@article{zhang_xu_liu_zhang_odle_lin_zhu_wang_liu_2019, title={EPA and DHA Inhibit Myogenesis and Downregulate the Expression of Muscle-related Genes in C2C12 Myoblasts}, volume={10}, ISSN={2073-4425}, url={http://dx.doi.org/10.3390/genes10010064}, DOI={10.3390/genes10010064}, abstractNote={This study was conducted to elucidate the biological effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on cell proliferation, differentiation and gene expression in C2C12 myoblasts. C2C12 were treated with various concentrations of EPA or DHA under proliferation and differentiation conditions. Cell viability was analyzed using cell counting kit-8 assays (CCK-8). The Edu assays were performed to analyze cell proliferation. To analyze cell differentiation, the expressions of myogenic marker genes were determined at the transcriptional and translational levels by qRT-PCR, immunoblotting and immunofluorescence. Global gene expression patterns were characterized using RNA-sequencing. Phosphorylation levels of ERK and Akt were examined by immunoblotting. Cell viability and proliferation was significantly inhibited after incubation with EPA (50 and 100 μM) or DHA (100 μM). Both EPA and DHA suppressed C2C12 myoblasts differentiation. RNA-sequencing analysis revealed that some muscle-related genes were significantly downregulated following EPA or DHA (50 μM) treatment, including insulin-like growth factor 2 (IGF-2), troponin T3 (Tnnt3), myoglobin (Mb), myosin light chain phosphorylatable fast skeletal muscle (Mylpf) and myosin heavy polypeptide 3 (Myh3). IGF-2 was crucial for the growth and differentiation of skeletal muscle and could activate the PI3K/Akt and the MAPK/ERK cascade. We found that EPA and DHA (50 μM) decreased the phosphorylation levels of ERK1/2 and Akt in C2C12 myoblasts. Thus, this study suggested that EPA and DHA exerted an inhibitory effect on myoblast proliferation and differentiation and downregulated muscle-related genes expression.}, number={1}, journal={Genes}, publisher={MDPI AG}, author={Zhang, Jing and Xu, Xin and Liu, Yan and Zhang, Lin and Odle, Jack and Lin, Xi and Zhu, Huiling and Wang, Xiuying and Liu, Yulan}, year={2019}, month={Jan}, pages={64} }
 @article{qiu_jiang_guo_zhang_burkey_zobel_reberg-horton_shew_hui_2019, title={Shifts in the Composition and Activities of Denitrifiers Dominate CO2 Stimulation of N2O Emissions}, volume={53}, ISSN={["1520-5851"]}, DOI={10.1021/acs.est.9b02983}, abstractNote={Elevated atmospheric CO2 (eCO2) often increases soil N2O emissions but the underlying mechanisms remain largely unknown. One hypothesis suggests that high N2O emissions may stem from increased denitrification induced by CO2-enhancement of plant carbon (C) allocation belowground. However, direct evidence illustrating linkages among N2O emissions, plant C allocation and denitrifying microbes under eCO2 is still lacking. We examined the impact of eCO2 on plant C allocation to roots and their associated arbuscular mycorrhizal fungi (AMF) and its subsequent effects on N2O emissions and denitrifying microbes in the presence of two distinct N sources, ammonium nitrogen (NH4+- N) and nitrate nitrogen (NO3--N). Our results showed that the form of the N inputs dominated the effects of eCO2 on N2O emissions: eCO2 significantly increased N2O emissions with NO3--N inputs but had no effect with NH4+-N inputs. eCO2 increased plant biomass N more with NH4+-N than NO3--N inputs, likely reducing microbial access to available N under NH4+-N inputs and/or contributing to higher N2O emissions under NO3--N inputs. While eCO2 enhanced root and mycorrhizal N uptake, it also increased N2O emissions under NO3--N inputs. Further, eCO2-enhancement of N2O emissions under NO3--N inputs concurred with a shift in the soil denitrifier community composition in favor of N2O-producing (nirK- and nirS-type) over N2O-consuming (nosZ-type) denitrifiers. Together, these results indicate that eCO2 stimulated N2O emissions mainly through altering plant N preference in favor of NH4+ over NO3- and thus stimulating soil denitrifiers and their activities. These findings suggest that effective management of N sources may mitigate N2O emissions by negating eCO2-stimulation of soil denitrifying microbes and their activities.}, number={19}, journal={ENVIRONMENTAL SCIENCE & TECHNOLOGY}, author={Qiu, Yunpeng and Jiang, Yu and Guo, Lijin and Zhang, Lin and Burkey, Kent O. and Zobel, Richard W. and Reberg-Horton, S. Chris and Shew, H. David and Hui, Shuijin}, year={2019}, month={Oct}, pages={11204–11213} }
 @article{kajikawa_nordone_zhang_stoeker_lavoy_klaenhammer_dean_2011, title={Dissimilar Properties of Two Recombinant Lactobacillus acidophilus Strains Displaying Salmonella FliC with Different Anchoring Motifs}, volume={77}, ISSN={["0099-2240"]}, DOI={10.1128/aem.05153-11}, abstractNote={ABSTRACT}, number={18}, journal={APPLIED AND ENVIRONMENTAL MICROBIOLOGY}, author={Kajikawa, Akinobu and Nordone, Shila K. and Zhang, Lin and Stoeker, Laura L. and LaVoy, Alora S. and Klaenhammer, Todd R. and Dean, Gregg A.}, year={2011}, month={Sep}, pages={6587–6596} }
 @article{mikkelsen_long_zhang_galemore_vandewoude_dean_2011, title={Partial Regulatory T Cell Depletion Prior to Acute Feline Immunodeficiency Virus Infection Does Not Alter Disease Pathogenesis}, volume={6}, ISSN={["1932-6203"]}, DOI={10.1371/journal.pone.0017183}, abstractNote={Feline immunodeficiency virus (FIV) infection in cats follows a disease course similar to HIV-1, including a short acute phase characterized by high viremia, and a prolonged asymptomatic phase characterized by low viremia and generalized immune dysfunction. CD4+CD25hiFoxP3+ immunosuppressive regulatory T (Treg) cells have been implicated as a possible cause of immune dysfunction during FIV and HIV-1 infection, as they are capable of modulating virus-specific and inflammatory immune responses. Additionally, the immunosuppressive capacity of feline Treg cells has been shown to be increased during FIV infection. We have previously shown that transient in vivo Treg cell depletion during asymptomatic FIV infection reveals FIV-specific immune responses suppressed by Treg cells. In this study, we sought to determine the immunological influence of Treg cells during acute FIV infection. We asked whether Treg cell depletion prior to infection with the highly pathogenic molecular clone FIV-C36 in cats could alter FIV pathogenesis. We report here that partial Treg cell depletion prior to FIV infection does not significantly change provirus, viremia, or CD4+ T cell levels in blood and lymphoid tissues during the acute phase of disease. The effects of anti-CD25 mAb treatment are truncated in cats acutely infected with FIV-C36 as compared to chronically infected cats or FIV-naïve cats, as Treg cell levels were heightened in all treatment groups included in the study within two weeks post-FIV infection. Our findings suggest that the influence of Treg cell suppression during FIV pathogenesis is most prominent after Treg cells are activated in the environment of established FIV infection.}, number={2}, journal={PLOS ONE}, author={Mikkelsen, S. Rochelle and Long, Julie M. and Zhang, Lin and Galemore, Erin R. and VandeWoude, Sue and Dean, Gregg A.}, year={2011}, month={Feb} }
 @article{ho_zhang_wei_seah_2009, title={Mycobacterium chelonae sensitisation induces CD4(+)-mediated cytotoxicity against BCG}, volume={39}, ISSN={["1521-4141"]}, DOI={10.1002/eji.200838933}, abstractNote={Abstract}, number={7}, journal={EUROPEAN JOURNAL OF IMMUNOLOGY}, author={Ho, Peiying and Zhang, Lin and Wei, Xing and Seah, Geok Teng}, year={2009}, month={Jul}, pages={1841–1849} }