bluuebunny/crossref_metadata_2025_split huggingface dataset:
Outcomes of induction of labour in nulliparous women at 38 to 39 weeks pregnancy by clinical indication: An observational study
Authors: de Vries Bradley Stephen , Barratt Alexandra , McGeechan Kevin , Tooher Jane , Wong Ebony , Phipps Hala , Gordon Adrienne , Hyett Jon Anthony 
Published: December 2018

BackgroundKnowledge of the outcomes of induction of labour for different indications is sparse.AimsTo describe the mode of birth and other outcomes for nulliparous women induced at 38–39 weeks gestational age by indication for induction of labour.Material and methodsThis was a retrospective observational study in a tertiary referral hospital, and a metropolitan teaching hospital in Sydney. The study population was nulliparous women with induction of labour at 38 or 39 completed weeks of pregnancy and a singleton, cephalic presenting baby planning a vaginal birth, from 2009 to 2016. The indication for induction of labour was classified into 12 groups. Mode of birth and other maternal and perinatal outcomes were described in each group, for women who spontaneously laboured at 38 or 39 weeks, and for women who gave birth from 40 completed weeks onward. The main outcome measure was mode of birth.ResultsThere were 3330 women with induction of labour at 38 or 39 weeks gestation. Rates of vaginal birth varied widely, ranging from 54% when the indication for induction was suspected large fetus, to 82% when the indication was suspected fetal compromise, and was 74% overall. Indications for caesarean delivery also varied by indication for induction. Among women giving birth ≥40 weeks gestational age, 75% had a vaginal birth.ConclusionsIn nulliparous women, rates of vaginal birth following induction of labour at 38 or 39 weeks gestation vary widely according to the indication for induction. These data are useful for antenatal counselling.
Immunotherapy with grass pollen tablets reduces medication dispensing for allergic rhinitis and asthma: A retrospective database study in France
Authors: Devillier Philippe , Molimard Mathieu , Ansolabehere Xavier , Bardoulat Isabelle , Coulombel Nicolas , Maurel Frédérique , Le Jeunne Philippe , Demoly Pascal 
Published: December 2018

AbstractBackgroundModerate‐to‐severe allergic rhinitis (AR) may increase the risk of developing or worsening asthma, whereas treatment of AR with subcutaneously or sublingual allergen immunotherapy (SLIT) may slow this progression.MethodsIn a retrospective real‐world analysis, prescription fulfilment data were gathered from French retail pharmacies between 1 March 2012 and 31 December 2016. Using linear regression analyses, patients having received at least two prescriptions of grass pollen SLIT tablets over at least 2 successive years were compared with control patients having received symptomatic medications only.ResultsA total of 1099 SLIT patients and 27 475 control patients were included in the main analysis. With regard to symptomatic AR medication dispensing, we observed a 50% decrease in the pre‐index/follow‐up ratio in the SLIT group, a 30% increase in the control group without age matching (P < 0.0001 vs SLIT) and a 20% increase in the control group with age matching (P < 0.0001 vs SLIT). During the follow‐up, 11 (1.8%) and 782 (5.3%) patients initiated asthma treatment in the SLIT and control groups, respectively. The relative risk of medication dispensing for new asthma was lower in the SLIT group (by 62.5% [29.1%‐80.1%] without age matching (P = 0.0025) and by 63.7% [31.5%‐80.7%] with age matching; P = 0.0018). SLIT was also associated with slower progression of asthma medication dispensing during the follow‐up period, relative to the control group (regression coefficient: −0.58 [−0.74 to 0.42] without age matching (P < 0.0001) and −0.61 [−0.76 to −0.46] with age matching; P < 0.0001).ConclusionPrescription of grass pollen SLIT tablets reduced the dispensing of AR and asthma medications in real life.
Inverted U‐shaped relationship between vitamin D and ever‐reported eczema in US adults
Authors: Wei Jia , Jaleel Tarannum , MacLeod Amanda S. , Ji John S. 
Published: December 2018

AbstractBackgroundEczema is a skin condition which affects up to 10% to 20% of people worldwide. Previous literature finds that low vitamin D levels may be a risk factor for eczema, but the association is not clear.MethodsWe used the cross‐sectional data from U.S. National Health and Nutrition Examination Survey 2005‐2006. Adults were defined as 20 years and older. The association between eczema and serum 25‐hydroxyvitamin D [25(OH)D] was estimated using multivariate logistic regression models adjusted for patient demographics, lifestyle variables, stress, and medical comorbidities. Restricted cubic spline analyses were performed to explore nonlinear relationship. We also stratified by race.ResultsA total of 3921 adults were included in the analysis. The prevalence of ever‐report of eczema was 7.94% in US adults. Reports of eczema were higher in people with higher socioeconomic status, depressive symptoms, previous history of asthma and hay fever, female, sampled in summer, and nonHispanic white. The logistic regression found higher odds ratio of eczema in vitamin D deficiency group (<50 nmol/L) compared to sufficiency group (>75 nmol/L) (OR = 1.81, 95% CI: 1.09‐3.01, P = 0.02). The spline analysis found an inverted U‐shaped relationship between eczema and serum 25(OH)D level. Eczema risk reached the highest at around 45 nmol/L, with decreasing risk in both directions away from this value. This relationship was absent in nonHispanic black population.ConclusionVitamin D is associated with reports of eczema in nonHispanic white population, but not in the nonHispanic black population in the United States.
Bacterial secretion of histamine within the gut influences immune responses within the lung
Authors: Barcik Weronika , Pugin Benoit , Brescó Marina Sabaté , Westermann Patrick , Rinaldi Arturo , Groeger David , Van Elst Dries , Sokolowska Milena , Krawczyk Krzysztof , Frei Remo , Ferstl Ruth , Wawrzyniak Marcin , Altunbulakli Can , Akdis Cezmi A. , O'Mahony Liam 
Published: December 2018

AbstractBackgroundHistamine is an important immunomodulator influencing both the innate and adaptive immune system. Certain host cells express the histidine decarboxylase enzyme (HDC), which is responsible for catalysing the decarboxylation of histidine to histamine. We and others have shown that bacterial strains can also express HDC and secrete histamine; however, the influence of bacterial‐derived histamine on the host immune responses distant to the gut is unclear.MethodsThe Escherichia coli BL21 (E coli BL21) strain was genetically modified to express the Morganella morganii (M morganii)‐derived HDC gene (E coli BL21_HTW). E coli BL21 and E coli BL21_HTW were gavaged to ovalbumin (OVA) sensitized and challenged mice to investigate the effect of bacterial‐derived histamine on lung inflammatory responses.ResultsOral administration of E coli BL21_HTW, which is able to secrete histamine, to wild‐type mice reduced lung eosinophilia and suppressed ex vivo OVA‐stimulated cytokine secretion from lung cells in the OVA respiratory inflammation mouse model. In histamine receptor 2 (H2R)‐deficient mice, administration of histamine‐secreting bacteria also reduced inflammatory cell numbers in bronchoalveolar lavage (BAL). However, the suppressive effect of bacterial‐derived histamine on BAL inflammation was lost in HDC‐deficient mice. This loss of activity was associated with increased expression of histamine degrading enzymes and reduced histamine receptor expression.ConclusionHistamine secretion from bacteria within the gut can have immunological consequences at distant mucosal sites, such as within the lung. These effects are influenced by host histamine receptor expression and the expression of histamine degrading enzymes.
Systematic review and meta‐analysis of the association between childhood physical activity and age at menarche
Authors: Calthorpe Lucia , Brage Soren , Ong Ken K. 
Published: December 2018

AbstractAimTo systematically appraise and summarise published evidence on the association between childhood physical activity (PA) and subsequent age at menarche (AAM).MethodsWe searched PubMed (1990–2018) for studies that reported the relationship between childhood PA and AAM. We performed tabular synthesis of population‐based studies and a random‐effects meta‐analysis of results of athlete/nonathlete studies.ResultsOne randomised controlled trial was identified, in which an intervention to prevent obesity reduced the likelihood of menarche during the two‐year study period (relative risk: 0.75, 95% CI: 0.66–0.87; n = 422 girls). One of five prospective cohort studies (total n = 4492) reported a significant association between self‐reported PA duration and subsequent menarche timing. Four of five historical cohort studies (total n = 89 470) reported significant associations between recalled premenarcheal PA and later AAM. Meta‐analysis across 12 athlete/nonathlete studies showed that menarche occurred 1.13 years later (95% CI: 0.80–1.47) in athletes compared to nonathletes.ConclusionThese findings suggest that AAM is a behaviourally modifiable trait. However, the quality of reported population‐based study evidence is low and estimation of the true relationship between childhood PA and AAM is likely confounded by concomitant changes in diet and lifestyle behaviours.
Cardiotrophin‐1 opposes renal fibrosis in mice: Potential prevention of chronic kidney disease
Authors: Perretta‐Tejedor Nuria , Muñoz‐Félix José M. , Düwel Annette , Quiros‐Luis Yaremi , Fernández‐Martín José L. , Morales Ana I. , López‐Hernández Francisco J. , López‐Novoa José M. , Martínez‐Salgado Carlos 
Published: December 2018

AbstractAimChronic kidney disease is characterized by tubulointerstitial fibrosis involving inflammation, tubular apoptosis, fibroblast proliferation and extracellular matrix accumulation. Cardiotrophin‐1, a member of the interleukin‐6 family of cytokines, protects several organs from damage by promoting survival and anti‐inflammatory effects. However, whether cardiotrophin‐1 participates in the response to chronic kidney injury leading to renal fibrosis is unknown.MethodsWe hypothesized and assessed the potential role of cardiotrophin‐1 in a mice model of tubulointerstitial fibrosis induced by unilateral ureteral obstruction (UUO).ResultsThree days after UUO, obstructed kidneys from cardiotrophin‐1−/− mice show higher expression of inflammatory markers IL‐1β, Cd68, ICAM‐1, COX‐2 and iNOs, higher activation of NF‐κB, higher amount of myofibroblasts and higher severity of tubular damage and apoptosis, compared with obstructed kidneys from wild‐type littermates. In a later stage, obstructed kidneys from cardiotrophin‐1−/− mice show higher fibrosis than obstructed kidneys from wild‐type mice. Interestingly, administration of exogenous cardiotrophin‐1 prevents the increased fibrosis resulting from the genetic knockout of cardiotrophin‐1 upon UUO, and supplementation of wild‐type mice with exogenous cardiotrophin‐1 further reduces the renal fibrosis induced by UUO. In vitro, renal myofibroblasts from cardiotrophin‐1−/− mice have higher collagen I and fibronectin expression and higher NF‐κB activation than wild‐type cells.ConclusionsCardiotrophin‐1 participates in the endogenous response that opposes renal damage by counteracting the inflammatory, apoptotic and fibrotic processes. And exogenous cardiotrophin‐1 is proposed as a candidate for the treatment and prevention of chronic renal fibrosis.
Letter: reduction in projected mortality or need for liver transplantation associated with bezafibrate add‐on in primary biliary cholangitis with incomplete UDCA response
Authors: Corpechot Christophe , Chazouillères Olivier , Lemoinne Sara , Rousseau Alexandra 
Published: December 2018

Linked ContentThis article is linked to Jones and Hansen, Cheung et al and Cheung et al papers. To view these articles, visit https://doi.org/10.1111/apt.13507, https://doi.org/10.1111/apt.13519 and https://doi.org/10.1111/apt.13465.
Letter: SPOSIB SB2—a Sicilian prospective observational study of IBD patients treated with infliximab biosimilar SB2
Authors: Macaluso Fabio Salvatore , Cappello Maria , Giuffrida Enrica , Fries Walter , Centritto Andrea , Privitera Antonio Carlo , Inserra Gaetano , Vassallo Roberto , Magnano Antonio , Vinci Elisa , Garufi Serena , Ventimiglia Marco , Renna Sara , Orlando Rosalba , Rizzuto Giulia , Cottone Mario , Orlando Ambrogio ,   Sicilian Network for Inflammatory Bowel Disease (SN‐IBD)
Published: December 2018

Linked ContentThis article is linked to Schmitz et al paper. To view these articles, visit https://doi.org/10.1111/apt.14453.
Condition mimicking peritoneal metastasis associated with preoperative staging laparoscopy in advanced gastric cancer
Authors: Ushimaru Yuki , Fujiwara Yoshiyuki , Shishido Yuji , Omori Takeshi , Yanagimoto Yoshitomo , Sugimura Keijirou , Moon Jeong‐Ho , Miyata Hiroshi , Yano Masahiko 
Published: December 2018

AbstractPreoperative staging laparoscopy is used to search for peritoneal dissemination or distant metastasis as part of the treatment strategy for advanced gastric cancer. We observed pseudo‐peritoneal metastasis during laparotomy in 6 of 49 patients in whom lack of peritoneal dissemination had been confirmed by preoperative staging laparoscopy. In all cases, suspected nodules were biopsied and subjected to rapid histological diagnosis. However, a definite malignant or benign diagnosis could not be obtained via a rapid histological examination during surgery. A final histological examination combined with immunohistological analysis using formalin‐fixed embedded tissues confirmed no malignancy after surgery in all cases. These rapidly growing nodules that mimic peritoneal metastasis are thought to be associated with the use of grasping forceps during staging laparoscopy. No cases have been reported in which peritoneal nodules mimicking peritoneal metastasis occurred after staging laparoscopy, and surgeons should consider this possibility in patients treated shortly after staging laparoscopy.
Pharmacogenomics research and clinical implementation in Brazil
Authors: Rodrigues‐Soares Fernanda , Suarez‐Kurtz Guilherme 
Published: December 2018

AbstractWe searched PubMed entries and the Lattes database of Brazilian Pharmacogenetics Network investigators, for pharmacogenetic/genomic (PGx) studies in the Brazilian population, focusing on the drugs and genes included in the Clinical Pharmacogenetics Implementation Consortium (CPIC) guidelines. Warfarin was the most extensively studied drug in a PGx context: a genomewide association study targeting warfarin stable dose identified significant signals in VKORC1 and CYP2C9, several PGx dosing algorithms were developed based on these and other genes, and the implications of population admixture on extrapolation of dosing recommendations in the CPIC guidelines were examined. A study in renal transplanted patients disclosed association of CYP3A5*6 and CYP3A5*7 with tacrolimus dosing, which led to addition of these variants to CYP3A5*3 in the CPIC tacrolimus guideline. Studies verified predisposition of HIV‐positive carriers of UGT1A1*28 to severe atazanavir‐induced hyperbilirubinaemia, intolerance to 5‐fluorouracyl in gastrointestinal cancer patients with deleterious DPYD variants, failure of HCV‐infected carriers of IFNL3 rs12979860 to obtain a sustained viral response to PEG‐IFN‐α, and hypersensitivity reactions to abacavir in HIV‐positive carriers of HLA‐B*57:01. No prospective analyses of drug therapy outcomes or cost‐effectiveness assessments of PGx‐guided therapy were found. In conclusion, the limited adoption of PGx‐informed drug prescription in Brazil reflects combination of recognized barriers to PGx implementation worldwide plus factors specific to the Brazilian population. The latter include rarity/absence of genetic variants on which international PGx guidelines are based (eg HLA‐B*15.02 for phenytoin and carbamazepine) and the caveat of extrapolating to the admixed Brazilian population, guidelines based on categorical variables, such as continental ancestry (eg warfarin guidelines), “race” or ethnicity.
Is Job Insecurity Higher in Leveraged Buyouts?
Authors: Bacon Nick , Hoque Kim , Wright Mike 
Published: December 2018

AbstractThis article assesses whether job insecurity is higher in leveraged buyouts (LBOs) than elsewhere. It draws on matched employer‐employee data from the British 2011 Workplace Employment Relations Study linked to data from the Centre for Management Buyout Research. The analysis finds no consistent evidence of higher job insecurity in LBOs as measured by workforce reduction practices (redundancy rates, job security/no‐compulsory redundancies policies and redundancy consultation), dismissal rates, labour use practices (non‐permanent employment contracts and outsourcing) and employees’ job security perceptions. Job insecurity is no higher in either current or former LBOs than elsewhere. Contrary to what might be expected, it is also no higher in private equity (PE)‐backed LBOs, management buy‐ins or high‐debt LBOs and there is only partial and weak evidence of higher job insecurity in short‐hold LBOs. Job insecurity is also no higher in perfect storm LBOs (PE‐backed management buy‐ins that are short‐holds with high‐debt). Concerns over the negative implications of LBOs for job security thus appear misplaced.
Recent advances in the histo‐molecular pathology of human prion disease
Authors: Baiardi Simone , Rossi Marcello , Capellari Sabina , Parchi Piero 
Published: December 2018

AbstractPrion diseases are progressive neurodegenerative disorders affecting humans and other mammalian species. The term prion, originally put forward to propose the concept that a protein could be infectious, refers to PrPSc, a misfolded isoform of the cellular prion protein (PrPC) that represents the pathogenetic hallmark of these disorders. The discovery that other proteins characterized by misfolding and seeded aggregation can spread from cell to cell, similarly to PrPSc, has increased interest in prion diseases. Among neurodegenerative disorders, however, prion diseases distinguish themselves for the broader phenotypic spectrum, the fastest disease progression and the existence of infectious forms that can be transmitted through the exposure to diseased tissues via ingestion, injection or transplantation. The main clinicopathological phenotypes of human prion disease include Creutzfeldt–Jakob disease, by far the most common, fatal insomnia, variably protease‐sensitive prionopathy, and Gerstmann–Sträussler–Scheinker disease. However, clinicopathological manifestations extend even beyond those predicted by this classification. Because of their transmissibility, the phenotypic diversity of prion diseases can also be propagated into syngenic hosts as prion strains with distinct characteristics, such as incubation period, pattern of PrPSc distribution and regional severity of histopathological changes in the brain. Increasing evidence indicates that different PrPSc conformers, forming distinct ordered aggregates, encipher the phenotypic variants related to prion strains. In this review, we summarize the most recent advances concerning the histo‐molecular pathology of human prion disease focusing on the phenotypic spectrum of the disease including co‐pathologies, the characterization of prion strains by experimental transmission and their correlation with the physicochemical properties of PrPSc aggregates.
A novel nitroalkene‐α‐tocopherol analogue inhibits inflammation and ameliorates atherosclerosis in Apo E knockout mice
Authors: Rodriguez‐Duarte Jorge , Galliussi Germán , Dapueto Rosina , Rossello Jessica , Malacrida Leonel , Kamaid Andrés , Schopfer Francisco J , Escande Carlos , López Gloria V , Batthyány Carlos 
Published: December 2018

Background and purposeAtherosclerosis is characterized by chronic low‐grade inflammation with concomitant lipid accumulation in the arterial wall. Anti‐inflammatory and anti‐atherogenic properties have been described for a novel class of endogenous nitroalkenes (nitrated‐unsaturated fatty acids), formed during inflammation and digestion/absorption processes. The lipid‐associated antioxidant α‐tocopherol is transported systemically by LDL particles including to the atheroma lesions. To capitalize on the overlapping and complementary salutary properties of endogenous nitroalkenes and α‐tocopherol, we designed and synthesized a novel nitroalkene‐α‐tocopherol analogue (NATOH) to address chronic inflammation and atherosclerosis, particularly at the lesion sites.Experimental approachWe synthesized NATOH, determined its electrophilicity and antioxidant capacity and studied its effects over pro‐inflammatory and cytoprotective pathways in macrophages in vitro. Moreover, we demonstrated its incorporation into lipoproteins and tissue both in vitro and in vivo, and determined its effect on atherosclerosis and inflammatory responses in vivo using the Apo E knockout mice model.Key resultsNATOH exhibited similar antioxidant capacity to α‐tocopherol and, due to the presence of the nitroalkenyl group, like endogenous nitroalkenes, it exerted electrophilic reactivity. NATOH was incorporated in vivo into the VLDL/LDL lipoproteins particles to reach the atheroma lesions. Furthermore, oral administration of NATOH down‐regulated NF‐κB‐dependent expression of pro‐inflammatory markers (including IL‐1β and adhesion molecules) and ameliorated atherosclerosis in Apo E knockout mice.Conclusions and implicationsIn toto, the data demonstrate a novel pharmacological strategy for the prevention of atherosclerosis based on a creative, natural and safe drug delivery system of a non‐conventional anti‐inflammatory compound (NATOH) with significant potential for clinical application.
Stimulation of histamine H4 receptors increases the production of IL‐9 in Th9 polarized cells
Authors: Schaper‐Gerhardt Katrin , Wohlert Mareike , Mommert Susanne , Kietzmann Manfred , Werfel Thomas , Gutzmer Ralf 
Published: December 2018

Background and PurposeTh9 cells represent a recently defined subset of CD4+ T‐helper cells, characterized by a high production of IL‐9. They are found at increased frequency in lesions of atopic dermatitis, where IL‐9 is also elevated. As histamine is up‐regulated in lesions of inflammatory skin diseases, we investigated the expression profile of histamine receptors and their functional role on Th9 cells.Experimental ApproachNaïve CD4+ T‐cells were purified from human peripheral blood mononuclear cells, using magnetic beads and further differentiated into Th9 cells. During differentiation, cells were additionally stimulated with histamine receptor agonists or left untreated. Histamine receptor expression as well as IL‐9 production was measured.Key ResultsAs proof of a successful differentiation, IL‐9 production was measured at mRNA and protein level. Expression of mRNA for histamine H1, H2 and H4 receptors were up‐regulated in differentiated Th9 cells compared to Th0 cells, while no mRNA for the H3 receptor was detectable. Stimulation of Th9 cells with histamine significantly up‐regulated expression of mRNA and protein for IL‐9 . Experiments with specific histamine receptor agonists and antagonists revealed that this up‐regulation was mediated by H4 receptors.Conclusions and ImplicationsIn summary, our study demonstrates a functional role for histamine H4 receptors on Th9 cells, which might amplify the pro‐inflammatory potency of these cells. Together with earlier studies on Th2 and Th17 cells, this study underlines the promising approach for the use of H4 receptor antagonists in inflammatory and allergic diseases such as atopic dermatitis.Linked ArticlesThis article is part of a themed section on New Uses for 21st Century. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.3/issuetoc