bluuebunny/crossref_metadata_2025_split huggingface dataset:
Are questionnaires reliable in diagnosing sleep-disordered breathing in university students?
Authors: Migacz E , Wichniak A , Kukwa W 
Published: September 2017

AbstractObjective:This study aimed to screen young adults for sleep-disordered breathing, and compare those with high and low risk for sleep-disordered breathing.Methods:A survey based on the Berlin questionnaire was completed by 330 university students, and the results were used to divide them into sleep-disordered breathing positive and sleep-disordered breathing negative groups. A representative group was selected from each cohort (positive group,n= 16; negative group,n= 21), and assessed with sleep study, ENT examination, the Nose Obstruction Symptom Evaluation scale, and the Epworth Sleepiness Scale.Results:Sleep-disordered breathing prevalence was 11.2 per cent in the questionnaire and 24 per cent according to the sleep study. The sleep-disordered breathing positive and negative groups significantly differed in terms of coexisting sleep-disordered breathing symptoms. There were no significant differences between the positive and negative groups with regard to sleep study parameters (apnoea/hypopnoea index, respiratory disturbance index, oxygen desaturation index, snoring intensity) and the Epworth Sleepiness Scale.Conclusion:Subjective and objective diagnostic tools revealed that sleep-disordered breathing is a common problem among young adults.
A (tidal-marine) boulder pavement in the late Cenozoic of Seymour Island, West Antarctica: contribution to the palaeogeographical and palaeoclimatic evolution of West Antarctica
Authors: Rocha-Campos Antonio C. , Kuchenbecker Matheus , Duleba Wania , Dos Santos Paulo Roberto , Canile Fernanda M. 
Published: September 2017

AbstractWe report here the discovery of a boulder pavement cropping out at the base of the Hobbs Glacier Formation (Miocene), on the northern sector of Seymour Island (Isla Marambio), West Antarctica, along the contact with the underlying La Meseta Formation (Eocene). The feature described has many points in common with boulder pavements developed in tidal-marine environments. The clasts of the pavement are mostly boulders and bear up to three sets of glacial striae on their bevelled truncated surfaces, but are not elongate parallel to them or bullet shaped. No diamictite body was identified associated with the boulder pavement. These features differ from those of boulder pavements described from terrestrially glaciated Cenozoic deposits and may indicate a shallow glaciomarine environment for the late Cenozoic of Seymour Island.
Avian pox in seabirds on Marion Island, southern Indian Ocean
Authors: Schoombie S. , Schoombie J. , Oosthuizen A. , Suleman E. , Jones M.G.W. , Pretorius L. , Dilley B.J. , Ryan P.G. 
Published: September 2017

AbstractAlbatrosses are among the most threatened groups of seabirds with the main land-based threats being alien invasive species, human disturbance and habitat degradation. Disease outbreaks in Antarctic and sub-Antarctic seabird populations are uncommon, but in the past few decades there has been an increase in reported cases. The sub-Antarctic Prince Edward Islands (46°S, 37°E) in the south-western Indian Ocean provide breeding grounds for many seabird species, including 44% of all wandering albatrosses (Diomedea exulans L.). In 2015, five wandering albatrosses and two penguins (Eudyptes chrysocome Forster and Aptenodytes patagonicus Miller) with pox-like lesions were observed on Marion Island, the larger of the two Prince Edward Islands. Despite intensive study of the wandering albatross population since the 1980s, the only previous records of such lesions are one case in 2006 and another in 2009 in white-chinned petrels (Procellaria aequinoctialis L.). Molecular and phylogenetic analysis of tissue samples from two albatross chicks confirmed the presence of avian pox virus (Avipoxvirus). This highlights the need for research into the diseases present on sub-Antarctic islands, for strict controls to limit the risk of accidental introduction of diseases through human activities and the need for effective conservation measures in the event of an outbreak.
The prevalence and factors associated with stunting among infants aged 6 months in a peri-urban South African community
Authors: Matsungo Tonderayi M , Kruger Herculina S , Faber Mieke , Rothman Marinel , Smuts Cornelius M 
Published: September 2017

AbstractObjectiveTo determine the prevalence and factors associated with stunting in 6-month-old South African infants.DesignThis cross-sectional study was part of the baseline of a randomized controlled trial. Weight-for-length, length-for-age and weight-for-ageZ-scores were based on the WHO classification. Blood samples were analysed for Hb, plasma ferritin and soluble transferrin receptor (sTfR). Socio-economic, breast-feeding and complementary feeding practices were assessed by questionnaire.Setting/SubjectsInfants aged 6 months (n750) from a peri-urban area of Matlosana Municipality, North West Province of South Africa.ResultsStunting, underweight, wasting and overweight affected 28·5, 11·1, 1·7 and 10·1 % of infants, respectively. Exclusive breast-feeding to 6 months of age was reported in 5·9 % of the infants. Multivariable binary logistic regression showed that birth weight (OR=0·12; 95 % CI 0·07, 0·21,P<0·001) and maternal height (OR=0·94; 95 % CI 0·91, 0·98,P=0·001) were inversely associated with stunting; while male sex (OR=1·73; 95 % CI 1·10, 2·70,P=0·014) was associated with higher odds for stunting. Stunting was also associated with higher plasma sTfR (>8·3 mg/l) concentrations.ConclusionsThe association between stunting and lower birth weight, shorter maternal height and male sex reflects possibly the intergenerational origins of stunting. Therefore, interventions that focus on improving preconceptual and maternal nutritional status, combined with strategies to promote appropriate infant feeding practices, may be an important strategy to prevent stunting in vulnerable settings.
Prospective associations between dietary patterns and body composition changes in European children: the IDEFICS study
Authors: Fernández-Alvira Juan Miguel , Bammann Karin , Eiben Gabriele , Hebestreit Antje , Kourides Yannis A , Kovacs Eva , Michels Nathalie , Pala Valeria , Reisch Lucia , Russo Paola , Veidebaum Tomas , Moreno Luis A , Börnhorst Claudia 
Published: September 2017

AbstractObjectiveTo describe dietary patterns by applying cluster analysis and to describe the cluster memberships of European children over time and their association with body composition changes.DesignThe analyses included k-means clustering based on the similarities between the relative frequencies of consumption of forty-three food items and regression models were fitted to assess the association between dietary patterns and body composition changes.SettingPrimary schools and pre-schools of selected regions in Italy, Estonia, Cyprus, Belgium, Sweden, Hungary, Germany and Spain.SubjectsParticipants (n 8341) in the baseline (2–9 years old) and follow-up (4–11 years old) surveys of the IDEFICS (Identification and prevention of Dietary- and lifestyle-induced health EFfects In Children and infantS) study.ResultsThree persistent clusters were obtained at baseline and follow-up. Children consistently allocated to the ‘processed’ cluster presented increased BMI (β=0·050; 95 % CI 0·006, 0·093), increased waist circumference (β=0·071; 95 % CI 0·001, 0·141) and increased fat mass gain (β=0·052; 95 % CI 0·014, 0·090) over time v. children allocated to the ‘healthy’ cluster. Being in the ‘processed’–‘sweet’ cluster combination was also linked to increased BMI (β=0·079; 95 % CI 0·015, 0·143), increased waist circumference (β=0·172; 95 % CI 0·069, 0·275) and increased fat mass gain (β=0·076; 95 % CI 0·019, 0·133) over time v. the ‘healthy’ cluster.ConclusionsChildren consistently showing a processed dietary pattern or changing from a processed pattern to a sweet pattern presented the most unfavourable changes in fat mass and abdominal fat. These findings support the need to promote overall healthy dietary habits in obesity prevention and health promotion programmes targeting children.
LncRNA ZNF503-AS1 promotes RPE differentiation by downregulating ZNF503 expression
Authors: Chen Xue , Jiang Chao , Qin Bing , Liu Guohua , Ji Jiangdong , Sun Xiantao , Xu Min , Ding Sijia , Zhu Meidong , Huang Guofu , Yan Biao , Zhao Chen 
Published: September 2017

AbstractLong noncoding RNAs (lncRNAs) have important roles in various biological processes. Our previous work has revealed that dedifferentiation of retinal pigment epithelium (RPE) cells contributes to the pathology of age-related macular degeneration (AMD). Herein, we show roles of lncRNAs in RPE differentiation. We used microarray to identify lncRNA expression profiles in human induced pluripotent stem cells (hiPSCs) and hiPSC-derived RPE cells. A total of 217 differentially expressed lncRNAs along with the differentiation were initially identified, among which 13 lncRNAs showed a consistent fold change of over 2. LncRNA ZNF503-AS1, located in the cytoplasm of RPE cells, was found consistently upregulated along with RPE differentiation, and downregulated in the RPE-choroid of AMD patients. In vitro study further suggested that ZNF503-AS1 insufficiency could inhibit RPE differentiation, and promote its proliferation and migration. As ZNF503-AS1 is transcribed from the antisense strand of the ZNF503 gene locus, we further revealed its regulatory role in ZNF503 expression. ZNF503-AS1 was reversely correlated with ZNF503 expression. Our results also suggested that ZNF503 could inhibit RPE differentiation, and promote its proliferation and migration. Thus, ZNF503-AS1 potentially promotes RPE differentiation through downregulation of ZNF503 expression. In addition, nuclear factor-κB was recognized as a potential upstream transcript factor for ZNF503-AS1, which might participate in promoting RPE differentiation by regulating the expression of ZNF503-AS1. Taken together, our study identifies a group of RPE differentiation relevant lncRNAs, and the potential role of ZNF503-AS1 in the pathology of atrophic AMD, which might help with the intervention of AMD patients.
The functional relationship between transglutaminase 2 and transforming growth factor β1 in the regulation of angiogenesis and endothelial–mesenchymal transition
Authors: Wang Zhuo , Perez Mileidys , Lee Eun-Seo , Kojima Soichi , Griffin Martin 
Published: September 2017

AbstractThe importance of transglutaminase 2 (TG2) in angiogenesis has been highlighted in recent studies, but other roles of this multi-functional enzyme in endothelial cell (EC) function still remains to be fully elucidated. We previously showed that the extracellular TG2 is involved in maintaining tubule formation in ECs by a mechanism involving matrix-bound vascular endothelial growth factor (VEGF) signalling. Here, by using the ECs and fibroblast co-culture and ECs 3D culture models, we demonstrate a further role for TG2 in both endothelial tubule formation and in tubule loss, which involves its role in the regulation of transforming growth factor β1 (TGFβ1) and Smad signalling. We demonstrate that inhibition of tubule formation by TG2 inhibitors can be restored by add-back of exogenous TGFβ1 at pg/ml levels and show that TG2 −/− mouse ECs are unable to form tubules in 3D culture and display negligible Smad signalling compared to wild-type cells. Loss of tubule formation in the TG2 −/− ECs can be reconstituted by transduction with TG2. We demonstrate that extracellular TG2 also has an important role in TGFβ1-induced transition of ECs into myofibroblast-like cells (endothelial–mesenchymal transition), resulting in loss of EC tubules and tubule formation. Our data also indicate that TG2 may have a role in regulating TGFβ signalling through entrapment of active TGFβ1 into the extracellular matrix. In conclusion, our work demonstrates that TG2 has multi-functional roles in ECs where its ability to fine-tune of TGFβ1 signalling means it can be involved in both endothelial tubule formation and tubule rarefaction.
Acceleration of pancreatic tumorigenesis under immunosuppressive microenvironment induced by Reg3g overexpression
Authors: Liu Xiulan , Zhou Zhongshi , Cheng Qi , Wang Hongjie , Cao Hui , Xu Qianqian , Tuo Yali , Jiang Li , Zou You , Ren Hongyu , Xiang Ming 
Published: September 2017

AbstractReg3g is a potential risk for pancreatic ductal adenocarcinoma (PDAC). We previously demonstrated that Reg3g promoted pancreatic carcinogenesis via a STAT3 signaling pathway in a murine model of chronic pancreatitis. Whether the immune response is involved in tumorigenesis induced by Reg3g remains unknown. In this study, Reg3g-regulated tumor immunity was evaluated in tumor-implanted murine models, immune cells, and tumor microenvironment. In mice that had been orthotopically or ectopically implanted with Panc02 cells, Reg3g overexpression increased EGFR and Ki67, diminished MHC-I and caspase-3 expression, and accelerated growth of tumors. By interacting with PD-1/PD-L1, Reg3g also promoted differentiation of Tregs and recruitment of MDSC, retarded maturation of DCs and inactivation of CD8+ T cells, and suppressed cross-priming of CD8+ T-cell responses by DCs in tumor-bearing mice. Knockdown of Reg3g delayed tumor development in normal mice, but not in CD8+ T-cell-deficient mice. In vitro, Reg3g upregulated EGFR in DCs, activated heme oxygenase-1 (Hmox1) involved JAK2/STAT3 signaling, raised levels of Th2 cytokines in and suppressed maturation of DCs, and enhanced tumor cell proliferation. These results reveal a novel role of Reg3g as an immunosuppressive promoter that weakens tumor-specific antigenicity and suppresses antitumor effects of CD8+ T cells in a murine model of pancreatic cancer. Reg3g produces these effects by activating the JAK2/STAT3 signaling pathway in DCs, triggering the generation of an immunosuppressive tumor microenvironment.
p73 is required for appropriate BMP-induced mesenchymal-to-epithelial transition during somatic cell reprogramming
Authors: Martin-Lopez Marta , Maeso-Alonso Laura , Fuertes-Alvarez Sandra , Balboa Diego , Rodríguez-Cortez Virginia , Weltner Jere , Diez-Prieto Inmaculada , Davis Andrew , Wu Yaning , Otonkoski Timo , Flores Elsa R , Menéndez Pablo , Marques Margarita M , Marin Maria C 
Published: September 2017

AbstractThe generation of induced pluripotent stem cells (iPSCs) by somatic cell reprogramming holds great potential for modeling human diseases. However, the reprogramming process remains very inefficient and a better understanding of its basic biology is required. The mesenchymal-to-epithelial transition (MET) has been recognized as a crucial step for the successful reprogramming of fibroblasts into iPSCs. It has been reported that the p53 tumor suppressor gene acts as a barrier of this process, while its homolog p63 acts as an enabling factor. In this regard, the information concerning the role of the third homolog, p73, during cell reprogramming is limited. Here, we derive total Trp73 knockout mouse embryonic fibroblasts, with or without Trp53, and examine their reprogramming capacity. We show that p73 is required for effective reprogramming by the Yamanaka factors, even in the absence of p53. Lack of p73 affects the early stages of reprogramming, impairing the MET and resulting in altered maturation and stabilization phases. Accordingly, the obtained p73-deficient iPSCs have a defective epithelial phenotype and alterations in the expression of pluripotency markers. We demonstrate that p73 deficiency impairs the MET, at least in part, by hindering BMP pathway activation. We report that p73 is a positive modulator of the BMP circuit, enhancing its activation by DNp73 repression of the Smad6 promoter. Collectively, these findings provide mechanistic insight into the MET process, proposing p73 as an enhancer of MET during cellular reprogramming.
The intracellular angiotensin system buffers deleterious effects of the extracellular paracrine system
Authors: Villar-Cheda Begoña , Costa-Besada Maria A , Valenzuela Rita , Perez-Costas Emma , Melendez-Ferro Miguel , Labandeira-Garcia Jose L 
Published: September 2017

AbstractThe ‘classical’ renin–angiotensin system (RAS) is a circulating system that controls blood pressure. Local/paracrine RAS, identified in a variety of tissues, including the brain, is involved in different functions and diseases, and RAS blockers are commonly used in clinical practice. A third type of RAS (intracellular/intracrine RAS) has been observed in some types of cells, including neurons. However, its role is still unknown. The present results indicate that in brain cells the intracellular RAS counteracts the intracellular superoxide/H2O2 and oxidative stress induced by the extracellular/paracrine angiotensin II acting on plasma membrane receptors. Activation of nuclear receptors by intracellular or internalized angiotensin triggers a number of mechanisms that protect the cell, such as an increase in the levels of protective angiotensin type 2 receptors, intracellular angiotensin, PGC-1α and IGF-1/SIRT1. Interestingly, this protective mechanism is altered in isolated nuclei from brains of aged animals. The present results indicate that at least in the brain, AT1 receptor blockers acting only on the extracellular or paracrine RAS may offer better protection of cells.
Perturbed cholesterol and vesicular trafficking associated with dengue blocking in Wolbachia-infected Aedes aegypti cells
Authors: Geoghegan Vincent , Stainton Kirsty , Rainey Stephanie M. , Ant Thomas H. , Dowle Adam A. , Larson Tony , Hester Svenja , Charles Philip D. , Thomas Benjamin , Sinkins Steven P. 
Published: September 2017

AbstractWolbachiaare intracellular maternally inherited bacteria that can spread through insect populations and block virus transmission by mosquitoes, providing an important approach to dengue control. To better understand the mechanisms of virus inhibition, we here perform proteomic quantification of the effects ofWolbachiainAedes aegyptimosquito cells and midgut. Perturbations are observed in vesicular trafficking, lipid metabolism and in the endoplasmic reticulum that could impact viral entry and replication.Wolbachia-infected cells display a differential cholesterol profile, including elevated levels of esterified cholesterol, that is consistent with perturbed intracellular cholesterol trafficking. Cyclodextrins have been shown to reverse lipid accumulation defects in cells with disrupted cholesterol homeostasis. Treatment ofWolbachia-infectedAe.aegypticells with 2-hydroxypropyl-β-cyclodextrin restores dengue replication inWolbachia-carrying cells, suggesting dengue is inhibited inWolbachia-infected cells by localised cholesterol accumulation. These results demonstrate parallels between the cellularWolbachiaviral inhibition phenotype and lipid storage genetic disorders.
BRCA2 suppresses replication stress-induced mitotic and G1 abnormalities through homologous recombination
Authors: Feng Weiran , Jasin Maria 
Published: September 2017

AbstractMutations in the tumor suppressor BRCA2 predominantly predispose to breast cancer. Paradoxically, while loss of BRCA2 promotes tumor formation, it also causes cell lethality, although how lethality is triggered is unclear. Here, we generate BRCA2 conditional non-transformed human mammary epithelial cell lines using CRISPR-Cas9. Cells are inviable upon BRCA2 loss, which leads to replication stress associated with under replication, causing mitotic abnormalities, 53BP1 nuclear body formation in the ensuing G1 phase, and G1 arrest. Unexpected from other systems, the role of BRCA2 in homologous recombination, but not in stalled replication fork protection, is primarily associated with supporting human mammary epithelial cell viability, and, moreover, preventing replication stress, a hallmark of pre-cancerous lesions. Thus, we uncover a DNA under replication-53BP1 nuclear body formation-G1 arrest axis as an unanticipated outcome of homologous recombination deficiency, which triggers cell lethality and, we propose, serves as a barrier that must be overcome for tumor formation.
Aqueous synthesis of functionalized copper sulfide quantum dots as near-infrared luminescent probes for detection of Hg2+, Ag+ and Au3+
Authors: Du Weilin , Liao Lei , Yang Li , Qin Aimiao , Liang Aihui 
Published: September 2017

AbstractStable water-soluble copper sulfide(Cu2S) quantum dots(QDs) with near-infrared emission were synthesized using N-acetyl-L-cysteine(NAC) as a modifier in aqueous solution and nitrogen atmosphere at room temperature. The product was characterized by TEM, XRD, XPS, FT-IR, FL and UV-VIS spectrometers. Effects of preparation conditions such as pH values, the molar ratio of reactants, temperature, and metal ions on the fluorescence properties of Cu2S QDs were discussed. Under optimal conditions, the prepared Cu2S QDs with average diameter about 2–5 nm show a near-infrared emission at 770 nm with the excitation wavelength of 466 nm, and have a good detection sensitivity for ions of Hg2+, Ag+ and Au3+, based on the characteristic of fluorescence quenching. The fluorescence quenching mechanism was proposed via electron transfer with cation exchange, which based on the theory of Hard-Soft-Acid-Base (HSAB) and Ksp value of metal–sulfide.
Cross-polarization coupling terahertz time-domain spectroscopy in a semiconductor based on the Hall effect
Authors: Hu Jiangsheng , Liu JinSong , Wang Kejia 
Published: September 2017

AbstractWe propose a new type of terahertz time-domain spectroscopy in an isotropic semiconductor wafer applied by a magnetic field in which two cross-polarization THz pulses couple with each other via the Hall effect. We built a classic theoretic model to describe cross-polarization coupling THz spectroscopy (CPCTS). Numerical simulations show that the magnetic field can clearly affect the spectral features of the two THz pulses via the Hall effect in which both the magnitude and direction of the magnetic field and the thickness of the wafer play important roles. Using CPCTS, we present an improved method that is non-contact to measure the material parameters, such as the damping constant and carrier density of a semiconductor wafer, and discuss the possibility of THz functional devices. Finally, we describe an experimental scheme to guide CPCTS.
Polyphenols journey through blood-brain barrier towards neuronal protection
Authors: Figueira I. , Garcia G. , Pimpão R. C. , Terrasso A. P. , Costa I. , Almeida A. F. , Tavares L. , Pais T. F. , Pinto P. , Ventura M. R. , Filipe A. , McDougall G. J. , Stewart D. , Kim K. S. , Palmela I. , Brites D. , Brito M. A. , Brito C. , Santos C. N. 
Published: September 2017

AbstractAge-related complications such as neurodegenerative disorders are increasing and remain cureless. The possibility of altering the progression or the development of these multifactorial diseases through diet is an emerging and attractive approach with increasing experimental support. We examined the potential of known bioavailable phenolic sulfates, arising from colonic metabolism of berries, to influence hallmarks of neurodegenerative processes. In silico predictions and in vitro transport studies across blood-brain barrier (BBB) endothelial cells, at circulating concentrations, provided evidence for differential transport, likely related to chemical structure. Moreover, endothelial metabolism of these phenolic sulfates produced a plethora of novel chemical entities with further potential bioactivies. Pre-conditioning with phenolic sulfates improved cellular responses to oxidative, excitotoxicity and inflammatory injuries and this attenuation of neuroinflammation was achieved via modulation of NF-κB pathway. Our results support the hypothesis that these small molecules, derived from dietary (poly)phenols may cross the BBB, reach brain cells, modulate microglia-mediated inflammation and exert neuroprotective effects, with potential for alleviation of neurodegenerative diseases.