A Novel Completely Local Repairable Code Algorithm Based on Erasure Code

Hadoop Distributed File System (HDFS) is widely used in massive data storage. Because of the disadvantage of the multi-copy strategy, the hardware expansion of HDFS cannot keep up with the continuous volume of big data. Now, the traditional data replication strategy has been gradually replaced by Erasure Code due to its smaller redundancy rate and storage overhead. However, compared with replicas, Erasure Code needs to read a certain amount of data blocks during the process of data recovery, resulting in a large amount of overhead for I/O and network. Based on the Reed-Solomon (RS) algorithm, we propose a novel Completely Local Repairable Code (CLRC) algorithm. By grouping RS coded blocks and generating local check blocks, CLRC algorithm can optimize the locality of the RS algorithm, which can reduce the cost of data recovery. Evaluations show that the CLRC algorithm can reduce the bandwidth and I/O consumption during the process of data recovery when a single block is damaged. What\u27s more, the cost of decoding time is only 59% of the RS algorithm

Storage of 1650 modes of single photons at telecom wavelength

To advance the full potential of quantum networks one should be able to distribute quantum resources over long distances at appreciable rates. As a consequence, all components in the networks need to have large multimode capacity to manipulate photonic quantum states. Towards this end, a multimode photonic quantum memory, especially one operating at telecom wavelength, remains a key challenge. Here we demonstrate a spectro-temporally multiplexed quantum memory at 1532 nm. Multimode quantum storage of telecom-band heralded single photons is realized by employing the atomic frequency comb protocol in a 10-m-long cryogenically cooled erbium doped silica fibre. The multiplexing encompasses five spectral channels - each 10 GHz wide - and in each of these up to 330 temporal modes, resulting in the simultaneous storage of 1650 modes of single photons. Our demonstrations open doors for high-rate quantum networks, which are essential for future quantum internet

Thrixspermum taeniophyllum (Orchidaceae, Epidendroideae), a new species from southwest China, based on molecular and morphological evidence

Thrixspermum taeniophyllum is described as a new orchid species from Wenchuan County, Sichuan Province of southwest China. It is morphologically similar to T. japonicum, but it differs from the latter in having branched stems, slightly fleshy strap-shaped leaves, longer inflorescences with 3–6 flowers and a capitate gynandrium with a lip-shaped mouth opening. Its species status is also supported by molecular phylogenetic analyses, based on nuclear ribosome internal transcribed spacer (nrITS) and three chloroplast DNA fragments (matK, psbA-trnH and trnL-F), which showed distinct systematic boundaries from the most morphologically similar T. japonicum and their morphological relatives T. saruwatarii and T. pygmaeum

High, in Contrast to Low Levels of Acute Stress Induce Depressive-like Behavior by Involving Astrocytic, in Addition to Microglial P2X7 Receptors in the Rodent Hippocampus

Extracellular adenosine 50-triphosphate (ATP) in the brain is suggested to be an etiological factor of major depressive disorder (MDD). It has been assumed that stress-released ATP stimulates P2X7 receptors (Rs) at the microglia, thereby causing neuroinflammation; however, other central nervous system (CNS) cell types such as astrocytes also possess P2X7Rs. In order to elucidate the possible involvement of the MDD-relevant hippocampal astrocytes in the development of a depressive-like state, we used various behavioral tests (tail suspension test [TST], forced swim test [FST], restraint stress, inescapable foot shock, unpredictable chronic mild stress [UCMS]), as well as fluorescence immunohistochemistry, and patch-clamp electrophysiology in wild-type (WT) and genetically manipulated rodents. The TST and FST resulted in learned helplessness manifested as a prolongation of the immobility time, while inescapable foot shock caused lower sucrose consumption as a sign of anhedonia. We confirmed the participation of P2X7Rs in the development of the depressive-like behaviors in all forms of acute (TST, FST, foot shock) and chronic stress (UCMS) in the rodent models used. Further, pharmacological agonists and antagonists acted in a different manner in rats and mice due to their diverse potencies at the respective receptor orthologs. In hippocampal slices of mice and rats, only foot shock increased the current responses to locally applied dibenzoyl-ATP (Bz-ATP) in CA1 astrocytes; in contrast, TST and restraint depressed these responses. Following stressful stimuli, immunohistochemistry demonstrated an increased co-localization of P2X7Rs with a microglial marker, but no change in co-localization with an astroglial marker. Pharmacological damage to the microglia and astroglia has proven the significance of the microglia for mediating all types of depression-like behavioral reactions, while the astroglia participated only in reactions induced by strong stressors, such as foot shock. Because, in addition to acute stressors, their chronic counterparts induce a depressive-like state in rodents via P2X7R activation, we suggest that our data may have relevance for the etiology of MDD in humans

Comparative Proteomic Approach Identifies Pkm2 and Cofilin-1 as Potential Diagnostic, Prognostic and Therapeutic Targets for Pulmonary Adenocarcinoma

Lung cancer is the leading cause of cancer-related death in the world. Non-small cell lung carcinomas (Non-SCLC) account for almost 80% of lung cancers, of which 40% were adenocarcinomas. For a better understanding of the molecular mechanisms behind the development and progression of lung cancer, particularly lung adenocarcinoma, we have used proteomics technology to search for candidate prognostic and therapeutic targets in pulmonary adenocarcinoma. The protein profile changes between human pulmonary adenocarcinoma tissue and paired surrounding normal tissue were analyzed using two-dimensional polyacrylamide gel electrophoresis (2-DE) based approach. Differentially expressed protein-spots were identified with ESI-Q-TOF MS/MS instruments. As a result, thirty two differentially expressed proteins (over 2-fold, p<0.05) were identified in pulmonary adenocarcinoma compared to normal tissues. Among them, two proteins (PKM2 and cofilin-1), significantly up-regulated in adenocarcinoma, were selected for detailed analysis. Immunohistochemical examination indicated that enhanced expression of PKM2 and cofilin-1 were correlated with the severity of epithelial dysplasia, as well as a relatively poor prognosis. Knockdown of PKM2 expression by RNA interference led to a significant suppression of cell growth and induction of apoptosis in pulmonary adenocarcinoma SPC-A1 cells in vitro, and tumor growth inhibition in vivo xenograft model (P<0.05). In addition, the shRNA expressing plasmid targeting cofilin-1 significantly inhibited tumor metastases and prolonged survival in LL/2 metastatic model. While additional works are needed to elucidate the biological significance and molecular mechanisms of these altered proteins identified in this study, PKM2 and cofilin-1 may serve as potential diagnostic and prognostic biomarkers, as well as therapeutic targets for pulmonary adenocarcinoma

The Role of Macrolide Antibiotics in Increasing Cardiovascular Risk

AbstractBackgroundLarge cohort studies provide conflicting evidence regarding the potential for oral macrolide antibiotics to increase the risk of serious cardiac events.ObjectivesThis study performed a meta-analysis to examine the link between macrolides and risk of sudden cardiac death (SCD) or ventricular tachyarrhythmias (VTA), cardiovascular death, and death from any cause.MethodsWe performed a search of published reports by using MEDLINE (January 1, 1966, to April 30, 2015) and EMBASE (January 1, 1980, to April 30, 2015) with no restrictions. Studies that reported relative risk (RR) estimates with 95% confidence intervals (CIs) for the associations of interest were included.ResultsThirty-three studies involving 20,779,963 participants were identified. Patients taking macrolides, compared with those who took no macrolides, experienced an increased risk of developing SCD or VTA (RR: 2.42; 95% CI: 1.61 to 3.63), SCD (RR: 2.52; 95% CI: 1.91 to 3.31), and cardiovascular death (RR: 1.31; 95% CI: 1.06 to 1.62). No association was found between macrolides use and all-cause death or any cardiovascular events. The RRs associated with SCD or VTA were 3.40 for azithromycin, 2.16 for clarithromycin, and 3.61 for erythromycin, respectively. RRs for cardiovascular death were 1.54 for azithromycin and 1.48 for clarithromycin. No association was noted between roxithromycin and adverse cardiac outcomes. Treatment with macrolides is associated with an absolute risk increase of 118.1 additional SCDs or VTA, and 38.2 additional cardiovascular deaths per 1 million treatment courses.ConclusionsAdministration of macrolide antibiotics is associated with increased risk for SCD or VTA and cardiovascular death but not increased all-cause mortality