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| 1 | Management of postoperative spinal infections显示文摘Postoperative surgical site infection(SSI) is a common complication after posterior lumbar spine surgery. This review details an approach to the prevention,diagnosis and treatment of SSIs. Factors contributing to the development of a SSI can be split into three categories:(1) microbiological factors;(2) factors related to the patient and their spinal pathology; and(3) factors relating to the surgical procedure. SSI is most commonly caused by Staphylococcus aureus. The virulence of the organism causing the SSI can affect its presentation. SSI can be prevented by careful adherence to aseptic technique,prophylactic antibiotics,avoiding myonecrosis by frequently releasing retractors and preoperatively optimizing modifiable patient factors. Increasing pain is commonly the only symptom of a SSI and can lead to a delay in diagnosis. C-reactive protein and magnetic resonance imaging can help establish the diagnosis. Treatment requires acquiring intra-operative cultures to guide future antibiotic therapy and surgical debridement of all necrotic tissue. A SSI can usually be adequately treated without removing spinalinstrumentation. A multidisciplinary approach to SSIs is important. It is useful to involve an infectious disease specialist and use minimum serial bactericidal titers to enhance the effectiveness of antibiotic therapy. A plastic surgeon should also be involved in those cases of severe infection that require repeat debridement and delayed closure. | Vishal Hegde Dennis S Meredith Christopher K Kepler Russel C Huang | 2012 | World Journal of Orthopedics2012，3，11： | 17 |
| 2 | In vivo radiometric analysis of glucose uptake and distribution in mouse bone显示文摘Bone formation and remodeling occurs throughout life and requires the sustained activity of osteoblasts and osteoclasts,particularly during periods of rapid bone growth.Despite increasing evidence linking bone cell activity to global energy homeostasis,little is known about the relative energy requirements or substrate utilization of bone cells.In these studies,we measured the uptake and distribution of glucose in the skeleton in vivo using positron-emitting^(18)F-fluorodeoxyglucose([^(18)F]-FDG) and non-invasive,high-resolution positron emission tomography/computed tomography(PET/CT) imaging and ex vivo autoradiography.Assessment of [^(18)F]-FDG uptake demonstrated that relative to other tissues bone accumulated a significant fraction of the total dose of the glucose analog.Skeletal accumulation was greatest in young mice undergoing the rapid bone formation that characterizes early development.PET/CT imaging revealed that [^(18)F]-FDG uptake was greatest in the epiphyseal and metaphyseal regions of long bones,which accords with the increased osteoblast numbers and activity at this skeletal site.Insulin administration significantly increased skeletal accumulation of [^(18)F]-FDG,while uptake was reduced in mice lacking the insulin receptor specifically in osteoblasts or fed a high-fat diet.Our results indicated that the skeleton is a site of significant glucose uptake and that its consumption by bone cells is subject to regulation by insulin and disturbances in whole-body metabolism. | Meredith L Zoch Diane S Abou Thomas L Clemens Daniel LJ Thorek Ryan C Riddle | 2016 | Bone Research2016，4，1： | 9 |
| 3 | Prolonged high-fat-diet feeding promotes non-alcoholic fatty liver disease and alters gut microbiota in mice显示文摘BACKGROUND Non-alcoholic fatty liver disease (NAFLD) has become an epidemic largely due to the worldwide increase in obesity. While lifestyle modifications and pharmacotherapies have been used to alleviate NAFLD, successful treatment options are limited. One of the main barriers to finding safe and effective drugs for long-term use in NAFLD is the fast initiation and progression of disease in the available preclinical models. Therefore, we are in need of preclinical models that (1) mimic the human manifestation of NAFLD and (2) have a longer progression time to allow for the design of superior treatments. AIM To characterize a model of prolonged high-fat diet (HFD) feeding for investigation of the long-term progression of NAFLD. METHODS In this study, we utilized prolonged HFD feeding to examine NAFLD features in C57BL/6 male mice. We fed mice with a HFD (60% fat, 20% protein, and 20% carbohydrate) for 80 wk to promote obesity (Old-HFD group, n = 18). A low-fat diet (LFD)(14% fat, 32% protein, and 54% carbohydrate) was administered for the same duration to age-matched mice (Old-LFD group, n = 15). An additional group of mice was maintained on the LFD (Young-LFD, n = 20) for a shorter duration (6 wk) to distinguish between age-dependent and age-independent effects. Liver, colon, adipose tissue, and feces were collected for histological and molecular assessments.RESULTS Prolonged HFD feeding led to obesity and insulin resistance. Histological analysis in the liver of HFD mice demonstrated steatosis, cell injury, portal and lobular inflammation and fibrosis. In addition, molecular analysis for markers of endoplasmic reticulum stress established that the liver tissue of HFD mice have increased phosphorylated Jnk and CHOP. Lastly, we evaluated the gut microbial composition of Old-LFD and Old-HFD. We observed that prolonged HFD feeding in mice increased the relative abundance of the Firmicutes phylum. At the genus level, we observed a significant increase in the abundance of Adercreutzia, Coprococcus, Dorea, and Ruminococcus and decreased relative abundance of Turicibacter and Anaeroplasma in HFD mice. CONCLUSION Overall, these data suggest that chronic HFD consumption in mice can mimic pathophysiological and some microbial events observed in NAFLD patients. | Kandy T Velázquez Reilly T Enos Jackie E Bader Alexander T Sougiannis Meredith S Carson Ioulia Chatzistamou James A Carson Prakash S Nagarkatti Mitzi Nagarkatti E Angela Murphy | 2019 | World Journal of Hepatology2019，11，8： | 6 |
| 4 | Oncogenic Kras is required for both the initiation and maintenance of pancreatic cancer in mice显示文摘 | Collins Meredith A Bednar Filip Zhang Yaqing Brisset Jean-Christophe Galbán Stefanie Galbán Craig J Rakshit Sabita Flannagan Karen S Adsay N Volkan di Magliano Marina Pasca | 2012 | EN2012，，： | 3 |
| 5 | 新加坡成人慢性呼吸系统疾病患者6分钟步行距离的最小临床重要差异值研究(英文)显示文摘目的:6 min步行距离(6MWD)是临床上常见的功能性运动能力测试,特别是对于慢性呼吸系统疾病患者。一些文献记载了关于白种人的6MWD的最小临床重要差异(MCID),但对亚洲人群的相关信息未见记载。本研究旨在建立亚洲成人慢性呼吸道疾病患者6MWD的最小临床重要差异。方法:采用'锚定'法和'分布'法对新加坡中央医院肺康复计划登记处的资料进行了分析。'锚定'法收集确诊为慢性呼吸道疾病的患者50例,其中男38例,女12例;平均年龄(64.2±12.3)岁,通过电话采访及使用整体变化评估量表(GROC)评价患者肺康复计划后的自觉改善程度,再将患者在肺康复计划中6MWD的改变数值与相对应的患者自觉改善程度进行比较,这种关系用操作特征曲线(ROC)统计表示。通过'分布'法确定6MWD的MCID,从门诊和住院的肺康复计划(PRP)参与者中检索医疗记录136例,其中男103例,女33例;平均年龄(60.1±14.1)岁。结果 :ROC曲线表明6MWD出现临床显著性变化的最佳临界值为17.4 m,其对应的敏感性为79.4%,特异性为81.3%,阳性似然比为4.23。由'分布'法确定6MWD的最小临床重要差异值为18.6 m。结论:18.6 m为新加坡华人6MWD的最小临床重要差异的估计值。 | Meredith T L YEUNG Alan W P WONG Katherine S L HUANG Alice Y M JONES | 2015 | 康复学报2015，25，1： | 3 |
| 6 | Abnormal nasal glandular secretion in recurrent sinusitis显示文摘 | JENEY E V RAPHAEL G D MEREDITH S D | 1990 | J Allergy Clin Immunol1990，86，： | 1 |
| 7 | Oral erythromyein and the risk of sudden death from cardiac causes显示文摘 | Ray WA Murray KT Meredith S | 2004 | N Engl J Med2004，351，11： | 1 |
| 8 | Modified amino acids and peptides as substrates for the intestinal peptide transporter Pep T1显示文摘 | Meredith D Temple C S Guha N | 2000 | Eur J Biochem2000，267，12： | 1 |
| 9 | Eukaryotic initiation factor 4D, the hypusine-containing protein, is conserved among eukaryotes 显示文摘 | Gordon E D Mora R Meredith S C | 1987 | J Biol Chem1987，262，16： | 1 |
| 10 | Oral erythromycin and the risk of sudden death from cardiac causes显示文摘 | Ray WA Murray KT Meredith S | 2004 | N Engl J Med2004，351，11： | 1 |
| 11 | The effects oftime-of-exposure of alginate-coated rat embryos to calciumchloride on in vitro development and pregnancy maintenance inewes with alginate-coated 4-or 8-cell embryos显示文摘 | MEREDITH S NICKS D K KIESLING D O | 1990 | Theriog-enology1990，33，： | 1 |
| 12 | Grain refinement of aluminium alloys by inoculation 显示文摘 | GREER A L COOPER P S MEREDITH M W SCHNEIDER W SCHUMACHER P SPITTLE J A | 2003 | Advanced Engineering Materials2003，5，： | 1 |
| 13 | Transient evoked otoacoustic emissions with contralateral stimulation in King-Kopetzky syndrome显示文摘 | Zhao F Meredith R Stephens S Ozcaglar H | | 0，，： | 1 |
| 14 | Optical Transitions and Visible Upconversion in Er^3+ Doped Niobic Tellurite Glass显示文摘 | Lin H Meredith G Jiang S B | 2003 | J Appl Phys2003，93，1： | 1 |
| 15 | Modeling PD pathogenesis in mice:advantages of a chronic MPTP protacol 显示文摘 | MEREDITH GE TOTTERDELL S POTASHKIN JA | 2008 | Parkinsonism Relat Disord2008，14，2： | 1 |
| 16 | Optical transitions and visible upconversion in Er^3+ doped niobic tellurite glass显示文摘 | LIN H MEREDITH G JIANG S | 2003 | J Appl Phys2003，93，1： | 1 |
| 17 | Mouse model of Parkinsonism:a comparison between subacute MPTP and chronic MPTP/probenecid treatment显示文摘 | Petroske E Meredith GE Callen S | 2001 | Neurosci2001，106，1： | 1 |
| 18 | Design and character- ization of a membrane permeable N-methyl amino acid- containing peptide that inhibits Af31-40 fibriUogenesis 显示文摘 | Gordon D J Tappe R Meredith S C | 2002 | J Pept Res2002，60，1： | 1 |
| 19 | Lysosomal malfunction accompanies alpha-synuclein aggregation in a progressive mouse model of Parkinson's disease 显示文摘 | Meredith G E Totterdell S Petroske E | 2002 | Brain Res2002，956，1： | 1 |
| 20 | Oral erythromycin and the risk of sudden death from cardiac causes显示文摘 | Ray WA Murray KT Meredith S | 2004 | N Engl J Med2004，351，： | 1 |
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