bluuebunny/crossref_metadata_2025_split huggingface dataset:
Preference Mapping of Lemon Lime Carbonated Beverages with Regular and Diet Beverage Consumers
Authors: Leksrisompong P. P. , Lopetcharat K. , Guthrie B. , Drake M. A. 
Published: January 2013

AbstractThe drivers of liking of lemon‐lime carbonated beverages were investigated with regular and diet beverage consumers. Ten beverages were selected from a category survey of commercial beverages using a D‐optimal procedure. Beverages were subjected to consumer testing (n = 101 regular beverage consumers, n = 100 diet beverage consumers). Segmentation of consumers was performed on overall liking scores followed by external preference mapping of selected samples. Diet beverage consumers liked 2 diet beverages more than regular beverage consumers. There were no differences in the overall liking scores between diet and regular beverage consumers for other products except for a sparkling beverage sweetened with juice which was more liked by regular beverage consumers. Three subtle but distinct consumer preference clusters were identified. Two segments had evenly distributed diet and regular beverage consumers but one segment had a greater percentage of regular beverage consumers (P < 0.05). The 3 preference segments were named: cluster 1 (C1) sweet taste and carbonation mouthfeel lovers, cluster 2 (C2) carbonation mouthfeel lovers, sweet and bitter taste acceptors, and cluster 3 (C3) bitter taste avoiders, mouthfeel and sweet taste lovers. User status (diet or regular beverage consumers) did not have a large impact on carbonated beverage liking. Instead, mouthfeel attributes were major drivers of liking when these beverages were tested in a blind tasting.Practical Application: Preference mapping of lemon‐lime carbonated beverage with diet and regular beverage consumers allowed the determination of drivers of liking of both populations. The understanding of how mouthfeel attributes, aromatics, and basic tastes impact liking or disliking of products was achieved. Preference drivers established in this study provide product developers of carbonated lemon‐lime beverages with additional information to develop beverages that may be suitable for different groups of consumers.
Differential mitochondrial proteome analysis of human lung adenocarcinoma and normal bronchial epithelium cell lines using quantitative mass spectrometry
Authors: Zhang Wei , Li Yanting , Yang Shuanying , Li Wei , Ming Zongjuan , Zhang Yuping , Hou Yanli , Niu Zequn , Rong Biaoxue , Zhang Xuede , Liu Xiaoli 
Published: January 2013

AbstractBackgroundLung cancer is one of the higher incidences of malignant tumors around the world. At present, tumor markers CEA, CA19‐9, and CA‐125 in serum are used for the diagnosis of lung cancer, however, fewer studies have shown tumor markers for early diagnosis. Therefore, using quantitative mass spectrometry, differential mitochondrial proteome analysis was performed, comparing human lung adenocarcinoma and normal bronchial epithelium cells.MethodsA human lung adenocarcinoma cell line A549 and a normal human bronchial epithelial cell line 16HBE were cultured in vitro. The cell mitochondria of the two cell lines were extracted and purified by differential centrifugation and percoll density gradient centrifugation. The integrity and purity of mitochondria were validated by electron microscopy and Western‐blot. The proteins/peptides from lung cancer cells and normal cells were marked by the same amount of relative and absolute quantification of ectopic tags (iTRAQ). The mixed samples were analyzed and identified by two‐dimensional liquid chromatography – tandem mass spectrometry (2D‐LC‐MS/MS). The proteome was analyzed with different bioinformatic tools.ResultsOne hundred and sixty‐one mitochondrial proteins were identified. One hundred and fifty‐three mitochondrial proteins, which were expressed differently between 16HBE cells and A549 cells, were identified. Sixty‐seven proteins were high expression, while 86 proteins were lower expression. Expression of three proteins: ornithine aminotransferase (OAT), heat shock protein beta90 (HSP90), and vimentin (VIM), was increased more than twice. Our results, in combination with the literature review, suggest that HSP90 and Vimentin may be the new tumor markers of lung cancer.
Heparin‐binding protein (HBP): an early marker of respiratory failure after trauma?
Authors: JOHANSSON J. , BRATTSTRÖM O. , SJÖBERG F. , LINDBOM L. , HERWALD H. , WEITZBERG E. , OLDNER A. 
Published: January 2013

BackgroundTrauma and its complications contribute to morbidity and mortality in the general population. Trauma victims are susceptible to acute respiratory distress syndrome (ARDS) and sepsis. Polymorphonuclear leucocytes (PMNs) are activated after trauma and there is substantial evidence of their involvement in the development of ARDS. Activated PMNs release heparin‐binding protein (HBP), a granule protein previously shown to be involved in acute inflammatory reactions. We hypothesised that there is an increase in plasma HBP content after trauma and that the increased levels are related to the severity of the trauma or later development of severe sepsis and organ failure (ARDS).Methods and MaterialWe investigated HBP in plasma samples within 36 h from trauma in 47 patients admitted to a level one trauma centre with a mean injury severity score (ISS) of 26 (21–34). ISS, admission sequential organ failure assessment (SOFA) and Acute Physiology and Chronic Health Evaluation (APACHE) II scores were recorded at admission. ARDS and presence of severe sepsis were determined daily during intensive care.ResultsWe found no correlation between individual maximal plasma HBP levels at admission and ISS, admission SOFA or APACHE II. We found, however, a correlation between HBP levels and development of ARDS (P = 0.026, n = 47), but not to severe sepsis.ConclusionHBP is a potential biomarker candidate for early detection of ARDS development after trauma. Further research is required to confirm a casual relationship between plasma HBP and the development of ARDS.
Cephalodiscusreproductive biology (Pterobranchia,Hemichordata)
Authors: Dilly Peter N. 
Published: January 2013

AbstractSexually mature adults and embryos and larvae ofCephalodiscus nigrescensandC.graciliswere studied by light and electron microscopy. Contrary to claims in the literature, individual coenecial cavities are inhabited by colonies of up to 15 joined zooids and not by single individuals, which is important for the interpretation of the mode of life of the related fossil group the graptolites. Some aspects of the reproductive apparatus and reproduction inCephalodiscusare reported. The ultrastructure of the spermatozoon is described for the first time. Coelom formation is by schizocoely. The structure of the larva at several developmental stages is illustrated. Not all fertilised eggs are destined to become motile larvae and some develop into zooids omitting the motile stage. The lumen of the oviduct is much larger than previously supposed. Spermatozoa are shed into the cavity of the coenecium. It is proposed that fertilisation takes place within the coenecium. The ultrastructure of the enigmatic black ‘CommaBody’ is described and a reproductive function is proposed. Budding takes place from a base common to several zooids. This base probably also serves as an attachment foot. Large masses of yolk have been discovered within the coelom of some zooids and muscle stalks. It is inconceivable that a colony ofCephalodiscus nigrescenscould survive unless it spent most of its life outside the coenecium.
Inhibition of MAO‐A and stimulation of behavioural activities in mice by the inactive prodrug form of the anti‐influenza agent oseltamivir
Authors: Hiasa Miki , Isoda Yumiko , Kishimoto Yasushi , Saitoh Kenta , Kimura Yasuaki , Kanai Motomu , Shibasaki Masakatsu , Hatakeyama Dai , Kirino Yutaka , Kuzuhara Takashi 
Published: January 2013

Background and PurposeOseltamivir is the most widely prescribed anti‐influenza medication. However, in rare instances, it has been reported to stimulate behavioural activities in adolescents. The goal of this study was to determine the molecular mechanism responsible for these behavioural activities.Experimental ApproachWe performed an in vitro assay of MAO‐A, the enzyme responsible for neurotransmitter degradation, using either the active form – oseltamivir carboxylate (OC) or the inactive prodrug – oseltamivir ethyl ester (OEE). We also analysed the docking of MAO‐A with OEE or OC in silico. Mouse behaviours after OEE or OC administration were monitored using automated video and computer analysis.Key ResultsOEE, but not OC, competitively and selectively inhibited human MAO‐A. The estimated Ki value was comparable with the Km values of native substrates of MAO‐A. Docking simulations in silico based on the tertiary structure of MAO‐A suggested that OEE could fit into the inner pocket of the enzyme. Behavioural monitoring using automated video analysis further revealed that OEE, not OC, significantly enhanced spontaneous behavioural activities in mice, such as jumping, rearing, sniffing, turning and walking.Conclusions and ImplicationsOur multilevel analyses suggested OEE to be the cause of the side effects associated with oseltamivir and revealed the molecular mechanism underlying the stimulated behaviours induced by oseltamivir in some circumstances.
Glutathione S‐transferase P1 Ile105Val polymorphism modulates allergen‐induced airway inflammation in human atopic asthmatics in vivo
Authors: Hoskins A. , Wu P. , Reiss S. , Dworski R. 
Published: January 2013

SummaryBackgroundGlutathione S‐transferase P1 is a Phase II cytoprotective and detoxifying enzyme that is widely expressed in human airways. The glutathione S‐transferase P1 Ile105Val polymorphism has been linked with atopic disorders and asthma. Yet, little remains known about the regulation of allergic inflammation by glutathione S‐transferase P1 in human asthmatics.ObjectiveTo establish the effect of the glutathione S‐transferase P1 Ile105Val polymorphism on allergen‐induced airway inflammation and oxidant stress, and non‐specific bronchial hyperresponsiveness to methacholine and reactivity to specific allergen in mild human atopic asthmatics in vivo.MethodsFive Val105/Val105, twelve Val105/Ile105 and twenty Ile105/Ile105 mild atopic asthmatics underwent methacholine challenge, inhaled allergen challenge and endobronchial allergen provocation through a bronchoscope. A panel of inflammatory cytokines and chemokines, F2‐isoprostanes and isofuranes, markers of oxidative stress, thromboxane B2 and immunoglobulin E were measured in bronchoalveolar lavage fluid at baseline and 24 h after allergen instillation.ResultsAsthmatics with glutathione S‐transferase P1 Val105/Val105 compared with asthmatics with the glutathione S‐transferase P1 Val105/Ile105 and Ile105/Ile105 had greater generation of acute phase cytokines (TNF‐α, IL‐6, CXCL8), IL‐12, CCL11, thromboxane B2 and immunoglobulin E at 24 h after local allergen challenge. The GSTP1 genotype had no effect on airway hyperresponsiveness to methacholine and the reactivity to specific allergen.ConclusionThe glutathione S‐transferase P1 Ile105Val polymorphism markedly modifies allergen‐provoked airway inflammation in atopic asthmatics in vivo. Modulation of the biochemical milieu in response to allergen provides a mechanistic explanation for regulatory effects of glutathione S‐transferase P1 polymorphism on airway pathophysiology, and may guide improvement of future therapeutic methods in human atopic asthmatics. These findings must me confirmed in a larger study population of asthmatics with various ethnicities.
Development of atopic disease and disturbed sleep in childhood and adolescence – a longitudinal population‐based study
Authors: Jernelöv S. , Lekander M. , Almqvist C. , Axelsson J. , Larsson H. 
Published: January 2013

SummaryBackgroundBoth atopic diseases and sleep disturbances have increased during recent decades, especially in children. Sleep is important for many aspects of immune regulation relevant in allergic diseases, and sleep disturbances are common in patients with such diseases. A connection between sleep disturbances and fatigue, and atopic disease is well established. However, the time course and putative causal relationships between these factors are obscure.ObjectiveWe aimed at investigating the developmental relationships between subjectively reported sleep disturbances and symptoms of atopic disease, from childhood to adolescence.MethodsThis longitudinal study used parent‐report questionnaire data on symptoms of atopic disease, and sleep disturbances, from the Twin Study of Child and Adolescent Development (TCHAD). Overall, 1480 twin pairs born in Sweden were approached first when children were 8–9 years old, and again later at 13–14 years old. Response rates were 75% and 72%. Data from the TCHAD questionnaires were linked to the Swedish Medical Birth Register based on personal identification numbers.ResultsBeing overtired at age 8 increased the risk [OR; 95% CI (2.59; 1.31–5.11)] to develop rhinitis symptoms at age 13, even when controlling for gender, previous rhinitis, Socio‐economic status, birth weight and other sleep disturbances at age 8. Likewise, symptoms of asthma at age 8 was an independent risk factor for being overtired at age 13 [OR; 95% CI (2.64; 1.44–4.84)], controlling for similar confounders.Conclusion & Clinical RelevanceThe findings from this study are consonant with the proposition that atopic disease and disturbed sleep are more than passively interrelated. Future research needs to delineate whether causal relationships between these problems are at hand and, if so, at what periods in development this applies. These results point to a need for clinicians to investigate sleep difficulties and treat impaired sleep in paediatric patients with atopic disease.
The effect of B cell depletion therapy on anti‐TSH receptor antibodies and clinical outcome in glucocorticoid‐refractory Graves' orbitopathy
Authors: Mitchell Anna L. , Gan Earn H. , Morris Margaret , Johnson Kim , Neoh Christopher , Dickinson A. Jane , Perros Petros , Pearce Simon H. S. 
Published: January 2013

SummaryObjectiveThis case series documents the response of nine individuals with glucocorticoid‐refractory Graves' orbitopathy (GO) to B cell depletion therapy with rituximab (RTX).ContextGraves' disease (GD) is one of the commonest autoimmune conditions and is frequently associated with inflammatory changes around the eyes (GO). GO frequently results in significant functional visual impairment, and in the most severe cases, it can result in permanent loss of sight. RTX is a therapeutic monoclonal antibody, which targets cell‐surface CD‐20, resulting in depletion of circulating B lymphocytes. It has been found to be useful for the treatment of a number of autoimmune conditions including, in preliminary studies, GO.Design and PatientsWe have treated nine individuals (1 male, 8 female, age range 37–87 years) with glucocorticoid‐resistant GO with RTX since 2008. RTX was administered in divided doses at fortnightly intervals, following 500 mg IV methylprednisolone pretreatment.MeasurementsEach patient underwent thorough assessment before and after RTX therapy, including thyroid function tests, B cell counts, thyroid autoantibody levels and detailed clinical assessment according to EUGOGO standard protocols. All patients have now been followed up for 16 months or more.ResultsThere was a significant reduction in thyrotropin receptor binding inhibitory immunoglobulin (TBII) levels in all patients following RTX treatment and a reduction in the clinical activity score (CAS) was seen in all cases. We also report striking improvement in pretibial thyroid dermopathy in one patient following RTX.ConclusionsThis case series adds to the growing literature demonstrating that RTX, administered in our patients with concomitant methylprednisolone, is safe and clinically effective in the treatment of active, moderate to severe and sight‐threatening GO. Randomized controlled trials are now needed to confirm the efficacy of RTX for GO.
Applying occupancy estimation and modelling to the analysis of atlas data
Authors: Sadoti Giancarlo , Zuckerberg Benjamin , Jarzyna Marta A. , Porter William F. 
Published: January 2013

AbstractAimBiological atlases are a globally widespread and effective means for documenting the distribution of numerous taxa and have been used to study many macroecological relationships. A common assumption when analysing atlas data is that species are detected perfectly (p = 1). This assumption is likely incorrect, but the application of methods to account for heterogeneous detectability (p < 1) has been difficult to implement. We provide an application of current methods of occupancy estimation and modelling to account for imperfect detection in the analysis of atlas data.LocationNew York, USA.MethodsWe employed multiseason occupancy models substituting spatial replicates for temporally repeated surveys to examine changes in distribution of the Canada Warbler (Cardellina canadensis) using breeding bird atlases from 1980–1985 and 2000–2005. We compared estimates from models accounting for p < 1 versus those assuming p = 1 in assessing statewide patterns of occupancy, colonization and extinction.ResultsWe found forest cover, observer effort, information on previous detections and the sampling year were important predictors of detection. Environmental predictors of statewide occupancy dynamics were similar among models accounting for p < 1 versus those assuming p = 1. Despite these similarities, site‐level estimates of occupancy from the model accounting for imperfect detection indicated 14% and 19% higher site occupancy in the 1980–1985 and 2000–2005 Atlases, respectively. In addition, relative to the model accounting for p < 1, the model assuming perfect detectability underestimated persistence and overestimated extinction between atlases. The model accounting for p < 1 had 0.3% and 7.9% higher accuracy in predicting occupancy in the 1980–1985 and 2000–2005 Atlases, respectively, than the models assuming p = 1.Main conclusionsOccupancy modelling and estimation can be successfully applied to broad‐scale surveys, such as atlases, that do not explicitly implement repeated visits to a survey block. Occupancy modelling allows for a more rigorous analysis of atlas data for exploring species–environmental relationships and modelling species distributions while accounting for imperfect detection.
Biallelic PDX1 (insulin promoter factor 1) mutations causing neonatal diabetes without exocrine pancreatic insufficiency
Authors: De Franco E. , Shaw‐Smith C. , Flanagan S. E. , Edghill E. L. , Wolf J. , Otte V. , Ebinger F. , Varthakavi P. , Vasanthi T. , Edvardsson S. , Hattersley A. T. , Ellard S. 
Published: January 2013

AbstractAimsRecessive PDX1 (IPF1) mutations are a rare cause of pancreatic agenesis, with three cases reported worldwide. A recent report described two cousins with a homozygous hypomorphic PDX1 mutation causing permanent neonatal diabetes with subclinical exocrine insufficiency. The aim of our study was to investigate the possibility of hypomorphic PDX1 mutations in a large cohort of patients with permanent neonatal diabetes and no reported pancreatic hypoplasia or exocrine insufficiency.MethodsPDX1 was sequenced in 103 probands with isolated permanent neonatal diabetes in whom ABCC8, KCNJ11 and INS mutations had been excluded.ResultsSequencing analysis identified biallelic PDX1 mutations in three of the 103 probands with permanent neonatal diabetes (2.9%). One proband and his affected brother were compound heterozygotes for a frameshift and a novel missense mutation (p.A34fsX191; c.98dupC and p.P87L; c.260C>T). The other two probands were homozygous for novel PDX1 missense mutations (p.A152G; c.455C>G and p.R176Q; c.527G>A). Both mutations affect highly conserved residues located within the homeobox domain. None of the four cases showed any evidence of exocrine pancreatic insufficiency, either clinically, or, where data were available, biochemically. In addition a heterozygous nonsense mutation (p.C18X; c.54C>A) was identified in a fourth case.ConclusionsThis study demonstrates that recessive PDX1 mutations are a rare but important cause of isolated permanent neonatal diabetes in patients without pancreatic hypoplasia/agenesis. Inclusion of the PDX1 gene in mutation screening for permanent neonatal diabetes is recommended as a genetic diagnosis reveals the mode of inheritance, allows accurate estimation of recurrence risks and confirms the requirement for insulin treatment.
The impact of hypoglycaemia on patients admitted to hospital with medical emergencies
Authors: Tan H. K. , Flanagan D. 
Published: January 2013

AbstractAimsTo quantify the frequency of biochemical hypoglycaemia in acutely unwell patients in the medical assessment unit and relate this to their subsequent outcomes.MethodsA retrospective audit was conducted on all emergency medical patients attending the medical assessment unit between November 2010 and April 2011. Capillary blood glucose measurements were obtained and electronically stored for all patients. Admission details, presence of diabetes, type of diabetes and treatment, length of stay in hospital and death in hospital were obtained from the hospital clinical coding data and electronic discharge summary. The incidence of hypoglycaemia in patients with and without diabetes was quantified. The mean age, length of stay and percentage of death in hospital were compared between groups with and without hypoglycaemia.ResultsOne hundred and thirty‐eight (9.5%) patients with diabetes and 70 (2.7%) patients without diabetes had an episode of hypoglycaemia in the medical assessment unit. Patients with diabetes and hypoglycaemia on admission had a significantly longer length of stay (mean ± sd) (10.3 ± 11.2 vs. 7.3 ± 9.5 days, P = 0.001) and higher rate of hospital mortality (14.5 vs. 5.2%, P < 0.001) compared with those without hypoglycaemia. Patients without diabetes with hypoglycaemia had a longer length of stay (mean ± sd) (9.1 ± 10.5 vs. 6.7 ± 9.9 days, P = 0.05) and a higher rate of hospital mortality (24.3 vs. 5.4%, P < 0.001) compared with those without hypoglycaemia.ConclusionHypoglycaemia is associated with an increased length of stay in hospital and an increased in‐hospital mortality rate. Hypoglycaemia may have contributed to the poorer outcome, but would also appear to be a marker of disease severity in unwell patients, especially patients with sepsis.