bluuebunny/crossref_metadata_2025_split huggingface dataset:
Why chronically ill children face challenges in regular classrooms: perspectives from nursing teachers in Japan
Authors: Seki Y. , Kakinuma A. , Kuchii T. , Ohira K. 
Published: October 2016

AbstractBackgroundChronically ill children are increasingly expected to join their peers in regular classrooms. However, sometimes schools do not provide adequate assistance. This study explores nursing teachers' thoughts and experiences on integrating such students into regular classrooms in Japan.MethodsWe analysed 79 essays written by nursing teachers collectively titled ‘The challenges of having chronically ill children in regular classrooms’. We conducted a qualitative study using Kinoshita's Modified Grounded Theory Approach.ResultsNursing teachers identified three main obstacles: insufficient resources to support chronically ill students, parents not playing a supporting role in aiding them at school and a regular classroom not being suitable for them. However, collaborating with the children's medical staff proved successful at integrating them into regular classrooms.ConclusionsGiven these obstacles, it seems very difficult for nursing teachers to lead the way toward establishing cooperative support systems for the children. Instructions from medical staff could empower teachers to set up such systems.
Characterization of resident lymphocytes in human pancreatic islets
Authors: Radenkovic M , Uvebrant K , Skog O , Sarmiento L , Avartsson J , Storm P , Vickman P , Bertilsson P-A , Fex M , Korgsgren O , Cilio C M 
Published: October 2016

Summary
The current view of type 1 diabetes (T1D) is that it is an immune-mediated disease where lymphocytes infiltrate the pancreatic islets, promote killing of beta cells and cause overt diabetes. Although tissue resident immune cells have been demonstrated in several organs, the composition of lymphocytes in human healthy pancreatic islets have been scarcely studied. Here we aimed to investigate the phenotype of immune cells associated with human islets of non-diabetic organ donors. A flow cytometry analysis of isolated islets from perfused pancreases (n = 38) was employed to identify alpha, beta, T, natural killer (NK) and B cells. Moreover, the expression of insulin and glucagon transcripts was evaluated by RNA sequencing. Up to 80% of the lymphocytes were CD3+ T cells with a remarkable bias towards CD8+ cells. Central memory and effector memory phenotypes dominated within the CD8+ and CD4+ T cells and most CD8+ T cells were positive for CD69 and up to 50–70% for CD103, both markers of resident memory cells. The frequency of B and NK cells was low in most islet preparations (12 and 3% of CD45+ cells, respectively), and the frequency of alpha and beta cells varied between donors and correlated clearly with insulin and glucagon mRNA expression. In conclusion, we demonstrated the predominance of canonical tissue resident memory CD8+ T cells associated with human islets. We believe that these results are important to understand more clearly the immunobiology of human islets and the disease-related phenotypes observed in diabetes.
Three immune‐mediated disease models induced by Theiler's virus: Multiple sclerosis, seizures and myocarditis
Authors: Tsunoda Ikuo , Sato Fumitaka , Omura Seiichi , Fujita Mitsugu , Sakiyama Namie , Park Ah‐Mee 
Published: October 2016

AbstractTheiler's murine encephalomyelitis virus (TMEV) infection has been used as a viral model for multiple sclerosis (MS), as TMEV can induce chronic inflammatory demyelinating lesions with viral persistence in the spinal cord of SJL/J mice. In contrast, when C57BL/6 mice are infected with TMEV, the mice can clear the virus from the central nervous system (CNS), without viral persistence or demyelination, but develop seizures and hippocampal sclerosis, which has been used as a viral model for seizures/epilepsy. In the two TMEV‐induced CNS disease models, not only viral infection, but also immune responses contribute to the pathogenesis. Interestingly, acquired immunity plays an effector role in the MS model, whereas innate immunity appears to contribute to the development of seizures. Recently, we have established the third TMEV‐induced disease model, a mouse model for viral myocarditis, using C3H mice. TMEV‐induced myocarditis is a triphasic disease, which mimics human myocarditis; phase I, mediated by viral replication in the heart and innate immunity; phase II, mediated by acquired immunity; and phase III, resulted from cardiac fibrosis. The genetic susceptibility to the aforementioned three models (MS, seizures and myocarditis) differs among mouse strains. We have compared and contrasted the three models induced by one single pathogen, TMEV, particularly in regard to the roles of T helper cells and natural killer T cells, which will give an insight into how interactions between the immune system and the host's genetic background determine the tissue tropism of virus and the development of virus‐induced organ‐specific immunopathology.
Left atrial changes in early stages of heart failure with preserved ejection fraction
Authors: Bytyçi Ibadete , Bajraktari Gani 
Published: October 2016

Background and AimIncreased left atrial (LA) mass was introduced as a compensatory mechanism in heart failure (HF) patients. Furthermore, atrial conduction time and LA emptying fraction is are deteriorated in HF with preserved ejection fraction (HFpEF). The aim of this study was to assess the early LA changes in HFpEF patients.MethodsIn 79 consecutive patients with HFpEF (age 61±8 years, NYHA class I–III, LV EF ≥45%), a complete 2‐dimensional, M‐mode, and Doppler echocardiographic study was performed. According to the diastolic dysfunction (DD), patients were divided into three groups: Group I—29 healthy subjects (control group); Group II—HFpEF patients with mild DD; and Group III—HFpEF patients with moderate DD.ResultsThe LV mass was increased (P<.05), septal s′, lateral s′, septal and lateral MAPSE were decreased (P<.05, for all), E/e′ ratio was increased (P<.001), LA mass and minimal volume were increased (P<.001, P<.05), LA emptying fraction was decreased (P<.05), and LA dyssynchrony was deteriorated (P<.05) in patients with mild DD compared to controls. These changes were of the same nature in patients with moderate LV DD.ConclusionsIn early stage of DD, in patients with HFpEF, in addition to LV hypertrophy and compromised LV longitudinal systolic function, the LA emptying fraction is reduced, LA mass and LAV min are increased and LA dyssynchrony is significant, despite normal LA dimensions. These findings suggest early LA function deterioration irrespective of normal cavity measurements, hence a need for optimum therapy.
Global meta‐analysis of native and nonindigenous trophic traits in aquatic ecosystems
Authors: McKnight Ella , García‐Berthou Emili , Srean Pao , Rius Marc 
Published: October 2016

AbstractEcologists have recently devoted their attention to the study of species traits and their role in the establishment and spread of nonindigenous species (NIS). However, research efforts have mostly focused on studies of terrestrial taxa, with lesser attention being dedicated to aquatic species. Aquatic habitats comprise of interconnected waterways, as well as exclusive introduction vectors that allow unparalleled artificial transport of species and their propagules. Consequently, species traits that commonly facilitate biological invasions in terrestrial systems may not be as represented in aquatic environments. We provide a global meta‐analysis of studies conducted in both marine and freshwater habitats. We selected studies that conducted experiments with native andNISunder common environmental conditions to allow detailed comparisons among species traits. In addition, we explored whether different factors such as species relatedness, functional feeding groups, latitude, climate, and experimental conditions could be linked to predictive traits. Our results show that species with traits that enhance consumption and growth have a substantially increased probability of establishing and spreading when entering novel ecosystems. Moreover, traits associated with predatory avoidance were more prevalent inNISand therefore favour invasive species in aquatic habitats. When we analysedNISinteracting with taxonomically distinctive native taxa, we found that consumption and growth were particularly important traits. This suggests that particular attention should be paid to newly introduced species for which there are no close relatives in the local biota. Finally, we found a bias towards studies conducted in temperate regions, and thus, more studies in other climatic regions are needed. We conclude that studies aiming at predicting future range shifts should consider trophic traits of aquaticNISas these traits are indicative of multiple interacting mechanisms involved in promoting species invasions.
Green method for determination of phenolic compounds in mung bean (Vigna radiata L.) based on near‐infrared spectroscopy and chemometrics
Authors: Meenu Maninder , Kamboj Uma , Sharma Anupma , Guha Paramita , Mishra Sunita 
Published: October 2016

SummaryMung bean grains exhibit high level of antioxidant activity due the presence of phenolic compounds. Near‐infrared spectroscopy (NIRS), in conjunction with chemometrics, was used to develop a rapid, nondestructive, chemical free and easy‐to‐use method to determine these compounds in sixty genotypes of mung bean. NIRS calibration curve with high‐performance liquid chromatography (HPLC) as reference method was used to determine phenolic compounds (catechin, chlorogenic acid, caffeic acid, p‐coumaric acid, t‐ferulic acid, vitexin, isovitexin, myricetin, quercetin and kaempferol). It was observed that partial least square regression (PLSR) model in the wavelength range of 1600–2500 nm with standard normal variate (SNV) and linear baseline correction (LBC) as preprocessing techniques can measure phenolic compound accurately (R2 > 0.987) with root‐mean‐square error less than 1.82%. This study shows that NIRS along with chemometrics is an accurate method to estimate the phenolic compounds rapidly and nondestructively.
The emerging roles of mannose‐binding lectin‐associated serine proteases (MASPs) in the lectin pathway of complement and beyond
Authors: Dobó József , Pál Gábor , Cervenak László , Gál Péter 
Published: October 2016

SummaryMannose‐binding lectin (MBL)‐associated serine proteases (MASPs) are the enzymatic constituents of the lectin pathway of the complement system. They are complexed with large pattern recognition molecules (PRMs) such as MBL, other collectins, and ficolins. The main function of two of the three MASPs has crystallized lately: MASP‐1 autoactivates first, then it activates MASP‐2, and finally both participate in the formation of the C4b2a convertase. In addition to this, both enzymes are involved in several other processes which are subject to intense research nowadays. Notably, MASP‐1, as a promiscuous enzyme, has been implicated in the coagulation cascade, in the kinin generating contact system, and in cellular activation through protease‐activated receptor (PAR) cleavage on endothelial cells. The third protease MASP‐3 has emerged recently as the protease responsible for pro‐factor D activation in resting blood, providing a fundamental link between two complement pathways. At present all three MASPs have at least one well‐defined role and several other possible functions were implicated. Defect or more likely over‐activation of MASPs may culminate into diseases such as ischemia–reperfusion injury (IRI); hence, MASPs are all potential targets of drug development.
Complement in removal of the dead – balancing inflammation
Authors: Martin Myriam , Blom Anna M. 
Published: October 2016

SummaryRecognition and removal of apoptotic and necrotic cells must be efficient and highly controlled to avoid excessive inflammation and autoimmune responses to self. The complement system, a crucial part of innate immunity, plays an important role in this process. Thus, apoptotic and necrotic cells are recognized by complement initiators such as C1q, mannose binding lectin, ficolins, and properdin. This triggers complement activation and opsonization of cells with fragments of C3b, which enhances phagocytosis and thus ensures silent removal. Importantly, the process is tightly controlled by the binding of complement inhibitors C4b‐binding protein and factor H, which attenuates late steps of complement activation and inflammation. Furthermore, factor H becomes actively internalized by apoptotic cells, where it catalyzes the cleavage of intracellular C3 to C3b. The intracellularly derived C3b additionally opsonizes the cell surface further supporting safe and fast clearance and thereby aids to prevent autoimmunity. Internalized factor H also binds nucleosomes and directs monocytes into production of anti‐inflammatory cytokines upon phagocytosis of such complexes. Disturbances in the complement‐mediated clearance of dying cells result in persistence of autoantigens and development of autoimmune diseases like systemic lupus erythematosus, and may also be involved in development of age‐related macula degeneration.
Old dogs—new tricks: immunoregulatory properties of C3 and C5 cleavage fragments
Authors: Verschoor Admar , Karsten Christian M. , Broadley Steven P. , Laumonnier Yves , Köhl Jörg 
Published: October 2016

SummaryThe activation of the complement system by canonical and non‐canonical mechanisms results in the generation of multiple C3 and C5 cleavage fragments including anaphylatoxins C3a and C5a as well as opsonizing C3b/iC3b. It is now well appreciated that anaphylatoxins not only act as pro‐inflammatory mediators but as immunoregulatory molecules that control the activation status of cells and tissue at several levels. Likewise, C3b/iC3b is more than the opsonizing fragment that facilitates engulfment and destruction of targets by phagocytes. In the circulation, it also facilitates the transport and delivery of bacteria and immune complexes to phagocytes, through a process known as immune adherence, with consequences for adaptive immunity. Here, we will discuss non‐classical immunoregulatory properties of C3 and C5 cleavage fragments. We highlight the influence of anaphylatoxins on Th2 and Th17 cell development during allergic asthma with a particular emphasis on their role in the modulation of CD11b+ conventional dendritic cells and monocyte‐derived dendritic cells. Furthermore, we discuss the control of anaphylatoxin‐mediated activation of dendritic cells and allergic effector cells by adaptive immune mechanisms that involve allergen‐specific IgG1 antibodies and plasma or regulatory T cell‐derived IL‐10 production. Finally, we take a fresh look at immune adherence with a particular focus on the development of antibacterial cytotoxic T‐cell responses.
Protection of host cells by complement regulators
Authors: Schmidt Christoph Q. , Lambris John D. , Ricklin Daniel 
Published: October 2016

SummaryThe complement cascade is an ancient immune‐surveillance system that not only provides protection from pathogen invasion but has also evolved to participate in physiological processes to maintain tissue homeostasis. The alternative pathway (AP) of complement activation is the evolutionarily oldest part of this innate immune cascade. It is unique in that it is continuously activated at a low level and arbitrarily probes foreign, modified‐self, and also unaltered self‐structures. This indiscriminate activation necessitates the presence of preformed regulators on autologous surfaces to spare self‐cells from the undirected nature of AP activation. Although the other two canonical complement activation routes, the classical and lectin pathways, initiate the cascade more specifically through pattern recognition, their activity still needs to be tightly controlled to avoid excessive reactivity. It is the perpetual duty of complement regulators to protect the self from damage inflicted by inadequate complement activation. Here, we review the role of complement regulators as preformed mediators of defense, explain their common and specialized functions, and discuss selected cases in which alterations in complement regulators lead to disease. Finally, rational engineering approaches using natural complement inhibitors as potential therapeutics are highlighted.
Pentraxins in the activation and regulation of innate immunity
Authors: Daigo Kenji , Inforzato Antonio , Barajon Isabella , Garlanda Cecilia , Bottazzi Barbara , Meri Seppo , Mantovani Alberto 
Published: October 2016

SummaryHumoral fluid phase pattern recognition molecules (PRMs) are a key component of the activation and regulation of innate immunity. Humoral PRMs are diverse. We focused on the long pentraxin PTX3 as a paradigmatic example of fluid phase PRMs. PTX3 acts as a functional ancestor of antibodies and plays a non‐redundant role in resistance against selected microbes in mouse and man and in the regulation of inflammation. This molecule interacts with complement components, thus modulating complement activation. In particular, PTX3 regulates complement‐driven macrophage‐mediated tumor progression, acting as an extrinsic oncosuppressor in preclinical models and selected human tumors. Evidence collected over the years suggests that PTX3 is a biomarker and potential therapeutic agent in humans, and pave the way to translation of this molecule into the clinic.
The versatile functions of complement C3‐derived ligands
Authors: Erdei Anna , Sándor Noémi , Mácsik‐Valent Bernadett , Lukácsi Szilvia , Kremlitzka Mariann , Bajtay Zsuzsa 
Published: October 2016

SummaryThe complement system is a major component of immune defense. Activation of the complement cascade by foreign substances and altered self‐structures may lead to the elimination of the activating agent, and during the enzymatic cascade, several biologically active fragments are generated. Most immune regulatory effects of complement are mediated by the activation products of C3, the central component. The indispensable role of C3 in opsonic phagocytosis as well as in the regulation of humoral immune response is known for long, while the involvement of complement in T‐cell biology have been revealed in the past few years. In this review, we discuss the immune modulatory functions of C3‐derived fragments focusing on their role in processes which have not been summarized so far. The importance of locally synthesized complement will receive special emphasis, as several immunological processes take place in tissues, where hepatocyte‐derived complement components might not be available at high concentrations. We also aim to call the attention to important differences between human and mouse systems regarding C3‐mediated processes.
RETRACTED: MicroRNA‐379 suppresses osteosarcoma progression by targeting PDK1
Authors: Li Zheng , Shen Jianxiong , Chan Matthew T. V. , Wu William Ka Kei 
Published: October 2016

AbstractOsteosarcoma is the most common primary bone tumour. Increasing evidence has demonstrated the pathogenic role of microRNA (miRNAs) dysregulation in tumour development. miR‐379 was previously reported to function as an oncogenic or tumour‐suppressing miRNA in a tissue‐dependent manner. However, its function in osteosarcoma remains unknown. In this study, we found that the expression of miR‐379 was downregulated in osteosarcoma tissues and cell lines. Further functional characterization revealed that miR‐379 suppressed osteosarcoma cell proliferation and invasion in vitro and retarded the growth of osteosarcoma xenografts in vivo. Mechanistically, PDK1 was identified as the direct target of miR‐379 in osteosarcoma, in which PDK1 expression was up‐regulated and showed inverse correlation with miR‐379. Enforced expression of PDK1 promoted osteosarcoma cell proliferation and rescued the anti‐proliferative effect of miR‐379. These data suggest that miR‐379 could function as a tumour‐suppressing miRNA via targeting PDK1 in osteosarcoma.
Association between irritability and bias in attention orienting to threat in children and adolescents
Authors: Salum Giovanni A. , Mogg Karin , Bradley Brendan P. , Stringaris Argyris , Gadelha Ary , Pan Pedro M. , Rohde Luis A. , Polanczyk Guilherme V. , Manfro Gisele G. , Pine Daniel S. , Leibenluft Ellen 
Published: October 2016

BackgroundIrritability, a frequent complaint in children with psychiatric disorders, reflects increased predisposition to anger. Preliminary work in pediatric clinical samples links irritability to attention bias to threat, and the current study examines this association in a large population‐based sample.MethodsWe studied 1,872 children (ages 6–14) using the Development and Well‐Being Assessment (DAWBA), Childhood Behavior Checklist (CBCL), and dot‐probe tasks. Irritability was defined using CBCL items that assessed temper tantrums and hot temper. The dot‐probe task assessed attention biases for threat‐related (angry face) stimuli. Multiple regression analysis was used to assess specificity of associations to irritability when adjusting for demographic variables and co‐occurring psychiatric traits. Propensity score matching analysis was used to increase causal inference when matching for demographic variables and co‐occurring psychiatric traits.ResultsIrritability was associated with increased attention bias toward threat‐related cues. Multiple regression analysis suggests associations between irritability and threat bias are independent from demographic variables, anxiety, and externalizing traits (attention‐deficit/hyperactivity, conduct, and headstrong/hurtful), but not from broad internalizing symptoms. Propensity score matching analysis indicated that this association was found for irritable versus nonirritable groups matched on demographic and co‐occurring traits including internalizing symptoms.ConclusionsIrritability in children is associated with biased attention toward threatening information. This finding, if replicated, warrants further investigation to examine the extent to which it contributes to chronic irritability and to explore possible treatment implications.
Precise Placement of Single‐Retainer Resin‐Bonded Fixed Dental Prostheses with an Innovative Splint Design
Authors: Stimmelmayr Michael , Stangl Martin , Kremzow‐Stangl Judith , Krennmair Gerald , Beuer Florian , Edelhoff Daniel , Güth Jan‐Frederik 
Published: October 2016

AbstractSingle‐retainer resin‐bonded fixed dental prostheses (RBFDPs) are difficult to position due to the pressure of soft tissue at the pontic area and the single‐retainer design. This clinical report describes an innovative technique for the insertion of single‐retainer RBFDPs. An incisal inserting splint is used to position the RBFDPs reliably. With the help of grooves in the buccal and incisal area of the splint, the precise positioning of the splint on the adjacent teeth and the RBFDP can be controlled. Also, a hole in the retainer wing region of the splint gives access for pressure application on the wing during the bonding process. With the aid of this method, 25 single‐retainer FBFDPs were inserted in the correct position in a case series. The splint described here allows the precise insertion of single‐retainer RBFDPs and simplifies delivery.