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World journal of Gastroenterology 2014年第26期20卷 8458-8470页

作者： Daniel Delitto Eva Vertes-George steven j hughes Kevin E Behrns jose G Trevino Department of Surgery University of Florida-Gainesville Department of Pathology University of Florida-Gainesville

Pancreatic ductal adenocarcinoma is the 4th leading cause of cancer deaths in the United States. The majority of patients are candidates only for palliative chemotherapy, which has proven largely ineffective in halting tumor progression. One proposed mechanism of chemoresistance involves signaling via the mesenchymal-epithelial transition factor protein (MET), a previously established pathway critical to cell proliferation and migration. Here, we review the literature to characterize the role of MET in the development of tumorigenesis, metastasis and chemoresistance, highlighting the potential of MET as a therapeutic target in pancreatic cancer. In this review, we characterize the role of c-Met in the development of tumorigenesis, metastasis and chemoresistance, highlighting the potential of c-Met as a therapeutic target in pancreatic cancer.

关键词： Pancreatic adenocarcinoma c-Met Chemoresistance Receptor tyrosine kinase

Feasibility of pancreatectomy following high-dose proton therapy for unresectable pancreatic cancer

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World journal of Gastrointestinal Surgery 2017年第4期9卷 103-108页

作者： Kathryn E Hitchcock R Charles Nichols Christopher G Morris Debashish Bose steven j hughes john A Stauffer Scott A Celinski Elizabeth A johnson Robert A Zaiden Nancy P Mendenhall Michael S Rutenberg Department of Radiation Oncology University of Florida Department of Surgical Oncology UF Health Cancer Center-Orlando Health Department of Surgery University of Florida Department of Surgery Mayo Clinic Department of Surgery Baylor University Medical Center at Dallas Department of Hematology/Oncology Mayo Clinic Department of Hematology/Oncology Baptist Health

AIM To review surgical outcomes for patients undergoing pancreatectomy after proton therapy with concomitant capecitabine for initially unresectable pancreatic *** From April 2010 to September 2013,15 patients with initially unresectable pancreatic cancer were treated withproton therapy with concomitant capecitabine at 1000 mg orally twice daily. All patients received 59.40 Gy(RBE) to the gross disease and 1 patient received 50.40 Gy(RBE) to high-risk nodal targets. There were no treatment interruptions and no chemotherapy dose reductions. Six patients achieved a radiographic response sufficient to justify surgical exploration,of whom 1 was identified as having intraperitoneal dissemination at the time of surgery and the planned pancreatectomy was aborted. Five patients underwent resection. Procedures included:Laparoscopic standard pancreaticoduodenectomy(n = 3),open pyloris-sparing pancreaticoduodenectomy(n = 1),and open distal pancreatectomy with irreversible electroporation(IRE) of a pancreatic head mass(n = 1). RESULTS The median patient age was 60 years(range,51-67). The median duration of surgery was 419 min(range,290-484),with a median estimated blood loss of 850 cm^3(range,300-2000),median ICU stay of 1 d(range,0-2),and median hospital stay of 10 d(range,5-14). Three patients were re-admitted to a hospital within 30 d after discharge for wound infection(n = 1),delayed gastric emptying(n = 1),and ischemic gastritis(n = 1). Two patients underwent R0 resections and demonstrated minimal residual disease in the final pathology specimen. One patient,after negative pancreatic head biopsies,underwent IRE followed by distal pancreatectomy with no tumor seen in the specimen. Two patients underwent R2 resections. Only 1 patient demonstrated ultimate local progression at the primary site. Median survival for the 5 resected patients was 24 mo(range,10-30).CONCLUSION Pancreatic resection for patients with initially unresectable cancers is feasible after

关键词： Pancreatic cancer Pancreatectomy Pancreas Proton therapy Radiotherapy

Oesophageal atresia: The growth gap

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World journal of Gastroenterology 2020年第12期26卷 1262-1272页

作者： Isabelle Traini jessica Menzies jennifer hughes steven Thomas Leach Usha Krishnan School of Women’s and Children’s Health University of New South WalesSydneyNSW 2052Australia Department of Nutrition and Dietetics Sydney Children’s HospitalRandwickNSW 2031Australia Department of Speech Pathology Sydney Children’s HospitalRandwickNSW 2031Australia Department of Paediatric Gastroenterology Sydney Children’s HospitalRandwickNSW 2031Australia

Poor growth is an under-recognised yet significant long-term sequelae of oesophageal atresia(OA)*** studies have specifically explored the reasons for growth impairment in this complex *** association between poor growth with younger age and fundoplication appears to have the strongest supportive evidence,highlighting the need for early involvement of a dietitian and speech pathologist,and consideration of optimal medical reflux management prior to referring for anti-reflux ***,it remains difficult to reach conclusions regarding other factors which may negatively influence growth,due to conflicting findings,inconsistent definitions and lack of validated tool *** swallowing and feeding difficulties are particularly frequent in younger children,their relationship with growth remains *** is possible that these morbidities impact on the diet of children with OA,but detailed analysis of dietary composition and quality,and its relationship with these complications and growth,has not yet been *** potential area of research in OA is the role of the microbiota in growth and *** the microbiota has been linked to growth impairment in other paediatric conditions,it is yet to be investigated in *** research is needed to identify the most important contributory factors to poor growth,the role of the intestinal microbiota,and effective interventions to maximise growth and nutritional outcomes in this cohort.

关键词： Oesophageal atresia Growth Malnutrition Feeding difficulty Dysphagia Microbiota

VARIABLE STEP-SIZE IMPLICIT-EXPLICIT LINEAR MULTISTEP METHODS FOR TIME-DEPENDENT PARTIAL DIFFERENTIAL EQUATIONS

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journal of Computational Mathematics 2008年第6期26卷 838-855页

作者： DongWang steven j. Ruuth Department of Civil and Environmental Engineering University of Illinois at Urbana-Champaign B231 Newmark Civil Engineering Laboratory Urbana IL 61801 USA Department of Mathematics Simon Fraser University Burnaby BC Canada V5A 1S6

Implicit-explicit （IMEX） linear multistep methods are popular techniques for solving partial differential equations （PDEs） with terms of different types. While fixed timestep versions of such schemes have been developed and studied, implicit-explicit schemes also naturally arise in general situations where the temporal smoothness of the solution changes. In this paper we consider easily implementable variable step-size implicit-explicit （VSIMEX） linear multistep methods for time-dependent PDEs. Families of order-p, pstep VSIMEX schemes are constructed and analyzed, where p ranges from 1 to 4. The corresponding schemes are simple to implement and have the property that they reduce to the classical IMEX schemes whenever constant time step-sizes are imposed. The methods are validated on the Burgers＇ equation. These results demonstrate that by varying the time step-size, VSIMEX methods can outperform their fixed time step counterparts while still maintaining good numerical behavior.

关键词： Implicit-explicit (IMEX) linear multistep methods Variable step-size Zero-stability Burgers' equation.

Mitogen-activated protein kinases mediate the oxidative burst and saponin synthesis induced by chitosan in cell cultures of Panax ginseng

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Science China(Life Sciences) 2004年第4期47卷 303-312页

作者： steven j. NEILL Centre for Research in Plant Science University of the West of England Bristol Coldharbour Lane Bristol BS16 1QY United Kingdom

Chitosan (CHN) specially induced the activities of 39 kD and 42 kD protein kinases in ginseng cells, which could be suppressed by an inhibitor of mitogen-activated protein kinase (MAPK) pathway, PD98059. The immunoprecipitation (IP) using MAPK antibody or kinase assay in vitro also showed that CHN-induced 42 kD and 39 kD protein kinases belonged to the MAPK family. PD98059 suppressed CHN-induced transcriptions of ginseng squalene synthase and ginseng squalene epoxidase genes (gss and gse), CHN-induced accumulation of β-Amyrin synthase (β-AS) and synthesis of saponin. These results showed that CHN-induced activities of MAPKs were necessary for the CHN-induced saponin synthesis. EGTA and LaCl3 suppressed CHN-induced 39 kD and 42 kD MAPK activities. Ruthenium red (RR) could suppress CHN-induced 39 kD activity. All of them suppressed CHN-induced saponin synthesis. These results indicated that CHN-induced increment of cytosolic calcium was necessary for CHN-induced saponin synthesis. PD98059 also suppressed CHN-induced oxidative burst (including the increment of activity of plasma membrane NADPH oxidase and production of H2O2), but diphenylene iodonium (DPI), dimethylthiourea (DMTU) and 2,5-dihydroxycinnamic acid methyl ester (DHC) could not suppress CHN-induced MAPK activities, which indicated that MAPK was possibly function upstream of CHN-induced oxidative burst. Keywords mitogen-activated protein kinase - chitosan - saponin

关键词： mitogen-activated protein kinase,chitosan,saponin.

Transport model for shale gas well leakage through the surrounding fractured zones of a longwall mine

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International journal of Mining Science and Technology 2020年第5期30卷 635-641页

作者： Kayode M.Ajayi steven j.Schatzel Centers for Disease Control and Prevention National Institute for Occupational Safety and HealthPittsburghPA 15236USA

The environmental risks associated with casing deformation in unconventional(shale)gas wells positioned in abutment pillars of longwall mines is a concern to many in the mining and gas well *** the recent interest in shale exploration and the proximity to longwall mining in Southwestern Pennsylvania,the risk to mine workers could be catastrophic as fractures in surrounding strata create pathways for transport of leaked ***,this research by the National Institute for Occupational Safety and Health(NIOSH)presents an analytical model of the gas transport through fractures in a low permeable *** derived equations are used to conduct parametric studies of specific transport conditions to understand the influence of stratum geology,fracture lengths,and the leaked gas properties on subsurface *** results indicated that the prediction that the subsurface gas flux decreases with an increase in fracture length is specifically for a non-gassy *** sub-transport trend could be significantly impacted by the stratum gas generation rate within specific fracture lengths,which emphasized the importance of the stratum *** findings provide new insights for improved understanding of subsurface gas transport to ensure mine safety.

关键词： Subsurface gas transport Longwall mining Shale gas well Analytical modeling Environmental risk Shale gas casing failure

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亚洲高山流域千年尺度地表剥蚀的制约因素

中国科学:地球科学 2025年第1期 75-94页

作者：杨业 steven A.BINNIE 徐胜刘丛强 Tibor j.DUNAI 天津大学地球系统科学学院表层地球系统科学研究院 Institute of Geology and Mineralogy University of Cologne

本研究利用前人1233个亚洲高山流域沉积物宇宙成因核素10Be数据统一计算了地表剥蚀速率,以约束构造、气候和地形如何影响和控制地表剥蚀过程.基于高程数据逐个像元的核素产率,使用蒙特卡洛模拟方法重新计算了10Be流域剥蚀速率.剥蚀速率... 详细信息

本研究利用前人1233个亚洲高山流域沉积物宇宙成因核素10Be数据统一计算了地表剥蚀速率,以约束构造、气候和地形如何影响和控制地表剥蚀过程.基于高程数据逐个像元的核素产率,使用蒙特卡洛模拟方法重新计算了10Be流域剥蚀速率.剥蚀速率变化范围从（7.4±0.7）mm ka-1（1σ;青藏高原内部）到（9,646744+777）mm ka-1（1σ;青藏高原南部）跨四个数量级,中位数为186mm ka-1.逐个像元计算的核素产率与传统模型使用质心坐标和平均高程计算的核素产率相比,后者96.6%核素产率被低估,其中高程差越大越被低估.两种方法计算的产率偏差可达40%,究其原因可能是流域高程分布不均和核素产率随海拔和纬度呈非线性变化.通过量化地表剥蚀速率与构造、气候、地形和岩性之间的相关性将有助于推演未知流域的剥蚀速率.从局部小尺度分析,亚热带台湾岛地区剥蚀速率可能主要受降水和新构造驱动的山体滑坡影响,而降水变化范围较窄的青藏高原东部的剥蚀速率主要受控于地形;冰川覆盖的高原地区剥蚀速率受冰川作用影响,如帕米尔、青藏高原内部和南部地区;青藏高原内部剥蚀速率较低是因为较低的降水和较高的侵蚀基准面,从而限制了河流的下切和地表起伏度演化.与局部小尺度强调单一主控因素不同,本研究对亚洲高山流域宏观大尺度进行量化分析发现:（1）地形指标（包括坡度、地形起伏度和河道陡峭指数）与剥蚀速率在千年尺度呈现一致的幂函数关系,而非简单线性;（2）剥蚀速率与气候（包括与海拔相关的降水、温度和植被覆盖度）和新构造活动（地震核密度分布）呈近似幂函数关系,为次要控制因素;（3）岩性与剥蚀速率没有明显的相关性,可能受限于流域复杂的岩性混合和低分辨率的可侵蚀指数数据.

关键词： 10Be剥蚀速率气候变化构造抬升地形梯度亚洲高山流域

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Compressive deformation of ultralong amyloid fibrils

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Acta Mechanica Sinica 2010年第6期26卷 977-986页

作者： Raffaella Paparcone steven Cranford Markus j.Buehler Laboratory for Atomistic and Molecular Mechanics

Involved in various neurodegenerative diseases, amyloid fibrils and plaques feature a hierarchical structure, ranging from the atomistic to the micrometer *** the atomistic level,a dense and organized hydrogen bond network is resembled in a beta-sheet rich secondary structure, which drives a remarkable stiffness in the range of 10-20GPa,larger than many other biological nanofibrils, a result confirmed by both experiment and ***, the understanding of how these exceptional mechanical properties transfer from the atomistic to the nanoscale remains *** we report a multiscale analysis that, from the atomistic-level structure of a single fibril,extends to the mesoscale level,reaching size scales of hundreds of *** use parameters directly derived from full atomistic simulations of Aβ（1-40） amyloid fibrils to parameterize a mesoscopic coarse-grained model,which is used to reproduce the elastic properties of amyloid *** then apply our mesoscopic model in an analysis of the buckling behavior of amyloid fibrils with different lengths and report a comparison with predictions from continuum beam theory. An important implication of our results is a severe reduction of the effective modulus due to buckling,an effect that could be important to interpret experimental results of ultralong amyloid *** model represents a powerful tool to mechanically characterize molecular structures on the order of hundreds of nanometers to micrometers on the basis of the underlying atomistic *** work provides insight into structural and mechanical properties of amyloid fibrils and may enable further analysis of larger-scale assemblies such as amyloidogenic bundles or plaques as found in disease states.

关键词： Amyloid Coarse-grain Molecular simulation Nanomechanics Materiomics

Reprogramming cholesterol metabolism in macrophages and its role in host defense against cholesterol-dependent cytolysins

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Cellular & Molecular Immunology 2022年第3期19卷 327-336页

作者： Min-Sub Lee steven j.Bensinger Department of Molecular and Medical Pharmacology University of CaliforniaLos AngelesCA90095USA Department of Microbiology Immunology and Molecular GeneticsUniversity of CaliforniaLos AngelesCA90095USA

Cholesterol is a critical lipid for all mammalian cells,ensuring proper membrane integrity,fluidity,and biochemical *** evidence indicates that macrophages rapidly and profoundly reprogram their cholesterol metabolism in response to activation signals to support host defense ***,our understanding of the molecular details underlying how and why cholesterol homeostasis is specifically reshaped during immune responses remains less well *** review discusses our current knowledge of cellular cholesterol homeostatic machinery and introduces emerging concepts regarding how plasma membrane cholesterol is partitioned into distinct *** then discuss how proinflammatory signals can markedly reshape the cholesterol metabolism of macrophages,with a focus on the differences between MyD88-dependent pattern recognition receptors and the interferon signaling *** also discuss recent work investigating the capacity of these proinflammatory signals to selectively reshape plasma membrane cholesterol *** examine how these changes in plasma membrane cholesterol metabolism influence sensitivity to a set of microbial pore-forming toxins known as cholesterol-dependent cytolysins that specifically target cholesterol for their effector *** also discuss whether lipid metabolic reprogramming can be leveraged for therapy to mitigate tissue damage mediated by cholesterol-dependent cytolysins in necrotizing fasciitis and other related *** expect that advancing our understanding of the crosstalk between metabolism and innate immunity will help explain how inflammation underlies metabolic diseases and highlight pathways that could be targeted to normalize metabolic homeostasis in disease states.

关键词： Cholesterol Macrophages Innate Immunity Metabolism

Autophagy gets in on the regulatory act

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journal of Molecular Cell Biology 2011年第2期3卷 76-77页

作者： steven K.Backues Daniel j.Klionsky Life Sciences Institute University of MichiganAnn ArborMI 48109-2216USA

Autophagy down-regulates the Wnt signal transduction pathway via targeted degradation of a key signaling *** may provide an explanation for autophagy’s role in tumor *** eukaryotic cell has at its disposal two primar... 详细信息

关键词： Autophagy targeted explanation