Aberrant KDM5B expression promotes aggressive breast cancer through MALAT1 overexpression and downregulation of hsa-miR-448

Relative expression of KDM5B, MALAT1, SNAIL, Vimentin and miR 448 normalized against GAPDH in MCF10A WT, MCF10A OE, MDA-MB-231 WT and MDA-MB-231 KD cells. Data are representative of 3 independent experiments and analyzed by student’s t-test. All data are shown as mean ± SEM. WT, wild type; OE, KDM5B overexpressed; KD, knockdown using shKDM5B clone II. (DOCX 519 kb

Spleen artery embolization increases the success of nonoperative management following blunt splenic injury

AbstractBackgroundSpleen artery embolization (SAE) may increase the success rate of nonoperative management (NOM). The present study investigated the clinical outcome after the installation of SAE in the management of blunt splenic injury.MethodsA retrospective review of hospital records was performed to enroll patients with blunt injury of the spleen. Demographic data and information about the injury severity score, organ injury scale, hospitalization days, management and final outcomes were evaluated. Patients were separated into early and late groups according to the year that SAE was selectively used (2003–2004 and 2005–2008).ResultsSix of eleven (55%) patients in the early group were successfully managed without surgery for blunt splenic injury, whereas all of the 38 patients (100%) in the late group were successfully managed without surgery. Eleven patients (11 of 38; 28.9%) received SAE in the late group. The rate of NOM increased from 55% in the early group to 100% in the late group (p < 0.001). Both early and late groups had similar injury severity score, length of hospitalization, blood transfusion, and complications, and there was no mortality.ConclusionPerformance of SAE for the patients with blunt splenic injury could increase the successful rate of NOM significantly and safely. An algorithm including the angioembolization might be beneficial in the management of patients with blunt spleen trauma

Thorium-doping induced superconductivity up to 56 K in Gd1-xThxFeAsO

Following the discovery of superconductivity in an iron-based arsenide LaO1-xFxFeAs with a superconducting transition temperature (Tc) of 26 K[1], Tc was pushed up surprisingly to above 40 K by either applying pressure[2] or replacing La with Sm[3], Ce[4], Nd[5] and Pr[6]. The maximum Tc has climbed to 55 K, observed in SmO1-xFxFeAs[7, 8] and SmFeAsO1-x[9]. The value of Tc was found to increase with decreasing lattice parameters in LnFeAsO1-xFx (Ln stands for the lanthanide elements) at an apparently optimal doping level. However, the F- doping in GdFeAsO is particularly difficult[10,11] due to the lattice mismatch between the Gd2O2 layers and Fe2As2 layers. Here we report observation of superconductivity with Tc as high as 56 K by the Th4+ substitution for Gd3+ in GdFeAsO. The incorporation of relatively large Th4+ ions relaxes the lattice mismatch, hence induces the high temperature superconductivity.Comment: 4 pages, 3 figure

Direct Radiofrequency Application Improves Pain and Gait in Collagenase-Induced Acute Achilles Tendon Injury

Radiofrequency (RF) is often used as a supplementary and alternative method to alleviate pain for chronic tendinopathy. Whether or how it would work for acute tendon injury is not addressed in the literatures. Through detailed pain and gait monitoring, we hypothesized that collagenase-induce acute tendinopathy model may be able to answer these questions. Gait parameters, including time, distance, and range of motion, were recorded and analyzed using a walking track equipped with a video-based system. Expression of substance P (SP), calcitonin gene related peptide (CGRP), and galanin were used as pain markers. Beta-III tubulin and Masson trichrome staining were used as to evaluate nerve sprouting, matrix tension, and degeneration in the tendon. Of fourteen analyzed parameters, RF significantly improved stance phase, step length, preswing, and intermediary toe-spread of gait. Improved gait related to the expression of substance P, CGRP, and reduced nerve fiber sprouting and matrix tension, but not galanin. The study indicates that direct RF application may be a valuable approach to improve gait and pain in acute tendon injury. Altered gait parameters may be used as references to evaluate therapeutic outcomes of RF or other treatment plan for tendinopathy

TNF-α Mediates Eosinophil Cationic Protein-induced Apoptosis in BEAS-2B Cells

<p>Abstract</p> <p>Background</p> <p>Eosinophilic granulocytes are important for the human immune system. Many cationic proteins with cytotoxic activities, such as eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN), are released from activated eosinophils. ECP, with low RNase activity, is widely used as a biomarker for asthma. ECP inhibits cell viability and induces apoptosis to cells. However, the specific pathway underlying the mechanisms of ECP-induced cytotoxicity remains unclear. This study investigated ECP-induced apoptosis in bronchial epithelial BEAS-2B cells and elucidated the specific pathway during apoptosis.</p> <p>Results</p> <p>To address the mechanisms involved in ECP-induced apoptosis in human BEAS-2B cells, investigation was carried out using chromatin condensation, cleavage of poly (ADP-ribose) polymerase (PARP), sub-G1 distribution in cell cycle, annexin V labeling, and general or specific caspase inhibitors. Caspase-8-dependent apoptosis was demonstrated by cleavage of caspase-8 after recombinant ECP treatment, accompanied with elevated level of tumor necrosis factor alpha (TNF-α). Moreover, ECP-induced apoptosis was effectively inhibited in the presence of neutralizing anti-TNF-α antibody.</p> <p>Conclusion</p> <p>In conclusion, our results have demonstrated that ECP increased TNF-α production in BEAS-2B cells and triggered apoptosis by caspase-8 activation through mitochondria-independent pathway.</p

miRTarBase update 2014: an information resource for experimentally validated miRNA-target interactions

MicroRNAs (miRNAs) are small non-coding RNA molecules capable of negatively regulating gene expression to control many cellular mechanisms. The miRTarBase database (http://mirtarbase.mbc.nctu.edu.tw/) provides the most current and comprehensive information of experimentally validated miRNA-target interactions. The database was launched in 2010 with data sources for >100 published studies in the identification of miRNA targets, molecular networks of miRNA targets and systems biology, and the current release (2013, version 4) includes significant expansions and enhancements over the initial release (2010, version 1). This article reports the current status of and recent improvements to the database, including (i) a 14-fold increase to miRNA-target interaction entries, (ii) a miRNA-target network, (iii) expression profile of miRNA and its target gene, (iv) miRNA target-associated diseases and (v) additional utilities including an upgrade reminder and an error reporting/user feedback system

Neuromuscular abnormality and autonomic dysfunction in patients with cerebrotendinous xanthomatosis

<p>Abstract</p> <p>Background</p> <p>Cerebrotendinous xanthomatosis (CTX) is a rare lipid-storage disease. Neuromuscular abnormality and autonomic system (ANS) dysfuction in CTX are rarely examined in large-scale studies in the literature. We studied the peripheral nervous system, myopathology, and autonomic system of four CTX patients and performed a literature review of the reported CTX patients with peripheral neuropathy.</p> <p>Methods</p> <p>Four biochemically and genetically confirmed CTX patients, belonging to two families, were included for study and all received nerve conduction study (NCS), muscle biopsy for histopathologic and ultrastructural study, skin biopsy for intraepidermal nerve fiber (INEF) density measurement, autonomic testings including sympathetic skin response, R-R interval variation and head-up tilt test using an automated tilt table to record the changes of blood pressure and heart rate in different postures. The Q-Sweat test was also applied for the detection of sweat amount and onset time of response. The clinical characteristics, study methods and results of 13 studies of peripheral neuropathy in CTX patients in the literature were also recorded for analysis.</p> <p>Results</p> <p>The results of NCS study showed axonal sensory-motor polyneuropathy in three CTX cases and mixed axonal and demyelinating sensor-motor polyneuropathy in one. The myopathological and histopathologic studies revealed mild denervation characteristics, but the ultrastructural study revealed changes of mitochondria and the membranous system, and increased amounts of glycogen, lipofuscin and lipid deposition. The ANS study revealed different degrees of abnormalities in the applied tests and the INEF density measurement showed small fiber neuropathy in three of the four CTX patients. The literature review of peripheral neuropathy in CTX revealed different types of peripheral neuropathy, of which axonal peripheral neuropathy was the most common.</p> <p>Conclusions</p> <p>Peripheral neuropathy, especially the subtype of axonal sensori-motor neuropathy, is common in patients with CTX. Evidence of lipid metabolic derangement in CTX can be reflected in ultrastructural studies of muscles. With an adequate multi-parametric evaluation, a high incidence of ANS abnormalities can be seen in this rare lipid-storage disease, and a high incidence of small fiber involvement is also reflected in the IENF density measurement of skin biopsies.</p