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| 1 | Recent advances in the diagnosis and treatment of acute myocardial infarction显示文摘The Third Universal Definition of Myocardial Infarction(MI) requires cardiac myocyte necrosis with an increase and/or a decrease in a patient's plasma of cardiac troponin(cT n) with at least one cT n measurement greater than the 99 th percentile of the upper normal reference limit during:(1) symptoms of myocardialischemia;(2) new significant electrocardiogram(ECG) ST-segment/T-wave changes or left bundle branch block;(3) the development of pathological ECG Q waves;(4) new loss of viable myocardium or regional wall motion abnormality identified by an imaging procedure; or(5) identification of intracoronary thrombus by angiography or autopsy.Myocardial infarction,when diagnosed,is now classified into five types.Detection of a rise and a fall of troponin are essential to the diagnosis of acute MI.However,high sensitivity troponin assays can increase the sensitivity but decrease the specificity of MI diagnosis.The ECG remains a cornerstone in the diagnosis of MI and should be frequently repeated,especially if the initial ECG is not diagnostic of MI.There have been significant advances in adjunctive pharmacotherapy,procedural techniques and stent technology in the treatment of patients with MIs.The routine use of antiplatelet agents such as clopidogrel,prasugrel or ticagrelor,in addition to aspirin,reduces patient morbidity and mortality.Percutaneous coronary intervention(PCI) in a timely manner is the primary treatment of patients with acute ST segment elevation MI.Drug eluting coronary stents are safe and beneficial with primary coronary intervention.Treatment with direct thrombin inhibitors during PCI is non-inferior to unfractionated heparin and glycoprotein Ⅱb/Ⅲa receptor antagonists and is associated with a significant reduction in bleeding.The intra-coronary use of a glycoprotein Ⅱb/Ⅲa antagonist can reduce infarct size.Pre- and post-conditioning techniques can provide additional cardioprotection.However,the incidence and mortality due to MI continues to be high despite all these recent advances.The initial ten year experience with autologous human bone marrow mononuclear cells(BMCs) in patients with MI showed modest but significant increases in left ventricular(LV) ejection fraction,decreases in LV endsystolic volume and reductions in MI size.These studies established that the intramyocardial or intracoronary administration of stem cells is safe.However,many of these studies consisted of small numbers of patients who were not randomized to BMCs or placebo.The recent LateT ime,Time,and Swiss Multicenter Trials in patientswith MI did not demonstrate significant improvement in patient LV ejection fraction with BMCs in comparison with placebo.Possible explanations include the early use of PCI in these patients,heterogeneous BMC populations which died prematurely from patients with chronic ischemic disease,red blood cell contamination which decreases BMC renewal,and heparin which decreases BMC migration.In contrast,cardiac stem cells from the right atrial appendage and ventricular septum and apex in the SCIPIO and CADUCEUS Trials appear to reduce patient MI size and increase viable myocardium.Additional clinical studies with cardiac stem cells are in progress. | Koushik Reddy Asma Khaliq Robert J Henning | 2015 | World Journal of Cardiology2015，7，5： | 107 |
| 2 | Osteonecrosis of the femoral head: An update in year 2012显示文摘Osteonecrosis is a phenomenon involving disruption to the vascular supply to the femoral head, resulting in articular surface collapse and eventual osteoarthritis. Although alcoholism, steroid use, and hip trauma remain the most common causes, several other etiologies for osteonecrosis have been identified. Basic science research utilizing animal models and stem cell applications continue to further elucidate the pathophysiology of osteonecrosis and promise novel treatment options in the future. Clinical studies evaluating modern joint-sparing procedures have demonstrated significant improvements in outcomes, but hip arthroplasty is still the most common procedure performed in these affected younger adults. Further advances in joint-preserving procedures are required and will be widely studied in the coming decade. | Anjan P Kaushik Anusuya Das Quanjun Cui | 2012 | World Journal of Orthopedics2012，3，5： | 68 |
| 3 | Biomolecular basis of the role of diabetes mellitus in osteoporosis and bone fractures显示文摘Osteoporosis has become a serious health problem throughout the world which is associated with an increased risk of bone fractures and mortality among the people of middle to old ages.Diabetes is also a major health problem among the people of all age ranges and the sufferers due to this abnormality increasing day by day.The aim of this review is to summarize the possible mechanisms through which diabetes may induce osteoporosis.Diabetes mellitus generally exerts its effect on different parts of the body including bone cells specially the osteoblast and osteoclast,muscles,retina of the eyes,adipose tissue,endocrine system specially parathyroid hormone(PTH) and estrogen,cytokines,nervous system and digestive system.Diabetes negatively regulates osteoblast differentiation and function while positively regulates osteoclast differentiation and function through the regulation of different intermediate factors and thereby decreases bone formation while increases bone resorption.Some factors such as diabetic neuropathy,reactive oxygen species,Vitamin D,PTH have their effects on muscle cells.Diabetes decreases the muscle strength through regulating these factors in various ways and ultimately increases the risk of fall that may cause bone fractures. | Bipradas Roy | 2013 | World Journal of Diabetes2013，4，4： | 41 |
| 4 | 菝葜活性成份对慢性盆腔炎大鼠子宫组织肿瘤坏死因子-ɑ和白介素-4的影响显示文摘目的探讨菝葜活性成份治疗慢性盆腔炎的作用机制。方法采用化学烧伤的方法建立慢性盆腔炎大鼠模型。对70只大鼠随机分为模型对照组,假手术组,空白对照组,菝葜活性成份高、中、低剂量组,金刚藤胶囊组。治疗14 d后,观察子宫肿胀率和抑制率,酶联免疫法检测各组大鼠子宫组织中TNF-α和IL-4的表达情况。结果光学显微镜下观察显示:菝葜活性成份高、中、低剂量组能降低大鼠子宫内膜的炎症细胞,促进其病变上皮细胞增生修复,减轻浆膜充血水肿。与模型对照组比较,菝葜活性成份高、中剂量组能降低慢性盆腔模型大鼠子宫的肿胀率(P<0.01);菝葜活性成份高、中、低剂量组子宫组织中TNF-α的含量明显降低(P<0.01);菝葜活性成份高、中剂量组子宫组织中IL-4的含量明显升高(P<0.01),菝葜活性成份低剂量组子宫组织中IL-4的含量升高(P<0.05)。结论菝葜活性成份能影响慢性盆腔炎大鼠子宫的肿胀率及子宫组织中TNF-α、IL-4的水平,这可能是菝葜活性成份治疗慢性盆腔炎症和缓解盆腔粘连的药理作用机制之一。 | 罗艳琴 马云 宋路瑶 罗红成 侯连兵 | 2014 | 南方医科大学学报2014，34，2： | 41 |
| 5 | Tumor necrosis factor-α and interleukin-6 in cirrhotic patients with spontaneous bacterial peritonitis显示文摘AIM:To evaluate the role of tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) in cirrhotic patients who have hepatic and renal impairment with spontaneous bacterial peritonitis(SBP).METHODS:We prospectively studied 120 cirrhotic patients with SBP and 80 cirrhotic patients with sterile ascitic fluid.They included 144 males and 56 females with ages ranging between 34 and 62 years.The diagnosis of cirrhosis was established by clinical and laboratory criteria that did not require histological confirmation.The severity of underlying liver disease was evaluated using Pugh's modification of Child's criteria(Child-Pugh scores).Ascitic fluid was sent to the laboratory for cell count,culture,sensitivity testing,and measurement of chemical elements(i.e.,albumin,glucose).Specimens were inoculated into aerobic and anaerobic blood culture bottles.Serum and ascitic fluid were also collected in sterile tubes at study entry(before the initiation of antibiotic treatment) and 48 h later.Assays for TNF-α and IL-6 in the serum and ascitic fluid were performed with an immunoenzymometric assay using manufacture's instructions.RESULTS:Cytokine levels in serum and ascitic fluid were significantly higher in the patients with SBP.(plasma TNF-α:135.35 ng/mL ± 11.21 ng/mL vs 92.86 ng/mL ± 17.56 ng/mL,P < 0.001;plasma IL-6:32.30 pg/mL ± 7.07 pg/mL vs 12.11 pg/mL ± 6.53 pg/mL,P < 0.001;ascitic fluid TNF-α:647.54 ± 107.11 ng/mL vs 238.43 ng/mL ± 65.42 ng/mL,P < 0.001);ascitic fluid IL-6:132.84 ng/mL ± 34.13 vs 40.41 ± 12.85 pg/mL,P < 0.001).About 48(40%) cirrhotic patients with SBP developed renal and hepatic impairment and showed significantly higher plasma and ascitic fluid cytokine levels at diagnosis of infection.[(plasma TNF-α:176.58 ± 17.84 vs 135.35 ± 11.21 ng/mL)(P < 0.001) and(IL-6:57.83 ± 7.85 vs 32.30 ± 7.07 pg/mL)(P < 0.001);ascitic fluid TNF-α:958.39 ± 135.72 vs 647.54 ± 107.11 ng/mL,(P < 0.001),ascitic fluid IL-6:654.74 ± 97.43 vs 132.84 ± 34.13 pg/mL,(P < 0.001)].Twenty nine patients(60.4%) with SBP and renal impairment died whereas,only four patients(5.55%) with SBP but without renal impairment died from gastrointestinal hemorrhage(P < 0.0005).CONCLUSION:It appears that TNF-α production may enhance liver cell injury and lead to renal impairment.This correlated well with the poor prognosis and significantly increased mortality associated with SBP in cirrhotic patients. | Muhammed AM Suliman Fawzy MH Khalil Salam SA Alkindi Anil V Pathare Ali AA Almadhani Neveen AAI Soliman | 2012 | World Journal of Gastrointestinal Pathophysiology2012，3，5： | 39 |
| 6 | Changes of gut bacteria and immune parameters in liver transplant recipients显示文摘BACKGROUND: Liver transplantation is one of the most effective therapeutic options for patients with end-stage liver diseases, and gut microbiota is actively involved in potential infections in pretransplant and posttransplant patients. However, the diversity of gut microbiota and its relationship with the immune parameter of liver transplantation recipients are not well understood. METHODS: We collected fresh feces and blood samples from 190 participants in China from November 2004 to May 2008, including 28 healthy volunteers, 51 cirrhotic patients and 111 liver-transplanted patients. Six interesting gut bacteria, plasma endotoxin, serum cytokines (i.e., tumor necrosis factor alpha and interleukin-6) and fecal secretory IgA (SIgA) were investigated by real-time quantitative PCR, chromogenic limulus amoebocyte assay, sandwich-type enzyme-linked immunosorbent assay and radioimmunoassay, respectively. RESULTS: All Eubacteria, Bifidobacterium spp., Faecalibacterium prausnitzii and Lactobacillus spp. were significantly lower in the liver transplantation recipients while Enterobacteriaceae and Enterococcus spp. were significantly higher (P<0.05). Except for Enterococcus spp., other bacteria showed a tendency to restore to normal level along with the time after liver transplantation. Plasma endotoxin, interleukin-6 and fecal SIgA in cirrhotic patients increased significantly, but not in liver transplantation recipients. Plasma endotoxin and interleukin-6 were negatively correlated with all Eubacteria and the Bacteroides-Prevotella group, while tumor necrosis factor alpha was not significantly correlated with these six gut bacteria in cirrhotic patients.CONCLUSIONS: Our study demonstrates that abundant gut bacteria were altered significantly in both cirrhotic and liver transplantation patients, while plasma endotoxin and interleukin-6 increased remarkably in cirrhotic patients, showing significant correlations with gut microbiota. Interestingly, our data show a tendency for these gut bacteria to restore to normal levels in liver transplantation recipients. | Zhong-Wen Wu, Zong-Xin Ling, Hai-Feng Lu, Jian Zuo, Ji-Fang Sheng, Shu-Sen Zheng and Lan-Juan Li State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Department of Infectious Diseases Key Lab of Combined Multiorgan Transplantation, Ministry of Public Health, Key Lab of Organ Transplantation and Department of Hepatobiliary and Pancreatic Surgery , First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China | 2012 | Hepatobiliary & Pancreatic Diseases International2012，11，1： | 37 |
| 7 | 非哺乳期乳腺炎的免疫学研究进展显示文摘乳腺慢性炎症是一种临床上较少见的乳腺炎性疾病,又称非哺乳期乳腺炎,近几年发病率有明显上升趋势。但由于临床医生对该病认识不足,且病因不明,从而导致目前对该病的检出率低,治愈率低。目前认为非哺乳期乳腺炎是一个免疫相关性疾病,有多种细胞及细胞因子参与疾病的发生、发展过程。各类细胞因子在非哺乳期乳腺炎的疾病进展的不同阶段,其血浆含量不同,并有一定规律。本文就肿瘤坏死因子-α,NK细胞,干扰素-γ,CD4+T细胞亚群,树突状细胞及趋化因子与非哺乳期乳腺炎之间的关系进行综述。 | 张超杰 孔成 | 2014 | 大连医科大学学报2014，36，4： | 39 |
| 8 | Effect of cholecystokinin on cytokines during endotoxic shock in rats显示文摘AIM To study the effect of cholecystokinin-octapeptide (CCK-8) on systemic hypotension and cytokine production in lipopolysaccharide (LPS)-induced endotoxic shock (ES) rats.``METHODS The changes of blood pressure were observed using physiological record instrument in four groups of rats: LPS (8 mg. kg-1, iv) induced ES; CCK-8 (40 μg.kg- 1 iv) pretreatment 10 min before LPS (8 mg. kg- 1);CCK-8 (40 μg.kg-1, iv) or normal saline (control) groups.Differences in tissue and circulating specificity of the proinflammatory cytokines (TNF-a, IL-l3 and IL-6) were assayed with ELISA kits.``RESULTS CCK-8 reversed LPS-induced decrease of mean artery blood pressure (MABP) in rats. Compared with control, LPS elevated the serum level of IL-6 significantly (3567_-687 ng.L-1 vs 128_+22 ng.L-1, P<0.01), while contents of TNF-a and IL- lβ elevated significantly (277 _± 86ng.L-1 vs not detectable and 43 ± 9 ng.L-1 vs notdetectable, P<0.01) but less extent than IL-6, CCK-8significantly inhibited the LPS-induced increase in serum TNF-a, IL-lβ and IL-6. LPS elevated spleen and lung content of IL-Iβ significantly (5184 ± 85 ng.L-1 vs 1047 ±21 ng.L-1 and 4050 ± 614 ng.L-1 vs not detectable,P<0,01). while levels of TNF-a and IL-6 also rosesignificantly but in less extent than IL-lβ. CCK-8 inhibited the LPS-induced increase of the cytokines in spleen and lung. in the heart, CCK-8 significantly inhibited LPS.induced increase of TNF-a (864 ± 123 ng. L-1 in CCK-8 +LPS group vs 1599_-227 ng-L-1 in LPS group, P<0.01),and IL-lβ (282 ± 93 ng-L-1 in CCK-8 + LPS group vs 621 ±145 ng.L-1 in LPS group, P<0.01).``CONCLUSION CCK-8 reverses ES, which may be relatedto its inhibitory effect on the overproduction of cytokines. | Yi-Ling Ling~1 Ai-Hong Meng~1 Xiao-Yun Zhao~1 Bao-En Shan~2 Jun-Lan Zhang~1 Xiao-Peng Zhang~3 1 Department of Pathophysiology,Hebei Medical University,Shijiazhuang 050017,Hebei Province,China2 Research Center of Fourth Hospital,Hebei Medical University,Shijiazhuang 050000,Hebei Province,China3 Department of Chest Surgery of Hebei Provincial People’s Hospital,Shijiazhuang 050000,Hebei Province,China | 2001 | World Journal of Gastroenterology2001，7，5： | 31 |
| 9 | Bedside index for severity in acute pancreatitis:comparison with other scoring systems in predicting severity and organ failure显示文摘BACKGROUND:The early identification of severe acute pancreatitis is important for the management and for improving outcomes.The bedside index for severity in acute pancreatitis(BISAP)has been considered as an accurate method for risk stratification in patients with acute pancreatitis.This study aimed to evaluate the comparative usefulness of the BISAP.METHODS:We retrospectively analyzed 303 patients with acute pancreatitis diagnosed at our hospital from March 2007to December 2010.BISAP,APACHE-II,Ranson criteria,and CT severity index(CTSI)of all patients were calculated.We stratified the number of patiants with severe pancreatitis,pancreatic necrosis,and organ failure as well as the number of deaths by BISAP score.We used the area under the receiveroperating curve(AUC)to compare BISAP with other scoring systems,C-reactive protein(CRP),hematocrit,and body mass index(BMI)with regard to prediction of severe acute pancreatitis,necrosis,organ failure,and death.RESULTS:Of the 303 patiants,31(10.2%)were classified as having severe acute pancreatitis.Organ failure occurred in 23(7.6%)patients,pancreatic necrosis in 40(13.2%),and death in6(2.0%).A BISAP score of 2 was a statistically significant cutoff value for the diagnosis of severe acute pancreatitis,organ failure,and mortality.AUCs for BISAP predicting severe pancreatitis and death were 0.80 and 0.86,respectively,which were similar to those for APACHE-II(0.80,0.87)and Ranson criteria(0.74,0.74)and greater than AUCs for CTSI(0.67,0.42).The AUC for organ failure predicted by BISAP,APACHE-II,Ranson criteria,and CTSI was 0.93,0.95,0.84 and 0.57,respectively.AUCs for BISAP predicting severity,organ failure,and death were greater than those for CRP(0.69,0.80,0.72),hematocrit(0.45,0.35,0.14),and BMI(0.41,0.47,0.17).CONCLUSION:The BISAP predicts severity,death,and especially organ failure in acute pancreatitis as well as APACHE-II does and better than Ranson criteria,CTSI,CRP,hematocrit,and BMI. | Ji Young Park Tae Joo Jeon Tae Hwan Ha Jin Tae Hwang Dong Hyun Sinn Tae-Hoon Oh Won Chang Shin Won-Choong | 2013 | Hepatobiliary & Pancreatic Diseases International2013，12，6： | 33 |
| 10 | Experimental study of“Tong Xia”purgative method in ameliorating lung injury in acute necrotizing pancreatitis显示文摘AIM To investigate the role of tumor necrosisfactor(TNF)in lung injury during acutenecrotizing pancreatitis(ANP),and thetherapeutic effect of'Tong Xia'purgativemethod in minimizing the severity of lung injury.METHODS Fourteen canines were randomlydivided into 3 groups:the'Tong Xia'treatmentgroup(n = 5)using Dachengqitang;salinecontrol group(n = 5),and the sham operationgroup(n = 4).TNF activity in serum and inbronchoalveolar lavage fluid(BALF),the serumendotoxin levels were measured,and theseverity of lung injury evaluated.RESULTS Elevation of TNF activity was moreprominent in BALF than in serum.TNF activity inserum at 6 and 12 hours and in BALI:wassignificantly decreased in the'Tong Xia'treatment group than in the saline control one(q=21.11,q=12.07,q=9.03,respectively,P<0.01)and the lung injury was significantlyalleviated at 12 hours as compared with that inthe saline group,manifested as amelioration otthe lung wet/ dry weight ratio,decrease inprotein concentration and neutrophils count inBALF,and improvement of pulmonaryinflammatory changes.A positive correlationwas demonstrated between serum TNF activity and endotoxin level.CONCLUSION Hypersecretion of TNF is shownto be one of the major causes of lung injuryduring ANP;'Tong Xia'purgative method couldalleviate the degree of lung injury mediated byTNF. | Xia Q Jiang JM Gong X Chen GY Li L Huang ZW | 2000 | World Journal of Gastroenterology2000，6，1： | 31 |
| 11 | Inflammatory bowel disease and cancer: The role of inflammation, immunosuppression, and cancer treatment显示文摘In patients with inflammatory bowel disease(IBD), chronic inflammation is a major risk factor for the development of gastrointestinal malignancies. The pathogenesis of colitis-associated cancer is distinct from sporadic colorectal carcinoma and the critical molecular mechanisms underlying this process have yet to be elucidated. Patients with IBD have also been shown to be at increased risk of developing extra-intestinal malignancies. Medical therapies that diminish the mucosal inflammatory response represent the foundation of treatment in IBD, and recent evidence supports their introduction earlier in the disease course. However, therapies that alter the immune system, often used for long durations, may also promote carcinogenesis. As the population of patients with IBD grows older, with longer duration of chronic inflammation and longer exposure to immunosuppression, there is an increasing risk of cancer development. Many of these patients will require cancer treatment, including chemotherapy, radiation, hormonal therapy, and surgery. Many patients will require further treatment for their IBD. This review seeks to explore the characteristics and risks of cancer in patients with IBD, and to evaluate the limited data on patients with IBD and cancer, including management of IBD after a diagnosis of cancer, the effects of cancer treatment on IBD, and the effect of IBD and medications for IBD on cancer outcomes. | Jordan E Axelrad Simon Lichtiger Vijay Yajnik | 2016 | World Journal of Gastroenterology2016，22，20： | 33 |
| 12 | Effect of hepatocyte apoptosis induced by TNF-α on acute severe hepatitis in mouse models显示文摘AIM To study the effect of hepatocyteapoptosis and necrosis induced by TNF-α on thepathogenesis of acute severe hepatitis(ASH).METHODS The model of ASH was prepared inD-galactosamine(GAIN)sensitized BALB/c miceby injection of either endotoxin(ET)or tumornecrosis factor-α(TNF-α).Morphologicalchanges of apoptotic hepatocytes were studiedby both light and electron microscope and in siteend labeling method(ISEL).Molecular biologicalchanges of DNA ladder were observed byelectrophoresis of extract from liver tissues.Biochemical changes were measured by alanineaminotransferase(ALT),asparticaminotransferase(AST)and TNF-α.The relationbetween apoptosis and necrosis was evaluatedsimultaneously.RESULTS The sequence of hepatocyteapoptosis,necrosis,and final death from ASHwas observed both in GAIN/ET and GAIN/TNF-agroup.Apoptosis was prominent at 3.5 h and 5 hafter injection of inducer,while necrosis becamedominant at 9 h after challenge.The appearanceof apoptosis was earlier in GAIN/TNF-α groupthan that in GAIN/ ET group.Pretreatment ofmice with antiTNF IgG1 may completely preventthe liver injury induced by GalN/ET.CONCLUSION TNF-α can cause liver damageby inducing hepatic apoptosis and necrosis inmice with endotoxemia. | Guo Qing Zang Xia Qiu Zhou Hong Yu Qing Xie Guo Ming Zhao Bin Wang Qing Guo Yue Qin Xiang Dan Liao Department of Infectious Diseases,Rujin Hospital,Shanghai Second Medical University,Shanghai 200025,China | 2000 | World Journal of Gastroenterology2000，6，5： | 30 |
| 13 | Urinary trypsin inhibitor attenuates hepatic ischemia-reperfusion injury by reducing nuclear factor-kappa B activation显示文摘BACKGROUND:Urinary trypsin inhibitor(UTI)inhibits the inflammatory response and protects against ischemia- reperfusion(I/R)injury.The inflammatory response is mediated by nuclear factor-kappa B(NF-κB)and its related target genes and products such as vascular endothelial cell adhesion molecule and CXC chemokines.We aimed to assess the roles of those mediators in a UTI-treated mouse model of hepatic I/R injury. METHODS:Treatment group 1(UTI given 5 minutes prior to liver ischemia),treatment group 2(UTI given 5 minutes after the anhepatic phase)and a control group were investigated.Blood and liver samples were obtained and compared at 1,3,6 and 24 hours after reperfusion. RESULTS:Attenuation of pathological hepatocellular damage was greater in the treatment groups than in the control group(P<0.05).Compared with the control group, the UTI treatment groups showed significantly lower serum alanine aminotransferase and aspartate aminotransferase levels,decreased myeloperoxidase activity,and reduced NF- κB activation.Also downregulated was the expression of tumor necrosis factor-alpha,cytokine-induced neutrophil chemoattractant,and macrophage inflammatory protein-2 at the mRNA level.P-selectin protein and intercellular adhesion molecule-1 protein expression were also downregulated.In addition,the treatment group 1 showed a better protective effect against I/R injury than the treatment group 2.CONCLUSIONS:UTI reduces NF-κB activation and downregulates the expression of its related mediators, followed by the inhibition of neutrophil aggregation and infiltration in hepatic I/R injury.The protective role of UTI is more effective in prevention than in treatment. | Wu, Yi-Jun Ling, Qi Zhou, Xin-Hui Wang, Yan Xie, Hai-Yang Yu, Ji-Ren Zheng, Shu-Sen | 2009 | Hepatobiliary & Pancreatic Diseases International2009，8，1： | 28 |
| 14 | Inflammatory pathways of importance for management of inflammatory bowel disease显示文摘Inflammatory bowel disease(IBD)is a group of chronic disorders of the gastrointestinal tract comprising Crohn’s disease(CD)and ulcerative colitis(UC).Their etiologies are unknown,but they are characterised by an imbalanced production of pro-inflammatory mediators,e.g.,tumor necrosis factor(TNF)-α,as well as increased recruitment of leukocytes to the site of inflammation.Advantages in understanding the role of the inflammatory pathways in IBD and an inadequate response to conventional therapy in a large portion of patients,has over the last two decades lead to new therapies which includes the TNF inhibitors(TNFi),designed to target and neutralise the effect of TNF-α.TNFi have shown to be efficient in treating moderate to severe CD and UC.However,convenient alternative therapeutics targeting other immune pathways are needed for patients with IBD refractory to conventional therapy including TNFi.Indeed,several therapeutics are currently under development,and have shown success in clinical trials.These include antibodies targeting and neutralising interleukin-12/23,small pharmacologic Janus kinase inhibitors designed to block intracellular signaling of several pro-inflammatory cytokines,antibodies targeting integrins,and small anti-adhesion molecules that block adhesion between leukocytes and the intestinal vascular endothelium,reducing their infiltration into the inflamed mucosa.In this review we have elucidated the major signaling pathways of clinical importance for IBD therapy and highlighted the new promising therapies available.As stated in this paper several new treatment options are under development for the treatment of CD and UC,however,no drug fits all patients.Hence,optimisations of treatment regimens are warranted for the benefit of the patients either through biomarker establishment or other rationales to maximise the effect of the broad range of mode-of-actions of the present and future drugs in IBD. | Jannie Pedersen Mehmet Coskun Christoffer Soendergaard Mohammad Salem Ole Haagen Nielsen | 2014 | World Journal of Gastroenterology2014，20，1： | 28 |
| 15 | Advances in prognostic factors in acute pancreatitis:a mini-review显示文摘BACKGROUND:Early assessment of the severity of acute pancreatitis is essential to the proper management of the disease.It is dependent on the criteria of the Atlanta classification system.DATA SOURCES:PubMed search of recent relevant articles was performed to identify information about the severity and prognosis of acute pancreatitis.RESULTS:The scoring systems included the Ranson's or Glasgow's criteria ≥3,the APACHE II classification system ≥8,and the Balthazar's criteria ≥4 according to the computed tomography enhanced scanning findings.The single factors on admission included age >65 years,obesity,hemoconcentration(>44%),abnormal chest X-ray,creatinine >2 mg/dl,C-reactive protein>150 mg/dl,procalcitonin >1.8 ng/ml,albumin <2.5 mg/dl,calcium <8.5 mg/dl,early hyperglycemia,increased intra-abdominal pressure,macrophage migration inhibitory factor,or a combination of IL-10 >50 pg/ml with calcium <6.6 mg/dl.CONCLUSION:The prediction of the severity of acute pancreatitis is largely based on well defined multiple factor scoring systems as well as several single risk factors. | Theodoros E Pavlidis Efstathios T Pavlidis Athanasios K Sakantamis | 2010 | Hepatobiliary & Pancreatic Diseases International2010，9，5： | 25 |
| 16 | Role of inflammatory response in liver diseases: Therapeutic strategies显示文摘Inflammation and tumorigenesis are tightly linked pathways impacting cancer development. Inflammasomes are key signalling platforms that detect pathogenic microorganisms, including hepatitis C virus(HCV) infection, and sterile stressors(oxidative stress, insulin resistance, lipotoxicity) able to activate pro-inflammatory cytokines interleukin-1β and IL-18. Most of the inflammasome complexes that have been described to date contain a NOD-like receptor sensor molecule. Redox state and autophagy can regulate inflammasome complex and, depending on the conditions, can be either pro-or antiapoptotic. Acute and chronic liver diseases are cytokinedriven diseases as several proinflammatory cytokines(IL-1α, IL-1β, tumor necrosis factor-alpha, and IL-6) are critically involved in inflammation, steatosis, fibrosis, and cancer development. NLRP3 inflammasome gain of function aggravates liver disease, resulting in severe liver fibrosis and highlighting this pathway in the pathogenesis of non-alcoholic fatty liver disease. On the other hand, HCV infection is the primary catalyst for progressive liver disease and development of liver cancer. It is well established that HCV-induced IL-1β production by hepatic macrophages plays a critical and central process that promotes liver inflammation and disease. In this review, we aim to clarify the role of the inflammasome in the aggravation of liver disease, and how selective blockade of this main pathway may be a useful strategy to delay fibrosis progression in liver diseases. | José A Del Campo Paloma Gallego Lourdes Grande | 2018 | World Journal of Hepatology2018，10，1： | 25 |
| 17 | The Change of Interleukin-6 and Tumor Necrosis Factor in Patients with Obstructive Sleep Apnea Syndrome显示文摘The levels of lipopolysaccharide (LPS) induced interleukin 6 (IL 6) and tumor necrosis factor α (TNF α) expression in culture of peripheral blood mononuclear cells (PBMC) and the plasma levels of IL 6 and TNF α in the patients with obstructive sleep apnea syndrome (OSAS) were measured and the relationship between OSAS and IL 6 or TNF α expression studied. Both IL 6 and TNF α were detected by using ELISA in 22 patients with OSAS and 16 normal controls. The levels of LPS induced IL 6 (787.82±151.97 pg/ml) and TNF α (4165.45±1501.43 pg/ml) expression in the supernatant of the culture of PBMC and plasma level of IL 6 (50.67±4.70 pg/ml) and TNF α (299.09±43.57 pg/ml) in the patients with OSAS were significantly higher than those in the normal controls (in the supernatant of the culture of PBMC: 562.69±197.54 pg/ml and 1596.25±403.08 pg/ml respectively; in the plasma: 12.69±2.75 pg/ml and 101.88±21.27 pg/ml respectively). There were significantly positive correlation between the levels of IL 6 and TNF α and the percentage of time of apnea and hyponea, as well as the percentage of time spending at SaO 2 below 90 % in the total sleep time. It was concluded that LPS induced IL 6 and TNF α levels as well as plasma IL 6 and TNF α levels in the patients with OSAS were up regulated, which may be associated with the pathogenesis of OSAS. | 刘辉国 刘瑾 熊盛道 沈关心 张珍祥 徐永健 | 2000 | Journal of Huazhong University of Science and Technology(Medical Sciences)2000，20，3： | 22 |
| 18 | Bone-marrow mesenchymal stem cells reduce rat intestinal ischemia-reperfusion injury, ZO-1 downregulation and tight junction disruption via a TNF-α-regulated mechanism显示文摘AIM: To investigate the effect of bone-marrow mesenchymal stem cells (BM MSCs) on the intestinal mucosa barrier in ischemia/reperfusion (I/R) injury. METHODS: BM MSCs were isolated from male Sprague-Dawley rats by density gradient centrifugation, cultured, and analyzed by flow cytometry. I/R injury was induced by occlusion of the superior mesenteric artery for 30 min. Rats were treated with saline, BM MSCs (via intramucosal injection) or tumor necrosis factor (TNF)-α blocking antibodies (via the tail vein). I/R injury was assessed using transmission electron microscopy, hematoxylin and eosin (HE) staining, immunohistochemistry, western blotting and enzyme linked immunosorbent assay.RESULTS: Intestinal permeability increased, tight junctions (TJs) were disrupted, and zona occludens 1 (ZO-1) was downregulated after I/R injury. BM MSCs reduced intestinal mucosal barrier destruction, ZO-1 downregulation, and TJ disruption. The morphological abnormalities after intestinal I/R injury positively correlated with serum TNF-α levels. Administration of anti-TNF-α IgG or anti-TNF-α receptor 1 antibodies attenuated the intestinal ultrastructural changes, ZO-1 downregulation, and TJ disruption. CONCLUSION: Altered serum TNF-α levels play an important role in the ability of BM MSCs to protect against intestinal I/R injury. | Zhong-Yang Shen Jing Zhang Hong-Li Song Wei-Ping Zheng | 2013 | World Journal of Gastroenterology2013，19，23： | 23 |
| 19 | 不同强度有氧运动对乳腺癌大鼠癌因性疲乏及血清IL-6、TNF-α、IL-1β水平的影响显示文摘目的:探讨不同强度有氧运动对雌鼠乳腺癌化疗所致癌因性疲乏及血清IL-6、TNF-α、IL-1β水平的影响。方法:将40只雌性SD大鼠随机分为正常组(N)、模型组(C)、低等强度运动组(L)、中等强度运动组(M)和高等强度运动组(H),每组8只。除正常组外,大鼠均建立乳腺癌癌因性疲乏模型。运动组大鼠分别接受10min、20min、25min的低、中、高三种不同强度的游泳运动,1次/d,6d/周,共6周。6周后处死大鼠检测其癌因性疲乏及血清中IL-6、TNF-α和IL-1β的值。结果:化疗后,与N组相比,C组和三个运动组大鼠均出现疲乏(P<0.05)。运动后,与C组相比,L组和M组大鼠癌因性疲乏缓解(P<0.05),H组大鼠癌因性疲乏增加(P<0.01);三个运动组IL-6含量均增加,其中M组和H组IL-6含量增加有显著性意义(P<0.01);L组和M组TNF-α和IL-1β的含量下降(P<0.01),H组TNF-α和IL-1β含量增加(P<0.05)。结论:中低强度有氧运动可以缓解大鼠的癌因性疲乏,提高抗炎性因子IL-6的水平,同时降低促炎性因子TNF-α和IL-1β的水平。而高等强度有氧运动则会增加癌因性疲乏。 | 何晓玲 邹凌云 曹瑶 宋祎 徐锦江 | 2015 | 中国康复医学杂志2015，30，9： | 23 |
| 20 | Receptor-interacting protein (RIP) kinase family显示文摘Receptor-interacting protein(RIP)kinases are a group of threonine/serine protein kinases with a relatively conserved kinase domain but distinct non-kinase regions.A number of different domain structures,such as death and caspase activation and recruitment domain(CARD)domains,were found in different RIP family members,and these domains should be keys in determining the specific function of each RIP kinase.It is known that RIP kinases participate in different biological processes,including those in innate immunity,but their downstream substrates are largely unknown.This review will give an overview of the structures and functions of RIP family members,and an update of recent progress in RIP kinase research. | Duanwu Zhang Juan Lin Jiahuai Han | 2010 | Cellular & Molecular Immunology2010，7，4： | 23 |
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