<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.jecm-online.com//inpress?rss=yes"><title>Journal of Experimental &amp; Clinical Medicine - Articles in Press</title><description>Journal of Experimental &amp; Clinical Medicine RSS feed: Articles in Press.    The  Journal of Experimental and Clinical Medicine (JECM)  aims
to publish high quality scientific research in the field of 
experimental
and clinical medicine, with the goal of promoting and
disseminating medical science knowledge to improve global
health. 
 

Articles on clinical, laboratory and social research in medicine
and other related fields that are of interest to the medical
profession 
are eligible for consideration. The  JECM  publishes
review articles, original articles, case reports, short communications,
and 
letters to the editor. The journal is published
every 2 months, with a total of 6 issues a year.   </description><link>http://www.jecm-online.com//inpress?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 Published by Elsevier Inc.  </dc:rights><prism:publicationName>Journal of Experimental &amp; Clinical Medicine</prism:publicationName><prism:issn>1878-3317</prism:issn><prism:publicationDate>2012-05-21</prism:publicationDate><prism:copyright> © 2012 Published by Elsevier Inc.  </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.jecm-online.com/article/PIIS1878331712000587/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecm-online.com/article/PIIS1878331712000599/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecm-online.com/article/PIIS1878331712000605/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecm-online.com/article/PIIS1878331712000629/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecm-online.com/article/PIIS1878331712000654/abstract?rss=yes"/><rdf:li rdf:resource="http://www.jecm-online.com/article/PIIS1878331711001690/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.jecm-online.com/article/PIIS1878331712000587/abstract?rss=yes"><title>Roles of Glycogen Synthase Kinase-3 in Alzheimer's Disease: From Pathology to Treatment Target - Corrected Proof</title><link>http://www.jecm-online.com/article/PIIS1878331712000587/abstract?rss=yes</link><description>Alzheimer's disease (AD) is a progressive neurodegenerative disorder with an unknown cause, and as of yet there is no effective treatment. The neuropathological hallmarks of AD include amyloid plaques and neurofibrillary tangle (NFT) deposits. There is evidentiary support for amyloid deposition being the primary influence driving AD pathogenesis, commonly referred to as the amyloid hypothesis of AD. But brain amyloid load is not correlated with AD severity; instead, NFT formation has been shown to be associated with disease progression. Therefore, advocates of the tau hypothesis strongly postulate that NFT accumulation is critical for neuronal loss and AD development. Hence, inhibition of NFT formation/accumulation is one of the treatment strategies to combat AD. NFTs consist of aggregations of paired helical hyperphosphorylated tau protein, one of the major microtubule-associated proteins. The hyperphosphorylation of tau impairs its normal maintenance function for cytoskeleton stability, and induces a toxic sequestration of normal tau and other microtubule-associated proteins. Glycogen synthase kinase-3 (GSK-3) is the main enzyme that phosphorylates tau, and an increase in GSK-3 activity has been observed in AD patients. GSK-3 inhibition by lithium, a major mood stabilizer that is used to treat bipolar disorder, has been shown to reduce tau phosphorylation and even decrease amyloid burden in the brain of AD animal models. This supports the notion of GSK-3 inhibition as a potential avenue for AD treatment.</description><dc:title>Roles of Glycogen Synthase Kinase-3 in Alzheimer's Disease: From Pathology to Treatment Target - Corrected Proof</dc:title><dc:creator>Hsing-Cheng Liu, Sy-Jye Leu, De-Maw Chuang</dc:creator><dc:identifier>10.1016/j.jecm.2012.04.001</dc:identifier><dc:source>Journal of Experimental &amp; Clinical Medicine (2012)</dc:source><dc:date>2012-05-21</dc:date><prism:publicationName>Journal of Experimental &amp; Clinical Medicine</prism:publicationName><prism:publicationDate>2012-05-21</prism:publicationDate><prism:section>REVIEW ARTICLE</prism:section></item><item rdf:about="http://www.jecm-online.com/article/PIIS1878331712000599/abstract?rss=yes"><title>Metformin as a Novel Component of Metronomic Chemotherapeutic Use: A Hypothesis - Corrected Proof</title><link>http://www.jecm-online.com/article/PIIS1878331712000599/abstract?rss=yes</link><description>The hypoglycemic agent metformin has been found to possess chemopreventive and direct antitumor properties. Several clinical studies worldwide are using it as a monotherapy or as an add-on therapy with chemotherapeutic drugs to determine prospectively its efficacy and safety in treating human cancer. In terms of its mechanism of action, metformin moderately inhibits electron transport in mitochondria to cause increased AMP:ATP ratios, which antagonize gluconeogenesis in hepatocytes, and to promote catabolism in most tissues through activating AMP-activated kinase (AMPK). Inhibition of mammalian target of rapamycin signaling through activation of AMPK has been suggested to mediate the antitumor effects of metformin. However, AMPK-independent growth-inhibitory properties of metformin on tumor cells have also been described, suggesting that antagonizing electron transport per se may be cytostatic or cytotoxic to cancer cells. In addition, metformin was hypothesized to display antiviral and antimalarial effects in 1950s, and recently it has been found to promote the generation of CD8 T memory lymphocytes, suggesting that its immune-activating effects may also contribute to its observed antitumor and chemopreventive properties. Chronic administration of metformin has an acceptable toxicity profile and is well tolerated by millions of patients with type 2 diabetes worldwide, suggesting that this agent could potentially be a therapeutic component with low intensity if given in continuous dosing/frequent usage schedules. These metronomic strategies show that metformin can inhibit tumor angiogenesis and activate antitumor immunity, indicating a potential therapeutic interaction with immune potentiation, antitumor effects, and an acceptable toxicity profile. Here, we review current knowledge on metformin's signaling, metabolic, and immune effects, as well as data from clinical drug trials, to discuss how the interplay may orchestrate the antitumor effects of this agent, particularly in combination with reduced-intensity or metronomic chemotherapeutic use.</description><dc:title>Metformin as a Novel Component of Metronomic Chemotherapeutic Use: A Hypothesis - Corrected Proof</dc:title><dc:creator>Jorge Eduardo Duque, Juliana Velez, Ismael Samudio, Enoch Lai</dc:creator><dc:identifier>10.1016/j.jecm.2012.04.002</dc:identifier><dc:source>Journal of Experimental &amp; Clinical Medicine (2012)</dc:source><dc:date>2012-05-21</dc:date><prism:publicationName>Journal of Experimental &amp; Clinical Medicine</prism:publicationName><prism:publicationDate>2012-05-21</prism:publicationDate><prism:section>REVIEW ARTICLE</prism:section></item><item rdf:about="http://www.jecm-online.com/article/PIIS1878331712000605/abstract?rss=yes"><title>The Roles of Adiponectin in Acute Kidney Injury - Corrected Proof</title><link>http://www.jecm-online.com/article/PIIS1878331712000605/abstract?rss=yes</link><description>Adiponectin (APN) is an adipokine shown to have potent antiobesity, antiatherosclerotic, suppression of macrophage-to-foam cell transformation, and inhibition of proinflammatory cytokines. Studies have revealed that plasma concentration of APN is approximately three times higher in patients with end-stage kidney disease than in healthy people. However, low plasma levels of the hormone have been shown to elicit a protective effect against inflammation in animal models of ischemia/reperfusion-induced acute renal failure. This review summarizes the possible molecular signaling pathways involved in the effects of APN accumulation in the circulation on acute kidney injury in humans and in rodents.</description><dc:title>The Roles of Adiponectin in Acute Kidney Injury - Corrected Proof</dc:title><dc:creator>Hsi-Hsien Chen, Yen-Chung Lin, Tzen-Wen Chen, Heng Lin</dc:creator><dc:identifier>10.1016/j.jecm.2012.04.003</dc:identifier><dc:source>Journal of Experimental &amp; Clinical Medicine (2012)</dc:source><dc:date>2012-05-21</dc:date><prism:publicationName>Journal of Experimental &amp; Clinical Medicine</prism:publicationName><prism:publicationDate>2012-05-21</prism:publicationDate><prism:section>REVIEW ARTICLE</prism:section></item><item rdf:about="http://www.jecm-online.com/article/PIIS1878331712000629/abstract?rss=yes"><title>Reducing Blood Culture Contamination Rates by Educational Intervention and one-on-one Feedback in the Emergency Department - Corrected Proof</title><link>http://www.jecm-online.com/article/PIIS1878331712000629/abstract?rss=yes</link><description>Background/Purpose: Blood culture specimens collected from patients in the emergency department (ED) can subsequently give the clinical physicians useful information and references for diagnosis and medication selection. If the isolates are found to be contaminants, the consequences are increased antibiotic use and inpatient hospital fees. The purpose of this research is to reduce blood culture contamination (BCC) rates in the ED.Methods: The effectiveness of educational intervention and one-on-one feedback to reduce BCC rates in the ED was assessed in a busy medical center in which blood cultures were obtained by nurses rather than trained phlebotomists.The study comprised two phases. The first phase was to ensure understanding of the correct methods for performing blood culture, and to measure the effectiveness of the educational intervention. The second phase was to continue the educational intervention plus to give one-on-one feedback of the BCC rates to the ED and individuals weekly.Results: The baseline BCC rate was 3.4% in the pre-intervention period. The BCC rate fell to 2.67% in Phase 1 (i.e., educational intervention only). The BCC rate fell to 2% in Phase 2 (i.e., educational intervention plus one-on-one feedback). Among the contaminants, coagulase-negative staphylococci (CoNS) fell from 62% before the intervention to 48% post-intervention.Conclusion: Educational intervention plus one-on-one feedback for decreasing BCC rates was more effective than an educational intervention alone in our study.</description><dc:title>Reducing Blood Culture Contamination Rates by Educational Intervention and one-on-one Feedback in the Emergency Department - Corrected Proof</dc:title><dc:creator>Chun-Mei Lin, Wen-Sen Lee, Fang-Yu Lin, Fang-Lan Yu, Tsong-Yih Ou, Sing-On Teng</dc:creator><dc:identifier>10.1016/j.jecm.2012.04.005</dc:identifier><dc:source>Journal of Experimental &amp; Clinical Medicine (2012)</dc:source><dc:date>2012-05-21</dc:date><prism:publicationName>Journal of Experimental &amp; Clinical Medicine</prism:publicationName><prism:publicationDate>2012-05-21</prism:publicationDate><prism:section>ORIGINAL ARTICLE</prism:section></item><item rdf:about="http://www.jecm-online.com/article/PIIS1878331712000654/abstract?rss=yes"><title>Correlates of Perceived Competitive Advantage among Hospital Management: A Multilevel Analysis - Corrected Proof</title><link>http://www.jecm-online.com/article/PIIS1878331712000654/abstract?rss=yes</link><description>Background/Purpose: As the hospital industry continues to undergo significant change and becomes an increasingly competitive environment, the concept of competitive advantage has received a considerable degree of attention in the healthcare literature. Using a multilevel modeling approach, this study evaluated the contributions of hospital characteristics and market competition on perceived competitive advantage of hospital managers in Taiwan.Methods: Data for this study were mainly collected using a questionnaire that was mailed to the top executives of 432 accredited hospitals in Taiwan in 2009. Valid responses were obtained from182 hospitals for an effective response rate of 42.1%.Results: Respondents indicated relatively moderate assessment of perceived competitive advantage (mean = 3.5, standard deviation = 0.72, on a five-point Likert scale). There were no significant correlations between the group-level predictor (competition of local healthcare market) and the individual-level ones. Results of multilevel analysis to simultaneously examine the effects of individual-level (hospital characteristics; level 1) and group-level (competition of local healthcare market; level 2) predictors on perceived competitive advantage indicated that the predictors at hospital level had a statistically significant effect on respondents' perception of competitive advantage of their hospitals. Nonetheless, there was insignificant market competition variation in perceived competitive advantage among respondents.Conclusion: We conducted a multilevel analysis that reflected the hierarchical structure of our data, where hospitals were nested within healthcare markets of different intensities of competition. Our results join a body of healthcare literature suggesting that hospital level is a significant predictor of hospital performance. However, we found no evidence of a strong relationship between the degree of local market competition and perceived competitive advantage of respondents. Taken together, the results of our empirical study shed light on some interesting issues regarding competitive advantage.</description><dc:title>Correlates of Perceived Competitive Advantage among Hospital Management: A Multilevel Analysis - Corrected Proof</dc:title><dc:creator>Kuo-Cherh Huang, Ning Lu, Wei-Jung Chang, Hui-Chih Chang, Jiun-Shyan Chen</dc:creator><dc:identifier>10.1016/j.jecm.2012.04.008</dc:identifier><dc:source>Journal of Experimental &amp; Clinical Medicine (2012)</dc:source><dc:date>2012-05-21</dc:date><prism:publicationName>Journal of Experimental &amp; Clinical Medicine</prism:publicationName><prism:publicationDate>2012-05-21</prism:publicationDate><prism:section>ORIGINAL ARTICLE</prism:section></item><item rdf:about="http://www.jecm-online.com/article/PIIS1878331711001690/abstract?rss=yes"><title>A Duplex PCR-RFLP Assay for Simultaneous Detection of FV Leiden and Prothrombin G20210A Mutations in Women with Recurrent Miscarriage - Corrected Proof</title><link>http://www.jecm-online.com/article/PIIS1878331711001690/abstract?rss=yes</link><description>Factor V Leiden (FV-Leiden) and prothrombin gene mutations (FII G20210A) are well-established independent risk factors for several pregnancy complications and may be associated with an increased risk of recurrent miscarriage. Molecular diagnosis testing for both mutations is widespread and need to be standardized. We have optimized a duplex polymerase chain reaction-restriction fragment length polymorphism assay (PCR-RFLP) for the simultaneous detection of both mutations in a single-tube single-enzyme digestion reaction for 35 women with recurrent miscarriage. This assay is a convenient method that should be applied in routine settings for detecting thrombophilia in women who are suffering from recurrent miscarriage.</description><dc:title>A Duplex PCR-RFLP Assay for Simultaneous Detection of FV Leiden and Prothrombin G20210A Mutations in Women with Recurrent Miscarriage - Corrected Proof</dc:title><dc:creator>Rim Frikha, Nouha Bouayed Abdelmoula, Tarek Rebai</dc:creator><dc:identifier>10.1016/j.jecm.2011.11.015</dc:identifier><dc:source>Journal of Experimental &amp; Clinical Medicine (2011)</dc:source><dc:date>2011-12-26</dc:date><prism:publicationName>Journal of Experimental &amp; Clinical Medicine</prism:publicationName><prism:publicationDate>2011-12-26</prism:publicationDate><prism:section>SHORT COMMUNICATION</prism:section></item></rdf:RDF>
