bluuebunny/crossref_metadata_2025_split huggingface dataset:
Examination time as a quality indicator of screening upper gastrointestinal endoscopy for asymptomatic examinees
Authors: Kawamura Takuji , Wada Hironori , Sakiyama Naokuni , Ueda Yuki , Shirakawa Atsushi , Okada Yusuke , Sanada Kasumi , Nakase Kojiro , Mandai Koichiro , Suzuki Azumi , Kamaguchi Mai , Morita Atsuhiro , Nishioji Kenichi , Tanaka Kiyohito , Mochizuki Naomi , Uno Koji , Yokota Isao , Kobayashi Masao , Yasuda Kenjiro 
Published: January 2017

Background and AimThe significance of examination time of esophagogastroduodenoscopy (EGD) for asymptomatic examinees is yet to be established. We aimed to clarify whether endoscopists who allot more examination time can detect higher numbers of neoplastic lesions among asymptomatic examinees.MethodsWe reviewed a database of consecutive examinees who underwent EGD in our hospital from April 2010 to September 2015. Staff endoscopists were classified into fast, moderate, and slow groups based on the mean examination time of EGD without a biopsy. Neoplastic lesion detection rate among these groups was compared using multiple logistic regression.ResultsOf the 55 786 consecutive examinees who underwent EGD, 15 763 asymptomatic examinees who were screened by staff doctors were analyzed. Mean examination time of 13 661 EGD without biopsy was 6.2 min (range, 2–18 min). When cut‐off times of 5 and 7 min were used, four endoscopists were classified into the fast (mean duration, 4.4 ± 1.0 min), 12 into the moderate (6.1 ± 1.4 min), and four into the slow (7.8 ± 1.9 min) groups. Neoplastic lesion detection rates in the fast, moderate, and slow groups were 0.57% (13/2288), 0.97% (99/10 180), and 0.94% (31/3295), respectively. Compared with that in the fast group, odds ratios for the neoplastic lesion detection rate in the moderate and slow groups were 1.90 (95% confidence interval [CI], 1.06–3.40) and 1.89 (95% CI, 0.98–3.64), respectively.ConclusionEndoscopists who do not allot adequate examination time may overlook neoplastic lesions in the upper gastrointestinal tract.
Mechanisms of the prevention and inhibition of the progression and development of non‐alcoholic steatohepatitis by genetic and pharmacological decoy receptor 3 supplementation
Authors: Lee Pei‐Chang , Yang Ling‐Yu , Wang Ying‐Wen , Huang Shiang‐Fen , Lee Kuei‐Chuan , Hsieh Yun‐Cheng , Yang Ying‐Ying , Hsieh Shie‐Liang , Hou Ming‐Chih , Lin Han‐Chieh , Lee Fa‐Yuah , Lee Shou‐Dong 
Published: January 2017

AimsTreatment of non‐alcoholic steatohepatitis (NASH) is difficult due to the absence of a proven treatment and its comprehensive mechanisms. In the NASH animal model, upregulated hepatic inflammation and oxidative stress, with the resultant M1 polarization of macrophages as well as imbalanced adipocytokines, all accelerate NASH progression. As a member of the tumor necrosis factor receptor superfamily, decoy receptor 3 (DcR3) not only neutralizes the death ligands, but also performs immune modulations. In this study, we aimed to investigate the possible non‐decoy effects of DcR3 on diet‐induced NASH mice.MethodsMethionine‐ and choline‐deficient (MCD) diet feeding for 9 weeks was applied to induce NASH in BALB/c mice. Decoy receptor 3 heterozygous transgenesis or pharmacological pretreatment with DcR3a for 1 month were designed as interventions. Intrahepatic inflammatory status as well as macrophage polarization, oxidative stress, and steatosis as well as lipogenic gene expression and fibrotic status were analyzed. Additionally, acute effects of DcR3a on HepG2 cells, Hep3B cells, and primary mouse hepatocytes in various MCD medium‐stimulated changes were also evaluated.ResultsBoth DcR3 genetic and pharmacologic supplement significantly reduced MCD diet‐induced hepatic M1 polarization. In addition, DcR3 supplement attenuated MCD diet‐increased hepatic inflammation, oxidative stress, adipocytokine imbalance, steatosis, and fibrogenesis. Moreover, acute DcR3a incubation in HepG2 cells, Hep3B cells, and mouse hepatocytes could normalize the expression of genes related to lipid oxidation along with inflammation and oxidative stress.ConclusionThe ability of DcR3 to attenuate hepatic steatosis and inflammation through its non‐decoy effects of immune modulation and oxidative stress attenuation makes it a potential treatment for NASH.
A role for the histone H2A deubiquitinase MYSM1 in maintenance of CD8+ T cells
Authors: Förster Michael , Boora Rupinder K. , Petrov Jessica C. , Fodil Nassima , Albanese Isabella , Kim Jamie , Gros Philippe , Nijnik Anastasia 
Published: January 2017

SummarySeveral previous studies outlined the importance of the histone H2A deubiquitinase MYSM1 in the regulation of stem cell quiescence and haematopoiesis. In this study we investigated the role of MYSM1 in T‐cell development. Using mouse models that allow conditional Mysm1 ablation at late stages of thymic development, we found that MYSM1 is intricately involved in the maintenance, activation and survival of CD8+ T cells. Mysm1 ablation resulted in a twofold reduction in CD8+ T‐cell numbers, and also led to a hyperactivated CD8+ T‐cell state accompanied by impaired proliferation and increased pro‐inflammatory cytokine production after ex vivo stimulation. These phenotypes coincided with an increased apoptosis and preferential up‐regulation of p53 tumour suppressor protein in CD8+ T cells. Lastly, we examined a model of experimental cerebral malaria, in which pathology is critically dependent on CD8+ T cells. In the mice conditionally deleted for Mysm1 in the T‐cell compartment, CD8+ T‐cell numbers remained reduced following infection, both in the periphery and in the brain, and the mice displayed improved survival after parasite challenge. Collectively, our data identify MYSM1 as a novel factor for CD8+ T cells in the immune system, increasing our understanding of the role of histone H2A deubiquitinases in cytotoxic T‐cell biology.
CHILD CARE PRICES AND MATERNAL EMPLOYMENT: A META‐ANALYSIS
Authors: Akgunduz Yusuf Emre , Plantenga Janneke 
Published: January 2017

AbstractThe literature estimates for labor force participation elasticity with regard to child care prices are extensive and varying. While some estimates imply substantial gains from child care subsidies, others find insignificant effects. To determine the causes of the variance, this paper reviews and analyzes the elasticity sizes using estimates from 36 peer‐reviewed articles and working papers in the literature. We start by reviewing the theoretical and empirical aspects related to participation elasticity with regard to child care costs, paying special attention to sample characteristics, methodological aspects, and macro level factors. We conclude by providing a meta‐regression using control variables based on our review of the literature to explain some of the differences between the estimates. As research builds on and improves the methods and assumptions in prior works, elasticity estimates have become smaller over time. This decline might also be partially explained by changes in labor market characteristics. In countries with high rates of part‐time work and very high or very low rates of female labor force participation, we find elasticity rates to be smaller.
Providing More but Receiving Less: Daughters in Intergenerational Exchange in Mainland China
Authors: Hu Anning 
Published: January 2017

AbstractThis study investigates the gender pattern of both downstream and upstream transfers between older parents and their children in China. Based on theories about the generation gap in the understandings of family norm and the heterogeneous effects of the social forces that encourage women to contribute more in elder care by generation, the author proposes a gender asymmetrical pattern in which the patrilineal norm governs parents' decisions of downstream transfers but exerts little effect on children's upstream support for parents. Capitalizing on a survey of the population older than 60 years, the author fitted several simultaneous equation models. Empirical results suggest that, all being equal, daughters provide more monetary and housework assistance to older parents than do sons, but daughters are comparatively disadvantaged in the probability of receiving either type of transfer from their parents. The pattern of “providing more but receiving less” for female caregivers affirms the gender asymmetrical pattern.
Two CYP716A subfamily cytochrome P450 monooxygenases of sweet basil play similar but nonredundant roles in ursane‐ and oleanane‐type pentacyclic triterpene biosynthesis
Authors: Misra Rajesh Chandra , Sharma Shubha , Sandeep  , Garg Anchal , Chanotiya Chandan Singh , Ghosh Sumit 
Published: January 2017

Summary

The medicinal plant sweet basil (Ocimum basilicum) accumulates bioactive ursane‐ and oleanane‐type pentacyclic triterpenes (PCTs), ursolic acid and oleanolic acid, respectively, in a spatio‐temporal manner; however, the biosynthetic enzymes and their contributions towards PCT biosynthesis remain to be elucidated.

Two CYP716A subfamily cytochrome P450 monooxygenases (CYP716A252 and CYP716A253) are identified from a methyl jasmonate‐responsive expression sequence tag collection and functionally characterized, employing yeast (Saccharomyces cerevisiae) expression platform and adapting virus‐induced gene silencing (VIGS) in sweet basil.

CYP716A252 and CYP716A253 catalyzed sequential three‐step oxidation at the C‐28 position of α‐amyrin and β‐amyrin to produce ursolic acid and oleanolic acid, respectively. Although CYP716A253 was more efficient than CYP716A252 for amyrin C‐28 oxidation in yeast, VIGS revealed essential roles for both of these CYP716As in constitutive biosynthesis of ursolic acid and oleanolic acid in sweet basil leaves. However, CYP716A253 played a major role in elicitor‐induced biosynthesis of ursolic acid and oleanolic acid.

Overall, the results suggest similar as well as distinct roles of CYP716A252 and CYP716A253 for the spatio‐temporal biosynthesis of PCTs. CYP716A252 and CYP716A253 might be useful for the alternative and sustainable production of PCTs in microbial host, besides increasing plant metabolite content through genetic modification.
Fourier Transform Infrared Imaging analysis of dental pulp inflammatory diseases
Authors: Giorgini E , Sabbatini S , Conti C , Rubini C , Rocchetti R , Fioroni M , Memè L , Orilisi G 
Published: January 2017

ObjectivesFourier Transform Infrared microspectroscopy let characterize the macromolecular composition and distribution of tissues and cells, by studying the interaction between infrared radiation and matter. Therefore, we hypothesize to exploit this analytical tool in the analysis of inflamed pulps, to detect the different biochemical features related to various degrees of inflammation.Materials and MethodsIR maps of 13 irreversible and 12 hyperplastic pulpitis, together with 10 normal pulps, were acquired, compared with histological findings and submitted to multivariate (HCA, PCA, SIMCA) and statistical (one‐way ANOVA) analysis. The fit of convoluted bands let calculate meaningful band area ratios (means ± s.d., P < 0.05).ResultsThe infrared imaging analysis pin‐pointed higher amounts of water and lower quantities of type I collagen in all inflamed pulps. Specific vibrational markers were defined for irreversible pulpitis (Lipids/Total Biomass, PhII/Total Biomass, CH2/CH3, and Ty/AII) and hyperplastic ones (OH/Total Biomass, Collagen/Total Biomass, and CH3 Collagen/Total Biomass).ConclusionThe study confirmed that FTIR microspectroscopy let discriminate tissues’ biological features. The infrared imaging analysis evidenced, in inflamed pulps, alterations in tissues’ structure and composition. Changes in lipid metabolism, increasing amounts of tyrosine, and the occurrence of phosphorylative processes were highlighted in irreversible pulpitis, while high amounts of water and low quantities of type I collagen were detected in hyperplastic samples.
Parasite excretory‐secretory products and their effects on metabolic syndrome
Authors: Crowe J. , Lumb F. E. , Harnett M. M. , Harnett W. 
Published: January 2017

SummaryObesity, one of the main causes of metabolic syndrome (MetS), is an increasingly common health and economic problem worldwide, and one of the major risk factors for developing type 2 diabetes and cardiovascular disease. Chronic, low‐grade inflammation is associated with MetS and obesity. A dominant type 2/anti‐inflammatory response is required for metabolic homoeostasis within adipose tissue: during obesity, this response is replaced by infiltrating, inflammatory macrophages and T cells. Helminths and certain protozoan parasites are able to manipulate the host immune response towards a TH2 immune phenotype that is beneficial for their survival, and there is emerging data that there is an inverse correlation between the incidence of MetS and helminth infections, suggesting that, as with autoimmune and allergic diseases, helminths may play a protective role against MetS disease. Within this review, we will focus primarily on the excretory‐secretory products that the parasites produce to modulate the immune system and discuss their potential use as therapeutics against MetS and its associated pathologies.
An Evidential Reasoning‐Based CREAM to Human Reliability Analysis in Maritime Accident Process
Authors: Wu Bing , Yan Xinping , Wang Yang , Soares C. Guedes 
Published: January 2017

AbstractThis article proposes a modified cognitive reliability and error analysis method (CREAM) for estimating the human error probability in the maritime accident process on the basis of an evidential reasoning approach. This modified CREAM is developed to precisely quantify the linguistic variables of the common performance conditions and to overcome the problem of ignoring the uncertainty caused by incomplete information in the existing CREAM models. Moreover, this article views maritime accident development from the sequential perspective, where a scenario‐ and barrier‐based framework is proposed to describe the maritime accident process. This evidential reasoning‐based CREAM approach together with the proposed accident development framework are applied to human reliability analysis of a ship capsizing accident. It will facilitate subjective human reliability analysis in different engineering systems where uncertainty exists in practice.
Arteriovenous Grafts: Much Maligned But in Need of Reconsideration?
Authors: Allon Michael 
Published: January 2017

AbstractThere are substantial variations in arteriovenous fistula (AVF) use among hemodialysis patients in different countries, in different regions of the U.S., and even in different hemodialysis units within a single metropolitan area. These variations persist after adjustment for patient demographics and comorbidities, suggesting that practice patterns play a major role in determining the frequency of AVF use. These observations led to vascular access guidelines urging nephrologists and surgeons to increase AVF creation in patients with chronic kidney disease. Over the past 20 years, as clinicians have adopted these guidelines, the prevalence of AVF use in hemodialysis patients has increased substantially. At the same time, clinicians have recognized important limitations of an unwavering “Fistula First” approach. First, a substantial proportion of AVFs fail to mature even when routine preoperative vascular mapping is used, leading to prolonged catheter dependence. Second, certain patient subgroups are at high risk for AVF nonmaturation. Third, nonmaturing AVFs frequently require interventions to promote their maturation. Fourth, AVFs that require such interventions have shortened cumulative patency. Fifth, arteriovenous grafts (AVG) have several advantages over AVFs, including lower primary failure rates, fewer interventions prior to successful cannulation, and shorter duration of catheter dependence with its associated risk of bacteremia. All these observations have led nephrologists to propose an individualized approach to vascular access, with AVG being preferred in patients who initiate hemodialysis with a catheter, particularly if they are at high risk for AVF nonmaturation and have a relatively short life expectancy.
Disseminated Acanthamoeba infection in a heart transplant recipient treated successfully with a miltefosine‐containing regimen: Case report and review of the literature
Authors: Brondfield Max N. , Reid Michael J.A. , Rutishauser Rachel L. , Cope Jennifer R. , Tang Jevon , Ritter Jana M. , Matanock Almea , Ali Ibne , Doernberg Sarah B. , Hilts‐Horeczko Alexandra , DeMarco Teresa , Klein Liviu , Babik Jennifer M. 
Published: January 2017

AbstractDisseminated acanthamoebiasis is a rare, often fatal, infection most commonly affecting immunocompromised patients. We report a case involving sinuses, skin, and bone in a 60‐year‐old woman 5 months after heart transplantation. She improved with a combination of flucytosine, fluconazole, miltefosine, and decreased immunosuppression. To our knowledge, this is the first case of successfully treated disseminated acanthamoebiasis in a heart transplant recipient and only the second successful use of miltefosine for this infection among solid organ transplant recipients. Acanthamoeba infection should be considered in transplant recipients with evidence of skin, central nervous system, and sinus infections that are unresponsive to antibiotics. Miltefosine may represent an effective component of a multidrug therapeutic regimen for the treatment of this amoebic infection.
Enteric glial activity regulates secretomotor function in the mouse colon but does not acutely affect gut permeability
Authors: Grubišić Vladimir , Gulbransen Brian D. 
Published: January 2017

Key points
The role of enteric glial cell activity in the acute regulation of epithelial barrier and secretomotor functions of the intestines under physiological conditions is not clear.
We used transgenic mice to modify glial activity and found that enteric glia significantly contribute to the neurogenic ion transport while glial activity does not appear to play a major role in the acute regulation of barrier function.
The selective activation of glial activity evoked electrogenic ion transport primarily through neural pathways and was sufficient to drive electrogenic ion transport to an extent equal to the direct activation of neurogenic ion transport.
These findings provide novel insight into the cellular mechanisms that control fluid transport homeostasis in the intestine and might provide novel therapeutic avenues for functional diarrheal diseases.
AbstractEnteric glial cells are often implicated in the regulation of epithelial barrier and secretomotor functions of the intestines. But whether glial cell activity regulates these functions acutely under physiological conditions is not clear. We addressed this issue by using transgenic animal models to modify the activity of enteric glia, either reducing glial expression of connexin 43 in Sox10::CreERT2+/−/Cx43f/f mice or activating glial calcium responses in GFAP::hM3Dq mice, and tested the effects on colonic barrier function and electrogenic ion transport in Ussing chambers. We assessed neuronal‐dependent and ‐independent contributions by activating or inhibiting neurogenic activity with veratridine and tetrodotoxin, respectively. Our results show that the reduction of glial Cx43 expression in Sox10::CreERT2+/−/Cx43f/f mice significantly reduced neurogenic ion transport. The selective glial activation in tissues from GFAP::hM3Dq mice evoked electrogenic ion transport to an extent equal to the direct activation of neurogenic ion transport with veratridine and glial driven responses consisted of both tetrodotoxin‐sensitive and ‐insensitive components. The selective glial stimulation did not affect transmural ion conductance or cell‐impermeant dye flux but the baseline ion conductance was more variable in Sox10::CreERT2+/−/Cx43f/f tissues. Together, our findings show that glial activity contributes to the regulation of electrogenic ion transport in the intestine through effects on neurons and possibly direct effects on epithelial cells. However, glial activity does not appear to play a major role in the acute regulation of barrier function. These findings provide novel insight into the cellular mechanisms that control fluid transport homeostasis in the intestine.
Human Cytomegalovirus Requires Epidermal Growth Factor Receptor Signaling To Enter and Initiate the Early Steps in the Establishment of Latency in CD34
+
Human Progenitor Cells
Authors: Kim Jung Heon , Collins-McMillen Donna , Buehler Jason C. , Goodrum Felicia D. , Yurochko Andrew D. 
Published: January 2017

ABSTRACT

The establishment of human cytomegalovirus (HCMV) latency and persistence relies on the successful infection of hematopoietic cells, which serve as sites of viral persistence and contribute to viral spread. Here, using blocking antibodies and pharmacological inhibitors, we document that HCMV activation of the epidermal growth factor receptor (EGFR) and downstream phosphatidylinositol 3-kinase (PI3K) mediates viral entry into CD34
+
human progenitor cells (HPCs), resulting in distinct cellular trafficking and nuclear translocation of the virus compared to that in other immune cells, such as we have documented in monocytes. We argue that the EGFR allows HCMV to regulate the cellular functions of these replication-restricted cells via its signaling activity following viral binding. In addition to regulating HCMV entry/trafficking, EGFR signaling may also shape the early steps required for the successful establishment of viral latency in CD34
+
cells, as pharmacological inhibition of EGFR increases the transcription of lytic IE1/IE2 mRNA while curbing the expression of latency-associated UL138 mRNA. EGFR signaling following infection of CD34
+
HPCs may also contribute to changes in hematopoietic potential, as treatment with the EGFR kinase (EGFRK) inhibitor AG1478 alters the expression of the cellular hematopoietic cytokine interleukin 12 (IL-12) in HCMV-infected cells but not in mock-infected cells. These findings, along with our previous work with monocytes, suggest that EGFR likely serves as an important determinant of HCMV tropism for select subsets of hematopoietic cells. Moreover, our new data suggest that EGFR is a key receptor for efficient viral entry and that the ensuing signaling regulates important early events required for successful infection of CD34
+
HPCs by HCMV.

IMPORTANCE
HCMV establishes lifelong persistence within the majority of the human population without causing overt pathogenesis in healthy individuals. Despite this, reactivation of HCMV from its latent reservoir in the bone marrow causes significant morbidity and mortality in immunologically compromised individuals, such as bone marrow and solid organ transplant patients. Lifelong persistent infection has also been linked with the development of various cardiovascular diseases in otherwise healthy individuals. Current HCMV therapeutics target lytic replication, but not the latent viral reservoir; thus, an understanding of the molecular basis for viral latency and persistence is paramount to controlling or eliminating HCMV infection. Here, we show that the viral signalosome activated by HCMV binding to its entry receptor, EGFR, in CD34
+
HPCs initiates early events necessary for successful latent infection of this cell type. EGFR and associated signaling players may therefore represent promising targets for mitigating HCMV persistence.