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68篇 您的检索式:作者名="Liat"
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1Treatment of hepatocellular carcinoma: Steps forward but still a long way to go显示文摘Hepatocellular carcinoma(HCC) is the fifth most common malignancy and the third cause of tumor associated deaths worldwide. HCC incidence rates are increasing in many parts of the world including developing and developed countries. Potentially curative treatments for HCC are resection and liver transplantation, but these are only suitable for patients with small tumors, meeting strict pre-defined criteria, or well-compensated liver disease. Early diagnosis of HCCcan be achieved by surveillance of at-risk populations. For patients with non-resectable disease treatments modalities include loco-ablative and systemic therapies. In this review we focus on treatment options in HCC and their allocation. Although significant research is in progress, to this date, the results are unsatisfactory with limited long-term survival. In the fight against this deadly disease, there is still a long way to go.Liat Mlynarsky Yoram Menachem Oren Shibolet 2015World Journal of Hepatology2015,7,3:13
2Nutritional issues in patients with obesity and cirrhosis显示文摘Obesity and metabolic syndrome are considered as responsible for a condition known as the non-alcoholic fatty liver disease that goes from simple accumulation of triglycerides to hepatic inflammation and may progress to cirrhosis.Patients with obesity also have an increased risk of primary liver malignancies and increased body mass index is a predictor of decompensation of liver cirrhosis.Sarcopenic obesity confers a risk of physical impairment and disability that is significantly higher than the risk induced by each of the two conditions alone as it has been shown to be an independent risk factor for chronicliver disease in patients with obesity and a prognostic negative marker for the evolution of liver cirrhosis and the results of liver transplantation.Cirrhotic patients with obesity are at high risk for depletion of various fat-soluble,water-soluble vitamins and trace elements and should be supplemented appropriately.Diet,physical activity and protein intake should be carefully monitored in these fragile patients according to recent recommendations.Bariatric surgery is sporadically used in patients with morbid obesity and cirrhosis also in the setting of liver transplantation.The risk of sarcopenia,micronutrient status,and the recommended supplementation in patients with obesity and cirrhosis are discussed in this review.Furthermore,the indications and contraindications of bariatric surgery-induced weight loss in the cirrhotic patient with obesity are discussed.Luigi Schiavo Luca Busetto Manuela Cesaretti Shira Zelber-Sagi Liat Deutsch Antonio Iannelli 2018World Journal of Gastroenterology2018,24,30:9
3Hepatocellular carcinoma in the post-hepatitis C virus era: Should we change the paradigm?显示文摘Hepatocellular carcinoma (HCC) is a common and deadly malignancy. The disease usually develops on a background of chronic liver disease. Until recently, the most common etiology was infection with the hepatitis C virus (HCV). The advent of direct-acting antiviral (DAA) therapies has been a major breakthrough in HCV treatment. Sustained virologic response can now be achieved in almost all treated patients, even in patients with a high risk for the development of HCC, such as the elderly or those with significant fibrosis. Early reports raised concerns of a high risk for HCC occurrence after DAA therapy both in patients with previous resection of tumors and those without previous tumors. As the World Health Organization’s goals for eradication of HCV are being endorsed worldwide, the elimination of HCV seems feasible. Simultaneous to the decrease in the burden of cirrhosis from HCV, non-alcoholic fatty liver disease (NAFLD) incidence has been increasing dramatically including significant increased incidence of cirrhosis and HCC in these patients. Surprisingly, a substantial proportion of patients with NAFLD were shown to develop HCC even in the absence of cirrhosis. Furthermore, HCC treatment and potential complications are known to be influenced by liver steatosis. These changes in etiology and epidemiology of HCC suggest the beginning of a new era: The post–HCV era. Changes may eventually undermine current practices of early detection, surveillance and management of HCC. We focused on the risk of HCC occurrence and recurrence in the post–HCV era, the surveillance needed after DAA therapy and current studies in HCC patients with NAFLD.Hadar Meringer Oren Shibolet Liat Deutsch 2019World Journal of Gastroenterology2019,25,29:6
4Germline mutation analysis of hPMS2 gene in Chinese families with hereditary nonpolyposis colorectal cancer显示文摘AIM: To study the germline mutation of hPMS2 gene in 26 unrelated Chinese hereditary nonpolyposis colorectal cancer (HNPCC) probands and to fulfill the screening strategy for HNPCC in Chinese. METHODS: Genomic DNA was extracted from the peripheral blood. To avoid the interference of pseudogene in detection of the remaining 11 exons (exon 1-5, 9, 11-15), long-range polymerase chain reaction (PCR) was conducted to amplify the complete coding region of hPMS2 gene firstly. Then 1/8 of the PCR productswere used as template to amplify the individual exon respectively and DNA sequencing was done. Direct DNA sequencing of the conventional PCR products of exon 6, 7, 8 and 10 of hPMS2 gene was performed. The same analysis was made in 130 healthy persons without family histories of HNPCC to further investigate the pathological effects of the detected missense mutation. RESULTS: One HNPCC proband fulf illed Bethesda guidelines and was found to carry the germline mutation of hPMS2 gene, which has not been reported in Chinese HNPCC families. It was a missense mutation at c.1532C>T of exon 11. It was detected in three controls as well with an occurrence rate of 2.3% (3/130). Since it could not be found in the PMS2-single nucleotide polymorphism (SNP) database, this missense mutation is a new SNP unreported up to date. Meanwhile, 260 reported SNPs of hPMS2 gene were detected in the 26 HNPCC probands. The 2nd and 5th exons were probably the hot SNP regions of hPMS2 gene in Chinese HNPCC families involving 53.1% of all reported SNP. CONCLUSION: The germline mutation of hPMS2 gene may be rare in Chinese HNPCC families. The 2nd and 5th exons are hot SNP regions of hPMS2 gene.Xia Sheng, Xiao-Yan Zhou, Xiang Du, Tai-Ming Zhang, WeiQi Sheng, Da-Ren Shi, Department of Pathology, Shanghai Cancer Center, Fudan University, Shanghai 200032, China Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China Heng-Hua Zhou, Department of Pathology, Shanghai Ninth People’s Hospital Affi liated to Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China San-Jun Cai, Department of Abdominal Surgery, Cancer Center, Fudan University, Shanghai 200032, China 2010World Journal of Gastroenterology2010,16,30:6
5Arachidyl amido cholanoic acid improves liver glucose and lipid homeostasis in nonalcoholic steatohepatitis via AMPK and mTOR regulation显示文摘BACKGROUND Arachidyl amido cholanoic acid(Aramchol)is a potent downregulator of hepatic stearoyl-CoA desaturase 1(SCD1)protein expression that reduces liver triglycerides and fibrosis in animal models of steatohepatitis.In a phase IIb clinical trial in patients with nonalcoholic steatohepatitis(NASH),52 wk of treatment with Aramchol reduced blood levels of glycated hemoglobin A1c,an indicator of glycemic control.AIM To assess lipid and glucose metabolism in mouse hepatocytes and in a NASH mouse model[induced with a 0.1%methionine and choline deficient diet(0.1MCD)]after treatment with Aramchol.METHODS Isolated primary mouse hepatocytes were incubated with 20μmol/L Aramchol or vehicle for 48 h.Subsequently,analyses were performed including Western blot,proteomics by mass spectrometry,and fluxomic analysis with 13C-uniformly labeled glucose.For the in vivo part of the study,male C57BL/6J mice were randomly fed a control or 0.1MCD for 4 wk and received 1 or 5 mg/kg/d Aramchol or vehicle by intragastric gavage for the last 2 wk.Liver metabolomics were assessed using ultra-high-performance liquid chromatography-time of flight-MS for the determination of glucose metabolism-related metabolites.RESULTS Combination of proteomics and Western blot analyses showed increased AMPK activity while the activity of nutrient sensor mTORC1 was decreased by Aramchol in hepatocytes.This translated into changes in the content of their downstream targets including proteins involved in fatty acid(FA)synthesis and oxidation[PACCα/β(S79),SCD1,CPT1A/B,HADHA,and HADHB],oxidative phosphorylation(NDUFA9,NDUFB11,NDUFS1,NDUFV1,ETFDH,and UQCRC2),tricarboxylic acid(TCA)cycle(MDH2,SUCLA2,and SUCLG2),and ribosome(P-p70S6K[T389]and P-S6[S235/S236]).Flux experiments with 13Cuniformely labeled glucose showed that TCA cycle cataplerosis was reduced by Aramchol in hepatocytes,as indicated by the increase in the number of rounds that malate remained in the TCA cycle.Finally,liver metabolomic analysis showed that glucose homeostasis was improved by Aramchol in 0.1MCD fed mice in a dose-dependent manner,showing normalization of glucose,G6P,F6P,UDP-glucose,and Rbl5P/Xyl5P.CONCLUSION Aramchol exerts its effect on glucose and lipid metabolism in NASH through activation of AMPK and inhibition of mTORC1,which in turn activate FAβ-oxidation and oxidative phosphorylation.David Fernández-Ramos Fernando Lopitz-Otsoa Laura Delacruz-Villar Jon Bilbao Martina Pagano Laura Mosca Maider Bizkarguenaga Marina Serrano-Macia Mikel Azkargorta Marta Iruarrizaga-Lejarreta Jesús Sot Darya Tsvirkun Sebastiaan Martijn van Liempd Felix M Goni Cristina Alonso María Luz Martínez-Chantar Felix Elortza Liat Hayardeny Shelly C Lu JoséM Mato 2020World Journal of Gastroenterology2020,26,34:5
6Older age, longer procedures and tandem endoscopic-ultrasound as risk factors for post-endoscopic retrograde cholangiopancreatography bacteremia显示文摘BACKGROUND Clinically significant post-endoscopic retrograde cholangiopancreatography(ERCP) bacteremia(PEB) occurs in up to 5% of cases, while antibiotic prophylaxis is recommended only when an ERCP is unlikely to achieve complete biliary drainage. However, the current recommendations may not cover all potential risk factors for PEB.AIM To identify novel risk factors for PEB and evaluate appropriateness of antibiotic prophylaxis.METHODS A retrospective study of 1082 ERCP procedures performed between January 2012-December 2013 in a single tertiary medical center. Data collection included: Demographic and clinical characteristics such as pre and post procedure antibiotic treatment and bacterial blood cultures. Exclusion criteria were:(1) Age < 18 years;(2) Positive bacterial blood culture before ERCP;(3) Scheduled antibiotic treatment prior to ERCP;(4) Hospitalization longer than 14 d before ERCP;and(5) missing critical data. Stepwise Logistic Regression analysis and Decision Tree algorithms were used for prediction modeling of PEB.RESULTS A total of 626 ERCPs performed in 434 patients were included. Mean age 66.49 ± 15.4 years and 46.5% were males. PEB prevalence was 3.7%. Antibiotic prophylaxis was administrated in 139/626(22.2%) cases but was indicated according to the guidelines only in 44/626(7%) cases. In all the PEB cases, prophylaxis was deemed not indicated. A stepwise logistic regression [receiver operating characteristic(ROC), 0.766], identified 3 variables as independent risk factors for PEB: Age at ERCP ≥ 75 years(OR, 3.780, 95%CI: 1.519-9.408, P = 0.004);Tandem EUS/ERCP with fine needle aspiration(FNA)(OR, 14.528, 95%CI: 3.571-59.095, P < 0.001);ERCP duration longer than 60 min(OR, 5.396, 95%CI: 1.86-15.656, P = 0.002). In a decision tree model(ROC, 0.778) the probability for PEB without any risk factors was 1% regardless of prophylaxis administration.CONCLUSION The prevalence of PEB in our study is similar to previous reports, despite the fact that antibiotic prophylaxis was administrated more readily than recommended. ERCP duration longer than 60 min, tandem EUS-ERCP with FNA and age above 75 years are significant risk factors for PEB. These factors should be further evaluated as indications for prophylactic antibiotic treatment before ERCP.Liat Deutsch Shay Matalon Adam Phillips Moshe Leshno Oren Shibolet Erwin Santo 2020World Journal of Gastroenterology2020,26,41:3
7Heparanase: busy at the cell surface显示文摘Liat Fux Neta Ilan Ralph D. Sanderson Israel Vlodavsky 2009Trends in Biochemical Sciences2009,,10:3
8Transitional cell carcin- oma of the renal pelvis: ureteroscopic and percutaneous approaeh显示文摘Liat sikos E N Dinlenc C Z Kapoor R 2001J Endourol2001,15,:1
9Cytokeratin 20 as a biomarker of gestational trophoblastic disease:diagnostic and prognostic significance显示文摘Rodica Stack Liat Drucker Ruth Zemer 2002Gynecologic Oncology2002,87,:1
10Funda- mental chemistry and engineering aspects of post-treat- ment processes for desalinated water--a review显示文摘Liat Bimhack Nikolay Voutchkov Ori Lahav 2011De- salination2011,273,1:1
11The Wingate anaerobic test cannot be used for the evaluation of growth hormone secretion in children with short stature显示文摘Purpose: To assess the growth hormone(GH) response to the Wingate anaerobic test(WAn T) among children with short stature and suspected GH deficiency. We hypothesized that the GH response to the WAn T would be similar to the GH response to a commonly used pharmacologic provocation test.Methods: Ten children(6 males and 4 females, age range 9.0–14.9 years) participated in the study. Each participant performed 2 tests: a standard all-out WAn T, cycling for 30 s against constant resistance, and a standardized pharmacologic test(clonidine or glucagon). Blood samples for GH were collected before and 10, 30, 45, and 60 min after the beginning of exercise. In addition, we collected pre-and post-exercise blood lactate levels.Results: There was a significant increase in GH levels after the WAn T, yet in 9 of 10 participants, this increase was below the threshold for GH sufficiency. Peak GH after the WAn T was significantly lower compared to the pharmacologic GH provocation tests(with 9 of 10 demonstrating GH-sufficient response).Conclusion: The traditional WAn T cannot be used as a GH provocation test. Further research is needed to develop anaerobic exercise protocols sufficient to promote GH secretion.Nitzan Dror Liat Oren Michal Pantanowitz Alon Eliakim Dan Nemet 2017Journal of Sport and Health Science2017,6,4:1
12Early events in the Fusarium verticillioides-maize interaction characterized by using a green fluorescent protein-expressing transgenic isolate显示文摘Liat O Smadar E David C 2003Applied and Environmental Microbiology2003,69,3:1
13Diagnosis and Treatment of Sleep Disorders in Older Adults显示文摘Sonia Ancoli-Israel Liat Ayalon 2006American Journal of Geriatric Psychiatry2006,,2:1
14Quality criteria for desalinated water and introduction of a novel, cost effec- tive and advantageous post treatment process 显示文摘Liat Birnhack Roni Penn Ori Lahav 2008Desal- ination2008,221,13:1
15Oral treatment with laquinimod augments regulatory T-cells and brain-derived neurotrophic factor expression and reduces injury in the CNS of mice with experimental autoimmune encephalomyelitis显示文摘Rina Aharoni Ravit Saada Raya Eilam Liat Hayardeny Michael Sela Ruth Arnon 2012Journal of Neuroimmunology (-)2012,,1:1
16Marital Power Relations,Resources and Gender Role Idelolgy:A Multivariate Model for Assessing Effects 显示文摘Kulik Liat 1999Journal of Comparative Family Studies1999,,:1
17Methotrexate success rates in progressing ectopic pregnancies: A reappraisal显示文摘Aviad Cohen Liat Zakar Yaron Gil Jonia Amer-Alshiek Guy Bibi Benny Almog Ishai Levin 2014American Journal of Obstetrics and Gynecology2014,,:1
18The development of memory for own- and other-race faces显示文摘Gail S. Goodman Liat Sayfan Jennifer S. Lee Marianne Sandhei Anita Walle-Olsen Svein Magnussen Kathy Pezdek Patricia Arredondo 2007Journal of Experimental Child Psychology2007,,4:1
19Quality criteria for desalinated water following post-treatment 显示文摘Ori Lahav Liat Bimhack 2007Desalination2007,207,13:1
20ATM-dependent activation of the gene encoding MAP kinase phosphatase 5 by radiomimetic DNA damage显示文摘ANAT B S SHARON R E LIAT Z 2002Oncogene2002,21,5:1
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