bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevalence and clinical characteristics of CMV coinfection among HIV infected individuals in Guinea‐Bissau: a cross‐sectional study
Authors: Grønborg Helene L. , Jespersen Sanne , Egedal Johanne H. , Correia Faustino G. , Medina Candida , Krarup Henrik , Hønge Bo L. , Wejse Christian ,   the Bissau HIV Cohort Study Group
Published: May 2018

AbstractObjectivesTo describe the prevalence of CMV in a cohort of HIV infected individuals in Guinea‐Bissau, West Africa and to evaluate differences in patients’ clinical characteristics associated with their CMV status.MethodsNewly diagnosed HIV infected adults were invited to participate in this cross‐sectional study, from May until December 2015. Enrolled patients were interviewed and underwent a full physical examination focusing on CMV disease manifestations. Blood samples were analysed for CMV serology, QuantiFERON‐CMV response and CMV DNA. Mortality follow‐up were registered for one year after inclusion.ResultsIn total, 180 patients were enrolled. Anti‐CMV IgG positivity was found in 100% (138/138) and 2.8% (4/138) were anti‐CMV IgM positive. A positive QuantiFERON‐CMV response was found in 85.7% (60/70) of the patients and 60.6% (83/137) had CMV viraemia. QuantiFERON‐CMV response and detectable CMV DNA were associated with lower CD4 cell count, older age and upper gastrointestinal complaints. During one year of follow‐up, the IRR for death among CMV DNA positive patients was 1.5 (P = 0.5).ConclusionsCMV coinfection was detected among all enrolled patients and CMV viraemia was highly prevalent. Only age and upper gastrointestinal complaints were associated with the patients’ CMV status.
Naturally acquired IgG antibodies to thrombospondin‐related anonymous protein of Plasmodium vivax (PvTRAP) in Thailand predominantly elicit immunological cross‐reactivity
Authors: Kosuwin Rattiporn , Feng Meng , Makiuchi Takashi , Putaporntip Chaturong , Tachibana Hiroshi , Jongwutiwes Somchai 
Published: May 2018

AbstractBackgroundThrombospondin‐related anonymous protein (TRAP) is a prime candidate for a malaria vaccine. Antibodies to Plasmodium vivax TRAP (PvTRAP) occur upon natural infection while specific antigenic domains remain to be addressed.MethodsThe PvTRAP sequences were determined from 73 P. vivax isolates from Tak and Ubon Ratchathani provinces collected in 2013. The recombinant proteins representing four variants each for domain II (A domain) and domain IV (thrombospondin repeat region) of PvTRAP circulating in these areas were used as antigens in enzyme‐linked immunosorbent assay against 246 serum samples from P. vivax‐infected patients in both provinces collected during 2013 and 2014.ResultsThe prevalence of total IgG antibodies to at least one variant antigen of domain II and domain IV was 63.8% and 71.5%, respectively. Differential IgG antibody responses to these variant antigens of each domain were observed. Total IgG antibody responses to the variant antigens of each domain upon pairwise comparisons were highly correlated, suggesting immunological cross‐reactivity in the majority of serum samples. A smaller proportion of serum samples contained non‐cross‐reactive antibodies to variants of each domain; particularly domain II in which amino acid differences significantly influenced antibody recognition. Previous malaria exposure positively affected antibody responses to domain IV. Positive seroconversion and rising antibody titres occurred within a few weeks after resolution of infections.ConclusionsBoth domains II and IV are targets of naturally acquired IgG antibodies. Despite sequence variation in these domains, most antibody responses were cross‐reactive. A cross‐sectional evaluation of antibodies to PvTRAP during acute infection could underestimate the seroprevalence.
Reviewer Acknowledgements
Authors: Smith Robert 
Published: May 2018

Journal of Education and Training Studies (JETS) would like to acknowledge the following reviewers for their assistance with peer review of manuscripts for this issue. Many authors, regardless of whether JETS publishes their work, appreciate the helpful feedback provided by the reviewers. Their comments and suggestions were of great help to the authors in improving the quality of their papers. Each of the reviewers listed below returned at least one review for this issue.Reviewers for Volume 6, Number 6 Brenda L. Shook, National University, USACagla Atmaca, Pamukkale University, TurkeyChris Prince Udochukwu Njoku, University of Nigeria, NigeriaErica D. Shifflet-Chila, Michigan State University, USAErkut Tutkun, Uludağ University, TurkeyFahrettin Sanal, Necmettin Erbakan University, TurkeyIntakhab Khan, King Abdulaziz University, Saudi ArabiaJohn Bosco Azigwe, Bolgatanga Polytechnic, GhanaKun-Hsi Liao, Taiwan Shoufu University, TaiwanMeral Seker, Alanya Alaaddin Keykubat University, TurkeyMin Gui, Wuhan University, ChinaOzgur Demirtas, Inonu University, TurkeyOzkan Kırmızı-Karabuk University, TurkeyRichard H. Martin, Mercer University, USASandro Sehic, Oneida BOCES, USAŞerife Vatansever, Uludağ University, TurkeyStamatis Papadakis, University of Crete, GreeceYeliz Doğru, İzmir Katip Çelebi University, Turkey Robert SmithEditorial AssistantOn behalf of,The Editorial Board of Journal of Education and Training StudiesRedfame Publishing9450 SW Gemini Dr. #99416Beaverton, OR 97008, USAURL: http://jets.redfame.com
Proposing Kluyvera georgiana as the Origin of the Plasmid-Mediated Resistance Gene
fosA4
Authors: Rodriguez Maria Margarita , Ghiglione Barbara , Power Pablo , Naas Thierry , Gutkind Gabriel 
Published: May 2018

ABSTRACT

A putative
fosA
gene in
Kluyvera georgiana
14751 showed 99% nucleotide identity with plasmid-encoded
fosA4
. Due to a single-nucleotide insertion translating to a truncated protein,
K. georgiana
14751
fosA
does not confer fosfomycin resistance. However, analysis of another genome deposit (
Kluyvera ascorbata
WCH1410) that could be recategorized as
K. georgiana
after phylogenetic analysis revealed a
fosA
gene 100% identical to the plasmid-borne
fosA4
gene. We suggest that
Kluyvera georgiana
represents the most probable origin of
fosA4
.
Immunomodulatory innate defence regulator (IDR) peptide alleviates airway inflammation and hyper-responsiveness
Authors: Piyadasa Hadeesha , Hemshekhar Mahadevappa , Altieri Anthony , Basu Sujata , van der Does Anne M , Halayko Andrew J , Hiemstra Pieter S , Mookherjee Neeloffer 
Published: May 2018

BackgroundExacerbation in asthma is associated with decreased expression of specific host defence peptides (HDPs) in the lungs. We examined the effects of a synthetic derivative of HDP, innate defence regulator (IDR) peptide IDR-1002, in house dust mite (HDM)-challenged murine model of asthma, in interleukin (IL)-33-challenged mice and in human primary bronchial epithelial cells (PBECs).MethodsIDR-1002 (6 mg/kg per mouse) was administered (subcutaneously) in HDM-challenged and/or IL-33-challenged BALB/c mice. Lung function analysis was performed with increasing dose of methacholine by flexiVent small animal ventilator, cell differentials in bronchoalveolar lavage performed by modified Wright-Giemsa staining, and cytokines monitored by MesoScale Discovery assay and ELISA. PBECs stimulated with tumour necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ), with or without IDR-1002, were analysed by western blots.ResultsIDR-1002 blunted HDM challenge-induced airway hyper-responsiveness (AHR), and lung leucocyte accumulation including that of eosinophils and neutrophils, in HDM-challenged mice. Concomitantly, IDR-1002 suppressed HDM-induced IL-33 in the lungs. IFN-γ/TNF-α-induced IL-33 production was abrogated by IDR-1002 in PBECs. Administration of IL-33 in HDM-challenged mice, or challenge with IL-33 alone, mitigated the ability of IDR-1002 to control leucocyte accumulation in the lungs, suggesting that the suppression of IL-33 is essential for the anti-inflammatory activity of IDR-1002. In contrast, the peptide significantly reduced either HDM, IL-33 or HDM+IL-33 co-challenge-induced AHR in vivo.ConclusionThis study demonstrates that an immunomodulatory IDR peptide controls the pathophysiology of asthma in a murine model. As IL-33 is implicated in steroid-refractory severe asthma, our findings on the effects of IDR-1002 may contribute to the development of novel therapies for steroid-refractory severe asthma.
Vaping versus JUULing: how the extraordinary growth and marketing of JUUL transformed the US retail e-cigarette market
Authors: Huang Jidong , Duan Zongshuan , Kwok Julian , Binns Steven , Vera Lisa E , Kim Yoonsang , Szczypka Glen , Emery Sherry L 
Published: May 2018

Background
While national surveys showed declines in e-cigarette use in the USA between 2015 and 2016, recent reports indicate that JUUL, a sleekly designed e-cigarette that looks like a USB drive, is increasingly being used by youth and young adults. However, the extent of JUUL’s growth and its marketing strategy have not been systematically examined.

Methods
A variety of data sources were used to examine JUUL retail sales in the USA and its marketing and promotion. Retail store scanner data were used to capture the retail sales of JUUL and other major e-cigarette brands for the period 2011–2017. A list of JUUL-related keywords was used to identify JUUL-related tweets on Twitter; to identify JUUL-related posts, hashtags and accounts on Instagram and to identify JUUL-related videos on YouTube.

Results
In the short 3-year period 2015–2017, JUUL has transformed from a little-known brand with minimum sales into the largest retail e-cigarette brand in the USA, lifting sales of the entire e-cigarette category. Its US$150 million retail sales in the last quarter of 2017 accounted for about 40% of e-cigarette retail market share. While marketing expenditures for JUUL were moderate, the sales growth of JUUL was accompanied by a variety of innovative, engaging and wide-reaching campaigns on Twitter, Instagram and YouTube, conducted by JUUL and its affiliated marketers.

Conclusions
The discrepancies between e-cigarette sales data and the prevalence of e-cigarette use from surveys highlight the challenges in tracking and understanding the use of new and emerging tobacco products. In a rapidly changing media environment, where successful and influential marketing campaigns can be conducted on social media at little cost, marketing expenditures alone may not fully capture the influence, reach and engagement of tobacco marketing.
Mature enteroendocrine cells contribute to basal and pathological stem cell dynamics in the small intestine
Authors: Sei Yoshitatsu , Feng Jianying , Samsel Leigh , White Ayla , Zhao Xilin , Yun Sajung , Citrin Deborah , McCoy J. Philip , Sundaresan Sinju , Hayes Michael M. , Merchant Juanita L. , Leiter Andrew , Wank Stephen A. 
Published: May 2018

Lgr5-expressing intestinal stem cells (ISCs) maintain continuous and rapid generation of the intestinal epithelium. Here, we present evidence that dedifferentiation of committed enteroendocrine cells (EECs) contributes to maintenance of the epithelium under both basal conditions and in response to injury. Lineage-tracing studies identified a subset of EECs that reside at +4 position for more than 2 wk, most of which were BrdU-label-retaining cells. Under basal conditions, cells derived from these EECs grow from the bottom of the crypt to generate intestinal epithelium according to neutral drift kinetics that is consistent with dedifferentiation of mature EECs to ISCs. The lineage tracing of EECs demonstrated reserve stem cell properties in response to radiation-induced injury with the generation of reparative EEC-derived epithelial patches. Finally, the enterochromaffin (EC) cell was the predominant EEC type participating in these stem cell dynamics. These results provide novel insights into the +4 reserve ISC hypothesis, stem cell dynamics of the intestinal epithelium, and in the development of EC-derived small intestinal tumors.NEW & NOTEWORTHY The current manuscript demonstrating that a subset of mature enteroendocrine cells (EECs), predominantly enterochromaffin cells, dedifferentiates to fully functional intestinal stem cells (ISCs) is novel, timely, and important. These cells dedifferentiate to ISCs not only in response to injury but also under basal homeostatic conditions. These novel findings provide a mechanism in which a specified cell can dedifferentiate and contribute to normal tissue plasticity as well as the development of EEC-derived intestinal tumors under pathologic conditions.
miR-155 accelerates proliferation of mouse hepatocytes during liver regeneration by directly targeting SOCS1
Authors: Lin Xia , Chen Li , Li Haiyan , Liu Yu , Guan Yanhong , Li Xiaoyan , Jia Zhenchang , Lin Xiaolin , Jia Junshuang , Sun Yan , Xiao Dong 
Published: May 2018

Liver regeneration after two-thirds partial hepatectomy (PH) is a clinically significant repair process for restoring proper liver architecture. Although microRNA-155 (miR-155) has been found to serve as a crucial microRNA regulator that controls liver cell function and proliferation, little is known about its specific role in the regenerating liver. Using a mouse model with miR-155 overexpression or miR-155 knockout, we investigated the molecular mechanisms of miR-155 in liver regeneration. We found a marked induction of miR-155 in C57BL/6 mice after PH. Furthermore, RL-m155 mice showed enhanced liver regeneration as a result of accelerated progression of hepatocytes into the cell cycle, mainly through an increase in cyclin levels. However, proliferation of hepatocytes was delayed in miR-155-deficient livers. Expression of suppressor of cytokine signaling 1 (SOCS1) was dramatically downregulated in the process of liver regeneration, and enhancement of SOCS1 contributed to impaired proliferation of hepatocytes. Additionally, in vitro and in vivo experiments showed that adenovirus- or adeno-associated virus-mediated overexpression of SOCS1 attenuated improved liver regeneration induced by miR-155 overexpression. Our study shows that miR-155 is a pro-proliferative regulator in liver regeneration by facilitating the cell cycle and directly targeting SOCS1. NEW & NOTEWORTHY Our findings suggest a microRNA-155 (miR-155)-mediated positive regulation pattern in liver regeneration. A series of in vivo and in vitro studies showed that miR-155 upregulation enhanced partial hepatectomy-induced proliferation of hepatocytes by promoting the cell cycle without inducing DNA damage or apoptosis. Suppressor of cytokine signaling 1, a target gene of miR-155, antagonized the proliferation-promoting effect of miR-155. Therefore, pharmacological intervention targeting miR-155 may be therapeutically beneficial in various liver diseases.
An enhancedLactobacillus reuteribiofilm formulation that increases protection against experimental necrotizing enterocolitis
Authors: Olson Jacob K. , Navarro Jason B. , Allen Jacob M. , McCulloh Christopher J. , Mashburn-Warren Lauren , Wang Yijie , Varaljay Vanessa A. , Bailey Michael T. , Goodman Steven D. , Besner Gail E. 
Published: May 2018

One significant drawback of current probiotic therapy for the prevention of necrotizing enterocolitis (NEC) is the need for at least daily administration because of poor probiotic persistence after enteral administration, increasing the risk of the probiotic bacteria causing bacteremia or sepsis if the intestines are already compromised. We previously showed that the effectiveness of Lactobacillus reuteri ( Lr) in preventing NEC is enhanced when Lr is grown as a biofilm on the surface of dextranomer microspheres (DM). Here we sought to test the efficacy of Lr administration by manipulating the Lr biofilm state with the addition of biofilm-promoting substances (sucrose and maltose) to DM or by mutating the Lr gtfW gene (encoding an enzyme central to biofilm production). Using an animal model of NEC, we determined that Lr adhered to sucrose- or maltose-loaded DM significantly reduced histologic injury, improved host survival, decreased intestinal permeability, reduced intestinal inflammation, and altered the gut microbiome compared with Lr adhered to unloaded DM. These effects were abolished when DM or GtfW were absent from the Lr inoculum. This demonstrates that a single dose of Lr in its biofilm state decreases NEC incidence. Importantly, preloading DM with sucrose or maltose further enhances Lr protection against NEC in a GtfW-dependent fashion, demonstrating the tunability of the approach and the potential to use other cargos to enhance future probiotic formulations.NEW & NOTEWORTHY Previous clinical trials of probiotics to prevent necrotizing enterocolitis have had variable results. In these studies, probiotics were delivered in their planktonic, free-living form. We have developed a novel probiotic delivery system in which Lactobacillus reuteri (Lr) is delivered in its biofilm state. In a model of experimental necrotizing enterocolitis, this formulation significantly reduces intestinal inflammation and permeability, improves survival, and preserves the natural gut microflora compared with the administration of Lr in its free-living form.
Expression of lysophosphatidic acid receptor 5 is necessary for the regulation of intestinal Na+/H+ exchanger 3 by lysophosphatidic acid in vivo
Authors: Jenkin Kayte A. , He Peijian , Yun C. Chris 
Published: May 2018

Lysophosphatidic acid (LPA) is a bioactive lipid molecule, which regulates a broad range of pathophysiological processes. Recent studies have demonstrated that LPA modulates electrolyte flux in the intestine, and its potential as an antidiarrheal agent has been suggested. Of six LPA receptors, LPA5 is highly expressed in the intestine. Recent studies by our group have demonstrated activation of Na+/H+ exchanger 3 (NHE3) by LPA5. However, much of what has been elucidated was achieved using colonic cell lines that were transfected to express LPA5. In the current study, we engineered a mouse that lacks LPA5 in intestinal epithelial cells, Lpar5ΔIEC, and investigated the role of LPA5 in NHE3 regulation and fluid absorption in vivo. The intestine of Lpar5ΔIEC mice appeared morphologically normal, and the stool frequency and fecal water content were unchanged compared with wild-type mice. Basal rates of NHE3 activity and fluid absorption and total NHE3 expression were not changed in Lpar5ΔIEC mice. However, LPA did not activate NHE3 activity or fluid absorption in Lpar5ΔIEC mice, providing direct evidence for the regulatory role of LPA5. NHE3 activation involves trafficking of NHE3 from the terminal web to microvilli, and this mobilization of NHE3 by LPA was abolished in Lpar5ΔIEC mice. Dysregulation of NHE3 was specific to LPA, and insulin and cholera toxin were able to stimulate and inhibit NHE3, respectively, in both wild-type and Lpar5ΔIEC mice. The current study for the first time demonstrates the necessity of LPA5 in LPA-mediated stimulation of NHE3 in vivo. NEW & NOTEWORTHY This study is the first to assess the role of LPA5 in NHE3 regulation and fluid absorption in vivo using a mouse that lacks LPA5 in intestinal epithelial cells, Lpar5ΔIEC. Basal rates of NHE3 activity and fluid absorption, and total NHE3 expression were not changed in Lpar5ΔIEC mice. However, LPA did not activate NHE3 activity or fluid absorption in Lpar5ΔIEC mice, providing direct evidence for the regulatory role of LPA5.
Inflammation-related differences in mucosa-associated microbiota and intestinal barrier function in colonic Crohn’s disease
Authors: Libertucci Josie , Dutta Usha , Kaur Sandeep , Jury Jennifer , Rossi Laura , Fontes Michelle E. , Shajib M. Sharif , Khan Waliul I. , Surette Michael G. , Verdu Elena F. , Armstrong David 
Published: May 2018

Crohn’s disease (CD), characterized by discontinuous intestinal injury and inflammation, has been associated with changes in luminal microbial composition and impaired barrier function. The relationships between visual features of intestinal injury, permeability, and the mucosa-associated microbiota are unclear. Individuals undergoing routine colonoscopy (controls) and patients with CD were evaluated by clinical parameters and confocal laser scanning endomicroscopic colonoscopy (CLE). Patients with CD were categorized as either CD with no injury (CD-NI) or CD with injury (CD-I). Colonic biopsies were taken from adjacent matched sites in all individuals, and CLE images from these sites were analyzed for vascular permeability. Microbial composition was evaluated by 16S rRNA gene sequencing of the V3 region, and the mycome was identified through internal transcribed spacer 2 sequencing. Subgroup analyses were performed for histology, paracellular permeability (Ussing chamber), and encroachment of bacteria (fluorescent in situ hybridization). CD-I patients showed an altered microbial community compared with both controls and CD-NI patients, with enrichment in Escherichia and a decrease in Firmicutes, including Lachnospira, Faecalibacterium, and Blautia. In CD-I patients, bacterial encroachment to host epithelial cells was greater in sites of injury than in matched biopsy sites. Biopsies from sites of injury also demonstrated greater vascular and paracellular permeability. Overall, CD-I patients showed an altered mucosal microbial community compared with CD-NI patients and controls. Matched biopsy samples in CD-I patients revealed that sites of injury, identified endoscopically, are characterized by increased encroachment of bacteria to host epithelial cells, associated with increased paracellular and vascular permeability, which may drive inflammation in CD.NEW & NOTEWORTHY Patients with Crohn’s disease (CD) with areas of colonic injury have an altered microbial community compared with patients who have no endoscopic evidence of injury or active disease. Although matched biopsies from patients with colonic injury show no differences in the mucosa-associated microbiota, injured sites are associated with increased permeability and increased encroachment. Our results support the notion that dysbiotic communities within patients with colonic injury cause or permit disruption of the mucosal and endothelial layers in CD.