bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transparency and effective e-Governance: a case of telecentres in the Indian State of Karnataka
Authors: Iyer Lakshmi Shankar , R.N. Subba Rao 
Published: November 2017

Purpose
It is the responsibility of any government to ensure efficient, transparent and reliable services to the common man through telecentres. The purpose of this study is to take into account the influence of people and process on transparency that leads to effective e-governance.

Design/methodology/approach
This study involved collecting data through questionnaire method from 400 citizens who visited the telecentres. Data were analysed by conducting chi-square test and independent sample t-test, and it was found that there exists significant influence of location on transparency.

Findings
The current study reiterates the fact from literature that transparency in transactions enables effective e-governance. Beneficiaries perceive that people and processes have influence on transparency.

Research limitations/implications
The research adds up to the literature in establishing that there exist differentials among the rural and urban population with respect to transparency. Results could be skewed, as there could be an impact of population density across urban and rural areas.

Practical implications
This study brings out a framework and an action plan for the government to implement and ensure transparency in processes leading to effective e-governance.

Social implications
The action plan ensures transparency in service delivery leading to effective e-governance. Increased transparency empowers citizens with increased trustworthiness towards services delivered through telecentres.

Originality/value
This paper fulfils the need for an action plan to assure citizens to use deliveries through telecentres with better transparency. The aspect of transparency is not being studied in the present context of service delivery by the government authorities in India. Moreover, the influence of transparency on e-governance is also under-explored.
Genomic data reveal high conservation but divergent evolutionary pattern of Polycomb/Trithorax group genes in arthropods
Authors: Jiang Feng , Liu Qing , Liu Xiang , Wang Xian‐Hui , Kang Le 
Published: November 2017

AbstractEpigenetic gene control is maintained by chromatin‐associated Polycomb group (PcG) and Trithorax group (TrxG) genes, which act antagonistically via the interplay between PcG and TrxG regulation to generate silenced or permissive transcriptional states. In this study, we searched for PcG/TrxG genes in 180 arthropod genomes, covering all the sequenced arthropod genomes at the time of conducting this study, to perform a global investigation of PcG/TrxG genes in a phylogenetic frame. Results of ancestral state reconstruction analysis revealed that the ancestor of arthropod species has an almost complete repertoire of PcG/TrxG genes, and most of these genes were seldom lost above order level. The domain diversity analysis indicated that the PcG/TrxG genes show variable extent of domain structure changes; some of these changes could be associated with lineage‐specific events. The likelihood ratio tests for selection pressure detected a number of PcG/TrxG genes which underwent episodic positive selection on the branch leading to the insects with holometabolous development. These results suggest that, despite their high conservation across arthropod species, different members of PcG/TrxG genes showed considerable differences in domain structure and sequence divergence in arthropod evolution. Our cross species comparisons using large‐scale genomic data provide insights into divergent evolutionary pattern on highly conserved genes in arthropods.
Comparison of anthropometrical parameters and dietary habits of young women with and without menstrual disorders
Authors: Łagowska Karolina , Kazmierczak Daria , Szymczak Katarzyna 
Published: November 2017

AimThe aim of this study was to assess the nutritional status and dietary habits of young women, in order to explore their relationship with the menstrual cycle and to determine the proportion of women with menstrual cycle irregularities.MethodsA total of 348 young women aged 15–25 years (19.7 ± 3.7 years) participated in the study and were assigned to a younger group (15–18 years; YG) or an older group (19–25 years; OG). Two subgroups were also distinguished: women with menstrual disorders (MD) and women with regular cycles (RC). Body mass, waist circumference, fat mass (FM), energy and nutrient intakes, and eating behaviour of the subjects were evaluated.ResultsIn both age groups, women with menstrual cycle disorders were more likely to have higher body weight, higher body mass index, larger waist circumference and higher body FM. The daily diets of these women contained larger quantities of animal protein and fat, including saturated fat (in OG), but were poorer in vitamins B1 and B6 (in YG) and in iron. Disinhibition was significantly more common in the MD group.ConclusionsThe results of this study suggest that nutritional habits and status can interfere with the course of the menstrual cycle in young women.
UNBS5162 inhibits the proliferation of human A549 non‐small‐cell lung cancer cells by promoting apoptosis
Authors: Liu Cuicui , Xing Jiaqiang , Gao Yujun 
Published: November 2017

BackgroundLung cancer is one of the most frequently diagnosed malignancies in the world, thus developing novel anticancer reagents for lung cancer treatment is critical.MethodsWe performed cell counting kit‐8 and cell colony formation assays to investigate the role of UNBS5162 in the proliferation of A549 cells. Invasion and migration assays were applied to study the inhibitory effect of UNBS5162 on non‐small cell lung cancer cells. To detect the effect of UNBS5162 on A549 cell apoptosis, Annexin‐V fluorescein isothiocyanate and propidium iodide staining methods were used. Protein expression was analyzed using Western blot assay.Results
UNBS5162 not only inhibited proliferation but also decreased invasion and migration in A549 cells. Most cells were intact (96.93%) under control conditions, but the number of intact cells decreased (84.8%) after 24 hours of treatment with UNBS5162, and the number of early and late apoptotic cells significantly increased (P < 0.05). Anti‐apoptotic protein Bcl‐2 expression in the UNBS5162 group was significantly decreased (P < 0.05), and expression of proapoptotic proteins Bim, Bax, and active caspase‐3 were significantly increased (P < 0.05) compared to the control. In the PI3K signaling pathway, phospo‐AKT and phospo‐mTOR levels were significantly decreased (P < 0.05), while S6K and Cyclin D1 protein levels were significantly decreased in UNBS5162 treated A549 cells (P < 0.05).ConclusionThese findings suggest that UNBS5162 could inhibit A549 cell proliferation and metastasis by inhibiting PI3K pathway mediated apoptosis.
Self‐reported marijuana use over 25 years and abdominal adiposity: the Coronary Artery Risk Development in Young Adults (CARDIA) Study
Authors: Bancks Michael P. , Auer Reto , Carr J. Jeffrey , Goff David C. , Kiefe Catarina , Rana Jamal S. , Reis Jared , Sidney Stephen , Terry James G. , Schreiner Pamela J. 
Published: November 2017

AbstractAimsWe investigated the association between cumulative lifetime and current marijuana use with total abdominal adipose tissue (AT), visceral AT, subcutaneous AT, intermuscular AT, and mean liver attenuation (LA) at mid‐life.DesignLongitudinal and cross‐sectional secondary data analysis of participants in the Coronary Artery Risk Development in Young Adults (CARDIA) Study.SettingCARDIA field centers in Birmingham, AL; Chicago, IL; Minneapolis, MN; and Oakland, CA, USA.ParticipantsCARDIA participants, aged 18–30 years in 1985–1986, who were present at the clinic examination in 2010–2011 (n = 2902).MeasurementsMarijuana use was assessed from responses to self‐administered questionnaires at 8 CARDIA examinations over 25 years, determined as cumulative marijuana‐years and current use status. Non‐contrast computed tomography imaging of the abdomen was obtained in 2010–2011.FindingsIn 2010–2011, 84% of participants reported a history of marijuana use with 11% reporting use within the past 30 days. Before adjustment, we observed greater cumulative marijuana use was associated with lower total abdominal and subcutaneous AT volume and lower LA and current marijuana use was associated with lower subcutaneous AT. However, after adjustment for age, sex, race, field center, cigarette pack‐years and current use, regular alcohol consumption, cumulative drink‐years, and physical activity, neither cumulative marijuana use nor current use showed an association with any abdominal adipose depot. Our estimates did not differ by age, sex, or race nor after accounting for cohort attrition.ConclusionNeither cumulative marijuana use nor current marijuana use is associated with total abdominal, visceral, subcutaneous, or intermuscular adipose tissue, or liver attenuation in mid‐life.
CBX3/heterochromatin protein 1 gamma is significantly upregulated in patients with non–small cell lung cancer
Authors: Chang Shih‐Chieh , Lai Yi‐Chun , Chen Yen‐Chung , Wang Nai‐Kuan , Wang Wei‐Shu , Lai Jiun‐I 
Published: November 2017

AbstractAimLung cancer is typically categorized into small cell lung cancer (SCLC) and non–small cell lung cancer (NSCLC). NSCLC comprises of the majority of lung cancer with a poor prognosis in advanced cases. Transcriptional profiling studies, including microarrays and RNA‐sequencing studies, have significantly enriched our knowledge of gene expression patterns in NSCLC. A recent transcriptional profiling study identified high prevalence ofCBX3/HP1‐gamma upregulation in human NSCLC samples.CBX3/HP1‐gamma is an isoform of the heterochromatin protein 1 family, which plays a role in heterochromatin formation and is linked to cancer.MethodsWe examined lung cancer samples from our hospital using immunohistochemistry forCBX3/HP1‐gamma staining. We also analyzed publicly available databases of NSCLC transcriptional profiling to validate our results.ResultsWe identified a high prevalence (77.2%) of samples with positive CBX3/HP1‐gamma staining by immunohistochemistry in NSCLC patient samples. Independently, we queried a publicly available dataset (GSE40419) containing RNA‐seq data from 77 patients. Upregulation ofCBX3/HP1‐gamma in tumor samples was present in 60.2% of the patients. A similar correlation was also observed in the The Cancer Genome Atlas (TCGA) database. Interestingly, we discovered a highly significant association between positiveCBX3/HP1‐gamma staining andEGFRmutation in our patient samples (40 of 42 patients,P < 0.001). Treatment ofEGFRmutant NSCLC cell lines with theEGFRinhibitor gefitinib failed to yield a change inCBX/HP1‐gamma expression, suggesting thatCBX/HP1‐gamma expression may be independent of EGFR downstream signaling.ConclusionWe report a significant upregulation ofCBX3/HP1‐gamma in NSCLC patients, and also a possible relationship betweenCBX3/HP1‐gamma expression andEGFRmutation.
Calcimimetic and calcilytic therapies for inherited disorders of the calcium‐sensing receptor signalling pathway
Authors: Hannan Fadil M , Olesen Mie K , Thakker Rajesh V 
Published: November 2017

The calcium‐sensing receptor (CaS receptor) plays a pivotal role in extracellular calcium homeostasis, and germline loss‐of‐function and gain‐of‐function mutations cause familial hypocalciuric hypercalcaemia (FHH) and autosomal dominant hypocalcaemia (ADH), respectively. CaS receptor signal transduction in the parathyroid glands is probably regulated by G‐protein subunit α11 (Gα11) and adaptor‐related protein complex‐2 σ‐subunit (AP2σ), and recent studies have identified germline mutations of these proteins as a cause of FHH and/or ADH. Calcimimetics and calcilytics are positive and negative allosteric modulators of the CaS receptor that have potential efficacy for symptomatic forms of FHH and ADH. Cellular studies have demonstrated that these compounds correct signalling and/or trafficking defects caused by mutant CaS receptor, Gα11 or AP2σ proteins. Moreover, mouse model studies indicate that calcilytics can rectify the hypocalcaemia and hypercalciuria associated with ADH, and patient‐based studies reveal calcimimetics to ameliorate symptomatic hypercalcaemia caused by FHH. Thus, calcimimetics and calcilytics represent targeted therapies for inherited disorders of the CaS receptor signalling pathway.Linked ArticlesThis article is part of a themed section on Molecular Pharmacology of GPCRs. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.21/issuetoc
PRN473, an inhibitor of Bruton's tyrosine kinase, inhibits neutrophil recruitment via inhibition of macrophage antigen‐1 signalling
Authors: Herter Jan M , Margraf Andreas , Volmering Stephanie , Correia Benedito Eduardo , Bradshaw J Michael , Bisconte Angelina , Hill Ronald J , Langrish Claire L , Lowell Clifford A , Zarbock Alexander 
Published: November 2017

Background and PurposeFollowing inflammatory stimuli, neutrophils are recruited to sites of inflammation and exert effector functions that often have deleterious effects on tissue integrity, which can lead to organ failure. Bruton's tyrosine kinase (Btk) is expressed in neutrophils and constitutes a promising pharmacological target for neutrophil‐mediated tissue damage. Here, we evaluate a selective reversible inhibitor of Btk, PRN473, for its ability to dampen neutrophil influx via inhibition of adhesion receptor signalling pathways.Experimental ApproachIn vitro assays were used to assess fMLP receptor 1 (Fpr‐1)‐mediated binding of ligands to the adhesion receptors macrophage antigen‐1 (Mac‐1) and lymphocyte function antigen‐1. Intravital microscopy of the murine cremaster was used to evaluate post‐adhesion strengthening and endoluminal crawling. Finally, neutrophil influx was visualized in a clinically relevant model of sterile liver injury in vivo. Btk knockout animals were used as points of reference for Btk functions.Key ResultsPharmacological inhibition of Btk by PRN473 reduced fMLP‐induced phosphorylation of Btk and Mac‐1 activation. Biochemical experiments demonstrated the specificity of the inhibitor. PRN473 (20 mg·kg−1) significantly reduced intravascular crawling and neutrophil recruitment into inflamed tissue in a model of sterile liver injury, down to levels seen in Btk‐deficient animals. A higher dose did not provide additional reduction of intravascular crawling and neutrophil recruitment.Conclusions and ImplicationsPRN473, a highly selective inhibitor of Btk, potently attenuates sterile liver injury by inhibiting the activation of the β2‐integrin Mac‐1 and subsequently neutrophil recruitment into inflamed tissue.
Sophocarpine attenuates wear particle‐induced implant loosening by inhibiting osteoclastogenesis and bone resorptionviasuppression of the NF‐κB signalling pathway in a rat model
Authors: Zhou Chen‐he , Shi Zhong‐li , Meng Jia‐hong , Hu Bin , Zhao Chen‐chen , Yang Yu‐te , Yu Wei , Chen Ze‐xin , Heng Boon Chin , Parkman Virginia‐Jeni Akila , Jiang Shuai , Zhu Han‐xiao , Wu Hao‐bo , Shen Wei‐liang , Yan Shi‐gui 
Published: November 2017

Background and PurposeAseptic prosthesis loosening, caused by wear particles, is one of the most common causes of arthroplasty failure. Extensive and over‐activated osteoclast formation and physiological functioning are regarded as the mechanism of prosthesis loosening. Therapeutic modalities based on inhibiting osteoclast formation and bone resorption have been confirmed to be an effective way of preventing aseptic prosthesis loosening. In this study, we have investigated the effects of sophocarpine (SPC, derived fromSophora flavescens) on preventing implant loosening and further explored the underlying mechanisms.Experimental ApproachThe effects of SPC in inhibiting osteoclastogenesis and bone resorption were evaluated in osteoclast formation, inducedin vitroby the receptor activator of NF‐κB ligand (RANKL). A rat femoral particle‐induced peri‐implant osteolysis model was established. Subsequently, micro‐CT, histology, mechanical testing and bone turnover were used to assess the effects of SPC in preventing implant loosening.Key ResultsIn vitro, we found that SPC suppressed osteoclast formation, bone resorption, F‐actin ring formation and osteoclast‐associated gene expression by inhibiting NF‐κB signalling, specifically by targeting IκB kinases. Ourin vivostudy showed that SPC prevented particle‐induced prosthesis loosening by inhibiting osteoclast formation, resulting in reduced periprosthetic bone loss, diminished pseudomembrane formation, improved bone‐implant contact, reduced bone resorption‐related turnover and enhanced stability of implants. Inhibition of NF‐κB signalling by SPC was confirmedin vivo.Conclusion and ImplicationsSPC can prevent implant loosening through inhibiting osteoclast formation and bone resorption. Thus, SPC might be a novel therapeutic agent to prevent prosthesis loosening and for osteolytic diseases.
Dimensionality of oppositional defiant disorder
Authors: Hukkelberg Silje S. , Ogden Terje 
Published: November 2017

BackgroundThe present study examined dimensionality of oppositional defiant disorder (ODD) using 10 alternative items using network analysis and confirmatory factor analysis.MethodsThe sample constituted 551 Norwegian children aged 2–12 and their parents. We used network analysis to investigate the connections between different symptoms. Next, we analysed data using traditional confirmatory factor methods, including the more recently proposed bifactor approach.ResultsThe bifactor model, with a strong general factor and three specific factors, provided the best model fit. Omega values did, however, reveal that only the general and the specific hurtful factor had satisfactory reliability. Network analysis showed that symptoms in general were positively connected within the ODD network. Strong connections between several symptoms within the irritable and hurtful cluster emerged, whereas some symptoms of the headstrong cluster seem to function as bridge nodes between the irritable and hurtful symptom clusters.ConclusionsThe findings support a bifactor model of ODD indicators, but omegas only gave support to the use of a general latent factor, and one specific factor. Network analysis did, however, provide some additional and interesting findings, revealing clusters of strongly connected symptoms and central bridge node symptoms. Implications of the results are discussed.
Dendritic cell phenotype in severe asthma reflects clinical responsiveness to glucocorticoids
Authors: Chambers E. S. , Nanzer A. M. , Pfeffer P. E. , Richards D. F. , Martineau A. R. , Griffiths C. J. , Corrigan C. J. , Hawrylowicz C. M. 
Published: November 2017

SummaryBackgroundSubsets of patients with severe asthma remain symptomatic despite prolonged, high‐dose glucocorticoid therapy. We hypothesized that the clinical glucocorticoid sensitivity of these asthmatics is reflected in differences in peripheral blood dendritic cell subsets.ObjectiveTo compare peripheral blood leucocyte populations using flow cytometry at baseline and after 2 weeks of systemic glucocorticoid (steroid) treatment to identify immunological differences between steroid‐sensitive (SS) and steroid‐resistant (SR) asthmatics.MethodsAdult severe asthmatics (SS n = 12; SR n = 23) were assessed for their response to 2 weeks of therapy with oral prednisolone. Peripheral blood was obtained before and after therapy and stained for lymphocyte (CD3, CD19, CD4, CD8 and Foxp3) and dendritic cell markers (Lineage negative [CD3, CD14, CD16, CD19, CD20, CD56], HLA‐DR+, CD304, CD11c, ILT3 and CD86).ResultsA higher median frequency of myeloid DCs (mDCs) but not plasmacytoid DCs (pDCs) was observed in the blood of SR as compared to SS asthmatics (P = .03). Glucocorticoid therapy significantly increased median B cell, but not T cell numbers in both cohorts, with a trend for increased numbers of Foxp3+ Tregs in SS (P = .07), but not SR subjects. Oral prednisolone therapy significantly reduced the median numbers and frequencies of total DCs and pDCs in both SS and SR asthmatics. Interestingly, the expression of HLA‐DR and ILT3 was also reduced on pDCs in all patients. In contrast, therapy increased the median frequency of mDCs in SS, but reduced it in SR asthmatics.ConclusionsMyeloid DC frequency is elevated in SR compared with SS asthmatics, and mDC shows a differential response to oral prednisolone therapy.
Magnesium boosts the memory restorative effect of environmental enrichment in Alzheimer's disease mice
Authors: Huang Ying , Huang Xian , Zhang Ling , Han Fang , Pang Ke‐Liang , Li Xue , Shen Jian‐Ying 
Published: November 2017

SummaryBackgroundEnvironmental enrichment (EE) has been shown to enhance cognitive function in mouse models of Alzheimer's disease (AD). Magnesium‐L‐threonate (MgT) is a compound with a newly discovered effect to rescue learning and memory function in aging and AD mice.AimTo study the additive therapeutic effect of EE combined with MgT (EM) and the potential mechanism underlying the effects.Materials and MethodsAPP/PS1 mice were treated with EE, MgT, or combination of EE and MgT (EM) and compared for restored memory function.ResultsEM was more effective in improving cognition and spatial memory than either treatment alone in either long‐term (12 months, started at 3 months old, which was before disease manifestation) or short‐term (3 months, started at 6 months old, which was after disease manifestation) treatment. The behavioral improvement has coincided with rescue of synaptic contacts in the hippocampal region of the AD mouse brain. Immunoblots also showed that EM but neither single treatment rescued the activity reduction in CaMKII and CREB, two important downstream molecules in the N‐methyl‐D‐aspartate receptor (NMDAR) pathway.ConclusionEnvironmental enrichment and MgT may synergistically improve recognition and spatial memory by reducing synaptic loss and restoring the NMDAR signaling pathway in AD mice, which suggests that combination of EE and MgT may be a novel therapeutic strategy for AD.
The Akkermansia muciniphila is a gut microbiota signature in psoriasis
Authors: Tan LiRong , Zhao Shuang , Zhu Wu , Wu Lisha , Li Jie , Shen MinXue , Lei Li , Chen Xiang , Peng Cong 
Published: November 2017

AbstractPsoriasis is an immune‐mediated chronic inflammatory skin disease. Although its pathogenesis is not fully understood, Th17 cells and the cytokines they produce, such as IL‐17, IL‐22 and IL‐23, play critical roles in the pathogenesis of psoriasis. Evidence has demonstrated that psoriasis has some common features, including immune responses (due to Th17 cells) and inflammatory cytokine profiles, with systematic diseases including inflammatory bowel diseases (IBDs) and obesity. Recently, studies have demonstrated that the gut microbiota plays a crucial role in host homoeostasis and immune response, particular in Th17 cells, but the role of the gut microbiota in psoriasis remains unclear. To study the relationship between gut microbiota and psoriasis, we analysed microbiota profiles in psoriasis using a 16S rDNA sequencing platform, and we found that the abundance of Akkermansia muciniphila was significantly reduced in patients with psoriasis. A. muciniphila is believed to have an important function in the pathogenesis of IBD and obesity; therefore, A. muciniphila, which is an indicator of health status, may be a key node for psoriasis as well as IBD and obesity. Taken together, our study identified that gut microbiota signature and function are significantly altered in the gut of patients with psoriasis, which provides a novel angle to understanding the pathogenesis of psoriasis.