with negative sheep serum. All rabbits that received the virus mixed with the positive sheep serum, either with or without complement, were protected from the infection while all rabbits in the control groups developed SA-MCF. The data indicate that this type of in vivo system, sheep or rabbits, can be used to assess antibody's ability to block OvHV-2 entry, which is a significant tool for the analysis of protective antibody responses to the virus.
  Journal of virological methods 12/2012; · 2.13 Impact Factor
• Article: Characterization of three small supernumerary marker chromosomes (sSMC) in humans.

  Jian Ou, Wei Wang, Thomas Liehr, Elisabeth Klein, Ahmed B Hamid, Fuxin Wang, Chengying Duan, Hong Li
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  ABSTRACT: In the present study, three prenatally detected small supernumerary marker chromosomes (sSMC) were identified by banding cytogenetics and characterized in detail by molecular cytogenetics. In one case an sSMC(10) leading to a pericentric partial trisomy and in two cases heterochromatic sSMC derived from chromosome 22 were characterized. Outcomes were reportedly normal for two of the three cases for whom this information was known.
  The journal of maternal-fetal & neonatal medicine: the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians 09/2012; · 1.36 Impact Factor
• Article: Shear stress augments the endothelial cell differentiation marker expression in late EPCs by upregulating integrins.

  Xiaodong Cui, Xiaoyun Zhang, Xiumei Guan, Hong Li, Xin Li, Hongyin Lu, Min Cheng
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  ABSTRACT: Vascular endothelial cell injury has been implicated in the onset of atherosclerosis. A number of previous studies have demonstrated that endothelial progenitor cells (EPCs), in particular late EPCs, play important roles in endothelial maintenance and repair. Recent evidence has revealed shear stress as a key regulator for EPC differentiation. However, the detailed events that contribute to the shear stress-induced EPC differentiation, in particular the mechanisms of mechanotransduction, remain to be identified. The present study was undertaken to further confirm the effects of shear stress on the late EPC differentiation, and to investigate the role of integrins in this procedure. Shear stress was observed to increase the expression of endothelial cell differentiation markers, such as vWF and CD31, in late EPCs isolated from rat bone marrow. Shear stress moreover enhanced the mRNA expression of integrin subunits β(1) and β(3) in a time-dependent manner, and also upregulated specific integrins in late EPCs plated on substrates containing various extracellular matrix (ECM) proteins. In addition, the shear stress-induced vWF and CD31 expression were found to be related to the levels of integrin β(1) and β(3), and were inhibited in late EPCs treated with RGD peptide (Gly-Arg-Gly-Asp-Asn-Pro, GRGDNP) that blocks the binding of integrins to the extracellular matrix. Additionally, this increase was also attenuated by both anti-β(1) integrin and anti-β(3) integrin antibodies. The integrin subunits β(1) and β(3) thus play important roles in regulating the shear stress-induced endothelial cell differentiation marker expression in late EPCs. This may provide novel insights into the mechanisms of mechanotransduction in shear stress-mediated late EPC differentiation.
  Biochemical and Biophysical Research Communications 07/2012; 425(2):419-25. · 2.48 Impact Factor
• Article: Hyperglycaemia exerts deleterious effects on late endothelial progenitor cell secretion actions.

  Jie Zhang, Xiaoyun Zhang, Hong Li, Xiaodong Cui, Xiumei Guan, Kexin Tang, Chengwen Jin, Min Cheng
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  ABSTRACT: Endothelial progenitor cells (EPCs) play a fundamental role in tissue regeneration and vascular repair both by differentiating into endothelial cells and by secretion of vasoactive substances that promote angiogenesis and maintain vascular homeostasis. It has previously been shown that hyperglycaemia impairs early and late EPC functions, such as differentiation, proliferation and adhesion. However, its role in the regulation of the production of vasoactive substances in EPCs, especially in late EPCs, is less well defined. We investigated the effects of hyperglycaemia on the production of vasodilator, fibrinolytic and angiogenic growth factors, and also on the activity of superoxide dismutase (SOD) in late EPCs. For this purpose, late EPCs were incubated with different concentrations of D-glucose (5-40 mmol/L) for 24 hr. Levels of nitric oxide (NO), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), prostaglandin I(2) (PGI(2)), vascular endothelial growth factor (VEGF) and the activity of SOD were measured by enzyme-linked immunosorbent assay (ELISA). Under high glucose stress conditions, late EPCs exhibited lower levels of NO, t-PA, PAI-1, PGI(2) and VEGF compared to control medium (5 mmol/L glucose). Moreover, high glucose was also observed to decrease the activity of SOD in late EPCs. These results suggest that hyperglycaemia-induced impairment of late EPC secretion functions could contribute to the development of vascular disease in diabetes.
  Diabetes & Vascular Disease Research 05/2012; · 2.12 Impact Factor
• Source

  Available from: PubMed Central

  Article: Advanced glycation end products impair the migration, adhesion and secretion potentials of late endothelial progenitor cells.

  Hong Li, Xiaoyun Zhang, Xiumei Guan, Xiaodong Cui, Yuliang Wang, Hairong Chu, Min Cheng
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  ABSTRACT: Endothelial progenitor cells (EPCs), especially late EPCs, play a critical role in endothelial maintenance and repair, and postnatal vasculogenesis. Advanced glycation end products (AGEs) have been shown to impair EPC functions, such as proliferation, migration and adhesion. However, their role in the regulation of the production of vasoactive substances in late EPCs is less well defined. Passages of 3~5 EPCs, namely late EPCs, were cultured with different concentrations (0~500 μg/ml) of AGEs, and the apoptosis, adhesion and migration were subsequently determined. The release of vasoactive substances, such as stromal cell-derived factor-1 (SDF-1), nitric oxide (NO), prostaglandin I2 (PGI2), plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (tPA), and in addition the activity of superoxide dismutase (SOD), were evaluated by ELISA. At the same time, the gene and protein expressions of CXCR4 were assayed by real-time RT-PCR and western-blot. AGEs promoted late EPC apoptosis. Moreover, AGEs impaired late EPC migration and adhesion in a concentration-dependent manner. Accordingly, the production of SDF-1 was decreased by AGEs. Although the CXCR4 expressions of late EPCs were up-regulated for AGE concentrations of 50, 100 or 200 μg/ml, a marked decrease was observed for the higher concentration of 500 μg/ml. Furthermore, co-culturing with AGEs decreased the levels of NO, t-PA, PGI2, and the activity of SOD but up-regulated the production of PAI-1. Our data provide evidence that AGEs play an important role in impairing late EPC functions, which could contribute to the development of vascular diseases in diabetes.
  Cardiovascular Diabetology 04/2012; 11:46. · 3.35 Impact Factor
• Article: Expression patterns and potential roles of SIRT1 in human medulloblastoma cells in vivo and in vitro.

  Jing-Xin Ma, Hong Li, Xiao-Ming Chen, Xiang-Hong Yang, Qian Wang, Mo-Li Wu, Qing-You Kong, Zai-Xia Li, Jia Liu
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  ABSTRACT: Medulloblastoma is a primitive neuroectodermal tumor, which originates in the cerebellum, presumably due to the alterations of some neurogenetic elements. Sirtuin 1 (SIRT1), a class III histone deacetylase (HDAC), regulates differentiation of neuronal stem cells but its status in medulloblastomas remains largely unknown. The current study aimed to address this issue by checking SIRT1 expression in noncancerous cerebellar tissues, medulloblastoma tissues and established cell lines. The roles of SIRT1 in proliferation and survival of UW228-3 medulloblastoma cells were analyzed by SIRT1 small interfering RNA (siRNA) transfection and SIRT1 inhibitor nicotinamide treatment. The results revealed that the frequency of SIRT1 expression in medulloblastoma tissues was 64.17% (77/120), while only one out of seven tumor-surrounding noncancerous cerebellar tissues showed restricted SIRT1 expression in the cells within the granule layer. Of the three morphological subtypes, the rates of SIRT1 detection in the large cell/anaplastic cell (79.07%; 34/43) and the classic medulloblastomas (60.29%; 41/68) are higher than that (22.22%; 2/9) in nodular/desmoplastic medulloblastomas (P < 0.01 and P < 0.05, respectively). Heterogeneous SIRT1 expression was commonly observed in classic medulloblastoma. Inhibition of SIRT1 expression by siRNA arrested 64.96% of UW228-3 medulloblastoma cells in the gap 1 (G1) phase and induced 14.53% of cells to apoptosis at the 48-h time point. Similarly, inhibition of SIRT1 enzymatic activity with nicotinamide brought about G1 arrest and apoptosis in a dose-related fashion. Our data thus indicate: (i) that SIRT1 may act as a G1-phase promoter and a survival factor in medulloblastoma cells; and (ii) that SIRT1 expression is correlated with the formation and prognosis of human medulloblastomas. In this context, SIRT1 would be a potential therapeutic target of medulloblastomas.
  Neuropathology 04/2012; · 2.02 Impact Factor
• Article: Andrographolide exerted its antimicrobial effects by upregulation of human β-defensin-2 induced through p38 MAPK and NF-κB pathway in human lung epithelial cells.

  Zhen-Jun Shao, Xiao-Wei Zheng, Ting Feng, Juan Huang, Jian Chen, Yi-Ying Wu, Li-Ming Zhou, Wen-Wei Tu, Hong Li
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  ABSTRACT: Andrographis paniculata (Burm. f) Nees is a traditional herbal medicine for the treatment of infection and inflammation in China. Andrographolide (andro) is one of the major components. Human β-defensin-2 (hBD-2) is an inducible antimicrobial peptide that plays an important role in innate immunity. The present study aimed to investigate the effect of andro on upregulation of hBD-2 and the key signaling pathways involved in andro-induced hBD-2 expression. Real-time reverse transcription - PCR and Western blot assays showed that andro (1.0-10 µmol/L) can upregulate the expression of hBD-2 in a dose-dependent manner. Further studies suggested that hBD-2 mRNA and protein expression in responsive to andro were attenuated by pretreatment with SB203580 (an inhibitor of p38 mitogen-activated protein kinase (p38 MAPK)), MG-132 (an inhibitor of nuclear factor κB (NF-κB)), and an NF-κB activator inhibitor, but not by an inhibitor of ERK (PD98059) or by an inhibitor of JNK(SP600125). Moreover, we found that a second p38 MAPK inhibitor (SB202190) significantly blocked andro-mediated hBD-2 induction in SPC-A-1 lung epithelial cells. Finally, the p-c-Jun transcription factor activity assay also showed that AP-1 activity was induced by andro compared with the untreated group. We conclude that andro may exert its antimicrobial effects by upregulating the expression of hBD-2 through the p38 MAPK and NF-κB pathway.
  Canadian Journal of Physiology and Pharmacology 04/2012; 90(5):647-53. · 1.95 Impact Factor
• Article: Distinct sulfonation activities in resveratrol-sensitive and resveratrol-insensitive human glioblastoma cells.

  Zheng Sun, Hong Li, Xiao-Hong Shu, Hui Shi, Xiao-Yan Chen, Qing-You Kong, Mo-Li Wu, Jia Liu
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  ABSTRACT: Glioblastoma multiforme (GBM) cells show different responses to resveratrol, for unknown reasons. Our data from human medulloblastoma cells and primary cultures of rat brain cells revealed an inverse correlation of sulfonation activity with resveratrol sensitivities, providing a clue to the underlying mechanisms of the variable sensitivities of GBM cells to resveratrol. In this study, we found that U251 cells were sensitive and LN229 cells were insensitive to resveratrol. Thus, these two cell lines were taken as comparable models for elucidating the influence of sulfonation activities on resveratrol sensitivity. HPLC showed identical resveratrol metabolic patterns in both cell lines. LC/MS and high-resolution mass MS analyses further demonstrated that resveratrol monosulfate generated by sulfotransferases (SULTs) was the major metabolite of human GBM cells. The levels of brain-associated SULT (SULT1A1, SULT1C2, and SULT4A1) expression in U251 cells were lower than those in LN229 cells, suggesting the inverse relationship of SULT-mediated sulfonation activity with high intracellular resveratrol bioavailability and resveratrol sensitivity of human GBM cells. Furthermore, immunohistochemical staining revealed reductions in expression of the three brain-associated SULTs in 72.8%, 47.5% and 66.3% of astrocytomas, respectively. Therefore, the levels of brain-associated SULTs and sulfonation activity mediated by them could be important parameters for evaluating the potential response of human GBM cells to resveratrol, and may have value in the personalized treatment of GBMs with resveratrol.
  FEBS Journal 04/2012; 279(13):2381-92. · 3.79 Impact Factor
• Article: Human serum albumin-coated lipid nanoparticles for delivery of siRNA to breast cancer.

  Longzhu Piao, Hong Li, Lesheng Teng, Bryant C Yung, Yasuro Sugimoto, Robert W Brueggemeier, Robert J Lee
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  ABSTRACT: Human serum albumin (HSA)-coated lipid nanoparticles (HSA-LNPs) loaded with phrGFP-targeted siRNA (HSA-LNPs-siRNA) were prepared and evaluated for gene downregulation effect in phrGFP-transfected breast cancer cells and the corresponding xenograft tumor model. HSA-LNPs-siRNA were successfully prepared with a particle size of 79.5±5.5 nm. In phrGFP-transfected MCF-7 cells, HSA-LNPs-siRNA significantly decreased cell fluorescence even in the presence of fetal bovine serum (FBS). Moreover, cell fluorescence and phrGFP mRNA expression were significantly downregulated by HSA-LNPs-siRNA in phrGFP-transfected MCF-7, MDA-MB-231, and SK-BR-3 cells in comparison with control or HSA-LNPs-siRNA (scrambled). In phrGFP-transfected MCF-7 xenograft tumor model, tumor fluorescence was significantly decreased after three IV administrations of HSA-LNPs-siRNA at a dose of 3 mg/kg in comparison with siRNA alone. HSA-LNPs-siRNA demonstrated a superior pharmacokinetic profile in comparison with siRNA at a dose of 1mg/kg. These results show that the novel nonviral carrier, HSA-LNPs, may be used for the delivery of siRNA to breast cancer cells.
  Nanomedicine: nanotechnology, biology, and medicine 04/2012; · 5.44 Impact Factor
• Article: Elevated profiles of Th22 cells and correlations with Th17 cells in patients with immune thrombocytopenia.

  Yu Hu, Haiyan Li, Lei Zhang, Baozhong Shan, Xingfang Xu, Hong Li, Xinguang Liu, Shuqian Xu, Shuang Yu, Daoxin Ma, Jun Peng, Ming Hou
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  ABSTRACT: T-helper (Th) 22 and Th17 cells are implicated in the pathogenesis of autoimmune diseases. However, the role of Th22 cells in the pathophysiology of immune thrombocytopenia (ITP) remains unclear. Th22, Th17 and Th1 cells in both ITP patients and healthy controls were examined by flow cytometry. Plasma interleukin-22 (IL-22) level was measured by enzyme linked immunosorbent assay (ELISA). Signal transducers and activators of transcription 3 (STAT-3) and transcription factor RAR-related organ receptor C (RORC) messenger RNA (mRNA) expressions were examined by quantitative reverse transcription polymerase chain reaction (RT-PCR). Th22 cells, Th17 cells, Th1 cells and plasma IL-22 were significantly higher in ITP patients than in healthy controls. Moreover, Th22 cells showed a positive correlation with the levels of plasma IL-22 as well as Th17 and Th1 cells in ITP patients. Significant up-regulations of both STAT-3 and RORC transcription factors were also observed. Additionally, the percentage of Th22 cells was higher in autoantibody-negative ITP patients than in autoantibody-positive patients. Our results demonstrate a possible role of Th22 cells in ITP, and thus, the blockade of IL-22 may be a reasonable therapeutic strategy for ITP.
  Human immunology 04/2012; 73(6):629-35. · 2.55 Impact Factor
• Article: Experimental induction of malignant catarrhal fever in pigs with ovine herpesvirus 2 by intranasal nebulization.

  Hong Li, Angela Brooking, Cristina W Cunha, Margaret A Highland, Donal O'Toole, Donald P Knowles, Naomi S Taus
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  ABSTRACT: Malignant catarrhal fever (MCF), a frequently fatal herpesviral disease primarily of ruminant species, has been sporadically reported in pigs. All cases of naturally occurring porcine MCF reported to date have been linked to ovine herpesvirus 2 (OvHV-2), a gammaherpesvirus in the genus Macavirus carried by sheep. Experimental induction of MCF by aerosolization of the virus in nasal secretions collected from infected sheep has been successful in bison, cattle and rabbits. The goals of this study were to determine the susceptibility of pigs to MCF following experimental intranasal inoculation of OvHV-2, and to characterize the disease. Twelve pigs in four groups were nebulized with 10(5), 10(6), 10(7), or 10(8) DNA copies of OvHV-2 from sheep nasal secretions. Three control pigs were nebulized with nasal secretions from uninfected sheep. Three additional pigs were inoculated intravenously with 10(7) DNA copies of OvHV-2 to evaluate this route of infection with cell-free virus. Seven of twelve intranasally challenged pigs became infected with OvHV-2. Five of these seven, all in higher dose groups, developed MCF. Lesions resembled those reported in natural cases of porcine MCF. The most striking and consistent histological lesions were in trachea, lung, kidney and brain. These comprised mucopurulent tracheitis, interstitial pneumonia, necrotizing arteritis-periarteritis, and nonpurulent meningoencephalitis. No infection was established in the intravenously challenged or control groups. The study showed that MCF can be experimentally induced in pigs by aerosol challenge using sheep nasal secretions containing OvHV-2. Domestic pigs are a natural clinically susceptible host for sheep-associated MCF. They represent a useful, cost-effective model for MCF research.
  Veterinary Microbiology 04/2012; 159(3-4):485-9. · 3.33 Impact Factor
• Article: Actin stabilization by jasplakinolide affects the function of bone marrow-derived late endothelial progenitor cells.

  Xiaoyun Zhang, Xiaodong Cui, Lixia Cheng, Xiumei Guan, Hong Li, Xin Li, Min Cheng
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  ABSTRACT: Bone marrow-derived endothelial progenitor cells (EPCs), especially late EPCs, play a critical role in endothelial maintenance and repair, and postnatal vasculogenesis. Although the actin cytoskeleton has been considered as a modulator that controls the function and modulation of stem cells, its role in the function of EPCs, and in particular late EPCs, remains poorly understood. Bone marrow-derived late EPCs were treated with jasplakinolide, a compound that stabilizes actin filaments. Cell apoptosis, proliferation, adhesion, migration, tube formation, nitric oxide (NO) production and endothelial NO synthase (eNOS) phosphorylation were subsequently assayed in vitro. Moreover, EPCs were locally infused into freshly balloon-injured carotid arteries, and the reendothelialization capacity was evaluated after 14 days. Jasplakinolide affected the actin distribution of late EPCs in a concentration and time dependent manner, and a moderate concentration of (100 nmol/l) jasplakinolide directly stabilized the actin filament of late EPCs. Actin stabilization by jasplakinolide enhanced the late EPC apoptosis induced by VEGF deprivation, and significantly impaired late EPC proliferation, adhesion, migration and tube formation. Furthermore, jasplakinolide attenuated the reendothelialization capacity of transplanted EPCs in the injured arterial segment in vivo. However, eNOS phosphorylation and NO production were increased in late EPCs treated with jasplakinolide. NO donor sodium nitroprusside (SNP) rescued the functional activities of jasplakinolide-stressed late EPCs while the endothelial NO synthase inhibitor L-NAME led to a further dysfunction induced by jasplakinolide in late EPCs. A moderate concentration of jasplakinolide results in an accumulation of actin filaments, enhancing the apoptosis induced by cytokine deprivation, and impairing the proliferation and function of late EPCs both in vitro and in vivo. NO donor reverses these impairments, suggesting the role of NO-related mechanisms in jasplakinolide-induced EPC downregulation. Actin cytoskeleton may thus play a pivotal role in regulating late EPC function.
  PLoS ONE 01/2012; 7(11):e50899. · 4.09 Impact Factor
• Article: Ionic Liquid Enhanced Solvent Extraction for Bitumen Recovery from Oil Sands

  Xingang Li, Wenjun Sun, Guozhong Wu, Lin He, Hong Li, Hong Sui
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  ABSTRACT: An ionic liquid (IL) with low viscosity, 1-ethyl-3-methyl imidazolium tetrafluoroborate ([Emim][BF4]), was used to enhance bitumen recovery from oil sands by solvent extraction using a composite solvent of n-heptane and acetone. Results demonstrated that [Emim][BF4] increased the bitumen recovery by up to 95% at room temperature. Much less clay fines in the recovered bitumen than those using solvent extraction without IL, and organic residue was not observed in the spent sands. This technology circumvented the issue of tailing water because only a small amount of water was used to recycle IL, and organic solvent could be readily regenerated by distillation. The low viscosity of [Emim][BF4] made it outperform other alternative ILs for application in the oil sand industry. Results also highlighted the role of acetone in this technology (i.e., decrease IL viscosity and reduce IL consumption). The optimal solvent extraction conditions were found to be stirring for 10 min at 450 rpm at 25 °C. The optimized ratio of acetone to n-heptane in the composite solvent and the ratio of organic solvents to oil sands was determined as 2:6 (v/v) and 4:1 (v/w), respectively.
  10/2011;
• Article: Characterization of ovine herpesvirus 2-induced malignant catarrhal fever in rabbits.

  Hong Li, Cristina W Cunha, Katherine L Gailbreath, Donal O'Toole, Stephen N White, Alain Vanderplasschen, Benjamin Dewals, Donald P Knowles, Naomi S Taus
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  ABSTRACT: Malignant catarrhal fever (MCF) is a frequently fatal lymphoproliferative disease syndrome primarily of ruminant species, caused by gammaherpesviruses in the genus Macavirus. Ovine herpesvirus 2 (OvHV-2), carried by sheep, causes sheep-associated MCF worldwide, while Alcelaphine herpesvirus 1 (AlHV-1), carried by wildebeest, causes wildebeest-associated MCF, mainly in Africa. Diseases in rabbits can be induced by both viruses, which are clinically and pathologically similar; however, recent studies revealed different expression of viral genes associated with latency or lytic replication during clinical disease between the two viruses. In this study, we further characterized experimentally induced MCF in rabbits by nebulization with OvHV-2 from sheep nasal secretions to elucidate the course of viral replication, along with in vivo incorporation of 5-Bromo-2'-Deoxyuridine (BrdU), to evaluate lymphoproliferation. All six rabbits nebulized with OvHV-2 developed MCF between 24 and 29 days post infection. OvHV-2 DNA levels in peripheral blood leukocytes (PBL) remained undetectable during the incubation period and increased dramatically a few days before onset of clinical signs. During the clinical stage, we found that predominantly lytic gene expression was detected in PBL and tissues, and both T and B cells were proliferating. The data showed that the viral gene expression profile and lymphoproliferation in rabbits with OvHV-2 induced MCF were different from that in rabbits with AlHV-1 induced MCF, suggesting that OvHV-2 and AlHV-1 may play a different role in MCF pathogenesis.
  Veterinary Microbiology 02/2011; 150(3-4):270-7. · 3.33 Impact Factor
• Source

  Available from: Naomi Taus

  Article: Malignant catarrhal Fever: understanding molecular diagnostics in context of epidemiology.

  Hong Li, Cristina W Cunha, Naomi S Taus
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  ABSTRACT: Malignant catarrhal fever (MCF) is a frequently fatal disease, primarily of ruminants, caused by a group of gammaherpesviruses. Due to complexities of pathogenesis and epidemiology in various species, which are either clinically-susceptible or reservoir hosts, veterinary clinicians face significant challenges in laboratory diagnostics. The recent development of specific assays for viral DNA and antibodies has expanded and improved the inventory of laboratory tests and opened new opportunities for use of MCF diagnostics. Issues related to understanding and implementing appropriate assays for specific diagnostic needs must be addressed in order to take advantage of molecular diagnostics in the laboratory.
  International Journal of Molecular Sciences 01/2011; 12(10):6881-93. · 2.60 Impact Factor
• Article: CD8(+)/perforin(+)/WC1(-) gammadelta T cells, not CD8(+) alphabeta T cells, infiltrate vasculitis lesions of American bison (Bison bison) with experimental sheep-associated malignant catarrhal fever.

  Danielle D Nelson, William C Davis, Wendy C Brown, Hong Li, Donal O'Toole, J Lindsay Oaks
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  ABSTRACT: Sheep-associated malignant catarrhal fever (SA-MCF) caused by ovine herpesvirus-2 (OvHV-2), a gamma-herpesvirus in the Macavirus genus, is a fatal disease associated with lymphoproliferation, lymphocytic vasculitis, and mucosal ulceration in clinically susceptible species. SA-MCF is an important threat to American bison (Bison bison) due to their high susceptibility to this disease. Currently, the pathogenesis of disease in SA-MCF is poorly understood, and the immunophenotype of lymphocytes that infiltrate the vascular lesions of bison and cattle with SA-MCF has been only partially defined. Previous single-color immunohistochemistry studies have demonstrated that CD8(+) cells and CD4(+) cells predominate within vascular infiltrates in cattle and bison. The CD8(+) cells detected in the vascular lesions of cattle and bison were assumed to be cytotoxic alphabeta T lymphocytes. However, polychromatic immunophenotyping analyses in this study showed that CD8(+)/perforin(+) gammadelta T cells, CD4(+)/perforin(-) alphabeta T cells, and B cells infiltrate vascular lesions in the urinary bladder, kidney, and liver of six bison with experimentally-induced SA-MCF. CD8(+) alphabeta T cells and WC1(+) gammadelta T cell cells were only infrequently and inconsistently identified. This study confirmed our hypothesis that the predominant CD8(+) lymphocytes infiltrating the vascular lesions of bison with SA-MCF are cytotoxic lymphocytes of the innate immune system, not CD8(+) alphabeta T cells. Results of the present study support the previous suggestions that MCF is fundamentally a disease of immune dysregulation.
  Veterinary Immunology and Immunopathology 08/2010; 136(3-4):284-91. · 2.08 Impact Factor
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  Available from: Naomi Taus

  Article: Sheep (Ovis aries) airway epithelial cells support ovine herpesvirus 2 lytic replication in vivo.

  Naomi S Taus, David A Schneider, J Lindsay Oaks, Huijun Yan, Katherine L Gailbreath, Donald P Knowles, Hong Li
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  ABSTRACT: Ovine herpesvirus 2 (OvHV-2) is the causative agent of sheep-associated malignant catarrhal fever (SA-MCF), a frequently fatal disease of some members of the order Artiodactyla. OvHV-2 is carried as a lifelong subclinical infection in sheep (Ovis aries). To date OvHV-2 has not been propagated in vitro and this has hampered studies of viral pathogenesis and efforts to develop a vaccine to protect animals from SA-MCF. Lytic OvHV-2 replication occurs in the lungs of experimentally infected sheep at early times post-inoculation (PI) and in the nasal cavities of naturally infected sheep during virus shedding episodes. Identification of specific cell types supporting lytic virus replication in vivo provides information that can be used in the development of an in vitro propagation system for the virus. Using fluorescence immunohistochemical techniques, we identified lytically infected alveolar epithelial cells in the lungs of sheep early during infection. Lytically infected epithelial cells were also detected in samples of nasal secretions collected from naturally infected sheep during episodes of virus shedding. This is the first reported identification in the natural reservoir species of specific cell types that support OvHV-2 lytic replication in vivo.
  Veterinary Microbiology 03/2010; 145(1-2):47-53. · 3.33 Impact Factor
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  Available from: Naomi Taus

  Article: Experimental nebulization of American bison (Bison bison) with low doses of ovine herpesvirus 2 from sheep nasal secretions.

  Katherine L Gailbreath, Donal O'Toole, Naomi S Taus, Donald P Knowles, J Lindsay Oaks, Hong Li
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  ABSTRACT: Malignant catarrhal fever (MCF), caused by ovine herpesvirus 2 (OvHV-2), is an important cause of mortality in ranched American bison and domestic cattle in North America. Previous studies showed that bison can be infected by intranasal nebulization with sheep nasal secretions containing OvHV-2 and provided preliminary information on viral doses required for infection and disease progression. The goals of this study were to establish optimal minimal infectious and minimal lethal doses of OvHV-2 by the intranasal route in bison, evaluate the influence of dose on incubation period and other clinical parameters and determine if bison seropositive for antibody against MCF-group viruses are resistant to developing MCF after intranasal challenge. In this study, the minimal infectious dose and minimal lethal dose overlap, suggesting that experimental production of subclinically infected bison is impractical. Dose is inversely related to both incubation period and the period between nebulization and first detection of >1000 OvHV-2 DNA copies/500 ng total DNA in peripheral blood leukocytes. Interestingly, all of the bison seropositive for anti-MCF-group viral antibody prior to inoculation died of MCF after nebulization. We conclude that previous exposure to an MCF-group virus does not necessarily provide resistance to OvHV-2-induced MCF in bison.
  Veterinary Microbiology 11/2009; 143(2-4):389-93. · 3.33 Impact Factor