bluuebunny/crossref_metadata_2025_split huggingface dataset:
OsSIDP366, a DUF1644 gene, positively regulates responses to drought and salt stresses in rice
Authors: Guo Chiming , Luo Chengke , Guo Lijia , Li Min , Guo Xiaoling , Zhang Yuxia , Wang Liangjiang , Chen Liang 
Published: July 2015

AbstractDomain of unknown function 1644 (DUF1644) is a highly conserved amino acid sequence motif present only in plants. Analysis of expression data of the family of DUF1644‐containing genes indicated that they may regulate responses to abiotic stress in rice. Here we present our discovery of the role of OsSIDP366, a member of the DUF1644 gene family, in response to drought and salinity stresses in rice. Transgenic rice plants overexpressing OsSIDP366 showed enhanced drought and salinity tolerance and reduced water loss as compared to that in the control, whereas plants with downregulated OsSIDP366 expression levels using RNA interference (RNAi) were more sensitive to salinity and drought treatments. The sensitivity to abscisic acid (ABA) treatment was not changed in OsSIDP366‐overexpressing plants, and OsSIDP366 expression was not affected in ABA‐deficient mutants. Subcellular localization analysis revealed that OsSIDP366 is presented in the cytoplasmic foci that colocalized with protein markers for both processing bodies (PBs) and stress granules (SGs) in rice protoplasts. Digital gene expression (DGE) profile analysis indicated that stress‐related genes such as SNAC1, OsHAK5 and PRs were upregulated in OsSIDP366‐overexpressing plants. These results suggest that OsSIDP366 may function as a regulator of the PBs/SGs and positively regulate salt and drought resistance in rice.
Plant Mediator complex and its critical functions in transcription regulation
Authors: Yang Yan , Li Ling , Qu Li‐Jia 
Published: July 2015

AbstractThe Mediator complex is an important component of the eukaryotic transcriptional machinery. As an essential link between transcription factors and RNA polymerase II, the Mediator complex transduces diverse signals to genes involved in different pathways. The plant Mediator complex was recently purified and comprises conserved and specific subunits. It functions in concert with transcription factors to modulate various responses. In this review, we summarize the recent advances in understanding the plant Mediator complex and its diverse roles in plant growth, development, defense, non‐coding RNA production, response to abiotic stresses, flowering, genomic stability and metabolic homeostasis. In addition, the transcription factors interacting with the Mediator complex are also highlighted.
Microglial Hv1 proton channel promotes cuprizone‐induced demyelination through oxidative damage
Authors: Liu Junli , Tian Daishi , Murugan Madhuvika , Eyo Ukpong B. , Dreyfus Cheryl F. , Wang Wei , Wu Long‐Jun 
Published: July 2015

AbstractNADPH oxidase (NOX)‐dependent reactive oxygen species (ROS) production in inflammatory cells including microglia plays an important role in demyelination and free radical‐mediated tissue injury in multiple sclerosis (MS). However, the mechanism underlying microglial ROS production and demyelination remains largely unknown. The voltage‐gated proton channel, Hv1, is selectively expressed in microglia and is required for NOX‐dependent ROS generation in the brain. In the present study, we sought to determine the role of microglial Hv1 proton channels in a mouse model of cuprizone‐induced demyelination, a model for MS. Following cuprizone exposure, wild‐type mice presented obvious demyelination, decreased myelin basic protein expression, loss of mature oligodendrocytes, and impaired motor coordination in comparison to mice on a normal chow diet. However, mice lacking Hv1 (Hv1−/−) are partially protected from demyelination and motor deficits compared with those in wild‐type mice. These rescued phenotypes in Hv1−/− mice in cuprizone‐induced demyelination is accompanied by reduced ROS production, ameliorated microglial activation, increased oligodendrocyte progenitor cell (NG2) proliferation, and increased number of mature oligodendrocytes. These results demonstrate that the Hv1 proton channel is required for cuprizone‐induced microglial oxidative damage and subsequent demyelination. Our study suggests that the microglial Hv1 proton channel is a unique target for controlling NOX‐dependent ROS production in the pathogenesis of MS.
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Hv1 proton channel is required for cuprizone‐induced microglial activation and ROS production. Mice lacking Hv1(Hv1−/−) have reduced ROS production, increased oligodendrocyte progenitor (NG2) proliferation, and are partially protected from demyelinatioin and motor deficits that follow curpizone exposure. These results suggest that Hv1 proton channel is a unique target for controlling NOX‐dependent ROS production in the pathogenesis of multiple sclerosis.
The mitochondrial uncoupling protein‐2 is a master regulator of both M1 and M2 microglial responses
Authors: De Simone Roberta , Ajmone‐Cat Maria Antonietta , Pandolfi Manuela , Bernardo Antonietta , De Nuccio Chiara , Minghetti Luisa , Visentin Sergio 
Published: July 2015

AbstractMicroglial activation is a dynamic process, central to neuroinflammation, which can have beneficial or pathogenic effects to human health. Mitochondria are key players in neuroinflammatory and neurodegenerative processes, common to most brain diseases. To the best of our knowledge on the role of mitochondria in the modulation of neuroinflammation, we focused on the mitochondrial uncoupling protein‐2 (UCP2), known to control mitochondrial functions and to be implicated in a variety of physiological and pathological processes. In primary microglial cultures, the M1 stimulus lipopolysaccharide induced an early and transitory decrease in UCP2 levels. The initial UCP2 down‐regulation was paralleled by mitochondrial inner membrane potential (mMP) depolarization and increased mitochondrial reactive oxygen species production. The key role of UCP2 in controlling mMP and reactive oxygen species production was confirmed by both pharmacological inhibition and down‐regulation by RNA interference. Additionally, UCP2‐silenced microglia stimulated with lipopolysaccharide showed an enhanced inflammatory response, characterized by a greater production of nitric oxide and interleukin‐6. UCP2 was differently regulated by M2 stimuli, as indicated by its persistent up‐regulation by interleukin‐4. In UCP2‐silenced microglia, interleukin‐4 failed to induce M2 genes (mannose receptor 1 and interleukin‐10) and to reduce M1 genes (inducible nitric oxide synthase and tumour necrosis factor‐α). Our findings indicate that UCP2 is central to the process of microglial activation, with opposite regulation of M1 and M2 responses, and point to UCP2 manipulation as a potential strategy for redirecting microglial response towards protective phenotypes in several brain diseases where neuroinflammation is recognized to contribute to neurodegeneration.
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We show that the mitochondrial uncoupling protein‐2 (UCP2) is central to the process of microglial activation, with opposite regulation of M1 and M2 responses. In UCP2‐silenced microglia, lipopolysaccharide (LPS) triggers an enhanced inflammatory response characterized by a greater expression of M1 genes, whereas interleukin‐4 (IL‐4) fails in inducing M2 genes and reducing M1 genes. We propose UCP2 manipulation as a potential strategy for redirecting microglial response towards protective phenotypes.
Pinnatoxins E, F and G target multiple nicotinic receptor subtypes
Authors: Hellyer Shane D. , Indurthi Dinesh , Balle Thomas , Runder‐Varga Vanda , Selwood Andrew I. , Tyndall Joel D.A. , Chebib Mary , Rhodes Lesley , Kerr D. Steven 
Published: July 2015

AbstractPinnatoxins are members of the cyclic imine group of marine phycotoxins that are highly toxic in in vivo rodent bioassays, causing rapid death due to respiratory depression. Recent studies have shown that pinnatoxins E, F and G, found in New Zealand and Australian shellfish, act as antagonists at muscle‐type nicotinic acetylcholine receptors (nAChRs) at the neuromuscular junction. In the present study, binding affinities and modes of these pinnatoxin isomers at neuronal and muscle nAChRs were assessed using radioligand binding, electrophysiological and molecular modelling techniques. Radioligand‐binding studies revealed that all three pinnatoxins bound with high affinity to muscle‐type nAChRs, as well as to the α7 and α4β2 neuronal receptors, with an order of affinity of muscle type > α7 > α4β2. The rank order of potency at all receptors was pinnatoxin F > G > E. Pinnatoxins F and G also antagonized ACh‐evoked responses in α7 and α4β2 neuronal receptors expressed in Xenopus oocytes. Molecular modelling revealed that pinnatoxins E, F and G make multiple hydrogen bond interactions with the binding site of muscle‐type and α7 receptors, with few interactions at the α4β2 binding site, reflecting the binding affinity and functional data. This study shows for the first time that pinnatoxins E, F and G bind to, and functionally antagonize neuronal nAChRs, with interactions potentially playing a role in pinnatoxin toxicity.
imageWe used a three‐pronged approach of radioligand binding, electrophysiological recording and molecular modelling to determine the nicotinic antagonist properties of the marine algal pinnatoxins E, F and G. These high‐affinity toxins bind to and antagonize muscle nicotinic receptors, as well as homomeric and heteromeric neuronal nicotinic receptors, and show a preference for homomeric neuronal and muscle‐type receptors over heteromeric neuronal receptors. Modelling of pinnatoxin/receptor interactions revealed potential determinants for binding to each of the receptor subtypes. This high‐affinity nicotinic binding presumably underlies the neuromuscular and CNS symptoms associated with pinnatoxin intoxication.
Subtle visuomotor difficulties in preclinical Alzheimer's disease
Authors: Mollica Maria A. , Navarra Jordi , Fernández‐Prieto Irune , Olives Jaume , Tort Adrià , Valech Natalia , Coll‐Padrós Nina , Molinuevo José L. , Rami Lorena 
Published: July 2015

BackgroundIndividuals with preclinical Alzheimer's disease (Pre‐AD) present nonimpaired cognition, as measured by standard neuropsychological tests. However, detecting subtle difficulties in cognitive functions may be necessary for an early diagnosis and intervention.ObjectivesA new computer‐based visuomotor coordination task (VMC) was developed to investigate the possible presence of early visuomotor difficulties in Pre‐AD individuals. Associations between VMC task performance and AD biomarkers were studied. The influence of ApoE status on participants’ performance was addressed, as well as the relationship between performance and subjective cognitive decline (SCD).MethodsSixty‐six cognitively normal (CN) elders (19 Pre‐AD and 47 control participants [CTR]) and 15 patients with AD performed the VMC task, which consisted in executing visually guided goal‐directed movements that required the coordination of the visual and motor systems. All participants underwent ApoE analysis and lumbar puncture. CN participants also completed an extensive standard neuropsychological battery.ResultsDespite presenting normal cognition in standard tests, Pre‐AD participants exhibited higher response times (RTs) to complete the VMC task than CTR (p < .01). Besides, patients with AD showed higher RTs than CTR (p < .001) and Pre‐AD (p < .05), and more errors than CTR (p < .005). RTs in ApoE4 carriers were higher than that observed in ApoE4 noncarriers (p < .01). In CN individuals, RTs were related to amyloid β‐protein 42 (AB42) biomarker (p < .01) and informant‐rated SCD (p < .01).ConclusionsThe VMC task is able to discriminate Pre‐AD from CTR individuals. Moreover, VMC results are associated with AB42 levels in CN individuals, suggesting that visuomotor dysfunction may be a sensitive marker of Pre‐AD.
The Evolution of World Health Organization's Initiatives for the Strengthening of Nursing and Midwifery
Authors: Ventura Carla Aparecida Arena , Mendes Isabel Amélia Costa , Fumincelli Laís , Trevizan Maria Auxiliadora 
Published: July 2015

AbstractPurposeTo describe the evolution in the resolutions approved by World Health Organization (WHO)’s World Health Assembly (WHA) to strengthen nursing and midwifery.MethodsQualitative and descriptive study, undertaken through a search of resolutions presented by WHA, on the WHO website, regarding the theme “strengthening of nursing and midwifery.” The resolutions on the theme “nursing and midwifery” were included, whose titles were available and whose full texts were accessed, excluding those on general health themes. The key words used were resolutions, strengthening, and nursing and midwifery. Among the 20 resolutions found, 12 were selected, adopted between 1948 and 2013, in accordance with the study inclusion criteria. The data were interpreted using thematic qualitative analysis, identifying and grouping the data in categories related to the study theme.FindingsBased on the content analysis of the 12 resolutions studied, three thematic categories were defined: “nursing and midwifery in primary health”; “role of nursing and midwifery in health for all”; and “nurses and midwives' professional training.”ConclusionsBased on the categories, the evolution in the strengthening of nursing and midwifery was demonstrated through the initiatives and resolutions approved by WHA, highlighting the importance of nurses and midwives as multiprofessional health team members and their fundamental role in the improvements of the health system. Therefore, in accordance with the needs of each country, the member states can implement strategies presented by the WHA resolutions to strengthen nursing and midwifery services.Clinical RelevanceThis study has relevance for the development of health policies considering the relevant contributions of nurses and midwives to healthcare systems and services, based on the analysis of WHO resolutions involving these professions.
Synaptic‐like vesicles and candidate transduction channels in mechanosensory terminals
Authors: Bewick Guy S. 
Published: July 2015

AbstractThis article summarises progress to date over an exciting and very enjoyable first 15 years of collaboration with Bob Banks. Our collaboration began when I contacted him with (to me) an unexpected observation that a dye used to mark recycling synaptic vesicle membrane at efferent terminals also labelled muscle spindle afferent terminals. This observation led to the re‐discovery of a system of small clear vesicles present in all vertebrate primary mechanosensory nerve terminals. These synaptic‐like vesicles (SLVs) have been, and continue to be, the major focus of our work. This article describes our characterisation of the properties and functional significance of these SLVs, combining our complementary skills: Bob's technical expertise and encyclopaedic knowledge of mechanosensation with my experience of synaptic vesicles and the development of the styryl pyridinium dyes, of which the most widely used is FM1‐43. On the way we have found that SLVs seem to be part of a constitutive glutamate secretory system necessary to maintain the stretch‐sensitivity of spindle endings. The glutamate activates a highly unusual glutamate receptor linked to phospholipase D activation, which we have termed the PLD‐mGluR. It has a totally distinct pharmacology first described in the hippocampus nearly 20 years ago but, like the SLVs that were first described over 50 years ago, has since been little researched. Yet, our evidence and literature searches suggest this glutamate/SLV/PLD‐mGluR system is a ubiquitous feature of mechanosensory endings and, at least for spindles, is essential for maintaining mechanosensory function. This article summarises how this system integrates with the classical model of mechanosensitive channels in spindles and other mechanosensory nerve terminals, including hair follicle afferents and baroreceptors controlling blood pressure. Finally, in this time when there is an imperative to show translational relevance, I describe how this fascinating system might actually be a useful therapeutic drug target for clinical conditions such as hypertension and muscle spasticity. This has been a fascinating 15‐year journey in collaboration with Bob who, as well as having an astute scientific mind, is also a great enthusiast, motivator and friend. I hope this exciting and enjoyable journey will continue well into the future.
Protein loss in human hair from combination straightening and coloring treatments
Authors: França‐Stefoni Simone Aparecida , Dario Michelli Ferrera , Sá‐Dias Tânia Cristina , Bedin Valcinir , de Almeida Adriano José , Baby André Rolim , Velasco Maria Valéria R. 
Published: July 2015

SummaryBackgroundHair chemical treatments, such as dyeing and straightening products, are known to cause damage that can be assessed by protein loss.ObjectivesThe aim of this study was to evaluate the hair protein loss caused by combined chemical treatments (dye and relaxer) using the validated bicinchoninic acid (BCA) method. Three kinds of straighteners, based on ammonium thioglycolate, guanidine hydroxide and sodium hydroxide, were evaluated and the least harmful combination indicated.MethodsCaucasian virgin dark brown hair tresses were treated with developed natural brown color oxidative hair dyeing and/or straightening commercial products based on ammonium thioglycolate, sodium hydroxide, or guanidine hydroxide. Protein loss quantification was assessed by the validated BCA method which has several advantages for quantifying protein loss in chemically treated hair.ResultsWhen both treatments (straightening and dyeing) were combined, a higher negative effect was observed, particularly for dyed hair treated with sodium hydroxide. In this case, a 356% increase in protein loss relative to virgin hair was observed and 208% in relation to only dyed hair. The combination of dying and relaxers based on ammonium thioglycolate or guanidine hydroxide caused a small increase in protein loss, suggesting that these straightening products could be the best alternatives for individuals wishing to combine both treatments.ConclusionsThese results indicated that when application of both types of products is desired, ammonium thioglycolate or guanidine hydroxide should be chosen for the straightening process.
Comparison of therapeutic effects of liposomal Tranexamic Acid and conventional Hydroquinone on melasma
Authors: Banihashemi Mahnaz , Zabolinejad Naghmeh , Jaafari Mahmoud Reza , Salehi Maryam , Jabari Asma 
Published: July 2015

SummaryBackgroundMelasma is one of the most common cosmetic disorders with skin darkening. Although several treatment modalities are available, none is satisfactorily used in management of this condition. Tranexamic acid (TA), a plasmin inhibitor, is reported to improve melasma when injected locally or used as oral and topical forms.AimThe aim of this study was to compare therapeutic effects of liposomal tranexamic acid and conventional hydroquinone on melasma.MethodsThirty women with bilateral melasma were enrolled in a split‐face trial lasting 12 weeks. Patients blindly applied 5% topical liposomal TA and 4% hydroquinone cream, to the designated sides of the face twice daily in addition to the assigned sunscreen in the morning. Skin pigmentation was measured using MASI (Melasma Area and Severity Index) at each visit separately for each side at the base line and every month until one month after treatment course. Data were obtained from patients file and were analyzed statistically using SPSS software, paired samples t‐test, and repeated measured ANOVA.ResultsTwenty‐three patients completed the study. The mean MASI scores significantly reduced in both treated sides (P < P = 0.001) after 12 week. A greater decrease was observed with 5% liposomal TA, although this difference was not statistically significant.Irritation occurred in three patients with hydroquinone, while no serious adverse events occurred with TA.ConclusionOn the basis of these results, topical liposomal TA can be used as a new, effective, safe, and promising therapeutic agent in melasma.
Effect of professional self‐concept on burnout among community health nurses in Chengdu, China: the mediator role of organisational commitment
Authors: Cao Xiaoyi , Chen Lin , Tian Lang , Diao Yongshu , Hu Xiuying 
Published: July 2015

Aims and objectivesTo examine the associations among professional self‐concept, organisational commitment and burnout, and to analyse the mediating role of organisational commitment on the relationship between professional self‐concept and burnout among community health nurses in Chengdu, China.BackgroundPrevious studies have focused on work environmental variables that contributed to burnout in nurses. However, no study has explored the mediating effect of organisational commitment on the correlation between professional self‐concept and burnout in community health nurses.DesignA cross‐sectional descriptive study.MethodsThis study was conducted at 36 community health centres in Chengdu, China with 485 nurses sampled using a two‐stage sampling method. The measures used in our study included Nurses’ Self‐concept Questionnaire, Organisational Commitment Scale and Maslach Burnout Inventory.ResultsThe results of structural equation model techniques indicated that, in the direct approach, positive professional self‐concept resulted in increased organisational commitment and reduced burnout. Higher organisational commitment resulted in less burnout. In the indirect approach, organisational commitment performed as a partial mediator on the correlation between professional self‐concept and burnout.ConclusionsPositive perception of professional self‐concept can result in reduced burnout via enhancing organisational commitment.Relevance to clinical practiceIt is crucial for nursing administrators to develop effective intervention strategies such as skills escalator training and assertive training, and establishing a supportive working environment to enhance nurses’ professional self‐concept and organisational commitment, and decrease burnout.
Motor vehicle collision‐related accidents in pregnancy
Authors: Azar Tania , Longo Cristina , Oddy Lisa , Abenhaim Haim Arie 
Published: July 2015

AbstractAimMotor vehicle accidents (MVA) are a major contributor of worldwide morbidity and mortality; however, relatively little is known about the incidence and consequences of traffic accidents on pregnant women. Our aim is to compare rates and outcomes of motor vehicle collision‐related accidents in pregnant women.Material and MethodsWe conducted a population‐based retrospective cohort study using the Healthcare Cost and Utilization Project Nationwide Inpatient Sample database from 2003 to 2011. The risk of different MVA and injuries were compared among pregnant and non‐pregnant subjects using conditional logistic regression.ResultsWe identified 5936 cases of collision‐related MVA in pregnancy and age‐matched them at a 1:10 ratio to 59 360 non‐pregnant women with collision‐related MVA. As compared to non‐pregnant women, pregnant women who were admitted after an MVA suffered less severe injuries and consequently required fewer therapeutic interventions and a shorter hospital stay. Pregnant women who had a collision‐related MVA were, however, at increased risk of requiring genitourinary surgery (odds ratio [OR], 1.45; 95% confidence interval [CI], 1.24–1.69). When restricted to women with a fracture, pregnant women were even more likely to require genitourinary surgery (OR, 2.93; 95%CI, 2.32–3.71) as well as require a blood transfusion (OR, 1.21; 95%CI, 1.01–1.44).ConclusionPregnant women admitted to hospital after a collision‐related MVA tend to sustain less severe injuries compared to non‐pregnant women. However, the influence of admissions for fetal monitoring, rather than maternal injury, could not be determined from our dataset. Pregnant women who experienced a collision‐related MVA also required less surgical intervention, with the exception of genitourinary surgery, which may be indicative of more cesarean deliveries.