bluuebunny/crossref_metadata_2025_split huggingface dataset:
Non‐adherence and measures to improve adherence in the topical treatment of psoriasis
Authors: Zschocke I. , Mrowietz U. , Karakasili E. , Reich K. 
Published: March 2014

AbstractPsoriasis is a chronic, recurrent immune‐mediated skin disease with a 2–3% prevalence in the Western population, which severely affects patients’ quality of life and poses a considerable socioeconomic challenge. The majority of individuals have psoriasis in limited areas and topical products are the mainstay of therapy according to existing guidelines. It is known that medication adherence rates are lower for topical treatment than for systemic treatment. Poor medication adherence is a major multidimensional problem for patients with chronic disorders as it is associated with unfavourable treatment outcomes, increased risk for development of concomitant diseases and inefficient use of health resources. Despite four decades of adherence research and the large number of studies that have identified the importance of medication non‐adherence, there are relatively few studies reporting and designing effective strategies to improve adherence. The aim of this article was to report and describe non‐adherence in the topical treatment of psoriasis, the factors that might contribute to this phenomenon, and which interventions have so far been developed for the management of chronic conditions. This article proposes that given that the barriers to medication adherence are complex and varied, solutions to improve adherence and thus clinical outcomes must be multifaceted and must also provide the possibility to be tailored according to each patient's individual needs. Such an individualized and comprehensive adherence‐enhancing intervention would probably enable the successful long‐term management of this disabling chronic condition.
Impairments of long‐term depression induction and motor coordination precede Aβ accumulation in the cerebellum of APPswe/PS1dE9 double transgenic mice
Authors: Kuwabara Yuki , Ishizeki Masato , Watamura Naoto , Toba Junya , Yoshii Aya , Inoue Takafumi , Ohshima Toshio 
Published: March 2014

AbstractAlzheimer's disease (AD) is a neurodegenerative disorder that represents the most common type of dementia among elderly people. Amyloid beta (Aβ) peptides in extracellular Aβ plaques, produced from the amyloid precursor protein (APP) via sequential processing by β‐ and γ‐secretases, impair hippocampal synaptic plasticity, and cause cognitive dysfunction in AD patients. Here, we report that Aβ peptides also impair another form of synaptic plasticity; cerebellar long‐term depression (LTD). In the cerebellum of commonly used AD mouse model, APPswe/PS1dE9 mice, Aβ plaques were detected from 8 months and profound accumulation of Aβ plaques was observed at 18 months of age. Biochemical analysis revealed relatively high levels of APP protein and Aβ in the cerebellum of APPswe/PS1dE9 mice. At pre‐Aβ accumulation stage, LTD induction, and motor coordination are disturbed. These results indicate that soluble Aβ oligomers disturb LTD induction and cerebellar function in AD mouse model.
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APPswe/PS1d9E mice, a commonly used Alzheimer's mouse model, have Aβ plaques in the cerebellum after 8 months old. We show that soluble Aβ impairs LTD induction in the cerebellar slice. APPswe/PS1d9E mice demonstrate defects of motor coordination and LTD induction in the cerebellum at the pre‐Aβ accumulation period.
Taxonomic Free Sorting: A Successful Method with Older Consumers and a Novel Approach to Preference Mapping
Authors: Withers C. , Methven L. , Qannari E.M. , Allen V.J. , Gosney M.A. , MacFie H.J.H. 
Published: March 2014

AbstractTaxonomic free sorting (TFS) is a fast, reliable and new technique in sensory science. The method extends the typical free sorting task where stimuli are grouped according to similarities, by asking respondents to combine their groups two at a time to produce a hierarchy. Previously, TFS has been used for the visual assessment of packaging whereas this study extends the range of potential uses of the technique to incorporate full sensory analysis by the target consumer, which, when combined with hedonic liking scores, was used to generate a novel preference map. Furthermore, to fully evaluate the efficacy of using the sorting method, the technique was evaluated with a healthy older adult consumer group. Participants sorted eight products into groups and described their reason at each stage as they combined those groups, producing a consumer‐specific vocabulary. This vocabulary was combined with hedonic data from a separate group of older adults, to give the external preference map. Taxonomic sorting is a simple, fast and effective method for use with older adults, and its combination with liking data can yield a preference map constructed entirely from target consumer data.Practical ApplicationsGenerating diagnostic sensory data directly from target consumers is a challenge in sensory science. Taxonomic free sorting (TFS) is a new and efficient sorting technique that aims to determine the sensory characteristics of products that are important to specific consumer cohorts. The hierarchical stages of TFS gives a better indication of the similarities and differences of a sample set and in this study was combined with consumer hedonic data to generate a preference map. In this study the attributes of the products assessed were provided directly by older consumers, without the need for training or prompting. TFS is a quick and effective method to give clear guidance of positive and negative characteristics of products according to the target consumer, as well as involving the specific consumer audience throughout the testing process.
The Effect of Tramadol and Indomethacin Coadministration on Gastric Barrier Function in Dogs
Authors: Hill T.L. , Lascelles B.D.X. , M. Law J. , Blikslager A.T. 
Published: March 2014

BackgroundTramadol is a centrally acting analgesic that is often used in conjunction with nonsteroidal anti‐inflammatory drugs (NSAIDs). The effect of coadministration of tramadol and indomethacin on gastric barrier function in dogs is unknown.Hypothesis/ObjectivesThat coadministration of a nonselective NSAID (indomethacin) and tramadol would decrease recovery of barrier function as compared with acid‐injured, indomethacin‐treated, and tramadol‐treated mucosa.AnimalsGastric mucosa of 10 humanely euthanized shelter dogs.MethodsEx vivo study. Mounted gastric mucosa was treated with indomethacin, tramadol, or both. Gastric barrier function, prostanoid production, and cyclooxygenase expression were quantified.ResultsIndomethacin decreased recovery of transepithelial electrical resistance after injury, although neither tramadol nor the coadministration of the two had an additional effect. Indomethacin inhibited production of gastroprotective prostanoids prostaglandin E2 (acid‐injured PGE2: 509.3 ± 158.3 pg/mL, indomethacin + acid injury PGE2: 182.9 ± 93.8 pg/mL, P < .001) and thromboxane B2 (acid‐injured TXB2: 233.2 ± 90.7 pg/mL, indomethacin + acid injury TXB2: 37.9 ± 16.8 pg/mL, P < .001), whereas tramadol had no significant effect (PGE2 P = .713, TXB2 P = .194). Neither drug had an effect on cyclooxygenase expression (COX‐1 P = .743, COX‐2 P = .705). Acid injury induced moderate to marked epithelial cell sloughing, which was unchanged by drug administration.Conclusions and Clinical ImportanceThere was no apparent interaction of tramadol and a nonselective cyclooxygenase in this ex vivo model. These results suggest that if there is an adverse interaction of the 2 drugs in vivo, it is unlikely to be via prostanoid inhibition.
Pro‐tumorigenic Effects of Transforming Growth Factor Beta 1 in Canine Osteosarcoma
Authors: Portela R.F. , Fadl‐Alla B.A. , Pondenis H.C. , Byrum M.L. , Garrett L.D. , Wycislo K.L. , Borst L.B. , Fan T.M. 
Published: March 2014

BackgroundTransforming growth factor beta 1 (TGFβ1) is a pleiotropic cytokine that contributes to reparative skeletal remodeling by inducing osteoblast proliferation, migration, and angiogenesis. Organic bone matrix is the largest bodily reservoir for latent TGFβ1, and active osteoblasts express cognate receptors for TGFβ1 (TGFβRI and TGFβRII). During malignant osteolysis, TGFβ1 is liberated from eroded bone matrix and promotes local progression of osteotropic solid tumors by its mitogenic and prosurvival activities.HypothesisCanine osteosarcoma (OS) cells will possess TGFβ1 signaling machinery. Blockade of TGFβ1 signaling will attenuate pro‐tumorigenic activities in OS cells. Naturally occurring primary OS samples will express cognate TGFβ1 receptors; and in dogs with OS, focal malignant osteolysis will contribute to circulating TGFβ1 concentrations.AnimalsThirty‐three dogs with appendicular OS.MethodsExpression of TGFβ1 and its cognate receptors, as well as the biologic effects of TGFβ1 blockade, was characterized in OS cells. Ten spontaneous OS samples were characterized for TGFβRI/II expressions by immunohistochemistry. In 33 dogs with OS, plasma TGFβ1 concentrations were quantified and correlated with bone resorption.ResultsCanine OS cells secrete TGFβ1, express cognate receptors, and TGFβ1 signaling blockade decreases proliferation, migration, and vascular endothelial growth factor secretion. Naturally occurring OS samples abundantly and uniformly express TGFβRI/II, and in OS‐bearing dogs, circulating TGFβ1 concentrations correlate with urine N‐telopeptide excretion.Conclusions and Clinical ImportanceCanine OS cells possess TGFβ1 signaling machinery, potentially allowing for the establishment of an autocrine and paracrine pro‐tumorigenic signaling loop. As such, TGFβ1 inhibitors might impede localized OS progression in dogs.
Drivers shaping the diversity and biogeography of total and active bacterial communities in the South China Sea
Authors: Zhang Yao , Zhao Zihao , Dai Minhan , Jiao Nianzhi , Herndl Gerhard J. 
Published: March 2014

AbstractTo test the hypothesis that different drivers shape the diversity and biogeography of the total and active bacterial community, we examined the bacterial community composition along two transects, one from the inner Pearl River estuary to the open waters of the South China Sea (SCS) and the other from the Luzon Strait to the SCS basin, using 454 pyrosequencing of the 16S rRNA and 16S rRNA gene (V1‐3 regions) and thereby characterizing the active and total bacterial community, respectively. The diversity and biogeographic patterns differed substantially between the active and total bacterial communities. Although the composition of both the total and active bacterial community was strongly correlated with environmental factors and weakly correlated with geographic distance, the active bacterial community displayed higher environmental sensitivity than the total community and particularly a greater distance effect largely caused by the active assemblage from deep waters. The 16S rRNA vs. rDNA relationships indicated that the active bacteria were low in relative abundance in the SCS. This might be due to a high competition between active bacterial taxa as indicated by our community network models. Based on these analyses, we speculate that high competition could cause some dispersal limitation of the active bacterial community resulting in a distinct distance‐decay relationship. Altogether, our results indicated that the biogeographic distribution of bacteria in the SCS is the result of both environmental control and distance decay.
A dual role of the transcriptional regulator TstR provides insights into cyanide detoxification in Lactobacillus brevis
Authors: Pagliai Fernando A. , Murdoch Caitlin C. , Brown Sara M. , Gonzalez Claudio F. , Lorca Graciela L. 
Published: March 2014

SummaryIn this study we uncover two genes in Lactobacillus brevis ATCC 367, tstT and tstR, encoding for a rhodanese and a transcriptional regulator involved in cyanide detoxification. TstT (LVIS_0852) belongs to a new class of thiosulphate:cyanide sulphurtransferases. We found that TstR (LVIS_0853) modulates both the expression and the activity of the downstream‐encoded tstT. The TstR binding site was identified at −1 to +33, from tstR transcriptional start site. EMSA revealed that sulphite, a product of the reaction catalysed by TstT, improved the interaction between TstR:PtstR, while Fe(III) disrupted this interaction. Site‐directed mutagenesis in TstR identified M64 as a key residue in sulphite recognition, while residues H136‐H139‐C167‐M171 formed a pocket for ferric iron co‐ordination. In addition to its role as a transcriptional repressor, TstR is also involved in regulating the thiosulphate:cyanide sulphurtransferase activity of TstT. A threefold increase in TstT activity was observed in the presence of TstR, which was enhanced by the addition of Fe(III). Overexpression of the tstRT operon was found to increase the cyanide tolerance of L. brevis and Escherichia coli. The protein–protein interaction between TstR and TstT described herein represents a novel mechanism for regulation of enzymatic activity by a transcriptional regulator.
Salicylic acid prevents Trichoderma harzianum from entering the vascular system of roots
Authors: Alonso‐Ramírez Ana , Poveda Jorge , Martín Ignacio , Hermosa Rosa , Monte Enrique , Nicolás Carlos 
Published: March 2014

SummaryTrichoderma is a soil‐borne fungal genus that includes species with a significant impact on agriculture and industrial processes. Some Trichoderma strains exert beneficial effects in plants through root colonization, although little is known about how this interaction takes place. To better understand this process, the root colonization of wild‐type Arabidopsis and the salicylic acid (SA)‐impaired mutant sid2 by a green fluorescent protein (GFP)‐marked Trichoderma harzianum strain was followed under confocal microscopy. Trichoderma harzianum GFP22 was able to penetrate the vascular tissue of the sid2 mutant because of the absence of callose deposition in the cell wall of root cells. In addition, a higher colonization of sid2 roots by GFP22 compared with that in Arabidopsis wild‐type roots was detected by real‐time polymerase chain reaction. These results, together with differences in the expression levels of plant defence genes in the roots of both interactions, support a key role for SA in Trichoderma early root colonization stages. We observed that, without the support of SA, plants were unable to prevent the arrival of the fungus in the vascular system and its spread into aerial parts, leading to later collapse.
Craniosynostosis surgery in an infant with a complex cyanotic cardiac defect
Authors: Bergmans Bas , Kammeraad Janneke A.E. , van Adrichem Leon N.A. , Staals Lonneke M. 
Published: March 2014

SummaryWe report on a case where craniosynostosis surgery for a left‐sided coronal synostosis was performed successfully on an 11‐month old infant with a hypoplastic left ventricle with a dysplastic mitral valve, double outlet right ventricle, transposition of the great arteries, atrial septal defect, multiple ventricular septal defects, and surgically applied pulmonary banding. Craniosynostosis surgery is considered high‐risk surgery, because of possible sudden and extensive blood loss, and is usually performed in cardiopulmonary healthy children. Children with congenital heart disease undergoing noncardiac surgery have an increased risk of perioperative morbidity and cardiac arrest. Patients with hypoplastic left heart syndrome are a high‐risk population when undergoing noncardiac surgery, in all stages of palliation. This infant would be undergoing a partial cavo‐pulmonary connection (PCPC) within a few months. With a PCPC, drainage of cranial vessels is dependent on passive flow via the superior caval vein directly into the pulmonary artery. Consequently, this could lead to an increased blood loss during craniosynostosis surgery. Therefore, it was decided to perform the craniosynostosis surgery first, before establishing a PCPC. When a child with CHD presents for high‐risk noncardiac surgery, future cardiac procedures and physiology also have to be taken into account. A multidisciplinary approach, involving pediatric cardiologists and pediatric anesthesiologists, is essential in making this decision.
Accounting for the Harm of Death
Authors: Purves Duncan 
Published: March 2014

AbstractI defend a theory of the way in which death is a harm to the person who dies that (i) fits into a larger, unified account of harm (so that death is not a special kind of harm but is harmful in the same way that any harmful event is harmful); and (ii) includes an account of the time of death's harmfulness, one that avoids the implications that death is a timeless harm and that people have levels of welfare at times at which they do not exist.
On the Mechanism Determining the Th1/Th2 Phenotype of an Immune Response, and its Pertinence to Strategies for the Prevention, and Treatment, of Certain Infectious Diseases
Authors: Bretscher P. A. 
Published: March 2014

AbstractIt is well recognized that the physiological/pathological consequences of an immune response, against a foreign or a self‐antigen, are often critically dependent on the class of immunity generated. Here we focus on how antigen interacts with the cells of the immune system to determine whether antigen predominantly generates Th1 or Th2 cells. We refer to this mechanism as the ‘decision criterion’ controlling the Th1/Th2 phenotype of the immune response. A plausible decision criterion should account for the variables of immunization known to affect the Th1/Th2 phenotype of the ensuing immune response. Documented variables include the nature of the antigen, in terms of its degree of foreignness, the dose of antigen and the time after immunization at which the Th1/Th2 phenotype of the immune response is assessed. These are quantitative variables made at the level of the system. In addition, the route of immunization is also critical. I describe a quantitative hypothesis as to the nature of the decision criterion, referred to as the Threshold Hypothesis. This hypothesis accounts for the quantitative variables of immunization known to affect the Th1/Th2 phenotype of the immune response generated. I suggest and illustrate how this is not true of competing, contemporary hypotheses. I outline studies testing predictions of the hypothesis and illustrate its potential utility in designing strategies to prevent or treat medical situations where a predominant Th1 response is required to contain an infection, such as those caused by HIV‐1 and by Mycobacterium tuberculosis, or to contain cancers.
IFNγ and Perforin Cooperate to Control Infection and Prevent Fatal Pathology During Persistent Gammaherpesvirus Infection in Mice
Authors: Bartholdy C. , Høgh‐Petersen M. , Storm P. , Holst P. J. , Ørskov C. , Christensen J. P. , Thomsen A. R. 
Published: March 2014

AbstractInfection with murine gammaherpesvirus 68 has become an accepted model for studying the virus/host interactions with regard to gammaherpesvirus infections. Previous studies using gene‐deficient mice have revealed that neither IFNγ nor perforin is essential in controlling the outcome of infection or the virus load during chronic infection in C57BL/6 mice. However, pronounced multiorgan fibrosis and splenic atrophy are observed in mice lacking IFNγ or the IFNγ receptor. To study the interplay between perforin and IFNγ in controlling the virus‐induced pathology and the viral load during chronic gammaherpesvirus infection, we infected IFNγ/perforin double‐deficient C57BL/6 mice and followed the course of infection. While absence of perforin prevented the splenic atrophy in IFNγ‐deficient mice, fibrosis did not disappear. Moreover, double‐deficient mice developed extreme splenomegaly, were unable to control the viral load and displayed chronic immune activation. Thus, IFNγ and perforin act in concert to minimize pathology and control the viral load in mice chronically infected with MHV68. Furthermore, while certain aspect of the virus‐induced pathology in IFNγ‐deficient mice may be alleviated in double‐deficient mice, other aspects are exaggerated, and the normal architecture of the spleen is completely destroyed. We believe that these findings add to the understanding of the virus/host interaction during chronic gammaherpes virus infection.
Interferon Lambda‐2 Levels in Sputum of Patients with Pulmonary Mycobacterium tuberculosis Infection
Authors: Travar M. , Vucic M. , Petkovic M. 
Published: March 2014

AbstractIn humans, there are three members of type III interferon family, designated as IFN‐λ1 (IL‐29), IFN‐λ2 (IL‐28A) and IFN‐λ3 (IL‐28B). Bacterial infections, including Mycobacterium tuberculosis infection, trigger the expression of interferon I and II genes, but little is known about their effect on IFN‐λ genes. It has been found that M. tuberculosis infection in A549 lung epithelial cells stimulate upregulation of IFN‐λ2 genes in vitro. The aim of this study was to determine the IFN‐λ2 levels in sputum of patients with active pulmonary tuberculosis comparing with levels in healthy persons sputum and sputum of persons with latent tuberculosis. IFN‐λ2 level in the samples was quantified with sandwich enzyme‐linked immunoassay kit for quantization of human IFN‐λ2 (IL‐28A). The IFN‐λ2 level in sputum of patients with pulmonary tuberculosis was significantly higher comparing with IFN‐λ2 levels in healthy group (P = 0.001) and latent tuberculosis group (P = 0.005). Logistic regression analysis has shown that IFN‐λ2 level in sputum is related to culture result (OR = 4.14; 95% CI = 1.28–17.5; P = 0.019). There was the correlation between Bartlett score and IFN‐λ2 levels in group with pulmonary tuberculosis (r = 0.641; P < 0.01). In conclusion, we have found that the inflammatory cells in sputum can be source of IFN‐λ after receptor stimulation by M. tuberculosis components.
Suppressed Expression of Homotypic Multinucleation, Extracellular Domains of CD172α (SIRP‐α) and CD47 (IAP) Receptors in TAMs UpRegulated by Hsp70–Peptide Complex in Dalton's Lymphoma
Authors: Gautam P. K. , Acharya A. 
Published: March 2014

AbstractCD172α and CD47 are members of glycoprotein expressed on macrophages and various immune cells, promote immune recognition and T cell stimulation that priming phagocytosis of pathogens and apoptotic bodies and malignant cell. Tumour‐releasing immunosuppressive factor promotes tumour growth and transforms the tumour resident M1 phenotype of macrophage to M2 phenotype (TAMs) that promotes tumour progression by downregulating the expression of different surface receptor including CD172α and CD47. Recent studies have reported that CD172α and CD47 are involved in the pathogenesis and promote malignancies such as lymphoma, leukaemia, melanoma, lung cancer and multiple myeloma, and their expression varies during infection and malignancies. Autologous Hsp70 is well recognized for its role in activating macrophages leading to enhance production of inflammatory cytokines. It has been observed that Hsp70 derived from normal tissues do not elicit tumour immunity, while Hsp70 preparation from tumour cell was able to elicit tumour immunity. However, the role of exogenous autologous hsp70 on the formation of giant cells is completely unknown. Therefore, in the present study, we sought to investigate the effect of Hsp70–peptide complex on the expression of CD172α and CD47 receptors in normal peritoneal macrophages (NMO) and TAMs. Finding shows that the expression of CD172α and CD47 enhances in TAMs and it reverts back the suppressed function of TAMs into M1 state of immunoregulatory phenotype that promotes tumour regression by enhanced multinucleation and phagocytosis of malignant cells and significantly enhances the homotypic fusion of macrophages and polykaryon formation in vitro by enhancing the expression of SIRPα and IAP.