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金刚石研磨和加工精度的实现

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航空制造技术 2012年第12期55卷 96-97页

作者： mark irvin 英格斯公司

"金刚石"这个词使人想到是"昂贵",但是用金刚石磨料进行研磨加工,却相对"低廉"——更少的金刚石研磨浆被消耗,每小时更低的运行成本,产生更少的废料,更短的加工时间,更低的废品率,更少的工序步骤.

关键词：金刚石研磨金刚石磨料运行成本研磨加工加工时间废品率磨浆工序废料

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产业集群协同创新赋能企业核心竞争力研究——以绿色食品产业集群为例

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江苏大学学报（社会科学版） 2022年第4期24卷 114-124页

作者：黄妍 mark irvin C.Celis 王国栋菲律宾莱西姆大学管理学菲律宾莱西姆大学不详

本研究在构建企业核心竞争力与外部可观测特征关系模型的基础上,基于淮安、宿迁、徐州地区880家绿色食品产业集群成员企业的调查数据,评价绿色食品产业集群协同创新对成员企业核心竞争力的赋能效应,诊断制约绿色食品产业集群协同创新的... 详细信息

本研究在构建企业核心竞争力与外部可观测特征关系模型的基础上,基于淮安、宿迁、徐州地区880家绿色食品产业集群成员企业的调查数据,评价绿色食品产业集群协同创新对成员企业核心竞争力的赋能效应,诊断制约绿色食品产业集群协同创新的主要因素。研究发现:企业深度参与产业集群协同创新,核心竞争力显著增强,赋能效果好;企业不具备协同创新条件,无协同创新实质活动,赋能效果差。在制约企业参与协同创新的主要因素中,资金最为关键。在技术层面需要加快推动绿色食品技术研发,在机制层面上需要以企业为创新主体,“产—学—研”“校—政—企”深度融合,完善成果转化、攻坚激励、要素保障等机制。

关键词：产业集群核心竞争力绿色食品产业协同创新区域发展分类系统

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Evolving concepts in bone infection: redefining “biofilm”,“acute vs. chronic osteomyelitis”, “the immune proteome” and “local antibiotic therapy”

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Bone Research 2019年第3期7卷 225-242页

作者： Elysia A. Masters Ryan P. Trombetta Karen L. de Mesy Bentley Brendan F Boyce Ann Lindley Gill Steven R. Gill Kohei Nishitani Masahiro Ishikawa Yugo Morita Hiromu Ito Sheila N. Bello-Irizarry mark Ninomiya James D. Brodell Jr. Charles C. Lee Stephanie P. Hao irvin Oh Chao Xie Hani A. Awad John L. Daiss John R. Owen Stephen L. Kates Edward M. Schwarz Gowrishankar Muthukrishnan Center for Musculoskeletal Research University of Rochester Medical Center Rochester NY USA Department of Biomedical Engineering University of Rochester Medical Center Rochester NY USA Department of Pathology and Laboratory Medicine University of Rochester Medical Center Rochester NY USA Department of Orthopaedics University of Rochester Medical Center Rochester NY USA Department of Microbiology & Immunology University of Rochester Medical Center Rochester NY USA Department of Orthopaedic Surgery Kyoto University Kyoto Japan Department of Orthopaedic Surgery Virginia Commonwealth University Medical Center Richmond VA USA

Osteomyelitis is a devastating disease caused by microbial infection of bone. While the frequency of infection following elective orthopedic surgery is low, rates of reinfection are disturbingly high. Staphylococcus aureus is responsible for the majority of chronic osteomyelitis cases and is often considered to be incurable due to bacterial persistence deep within bone. Unfortunately, there is no consensus on clinical classifications of osteomyelitis and the ensuing treatment algorithm. Given the high patient morbidity,mortality, and economic burden caused by osteomyelitis, it is important to elucidate mechanisms of bone infection to inform novel strategies for prevention and curative treatment. Recent discoveries in this field have identified three distinct reservoirs of bacterial biofilm including: Staphylococcal abscess communities in the local soft tissue and bone marrow, glycocalyx formation on implant hardware and necrotic tissue, and colonization of the osteocyte-lacuno canalicular network(OLCN) of cortical bone. In contrast, *** intracellular persistence in bone cells has not been substantiated in vivo, which challenges this mode of chronic osteomyelitis. There have also been major advances in our understanding of the immune proteome against S. aureus, from clinical studies of serum antibodies and media enriched for newly synthesized antibodies(MENSA), which may provide new opportunities for osteomyelitis diagnosis, prognosis, and vaccine development. Finally, novel therapies such as antimicrobial implant coatings and antibiotic impregnated 3D-printed scaffolds represent promising strategies for preventing and managing this devastating disease. Here, we review these recent advances and highlight translational opportunities towards a cure.

关键词： disease caused by soft tissue necrotic tissuel

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Glucagon receptor gene mutations with hyperglucagonemia but without the glucagonoma syndrome

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World Journal of Gastrointestinal Surgery 2015年第4期7卷 60-66页

作者： Helen C Miller mark Kidd irvin M Modlin Patrizia Cohen Roberto Dina Panagiotis Drymousis Panagiotis Vlavianos Günter Klöppel Andrea Frilling Department of Surgery and Cancer Imperial College LondonLondon W12 0HSUnited Kingdom Department of Surgery Yale UniversityNew HavenCT 06510United States Emeritus Yale University School of MedicineNew HavenCT 06510United States Department of Histopathology Imperial College LondonLondon W12 0HSUnited Kingdom Department of Gastroenterology Imperial College LondonLondon W12 0HSUnited Kingdom Department of Pathology Technical University of Munich81675 MunichGermany

Pancreatic neoplasms producing exclusively glucagon associated with glucagon cell hyperplasia of the islets and not related to hereditary endocrine syndromes have been recently described. They represent a novel entity within the panel of non-syndromic disorders associated with hyperglucagonemia. This case report describes a 36-year-old female with a 10 years history of nonspecific abdominal pain. No underlying cause was evident despite extensive diagnostic work-up. More recently she was diagnosed with gall bladder stones. Abdominal ultrasound, computerised tomography and magnetic resonance imaging revealed no pathologic findings apart from cholelithiasis. Endoscopic ultrasound revealed a 5.5 mm pancreatic lesion. Fine needle aspiration showed cells focally expressing chromogranin, suggestive but not diagnostic of a low grade neuroendocrine tumor. Octreo Scan was negative. Serum glucagon was elevated to 66 pmol/L(normal: 0-50 pmol/L). Other gut hormones, chromogranin A and chromogranin B were normal. Cholecystectomy and enucleation of the pancreatic lesion were undertaken. Postoperatively, abdominal symptoms resolved and serum glucagon dropped to 7 pmol/L. Although H and E staining confirmed normal pancreatic tissue, immunohistochemistry was initially thought to be suggestive of alpha cell hyperplasia. A count of glucagon positive cells from 5 islets, compared to 5 islets from 5 normal pancreata indicated that islet size and glucagon cell ratios were increased, however still within the wide range of normal physiological findings. Glucagon receptor gene(GCGR) sequencing revealed a heterozygous deletion,K349_G359del and 4 missense mutations. This case may potentially represent a progenitor stage of glucagon cell adenomatosis with hyperglucagonemia in the absence of glucagonoma syndrome. The identification of novel GCGR mutations suggests that these may represent the underlying cause of this condition.

关键词： Hyperglucagonemia Glucagon receptorgene Mutation Adenomatosis Pancreas

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