Ningxia Medical College

Xinhui, China

Ningxia Medical College

Xinhui, China

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Luan L.,Fudan University | Xue R.,Fudan University | Lu C.,Fudan University | Cui A.,Ningxia Medical College | And 8 more authors.
Autoimmunity | Year: 2016

Type 1 diabetes mellitus (T1DM) is an autoimmune disease characterized by an autoimmune-mediated loss of insulin secreting β-cells. Each B lymphocyte clone that escapes immune tolerance produces a specific antibody. No specific treatment against autoantibodies is available for autoimmune diseases. We have developed a strategy to produce an antiserum against autoantibodies for the treatment of T1DM. Non-obese diabetic (NOD) but not Balb/c mouse serum contains autoantibodies. Antisera were produced by immunizing Balb/c mice with affinity-purified IgG from NOD or BALB/c mice along with the immune adjuvant (hereafter, NIgG or BIgG, respectively). A bolus administration of NIgG significantly reduced serum autoantibodies, autoantibody-positive B lymphocytes in the spleens of NOD mice, mortality and morbidity of diabetes, blood glucose and islet immune infiltration, whereas it increased islet mass in NOD mice for at least 26 weeks. NIgG antiserum treatment has no significant effect on CD3+, CD4+ or CD8+ T cells and B220+ or CD19+ B cells. BIgG also imparted a moderate therapeutic effect, although it was considerably lower than that of NIgG. NIgG did not cross-react with allogeneic serum. NIgG showed no effect on Balb/c mice. The results show the feasibility of producing antiserum against autoantibodies to prevent and treat autoimmune-induced T1DM with a single bolus administration. © 2015 Taylor & Francis.


PubMed | Fudan University, Ningxia Medical College and Shanghai JiaoTong University
Type: Journal Article | Journal: Autoimmunity | Year: 2016

Type 1 diabetes mellitus (T1DM) is an autoimmune disease characterized by an autoimmune-mediated loss of insulin secreting -cells. Each B lymphocyte clone that escapes immune tolerance produces a specific antibody. No specific treatment against autoantibodies is available for autoimmune diseases. We have developed a strategy to produce an antiserum against autoantibodies for the treatment of T1DM. Non-obese diabetic (NOD) but not Balb/c mouse serum contains autoantibodies. Antisera were produced by immunizing Balb/c mice with affinity-purified IgG from NOD or BALB/c mice along with the immune adjuvant (hereafter, NIgG or BIgG, respectively). A bolus administration of NIgG significantly reduced serum autoantibodies, autoantibody-positive B lymphocytes in the spleens of NOD mice, mortality and morbidity of diabetes, blood glucose and islet immune infiltration, whereas it increased islet mass in NOD mice for at least 26 weeks. NIgG antiserum treatment has no significant effect on CD3(+), CD4(+) or CD8(+) T cells and B220(+) or CD19(+) B cells. BIgG also imparted a moderate therapeutic effect, although it was considerably lower than that of NIgG. NIgG did not cross-react with allogeneic serum. NIgG showed no effect on Balb/c mice. The results show the feasibility of producing antiserum against autoantibodies to prevent and treat autoimmune-induced T1DM with a single bolus administration.


Sui Y.,Ningxia Medical College
Yi chuan = Hereditas / Zhongguo yi chuan xue hui bian ji | Year: 2010

To investigate the roles of human REV3 gene in proliferation and genomic stability, we experimentally suppressed the REV3 expression in human colon cancer cells (SW480) by the interference RNA technology (RNAi) as monitored by real-time RT-PCR. Compared to untreated or mock-treated cells, ablation of REV3 significantly reduced cell growth rate, micronucleus formation and the frequency of sister chromatid exchange. Whereas the differences between untreated and mock-treated controls were insignificant. Indicators of cell cycle, proliferation and the expression of genetic information in cells of case group, which displayed lower-level expression of REV3, were extremely lower than the control group, and the difference was significant (P<0.05). Differences in the two control groups were not significant. This suggested that the reduced expression of REV3 may affect the growth and proliferation of colon cancer cells (SW480), and, to some extent, contribute to suppression of the genetic instability occurred in micronuclei and sister chromatids. Based on the results from this study, REV3 plays an important role in different cellular growth periods and physiological conditions, and its differential expression directly affects the development of human colon cancer cells.


Feng N.-C.,Central South University | Feng N.-C.,Ningxia Medical College | Guo X.-Y.,Central South University | Liang S.,Central South University
Transactions of Nonferrous Metals Society of China (English Edition) | Year: 2010

Copper adsorption by orange peel, which was chemically modified with sodium hydroxide, was investigated. The adsorbent was characterized using surface area analyzer, infrared spectroscopy and scanning electron microscopy. Total negative charge and zeta potentials on the adsorbent surface were determined. Equilibrium isotherms and kinetics were obtained and the effects of solution pH value, adsorbent concentration and temperature were studied in batch experiments. Column experiments were performed to study practical applicability, and breakthrough curves were obtained. Equilibrium is well described by Langmuir and Freundlich isotherms, and kinetics is found to fit pseudo-second order type adsorption kinetics. According to Langmuir equation, the maximum adsorption capacity for Cu(II) is 50.25 mg/g at pH value of 5.3. The results show additional chemical modification of the adsorbent by NaOH and the increased adsorption capacity.


Liang S.,Central South University | Guo X.-Y.,Central South University | Feng N.-C.,Ningxia Medical College | Tian Q.-H.,Central South University
Transactions of Nonferrous Metals Society of China (English Edition) | Year: 2010

Preparation of orange peel xanthate and its adsorption behaviors of five heavy metals (Cu2+, Cd2+, Pb2+, Zn2+ and Ni2+) were studied. FTIR spectra, Zeta potentials and TG analysis were used to characterize prepared orange peel xanthate. Effects of various parameters including equilibrium pH, initial metal ion concentration and adsorption time on the adsorption processes for the five metal ions were investigated. It was found that for all five metal ions, the adsorption isotherms agreed Langmuir model very well and the maximum adsorption capacities of Cu2+, Cd2+, Pb2+, Zn2+ and Ni2+ were obtained as 77.60, 76.57, 218.34, 49.85 and 15.45 mg/g, respectively. All adsorption processes can attain equilibrium within 20 min and kinetics was well fitted by psesudo-second order equation. It is proposed that the adsorption mechanism was complexation.


Nishina T.,Juntendo University | Komazawa-Sakon S.,Juntendo University | Yanaka S.,Tokyo Medical University | Piao X.,Juntendo University | And 15 more authors.
Science Signaling | Year: 2012

Apoptotic cells can stimulate the compensatory proliferation of surrounding cells to maintain tissue homeostasis. Although oxidative stress is associated with apoptosis and necrosis, whether it contributes to compensatory proliferation is unknown. Here, we showed that interleukin-11 (IL-11), a member of the IL-6 family of proinflammatory cytokines, was produced by cells in an oxidative stress-dependent manner. IL-11 production depended on the activation in dying cells of extracellular signal-regulated kinase 2, which in turn caused the phosphorylation and accumulation of the transcription factor Fra-1 by preventing its proteasome-dependent degradation. Fra-1 was subsequently recruited to the Il11 promoter and activated gene transcription. Upon acute liver injury in mice, IL-11 was mainly produced by hepatocytes in response to reactive oxygen species that were presumably released from dying hepatocytes. IL-11 that was secreted by the dying cells then induced the phosphorylation of the transcription factor STAT3 in adjacent healthy hepatocytes, which resulted in their compensatory proliferation. Furthermore, an IL-11 receptor (IL-11R) agonist enhanced the proliferation of hepatocytes and ameliorated oxidative stress upon acetaminophen-induced liver injury. Conversely, the effects of acetaminophen were exacerbated in mice deficient in the IL-11R a subunit. Together, these results suggest that IL-11 provides a functional link between oxidative stress and compensatory proliferation.


Kwan P.,Royal Melbourne Hospital | Kwan P.,Chinese University of Hong Kong | Wang W.,Capital Medical University | Wu J.,Capital Medical University | And 12 more authors.
Epilepsia | Year: 2013

Summary Purpose: To evaluate the long-term outcome of phenobarbital treatment for convulsive epilepsy in rural China, and to explore factors associated with overall seizure outcomes. Methods: We carried out follow-up assessments of people who took part in an epilepsy community management program conducted in rural counties of six provinces in China. People with convulsive epilepsy who were previously untreated (or on irregular treatment) were commenced on regular treatment with phenobarbital. Information was collected using a standardized questionnaire by face-to-face interviews of the individuals (and their families where necessary). Information collected included treatment status, medication change, seizure frequency, and mortality. Key Findings: Among the 2,455 people who participated in the original program, outcomes were successfully ascertained during the follow-up assessment in 1986. Among them, 206 had died. Information on treatment response was obtained in 1,780 (56% male; mean age 33.9 years, range 3-84; mean duration of follow-up 6.4 years). Among them, 939 (53%) were still taking phenobarbital. The most common reasons for stopping phenobarbital were seizure freedom or substantial seizure reduction, socioeconomic reasons, and personal preference. Four hundred fifty-three individuals (25%) became seizure-free for at least 1 year while taking phenobarbital, 88% of whom did so at daily doses of 120 mg or below. Four hundred six (23%) reported adverse events, which led to withdrawal of phenobarbital in <1%. The most common adverse effects were malaise/somnolence (7.4%), dizziness (3%), and lethargy (2.6%). At the follow-up assessment, 688 (39%) individuals had been seizure free for at least the previous year. People with persistent seizures had significantly longer duration of epilepsy and higher number of seizures in the 12 months before treatment. People who were taking AED treatment irregularly at recruitment were less likely to become seizure-free. Significance: We observed long-term benefits of regular treatment with phenobarbital for convulsive epilepsy in rural China. One hundred years after the discovery of its antiepileptic effect, phenobarbital is still playing an important role in the management of epilepsy. © Wiley Periodicals, Inc. © 2012 International League Against Epilepsy.


Wu Y.,Fudan University | Wu Y.,Ningxia Medical College | Zhang X.,Fudan University | Kang X.,Fudan University | And 9 more authors.
Clinical and Experimental Pharmacology and Physiology | Year: 2013

Summary: Oxidative stress caused by cellular accumulation of reactive oxygen species (ROS) is a major contributor to disease and cell death. However, how induced pluripotent stem cells (iPSC) respond to different levels of oxidative stress is largely unknown. Here, we investigated the effect of H2O2-induced oxidative stress on iPSC function in vitro. Mouse iPSC were treated with H2O2 (25-100 μmol/L). IPSC adhesion, migration, viability, apoptosis and senescence were analysed. Expression of adhesion-related genes, stress defence genes, and osteoblast- and adipocyte-associated genes were determined by reverse transcription polymerase chain reaction. The present study found that H2O2 (25-100 μmol/L) decreased iPSC adhesion to matrix proteins and endothelial cells, and downregulated gene expression levels of adhesion-related molecules, such as integrin alpha 7, cadherin 1 and 5, melanoma cell adhesion molecule, vascular cell adhesion molecule 1, and monocyte chemoattractant protein-1. H2O2 (100 μmol/L) decreased iPSC viability and inhibited the capacity of iPSC migration and transendothelial migration. iPSC were sensitive to H2O2-induced G2/M arrest, senescence and apoptosis when exposed to H2O2 at concentrations above 25 μmol/L. H2O2 increased the expression of stress defence genes, including catalase, cytochrome B alpha, lactoperoxidase and thioredoxin domain containing 2. H2O2 upregulated the expression of osteoblast- and adipocyte-associated genes in iPSC during their differentiation; however, short-term H2O2-induced oxidative stress did not affect the protein expression of the pluripotency markers, octamer-binding transcription factor 4 and sex-determining region Y-box 2. The present results suggest that iPSC are sensitive to H2O2 toxicity, and inhibition of oxidative stress might be a strategy for improving their functions. © 2013 Wiley Publishing Asia Pty Ltd.


Lekes N.,McGill University | Gingras I.,McGill University | Philippe F.L.,McGill University | Koestner R.,McGill University | Fang J.,Ningxia Medical College
Journal of Youth and Adolescence | Year: 2010

Self-determination theory proposes that prioritizing intrinsic life goals, such as community involvement, is related to well-being, whereas focusing on extrinsic life goals, such as financial success, is associated with lower well-being and that parenting influences the type of life goals that youth adopt. In a sample of 515 Chinese (56% female, mean age = 15.50) and 567 North American (52% male, mean age = 14.17) adolescents, a model of the relationships between parenting, life goals, and well-being was investigated and confirmed for intrinsic life goals. Across societies, autonomy-supportive parenting was associated with the endorsement of intrinsic life goals, which in turn was associated with well-being. Intrinsic life goals partially mediated the relationship between parental autonomy-support and well-being. These findings suggest that, cross-culturally, prioritizing intrinsic life goals is related to increased well-being among adolescents and that parents could encourage intrinsic life goals by being supportive of their children's autonomy. © 2009 Springer Science+Business Media, LLC.


Piao X.,Juntendo University | Komazawa-Sakon S.,Juntendo University | Nishina T.,Juntendo University | Koike M.,Juntendo University | And 13 more authors.
Science Signaling | Year: 2012

As a catalytically inactive homolog of caspase-8, a proapoptotic initiator caspase, c-FLIP blocks apoptosis by binding to and inhibiting caspase-8. The transcription factor nuclear factor κB (NF-κB) plays a pivotal role in maintaining the homeostasis of the intestine and the liver by preventing death receptor-induced apoptosis, and c-FLIP plays a role in the NF-κB-dependent protection of cells from death receptor signaling. Because c-Flip-deficient mice die in utero, we generated conditional c-Flip-deficient mice to investigate the contribution of c-FLIP to homeostasis of the intestine and the liver at developmental and postnatal stages. Intestinal epithelial cell (IEC)- or hepatocyte-specific deletion of c-Flip resulted in perinatal lethality as a result of the enhanced apoptosis and programmed necrosis of the IECs and the hepatocytes. Deficiency in the gene encoding tumor necrosis factor-α (TNF-α) receptor 1 (Tnfr1) partially rescued perinatal lethality and the development of colitis in IEC-specific c-Flip-deficient mice but did not rescue perinatal lethality in hepatocyte-specific c-Flip-deficient mice. Moreover, adult mice with interferon (IFN)-inducible deficiency in c-Flip died from hepatitis soon after depletion of c-FLIP. Pretreatment of IFN-inducible c-Flip-deficient mice with a mixture of neutralizing antibodies against TNF-α, Fas ligand (FasL), and TNF-related apoptosis-inducing ligand (TRAIL) prevented hepatitis. Together, these results suggest that c-FLIP controls the homeostasis of IECs and hepatocytes by preventing cell death induced by TNF-α, FasL, and TRAIL.

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