bluuebunny/crossref_metadata_2025_split huggingface dataset:
Demographic and lifestyle factors associated with adherence to the Mediterranean diet in relation to overweight/obesity among Israeli adolescents: findings from the Mabat Israeli national youth health and nutrition survey
Authors: Peng Wen , Goldsmith Rebecca , Berry Elliot M 
Published: November 2016

AbstractObjectiveTo investigate demographic and lifestyle factors associated with adherence to the Mediterranean diet (MD) in Israeli adolescents.DesignCross-sectional.SettingSchool-based.SubjectsSchoolchildren (n 5268) aged 11–19 years answered self-administered questionnaires on food consumption, eating habits and lifestyle; a subset (n 578) also completed 24 h food recalls.ResultsUsing a modified KIDMED index, 25·5 % of the students had poor, 55·2 % had average and 19·3 % had good MD adherence. Jewish middle-school children had the highest proportion (28·2 %) of poor MD adherence. Olive oil usage, derived from 24 h food recalls, was 18·1 % in Jewish families v. 71·1 % in Arab homes. In Jewish boys, the odds (OR; 95 % CI) of having poor MD adherence was higher in those who watched television/videos/listened to music for ≥2 h/d (1·25; 0·98, 1·58) and those who sometimes/don’t read food labels (1·69; 1·31, 2·18). In Jewish girls, the odds for having poor MD adherence was significantly higher in those whose mother’s schooling was <12 years (2·06; 1·41, 3·00) and those who sometimes/don’t read food labels (1·35; 1·08, 1·69). In Arab boys, watching television/videos/listening to music for ≥2 h/d was significantly associated with poor MD adherence (1·89; 1·16, 3·07). In Arab girls, no aerobic activity or ball games weekly was associated with poor MD adherence (1·38; 0·91, 2·09).ConclusionsIsraeli adolescents had overall a high rate of poor MD adherence. Jewish middle-school children were at the highest risk. Interventions aimed at increasing physical activity, reducing sedentary time, improving mother’s education and promoting reading of food labels are recommended.
The effects of restaurant nutrition menu labelling on college students’ healthy eating behaviours
Authors: Roseman Mary G , Joung Hyun-Woo , Choi Eun-Kyong (Cindy) , Kim Hak-Seon 
Published: November 2016

AbstractObjectiveAccording to the US Affordable Care Act, restaurant chains are required to provide energy (calorie) and other nutrition information on their menu. The current study examined the impact of menu labelling containing calorie information and recommended daily calorie intake, along with subjective nutrition knowledge, on intention to select lower-calorie foods prior to the implementation of the Affordable Care Act.DesignFull factorial experimental design with participants exposed to four variants of a sample menu in a 2 (presence v. absence of calorie information) ×2 (presence v. absence of recommended daily calorie intake).SettingLarge, public university in the Southwest USA.SubjectsPrimarily undergraduate college students.ResultsMajority of participants were 19–23 years of age (mean 21·8 (sd 3·6) years). Menu information about calorie content and respondents’ subjective nutrition knowledge had a significantly positive impact on students’ intention to select lower-calorie foods (β=0·24, P<0·001 and β=0·33, P<0·001, respectively); however, recommended daily calorie intake information on the menu board did not influence students’ intention to select lower-calorie foods (β=0·10, P=0·105). Gender played a significant role on purchase intent for lower-calorie menu items, with females more affected by the calorie information than males (β=0·37, P<0·001).ConclusionsFindings support the role menu labelling can play in encouraging a healthier lifestyle for college students. College students who are Generation Y desire healthier menu options and accept nutritional labels on restaurant menus as a way to easily and expediently obtain nutrition information.
Rapidly cycling Lgr5+ stem cells are exquisitely sensitive to extrinsic dietary factors that modulate colon cancer risk
Authors: Kim Eunjoo , Davidson Laurie A , Zoh Roger S , Hensel Martha E , Salinas Michael L , Patil Bhimanagouda S , Jayaprakasha Guddadarangavvanahally K , Callaway Evelyn S , Allred Clinton D , Turner Nancy D , Weeks Brad R , Chapkin Robert S 
Published: November 2016

AbstractThe majority of colon tumors are driven by aberrant Wnt signaling in intestinal stem cells, which mediates an efficient route toward initiating intestinal cancer. Natural lipophilic polyphenols and long-chain polyunsaturated fatty acids (PUFAs) generally suppress Wnt- and NF-κB- (nuclear factor-κ light-chain enhancer of activated B-cell) related pathways. However, the effects of these extrinsic agents on colonic leucine-rich repeat-containing G-protein-coupled receptor 5-positive (Lgr5+) stem cells, the cells of origin of colon cancer, have not been documented to date. Therefore, we examined the effect of n-3 PUFA and polyphenol (curcumin) combination on Lgr5+ stem cells during tumor initiation and progression in the colon compared with an n-6 PUFA-enriched control diet. Lgr5-EGFP-IRES-creERT2 knock-in mice were fed diets containing n-6 PUFA (control), n-3 PUFA, n-6 PUFA+curcumin or n-3 PUFA+curcumin for 3 weeks, followed by 6 azoxymethane (AOM) injections, and terminated 17 weeks after the last injection. To further elucidate the effects of the dietary bioactives at the tumor initiation stage, Lgr5+ stem cells were also assessed at 12 and 24 h post AOM injection. Only n-3 PUFA+curcumin feeding reduced nuclear β-catenin in aberrant crypt foci (by threefold) compared with control at the progression time point. n-3 PUFA+curcumin synergistically increased targeted apoptosis in DNA-damaged Lgr5+ stem cells by 4.5-fold compared with control at 12 h and maximally reduced damaged Lgr5+ stem cells at 24 h, down to the level observed in saline-treated mice. Finally, RNAseq analysis indicated that p53 signaling in Lgr5+ stem cells from mice exposed to AOM was uniquely upregulated only following n-3 PUFA+curcumin cotreatment. These novel findings demonstrate that Lgr5+ stem cells are uniquely responsive to external dietary cues following the induction of DNA damage, providing a therapeutic strategy for eliminating damaged Lgr5+ stem cells to reduce colon cancer initiation.
A link between adipogenesis and innate immunity: RNase-L promotes 3T3-L1 adipogenesis by destabilizing Pref-1 mRNA
Authors: Wang Yi-Ting , Chiang Hou-Hsien , Huang Ying-Shing , Hsu Chia-Lang , Yang Po-Jen , Juan Hsueh-Fen , Yang Wei-Shiung 
Published: November 2016

AbstractRibonuclease L (RNase-L) is an endoribonuclease well known for its roles in innate immunity. Recently it has been shown to regulate several cellular functions by modulating the levels of specific mRNAs. In this study, we investigated whether RNase-L may regulate adipocyte functions. We showed that knockdown of RNase-L reduced 3T3-L1 adipocyte differentiation and lipid accumulation. After mRNA profiling, we found that upregulation of Pref-1 mRNA, an inhibitory regulator of adipogenesis, could explain the reduced adipocyte differentiation with RNase-L downregulation. The signaling molecules downstream to Pref-1, including focal adhesion kinase, extracellular signal-regulated kinases and SRY-box 9, were activated by RNase-L suppression. The presence of Pref-1 mRNA was detected in the mRNP complexes precipitated by anti-RNase-L antibody. Moreover, the Pref-1 mRNA decay rate was raised by elevated RNase-L ribonuclease activity. Finally, in stable cell clones with RNase-L silencing, suppression of Pref-1 mRNA by specific siRNA partially recovered the adipocyte differentiation phenotype. Consistent with our findings, meta-analysis of 45 public array datasets from seven independent studies showed a significant negative relationship between RNase-L and Pref-1 mRNA levels in mouse adipose tissues. Higher RNase-L and lower Pref-1 mRNAs were found in the adipose tissues of high-fat diet mice compared to those of ND mice. In line with this, our animal data also showed that the adipose tissues of obese rats contained higher RNase-L and lower Pref-1 expression in comparison to that of lean rats. This study demonstrated that Pref-1 mRNA is a novel substrate of RNase-L. RNase-L is involved in adipocyte differentiation through destabilizing Pref-1 mRNA, thus offering a new link among RNA metabolism, innate immunity and adipogenesis in obesity progression.
The control of male fertility by spermatid-specific factors: searching for contraceptive targets from spermatozoon’s head to tail
Authors: Chen Su-Ren , Batool Aalia , Wang Yu-Qian , Hao Xiao-Xia , Chang Chawn-Shang , Cheng C Yan , Liu Yi-Xun 
Published: November 2016

AbstractMale infertility due to abnormal spermatozoa has been reported in both animals and humans, but its pathogenic causes, including genetic abnormalities, remain largely unknown. On the other hand, contraceptive options for men are limited, and a specific, reversible and safe method of male contraception has been a long-standing quest in medicine. Some progress has recently been made in exploring the effects of spermatid-specifical genetic factors in controlling male fertility. A comprehensive search of PubMed for articles and reviews published in English before July 2016 was carried out using the search terms ‘spermiogenesis failure’, ‘globozoospermia’, ‘spermatid-specific’, ‘acrosome’, ‘infertile’, ‘manchette’, ‘sperm connecting piece’, ‘sperm annulus’, ‘sperm ADAMs’, ‘flagellar abnormalities’, ‘sperm motility loss’, ‘sperm ion exchanger’ and ‘contraceptive targets’. Importantly, we have opted to focus on articles regarding spermatid-specific factors. Genetic studies to define the structure and physiology of sperm have shown that spermatozoa appear to be one of the most promising contraceptive targets. Here we summarize how these spermatid-specific factors regulate spermiogenesis and categorize them according to their localization and function from spermatid head to tail (e.g., acrosome, manchette, head-tail conjunction, annulus, principal piece of tail). In addition, we emphatically introduce small-molecule contraceptives, such as BRDT and PPP3CC/PPP3R2, which are currently being developed to target spermatogenic-specific proteins. We suggest that blocking the differentiation of haploid germ cells, which rarely affects early spermatogenic cell types and the testicular microenvironment, is a better choice than spermatogenic-specific proteins. The studies described here provide valuable information regarding the genetic and molecular defects causing male mouse infertility to improve our understanding of the importance of spermatid-specific factors in controlling fertility. Although a male contraceptive ‘pill’ is still many years away, research into the production of new small-molecule contraceptives targeting spermatid-specific proteins is the right avenue.
RIPK1 protects from TNF-α-mediated liver damage during hepatitis
Authors: Filliol Aveline , Piquet-Pellorce Claire , Le Seyec Jacques , Farooq Muhammad , Genet Valentine , Lucas-Clerc Catherine , Bertin John , Gough Peter J , Dimanche-Boitrel Marie-Thérèse , Vandenabeele Peter , Bertrand Mathieu JM , Samson Michel 
Published: November 2016

AbstractCell death of hepatocytes is a prominent characteristic in the pathogenesis of liver disease, while hepatolysis is a starting point of inflammation in hepatitis and loss of hepatic function. However, the precise molecular mechanisms of hepatocyte cell death, the role of the cytokines of hepatic microenvironment and the involvement of intracellular kinases, remain unclear. Tumor necrosis factor alpha (TNF-α) is a key cytokine involved in cell death or survival pathways and the role of RIPK1 has been associated to the TNF-α-dependent signaling pathway. We took advantage of two different deficient mouse lines, the RIPK1 kinase dead knock-in mice (Ripk1K45A) and the conditional knockout mice lacking RIPK1 only in liver parenchymal cells (Ripk1LPC-KO), to characterize the role of RIPK1 and TNF-α in hepatitis induced by concanavalin A (ConA). Our results show that RIPK1 is dispensable for liver homeostasis under steady-state conditions but in contrast, RIPK1 kinase activity contributes to caspase-independent cell death induction following ConA injection and RIPK1 also serves as a scaffold, protecting hepatocytes from massive apoptotic cell death in this model. In the Ripk1LPC-KO mice challenged with ConA, TNF-α triggers apoptosis, responsible for the observed severe hepatitis. Mechanism potentially involves both TNF-independent canonical NF-κB activation, as well as TNF-dependent, but canonical NF-κB-independent mechanisms. In conclusion, our results suggest that RIPK1 kinase activity is a pertinent therapeutic target to protect liver against excessive cell death in liver diseases.
Mechanism for rapid growth of organic–inorganic halide perovskite crystals
Authors: Nayak Pabitra K. , Moore David T. , Wenger Bernard , Nayak Simantini , Haghighirad Amir A. , Fineberg Adam , Noel Nakita K. , Reid Obadiah G. , Rumbles Garry , Kukura Philipp , Vincent Kylie A. , Snaith Henry J. 
Published: November 2016

AbstractOptoelectronic devices based on hybrid halide perovskites have shown remarkable progress to high performance. However, despite their apparent success, there remain many open questions about their intrinsic properties. Single crystals are often seen as the ideal platform for understanding the limits of crystalline materials, and recent reports of rapid, high-temperature crystallization of single crystals should enable a variety of studies. Here we explore the mechanism of this crystallization and find that it is due to reversible changes in the solution where breaking up of colloids, and a change in the solvent strength, leads to supersaturation and subsequent crystallization. We use this knowledge to demonstrate a broader range of processing parameters and show that these can lead to improved crystal quality. Our findings are therefore of central importance to enable the continued advancement of perovskite optoelectronics and to the improved reproducibility through a better understanding of factors influencing and controlling crystallization.
Biphasic regulation of chondrocytes by Rela through induction of anti-apoptotic and catabolic target genes
Authors: Kobayashi Hiroshi , Chang Song Ho , Mori Daisuke , Itoh Shozo , Hirata Makoto , Hosaka Yoko , Taniguchi Yuki , Okada Keita , Mori Yoshifumi , Yano Fumiko , Chung Ung-il , Akiyama Haruhiko , Kawaguchi Hiroshi , Tanaka Sakae , Saito Taku 
Published: November 2016

AbstractIn vitrostudies have shown that Rela/p65, a key subunit mediating NF-κB signalling, is involved in chondrogenic differentiation, cell survival and catabolic enzyme production. Here, we analysein vivofunctions of Rela in embryonic limbs and adult articular cartilage, and find that Rela protects chondrocytes from apoptosis through induction of anti-apoptotic genes includingPik3r1. During skeletal development, homozygous knockout ofRelaleads to impaired growth through enhanced chondrocyte apoptosis, whereas heterozygous knockout ofReladoes not alter growth. In articular cartilage, homozygous knockout ofRelaat 7 weeks leads to marked acceleration of osteoarthritis through enhanced chondrocyte apoptosis, whereas heterozygous knockout ofRelaresults in suppression of osteoarthritis development through inhibition of catabolic gene expression. Haploinsufficiency or a low dose of an IKK inhibitor suppresses catabolic gene expression, but does not alter anti-apoptotic gene expression. The biphasic regulation of chondrocytes by Rela contributes to understanding the pathophysiology of osteoarthritis.
Charge-specific size-dependent separation of water-soluble organic molecules by fluorinated nanoporous networks
Authors: Byun Jeehye , Patel Hasmukh A. , Thirion Damien , Yavuz Cafer T. 
Published: November 2016

AbstractMolecular architecture in nanoscale spaces can lead to selective chemical interactions and separation of species with similar sizes and functionality. Substrate specific sorbent chemistry is well known through highly crystalline ordered structures such as zeolites, metal organic frameworks and widely available nanoporous carbons. Size and charge-dependent separation of aqueous molecular contaminants, on the contrary, have not been adequately developed. Here we report a charge-specific size-dependent separation of water-soluble molecules through an ultra-microporous polymeric network that features fluorines as the predominant surface functional groups. Treatment of similarly sized organic molecules with and without charges shows that fluorine interacts with charges favourably. Control experiments using similarly constructed frameworks with or without fluorines verify the fluorine-cation interactions. Lack of a σ-hole for fluorine atoms is suggested to be responsible for this distinct property, and future applications of this discovery, such as desalination and mixed matrix membranes, may be expected to follow.
Glacial isostatic uplift of the European Alps
Authors: Mey Jürgen , Scherler Dirk , Wickert Andrew D. , Egholm David L. , Tesauro Magdala , Schildgen Taylor F. , Strecker Manfred R. 
Published: November 2016

AbstractFollowing the last glacial maximum (LGM), the demise of continental ice sheets induced crustal rebound in tectonically stable regions of North America and Scandinavia that is still ongoing. Unlike the ice sheets, the Alpine ice cap developed in an orogen where the measured uplift is potentially attributed to tectonic shortening, lithospheric delamination and unloading due to deglaciation and erosion. Here we show that ∼90% of the geodetically measured rock uplift in the Alps can be explained by the Earth’s viscoelastic response to LGM deglaciation. We modelled rock uplift by reconstructing the Alpine ice cap, while accounting for postglacial erosion, sediment deposition and spatial variations in lithospheric rigidity. Clusters of excessive uplift in the Rhône Valley and in the Eastern Alps delineate regions potentially affected by mantle processes, crustal heterogeneity and active tectonics. Our study shows that even small LGM ice caps can dominate present-day rock uplift in tectonically active regions.
Crystal structure of bacterial haem importer complex in the inward-facing conformation
Authors: Naoe Youichi , Nakamura Nozomi , Doi Akihiro , Sawabe Mia , Nakamura Hiro , Shiro Yoshitsugu , Sugimoto Hiroshi 
Published: November 2016

AbstractPathogenic bacteria remove iron from the haem of host tissues and use it as a catalytic center of many enzymes. Haem uptake by pathogenic bacteria is facilitated by the membrane-integrated haem importer, which belongs to the type II ATP-binding cassette (ABC) transporter. Here we present crystal structures of Burkholderia cenocepacia haem importer BhuUV complexed with the periplasmic haem-binding protein BhuT and in the absence of BhuT. The transmembrane helices of these structures show an inward-facing conformation, in which the cytoplasmic gate of the haem translocation pathway is completely open. Since this conformation is found in both the haem- and nucleotide-free form, the structure of BhuUV-T provides the post-translocation state and the missing piece in the transport cycle of the type II importer. Structural comparison with the outward-facing conformation reported for the haem importer ortholog HmuUV from Yersenia pestis gives mechanistic insights into conformational transitions and haem secretion during the haem transport cycle.
Metformin decreases progerin expression and alleviates pathological defects of Hutchinson–Gilford progeria syndrome cells
Authors: Egesipe Anne-Laure , Blondel Sophie , Lo Cicero Alessandra , Jaskowiak Anne-Laure , Navarro Claire , Sandre-Giovannoli Annachiara De , Levy Nicolas , Peschanski Marc , Nissan Xavier 
Published: November 2016

AbstractHutchinson–Gilford progeria syndrome (HGPS) is a rare genetic disorder that causes systemic accelerated aging in children. This syndrome is due to a mutation in the LMNA gene that leads to the production of a truncated and toxic form of lamin A called progerin. Because the balance between the A-type lamins is controlled by the RNA-binding protein SRSF1, we have hypothesized that its inhibition may have therapeutic effects for HGPS. For this purpose, we evaluated the antidiabetic drug metformin and demonstrated that 48 h treatment with 5 mmol/l metformin decreases SRSF1 and progerin expression in mesenchymal stem cells derived from HGPS induced pluripotent stem cells (HGPS MSCs). The effect of metformin on progerin was then confirmed in several in vitro models of HGPS, i.e., human primary HGPS fibroblasts, LmnaG609G/G609G mouse fibroblasts and healthy MSCs previously treated with a PMO (phosphorodiamidate morpholino oligonucleotide) that induces progerin. This was accompanied by an improvement in two in vitro phenotypes associated with the disease: nuclear shape abnormalities and premature osteoblastic differentiation of HGPS MSCs. Overall, these results suggest a novel approach towards therapeutics for HGPS that can be added to the currently assayed treatments that target other molecular defects associated with the disease.
Cellulase from Trichoderma harzianum interacts with roots and triggers induced systemic resistance to foliar disease in maize
Authors: Saravanakumar Kandasamy , Fan Lili , Fu Kehe , Yu Chuanjin , Wang Meng , Xia Hai , Sun Jianan , Li Yaqian , Chen Jie 
Published: November 2016

AbstractTrichoderma harzianum is well known to exhibit induced systemic resistance (ISR) to Curvularia leaf spot. We previously reported that a C6 zinc finger protein (Thc6) is responsible for a major contribution to the ISR to the leaf disease, but the types of effectors and the signals mediated by Thc6 from Trichoderma are unclear. In this work, we demonstrated that two hydrolases, Thph1 and Thph2, from T. harzianum were regulated by Thc6. Furthermore, an electrophoretic mobility shift assay (EMSA) study revealed that Thc6 regulated mRNA expression by binding to GGCTAA and GGCTAAA in the promoters of the Thph1 and Thph2 genes, respectively. Moreover, the Thph1 and Thph2 proteins triggered the transient production of reactive oxygen species (ROS) and elevated the free cytosolic calcium levels in maize leaf. Furthermore, the genes related to the jasmonate/ethylene signaling pathway were up-regulated in the wild-type maize strain. However, the ΔThph1- or ΔThph2-deletion mutants could not activate the immune defense-related genes in maize to protect against leaf disease. Therefore, we conclude that functional Thph1 and Thph2 may be required in T. harzianum to activate ISR in maize.