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Articles by J Ma
Total Records ( 12 ) for J Ma
  Y Xie , M Wu , R Song , J Ma , Y Shi , W Qin and Y. Jin
 

Regulatory T (Treg) cells are a subpopulation of T cells that not only prevent autoimmunity, but also control a wide range of T cell-dependent immune responses. Glucocorticoid treatment (dexamethasone, or Dex) has been reported to amplify IL-2-mediated selective in vivo expansion of Treg cells. We simultaneously administered Dex and IL-2 to the donor in a murine allogeneic lymphocyte transplantation model to expand functional suppressive CD4+CD25+FOXP3+ T cells in the graft and to raise the regulatory T cell/effector T cell (Treg/Teff) ratio to prevent graft-versus-host disease (GVHD). After combined treatment of the donor with Dex (5 mg/kg/day) and IL-2 (300,000 IU/mouse/day) for 3 days, grafts were subjected to flow cytometric analysis, and transplantation was carried out from male C57BL/6 mice to female BALB/c mice aged 8–12 weeks. Results showed that short-term simultaneous administration of Dex and IL-2 markedly expanded functional suppressive CD4+CD25+FOXP3+ T cells in the murine spleen. In this murine allogeneic transplantation model, the grafts from donors with Dex and IL-2 pre-treatment led to a longer survival time for the recipients than for the control group (median survival time > 60 day vs. 12 day, P = 0.0002). The ratio of Treg/Teff also increased remarkably (0.43 ± 0.15 vs. 0.14 ± 0.01, P = 0.01). This study demonstrated that co-stimulation with Dex and IL-2 selectively expanded functional CD4+CD25+FOXP3+ T cells in vivo, and that grafts from donors pre-treated with Dex and IL-2 led to longer survival time and greater suppression of GVHD after allogeneic transplantation. Thus, GVHD can be suppressed by the specific expansion of regulatory T cells with Dex and IL-2 in graft donors.

  J Ma , K Berra , W. L Haskell , L Klieman , S Hyde , M. W Smith , L Xiao and R. S. Stafford
 

Background  Case management (CM) is a systematic approach to supplement physician-centered efforts to prevent cardiovascular disease (CVD). Research is limited on its implementation and efficacy in low-income, ethnic minority populations.

Methods  We conducted a randomized clinical trial to evaluate a nurse- and dietitian-led CM program for reducing major CVD risk factors in low-income, primarily ethnic minority patients in a county health care system, 63.0% of whom had type 2 diabetes mellitus. The primary outcome was the Framingham risk score (FRS).

Results  A total of 419 patients at elevated risk of CVD events were randomized and followed up for a mean of 16 months (81.4% retention). The mean FRS was significantly lower for the CM vs usual care group at follow-up (7.80 [95% confidence interval, 7.21-8.38] vs 8.93 [8.36-9.49]; P = .001) after adjusting for baseline FRS. This is equivalent to 5 fewer heart disease events per 1000 individuals per year attributable to the intervention or to 200 individuals receiving the intervention to prevent 1 event per year. The pattern of group differences in the FRS was similar in subgroups defined a priori by sex and ethnicity. The main driver of these differences was lowering the mean (SD) systolic (–4.2 [18.5] vs 2.6 [22.7] mm Hg; P = .003) and diastolic (–6.0 [11.6] vs –3.0 [11.7] mm Hg; P = .02) blood pressures for the CM vs usual care group.

Conclusion  Nurse and dietitian CM targeting multifactor risk reduction can lead to modest improvements in CVD risk factors among high-risk patients in low-income, ethnic minority populations receiving care in county health clinics.

Trial Registration  clinicaltrials.gov Identifier: NCT00128687

  Y Dai , L Qiao , K. W Chan , M Yang , J Ye , J Ma , B Zou , Q Gu , J Wang , R Pang , H.Y Lan and B. C.Y. Wong
 

Down-regulation of XIAP (X-linked inhibitor of apoptosis protein) sensitizes colon cancer cells to the anticancer effect of peroxisome proliferator-activated receptor- (PPAR) ligands in mice. The aims of this study were to evaluate the effect of embelin (2,5-dihydroxy-3-undecyl-1,4-benzoquinone), an antagonist of XIAP, on colon cancer, with a particular focus on whether PPAR is required for embelin to exert its effect. A dominant-negative PPAR was used to antagonize endogenous PPAR in HCT116 cells. Cells were treated with or without embelin. Cell proliferation, apoptosis, and nuclear factor-B (NF-B) activity were measured. For in vivo studies, 1,2-dimethylhydrazine dihydrochloride (DMH) was s.c. injected to induce colon cancer in PPAR+/+ and PPAR+/– mice. Mice were fed embelin daily for 10 days before DMH injection, and continued for 30 more weeks. Embelin inhibited proliferation and induced apoptosis in HCT116 cells with marked up-regulation of PPAR. In addition, embelin significantly inhibited the expressions of survivin, cyclin D1, and c-Myc. These effects were partially dependent on PPAR. PPAR+/– mice were more susceptible to DMH-induced colon carcinogenesis than PPAR+/+ mice, and embelin significantly reduced the incidence of colon cancer in PPAR+/+ mice but not in PPAR+/– mice. Embelin inhibited NF-B activity in PPAR+/+ mice but marginally so in PPAR+/– mice. Thus, reduced expression of PPAR significantly sensitizes colonic tissues to the carcinogenic effect of DMH. Embelin inhibits chemical carcinogen-induced colon carcinogenesis, but this effect is partially dependent on the presence of functional PPAR, indicating that PPAR is a necessary signaling pathway involved in the antitumor activity of normal organisms. [Cancer Res 2009;69(11):4776–83]

  J Wang , Q Gu , M Li , W Zhang , M Yang , B Zou , S Chan , L Qiao , B Jiang , S Tu , J Ma , I. F Hung , H. Y Lan and B. C.Y. Wong
 

Background and aims: X-linked inhibitor of apoptosis-associated factor 1 (XAF1) was first recognized as an antagonist of X-linked inhibitor of apoptosis in suppressing caspase 3 activity. It has lower expression in cancer cells than normal tissue. Overexpression of XAF1 can inhibit cancer cell growth and sensitize tumor necrosis factor-related apoptosis-inducing ligand- or etoposide-induced apoptosis. The aim of this study is to elucidate the mechanism of XAF1 in regulating cell growth. Methods: Stable transfectants of gastrointestinal (GI) cancer cell lines AGS and SW1116 expressing XAF1 and vector control were generated. Cell growth, apoptosis, mitotic status and cell cycle distribution were assessed. The interaction between XAF1 and G2/M checkpoint proteins was evaluated by immunoblotting, kinase assay and co-immunoprecipitation assay. Mitotic catastrophe was identified by occurrence of aberrant nuclei and centrosomal amplification. Results: Our results showed that overexpression of XAF1 suppressed serum-dependent cancer cell growth, induced mitotic catastrophe and G2/M cell cycle arrest. Interestingly, XAF1 was predominantly expressed in G2/M phase after cell cycle synchronization. XAF1 interacted with and activated checkpoint kinase 1 (Chk1), inactivated Cdc25C and lead to inactivation of Cdc2–cyclin B complex. Suppression of Chk1 abrogated XAF1-induced G2/M arrest. Conclusions: Our findings implicate XAF1 as a novel cell cycle modulator that is recruited in G2/M phase and thus unravel a novel function pathway of XAF1, suggesting the potential role of XAF1 as the target for the management of GI cancers.

  L Dossus , R Kaaks , F Canzian , D Albanes , S. I Berndt , H Boeing , J Buring , S. J Chanock , F Clavel Chapelon , H. S Feigelson , J. M Gaziano , E Giovannucci , C Gonzalez , C. A Haiman , G Hallmans , S. E Hankinson , R. B Hayes , B. E Henderson , R. N Hoover , D. J Hunter , K. T Khaw , L. N Kolonel , P Kraft , J Ma , L Le Marchand , E Lund , P. H.M Peeters , M Stampfer , D. O Stram , G Thomas , M. J Thun , A Tjonneland , D Trichopoulos , R Tumino , E Riboli , J Virtamo , S. J Weinstein , M Yeager , R. G Ziegler and D. G. Cox
 

Genes involved in the inflammation pathway have been associated with cancer risk. Genetic variants in the interleukin-6 (IL6) and prostaglandin-endoperoxide synthase-2 (PTGS2, encoding for the COX-2 enzyme) genes, in particular, have been related to several cancer types, including breast and prostate cancers. We conducted a study within the Breast and Prostate Cancer Cohort Consortium to examine the association between IL6 and PTGS2 polymorphisms and breast and prostate cancer risk. Twenty-seven polymorphisms, selected by pairwise tagging, were genotyped on 6292 breast cancer cases and 8135 matched controls and 8008 prostate cancer cases and 8604 matched controls. The large sample sizes and comprehensive single nucleotide polymorphism tagging in this study gave us excellent power to detect modest effects for common variants. After adjustment for multiple testing, none of the associations examined remained statistically significant at P = 0.01. In analyses not adjusted for multiple testing, one IL6 polymorphism (rs6949149) was marginally associated with breast cancer risk (TT versus GG, odds ratios (OR): 1.32; 99% confidence intervals (CI): 1.00–1.74, Ptrend = 0.003) and two were marginally associated with prostate cancer risk (rs6969502-AA versus rs6969502-GG, OR: 0.87, 99% CI: 0.75–1.02; Ptrend = 0.002 and rs7805828-AA versus rs7805828-GG, OR: 1.11, 99% CI: 0.99–1.26; Ptrend = 0.007). An increase in breast cancer risk was observed for the PTGS2 polymorphism rs7550380 (TT versus GG, OR: 1.38, 99% CI: 1.04–1.83). No association was observed between PTGS2 polymorphisms and prostate cancer risk. In conclusion, common genetic variation in these two genes might play at best a limited role in breast and prostate cancers.

  L Zhang , T Deng , X Li , H Liu , H Zhou , J Ma , M Wu , M Zhou , S Shen , Z Niu , W Zhang , L Shi , B Xiang , J Lu , L Wang , D Li , H Tang and G. Li
 

microRNAs (miRNAs) are small non-coding RNAs and have been implicated in the pathology of various diseases, including cancer. Here we report that the miRNA profiles have been changed after knockdown of one of the most important oncogene c-MYC or re-expression of a candidate tumor suppressor gene SPLUNC1 in nasopharyngeal carcinoma (NPC) cells. Both c-MYC knockdown and SPLUNC1 re-expression can down-regulate microRNA-141 (miR-141). miR-141 is up-regulated in NPC specimens in comparison with normal nasopharyngeal epithelium. Inhibition of miR-141 could affect cell cycle, apoptosis, cell growth, migration and invasion in NPC cells. We found that BRD3, UBAP1 and PTEN are potential targets of miR-141, which had been confirmed following luciferase reporter assays and western blotting. BRD3 and UBAP1 are both involved in NPC carcinogenesis as confirmed through our previous studies and PTEN is a crucial tumor suppressor in many tumor types. BRD3 is involved in the regulation of the Rb/E2F pathway. Inhibition of miR-141 could affect some important molecules in the Rb/E2F, JNK2 and AKT pathways. It is well known that carcinogenesis of NPC is involved in the networks of genetic and epigenetic alteration events. We propose that miR-141- and tumor-related genes c-MYC, SPLUNC1, BRD3, UBAP1 and PTEN may constitute a gene–miRNA network to contribute to NPC development.

  J. H Page , J Ma , S. E Chiuve , M. J Stampfer , J Selhub , J. E Manson and E. B. Rimm
 

Background— We prospectively evaluated the relationships between fasting plasma levels of vitamin B6, as pyridoxal phosphate, and subsequent myocardial infarction risk in women.

Methods and Results— Among 32 826 women who provided blood samples between 1989 and 1990 (27% of the original 1976 cohort), 239 were diagnosed with incident myocardial infarction (fatal and nonfatal) after blood collection but before July 1998. Of these women, 144 had provided a sample after fasting >10 hours. Cases were matched 1:2 by age, cigarette smoking status, and month of and fasting status at the time of blood collection with controls from the same cohort. Conditional logistic regression was used to adjust for potential confounders, including traditional coronary risk factors, anthropometric factors, dietary intake, and selected biomarkers. Median age at blood collection was 63 years. Plasma levels of pyridoxal phosphate were inversely associated with risk of myocardial infarction; the multivariable-adjusted rate ratio for the highest compared with the lowest quartiles (>70 versus <27.9 pmol/mL) was 0.22 (95% confidence interval, 0.09 to 0.55; P for trend=0.05). The association varied by age: among women who were <60 years of age at blood sampling, the rate ratio comparing the highest and lowest quartiles was 0.05 (95% confidence interval, 0.004 to 0.61), whereas among older women, the corresponding rate ratio was 0.36 (95% confidence interval, 0.13 to 1.02).

Conclusions— Fasting plasma concentration of pyridoxal phosphate was inversely associated with myocardial infarction risk, an effect that was in part independent of dietary B6 intake. In addition to dietary vitamin B6 intake, there are other determinants of plasma vitamin B6 status, and these factors warrant further research.

  X Wang , W Xie , Y Zhang , P Lin , L Han , P Han , Y Wang , Z Chen , G Ji , M Zheng , N Weisleder , R. P Xiao , H Takeshima , J Ma and H. Cheng
 

Rationale: Unrepaired cardiomyocyte membrane injury causes irreplaceable cell loss, leading to myocardial fibrosis and eventually heart failure. However, the cellular and molecular mechanisms of cardiac membrane repair are largely unknown. MG53, a newly identified striated muscle-specific protein, is involved in skeletal muscle membrane repair. But the role of MG53 in the heart has not been determined.

Objective: We sought to investigate whether MG53 mediates membrane repair in cardiomyocytes and, if so, the cellular and molecular mechanism underlying MG53-mediated membrane repair in cardiomyocytes. Moreover, we determined possible cardioprotective effect of MG53-mediated membrane repair.

Methods and Results: We demonstrated that MG53 is crucial to the emergency membrane repair response in cardiomyocytes and protects the heart from stress-induced loss of cardiomyocytes. Disruption of the sarcolemmal membrane by mechanical, electric, chemical, or metabolic insults caused rapid and robust translocation of MG53 toward the injury sites. Ablation of MG53 prevented sarcolemmal resealing after infrared laser–induced membrane damage in intact heart, and exacerbated mitochondrial dysfunction and loss of cardiomyocytes during ischemia/reperfusion injury. Unexpectedly, the MG53-mediated cardiac membrane repair was mediated by a cholesterol-dependent mechanism: depletion of membrane cholesterol abolished, and its recovery restored injury-induced membrane translocation of MG53. The redox status of MG53 did not affect initiation of MG53 translocation, whereas MG53 oxidation conferred stability to the membrane repair patch.

Conclusions: Thus, cholesterol-dependent MG53-mediated membrane repair is a vital, heretofore unappreciated cardioprotective mechanism against a multitude of insults and may bear important therapeutic implications.

  L Cheng , Y Chen , C Chen , J Ma , L Shu , A. V Vasilakos and N. Xiong
 

Considering sensor nodes deployed densely and uniformly a mobile sink moving through the sensing field queries a specific area of interest for monitoring information. The Query packet, injected by the mobile sink, is routed to the specific area and the corresponding Response packet is expected to return via multi-hop communication. In this paper, we analyze such a network model to address the problem of efficient data collection for mobile wireless monitoring applications. We first propose a meeting position-aware routing (MPAR) protocol for routing the Response packet efficiently and then propose an efficient query-based data collection scheme (QBDCS) for mobile wireless monitoring applications based on the MPAR. In order to minimize the energy consumption and packet delivery latency, the QBDCS chooses the optimal query time of injecting the Query packet and tailors the routing mechanism for sensor nodes forwarding packets. Simulation study has verified the analysis and demonstrated that the QBDCS can significantly reduce the energy consumption and end to end delivery latency.

  T Dai , M Patel Chamberlin , R Natarajan , I Todorov , J Ma , J LaPage , L Phillips , C. C Nast , D Becerra , P Chuang , L Tong , J de Belleroche , D. J Wells , Y Wang and S. G. Adler
 

β-Cell apoptosis occurs in diabetes mellitus (DM). Heat shock protein (HSP) 27 (human homolog of rodent HSP25) mitigates stress-induced apoptosis but has not been studied in β-cells. We tested whether HSP27 overexpression attenuates streptozotocin (SZ)-induced DM in vivo and cytokine-induced islet apoptosis in vitro. DM was ascertained by ip glucose tolerance testing, and fasting serum insulin/glucose was measured. Pancreas was stained for insulin, HSP27, and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling, and insulin content was measured. HSP25/27 was measured by immunoblotting, isoelectric focusing, and RT-PCR. Islet HSP25/27 oligomerization and inhibitory B protein kinase (nuclear factor B essential modulator) binding were assessed by coimmunoprecipitation. HSP27 transgene (TG) in pancreas localized predominantly in β-cells. Baseline pancreatic insulin levels in wild-type (WT) and HSP27TG mice were similar, but lower in WT than HSP27TG after SZ (P < 0.01). Intraperitoneal glucose tolerance testing confirmed protection from SZ-DM in HSP27TG. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling and inducible nitric oxide synthase staining were increased in WT vs. HSP27TG islets (P < 0.05) after SZ. Caspase-3 activity was lower in islets from HSP27TG vs. WT mice after cytokine stress in vitro (P < 0.05). There was more HSP25 plus 27 protein from HSP27TG islets than HSP25 from WT (P < 0.01). HSP25 protein but not mRNA was increased in HSP27TG mice. Isoelectric focusing showed similar relative HSP phosphorylation in HSP27TG and WT (P > 0.05). HSP27 bound native HSP25 in TG islets; both bound to inhibitory B protein kinase (nuclear factor B essential modulator). These data show islet protection by HSP27 by mitigation of apoptosis, possibly through nuclear factor B regulation.

  J. R Stark , G Judson , J. F Alderete , V Mundodi , A. S Kucknoor , E. L Giovannucci , E. A Platz , S Sutcliffe , K Fall , T Kurth , J Ma , M. J Stampfer and L. A. Mucci
  Background

A recent nested case–control study found that the presence of antibodies against Trichomonas vaginalis, a common nonviral sexually transmitted infection, was positively associated with subsequent incidence of prostate cancer. We confirmed these findings in an independent population and related serostatus for antibodies against T vaginalis to prostate cancer incidence and mortality.

Methods

We conducted a case–control study nested within the Physicians’ Health Study that included 673 case subjects with prostate cancer and 673 individually matched control subjects who had available plasma samples. Plasma from blood samples collected at baseline was assayed for antibodies against T vaginalis with an enzyme-linked immunosorbent assay. We used conditional logistic regression to estimate the odds ratios (ORs) of incident prostate cancer, extraprostatic prostate cancer, and cancer that would ultimately progress to bony metastases or prostate cancer–specific death.

Results

Although not statistically significant, the magnitude of the association between T vaginalis–seropositive status and overall prostate cancer risk (OR = 1.23, 95% confidence interval [CI] = 0.94 to 1.61) was similar to that reported previously. Furthermore, a seropositive status was associated with statistically significantly increased risks of extraprostatic prostate cancer (OR = 2.17, 95% CI = 1.08 to 4.37) and of cancer that would ultimately progress to bony metastases or prostate cancer–specific death (OR = 2.69, 95% CI = 1.37 to 5.28).

Conclusions

This large prospective case–control study obtained further support for an association between a seropositive status for antibodies against T vaginalis and the risk of prostate cancer, with statistically significant associations identified for the risk of extraprostatic prostate cancer and for clinically relevant, potentially lethal prostate cancer.

  M. X Zhu , J Ma , J Parrington , P. J Calcraft , A Galione and A. M. Evans
 

Recently, we identified, for the first time, two-pore channels (TPCs, TPCN for gene name) as a novel family of nicotinic acid adenine dinucleotide phosphate (NAADP)-gated, endolysosome-targeted calcium release channels. Significantly, three subtypes of TPCs have been characterized, TPC1-3, with each being targeted to discrete acidic calcium stores, namely lysosomes (TPC2) and endosomes (TPC1 and TPC3). That TPCs act as NAADP-gated calcium release channels is clear, given that NAADP binds to high- and low-affinity sites associated with TPC2 and thereby induces calcium release and homologous desensitization, as observed in the case of endogenous NAADP receptors. Moreover, NAADP-evoked calcium signals via TPC2 are ablated by short hairpin RNA knockdown of TPC2 and by depletion of acidic calcium stores with bafilomycin. Importantly, however, NAADP-evoked calcium signals were biphasic in nature, with an initial phase of calcium release from lysosomes via TPC2, being subsequently amplified by calcium-induced calcium release (CICR) from the endoplasmic reticulum (ER). In marked contrast, calcium release via endosome-targeted TPC1 induced only spatially restricted calcium signals that were not amplified by CICR from the ER. These findings provide new insights into the mechanisms that cells may utilize to "filter" calcium signals via junctional complexes to determine whether a given signal remains local or is converted into a propagating global signal. Essentially, endosomes and lysosomes represent vesicular calcium stores, quite unlike the ER network, and TPCs do not themselves support CICR or, therefore, propagating regenerative calcium waves. Thus "quantal" vesicular calcium release via TPCs must subsequently recruit inositol 1,4,5-trisphoshpate receptors and/or ryanodine receptors on the ER by CICR to evoke a propagating calcium wave. This may call for a revision of current views on the mechanisms of intracellular calcium signaling. The purpose of this review is, therefore, to provide an appropriate framework for future studies in this area.

 
 
 
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