bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abscisic Acid-Induced Resistance against the Brown Spot Pathogen Cochliobolus miyabeanus in Rice Involves MAP Kinase-Mediated Repression of Ethylene Signaling
Authors: De Vleesschauwer David , Yang Yinong , Vera Cruz Casiana , Höfte Monica 
Published: February 2010

Abstract
The plant hormone abscisic acid (ABA) is involved in an array of plant processes, including the regulation of gene expression during adaptive responses to various environmental cues. Apart from its well-established role in abiotic stress adaptation, emerging evidence indicates that ABA is also prominently involved in the regulation and integration of pathogen defense responses. Here, we demonstrate that exogenously administered ABA enhances basal resistance of rice (Oryza sativa) against the brown spot-causing ascomycete Cochliobolus miyabeanus. Microscopic analysis of early infection events in control and ABA-treated plants revealed that this ABA-inducible resistance (ABA-IR) is based on restriction of fungal progression in the mesophyll. We also show that ABA-IR does not rely on boosted expression of salicylic acid-, jasmonic acid -, or callose-dependent resistance mechanisms but, instead, requires a functional Gα-protein. In addition, several lines of evidence are presented suggesting that ABA steers its positive effect on brown spot resistance through antagonistic cross talk with the ethylene (ET) response pathway. Exogenous ethephon application enhances susceptibility, whereas genetic disruption of ET signaling renders plants less vulnerable to C. miyabeanus attack, thereby inducing a level of resistance similar to that observed on ABA-treated wild-type plants. Moreover, ABA treatment alleviates C. miyabeanus-induced activation of the ET reporter gene EBP89, while derepression of pathogen-triggered EBP89 transcription via RNA interference-mediated knockdown of OsMPK5, an ABA-primed mitogen-activated protein kinase gene, compromises ABA-IR. Collectively, these data favor a model whereby exogenous ABA enhances resistance against C. miyabeanus at least in part by suppressing pathogen-induced ET action in an OsMPK5-dependent manner.
A Novel MYBS3-Dependent Pathway Confers Cold Tolerance in Rice
Authors: Su Chin-Fen , Wang Yi-Chieh , Hsieh Tsai-Hung , Lu Chung-An , Tseng Tung-Hai , Yu Su-May 
Published: February 2010

Abstract
Rice (Oryza sativa) seedlings are particularly sensitive to chilling in early spring in temperate and subtropical zones and in high-elevation areas. Improvement of chilling tolerance in rice may significantly increase rice production. MYBS3 is a single DNA-binding repeat MYB transcription factor previously shown to mediate sugar signaling in rice. In this study, we observed that MYBS3 also plays a critical role in cold adaptation in rice. Gain- and loss-of-function analyses indicated that MYBS3 was sufficient and necessary for enhancing cold tolerance in rice. Transgenic rice constitutively overexpressing MYBS3 tolerated 4°C for at least 1 week and exhibited no yield penalty in normal field conditions. Transcription profiling of transgenic rice overexpressing or underexpressing MYBS3 led to the identification of many genes in the MYBS3-mediated cold signaling pathway. Several genes activated by MYBS3 as well as inducible by cold have previously been implicated in various abiotic stress responses and/or tolerance in rice and other plant species. Surprisingly, MYBS3 repressed the well-known DREB1/CBF-dependent cold signaling pathway in rice, and the repression appears to act at the transcriptional level. DREB1 responded quickly and transiently while MYBS3 responded slowly to cold stress, which suggests that distinct pathways act sequentially and complementarily for adapting short- and long-term cold stress in rice. Our studies thus reveal a hitherto undiscovered novel pathway that controls cold adaptation in rice.
Contextual risk, maternal parenting and adolescent externalizing behaviour problems: the role of emotion regulation
Authors: Walton A. , Flouri E. 
Published: February 2010

AbstractBackground  The objective of this study was to test if emotion regulation mediates the association between mothers' parenting and adolescents' externalizing behaviour problems (conduct problems and hyperactivity). The parenting dimensions were warmth, psychological control and behavioural control (measured with knowledge, monitoring and discipline). Adjustment was made for contextual risk (measured with the number of proximal adverse life events experienced), gender, age and English as an additional language.Method  Data were from a UK community sample of adolescents aged 11–18 from a comprehensive school in a disadvantaged area.Results  At the multivariate level, none of the parenting variables predicted hyperactivity, which was associated only with difficulties in emotion regulation, contextual risk and English as a first language. The parenting variables predicting conduct problems at the multivariate level were warmth and knowledge. Knowledge did not predict emotion regulation. However, warmth predicted emotion regulation, which was negatively associated with conduct problems. Contextual risk was a significant predictor of both difficulties in emotion regulation and externalizing behaviour problems. Its effect on conduct problems was independent of parenting and was not via its association with difficulties in emotion regulation.Conclusions  The findings add to the evidence for the importance of maternal warmth and contextual risk for both regulated emotion and regulated behaviour. The small maternal control effects on both emotion regulation and externalizing behaviour could suggest the importance of paternal control for adolescent outcomes.
Testicular dysgenesis syndrome comprises some but not all cases of hypospadias and impaired spermatogenesis
Authors: Jørgensen N. , Meyts E. Rajpert‐De , Main K. M. , Skakkebæk N. E. 
Published: February 2010

SummaryIn 2001, when the testicular dysgenesis syndrome (TDS) concept was proposed, it suggested that impaired development of foetal testes could lead to increased risks of cryptorchidism, hypospadias, decreased spermatogenesis or testis cancer. The TDS concept links the pathogenesis of the four disorders together, but does not imply that all affected men develop all four symptoms. The least affected men may merely have a slightly reduced spermatogenic capacity, and only the most severely affected may present all symptoms. A majority of cases of testicular germ cell cancers (TGCC) and cryptorchidism are most likely caused by TDS. However, the frequency of the syndrome in the general population and to what extent poor semen quality and hypospadias are actually biologically related through a foetal mechanism remain unresolved. Hypospadias and impaired spermatogenesis can be classified as TDS if combined with cryptorchidism or TGCC. By contrast, recent studies demonstrated that among men with isolated hypospadias, only a fraction of cases are linked to TDS. There is no doubt that TDS contributes to impaired semen quality. This is most obvious for cases with visible dysgenetic features in testis histology, but in the majority of men with impaired semen quality as the only symptom, an association with TDS is less clear. Such cases have a very heterogeneous aetiology and may be caused by a host of other – often post‐natal‐factors. In conclusion, the TDS as a holistic concept has inspired new research activities and led to a better understanding of the early origin of male reproductive problems, but it clearly encompasses only a fraction of cases of hypospadias and impaired spermatogenesis.
Atomic force microscopy: probing the spatial organization, interactions and elasticity of microbial cell envelopes at molecular resolution
Authors: Scheuring Simon , Dufrêne Yves F. 
Published: February 2010

SummaryAlthough much is known about the structure and biosynthesis of microbial cell envelope constituents, the three‐dimensional organization, assembly and interactions of the individual components remain poorly understood. How do cell walls remodel during cell growth or incubation with drugs? What is the supramolecular architecture of proteins in bacterial surface layers, in outer membranes and in intracytoplasmic membranes? What is the spatial arrangement of cell surface receptors, clustered or homogeneous? What are the adhesive and mechanical properties of cell surface proteins and how are they related to function? Traditionally, these questions have been difficult – or impossible – to address owing to the lack of high‐resolution single‐cell and single‐molecule probing techniques. With its ability to observe and force probe the cell envelope down to the molecular level under physiological conditions, atomic force microscopy (AFM) has recently offered new opportunities in molecular microbiology. While high‐resolution AFM imaging is a powerful tool for visualizing the architecture of cells and membranes in buffer solution, force spectroscopy offers a means to analyse the localization, interactions and elasticity of their individual constituents. These nanoscale experiments complement microscopy, genetics and biochemical methods traditionally used to analyse the microbial envelope.
Staphylococcus aureus enterotoxin B augments granulocyte migration and survival via airway epithelial cell activation
Authors: Huvenne W. , Callebaut I. , Reekmans K. , Hens G. , Bobic S. , Jorissen M. , Bullens D. M. A. , Ceuppens J. L. , Bachert C. , Hellings P. W. 
Published: February 2010

To cite this article: Huvenne W, Callebaut I, Reekmans K, Hens G, Bobic S, Jorissen M, Bullens DMA, Ceuppens JL, Bachert C, Hellings PW. Staphylococcus aureus enterotoxin B augments granulocyte migration and survival via airway epithelial cell activation. Allergy 2010; 65: 1013–1020.AbstractBackground:  Staphylococcus aureus enterotoxin B (SEB) has recently been postulated to be involved in the pathology of granulocyte‐dominated disease. Studying the immunologic interaction between SEB and airway epithelial cells in immortalized cell lines or long‐term epithelial cell cultures has obvious disadvantages.Methods:  We used a novel technique of freshly isolated and purified human nasal epithelial cells (HNEC) from healthy, nonallergic individuals, which were incubated for 24 h without/with SEB at different concentrations. Chemokine production was evaluated in the supernatant using Cytometric Bead Array. The chemotactic activity of the supernatant was studied in vitro using a Boyden chamber. Survival was evaluated with flow cytometry, using propidium iodide to identify dead cells.Results:  Staphylococcus aureus enterotoxin B showed a dose‐dependent induction of interferon‐inducible protein‐10, monokine induced by interferon‐γ, regulated upon activation normal T cell expressed and secreted, monocyte chemoattractant protein 1 (MCP‐1) and granulocyte colony stimulating factor production by epithelial cells in vitro. The supernatant of epithelial cells had chemotactic activity for granulocytes in vitro, which was enhanced in the supernatant of SEB‐stimulated epithelial cells. Reduced number of propidium iodide positive granulocytes was found in the conditions where supernatant of SEB‐stimulated epithelial cells was applied.Conclusion:  Staphylococcus aureus enterotoxin B exerts a direct pro‐inflammatory effect on HNEC, with induction of chemokine and growth factor release, resulting in the migration and prolonged survival of granulocytes in vitro.
Stratum corneum lipids, skin barrier function and filaggrin mutations in patients with atopic eczema
Authors: Jungersted J. M. , Scheer H. , Mempel M. , Baurecht H. , Cifuentes L. , Høgh J. K. , Hellgren L. I. , Jemec G. B. E. , Agner T. , Weidinger S. 
Published: February 2010

To cite this article: Jungersted JM, Scheer H, Mempel M, Baurecht H, Cifuentes L, Høgh JK, Hellgren LI, Jemec GBE, Agner T, Weidinger S. Stratum corneum lipids, skin barrier function and filaggrin mutations in patients with atopic eczema. Allergy 2010; 65: 911–918.AbstractBackground:  Prior to the discovery of filaggrin (FLG) mutations, evidence for an impaired skin barrier in atopic dermatitis (AD) has been documented, and changes in ceramide profile, altered skin pH and increased trans‐epidermal water loss (TEWL) in patients with AD have been reported. Until now, no studies have analysed stratum corneum (SC) lipids combined with skin barrier parameters in subjects of known FLG genotype.Methods:  A cohort of 49 German individuals genotyped for the most common FLG mutations (R501X, 2282del4) had SC samples taken for lipid analysis by high‐performance thin layer chromatography. In addition, TEWL, erythema, skin hydration and pH were measured. In 27 of the 49 individuals, a 24‐h irritation patch test with sodium lauryl sulphate was performed. For the analysis, both the AD group and the control group were stratified by FLG mutation status (FLGmut/FLGwt).Results:  In the FLGmut AD group, significantly lower levels of ceramide 4 and significantly higher levels of ceramide 7 were observed when compared to both healthy control groups. However, ceramide 7 levels also significantly differed between FLGwt AD and FLGwt controls, as did ceramide 1 levels. No significant differences were observed for ceramide 2, 3, 5 and 6. FLGmut individuals had significantly higher skin pH values than individuals not carrying FLG mutations. Patients with AD with FLG mutations had significantly higher erythema compared to patients with AD without FLG mutations.Conclusion:  Our results confirm previous observations of altered ceramide levels in AD, which however appear to show no clear relationship with FLG mutations.
Novel and recurrent p14ARF mutations in Italian familial melanoma
Authors: Binni F , Antigoni I , De Simone P , Majore S , Silipo V , Crisi A , Amantea A , Pacchiarini D , Castori M , De Bernardo C , Catricalà C , Grammatico P 
Published: February 2010

Binni F, Antigoni I, De Simone P, Majore S, Silipo V, Crisi A, Amantea A, Pacchiarini D, Castori M, De Bernardo C, Catricalà C, Grammatico P. Novel and recurrent p14ARF mutations in Italian familial melanoma.CDKN2A and CDK4 are the only known high‐penetrant genes conferring proneness to cutaneous melanoma. The CDKN2A locus consists of four exons and encodes several alternate transcripts, two of which are p16INK4a and p14ARF, and originate from different open reading frames. Exon 1α is specific for p16INK4a, while exon 1β characterizes p14ARF. Most CDKN2A mutations are located in exons 1α and 2, while exon 1β variations have been identified in rare melanoma‐prone pedigrees. In a previous study, we investigated 155 Italian melanoma cases, including 94 familial melanomas (FAMs) and 61 sporadic multiple primary melanomas (MPMs), for p16INK4a/CDK4 germline alterations and identified 15 p16INK4a and 1 CDK4 point mutations. In the present work, we extended our search to p14ARF mutations and CDKN2A deletions in the remaining samples. We identified the recurrent g.193+1G> A mutation in two FAM cases, while an additional pedigree displayed the previously undescribed variant g.161G> A. Multiplex ligation‐dependent probe amplification (MLPA) screening for copy variations resulted negative in all cases. In Italy, the overall frequency of p14ARF mutations is 3.2% in FAM and 0% in sporadic MPM. Re‐evaluation of our patients' cohort emphasizes that the chance of identifying CDKN2A/CDK4 mutations in FAM is mainly influenced by the number of affected family members and the presence of one or more MPM cases. Accordingly, mutation rate rises to 61% in selected cases. Further studies are expected in order to investigate CDKN2A rarer mutations, including atypical deletions and inherited epimutations.
Dopamine‐mediated inhibition of renal Na+/K+‐ATPase in HK‐2 cells is reduced by ouabain
Authors: Zhang Yu‐Rong , Yuan Zu‐Yi 
Published: February 2010

Summary1. Abnormal renal sodium handling is considered a major contributing factor in hypertension associated with chronic ouabain treatment. However, the molecular mechanisms involved in abnormal renal sodium handling have not been elucidated. Therefore, we investigated whether chronic ouabain treatment perturbs dopamine D1receptor function.2. The expression and phosphorylation levels of the D1receptor in cells of the human proximal tubule cell line (HK‐2) were determined using western blot analysis and reverse transcription polymerase chain reaction. The activity of the renal sodium/potassium pump (Na+/K+‐ATPase) was measured using a colourimetric assay, and cyclic adenosine monophosphate accumulation was determined by performing a radioimmunoassay.3. We showed that chronic ouabain treatment decreased the protein and mRNA expression levels of the D1receptor and increased the basal phosphorylation of the D1receptor in HK‐2 cells. We also showed that in the presence of ouabain, HK‐2 cells did not reveal the cyclic adenosine monophosphate accumulation and Na+/K+‐ATPase inhibition induced by the D1receptor agonist fenoldopam.4. We hypothesize that the ouabain‐induced decrease in renal D1receptor function is responsible for the increase in renal sodium reabsorption, which eventually leads to ouabain‐induced hypertension.
Inhibitory effect of resveratrol derivative BTM‐0512 on high glucose‐induced cell senescence involves dimethylaminohydrolase/asymmetric dimethylarginine pathway
Authors: Yuan Qiong , Peng Jun , Liu Si‐Yu , Wang Chen‐Jing , Xiang Da‐Xiong , Xiong Xiao‐Ming , Hu Chang‐Ping , Li Yuan‐Jian 
Published: February 2010

Summary1. It has been reported that resveratrol exerts the inhibitory effects on aging through activation of sirtuin 1 (SIRT1) and dimethylarginine dimethylaminohydrolase (DDAH)/asymmetric dimethylarginine (ADMA) pathway involved in the high glucose‐induced endothelial cell senescence.2. The aims of this work were to explore whether BTM‐0512, a novel derivative of resveratrol, was able to exert the beneficial effect on high glucose‐induced cellular senescence through regulating the DDAH/ADMA pathway and to explore whether the regulatory effect of BTM‐0512 on DDAH/ADMA pathway was related to the activation of SIRT1.3. The senescence model of endothelial cells was induced by high glucose and the cells were collected for the determination of β‐galactosidase and DDAH activity, ADMA level, DDAH and SIRT1 mRNA expression.4. The results showed that high glucose significantly increased the ratio of senescent cells concomitantly with the decreased DDAH activity, the downregulated DDAH2 and SIRT1 mRNA expressions and the increased ADMA levels, which were attenuated by pretreatment with BTM‐0512.5. The beneficial effects of BTM‐0512 on high glucose‐induced senescence were blocked by splimtomicin, the specific inhibitor of SIRT1, or by silencing DDAH2 expression.6. The results suggest that BTM‐0512 was able to exert the beneficial effects on high glucose‐induced cellular senescence through regulating the DDAH/ADMA pathway, and its regulatory effect on DDAH/ADMA pathway was related to the activation of SIRT1.
Effects of flecainide and quinidine on action potential and ventricular arrhythmogenic properties in Scn3b knockout mice
Authors: Hakim Parvez , Thresher Rosemary , Grace Andrew A , Huang Christopher L‐H 
Published: February 2010

Summary1. Flecainide and quinidine exert contrasting pro‐arrhythmic and anti‐arrhythmic effects in mouse hearts containing the loss‐of‐function, Scn5a+/−, and the gain‐of‐function, Scn5a+/ΔKPQ, mutations in their sodium channel α‐subunits.2.  The following properties were accordingly compared in wild‐type and Scn3b−/− hearts modelling modifications in the β‐subunit, before and after introduction of either agent: (i) ventricular arrhythmogenecity and effective refractory periods (VERP) in response to programmed electrical stimulation (PES); (ii) monophasic action potential waveforms recorded from the left ventricular epicardium and endocardium; (iii) action potential durations (APD) obtained from the monophasic action potentials; and (iv) critical intervals derived from the APD and VERP values.3.  Ventricular tachycardia was induced by PES in 11 out of 15 Scn3b−/− hearts and 0 out of 17 wild‐type hearts. This incidence was reduced to three out of eight Scn3b−/− hearts but increased to three out of eight wild‐type hearts with flecainide.4. Arrhythmogenic incidence was reduced to two out of eight Scn3b−/− hearts and remained at 0 out of eight wild‐type hearts in the presence of quinidine.5. Ventricular effective refractory periods were prolonged and endocardial and epicardial APD shortened, resulting in negative critical intervals in both Scn3b−/− and wild‐type hearts treated by either flecainide or quinidine. Nevertheless, endocardial APD remained consistently longer than epicardial APD, leaving similar, positive endocardial–epicardial, differences, ΔAPD, in treated and untreated Scn3b−/− and wild‐type hearts.6. It is concluded that both flecainide and quinidine exert anti‐arrhythmogenic effects in Scn3b−/− hearts, doing so through modifying VERP rather than ΔAPD, in contrast to their differing effects in Scn5a+/− and Scn5a+/ΔKPQ hearts.
Erythropoietin inhibits γ‐irradiation‐induced apoptosis by upregulation of Bcl‐2 and decreasing the activation of caspase 3 in human UT‐7/erythropoietin cell line
Authors: Liu Yuan‐Yuan , She Zhen‐Jue , Yao Ming‐Hui 
Published: February 2010

Summary1. Erythropoietin (EPO) can reverse radiotherapy‐induced anaemia by stimulating bone marrow cells to produce erythrocytes. However, there are limited studies that address the mechanisms by which EPO exerts its beneficial effects in radiotherapy‐induced anaemia. In the present study, we used a human bone marrow‐derived EPO‐dependent leukaemia cell line UT‐7/EPO that progressed further in erythroid development to evaluate the anti‐apoptotic effects of EPO on irradiated human erythroid progenitor.2. The UT‐7/EPO cells exposed to γ‐irradiation were cultured in the presence or absence of EPO at a concentration of 7 U/mL. The cell viability, cell apoptosis and the expression of apoptosis‐related proteins Bcl‐2, Bax and caspase 3 were examined.3. The results showed that EPO protected the viability of human UT‐7/EPO cells exposed to γ‐irradiation. EPO significantly inhibited γ‐irradiation‐induced apoptosis in human UT‐7/EPO cells: a significant decrease in the percentage of apoptotic cells was observed (62, 69 and 62% at 24, 48 and 72 h, respectively). Furthermore, EPO significantly increased the expression of Bcl‐2 protein and the relative Bcl‐2/Bax ratio, and decreased the activation of caspase 3 and formation of the p17 and p12 cleavage in similar conditions.4. In conclusion, EPO exerts anti‐apoptotic effects on irradiated human UT‐7/EPO cells through upregulation of Bcl‐2 protein and the relative Bcl‐2/Bax ratio, and by decreasing the activation of caspase 3. These findings may contribute to our understanding of the beneficial function of EPO in radiotherapy‐induced anaemia.