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| 1 | Overview of macroautophagy regulation in mammalian cells显示文摘Macroautophagy 是 multistep, vacuolar,在 lysosomal 分隔空间终止的降级小径,和它具有在织物动态平衡的基本重要性。在这评论,我们在我们 autophagosomes 的形成的理解根据最近的进展考虑 macroautophagy,它是扣押的 double-membrane-bound 液泡细胞质的货物并且把他们送到 lysosomes。在大多数情况中,这最后的步被成熟步在哪个 autophagosomes 与 endocytic 小径交往期间先于。AuTophaGy 相关的基因的发现极大地关于为 autophagosome 形成负责的机制增加了我们的知识,并且也在 autophagosome 成熟的分子的方面的理解有进步。最后,因为 Atg 建筑群的活动被蛋白质 kinases 指向的发现, autophagy 的规定现在更好被理解,并且由于经由在调整 autophagy 基因的表示的抄写因素的原子规定的重要性。 | Maryam Mehrpour | 2010 | Cell Research2010，20，7： | 66 |
| 2 | WNT signaling regulates self-renewal and differentiation of prostate cancer cells with stem cell characteristics显示文摘有干细胞特征的前列腺癌症房间被他们在非支持者文化从单个房间形成自我更新的 prostaspheres 的能力在人的前列腺癌症房间线识别。Prostaspheres 展出了增长,区别和茎的异构的表示联系房间的制造者 CD44, ABCG2 和 CD133。有 WNT 禁止者的治疗减少了 prostasphere 尺寸和自强。相反,引起的 Wnt3a 的增加增加了 prostasphere 尺寸和自强,它与原子尾 - catenin 的重要增加被联系,角质素 18, CD133 和 CD44 表示。作为 LNCaP 和 C4-2B 癌症房间快车雄激素受体的一个高比例,我们决定了雄激素受体对手 bicalutamide 的效果。雄激素受体抑制减少了 prostasphere 尺寸和 PSA 的表示,但是没禁止 prostasphere 形成。这些效果与有干细胞特征和放大房间的运输的雄激素依赖者增长的房间的雄激素无关的自强一致。作为发信号的受动器尾 - catenin 能也与雄激素受体联系的正规 WNT,我们为包含在 WNT 和雄激素受体活动之间的平衡的瘤繁殖建议一个模型。那将与干细胞特征和开车运输放大房间增长和区别影响一个癌症房间的自强。在结论,我们提供那项 WNT 活动独立于雄激素受体活动与干细胞特征调整前列腺癌症房间的自强的证据。WNT 发信号的抑制因此有潜力与干细胞特征减少前列腺癌症房间的自强并且改进治疗学的结果。 | Isabelle Bisson David M Prowse | 2009 | Cell Research2009，，6： | 37 |
| 3 | SJWD14121600000297显示文摘 | Jacques Ferlay Isabelle Soerjomataram Rajesh Dikshit Sultan Eser Colin Mathers Marise Rebelo Donald Maxwell Parkin David Forman Freddie Bray | 2015 | Int. J. Cancer2015，，5： | 31 |
| 4 | Overlapping expression of microRNAs in human embryonic colon and colorectal cancer显示文摘MicroRNAs (miRNAs ) 为调整房间区别并且维持干细胞的 pluripotent 状态是必要的。尽管特定的 miRNAs 的 dysregulation 与癌症的某些类型被联系了,到日期,没有证据连接了 miRNA 表示在胚胎并且肿瘤纸巾。我们在人的胚胎的结肠组织,并且在 colorectal 癌症估计了成熟 miRNAs 的表示并且配对正常结肠组织。重叠 miRNA 表示在胚胎的结肠的 mucosa 和 colorectal 癌症之间被检测。我们发现了 miR-17-92 聚类,调整在两个盒子中的房间增长并且它的目标, E2F1,在人的冒号开发和结肠的 carcinogenesis 展出表示的一个类似的模式。在 situ,杂交在地窟祖先分隔空间证实了 miR-17-5p 的表示的高水平。我们断定 miRNA 小径在胚胎的开发和结肠的上皮的肿瘤的转变起一个主要作用。 | Mariano Monzo Alfons Navarro Eva Bandres Rosa Artells Isabel Moreno Bemat Gel Rafael Ibeas Jose Moreno Francisco Martinez Tania Diaz Antonio Martinez Olga Balague Jesus Garcia-Foncillas | 2008 | Cell Research2008，18，8： | 32 |
| 5 | Risk factors associated with the development of ischemic colitis显示文摘AIM:To ascertain the role of cardiovascular risk factors,cardiovascular diseases,standard treatments and other diseases in the development of ischemic colitis(IC).METHODS:A retrospective,case-control study was designed,using matched data and covering 161 incident cases of IC who required admission to our hospital from 1998 through 2003.IC was diagnosed on the basis of endoscopic findings and diagnostic or compatible his-tology.Controls were randomly chosen from a cohort of patients who were admitted in the same period and required a colonoscopy,excluding those with diagnosis of colitis.Cases were matched with controls(ratio 1:2),by age and sex.A conditional logistic regression was performed.RESULTS:A total of 483 patients(161 cases,322 con-trols)were included;mean age 75.67±10.03 years,55.9%women.The principal indications for colonos-copy in the control group were lower gastrointestinal hemorrhage(35.4%),anemia(33.9%),abdominal pain(19.9%)and diarrhea(9.6%).The endoscopic findings in this group were hemorrhoids(25.5%),diverticular disease(30.4%),polyps(19.9%)and colorectal cancer(10.2%).The following variables were associated with IC in the univariate analysis:arterial hypertension(P= 0.033);dyslipidemia(P<0.001);diabetes mellitus(P =0.025);peripheral arterial disease(P=0.004);heart failure(P=0.026);treatment with hypotensive drugs(P=0.023);angiotensin-converting enzyme inhibitors;(P=0.018);calcium channel antagonists(P=0.028);and acetylsalicylic acid(ASA)(P<0.001).Finally,the following variables were independently associated with the development of IC:diabetes mellitus[odds ratio(OR)1.76,95%confidence interval(CI):1.001-3.077,P=0.046];dyslipidemia(OR 2.12,95%CI:1.26-3.57,P=0.004);heart failure(OR 3.17,95%CI:1.31-7.68,P=0.01);peripheral arterial disease(OR 4.1,95%CI:1.32-12.72,P=0.015);treatment with digoxin(digitalis)(OR 0.27,95%CI:0.084-0.857,P=0.026);and ASA(OR 1.97,95%CI:1.16-3.36,P=0.012).CONCLUSION:The development of an episode of IC was independently associated with diabetes,dyslipid-emia,presence of heart failure,peripheral arterial dis-ease and treatment with digoxin or ASA. | Joaquín Cubiella Fernández Luisa Núez Calvo Elvira González Vázquez Maria Jesús García García Maria Teresa Alves Pérez Isabel Martínez Silva Javier Fernández Seara | 2010 | World Journal of Gastroenterology2010，16，36： | 27 |
| 6 | Dysregulation of apoptosis in hepatocellular carcinoma cells显示文摘Hepatocellular carcinoma (HCC) is a major health problem, being the sixth most common cancer world-wide. Dysregulation of the balance between proliferation and cell death represents a pro-tumorigenic principle in human hepatocarcinogenesis. This review updates the recent relevant contributions reporting molecular alterations for HCC that induce an imbalance in the regulation of apoptosis. Alterations in the expression and/or activation of p53 are frequent in HCC cells, which confer on them resistance to chemotherapeutic drugs. Many HCCs are also insensitive to apoptosis induced either by death receptor ligands, such as FasL or TRAIL, or by transforming growth factor-beta (TGF-β). Although the expression of some pro-apoptotic genes is decreased, the balance between death and survival is dysregulated in HCC mainly due to overactivation of anti-apoptotic pathways. Indeed, some molecules involved in counteracting apoptosis, such as Bcl-XL, Mcl-1, c-IAP1, XIAP or survivin are over-expressed in HCC cells. Furthermore, some growth factors that mediate cell survival are upregulated in HCC, as well as the molecules involved in the machinery responsible for cleavage of their proforms to an active peptide. The expression and/or activation of the JAK/STAT, PI3K/AKT and RAS/ERKs pathways are enhanced in many HCC cells, conferring on them resistance to apoptotic stimuli. Finally, recent evidence indicates that inflammatory processes, as well as the epithelial-mesenchymal transitions that occur in HCC cells to facilitate their dissemination, are related to cell survival. Therefore, therapeutic strategies to selectively inhibit anti-apoptotic signals in liver tumor cells have the potential to provide powerful tools to treat HCC. | Isabel Fabregat | 2009 | World Journal of Gastroenterology2009，15，5： | 28 |
| 7 | Obesity leads to higher risk of sperm DNA damage in infertile patients显示文摘在在富饶上的男营养的影响的过去几年有成长兴趣。不孕被连接了到男过重或肥胖,并且常规精液参数值似乎在高身体团索引(BMI ) 的情况下被改变。在精子 DNA 正直上估计 BMI 的影响的一些研究被出版了,但是他们没导致强壮的一致。我们的目的是进一步探索在精子 DNA 正直和 BMI 之间的关系,通过 3 年的 multicentre 研究。在 subfertile 夫妇的 330 个男搭挡被包括。用标记的终端 uridine 刻痕结束(TUNEL ) 试金,我们在肥胖的人观察了精子 DNA 损坏的增加的率(机会比率(95 %信心间隔) :2.5 (1.2-5.1 )) 。 | Charlotte Dupont Celine Fauret Nathalie Sermondade Marouane Boubaya Florence Eustache Patrice Clement Pascal Briot Isabelle Berthaut Vincent Levy Isabelle Cedrin-Durnerin Brigitte Benzacken Pascale Chavatte-Palmer Rachel Levy | 2013 | Asian Journal of Andrology2013，15，5： | 27 |
| 8 | Interleukin-33 drives hepatic fibrosis through activation of hepatic stellate cells显示文摘Liver fibrosis is a consequence of chronic liver disease,causing morbidity and mortality.Interleukin-33(IL-33)is a critical mediator of inflammation,which may be involved in the development of liver fibrosis.Here,we investigated the role of IL-33 in human patients and experimental bile-duct ligation(BDL)-induced fibrosis in mice.We report increased hepatic IL-33 expression in the murine BDL model of fibrosis and in surgical samples obtained from patients with liver fibrosis.Liver injury,inflammatory cell infiltration and fibrosis were reduced in the absence of the IL-33/ST2 receptor,and the activation of hepatic stellate cells(HSCs)was decreased in ST2-deficient mice.Recombinant IL-33 activated HSCs isolated from C57BL/6 mice,leading to the expression of IL-6,TGF-β,α-SMA and collagen,which was abrogated in the absence of ST2 or by pharmacological inhibition of MAPK signaling.Finally,administration of recombinant IL-33 significantly increased hepatic inflammation in sham-operated BL6 mice but did not enhance BDL-induced hepatic inflammation and fibrosis.In conclusion,BDL-induced liver inflammation and fibrosis are dependent on ST2 signaling in HSCs,and therefore,the IL-33/ST2 pathway may be a potential therapeutic target in human patients with chronic hepatitis and liver fibrosis. | Zhongming Tan Qianghui Liu Runqiu Jiang Long Lv Siamak S Shoto Isabelle Maillet Valerie Quesniaux Junwei Tang Wenjie Zhang Beicheng Sun Bernhard Ryffel | 2018 | Cellular & Molecular Immunology2018，15，4： | 24 |
| 9 | Helicobacter pylori and oral pathology:Relationship with the gastric infection显示文摘Helicobacter pylori(H.pylori)has been found in the oral cavity and stomach,and its infection is one of the most frequent worldwide.We reviewed the literature and conducted a Topic Highlight,which identified studies reporting an association between H.pylori-infection in the oral cavity and H.pylori-positive stomach bacterium.This work was designed to determine whether H.pylori is the etiologic agent in periodontal disease,recurrent aphthous stomatitis(RAS),squamous cell carcinoma,burning and halitosis.Record selection focused on the highest quality studies and meta-analyses.We selected 48 articles reporting on the association between saliva and plaque and H.pylori-infection.In order to assess periodontal disease data,we included 12 clinical trials and 1 meta-analysis.We evaluated 13 published articles that addressed the potential association with RAS,and 6 with squamous cell carcinoma.Fourteen publications focused on our questions on burning and halitosis.There is a close relation between H.pylori infection in the oral cavity and the stomach.The mouth is the first extra-gastric reservoir.Regarding the role of H.pylori in the etiology of squamous cell carcinoma,no evidence is still available. | Isabel Adler Andrea Muio Silvia Aguas Laura Harada Mariana Diaz Adriana Lence Mario Labbrozzi Juan Manuel Muio Boris Elsner Alejandra Avagnina Valeria Denninghoff | 2014 | World Journal of Gastroenterology2014，20，29： | 21 |
| 10 | TNF-α Induces Transient Resistance to Fas-Induced Apoptosis in Eosinophilic Acute Myeloid Leukemia Cells显示文摘Tumor necrosis factor α (TNF-α) has been recognized as an activator of nuclear factor κB (NF-κB), a factor implicated in the protection of many cell types from apoptosis. We and others have presented evidence to suggest that Fas-induced apoptosis may be an important aspect of the resolution of inflammation, and that delayed resolution of inflammation may be directly associated with NF-κB-dependent resistance to Fas. Because TNF-α activates NF-κB in many cell types including inflammatory cells such as eosinophils, we examined effects of TNF-α signaling on the Fas-mediated killing of an eosinophilic cell line AML14. While agonist anti-Fas (CH11) treatment induced apoptosis in AML14 cells, no significant cell death occurred in response to TNF-α alone. Electrophoretic mobility shift assay (EMSA) revealed that TNF-α induced NF-κB transactivation in AML14 cells in a time- and dose-dependent fashion, and subsequent supershift assays indicated that the translocated NF-κB was the heterodimer p65 (RelA)/p50. Pre-treatment of cells with TNF-α dramatically decreased the CH11-induced cell death in a transient fashion, accompanied by suppression of activation of caspase-8 and caspase-3 activation. Inhibition of NF-κB transactivation by inhibitors, BAY 11-7085 and parthenolide, reversed the suppression of Fas-mediated apoptosis by TNF-α. Furthermore, TNF-α up-regulated X-linked inhibitor of apoptosis protein (XIAP) transiently and XIAP levels were correlated with the temporal pattern of TNF-α protection against Fas-mediated apoptosis. This finding suggested that TNF-α may contribute to the prolonged survival of inflammatory cells by suppression of Fas-mediated apoptosis, the process involved with NF-κB transactivation,anti-apoptotic XIAP up-regulation and caspase | Yimin Qin Sogyong Auh Lyubov Blokh Catherine Long Isabelle Gagnon Kimm J. Hamann | 2007 | Cellular & Molecular Immunology2007，4，1： | 19 |
| 11 | Exogenous neural stem cell transplantation for cerebral ischemia显示文摘Cerebral ischemic injury is the main manifestation of stroke,and its incidence in stroke patients is 70–80%.Although ischemic stroke can be treated with tissue-type plasminogen activator,its time window of effectiveness is narrow.Therefore,the incidence of paralysis,hypoesthesia,aphasia,dysphagia,and cognitive impairment caused by cerebral ischemia is high.Nerve tissue regeneration can promote the recovery of the aforementioned dysfunction.Neural stem cells can participate in the reconstruction of the damaged nervous system and promote the recovery of nervous function during self-repair of damaged brain tissue.Neural stem cell transplantation for ischemic stroke has been a hot topic for more than 10 years.This review discusses the treatment of ischemic stroke with neural stem cells,as well as the mechanisms of their involvement in stroke treatment. | Ling-Yi Liao Benson Wui-Man Lau Dalinda Isabel Sánchez-Vidana Qiang Gao | 2019 | Neural Regeneration Research2019，14，7： | 19 |
| 12 | Assessment of drug-induced hepatotoxicity in clinical practice: A challenge for gastroenterologists显示文摘Currently, pharmaceutical preparations are serious contributors to liver disease; hepatotoxicity ranking as the most frequent cause for acute liver failure and post-commercialization regulatory decisions. The diagnosis of hepatotoxicity remains a difficult task because of the lack of reliable markers for use in general clinical practice. To incriminate any given drug in an episode of liver dysfunction is a step-by-step process that requires a high degree of suspicion, compatible chronology, awareness of the drug’s hepatotoxic potential, the exclusion of alternative causes of liver damage and the ability to detect the presence of subtle data that favors a toxic etiology. This process is time-consuming and the final result is frequently inaccurate. Diagnostic algorithms may add consistency to the diagnostic process by translating the suspicion into a quantitative score. Such scales are useful since they provide a framework that emphasizes the features that merit attention in cases of suspected hepatic adverse reaction as well. Current efforts in collecting bona fide cases of drug-induced hepatotoxicity will make refinements of existing scales feasible. It is now relatively easy to accommodate relevant data within the scoring system and to delete low-impact items. Efforts should also be directed toward the development of an abridged instrument for use in evaluating suspected drug-induced hepatotoxicity at the very beginning of the diagnosis and treatment process when clinical decisions need to be made. The instrument chosen would enable a confident diagnosis to be made on admission of the patient and treatment to be fine-tuned as further information is collected. | Raúl J Andrade Mercedes Robles Alejandra Fernández-Castaer Susana López-Ortega M Carmen López-Vega M Isabel Lucena | 2007 | World Journal of Gastroenterology2007，13，3： | 18 |
| 13 | SJWD14121600000297显示文摘 | Jacques Ferlay Isabelle Soerjomataram Rajesh Dikshit Sultan Eser Colin Mathers Marise Rebelo Donald Maxwell Parkin David Forman Freddie Bray | 2015 | Cancer2015，，5： | 15 |
| 14 | Consequences of gestational and pregestational diabetes on placental function and birth weight显示文摘Maternal diabetes constitutes an unfavorable environment for embryonic and fetoplacental development. Despite current treatments, pregnant women with pregestational diabetes are at increased risk for congenital malformations, materno-fetal complications, placental abnormalities and intrauterine malprogramming. The complications during pregnancy concern the mother (gravidic hypertension and/or preeclampsia, cesarean section) and the fetus (macrosomia or intrauterine growth restriction, shoulder dystocia, hypoglycemia and respiratory distress). The fetoplacental impairment and intrauterine programming of diseases in the offspring's later life induced by gestational diabetes are similar to those induced by type 1 and type 2 diabetes mellitus. Despite the existence of several developmental and morphological differences in the placenta from rodents and women, there are similarities in the alterations induced by maternal diabetes in the placenta from diabetic patients and diabetic experimental models. From both human and rodent diabetic experimentalmodels, it has been suggested that the placenta is a compromised target that largely suffers the impact of maternal diabetes. Depending on the maternal metabolic and proin ammatory derangements, macrosomia is explained by an excessive availability of nutrients and an increase in fetal insulin release, a phenotype related to the programming of glucose intolerance. The degree of fetal damage and placental dysfunction and the availability and utilisation of fetal substrates can lead to the induction of macrosomia or intrauterine growth restriction. In maternal diabetes, both the maternal environment and the genetic background are important in the complex and multifactorial processes that induce damage to the embryo, the placenta, the fetus and the offspring. Nevertheless, further research is needed to better understand the mechanisms that govern the early embryo development, the induction of congenital anomalies and fetal overgrowth in maternal diabetes. | Anne Vambergue Isabelle Fajardy | 2011 | World Journal of Diabetes2011，2，11： | 14 |
| 15 | Laboratory pull-out tests on fully grouted rock bolts and cable bolts:Results and lessons learned显示文摘Laboratory pull-out tests were conducted on the following rock bolts and cable bolts:steel rebars,smooth steel bars,fiberglass reinforced polymer threaded bolts,flexible cable bolts,IR5/IN special cable bolts and Mini-cage cable bolts.The diameter of the tested bolts was between 16 mm and 26 mm.The bolts were grouted in a sandstone sample using resin or cement grouts.The tests were conducted under either constant radial stiffness or constant confining pressure boundary conditions applied on the outer surface of the rock sample.In most tests,the rate of displacement was about 0.02 mm/s.The tests were performed using a pull-out bench that allows testing a wide range of parameters.This paper provides an extensive database of laboratory pull-out test results and confirms the influence of the confining pressure and the embedment length on the pull-out response(rock bolts and cable bolts).It also highlights the sensitivity of the results to the operating conditions and to the behavior of the sample as a whole,which cannot be neglected when the test results are used to assess the bolt-grout or the grouterock interface. | Isabelle Thenevin Laura Blanco-Martín Faouzi Hadj-Hassen Jacques Schleifer Zbigniew Lubosik Aleksander Wrana | 2017 | Journal of Rock Mechanics and Geotechnical Engineering2017，9，5： | 14 |
| 16 | Oxidative damage in the progression of chronic liver disease to hepatocellular carcinoma:An intricate pathway显示文摘The histo-pathologic and molecular mechanisms leading to initiation and progression of hepatocellular carcinoma(HCC)are still ill-defined;however,there is increasing evidence that the gradual accumulation of mutations,genetic and epigenetic changes which occur in preneoplastic hepatocytes results in the development of dysplastic foci,nodules,and finally,overt HCC.As well as many other neoplasias,liver cancer is considered an'inflammatory cancer',arising from a context of inflammation,and characterized by inflammation-related mechanisms that favor tumor cell survival,proliferation,and invasion.Molecular mechanisms that link inflammation and neoplasia have been widely investigated,and it has been well established that inflammatory cells recruited at these sites with ongoing inflammatory activity release chemokines that enhance the production of reactive oxygen species.The latter,in turn,probably have a major pathogenic role in the continuum starting from hepatitis followed by chronic inflammation,and ultimately leading to cancer.The relationship amongst chronic liver injury,free radical production,and development of HCC is explored in the present review,particularly in the light of the complex network that involves oxidative DNA damage,cytokine synthesis,telomere dysfunction,and microRNA regulation. | Romilda Cardin Marika Piciocchi Marina Bortolami Andromachi Kotsafti Luisa Barzon Enrico Lavezzo Alessandro Sinigaglia Kryssia Isabel Rodriguez-Castro Massimo Rugge Fabio Farinati | 2014 | World Journal of Gastroenterology2014，20，12： | 14 |
| 17 | Nutrition therapy:Integral part of liver transplant care显示文摘Managing malnutrition before liver transplantation(LTx) while on the waiting list and, excessive weight gain/metabolic disturbances in post-surgery are still a challenge in LTx care. The aim of this review is to support an interdisciplinary nutrition approach of these patients. Cirrhotic patients are frequently malnourished before LTx and this is associated with a poor prognosis. Although the relation between nutritional status versus survival, successful operation and recovery after LTx is well established, prevalence of malnutrition before the operation is still very high. Emerging research has also demonstrated that sarcopenia pre and post-transplant is highly prevalent, despite the weight gain in the postoperative period. The diagnosis of the nutritional status is the first step to address the adequate nutritional therapy. Nutritional recommendations and therapy to manage the nutritional status of LTx patients are discussed in this review, regarding counseling on adequate diets and findings of the latest research on using certain immunonutrients in these patients(branched chain amino-acids, pre and probiotics). Nutrition associated complications observed after transplantation is also described. They are commonly related to the adverse effects of immunosuppressive drugs, leading to hyperkalemia, hyperglycemia and weight gain. Excessive weight gain and post-transplant metabolic disorders have long been described in post-LTx and should be addressed in order to reduce associated morbidity and mortality. | Lucilene Rezende Anastácio Maria Isabel Toulson Davisson Correia | 2016 | World Journal of Gastroenterology2016，22，4： | 14 |
| 18 | 国际糖尿病足工作组:糖尿病足溃疡预防指南——《国际糖尿病足工作组:糖尿病足防治国际指南(2019)》的一部分显示文摘国际糖尿病足工作组(IWGDF)1999年发布了关于预防和管理糖尿病足病的循证指南。该指南旨在预防糖尿病患者的足部溃疡,并在2015年,IWGDF对预防指南进行了更新。我们遵循GRADE(grading of recommendations assessment development and evaluation)的评分方法,采用以患者为观察对象、有干预措施、与对照组进行比较、观察结局(patient-intervention-comparison-outcome,PICO)的方法来设计临床问题和关键成果,对医学科学文献进行系统评价,并撰写推荐意见及其理由。这些推荐基于系统评价中发现的证据质量、专家意见,以及益处及危害的权重、患者偏好、可行性和适用性以及与干预相关成本的权衡。我们建议对处于极低溃疡风险的患者每年做一次筛查,了解其是否有周围神经病变和外周血管病变,对高风险人群检查的频率要更高,以筛查其他危险因素。为了预防足溃疡,要对有危险因素的患者进行健康教育,教育患者适当地对足部进行自我护理以及对溃疡前症状进行有效治疗。指导中高危患者穿着合适的治疗鞋,并对其足部皮肤温度进行监测。处方治疗鞋在行走过程中具有明显的减轻足底压力的效果,能够防止足底溃疡复发。急性足溃疡或即将发生的足溃疡保守治疗失败,应考虑手术干预。我们不建议使用神经松解减压术。对高危患者给予综合足部医疗护理,以防溃疡复发。贯彻这些推荐将有助于医疗专业人员对有足溃疡风险的糖尿病患者提供更好的护理,降低糖尿病足溃疡的发生率,使足部健康维持更长的时间即增加无足病的天数,显著减少糖尿病患者和医疗机构的负担。 | Sicco A.Bus Larry A.Lavery Matilde Monteiro-Soares Anne Rasmussen Anita Raspovic Isabel C.N.Sacco Jaap J.van Netten 无 罗颖琪 李炳辉(译) 许樟荣(审校) | 2019 | 感染.炎症.修复2019，20，3： | 14 |
| 19 | 温度对海带幼孢子体生长和光合作用的影响显示文摘根据欧盟项目的总体研究计划 ,在室内和围隔实验中研究了海带幼孢子体在不同温度条件下的生长情况和光合作用曲线 ,得出幼孢子体在 15°C下生长情况最好 ,而且其长度和重量的日增加量均和温度有线性相关关系。 Pm 值在 15℃时为 5 79mol O2 / (g DW· h) ,围隔实验中为 6 4 2 (mol O2 / (g DW· h)。由于围隔实验海区的光照强于室内 ,使得围隔中海带的光合作用曲线其光饱和点高于室内实验海带的光饱和点。海带光饱和参数 (Ik)与温度有线性相关关系 (R2 =0 .736 7,p<0 .0 5 )。5℃时 ,Ik 值平均为 96μE/ (m2 · s) ,10℃时为 71μE/ (m2 · s) ,15℃时为 31μE/ (m2 · s)。呼吸速率 R值在 5℃时最低 ,为 5 4μmol O2 / (g DW·h) ,10℃、15℃和围隔中均高于 5℃时的呼吸速率 ,并且在 10℃达到最高。本次实验研究得出的生长和光合作用参数将有助于合理确定桑沟湾中海带的养殖容量。 | 朱明远 吴荣军 李瑞香 岳国锋 孙丕喜 Jean-Marc Deslous-Paoli Isabelle Auby | 2004 | 生态学报2004，24，1： | 14 |
| 20 | Therapy with stem cells in inflammatory bowel disease显示文摘Inflammatory bowel disease(IBD) affects a part of the young population and has a strong impact upon quality of life. The underlying etiology is not known, and the existing treatments are not curative. Furthermore, a significant percentage of patients are refractory to therapy. In recent years there have been great advances in our knowledge of stem cells and their therapeutic applications. In this context, autologous hematopoietic stem cell transplantation(HSCT) has been used in application to severe refractory Crohn's disease(CD), with encouraging results. Allogenic HSCT would correct the genetic defects of the immune system, but is currently not accepted for the treatment of IBD because of its considerable risks. Mesenchymal stem cells(MSCs) have immune regulatory and regenerative properties, and low immunogenicity(both autologous and allogenic MSCs). Based on these properties, MSCs have been used via the systemic route in IBD with promising results, though it is still too soon to draw firm conclusions. Their local administration in perianal CD is the field where most progress has been made in recent years, with encouraging results. The next few years will be decisive for defining the role of such therapy in the management of IBD. | María del Pilar Martínez-Montiel Gonzalo Jesús Gómez-Gómez Ana Isabel Flores | 2014 | World Journal of Gastroenterology2014，20，5： | 13 |
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