bluuebunny/crossref_metadata_2025_split huggingface dataset:
Optimizing de novo common wheat transcriptome assembly using short-read RNA-Seq data
Authors: Duan Jialei , Xia Chuan , Zhao Guangyao , Jia Jizeng , Kong Xiuying 
Published: August 2012

Abstract

Background
Rapid advances in next-generation sequencing methods have provided new opportunities for transcriptome sequencing (RNA-Seq). The unprecedented sequencing depth provided by RNA-Seq makes it a powerful and cost-efficient method for transcriptome study, and it has been widely used in model organisms and non-model organisms to identify and quantify RNA. For non-model organisms lacking well-defined genomes, de novo assembly is typically required for downstream RNA-Seq analyses, including SNP discovery and identification of genes differentially expressed by phenotypes. Although RNA-Seq has been successfully used to sequence many non-model organisms, the results of de novo assembly from short reads can still be improved by using recent bioinformatic developments.

Results
In this study, we used 212.6 million pair-end reads, which accounted for 16.2 Gb, to assemble the hexaploid wheat transcriptome. Two state-of-the-art assemblers, Trinity and Trans-ABySS, which use the single and multiple k-mer methods, respectively, were used, and the whole de novo assembly process was divided into the following four steps: pre-assembly, merging different samples, removal of redundancy and scaffolding. We documented every detail of these steps and how these steps influenced assembly performance to gain insight into transcriptome assembly from short reads. After optimization, the assembled transcripts were comparable to Sanger-derived ESTs in terms of both continuity and accuracy. We also provided considerable new wheat transcript data to the community.

Conclusions
It is feasible to assemble the hexaploid wheat transcriptome from short reads. Special attention should be paid to dealing with multiple samples to balance the spectrum of expression levels and redundancy. To obtain an accurate overview of RNA profiling, removal of redundancy may be crucial in de novo assembly.
Pediatric first aid knowledge and attitudes among staff in the preschools of Shanghai, China
Authors: Li Feng , Jiang Fan , Jin Xingming , Qiu Yulan , Shen Xiaoming 
Published: August 2012

AbstractBackgroundUnintentional injury remains the leading cause of morbidity and mortality among children worldwide. The aims of this study were to assess a baseline level of first aid knowledge and overall attitudes regarding first aid among staff members in Shanghai preschools.MethodsA cross-sectional study was carried out among the staff members at selected preschools. A stratified random sampling method was first used to identify suitable subjects. Data were obtained using a multiple-choice questionnaire. A standardized collection of demographics was performed and participants were given the aforementioned questionnaire to indicate knowledge of and attitudes toward first aid.Results1067 subjects completed the questionnaire. None of the surveyed employees answered all questions correctly; only 39 individuals (3.7%) achieved passing scores. The relative number of correct answers to specific questions ranged from 16.5% to 90.2%. In particular, subjects lacked knowledge regarding first aid for convulsive seizures (only 16.5% answered correctly), chemical injuries to the eye (23%), inhaled poison (27.6%), and choking and coughing (30.1%). A multiple linear regression analysis showed scores were significantly higher among staff members with more education, those who had received first aid training before or were already healthcare providers, younger employees, and staff members from rural districts. Most employees agreed that giving first aid was helpful; the vast majority felt that it was important and useful for them to learn pediatric first aid.ConclusionsThe level of first-aid knowledge among preschool staffs in Shanghai was low. There is an urgent need to educate staff members regarding first aid practices and the various risk factors relating to specific injuries.
Income-related inequality in health insurance coverage: analysis of China Health and Nutrition Survey of 2006 and 2009
Authors: Liu Jinan , Shi Lizheng , Meng Qingyue , Khan M Mahmud 
Published: August 2012

Abstract

Introduction
China introduced the urban resident basic medical insurance (URBMI) in 2007 to cover children and urban unemployed adults, in addition to the new cooperative medical scheme (NCMS) for rural residents in 2003 and the basic health insurance scheme (BHIS) for urban employees in 1998. This study examined whether the overall income-related inequality in health insurance coverage improved during 2006 and 2009 in China.

Methods
The China Health and Nutrition Survey (CHNS) data of 2006 and 2009 were used to create the concentration curve and the concentration index. GEE logistic regression was used to model the health insurance coverage as dependent variable and household income per capita as independent variable, controlling for individuals' age, gender, marital status, educational attainment, employment status, year 2009 (Y2009), household size, retirement status, and geographic variations. The change in the income-related inequality in 2009 was estimated using the interaction term of income*Y2009.

Results
In 2006, 49.7% (4,712/9,476) respondents had health insurance: 13.4% with BHIS and 28.4% with NCMS. In 2009, 90.8% (8,964/9,863) had health insurance: 10.1% with URBMI, 18.3% with BHIS, and 57.6% with NCMS. The BHIS, URBMI, and NCMS programs had different patterns of population coverage over 10 income deciles. The concentration index was 0.15 in 2006 and 0.04 in 2009. The dominance test showed that the concentration curves were significantly different between 2006 and 2009 (p < 0.05). An income increase per capita by 10,000 RMB was associated with 25.5% more likely to have health insurance coverage (odds ratio = 1.255, 95% confidence interval: [1.130-1.393]). In 2009, there was significant improvement in the income-related inequality (p < 0.001).

Discussions
Comparing 2009 to 2006, the income inequality in health insurance coverage was largely corrected in China through rapid expansion of CHNS in rural areas and initiation of URBMI in urban areas.
Obesity, Inflammation and Acute Myocardial Infarction - Expression of leptin, IL-6 and high sensitivity-CRP in Chennai based population
Authors: Rajendran Karthick , Devarajan Nalini , Ganesan Manohar , Ragunathan Malathi 
Published: August 2012

Abstract

Background
Obesity, characterised by increased fat mass and is currently regarded as a pro-inflammatory state and often associated with increased risk of cardiovascular diseases (CVD) including Myocardial infarction. There is an upregulation of inflammatory markers such as interleukin-6, interleukin-6 receptor and acute phase protein CRP in Acute Myocardial Infarction (AMI) patients but the exact mechanism linking obesity and inflammation is not known. It is of our interest to investigate if serum leptin (ob gene product) is associated with AMI and correlated with inflammatory proteins namely Interleukin-6 (IL-6) and high sensitivity - C reactive protein (hs-CRP).

Results
Serum leptin levels were significantly higher in AMI patients when compared to Non-CVD controls. IL-6 and hs-CRP were also elevated in the AMI group and leptin correlated positively with IL-6 and hs-CRP. Incidentally this is the first report from Chennai based population, India.

Conclusions
The strong correlation between serum levels of leptin and IL-6 implicates an involvement of leptin in the upregulation of inflammatory cytokines during AMI. We hypothesise that the increase in values of IL-6, hs-CRP and their correlation to leptin in AMI patients could be due to participation of leptin in the signaling cascade after myocardial ischemia.
Throughput and reliability analysis of a scalable broadcast MAC for distributed wireless networks
Authors: Pudasaini Subodh , Shin Seokjoo , Kim Kiseon 
Published: August 2012

Abstract
In carrier-sense-multiple-access-based distributed wireless networks, the legacy mechanism of arbitrating the access attempts of multiple broadcast users (using a fixed-size temporal contention window consisting of multiple contention slots having uniform selection probability) has been well understood to be inefficient in avoiding collisions, especially when the network is large. Recently, it has been found that this inefficiency can be mitigated by exploiting an additional degree of freedom (DoF) over the contention window, referred to as contention slot selection distribution (CSSD). In this article, the authors examine how the additional DoF contributes to enhancing network performance and quantify the performance gains that the network can achieve in terms of easily understandable performance indicators like network throughput efficiency and broadcast reliability. A discrete-time Markov chain is formulated to characterize the access arbitration process involving a reverse exponential CSSD and its steady-state solution is fed to a renewal-reward process-based network model to estimate the performances of interest. Validated numerical results are presented which confirm that this new channel access arbitration mechanism can significantly enhance the scalability of distributed broadcast networks.
TWIST1 associates with NF-κB subunit RELA via carboxyl-terminal WR domain to promote cell autonomous invasion through IL8 production
Authors: Li Shan , Kendall Stephen E , Raices Raquel , Finlay James , Covarrubias Maricela , Liu Zheng , Lowe Gina , Lin Yu-Huey , Teh Yuan Han , Leigh Victoria , Dhillon Simi , Flanagan Steven , Aboody Karen S , Glackin Carlotta A 
Published: August 2012

Abstract

Background
Metastasis is the primary cause of death for cancer patients. TWIST1, an evolutionarily conserved basic helix-loop-helix (bHLH) transcription factor, is a strong promoter of metastatic spread and its expression is elevated in many advanced human carcinomas. However, the molecular events triggered by TWIST1 to motivate dissemination of cancer cells are largely unknown.

Results
Here we show that TWIST1 induces the production of interleukin 8 (IL8), which activates matrix metalloproteinases and promotes invasion of breast epithelial and cancer cells. In this novel mechanism, TWIST1-mediated IL8 transcription is induced through the TWIST1 carboxy-terminal WR (Trp-Arg) domain instead of the classic DNA binding bHLH domain. Co-immunoprecipitation analyses revealed that the WR domain mediates the formation of a protein complex comprised of TWIST1 and the nuclear factor-kappaB (NF-κB) subunit RELA (p65/NF-κB3), which synergistically activates the transcriptional activity of NF-κB. This activation leads to increased DNA binding affinity of RELA to the IL8 promoter and thus induces the expression of the cytokine. Blockage of IL8 signaling by IL8 neutralizing antibodies or receptor inhibition reduced the invasiveness of both breast epithelial and cancer cells, indicating that TWIST1 induces autonomous cell invasion by establishing an IL8 antocrine loop.

Conclusions
Our data demonstrate that the TWIST1 WR domain plays a critical role in TWIST1-induced IL8 expression through interactions with and activation of NF-κB. The produced IL8 signals through an autocrine loop and promotes extracellular matrix degradation to enable cell invasion across the basement membrane.
Complement activation in the injured central nervous system: another dual-edged sword?
Authors: Brennan Faith H , Anderson Aileen J , Taylor Stephen M , Woodruff Trent M , Ruitenberg Marc J 
Published: August 2012

AbstractThe complement system, a major component of the innate immune system, is becoming increasingly recognised as a key participant in physiology and disease. The awareness that immunological mediators support various aspects of both normal central nervous system (CNS) function and pathology has led to a renaissance of complement research in neuroscience. Various studies have revealed particularly novel findings on the wide-ranging involvement of complement in neural development, synapse elimination and maturation of neural networks, as well as the progression of pathology in a range of chronic neurodegenerative disorders, and more recently, neurotraumatic events, where rapid disruption of neuronal homeostasis potently triggers complement activation. The purpose of this review is to summarise recent findings on complement activation and acquired brain or spinal cord injury, i.e. ischaemic-reperfusion injury or stroke, traumatic brain injury (TBI) and spinal cord injury (SCI), highlighting the potential for complement-targeted therapeutics to alleviate the devastating consequences of these neurological conditions.
Female attractiveness affects paternal investment: experimental evidence for male differential allocation in blue tits
Authors: Mahr Katharina , Griggio Matteo , Granatiero Michela , Hoi Herbert 
Published: August 2012

AbstractIntroductionThe differential allocation hypothesis (DAH) predicts that individuals should adjust their parental investment to their current mate’s quality. Although in principle the DAH holds for both sexes, male adjustment of parental investment has only been tested in a few experimental studies, revealing contradictory results. We conducted a field experiment to test whether male blue tits (Cyanistes caeruleus) allocate their parental effort in relation to female ornamentation (ultraviolet colouration of the crown), as predicted by the DAH.ResultsWe reduced the UV reflectance in a sample of females and compared parental care by their mates with that of males paired to sham-manipulated control females. As predicted by the DAH our results demonstrate that males paired with UV-reduced females invested less in feeding effort but did not defend the chicks less than males paired with control females.ConclusionsTo our knowledge, this is one of the first studies providing support for male differential allocation in response to female ornamentation.
Suppression of dynamin GTPase decreases α-synuclein uptake by neuronal and oligodendroglial cells: a potent therapeutic target for synucleinopathy
Authors: Konno Masatoshi , Hasegawa Takafumi , Baba Toru , Miura Emiko , Sugeno Naoto , Kikuchi Akio , Fiesel Fabienne C , Sasaki Tsutomu , Aoki Masashi , Itoyama Yasuto , Takeda Atsushi 
Published: August 2012

Abstract

Background
The intracellular deposition of misfolded proteins is a common neuropathological hallmark of most neurodegenerative disorders. Increasing evidence suggests that these pathogenic proteins may spread to neighboring cells and induce the propagation of neurodegeneration.

Results
In this study, we have demonstrated that α-synuclein (αSYN), a major constituent of intracellular inclusions in synucleinopathies, was taken up by neuronal and oligodendroglial cells in both a time- and concentration-dependent manner. Once incorporated, the extracellular αSYN was immediately assembled into high-molecular-weight oligomers and subsequently formed cytoplasmic inclusion bodies. Furthermore, αSYN uptake by neurons and cells of the oligodendroglial lineage was markedly decreased by the genetic suppression and pharmacological inhibition of the dynamin GTPases, suggesting the involvement of the endocytic pathway in this process.

Conclusions
Our findings shed light on the mode of αSYN uptake by neuronal and oligodendroglial cells and identify therapeutic strategies aimed at reducing the propagation of protein misfolding.
L166P mutant DJ-1 promotes cell death by dissociating Bax from mitochondrial Bcl-XL
Authors: Ren Haigang , Fu Kai , Mu Chenchen , Zhen Xuechu , Wang Guanghui 
Published: August 2012

AbstractBackgroundMutations or deletions in DJ-1/PARK7 gene are causative for recessive forms of early onset Parkinson’s disease (PD). Wild-type DJ-1 has cytoprotective roles against cell death through multiple pathways. The most commonly studied mutant DJ-1(L166P) shifts its subcellular distribution to mitochondria and renders cells more susceptible to cell death under stress stimuli. We previously reported that wild-type DJ-1 binds to Bcl-XLand stabilizes it against ultraviolet B (UVB) irradiation-induced rapid degradation. However, the mechanisms by which mitochondrial DJ-1(L166P) promotes cell death under death stimuli are largely unknown.ResultsWe show that DJ-1(L166P) is more prone to localize in mitochondria and it binds to Bcl-XLmore strongly than wild-type DJ-1. In addition, UVB irradiation significantly promotes DJ-1(L166P) translocation to mitochondria and binding to Bcl-XL. DJ-1(L166P) but not wild-type DJ-1 dissociates Bax from Bcl-XL, thereby leading to Bax enrichment at outer mitochondrial membrane and promoting mitochondrial apoptosis pathway in response to UVB irradiation.ConclusionOur findings suggest that wild-type DJ-1 protects cells and DJ-1(L166P) impairs cells by differentially regulating mitochondrial Bax/Bcl-XLfunctions.
Compatibility of SYTO 13 and Hoechst 33342 for longitudinal imaging of neuron viability and cell death
Authors: Hubbard Kyle S , Gut Ian M , Scheeler Stephen M , Lyman Megan E , McNutt Patrick M 
Published: August 2012

Abstract

Background
Simultaneous use of cell-permeant and impermeant fluorescent nuclear dyes is a common method to study cell viability and cell death progression. Although these assays are usually conducted as end-point studies, time-lapse imaging offers a powerful technique to distinguish temporal changes in cell viability at single-cell resolution. SYTO 13 and Hoechst 33342 are two commonly used cell-permeant nuclear dyes; however their suitability for live imaging has not been well characterized. We compare end-point assays with time-lapse imaging studies over a 6 h period to evaluate the compatibility of these two dyes with longitudinal imaging, using both control neurons and an apoptotic neuron model.

Findings
In longitudinal assays of untreated neurons, SYTO 13 addition caused acute necrosis within 3 h, whereas neurons imaged with Hoechst remained viable for at least 6 h. In a staurosporine-induced apoptotic model of neurotoxicity, determinations of the mode of cell death and measurements of nuclear size were identical between longitudinal studies using Hoechst and end-point assays. Alternatively, longitudinal studies using 500 nM or 5 nM SYTO 13 were not consistent with end-point assays.

Conclusions
SYTO 13 is acutely neurotoxic and when used in longitudinal studies, masked end-stage morphologic evidence of apoptotic cell death. In contrast, a single application of Hoechst evoked no evidence of toxicity over a 6 h period, and was consistent with end-point characterizations of cell viability and nuclear morphology. For longitudinal characterization of acute cell death, Hoechst is a superior option.
Uncommon cavernous malformation of the optic chiasm: a case report
Authors: Ning Xianbin , Xu Kan , Luo Qi , Qu Limei , Yu Jinlu 
Published: August 2012

Abstract
Cavernous malformation (CM) is a vascular malformation disorder characterized by a berry-like mass of expanded blood vessels. CM, originating from the optic chiasm. usually leads to chiasma syndrome presenting with bitemporal hemianopsia. We report a 28-year-old male presenting with left homonymous hemianopsia. Magnetic resonance imaging (MRI) revealed an occupied lesion located in the right side of the optic chiasm, and a clinical diagnosis of chiasmal CM was made. Microsurgical excision was performed via anterolateral pterional craniotomy. The patient showed good recovery with slight improvement of the visual field deficits after the operation. No CM recurrence was discovered during the follow-up MRI scans.
Persistence of disseminated tumor cells after neoadjuvant treatment for locally advanced breast cancer predicts poor survival
Authors: Mathiesen Randi R , Borgen Elin , Renolen Anne , Løkkevik Erik , Nesland Jahn M , Anker Gun , Østenstad Bjørn , Lundgren Steinar , Risberg Terje , Mjaaland Ingvil , Kvalheim Gunnar , Lønning Per Eystein , Naume Bjørn 
Published: August 2012

Abstract
Introduction
Presence of disseminated tumor cells (DTCs) in bone marrow (BM) and circulating tumor cells (CTC) in peripheral blood (PB) predicts reduced survival in early breast cancer. The aim of this study was to determine the presence of and alterations in DTC- and CTC-status in locally advanced breast cancer patients undergoing neoadjuvant chemotherapy (NACT) and to evaluate their prognostic impact.

Methods
Bone marrow and peripheral blood were collected before NACT (BM1: n = 231/PB1: n = 219), at surgery (BM2: n = 69/PB2: n = 71), and after 12 months from start of NACT (BM3: n = 162/PB3: n = 141). Patients were included from 1997 to 2003 and followed until 2009 (or ten years follow-up). DTC- and CTC-status were determined by morphological evaluation of immunocytochemically detected cytokeratin-positive cells. The prognostic significance of DTCs/CTCs was assessed by univariate and multivariate Cox-regression analyses.

Results
Before NACT, DTCs and CTCs were detected in 21.2% and 4.9% of the patients, respectively. At surgery, 15.9% and 1.4% had DTC- and CTC-presence, compared to 26.5% and 4.3% at 12 months from start of NACT. Of patients for whom DTC results both before NACT and at 12 months were available, concordant results were observed in 68%, and 14 out of 65 had positive DTC-status at both time points. Presence of ≥ 1 DTC 12 months from start of NACT, but not at other time points, predicted reduced disease-free survival (DFS; HR 2.3, p = 0.003), breast cancer-specific survival (BCSS; HR 3.0, p < 0.001) and overall survival (OS; HR 2.8, p < 0.001). Before NACT, presence of ≥ 3 DTCs was also associated with unfavorable outcome, and reduced BCSS was observed for CTC-positive patients (HR 2.2, p = 0.046). In multivariate analysis, DTC status (</≥ 1 DTC) at 12 months after start of NACT remained as a prognostic factor for both DFS (HR 2.2, p = 0.005), BCSS (HR 2.6, p = 0.002) and OS (HR 2.6, p = 0.002). The survival for patients with change in DTC-status was determined by the DTC-status at 12 months.

Conclusion
Presence of DTCs after NACT indicated high risk for relapse and death, irrespective of the DTC-status before treatment. The results supports the potential use of DTC analysis as a monitoring tool during follow up, for selection of patients to secondary treatment intervention within clinical trials.