bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression Profile of Long Noncoding RNAs in Peripheral Blood Mononuclear Cells from Multiple Sclerosis Patients
Authors: Zhang Fang , Gao Chao , Ma Xiao‐Feng , Peng Xiao‐Lin , Zhang Rong‐Xin , Kong De‐Xin , Simard Alain R. , Hao Jun‐Wei 
Published: February 2016

SummaryAimsLong noncoding RNAs (lncRNAs) play a key role in regulating immunological functions. Their impact on the chronic inflammatory disease multiple sclerosis (MS), however, remains unknown. We investigated the expression of lncRNAs in peripheral blood mononuclear cells (PBMCs) of patients with MS and attempt to explain their possible role in the process of MS.MethodsFor this study, we recruited 26 patients with MS according to the revised McDonald criteria. Then, we randomly chose 6 patients for microarray analysis. Microarray assays identified outstanding differences in lncRNA expression, which were verified through real‐time PCR. LncRNA functions were annotated for target genes using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, and regulatory relationships between lncRNAs and target genes were analyzed using the “cis” and “trans” model.ResultsThere were 2353 upregulated lncRNAs, 389 downregulated lncRNAs, 1037 upregulated mRNAs, and 279 downregulated mRNAs in patients with MS compared to healthy control subjects (fold change >2.0). Real‐time PCR results of six aberrant lncRNAs were consistent with the microarray data. The coexpression network comprised 864 lncRNAs and 628 mRNAs. Among differentially expressed lncRNAs, 10 lncRNAs were predicted to have 10 cis‐regulated target genes, and 33 lncRNAs might regulate their trans target genes.ConclusionsWe identified a subset of dysregulated lncRNAs and mRNAs. The differentially expressed lncRNAs may be important in the process of MS. However, the specific molecular mechanisms and biological functions of these lncRNAs in the pathogenesis of MS need further study.
Vessel Dilation Attenuates Endothelial Dysfunction Following Middle Cerebral Artery Occlusion in Hyperglycemic Rats
Authors: Mu Zhi‐Hao , Jiang Zhen , Lin Xiao‐Jie , Wang Li‐Ping , Xi Yan , Zhang Zhi‐Jun , Wang Yong‐Ting , Yang Guo‐Yuan 
Published: February 2016

SummaryObjectivesDynamically observe cerebral vascular changes in hyperglycemic rats in vivo and explore the effect of diabetes on endothelial function after ischemic stroke.BackgroundDiabetes affects both large and small vessels in the brain, but the dynamic process and mechanism are unclear.MethodsWe investigated the structural and functional changes of brain vasculature in living hyperglycemic rats and their impact on stroke outcomes via a novel technique: synchrotron radiation angiography. We also examined the effect of prolonged fasudil treatment on arterial reactivity and hemorrhagic transformation. Adult Sprague Dawley rats were treated by streptozotocin to induce type 1 diabetes. These hyperglycemic rats received fasudil pretreatment and then underwent transient middle cerebral artery occlusion.ResultsWe found that diabetes caused arteries narrowing in the circus Willis as early as 2 weeks after streptozotocin injection (P < 0.05). These vessels were further constricted after middle cerebral artery occlusion. L‐NAME could induce regional constrictions and impaired relaxation in hyperglycemic animals. Furthermore, hemorrhagic transformation was also increased in the hyperglycemic rats compared to the control (P < 0.05). In fasudil‐treated rats, the internal carotid artery narrowing was ameliorated and L‐NAME‐induced regional constriction was abolished. Importantly, stroke prognosis was improved in fasudil‐treated rats compared to the control (P < 0.05).ConclusionsOur dynamic angiographic data demonstrated that diabetes could impair the cerebral arterial reactivity. Prolonged fasudil treatment could attenuate arterial dysfunction and improve the prognosis of ischemic stroke by affecting both the large and small vasculature.
The Neural Basis of Postural Instability Gait Disorder Subtype of Parkinson's Disease: A PET and fMRI Study
Authors: Zhang Li , Li Tian‐Nv , Yuan Yong‐Sheng , Jiang Si‐Ming , Tong Qing , Wang Min , Wang Jian‐Wei , Chen Hua‐Jun , Ding Jian , Xu Qin‐Rong , Zhang Ke‐Zhong 
Published: February 2016

SummaryAimsThe aim of this study is to further uncover the neural basis of postural instability gait disorder (PIGD) subtype of Parkinson's disease.MethodsWith F‐18 fluorodeoxyglucose PET (FDG‐PET), brain glucose metabolism of patients with PIGD (n = 15) was compared with healthy controls (n = 17) and tremor‐dominant (TD) patients (n = 15), and the correlation between metabolism and PIGD symptoms was also assessed. Within PIGD symptom‐correlated hypometabolic areas, the relationship of functional connectivity (FC) with motor and cognitive symptoms was examined by using functional MRI.ResultsCompared with controls, patients with PIGD displayed a distributed pattern of brain hypometabolism including striatal, frontal, and parietal areas. Relative to the pattern of TD patients, the pattern of patients with PIGD had additional metabolic decreases in caudate and inferior parietal lobule (IPL, Brodmann area [BA] 40). In PIGD group, the metabolic reductions in IPL (BA 40), middle frontal gyrus (MFG, BA 9) and fusiform gyrus (FG, BA 20) were associated with severe PIGD symptoms. Regions showing such correlation were chosen for further seed‐based FC analysis. Decreased FC within the prefrontal–parietal network (between the MFG and IPL) was associated with severe PIGD symptoms.ConclusionThe involvement of the caudate, FG, and prefrontal–parietal network may be associated with the prominent gait impairments of PIGD subtype. Our findings expand the pathophysiological knowledge of PIGD subtype and provide valuable information for potential neuromodulation therapies alleviating gait disorders.
The Cannabinoid CB1/CB2 Agonist WIN55212.2 Promotes Oligodendrocyte Differentiation In Vitro and Neuroprotection During the Cuprizone‐Induced Central Nervous System Demyelination
Authors: Tomas‐Roig Jordi , Wirths Oliver , Salinas‐Riester Gabriela , Havemann‐Reinecke Ursula 
Published: February 2016

SummaryAim and methodsDifferent types of insults to the CNS lead to axon demyelination. Remyelination occurs when the CNS attempts to recover from myelin loss and requires the activation of oligodendrocyte precursor cells. With the rationale that CB1 receptor is expressed in oligodendrocytes and marijuana consumption alters CNS myelination, we study the effects of the cannabinoid agonist WIN55212.2 in (1) an in vitro model of oligodendrocyte differentiation and (2) the cuprizone model for demyelination.ResultsThe synthetic cannabinoid agonist WIN55212.2 at 1 μM increased the myelin basic protein mRNA and protein expression in vitro. During cuprizone‐induced acute demyelination, the administration of 0.5 mg/kg WIN55212.2 confers more myelinated axons, increased the expression of retinoid X receptor alpha, and declined nogo receptor expression. Controversially, 1 mg/kg of the drug increased the number of demyelinated axons and reduced the expression of nerve growth factor inducible, calreticulin and myelin‐related genes coupling specifically with a decrease in 2′,3′‐cyclic nucleotide 3′ phosphodiesterase expression.ConclusionThe cannabinoid agonist WIN55212.2 promotes oligodendrocyte differentiation in vitro. Moreover, 0.5 mg/kg of the drug confers neuroprotection during cuprizone‐induced demyelination, while 1 mg/kg aggravates the demyelination process.
Presymptomatic MPTP Mice Show Neurotrophic S100B/mRAGE Striatal Levels
Authors: Viana Sofia D. , Fernandes Rosa C. , Canas Paula M. , Silva Andréa M. , Carvalho Félix , Ali Syed F. , Fontes Ribeiro Carlos A. , Pereira Frederico C. 
Published: February 2016

SummaryAimsAstrocytic S100B and receptor for advanced glycation endproducts (RAGE) have been implicated in Parkinson׳s disease (PD) pathogenesis through yet unclear mechanisms. This study attempted to characterize S100B/mRAGE (signaling isoform) axis in a dying‐back dopaminergic (DAergic) axonopathy setting, which mimics an early event of PD pathology.MethodsC57BL/6 mice were submitted to a chronic MPTP paradigm (20 mg/kg i.p., 2 i.d‐12 h apart, 5 days/week for 2 weeks) and euthanized 7 days posttreatment to assess mRAGE cellular distribution and S100B/mRAGE density in striatum, after probing their locomotor activity (pole test and rotarod). Dopaminergic status, oxidative stress, and gliosis were also measured (HPLC‐ED, WB, IHC).ResultsThis MPTP regimen triggered increased oxidative stress (augmented HNE levels), gliosis (GS/Iba1‐reactive morphology), loss of DAergic fibers (decreased tyrosine hydroxylase levels), and severe hypodopaminergia. Biochemical deficits were not translated into motor abnormalities, mimicking a presymptomatic PD period. Remarkably, striatal neurotrophic S100B/mRAGE levels and major neuronal mRAGE localization coexist with compensatory responses (3‐fold increase in DA turnover), which are important to maintain normal motor function.ConclusionOur findings rule out the involvement of S100B/mRAGE axis in striatal reactive gliosis, DAergic axonopathy and warrant further exploration of its neurotrophic effects in a presymptomatic compensatory PD stage, which is a fundamental period for successful implementation of therapeutic strategies.
Distinct molecular signatures of mild extrinsic and intrinsic atopic dermatitis
Authors: Martel Britta C. , Litman Thomas , Hald Andreas , Norsgaard Hanne , Lovato Paola , Dyring‐Andersen Beatrice , Skov Lone , Thestrup‐Pedersen Kristian , Skov Søren , Skak Kresten , Poulsen Lars K. 
Published: February 2016

AbstractAtopic dermatitis (AD) is a common inflammatory skin disease with underlying defects in epidermal function and immune responses. In this study, we used microarray analysis to investigate differences in gene expression in lesional skin from patients with mild extrinsic or intrinsic AD compared to skin from healthy controls and from lesional psoriasis skin. The primary aim was to identify differentially expressed genes involved in skin barrier formation and inflammation, and to compare our results with those reported for patients with moderate and severe AD. In contrast to severe AD, expression of the majority of genes associated with skin barrier formation was unchanged or upregulated in patients with mild AD compared to normal healthy skin. Among these, no significant differences in the expression of filaggrin (FLG) and loricrin at both mRNA and protein level were found in lesional skin from patients with mild AD, despite the presence of heterozygous FLG mutations in the majority of patients with mild extrinsic AD. Several inflammation‐associated genes such as S100A9, MMP12, CXCL10 and CCL18 were highly expressed in lesional skin from patients with mild psoriasis and were also increased in patients with mild extrinsic and intrinsic AD similar to previous reports for severe AD. Interestingly, expression of genes involved in inflammatory responses in intrinsic AD resembled that of psoriasis more than that of extrinsic AD. Overall, differences in expression of inflammation‐associated genes found among patients with mild intrinsic and extrinsic AD correlated with previous findings for patients with severe intrinsic and extrinsic AD.
Numerical characterization of compact pipe specimen for stretch zone width assessment
Authors: Mahajan G. , Saxena S. , Mohanty A. 
Published: February 2016

AbstractPresent work focuses on evaluating the suitability of newly proposed compact pipe (CP) fracture specimen geometry for determining critical SZW. The effect of varying the parameter of CP specimen (outer diameter, thickness, a/W ratio and straight and radial crack front) on critical SZW have been studied. It is found that SZWc values decreases slightly with the increase in outer diameter of CP specimen. In CP specimen, thickness greater than a specified value is to be used for geometry independent evaluation of SZWc. Critical SZW shows significant variation with a/W ratio, straight and radial crack front. The CP specimen and Three Point Bend (TPB) specimen also compared in terms of stress tri‐axiality.
Island species–area relationships and species accumulation curves are not equivalent: an analysis of habitat island datasets
Authors: Matthews Thomas J. , Triantis Kostas A. , Rigal François , Borregaard Michael K. , Guilhaumon François , Whittaker Robert J. 
Published: February 2016

AbstractAimThe relationship between species number and area is of fundamental importance in macroecology and conservation science, yet the implications of different means of quantitative depiction of the relationship remain contentious. We set out (1) to establish the variation in form of the relationship between two distinct methods applied to the same habitat island datasets, (2) to explore the relevance of several key dataset properties for variation in the parameters of these relationships, and (3) to assess the implications for application of the resulting models.LocationsGlobal.MethodsThrough literature search we compiled 97 habitat island datasets. For each we analysed the form of the island species–area relationship (ISAR) and several versions of species accumulation curve (SAC), giving priority to a randomized form (Ran‐SAC). Having established the validity of the power model, we compared the slopes (z‐values) between the ISAR and the SAC for each dataset. We used boosted regression tree and simulation analyses to investigate the effect of nestedness and other variables in driving observed differences in z‐values between ISARs and SACs.ResultsThe Ran‐SAC was steeper than the ISAR in 77% of datasets. The differences were primarily driven by the degree of nestedness, although other variables (e.g. the number of islands in a dataset) were also important. The ISAR was often a poor predictor of archipelago species richness.Main conclusionsSlopes of the ISAR and SAC for the same data set can vary substantially, revealing their non‐equivalence, with implications for applications of species–area curve parameters in conservation science. For example, the ISAR was a poor predictor of archipelagic richness in datasets with a low degree of nestedness. Caution should be employed when using the ISAR for the purposes of extrapolation and prediction in habitat island systems.
Von Willebrand factor for menorrhagia: a survey and literature review
Authors: Ragni M. V. , Machin N. , Malec L. M. , James A. H. , Kessler C. M. , Konkle B. A. , Kouides P. A. , Neff A. T. , Philipp C. S. , Brambilla D. J. 
Published: February 2016

Backgroundvon Willebrand disease (VWD) is the most common congenital bleeding disorder. In women, menorrhagia is the most common bleeding symptom, and is disabling with iron deficiency anaemia, high health cost and poor quality of life. Current hormonal and non‐hormonal therapies are limited by ineffectiveness and intolerance. Few data exist regarding von Willebrand factor (VWF), typically prescribed when other treatments fail. The lack of effective therapy for menorrhagia remains the greatest unmet healthcare need in women with VWD. Better therapies are needed to treat women with menorrhagia.MethodsWe conducted a survey of US haemophilia treatment centres (HTCs) and a literature review using medical subject heading (MeSH) search terms ‘von Willebrand factor,’ ‘menorrhagia’ and ‘von Willebrand disease’ to assess the use of VWF in menorrhagia. Analysis was by descriptive statistics.ResultsOf 83 surveys distributed to HTC MDs, 20 (24.1%) provided sufficient data for analysis. Of 1321 women with VWD seen during 2011–2014, 816 (61.8%) had menorrhagia, for which combined oral contraceptives, tranexamic acid and desmopressin were the most common first‐line therapies for menorrhagia, whereas VWF was third‐line therapy reported in 13 women (1.6%). Together with data from 88 women from six published studies, VWF safely reduced menorrhagia in 101 women at a dose of 33–100 IU kg−1 on day 1–6 of menstrual cycle.ConclusionsThis represents the largest VWD menorrhagia treatment experience to date. VWF safely and effectively reduces menorrhagia in women with VWD. A prospective clinical trial is planned to confirm these findings.
Persistent left superior vena cava: Two case reports and a review from nephrologists’ perspective
Authors: Sahutoglu Tuncay , Sakaci Tamer , Kara Ekrem , Ahbap Elbis , Basturk Taner , Koc Yener , Sevinc Mustafa , Akgol Cuneyt , Kayarlar Arzu Ozdemir , Ucar Zuhal Atan , Caglayan Feyza Bayraktar , Hasbal Nuri Baris , Nazif Perin , Isleem Mahmoud , Sahutoglu Elif , Unsal Abdulkadir 
Published: February 2016

AbstractThoracic venous anomalies without congenital heart anomalies are present in minority of the population, but they are frequent enough to be encountered while placing hemodialysis catheters through the jugular or subclavian veins. Persistent left superior vena cava is the most commonly seen anomaly and it is rarely noticed before the observation of an unusual course of hemodialysis catheter or guidewire on chest X‐ray. We present two patients with previously unspotted persistent left superior vena cava and uncomplicated hemodialysis catheter insertions through the internal jugular veins with good catheter functions. Review of the relevant literature from a nephrologists’ perspective with technical aspects is provided.
The H3F3 K36M mutant antibody is a sensitive and specific marker for the diagnosis of chondroblastoma
Authors: Amary M Fernanda , Berisha Fitim , Mozela Rafael , Gibbons Rebecca , Guttridge Alice , O'Donnell Paul , Baumhoer Daniel , Tirabosco Roberto , Flanagan Adrienne M 
Published: February 2016

AimsWe recently reported that 95% of chondroblastomas harbour a p.K36M mutation in either H3F3A (chromosome 1) or H3F3B (chromosome 17), with the majority involving H3F3B. The aim of this study was to assess the expression of the K36M‐mutated protein by immunohistochemistry in a large group of tumours.Methods and resultsOne thousand eight hundred and ninety‐four tumours, including 85 chondroblastomas and 10 clear‐cell chondrosarcomas, were studied; of these, 82 chondroblastomas and one clear‐cell chondrosarcoma known to harbour the H3F3 p.K36M mutation expressed the mutated protein. Three chondroblastomas and nine clear‐cell chondrosarcomas wild type for H3F3A/H3F3B were negative for p.K36M immunoexpression. The remaining 1799 cases tested, 545 of which were known to be wild type for the H3F3A and H3F3B p.K36M mutations, included 1047 primary bone tumours, and 507 soft tissue and joint tumours. Two hundred and forty‐five other tumour types not expected to harbour the mutation were negative for p.K36M immunoexpression.ConclusionsOur data demonstrate the specificity and sensitivity of this immunomarker, and will be a useful adjunct for reaching a diagnosis of chondroblastoma.
Increased expression of senescence markers p14ARF and p16INK4a in breast cancer is associated with an increased risk of disease recurrence and poor survival outcome
Authors: Pare Rahmawati , Shin Joo‐Shik , Lee Cheok Soon 
Published: February 2016

AimsBreast cancer is a hormonally driven disease. Cellular senescence is an age‐related irreversible cell cycle arrest at the G1 phase upon induction. The aim of this study was to characterize the expression patterns of the senescence markers p14ARF, p16INK4a and p21WAF1/Cip1 during breast cancer progression in a large patient cohort.Methods and resultsWe conducted a retrospective study of 1080 patients with invasive ductal carcinoma, no special type, over an 11‐year period. We performed immunohistochemical staining on tissue microarrays that included normal, benign hyperplasia, ductal carcinoma in situ and invasive ductal carcinoma tissue from each patient. Invasive ductal carcinomas showed higher expression of p14ARF and p16INK4a but lower expression of p21WAF1/Cip1 than non‐malignant tissues. There were significant correlations of normal, benign, preinvasive and malignant tissues with p14ARF, p16INK4a and p21WAF1/Cip1 expression (P < 0.05). Univariate comparison showed a correlation between high p16INK4a expression and poor survival (P = 0.000) and an increased risk of relapse (P = 0.000), whereas high p14ARF expression correlated only with an increased risk of relapse (P = 0.038). Multivariate analysis showed p16INK4a to be an important prognostic factor for overall survival (P = 0.011) and disease‐free survival (P = 0.004), with p14ARF also being a significant prognostic factor for disease‐free survival (P = 0.043). Moreover, patients showing both high p16INK4a expression and and high p14ARF expression had an adjusted three‐fold increased risk of disease recurrence (P < 0.05) and a two‐fold increased risk of all‐cause‐related death (P < 0.05).ConclusionsThese finding suggest p16INK4a expression and p14ARF expression may play an important role in the progression of proliferative breast tissue to invasive cancer, and may be useful as prognostic factors.
A cross‐sectional study of dentine sensitivity in periodontitis patients in Trinidad and Tobago
Authors: Ramlogan S , Raman V , Rees JS , Legall G 
Published: February 2016

AbstractObjectiveThis cross‐sectional study aimed to determine the prevalence, distribution and associated factors of dentine sensitivity (DS) among periodontitis patients in Trinidad.MethodsSequential patients meeting the periodontitis criteria (BPE 4/4*) were included and completed a questionnaire on DS prior to a full periodontal examination. Clinically elicited symptoms of DS and presence of cervical tooth wear were recorded.ResultsDS prevalence was 73.1% (n = 130; mean age 50 years). Mean number of sensitive teeth increased with increased severity of gingival recession. Most common initiating factors of DS were cold stimuli (70.5%), brushing (25.3%) and sour food (11.6%). Correlations were obtained for DS and race, toothbrush texture hardness, cervical tooth wear and gingival recession severity (P < 0.05; binary logistic regression). Cervical tooth wear was recorded in 46.3% of DS patients. Full‐mouth plaque scores (FMPS) and full‐mouth bleeding scores (FMBS) were statistically significantly (P < 0.05; Mann–Whitney U) test lower for DS versus non‐DS patients. Patients reported a low usage (27.4%) and satisfaction (53.8%) rating for desensitizing agents.ConclusionsThe high prevalence of DS was comparable to other studies on periodontitis patients. Progressive periodontal disease and toothbrush abrasion were possible aetiological factors for DS in this study. Knowledge of local dietary practices and the role of acidic (sour) foods in eliciting DS may aid in management. The high prevalence of cervical tooth wear and the lower FMPS and FMBS among DS patients may reflect more aggressive tooth brushing. DS does not seem to be a limitation to plaque control in DS versus non‐DS patients in this study.