bluuebunny/crossref_metadata_2025_split huggingface dataset:
Identification of Lens culinaris defense genes responsive to the anthracnose pathogen Colletotrichum truncatum
Authors: Bhadauria Vijai , Bett Kirstin E , Zhou Tengsheng , Vandenberg Albert , Wei Yangdou , Banniza Sabine 
Published: April 2013

AbstractBackgroundAnthracnose of lentil, caused by the hemibiotrophic fungal pathogenColletotrichum truncatumis a serious threat to lentil production in western Canada.Colletotrichum truncatumemploys a bi-phasic infection strategy characterized by initial symptomless biotrophic and subsequent destructive necrotrophic colonization of its host. The transition from biotrophy to necrotrophy (known as the biotrophy-necrotrophy switch [BNS]) is critical in anthracnose development. Understanding plant responses during the BNS is the key to designing a strategy for incorporating resistance against hemibiotrophic pathogens either via introgression of resistance genes or quantitative trait loci contributing to host defense into elite cultivars, or via incorporation of resistance by biotechnological means.ResultsThein plantaBNS ofC. truncatumwas determined by histochemical analysis of infected lentil leaf tissues in time-course experiments. A total of 2852 lentil expressed sequence tags (ESTs) derived fromC. truncatum-infected leaf tissues were analyzed to catalogue defense related genes. These ESTs could be assembled into 1682 unigenes. Of these, 101 unigenes encoded membrane and transport associated proteins, 159 encoded proteins implicated in signal transduction and 387 were predicted to be stress and defense related proteins (GenBank accessions: JG293480 to JG293479). The most abundant class of defense related proteins contained pathogenesis related proteins (encoded by 125 ESTs) followed by heat shock proteins, glutathione S-transferase, protein kinases, protein phosphatase, zinc finger proteins, peroxidase, GTP binding proteins, resistance proteins and syringolide-induced proteins. Quantitative RT-PCR was conducted to compare the expression of two resistance genes of the NBS-LRR class in susceptible and partially resistant genotypes. One (contig186) was induced 6 days post-inoculation (dpi) in a susceptible host genotype (Eston) whereas the mRNA level of another (LT21-1990) peaked 4 dpi in a partially resistant host genotype (Robin), suggesting roles in conditioning the susceptibility and conferring tolerance to the pathogen, respectively.ConclusionsData obtained in this study suggest that lentil cells recognizeC. truncatumat the BNS and in response, mount an inducible defense as evident by a high number of transcripts (23% of the total pathogen-responsive lentil transcriptome) encoding defense related proteins. Temporal expression polymorphism of defense related genes could be used to distinguish the response of a lentil genotype as susceptible or resistant.
ContigScape: a Cytoscape plugin facilitating microbial genome gap closing
Authors: Tang Biao , Wang Qi , Yang Minjun , Xie Feng , Zhu Yongqiang , Zhuo Ying , Wang Shengyue , Gao Hong , Ding Xiaoming , Zhang Lixin , Zhao Guoping , Zheng Huajun 
Published: April 2013

Abstract

Background
With the emergence of next-generation sequencing, the availability of prokaryotic genome sequences is expanding rapidly. A total of 5,276 genomes have been released since 2008, yet only 1,692 genomes were complete. The final phase of microbial genome sequencing, particularly gap closing, is frequently the rate-limiting step either because of complex genomic structures that cause sequence bias even with high genomic coverage, or the presence of repeat sequences that may cause gaps in assembly.

Results
We have developed a Cytoscape plugin to facilitate gap closing for high-throughput sequencing data from microbial genomes. This plugin is capable of interactively displaying the relationships among genomic contigs derived from various sequencing formats. The sequence contigs of plasmids and special repeats (IS elements, ribosomal RNAs, terminal repeats, etc.) can be displayed as well.

Conclusions
Displaying relationships between contigs using graphs in Cytoscape rather than tables provides a more straightforward visual representation. This will facilitate a faster and more precise determination of the linkages among contigs and greatly improve the efficiency of gap closing.
Effects of insulin and IGF-I on growth hormone- induced STAT5 activation in 3T3-F442A adipocytes
Authors: Zhang Yuchao , Liu Yuantao , Li Xia , Gao Weina , Zhang Wenjie , Guan Qingbo , Jiang Jing , Frank Stuart J , Wang Xiangdong 
Published: April 2013

Abstract

Background
Growth hormone (GH) and insulin signaling pathways are known important regulators of adipose homeostasis. The cross-talk between GH and insulin signaling pathways in mature adipocytes is poorly understood.

Methods
In the present study, the impact of insulin on GH-mediated signaling in differentiated 3T3-F442A adipocytes and primary mice adipocytes was examined.

Results
Insulin alone did not induce STAT5 tyrosine phosphorylation, but enhanced GH-induced STAT5 activation. This effect was more pronounced when insulin was added 20 min prior to GH treatment. The above results were further confirmed by in vivo study, showing that insulin pretreatment potentiated GH- induced STAT5 tyrosine phosphorylation in visceral adipose tissues of C57/BL6 mice. In addition, our in vitro results showed that IGF-I had similar potentiating effect as insulin on GH-induced STAT5 activation. In vitro, insulin and IGF-I had an additive effect on GH- induced MAPK activation.

Conclusion
These results indicate that both insulin and IGF-I specifically potentiated GH mediated STAT5 activation in mature adipose cells. These findings suggest that insulin and GH, usually with antagonistic functions, might act synergistically to regulate some specific functions in mature adipocytes.
Ancient origin of somatic and visceral neurons
Authors: Nomaksteinsky Marc , Kassabov Stefan , Chettouh Zoubida , Stoeklé Henri-Corto , Bonnaud Laure , Fortin Gilles , Kandel Eric R , Brunet Jean-François 
Published: April 2013

Abstract

Background
A key to understanding the evolution of the nervous system on a large phylogenetic scale is the identification of homologous neuronal types. Here, we focus this search on the sensory and motor neurons of bilaterians, exploiting their well-defined molecular signatures in vertebrates. Sensorimotor circuits in vertebrates are of two types: somatic (that sense the environment and respond by shaping bodily motions) and visceral (that sense the interior milieu and respond by regulating vital functions). These circuits differ by a small set of largely dedicated transcriptional determinants: Brn3 is expressed in many somatic sensory neurons, first and second order (among which mechanoreceptors are uniquely marked by the Brn3+/Islet1+/Drgx+ signature), somatic motoneurons uniquely co-express Lhx3/4 and Mnx1, while the vast majority of neurons, sensory and motor, involved in respiration, blood circulation or digestion are molecularly defined by their expression and dependence on the pan-visceral determinant Phox2b.

Results
We explore the status of the sensorimotor transcriptional code of vertebrates in mollusks, a lophotrochozoa clade that provides a rich repertoire of physiologically identified neurons. In the gastropods Lymnaea stagnalis and Aplysia californica, we show that homologues of Brn3, Drgx, Islet1, Mnx1, Lhx3/4 and Phox2b differentially mark neurons with mechanoreceptive, locomotory and cardiorespiratory functions. Moreover, in the cephalopod Sepia officinalis, we show that Phox2 marks the stellate ganglion (in line with the respiratory — that is, visceral— ancestral role of the mantle, its target organ), while the anterior pedal ganglion, which controls the prehensile and locomotory arms, expresses Mnx.

Conclusions
Despite considerable divergence in overall neural architecture, a molecular underpinning for the functional allocation of neurons to interactions with the environment or to homeostasis was inherited from the urbilaterian ancestor by contemporary protostomes and deuterostomes.
Comparative expression of Toll-like receptors and inflammatory cytokines in pigs infected with different virulent porcine reproductive and respiratory syndrome virus isolates
Authors: Zhang Lili , Liu Jie , Bai Juan , Wang Xiaoye , Li Yufeng , Jiang Ping 
Published: April 2013

AbstractBackgroundPorcine reproductive and respiratory syndrome virus (PRRSV) is largely responsible for heavy economic losses in the swine industry worldwide because of its high mutation rate and subsequent emergence of virulent strains. However, the immunological and pathological responses of pigs to PRRSV strains with different virulence have not been completely elucidated.MethodsTwenty-four piglets were divided into 4 groups (n = 6 each) and inoculated with highly pathogenic PRRSV isolate BB0907 (HP), low pathogenic PRRSV NT0801 (LP), LP derivative strain NT0801-F70 (LP-der), and DMEM medium (control), respectively. The changes in TLR2, 3, 7, and 8 gene expression and TNF-α, IL-1β, IL-6, IFN-γ, and IL-10 secretion were evaluated using real-time PCR and ELISA at 6, 9, and 15 days post inoculation (d.p.i.). The cytokine levels were evaluated in the supernatants of porcine alveolar macrophages (PAMs) and peripheral blood mononuclear cells (PBMCs) following stimulation with LTA, poly(I:C), CL097, and PRRSV individually.ResultsHP caused more severe clinical signs and pathological lesions in swine than LP and LP-der had almost no virulence compared with LP. The serum levels of IL-1β, IL-6, TNF-α, and IFN-γ were increased in HP-infected piglets, which were greater than in those infected with LP or LP-der. The mRNA levels of TLR3, 7, and 8 were significantly up-regulated in PAMs in HP-infected pigs compared to those in groups LP and LP-der. Furthermore, TNF-α and IL-1β secretion in PAMs from group LP was statistically greater than those from the control group after stimulation with either poly(I:C) or CL097. Meanwhile, TNF-α, IL-1β, and IL-6 levels in CL097-stimulated PBMCs from HP-infected pigs were markedly higher than those from the LP- and LP-der-infected groups.ConclusionsWe found that HP was a stronger inducer of TLR 3, 7, and 8 expression and IL-1β, IL-6, TNF-α, and IFN-γ production compared to LP and LP-der. HP enhanced production of TNF-α, IL-1β, and IL-6 in PBMCs following CL097-stimulation more than LP and LP-der, whereas LP enhanced the secretion of TNF-α and IL-1β in poly(I:C)- and CL097-stimulated PAMs. Our data regarding cellular reactivity to different isolates should be useful in the development of more efficacious vaccines.
Upregulation of microRNA-224 is associated with aggressive progression and poor prognosis in human cervical cancer
Authors: Shen Shu-na , Wang Ling-feng , Jia Yong-feng , Hao Yu-qing , Zhang Lin , Wang Hui 
Published: April 2013

Abstract

Objective
Accumulating evidence for differential expression of microRNA-224 (miR-224) in various types of human cancer suggests that it may be play a crucial role in tumor biology. The previous microarray detection also shown that miR-224 was one of miRNAs with significant upregulation in cervical cancer tissues relative to adjacent normal tissues. However, little is known about the function of miR-224 in human cervical cancer. The aim of this study was to investigate the clinical significance of miR-224 expression in cervical cancer.

Methods
MiR-224 expression in 126 pairs of fresh human cervical cancer and adjacent normal tissues was measured by real-time quantitative RT-PCR assay.

Results
miR-224 expression was significantly upregulated in cervical cancer tissues when compared with corresponding adjacent normal tissues (P < 0.001). It was also significantly higher in the cancerous tissues of patients with advanced FIGO stage cervical cancer than those with early FIGO stage (P = 0.02). In addition, miR-224 was expressed at significantly higher levels in lymph node metastasis-positive patients than in lymph node metastasis-negative patients (P = 0.008). Moreover, we found that lesser differentiated tumors expressed higher miR-224 (P = 0.03). Finally, there were sufficient evidence to confirm its value in the status of vascular invasion (P = 0.01) and human papillomavirus (HPV) infection (P = 0.02) in cervical cancer. More importantly, Kaplan-Meier analysis showed that cervical cancer patients with high miR-224 expression tend to have shorter overall survival. In multivariate analysis stratified for known prognostic variables, miR-224 was identified as an independent prognostic marker.

Conclusion
Our data indicated that miR-224 upregulation was associated with aggressive progression and poor prognosis in cervical cancer. MiR-224 was identified for the first time as an independent marker for predicting the clinical outcome of cervical cancer patients.

Virtual slides
The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/2170449349527493
Abnormal interneuron development in disrupted-in-schizophrenia-1 L100P mutant mice
Authors: Lee Frankie HF , Zai Clement C , Cordes Sabine P , Roder John C , Wong Albert HC 
Published: April 2013

Abstract

Background
Interneuron deficits are one of the most consistent findings in post-mortem studies of schizophrenia patients and are likely important in the cognitive deficits associated with schizophrenia. Disrupted-in-Schizophrenia 1 (DISC1), a strong susceptibility gene for schizophrenia and other mental illnesses, is involved in neurodevelopment, including that of interneurons. However, the mechanism by which DISC1 regulates interneuron development remains unknown. In this study, we analyzed interneuron histology in the Disc1-L100P single point mutation mouse, that was previously shown to have behavioral abnormalities and cortical developmental defects related to schizophrenia.

Results
We sought to determine whether a Disc1-L100P point mutation in the mouse would alter interneuron density and location. First, we examined interneuron position in the developing mouse cortex during embryonic days 14–16 as an indicator of interneuron tangential migration, and found striking migration deficits in Disc1-L100P mutants. Further analysis of adult brains revealed that the Disc1-L100P mutants have selective alterations of calbindin- and parvalbumin-expressing interneurons in the cortex and hippocampus, decreased GAD67/PV co-localization and mis-positioned interneurons across the neocortex when compared to wild-type littermates.

Conclusion
Our results are consistent with the anomalies seen in post-mortem schizophrenia studies and other Disc1 mutant mouse models. Future research is required to determine the specific mechanisms underlying these cellular deficits. Overall, these findings provide further evidence that DISC1 participates in interneuron development and add to our understanding of how DISC1 variants can affect susceptibility to psychiatric illness.
A systematic map protocol: which components or attributes of biodiversity affect which dimensions of poverty?
Authors: Roe Dilys , Sandbrook Chris , Fancourt Max , Schulte Bjorn , Munroe Robert , Sibanda Mxolisi 
Published: April 2013

Abstract
Background
The assumption that biodiversity and ecosystem services can help in efforts to tackle poverty is implicit in international targets set for biodiversity conservation (by the Convention on Biological Diversity) and for poverty reduction (enshrined in the Millennium Development Goals). The 2010 United Nations General Assembly further stressed the linkage, claiming: “preserving biodiversity is inseparable from the fight against poverty.” Nevertheless the evidence-base on biodiversity – poverty links is not as robust as one might assume. Studies in the academic and “grey” literature have used diverse methods and metrics, different components of biodiversity and dimensions of poverty have been studied, and the scale of impact has rarely been assessed.

Methods/Design
This systematic map protocol sets out the proposed methodology for exploring the primary question: Which components or attributes of biodiversity affect (positively or negatively) which dimensions of poverty? The overall aim of our review is to unpack the broad claims and assumptions that are made about biodiversity-poverty links such as those above, and provide researchers, policy-makers and practitioners with a methodical overview of the type and quantity of evidence. The online databases SCOPUS and Web of Science will be searched for relevant peer-reviewed literature using search terms and Boolean search operators. Relevant grey literature will be identified through the membership and resources of the Poverty and Conservation Learning Group. The literature searches will be followed by a title and abstract level search using inclusion and exclusion criteria. Data will be extracted from the final list of papers using a questionnaire established through literature review and an expert workshop. A report and online database will be produced based on the results of the review.
Primary Granulocyte Colony-Stimulating Factor Prophylaxis During the First Two Cycles Only or Throughout All Chemotherapy Cycles in Patients With Breast Cancer at Risk for Febrile Neutropenia
Authors: Aarts Maureen J. , Peters Frank P. , Mandigers Caroline M. , Dercksen M. Wouter , Stouthard Jacqueline M. , Nortier Hans J. , van Laarhoven Hanneke W. , van Warmerdam Laurence J. , van de Wouw Agnes J. , Jacobs Esther M. , Mattijssen Vera , van der Rijt Carin C. , Smilde Tineke J. , van der Velden Annette W. , Temizkan Mehmet , Batman Erdogan , Muller Erik W. , van Gastel Saskia M. , Borm George F. , Tjan-Heijnen Vivianne C.G. 
Published: April 2013

Purpose Early breast cancer is commonly treated with anthracyclines and taxanes. However, combining these drugs increases the risk of myelotoxicity and may require granulocyte colony-stimulating factor (G-CSF) support. The highest incidence of febrile neutropenia (FN) and largest benefit of G-CSF during the first cycles of chemotherapy lead to questions about the effectiveness of continued use of G-CSF throughout later cycles of chemotherapy. Patients and Methods In a multicenter study, patients with breast cancer who were considered fit enough to receive 3-weekly polychemotherapy, but also had > 20% risk for FN, were randomly assigned to primary G-CSF prophylaxis during the first two chemotherapy cycles only (experimental arm) or to primary G-CSF prophylaxis throughout all chemotherapy cycles (standard arm). The noninferiority hypothesis was that the incidence of FN would be maximally 7.5% higher in the experimental compared with the standard arm. Results After inclusion of 167 eligible patients, the independent data monitoring committee advised premature study closure. Of 84 patients randomly assigned to G-CSF throughout all chemotherapy cycles, eight (10%) experienced an episode of FN. In contrast, of 83 patients randomly assigned to G-CSF during the first two cycles only, 30 (36%) had an FN episode (95% CI, 0.13 to 0.54), with a peak incidence of 24% in the third cycle (ie, first cycle without G-CSF prophylaxis). Conclusion In patients with early breast cancer at high risk for FN, continued use of primary G-CSF prophylaxis during all chemotherapy cycles is of clinical relevance and thus cannot be abandoned.
High-Dose Cytarabine Consolidation With or Without Additional Amsacrine and Mitoxantrone in Acute Myeloid Leukemia: Results of the Prospective Randomized AML2003 Trial
Authors: Schaich Markus , Parmentier Stefani , Kramer Michael , Illmer Thomas , Stölzel Friedrich , Röllig Christoph , Thiede Christian , Hänel Mathias , Schäfer-Eckart Kerstin , Aulitzky Walter , Einsele Hermann , Ho Anthony D. , Serve Hubert , Berdel Wolfgang E. , Mayer Jiri , Schmitz Norbert , Krause Stefan W. , Neubauer Andreas , Baldus Claudia D. , Schetelig Johannes , Bornhäuser Martin , Ehninger Gerhard 
Published: April 2013

Purpose To assess the treatment outcome benefit of multiagent consolidation in young adults with acute myeloid leukemia (AML) in a prospective, randomized, multicenter trial. Patients and Methods Between December 2003 and November 2009, 1,179 patients (median age, 48 years; range, 16 to 60 years) with untreated AML were randomly assigned at diagnosis to receive either standard high-dose cytarabine consolidation with three cycles of 18 g/m2 (3× HD-AraC) or multiagent consolidation with two cycles of mitoxantrone (30 mg/m2) plus cytarabine (12 g/m2) and one cycle of amsacrine (500 mg/m2) plus cytarabine (10 g/m2; MAC/MAMAC/MAC). Allogeneic and autologous hematopoietic stem-cell transplantations were performed in a risk-adapted and priority-based manner. Results After double induction therapy using a 3 + 7 regimen including standard-dose cytarabine and daunorubicin, complete remission was achieved in 65% of patients. In the primary efficacy population of patients evaluable for consolidation outcomes, consolidation with either 3× HD-AraC or MAC/MAMC/MAC did not result in any significant difference in 3-year overall (69% v 64%; P = .18) or disease-free survival (46% v 48%; P = .99) according to the intention-to-treat analysis. Furthermore, MAC/MAMAC/MAC led to additional GI and hepatic toxicity and a higher rate of infection and bleeding, resulting in significantly shorter 3-year overall survival in the per-protocol analysis compared with 3× HD-AraC (63% v 72%; P = .04). Conclusion In younger adults with AML, multiagent consolidation using mitoxantrone and amsacrine in combination with high-dose cytarabine does not improve treatment outcome and confers additional toxicity.
Reconstruction using femoral head allograft in revision total knee replacement
Authors: Wang J-W. , Hsu C-H. , Huang C-C. , Lin P-C. , Chen W-S. 
Published: April 2013

Structural allografts may be used to manage uncontained bone defects in revision total knee replacement (TKR). However, the availability of cadaver grafts is limited in some areas of Asia. The aim of this study was to evaluate the mid-term outcome of the use of femoral head allografts for the reconstruction of uncontained defects in revision TKR, focusing on complications related to the graft.We retrospectively reviewed 28 patients (30 TKRs) with Anderson Orthopaedic Research Institute (AORI) type 3 bone defects, who underwent revision using femoral head allografts and stemmed components. The mean number of femoral heads used was 1.7 (1 to 3). The allograft–host junctions were packed with cancellous autograft.At a mean follow-up of 76 months (38 to 136) the mean American Knee Society knee score improved from 37.2 (17 to 60) pre-operatively to 90 (83 to 100) (p < 0.001). The mean function score improved from 26.5 (0 to 50) pre-operatively to 81 (60 to 100) (p < 0.001). All the grafts healed to the host bone. The mean time to healing of the graft was 6.6 months (4 to 16). There have been no complications of collapse of the graft, nonunion, infection or implant loosening. No revision surgery was required.The use of femoral head allografts in conjunction with a stemmed component and autogenous bone graft in revision TKR in patients with uncontained bone defects resulted in a high rate of healing of the graft with minimal complications and a satisfactory outcome. Longer follow-up is needed to observe the evolution of the graft.Cite this article: Bone Joint J 2013;95-B:643–8.