bluuebunny/crossref_metadata_2025_split huggingface dataset:
Real‐world practice and Expectation of Asia‐Pacific physicians and patients in Helicobacter Pylori eradication (REAP‐HP Survey)
Authors: Chuah Yoen‐Young , Wu Deng‐Chyang , Chuah Seng‐Kee , Yang Jyh‐Chin , Lee Tzong‐Hsi , Yeh Hong‐Zen , Chen Chan‐Lin , Liu Yu‐Hwa , Hsu Ping‐I 
Published: February 2017

AbstractObjectiveThe aims of the study were: 1, to survey the most popular anti‐H. pylori regimens in Asia‐Pacific region and the real‐world effectiveness of these regimens; and 2, to investigate the expectation gaps of eradication rate between physicians and patients.DesignA questionnaire was distributed to Asia‐Pacific physicians who attended the Asia‐Pacific Digestive Week 2015 meeting. Reported eradication rates from the literatures were compared with real‐world rates of surveyed popular regimens within the region. In addition, a questionnaire was distributed to H. pylori‐infected patients in three regions of Taiwan.ResultsA total of 691 physicians and 539 patients participated in the survey. The top five most commonly used regimens were 7‐day clarithromycin‐based standard triple therapy (50.4%), 14‐day clarithromycin‐based standard triple therapy (31.0%), 10‐day sequential therapy (6.1%), 14‐day bismuth quadruple therapy (3.9%), and 14‐day hybrid therapy (3.6%). All countries except for China had a significant gap between the expectation of physicians on anti‐H. pylori therapy and the real‐world eradication rate of most commonly adopted regimens (all P value <.05). The expectation on minimal eradication rate among patients was higher than that of physicians (91.4% vs 86.5%, P<.001).ConclusionsIt is time for physicians in Asia‐Pacific countries to adopt newer and more efficacious anti‐H. pylori regimens to meet the Kyoto consensus recommendation and their patients’ expectations.
International trends in health science librarianship part 20: Russia
Authors: Murphy Jeannette , Jargin Serge 
Published: February 2017

AbstractThis is the last in a series of articles exploring international trends in health science librarianship in the 21st century. The focus of the present issue is Russia. The next feature column will initiate a new series entitled New Directions in Health Science Librarianship. The first contribution will be from Australia.JM
Extracellular histones disarrange vasoactive mediators release through a COX‐NOS interaction in human endothelial cells
Authors: Pérez‐Cremades Daniel , Bueno‐Betí Carlos , García‐Giménez José Luis , Ibañez‐Cabellos José Santiago , Hermenegildo Carlos , Pallardó Federico V. , Novella Susana 
Published: February 2017

AbstractExtracellular histones are mediators of inflammation, tissue injury and organ dysfunction. Interactions between circulating histones and vascular endothelial cells are key events in histone‐mediated pathologies. Our aim was to investigate the implication of extracellular histones in the production of the major vasoactive compounds released by human endothelial cells (HUVECs), prostanoids and nitric oxide (NO). HUVEC exposed to increasing concentrations of histones (0.001 to 100 μg/ml) for 4 hrs induced prostacyclin (PGI2) production in a dose‐dependent manner and decreased thromboxane A2 (TXA2) release at 100 μg/ml. Extracellular histones raised cyclooxygenase‐2 (COX‐2) and prostacyclin synthase (PGIS) mRNA and protein expression, decreased COX‐1 mRNA levels and did not change thromboxane A2 synthase (TXAS) expression. Moreover, extracellular histones decreased both, eNOS expression and NO production in HUVEC. The impaired NO production was related to COX‐2 activity and superoxide production since was reversed after celecoxib (10 μmol/l) and tempol (100 μmol/l) treatments, respectively. In conclusion, our findings suggest that extracellular histones stimulate the release of endothelial‐dependent mediators through an up‐regulation in COX‐2‐PGIS‐PGI2 pathway which involves a COX‐2‐dependent superoxide production that decreases the activity of eNOS and the NO production. These effects may contribute to the endothelial cell dysfunction observed in histone‐mediated pathologies.
Association of leptin and leptin receptor gene polymorphisms with systemic lupus erythematosus in a Chinese population
Authors: Li Hong‐Miao , Zhang Tian‐Ping , Leng Rui‐Xue , Li Xiang‐Pei , Wang De‐Guang , Li Xiao‐Mei , Ye Dong‐Qing , Pan Hai‐Feng 
Published: February 2017

AbstractTo explore the association of LEP and leptin receptor (LEPR) gene single‐nucleotide polymorphisms (SNPs) with susceptibility to systemic lupus erythematosus (SLE) in a Chinese population. Four LEP SNPs (rs11761556, rs12706832, rs2071045 and rs2167270) and nine LEPR SNPs (rs10749754, rs1137100, rs1137101, rs13306519, rs8179183, rs1805096, rs3790434, rs3806318 and rs7518632) were genotyped in a cohort of 633 patients with SLE and 559 healthy controls. Genotyping of SNPs was performed with improved multiple ligase detection reaction (iMLDR). No significant differences were detected for the distribution of allele and genotype frequencies of all 13 SNPs between patients with SLE and controls. The genotype effects of recessive, dominant and additive models were also analysed, but no significant evidence for association was detected. However, further analysis in patients with SLE showed that the TT genotype and T allele frequencies of the LEP rs2071045 polymorphism were nominally significantly higher in patients with pericarditis (P = 0.012, P = 0.011, respectively). In LEPR, the GA/AA genotype and A allele frequencies of the rs1137100 polymorphism were both nominally associated with photosensitivity in patients with SLE (P = 0.043, P = 0.018, respectively). Moreover, the genotype and allele distribution of rs3806318 were also nominally associated with photosensitivity in patients with SLE (P = 0.013, P = 0.008, respectively). No significant differences in serum leptin levels were observed in patients with SLE with different genotypes. In summary, LEP and LEPR SNPs are not associated with genetic susceptibility to SLE, but may contribute to some specific clinical phenotype of this disease; further studies are necessary to elucidate the exact role of LEP and LEPR genes in the pathogenesis of SLE.
Carbenoxolone inhibits TRPV4 channel‐initiated oxidative urothelial injury and ameliorates cyclophosphamide‐induced bladder dysfunction
Authors: Zhang Xiling , Gao Shan , Tanaka Masayoshi , Zhang Zhen , Huang Yanru , Mitsui Takahiko , Kamiyama Manabu , Koizumi Schuichi , Fan Jianglin , Takeda Masayuki , Yao Jian 
Published: February 2017

AbstractCarbenoxolone (CBX) is a clinically prescribed drug for the treatment of digestive ulcer and inflammation. It is also a widely used pharmacological inhibitor of several channels in basic research. Given that the overactivity of several channels, including those inhibitable by CBX, underlies bladder dysfunction, we tested the potential therapeutic application and mechanism of CBX in the treatment of voiding dysfunction. In a mouse model of cystitis induced by cyclophosphamide (CYP), CBX administration prevented the CYP‐elicited increase in bladder weight, oedema, haemorrhage, and urothelial injury. CBX also greatly improved micturition pattern, as manifested by the apparently decreased micturition frequency and increased micturition volume. Western blot results showed that CBX suppressed CYP‐induced increase in protein carbonyls, COX‐2, and iNOS. Further analysis using cultured urothelial cells revealed that acrolein, the major metabolite of CYP, caused protein oxidation, p38 activation, and urothelial injury. These effects of acrolein were reproduced by TRPV4 agonists and significantly prevented by antioxidant NAC, p38 inhibitor SB203580, TRPV4 antagonist RN‐1734, and CBX. Further studies showed that CBX potently suppressed TRPV4 agonist‐initiated calcium influx and subsequent cell injury. CBX attenuated CYP‐induced cystitis in vivo and reduced acrolein‐induced cell injury in vitro, through mechanisms involving inhibition of TRPV4 channels and attenuation of the channel‐mediated oxidative stress. CBX might be a promising agent for the treatment of bladder dysfunction.
Obesity and metabolic dysfunction severely influence prostate cell function: role of insulin and IGF1
Authors: L‐López Fernando , Sarmento‐Cabral André , Herrero‐Aguayo Vicente , Gahete Manuel D. , Castaño Justo P. , Luque Raúl M. 
Published: February 2017

AbstractObesity is a major health problem that courses with severe comorbidities and a drastic impairment of homeostasis and function of several organs, including the prostate gland (PG). The endocrine–metabolic regulatory axis comprising growth hormone (GH), insulin and IGF1, which is drastically altered under extreme metabolic conditions such as obesity, also plays relevant roles in the development, modulation and homeostasis of the PG. However, its implication in the pathophysiological interplay between obesity and prostate function is still to be elucidated. To explore this association, we used a high fat–diet obese mouse model, as well as in vitro primary cultures of normal‐mouse PG cells and human prostate cancer cell lines. This approach revealed that most of the components of the GH/insulin/IGF1 regulatory axis are present in PGs, where their expression pattern is altered under obesity conditions and after an acute insulin treatment (e.g. Igfbp3), which might have some pathophysiological implications. Moreover, our results demonstrate, for the first time, that the PG becomes severely insulin resistant under diet‐induced obesity in mice. Finally, use of in vitro approaches served to confirm and expand the conception that insulin and IGF1 play a direct, relevant role in the control of normal and pathological PG cell function. Altogether, these results uncover a fine, germane crosstalk between the endocrine–metabolic status and the development and homeostasis of the PG, wherein key components of the GH, insulin and IGF1 axes could play a relevant pathophysiological role.
Up‐regulation of glycolysis promotes the stemness and EMT phenotypes in gemcitabine‐resistant pancreatic cancer cells
Authors: Zhao Hengqiang , Duan Qingke , Zhang Zhengle , Li Hehe , Wu Heshui , Shen Qiang , Wang Chunyou , Yin Tao 
Published: February 2017

AbstractCancer stem cells (CSCs) and epithelial–mesenchymal transition (EMT)‐type cells are considered as underlying causes of chemoresistance, tumour recurrence and metastasis in pancreatic cancer. We aimed to describe the mechanisms – particularly glycolysis – involved in the regulation of the CSC and EMT phenotypes. We used a gemcitabine‐resistant (GR) Patu8988 cell line, which exhibited clear CSC and EMT phenotypes and showed reliance on glycolysis. Inhibition of glycolysis using 2‐deoxy‐D‐glucose (2‐DG) significantly enhanced the cytotoxicity of gemcitabine and inhibited the CSC and EMT phenotypes in GR cells both in vitro and in vivo. Intriguingly, the use of the reactive oxygen species (ROS) scavenger N‐acetylcysteine (NAC) restored the CSC and EMT phenotypes. H2O2 produced changes similar to those of 2‐DG, indicating that ROS were involved in the acquired cancer stemness and EMT phenotypes of GR cells. Moreover, doublecortin‐like kinase 1 (DCLK1), a pancreatic CSC marker, was highly expressed and regulated the stemness and EMT phenotypes in GR cell. Both 2‐DG and H2O2 treatment suppressed DCLK1 expression, which was also rescued by NAC. Together, these findings revealed that glycolysis promotes the expression of DCLK1 and maintains the CSC and EMT phenotypes via maintenance of low ROS levels in chemoresistant GR cells. The glycolysis‐ROS‐DCLK1 pathway may be potential targets for reversing the malignant behaviour of pancreatic cancer.
Reduced hair cortisol after maltreatment mediates externalizing symptoms in middle childhood and adolescence
Authors: White Lars O. , Ising Marcus , von Klitzing Kai , Sierau Susan , Michel Andrea , Klein Annette M. , Andreas Anna , Keil Jan , Quintero Leonhard , Müller‐Myhsok Bertram , Uhr Manfred , Gausche Ruth , Manly Jody T. , Crowley Michael J. , Kirschbaum Clemens , Stalder Tobias 
Published: February 2017

BackgroundThe enduring impact of childhood maltreatment on biological systems and ensuing psychopathology remains incompletely understood. Long‐term effects of stress may be reflected in cumulative cortisol secretion over several months, which is now quantifiable via hair cortisol concentrations (HCC). We conducted a first comprehensive investigation utilizing the potential of hair cortisol analysis in a large sample of maltreated and nonmaltreated children and adolescents.MethodParticipants included 537 children and adolescents (3–16 years; 272 females) with maltreatment (n = 245) or without maltreatment histories (n = 292). Maltreated subjects were recruited from child protection services (CPS; n = 95), youth psychiatric services (n = 56), and the community (n = 94). Maltreatment was coded using the Maltreatment Classification System drawing on caregiver interviews and complemented with CPS records. Caregivers and teachers reported on child mental health. HCC were assessed in the first 3 cm hair segment.ResultsAnalyses uniformly supported that maltreatment coincides with a gradual and dose‐dependent reduction in HCC from 9 to 10 years onwards relative to nonmaltreated controls. This pattern emerged consistently from both group comparisons between maltreated and nonmaltreated subjects (27.6% HCC reduction in maltreated 9–16‐year‐olds) and dimensional analyses within maltreated subjects, with lower HCC related to greater maltreatment chronicity and number of subtypes. Moreover, both group comparisons and dimensional analyses within maltreated youth revealed that relative HCC reduction mediates the effect of maltreatment on externalizing symptoms.ConclusionsFrom middle childhood onwards, maltreatment coincides with a relative reduction in cortisol secretion, which, in turn, may predispose to externalizing symptoms.
‘Mixed blessings’: parental religiousness, parenting, and child adjustment in global perspective
Authors: Bornstein Marc H. , Putnick Diane L. , Lansford Jennifer E. , Al‐Hassan Suha M. , Bacchini Dario , Bombi Anna Silvia , Chang Lei , Deater‐Deckard Kirby , Di Giunta Laura , Dodge Kenneth A. , Malone Patrick S. , Oburu Paul , Pastorelli Concetta , Skinner Ann T. , Sorbring Emma , Steinberg Laurence , Tapanya Sombat , Tirado Liliana Maria Uribe , Zelli Arnaldo , Alampay Liane Peña 
Published: February 2017

BackgroundMost studies of the effects of parental religiousness on parenting and child development focus on a particular religion or cultural group, which limits generalizations that can be made about the effects of parental religiousness on family life.MethodsWe assessed the associations among parental religiousness, parenting, and children's adjustment in a 3‐year longitudinal investigation of 1,198 families from nine countries. We included four religions (Catholicism, Protestantism, Buddhism, and Islam) plus unaffiliated parents, two positive (efficacy and warmth) and two negative (control and rejection) parenting practices, and two positive (social competence and school performance) and two negative (internalizing and externalizing) child outcomes. Parents and children were informants.ResultsGreater parent religiousness had both positive and negative associations with parenting and child adjustment. Greater parent religiousness when children were age 8 was associated with higher parental efficacy at age 9 and, in turn, children's better social competence and school performance and fewer child internalizing and externalizing problems at age 10. However, greater parent religiousness at age 8 was also associated with more parental control at age 9, which in turn was associated with more child internalizing and externalizing problems at age 10. Parental warmth and rejection had inconsistent relations with parental religiousness and child outcomes depending on the informant. With a few exceptions, similar patterns of results held for all four religions and the unaffiliated, nine sites, mothers and fathers, girls and boys, and controlling for demographic covariates.ConclusionsParents and children agree that parental religiousness is associated with more controlling parenting and, in turn, increased child problem behaviors. However, children see religiousness as related to parental rejection, whereas parents see religiousness as related to parental efficacy and warmth, which have different associations with child functioning. Studying both parent and child views of religiousness and parenting are important to understand the effects of parental religiousness on parents and children.
Nutritional, microbiological and psychosocial implications of the low FODMAP diet
Authors: Staudacher Heidi Maria 
Published: February 2017

AbstractDietary restriction of certain fermentable carbohydrates (low fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) diet) is effective for managing symptoms of irritable bowel syndrome (IBS). However, there are potential consequences of this diet that relate to its impact on nutritional, microbiological, and health‐related quality of life outcomes. Evidence suggests that the low FODMAP diet leads to some alterations in nutrient intake. For example, carbohydrate intake is reduced, and there is a decrease in the proportion of patients meeting the recommended intake for calcium. Intake of other macro and micro‐nutrients appears to be adequate in the short term. As well as the impact on nutrient intake, extensive dietary modification can have a pronounced impact on the gastrointestinal microbiota. Indeed, recent data suggests the diet markedly reduces luminal Bifidobacteria concentration, and there is limited evidence that it reduces total bacteria abundance and concentration of other bacterial groups, for example, Faecalibacterium prausnitzii. Finally, despite the evidence for its clinical effectiveness in patients with IBS, the restrictive nature of the diet could pose a significant burden on patients, thereby limiting improvements, or indeed worsening health‐related quality of life. In conclusion, while robust evidence supports the clinical effectiveness of the low FODMAP diet, it is important, considering the likelihood of its continued widespread use in IBS and other functional bowel disorders, that we extend our understanding of the impact of the diet on endpoints that may have potential consequences for long term health.
FODMAPs: food composition, defining cutoff values and international application
Authors: Varney Jane , Barrett Jacqueline , Scarlata Kate , Catsos Patsy , Gibson Peter R , Muir Jane G 
Published: February 2017

AbstractThe low‐FODMAP diet is a new dietary therapy for the management of irritable bowel syndrome that is gaining in popularity around the world. Developing the low‐FODMAP diet required not only extensive food composition data but also the establishment of “cutoff values” to classify foods as low‐FODMAP. These cutoff values relate to each particular FODMAP present in a food, including oligosaccharides (fructans and galacto‐oligosaccharides), sugar polyols (mannitol and sorbitol), lactose, and fructose in excess of glucose. Cutoff values were derived by considering the FODMAP levels in typical serving sizes of foods that commonly trigger symptoms in individuals with irritable bowel syndrome, as well as foods that were generally well tolerated. The reliability of these FODMAP cutoff values has been tested in a number of dietary studies. The development of the techniques to quantify the FODMAP content of foods has greatly advanced our understanding of food composition. FODMAP composition is affected by food processing techniques and ingredient selection. In the USA, the use of high‐fructose corn syrups may contribute to the higher FODMAP levels detected (via excess fructose) in some processed foods. Because food processing techniques and ingredients can vary between countries, more comprehensive food composition data are needed for this diet to be more easily implemented internationally.
Prebiotic inulin‐type fructans and galacto‐oligosaccharides: definition, specificity, function, and application in gastrointestinal disorders
Authors: Wilson Bridgette , Whelan Kevin 
Published: February 2017

AbstractPrebiotics are non‐digestible selectively fermented dietary fibers that specifically promote the growth of one or more bacterial genera in the gastrointestinal tract and thus provide health benefit to the host. The two most investigated prebiotics being the inulin‐type fructans and galacto‐oligosaccharides. Prebiotic specificity is mediated through species‐specific gene clusters within saccharolytic bacteria controlled by signaling sensors for various substrates. Prebiotic health benefits are attributed to immune regulation and bacterial metabolite production. In humans, prebiotic supplementation leads to increased growth of specific gut microbiota (e.g., bifidobacteria), immune modulation, and depending on the bacterial augmentation, short‐chain fatty acid production. Irritable bowel syndrome and Crohn's disease are gastrointestinal disorders associated with reductions in some gut bacteria and greater mucosal inflammation. Prebiotic supplementation studies have shown some promise at low doses for modulation of the gut bacteria and reduction of symptoms in IBS; however, larger doses may have neutral or negative impact on symptoms. Studies in Crohn's disease have not shown benefit to bacterial modulation or inflammatory response with prebiotic supplementation. Dietary restriction of fermentable carbohydrates (low FODMAP diet), which restricts some naturally occurring prebiotics from the diet, has shown efficacy in improving symptoms in irritable bowel syndrome, but it lowers the numbers of some key gut microbiota. Further research is required on the effect of prebiotics in gastrointestinal disorders and, in particular, on their use in conjunction with the low FODMAP diet.
Non‐coeliac gluten sensitivity
Authors: Gibson Peter R , Skodje Gry I , Lundin Knut E A 
Published: February 2017

AbstractIrritable bowel syndrome‐like symptoms in response to wheat ingestion is common and well described, but whether the reaction is due to gluten (i.e., non‐coeliac gluten sensitivity), other wheat proteins, or FODMAPs (mostly fructans) alone or in combinations has not been clearly defined. Exclusion of coeliac disease in the presence of negative serology, and normal villous architecture but increased density of intraepithelial lymphocytes on duodenal biopsies, is difficult. Furthermore, the confidence by which a positive diagnosis is made or non‐coeliac gluten sensitivity is excluded by blinded placebo‐controlled rechallenge with wheat protein is reduced by strong nocebo responses generally found in patients with self‐reported non‐coeliac gluten sensitivity. The absence of a clear biological mechanism of action and difficulties with the design and interpretation of research studies have plunged this entity into even deeper controversy. In the absence of clarity in its diagnosis, the epidemiology, prognosis, and therapeutic approaches to a patient who may be gluten sensitive remain to be determined. Adequate understanding of the issues surrounding the controversy and further research will slowly unravel the truth behind the problem.