Ningxia Medical College

Xinhui, China

Ningxia Medical College

Xinhui, China
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Ito M.,Juntendo University | Seki T.,Tohoku University | Liu J.,Ningxia Medical College | Nakamura K.,Juntendo University | And 4 more authors.
Synapse | Year: 2010

Electroconvulsive therapy (ECT) is known as a successful treatment for severe depression. Despite great efforts, the biological mechanisms underlying the beneficial effects of ECT remain largely unclear. In this study, animals received a single, 10, or 20 applications of electroconvulsive seizure (ECS), and then cell proliferation and apoptosis were investigated in the subgranular zone (SGZ) of the dentate gyrus. We analyzed whether a series of ECSs could induce changes in the dentate gyrus in a dose-response fashion. A single-ECS seizure significantly increased cell proliferation in the SGZ by ~2.3-fold compared to sham treatment. After 10 ECSs, a significant increase in cell proliferation was observed in the SGZ by ~2.4-fold compared to sham treatment. Moreover, 10 ECSs induced a significant increase in cell proliferation by 1.3-fold compared to a single-ECS group. However, cell proliferation did not differ between the group with 20 ECSs and sham group. In addition, a significant increase in the number of apoptotic cells was found in the group with 10 ECSs, whereas no significant change in it was found in either a single ECS or 20 ECSs group compared to sham treatment. These findings indicate that the optimal number of treatments and duration of stimulation requires investigation. Further studies are needed to elucidate the intracellular mechanisms underlying both effective and excessive ECT. © 2010 Wiley-Liss, Inc.


Wang C.,Capital Medical University | Liu Y.,Central South University | Yang Q.,Central South University | Dai X.,Ningxia Medical College | And 5 more authors.
International Journal of Stroke | Year: 2013

Background: The prevalence rate of overweight and obese has been escalating over the past two decades in China. Even so, the association between obesity and stroke still remains unclear to some extent. Aims: The aim of this study was to elucidate the association between body mass index and stroke in a large Chinese population cohort. Methods: A cohort of 26607 Chinese people, aged over 35 years, was investigated in 1987. Baseline information of body weight and height was used to calculate BMI (weight in kilograms divided by height in meters squared, kg/m2). Cox proportional hazards model was fitted to estimate hazard ratios of stroke adjusted for age, educational level, smoking and alcohol consumption. Results: The 11-year follow-up revealed (241149 person-years) a total of 1108 stroke events (614 ischemic, 451 hemorrhagic, and 44 undefined stroke). Body mass index≥30·0 was an independent risk factor for stroke both in men and women. Compared with normal weight, hazard ratios for total stroke were 0·74 in men underweight (95% confidence interval: 0·53∼1·03), 1·63 overweight (95% confidence interval: 1·35∼1·96), and 2·20 with obesity (95% confidence interval: 1·47∼3·30); and with ischemic stroke, hazard ratios were 0·52 in those underweight (95% confidence interval: 0·30∼0·89), 2·08 overweight (95% confidence interval: 1·65∼2·62), and 3·80 with obesity (95% confidence interval: 2·47∼5·86). In women, the corresponding hazard ratios for total stroke were 0·79 underweight (95% confidence interval: 0·58∼1·07), 1·42 overweight (95% confidence interval: 1·16∼1·73), and 1·57 with obesity (95% confidence interval: 1·06∼2·31); and for those with ischemic stroke, 0·92 underweight (95% confidence interval: 0·59∼1·43), 1·90 overweight (95% confidence interval: 1·44∼2·50), and 2·42 with obesity (95% confidence interval: 1·50∼3·93). There appeared an evident dose-response relationship between body mass index and the risk of developing stroke, which still appeared, however, adjusted low for hypertension, diabetes, and heart disease. Decreased risk for stroke in the leanest group was confined to men only. No association was found between body mass index and hemorrhagic stroke in both genders. Conclusions: Our data suggest that body mass index was an independent risk factor for total and ischemic stroke but not for hemorrhagic stroke in both genders. Association between body mass index and stroke was extremely mediated by hypertension, diabetes, and heart disease. Decreased risk for the leanest group was confined to men. © 2012 World Stroke Organization.


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.


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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