Search

Objective To comprehensively evaluate diagnostic algorithms for myocardial infarction using a high-sensitivity cardiac troponin I (hs-cTnI) assay. Patients and methods We prospectively enrolled patients with suspected myocardial infarction without ST-segment elevation from nine emergency departments in Japan. The diagnostic algorithms evaluated: (i) based on hs-cTnI alone, such as the European Society of Cardiology (ESC) 0/1-h or 0/2-h and High-STEACS pathways; or (ii) used medical history and physical findings, such as the ADAPT, EDACS, HEART, and GRACE pathways. We evaluated the negative predictive value (NPV), sensitivity as safety measures, and proportion of patients classified as low or high-risk as an efficiency measure for a primary outcome of type 1 myocardial infarction or cardiac death within 30 days. Results We included 437 patients, and the hs-cTnI was collected at 0 and 1 hours in 407 patients and at 0 and 2 hours in 394. The primary outcome occurred in 8.1% (33/407) and 6.9% (27/394) of patients, respectively. All the algorithms classified low-risk patients without missing those with the primary outcome, except for the GRACE pathway. The hs-cTnI-based algorithms classified more patients as low-risk: the ESC 0/1-h 45.7%; the ESC 0/2-h 50.5%; the High-STEACS pathway 68.5%, than those using history and physical findings (15–30%). The High-STEACS pathway ruled out more patients (20.5%) by hs-cTnI measurement at 0 hours than the ESC 0/1-h and 0/2-h algorithms (7.4%). Conclusions The hs-cTnI algorithms, especially the High-STEACS pathway, had excellent safety performance for the early diagnosis of myocardial infarction and offered the greatest improvement in efficiency. [ABSTRACT FROM AUTHOR]

The genus Vanoverberghia currently includes three species namely V. sepulchrei and V. rubrobracteata from the Philippines and V. sasakiana from Taiwan. New material targeting the Alpinia eubractea clade of the tribe Alpinieae was used to test the monophyly of Vanoverberghia. A combined analysis of the ITS and trnK/matK regions reveals that these three species form a strongly supported monophyletic clade with Alpinia diversifolia and Alpinia vanoverberghii. The morphological descriptions of all species were updated after examining recent collections and comparing with types and protologues. The original description of A. diversifolia did not include information on the flowers which are described here. The morphology of A. diversifolia and A. vanoverberghii is for most parts in accordance with the previous perception of the genus but a few characters are added and a recircumscription of Vanoverberghia is subsequently provided here. Vanoverberghia diversifolia is reinstated and A. vanoverberghii is combined in Vanoverberghia. Furthermore, collections from northern Luzon documents the presence of V. sasakiana and all species of Vanoverberghia thus occur in the Philippines. A key to the five species is provided including a comprehensive taxonomic revision and designation of three lectotypes. [ABSTRACT FROM AUTHOR]

We have identified LIM-kinase (LIMK1 and LIMK2), the only known catalytic protein among LIM-family molecules. Both LIMK1 and LIMK2 phosphorylate (inactivate) cofilin, an actin depolymerizing factor, and induce actin cytoskeleton reorganization. We as well as others concurrently demonstrated that LIMK activation was regulated by the Rho family of GTPases, and LIMK1 and LIMK2 share the distinct functional portion in Rho GTPases-mediated actin dynamics. Although evidence for their physiological significance is tenuous, several studies have focused on understanding LIMK functions, particularly in meiosis and mitosis. This review addresses recent LIMK findings, with emphasis on spermatogenesis studies, upon which future studies can shed light on the role of the LIMK/actin system in meiosis and mitosis. Copyright © 2003 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Purpose: Long non-coding RNAs (lncRNAs) constitute a group of non-coding RNAs longer than 200 nucleotides. LncRNAs are able to regulate almost every stage of gene expression, from epigenetic modification to post-transcriptional regulation. Recent landmark studies revealed that lncRNAs are involved in cardiac development. However, the role of lncRNAs in cardiac diseases is unknown. Here, we investigated the regulation of lncRNAs in the hypertrophied heart.Methods: Wild-type and adenosine A2a receptor overexpressing mice (A2a-Tg) were subjected to transverse aortic constriction (TAC) as a model of cardiac hypertrophy or doxorubicin treatment as a model of cardiotoxicity. Hearts were harvested and expression of lncRNAs was investigated using Affymetrix Mouse Gene 1.0 ST microarrays. A specific analytical pipeline was developed to extract from these microarrays the data related to lncRNAs.Results: Analysis of microarray data identified 2 lncRNAs up-regulated and 3 down-regulated in the hearts of A2a-Tg mice subjected to TAC. Quantitative PCR showed that expression of the lncRNA 2900055J20Rik was highly down-regulated in A2a-Tg mice compared to wild-type littermates (-3.5-fold, P<0.001). To confirm the association between 2900055J20Rik and cardiac hypertrophy, we used a public microarray dataset from mice subjected to TAC. In this public dataset, expression of 2900055J20Rik was found to be up-regulated in TAC mice compared to sham-operated animals (6-fold after 28 days, P<0.01). Interestingly, administration of the BET bromodomain inhibitor JQ1, a suppressor of cardiac hypertrophy, resulted in a decrease of 2900055J20Rik expression 3, 11 and 28 days after treatment onset (P<0.01). Finally, to investigate the effect of adenosine on the expression of 2900055J20Rik in another model of cardiac stress, wild-type and A2a-Tg mice were treated with doxorubicin. As it was observed in TAC mice, expression of 2900055J20Rik was down-regulated upon overexpression of the adenosine A2a receptor in doxorubicin-treated animals (2-fold, P=0.03).Conclusions: First, we have shown that data on lncRNAs can be obtained from traditional gene expression microarrays. Second, lncRNAs are regulated in the hypertrophied heart and can be modulated by cardioprotective molecules (adenosine and JQ1). Third, we have identified the lncRNA 2900055J20Rik which may be involved in regulation of cardiac hypertrophy. These observations motivate further investigation of the therapeutic value of lncRNAs in the diseased heart. [ABSTRACT FROM PUBLISHER]