关键词： 协同过滤   电子商务   个性化推荐   聚类  

摘要： 针对传统的协同过滤算法在电子商务系统中存在数据稀疏性和扩展性方面的问题,提出了一种混合用户和项目协同过滤的电子商务个性化推荐算法。该算法采用聚类技术,将基于用户协同过滤和基于项目的协同过滤结合起来进行双重聚类,结合基于用户协同过滤和基于项目协同过滤两方面的优点,从而获得更好的性能。实验表明,通过与其他推荐算法的比较,文中算法具有较高的推荐质量,更好的准确率和召回率。

关键词： CBM management   E-maintenance   Failure Mode Symptom Analysis (FMSA)   Detection   Diagnosis   Prognosis  

摘要： CBM (Condition Based Maintenance) solutions are increasingly present in industrial systems due to two main circumstances: rapid evolution, without precedents, in the capture and analysis of data and significant cost reduction of supporting technologies. CBM programs in industrial systems can become extremely complex, especially when considering the effective introduction of new capabilities provided by PHM (Prognostics and Health Management) and E-maintenance disciplines. In this scenario, any CBM solution involves the management of numerous technical aspects, that the maintenance manager needs to understand, in order to be implemented properly and effectively, according to the company's strategy. This paper provides a comprehensive representation of the key components of a generic CBM solution, this is presented using a framework or supporting structure for an effective management of the. CBM programs. The concept "symptom of failure", its corresponding analysis techniques (introduced by ISO 13379-1 and linked with RCM/FMEA analysis), and other international standard for CBM open-software application development (for instance, ISO 13374 and OSA-CBM), are used in the paper for the development of the framework. An original template has been developed, adopting the formal structure of RCM analysis templates, to integrate the information of the PHM techniques used to capture the failure mode behaviour and to manage maintenance. Finally, a case study describes the framework using the referred template. (C) 2016 Elsevier B.V. All rights reserved.

关键词： Pervasive healthcare   Archetypes   openEHR   Software agents   Semantic interoperability  

摘要： Background and objective: In Pervasive Healthcare, novel information and communication technologies are applied to support the provision of health services anywhere, at anytime and to anyone. Since health systems may offer their health records in different electronic formats, the openEHR Foundation prescribes the use of archetypes for describing clinical knowledge in order to achieve semantic interoperability between these systems. Software agents have been applied to simulate human skills in some healthcare procedures. This paper presents a methodology, based on the use of openEHR archetypes and agent technology, which aims to overcome the weaknesses typically found in legacy healthcare systems, thereby adding value to the systems. Methods: This methodology was applied in the design of an agent-based system, which was used in a realistic healthcare scenario in which a medical staff meeting to prepare a cardiac surgery has been supported. We conducted experiments with this system in a distributed environment composed by three cardiology clinics and a center of cardiac surgery, all located in the city of Marilia (Sao Paulo, Brazil). We evaluated this system according to the Technology Acceptance Model. Results: The case study confirmed the acceptance of our agent-based system by healthcare professionals and patients, who reacted positively with respect to the usefulness of this system in particular, and with respect to task delegation to software agents in general. The case study also showed that a software agent-based interface and a tools-based alternative must be provided to the end users, which should allow them to perform the tasks themselves or to delegate these tasks to other people. Conclusions: A Pervasive Healthcare model requires efficient and secure information exchange between healthcare providers. The proposed methodology allows designers to build communication systems for the message exchange among heterogeneous healthcare systems, and to shift from sy

关键词： H2S   Barrier integrity   Inflammation  

摘要： Intestinal barrier involves in the pathogeny of inflammatory bowel disease (IBD) and hydrogen sulfide (H2S) has been reported to improve intestinal barrier integrity. Thus, this study investigated the effects of GYY4137, a slow release H2S donor, on DSS-induced inflammation and intestinal dysfunction. In vitro model, cellular permeability was significantly increased and expression of tight junctions (ZO-1, Cauldin4, and Occludin) was downregulated in Caco-2 cells. GYY4137 treatment markedly attenuated DSS-induced inflammation and barrier dysfunction. Cystathionine beta-synthase (CBS)-siRNA transfection further demonstrated that endogenous H2S system involves in DSS-induced inflammation and mediates barrier function. In vivo model, DSS exposure caused colonic inflammation and injury in mice and GYY4137 injection alleviated inflammatory response and improved intestinal barrier via reducing intestinal permeability and upregulating of tight junctions. In conclusion, endogenous H2S system involves in DSS-induced inflammation and H2S addition alleviated inflammation and intestinal dysfunction in vitro and in vivo. (C) 2016 Elsevier B.V. All rights reserved.

关键词： Inflammatory bowel disease   Neutrophil   beta-AR   Catecholamine  

摘要： Inflammatory bowel disease (IBD) is a chronic intestinal inflammatory condition. Psychological stress has been postulated to affect the clinical symptoms and recurrence of IBD. The exact molecular mechanisms are not fully understood. In the present study, we demonstrate that psychological stress promotes neutrophil infiltration into colon tissues in dextran sulfate sodium (DSS)-induced colitis model. The psychological stress resulted in abnormal expression of the proinflammatory cytokines (IL-1 beta, IL-6, IL-17A, and IL-22) and neutrophil chemokines (CXCL1 and CXCL2) and overactivation of the STAT3 inflammatory signaling pathway. Under chronic unpredictable stress, the adrenergic nervous system was markedly activated, as the expression of tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis, in bone marrow and colonic epithelium was enhanced, especially in the myenteric ganglia. The beta-AR agonist isoproterenol mimicked the effects of psychological stress on neutrophilia, neutrophil infiltration, and colonic damage in DSS-induced colitis. The beta 1-AR/62-AR inhibitor propranolol reduced the numbers of the neutrophils in the circulation, suppressed neutrophil infiltration into colonic tissues, and attenuated the colonic tissue damage promoted by chronic stress. Propranolol also abolished stress induced upregulation of proinflammatory cytokines and neutrophil chemokines. Our data reveal a close linkage between the beta 1-AR/beta 2-AR activation and neutrophil trafficking and also suggest the critical roles of adrenergic nervous system in exacerbation of inflammation and damage of colonic tissues in experimental colitis. The current study provides a new insight into the mechanisms underlying the association of psychological stress with excessive inflammatory response and pathophysiological consequences in IBD. The findings also suggest a potential application of neuroprotective agents to prevent relapsing immune activation in the treatment of

关键词： 决策支持   数据仓库   联机分析处理   数据挖掘  

摘要： 根据医院管理需求,把医院分散在各个业务系统的数据进行整合,建立了决策支持系统,对医院的日常管理提供决策依据,文章描述了系统建设的意义,并对系统设计部分和数据挖掘分析作了详尽的探讨。

关键词： Anatomy   Animal cells   Autophagic cell death   Biochemistry   Biology and life sciences   Blood cells   Cell biology   Cell death   Cell processes   Cellular types   Colitis   Colon   Diagnostic medicine   Digestive system   Gastroenterology and hepatology   Gastrointestinal tract   Gene expression   Gene regulation   Genetics   Immune cells   Immune response   Immune system proteins   Immunology   Inflammasomes   Inflammation   Inflammatory bowel disease   Macrophages   Medicine and health sciences   Non-coding RNA   Nucleic acids   Pathology and laboratory medicine   Proteins   Research Article   RNA   Signs and symptoms   Small interfering RNAs   White blood cells  

摘要： Activation of cannabinoid receptor 2 (CB2R) ameliorates inflammation, but the underlying mechanism remains unclear. In the present study, we examined whether activation of CB2R could suppress the nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome. In peritoneal macrophages isolated from C57BL/6 mice, LPS/DSS challenge for 24 h increased the expression of the components of NLRP3 inflammasome NLRP3, Casp-1 p20/Casp-1 p45 ratio, proIL-1 beta and IL-1 beta and also enhanced autophagy (LC3-II/LC3-I ratio, Beclin-1 and SQSTM1). Pretreatment of peritoneal macrophages with HU 308, a selective CB2R agonist, attenuated LPS/DSS-induced NLRP3 inflammasome activation, but further enhanced autophagy. In comparison with wild-type (WT) control, peritoneal macrophages from CB2R knockout (KO) mice had more robust NLRP3 inflammasome activation and attenuated autophagy upon LPS/DSS challenge. Knockdown autophagy-related gene 5 (Atg5) with a siRNA in peritoneal macrophages attenuated the inhibitory effects of HU 308 on LPS/DSS-induced NLRP3 inflammasome activation in vitro. In vivo, HU308 treatment attenuated DSS-induced colitis mice associated with reduced colon inflammation and inhibited NLRP3 inflammasome activation in wild-type mice. In CB2R KO mice, DSS-induced inflammation and NLRP3 inflammasome activation were more pronounced than those in WT control. Finally, we demonstrated that AMPK-mTOR-P70S6K signaling pathway was involved in this CB2R-mediated process. We conclude that activation of CB2R ameliorates DSS-induced colitis through enhancing autophagy that may inhibit NLRP3 inflammasome activation in macrophages.

关键词： ANXA1   Intestinal epithelial cells   Colitis   Natural killer cells   NKG2A  

摘要： Inflammatory bowel disease (IBD) arises when intestinal immune homeostasis is broken, the maintenance of such homeostasis is principally controlled by cross talk between commensal bacteria, mucosa] immune cells and intestinal epithelial cells (IECs). IECs can prevent the contact between luminal bacteria with immune cells through the formation of a physical barrier and the expression of antimicrobial peptides to maintain intestinal immune homeostasis. During Colitis the IECs can express increased ANXA1, which is important for regeneration of intestinal mucosa and function as a potent anti-inflammatory protein. Natural Killer (NK) cells can also suppress the progression of colitis. It is uncertain about the effect of the cross-talk between injured IECs and recruited NK cells during colitis. In this study, the expression of ANXA1 in IECS from DSS treated mice was increased, and more NK cells were recruited to intestinal mucosa. In addition, the expression of NKG2A was upregulated when co-cultured with NK cells. The results further proved that overexpression of NKG2A in NK cells was important for inhibiting the recruitment and activity of neutrophils to alleviate DSS-induced colitis. Here, we provide a new anti-inflammation mechanism about ANXA1 secreted from injured IECs, where ANXA1 can stimulate the expression of NKG2A in NK cells that affect the recruitment and activity of neutrophils necessary for pathology of colitis. (C) 2016 Elsevier Inc. All rights reserved.