http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Xiaoyan Feng,Xin Wen,Ling Li,Zhenchang Sun,Xin Li,Lei Zhang,Jingjing Wu,Xiaorui Fu,Xinhua Wang,Hui Yu,Xinran Ma,Xudong Zhang,Xinli Xie,Xingmin Han,Mingzhi Zhang 대한암학회 2021 Cancer Research and Treatment Vol.53 No.3
Purpose There is no optimal prognostic model for T-cell lymphoblastic lymphoma (T-LBL). Here, we discussed the predictive value of total metabolic tumor volume (TMTV) and total lesion glycolysis (TLG) measured on 18F-fluorodeoxyglucose positron emission tomography–computed tomography (PET-CT) in T-LBL.Materials and Methods Thirty-seven treatment naïve T-LBL patients with PET-CT scans were enrolled. TMTV was obtained using the 41% maximum standardized uptake value (SUVmax) threshold method, and TLG was measured as metabolic tumor volume multiplied by the mean SUV. Progression-free survival (PFS) and overall survival (OS) were analyzed by Kaplan-Meier curves and compared by the log-rank test.Results The optimal cutoff values for SUVmax, TMTV, and TLG were 12.7, 302 cm3, and 890, respectively. A high SUVmax, TMTV, and TLG indicated a shorten PFS and OS. On multivariable analysis, TMTV ≥ 302 cm3, and central nervous system (CNS) involvement predicted inferior PFS, while high SUVmax, TLG and CNS involvement were associated with worse OS. Subsequently, we generated a risk model comprising high SUVmax, TMTV or TLG and CNS involvement, which stratified the population into three risk groups, which had significantly different median PFS of not reached, 14 months, and 7 months for low-risk group, mediate-risk group, and high-risk group, respectively (p < 0.001). Median OS were not reached, 27 months, and 13 months, respectively (p < 0.001).Conclusion Baseline SUVmax, TMTV, and TLG measured on PET-CT are strong predictors of worse outcome in T-LBL. A risk model integrating these three parameters with CNS involvement identifies patients at high risk of disease progression.
( Hyeun Bum Kim ),( Yuankai Wang ),( Xingmin Sun ) 한국미생물 · 생명공학회 2016 Journal of microbiology and biotechnology Vol.26 No.3
We investigated the increased risk of Clostridium difficile infection (CDI) caused by the combined use of antibiotics and an immunosuppressive drug in a mouse model. Our data showed that an approximate return to pretreatment conditions of gut microbiota occurred within days after cessation of the antibiotic treatment, whereas the recovery of gut microbiota was delayed with the combined treatment of antibiotics and dexamethasone, leading to an increased severity of CDI. An alteration of gut microbiota is a key player in CDI. Therefore, our data implied that immunosuppressive drugs can increase the risk of CDI through the delayed recovery of altered gut microbiota.
Wang, Yuan-Kai,Yan, Ya-Xian,Kim, Hyeun Bum,Ju, Xianghong,Zhao, Song,Zhang, Keshan,Tzipori, Saul,Sun, Xingmin TaylorFrancis 2015 Human Vaccines & Immunotherapeutics Vol.11 No.9
<P><I>Clostridium difficile</I> is the major cause of hospital-acquired infectious diarrhea and colitis in developed countries. The pathogenicity of <I>C. difficile</I> is mainly mediated by the release of 2 large potent exotoxins, toxin A (TcdA) and toxin B (TcdB), both of which require neutralization to prevent disease occurrence. We have generated a novel chimeric protein, designated mTcd138, comprised of the glucosyltransferase and cysteine proteinase domains of TcdB and the receptor binding domain of TcdA and expressed it in <I>Bacillus megaterium</I>. To ensure that mTcd138 is atoxic, 2 point mutations were introduced to the glucosyltransferase domain of TcdB, which essentially eliminates toxicity of mTcd138. Parenteral immunizations of mice and hamsters with mTcd138 induced protective antibodies to both toxins and provided protection against infection with the hyper-virulent <I>C. difficile</I> strain UK6.</P>
Hyperimmune Bovine Colostrum as a Novel Therapy to Combat <i>Clostridium difficile</i> Infection
Sponseller, Jerlyn K.,Steele, Jennifer A.,Schmidt, Diane J.,Kim, Hyeun Bum,Beamer, Gillian,Sun, Xingmin,Tzipori, Saul Oxford University Press 2015 The Journal of Infectious Diseases Vol.211 No.8
<P><B><I>Background.</I></B> <I>Clostridium difficile</I> is a primary cause of antibiotic-associated diarrhea that typically develops when gut microbiota is altered. Conventional treatment for <I>C. difficile</I> infection (CDI) is additional antimicrobial administration, which further disrupts normal intestinal microbiota, often resulting in poor treatment outcomes.</P><P><B><I>Methods.</I></B> A pregnant dairy cow was repeatedly immunized with recombinant mutants of toxins A and B produced by <I>C. difficile</I>, and the resultant hyperimmune bovine colostrum (HBC) was evaluated for therapeutic efficacy in gnotobiotic piglets with diarrhea due to CDI. Control piglets received nonimmune colostrum. To determine the impact of HBC on gut microbiota, 1 of 2 groups of piglets transplanted with normal human gut microbiota was treated with HBC.</P><P><B><I>Results.</I></B> Nonimmune colostrum–treated piglets developed moderate to severe diarrhea and colitis. In contrast, HBC-treated piglets had mild or no diarrhea and mild or no colitis. Lyophilization had no detectable impact on HBC efficacy. HBC had no discernible effect on the composition of normal human gut microbiota in the porcine intestinal tract.</P><P><B><I>Conclusions.</I></B> HBC provides an oral, cost-effective, and safe alternative to antibiotic therapy for CDI. By preserving intestinal microbiota, HBC may be more efficacious than antibiotics. Additional studies are warranted to establish HBC as a viable immunotherapeutic agent for human use against CDI.</P>
Peng, Zhong,Jin, Dazhi,Kim, Hyeun Bum,Stratton, Charles W.,Wu, Bin,Tang, Yi-Wei,Sun, Xingmin American Society for Microbiology 2017 Journal of clinical microbiology Vol.55 No.7
<P>Oral antibiotics such as metronidazole, vancomycin and fidaxomicin are therapies of choice for Clostridium difficile infection. Several important mechanisms for C. difficile antibiotic resistance have been described, including the acquisition of antibiotic resistance genes via the transfer of mobile genetic elements, selective pressure in vivo resulting in gene mutations, altered expression of redox-active proteins, iron metabolism, and DNA repair, as well as via biofilm formation. This update summarizes new information published since 2010 on phenotypic and genotypic resistance mechanisms in C. difficile and addresses susceptibility test methods and other strategies to counter antibiotic resistance of C. difficile.</P>