bluuebunny/crossref_metadata_2025_split huggingface dataset:
Risk of developing advanced colorectal neoplasia after removing high‐risk adenoma detected at index colonoscopy in young patients: A KASID study
Authors: Park Soo‐Kyung , Kim Nam Hee , Jung Yoon Suk , Kim Won Hee , Eun Chang Soo , Ko Bong Min , Seo Geom Seog , Cha Jae Myung , Park Jae Jun , Kim Kyeong Ok , Moon Chang Mo , Jung Yoonho , Kim Eun Soo , Jeon Seong Ran , Lee Chang Kyun , Park Dong Il ,   Intestinal cancer study group of the Korean Association for the Study of Intestinal Diseases (KASID)
Published: September 2015

AbstractBackground and Aim:Advanced adenoma (> 10 mm in diameter, villous structure, or high‐grade dysplasia) in young patients may have different characteristics and prognosis compared with those in older patients. We aimed to compare the incidence of colorectal neoplasms in young patients with older patients after removing high‐risk adenoma (advance adenoma or ≥ 3 adenomas).Methods:A retrospective, multicenter study was conducted at 13 university hospitals in Korea. The 1479 patients who removed high‐risk adenoma at index colonoscopy and followed by surveillance colonoscopy ≥ 2.5 years after were included. The cumulative incidence of overall and advanced colorectal neoplasms was compared according to the age groups (group 1: < 50 years, group 2: 50–70 years, and group 3: ≥ 70 years).Results:The prevalence of advance adenoma detected at index colonoscopy was significantly higher in group 1 than in groups 2 and 3 (85.4%, 78.1%, and 77.2%, respectively; P = 0.035). The 5 years cumulative incidence of overall and advanced colorectal neoplasms were 61.9%, 67.9%, and 74.7% (P < 0.001), and 11.7%, 17.9%, and 27.1% (P = 0.001) in groups 1, 2, and 3, respectively. In multivariate analysis, age > 70 years was a significant risk factor for developing overall (hazard ratio [HR] 1.41, 95% confidence interval [CI] 1.12–1.82, P = 0.004) and advanced colorectal neoplasms (HR = 2.56, 95% CI 1.43–4.59, P = 0.002).Conclusion:The cumulative incidence of overall and advanced colorectal neoplasms was significantly higher in older patients than in young patient groups. Age was a significant risk factor for developing colorectal neoplasms after removing high‐risk adenoma.
Crohn's disease prognosis and early immunomodulator therapy: Results from the CONNECT study
Authors: Kim Bun , Cheon Jae Hee , Moon Hyun Jin , Park Yi Rang , Ye Byong Duk , Yang Suk‐Kyun , Seo Geom Seog , Jang Byung Ik , Kim You Sun , Kim Joo Sung , Han Dong Soo , Kim Young‐Ho , Kim Won Ho 
Published: September 2015

AbstractBackground:It is unknown whether the treatment initiating time of immunomodulators such as thiopurines affects the course of Crohn's disease (CD). We evaluated the efficacy of early immunomodulator therapy (EIT) on the prognosis of patients with CD.Methods:We retrospectively analyzed 1157 patients with CD who were enrolled in the CrOhn's disease cliNical NEtwork and CohorT study and received immunomodulator therapy. The patients were divided into an EIT group and a conventional therapy group based on whether immunomodulators were initiated within six months after being diagnosed with CD. We compared the rates of intestinal surgery, bowel complications, and hospitalization because of CD between the groups.Results:Patient age at diagnosis and sex were not significantly different between the two groups. The mean duration of follow‐up was 105.8 ± 51.5 months. A Kaplan–Meier analysis identified that the EIT group was superior to the conventional therapy group in terms of delaying surgery (P = 0.017). In multivariate analysis, EIT was an independent predicting factor associated with delaying the onset of complications (P = 0.050). Patients were divided into two groups based on the year of CD diagnosis: from 1982 to 1999 (A) and from 2000 to 2008 (B). In group A, the time from diagnosis to the start of immunomodulatory therapy was longer (P < 0.001), and the time to first intestinal surgery was shorter than group B (P = 0.002).Conclusions:The early use of immunomodulators was associated with a good prognosis as defined by a need for surgery and the occurrence of complications in CD in our multicenter study.
Metabotropic GABAB receptors mediate GABA inhibition of acetylcholine release in the rat neuromuscular junction
Authors: Malomouzh Artem I. , Petrov Konstantin A. , Nurullin Leniz F. , Nikolsky Evgeny E. 
Published: September 2015

AbstractGamma‐aminobutyric acid (GABA) is an amino acid which acts as a neurotransmitter in the central nervous system. Here, we studied the effects of GABA on non‐quantal, spontaneous, and evoked quantal acetylcholine (ACh) release from motor nerve endings. We found that while the application of 10 μM of GABA had no effect on spontaneous quantal ACh release, as detected by the frequency of miniature endplate potentials, GABA reduced the non‐quantal ACh release by 57%, as determined by the H‐effect value. Finally, the evoked quantal ACh release, estimated by calculating the quantal content of full‐sized endplate potentials (EPPs), was reduced by 34%. GABA's inhibitory effect remained unchanged after pre‐incubation with picrotoxin, an ionotropic GABAA receptor blocker, but was attenuated following application of the GABAB receptor blocker CGP 55845, which itself had no effect on ACh release. An inhibitor of phospholipase C, U73122, completely prevented the GABA‐induced decrease in ACh release. Immunofluorescence demonstrated the presence of both subunits of the GABAB receptor (GABABR1 and GABABR2) in the neuromuscular junction. These findings suggest that metabotropic GABAB receptors are expressed in the mammalian neuromuscular synapse and their activation results in a phospholipase C‐mediated reduction in the intensity of non‐quantal and evoked quantal ACh release.
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We investigated the effect of gamma‐aminobutyric acid (GABA) on neuromuscular transmission. GABA reduced the non‐quantal and evoked quantal release of acetylcholine. These effects are mediated by GABAB receptors and are implemented via phospholipase C (PLC) activation. Our findings suggest that in the mammalian neuromuscular synapse, metabotropic GABAB receptors are expressed and their activation results in a reduction in the intensity of acetylcholine release.
Gene expression profiling of the inner ear
Authors: Schimmang Thomas , Maconochie Mark 
Published: September 2015

AbstractThe identification of transcriptional differences has served as an important starting point in understanding the molecular mechanisms behind biological processes and systems. The developmental biology of the inner ear, the biology of hearing and of course the pathology of deafness are all processes that warrant a molecular description if we are to improve human health. To this end, technological innovation has meant that larger scale analysis of gene transcription has been possible for a number of years now, extending our molecular analysis of genes to beyond those that are currently in vogue for a given system. In this review, some of the contributions gene profiling has made to understanding developmental, pathological and physiological processes in the inner ear are highlighted.
Monitoring a ‘metabolic shift’ after surgical resection of oral squamous cell carcinomas by serum lactate dehydrogenase
Authors: Grimm M. , Krimmel M. , Hoefert S. , Kraut W. , Calgéer B. , Biegner T. , Teriete P. , Munz A. , Reinert S. 
Published: September 2015

ObjectivesMonitoring surgical removal of oral squamous cell carcinomas (OSCC) is being routinely performed through clinical and imaging follow‐up. We analyzed the potential use of serum lactate, lactate dehydrogenase (LDH), and LDH isoenzymes (LDH 1‐5) as biomarkers in blood for the monitoring of surgical removal of OSCC.Materials and MethodsSerum lactate, LDH, and LDH isoenzymes (LDH 1‐5) have been prospectively assessed in healthy individuals (n = 19), patients with OSCC (n = 34: primary OSCC, n = 32 and recurrent OSCC, n = 2) before surgery and after curative tumor resection (n = 26). LDHA and LDHB expressions were analyzed by immunohistochemistry (IHC) in the same OSCC tumor specimen.ResultsPositive LDHA tumor tissue expression measured by IHC (n = 34/34, 100%) was significantly associated with increased serum LDH‐5 (n = 24/34, 71%, P = 0.0258) but weak significantly associated with increased total serum LDH (n = 23/34, 68%, P = 0.0592). Positive LDHB tumor tissue expression measured by IHC (n = 25/34, 74%) was significantly associated with increased total serum LDH (P = 0.0172). After surgery, serum LDH and LDH‐5 isoenzyme significantly decreased and LDH‐1 significantly increased in the aftercare. A significantly inverse correlation of LDHA with LDHB IHC scores was found (P < 0.0001).ConclusionsThe association of LDHA and LDHB measured by IHC with serum LDH indicates that analyzing this enzyme could serve as a favorable ‘liquid biopsy’ (non‐invasive diagnostic tool) for OSCC.
Peginterferon add‐on results in more HBsAg decline compared to monotherapy in HBeAg‐positive chronic hepatitis B patients
Authors: Brouwer W. P. , Sonneveld M. J. , Xie Q. , Guo S. , Zhang N. , Zeuzem S. , Tabak F. , Zhang Q. , Simon K. , Akarca U. S. , Streinu‐Cercel A. , Hansen B. E. , Janssen H. L. A. 
Published: September 2015

SummaryIt is unknown whether peginterferon (PEG‐IFN) add‐on to entecavir (ETV) leads to more HBsAg decline compared to PEG‐IFN monotherapy or combination therapy, and whether ETV therapy may prevent HBsAg increase after PEG‐IFN cessation. We performed a post hoc analysis of 396 HBeAg‐positive patients treated for 72 weeks with ETV + 24 weeks PEG‐IFN add‐on from week 24 to 48 (add‐on, n = 85), 72 weeks with ETV monotherapy (n = 90), 52 weeks with PEG‐IFN monotherapy (n = 111) and 52 weeks PEG‐IFN + lamivudine (combination, n = 110) within 2 randomized trials. HBsAg decline was assessed at the end of PEG‐IFN (EOP) and 6 months after PEG‐IFN (EOF) discontinuation. Differences in baseline characteristics were accounted for using inversed probability of treatment weights. At EOP, a HBsAg reduction of ≥1log10 IU/mL was more frequently achieved for patients in the add‐on or combination therapy arms (both 36%), compared to PEG‐IFN mono (20%) or ETV (8%) (add‐on vs PEG‐IFN mono P = 0.050). At EOF, the HBsAg reduction ≥1log10 IU/mL was only sustained in patients treated with ETV consolidation (add‐on vs combination and PEG‐IFN mono: 40% vs 23% and 18%, P = 0.029 and P = 0.003, respectively). For add‐on, combination, PEG‐IFN mono and ETV, the mean HBsAg‐level change at EOF was −0.84, −0.81, −0.68 and −0.33 log10 IU/mL, respectively (P > 0.05 for PEG‐IFN arms). HBeAg loss at EOF was 36%, 31%, 33% and 20%, respectively (P > 0.05). PEG‐IFN add‐on for 24 weeks results in more on‐treatment HBsAg decline than does 52 weeks of PEG‐IFN monotherapy. ETV therapy may maintain the HBsAg reduction achieved with PEG‐IFN.
Relationship between Plasma Fibroblast Growth Factor‐23 Concentration and Survival Time in Cats with Chronic Kidney Disease
Authors: Geddes R.F. , Elliott J. , Syme H.M. 
Published: September 2015

BackgroundFibroblast growth factor‐23 (FGF‐23) and parathyroid hormone (PTH) are commonly increased in cats with azotemic chronic kidney disease (CKD). Both are predictors of survival time in human patients, but these relationships have not previously been examined in the cat.ObjectivesTo investigate the relationship between plasma FGF‐23 and PTH concentrations at diagnosis of CKD in cats with survival time and with disease progression over 12 months.Animals214 azotemic, client‐owned cats (≥9 years).MethodsRetrospective study: Biochemical and urinary variables at diagnosis of azotemic CKD, including plasma FGF‐23 and PTH concentrations were assessed as predictors of survival time (all‐cause mortality) using Cox regression, and as predictors of CKD progression over 12 months using logistic regression.ResultsIn the final multivariable Cox regression model, survival was negatively associated with plasma creatinine (P = .002) and FGF‐23 concentrations (P = .014), urine protein‐to‐creatinine ratio (P < .001) and age (P < .001). Survival was positively associated with PCV (P = .004). In the final multivariable logistic regression model, independent predictors of CKD progression included logFGF‐23 and age. Neither plasma phosphate nor PTH was found to be an independent predictor of survival time or of CKD progression.Conclusions and Clinical ImportancePlasma FGF‐23 concentration is a novel prognostic indicator in cats with CKD, independent of other factors including plasma creatinine and phosphate concentrations. Further work is required to assess if FGF‐23 contributes directly to CKD progression, but regardless these findings may make FGF‐23 a useful biomarker for predicting poorer outcomes in cats with CKD.
Population genetic structure of a common host predicts the spread of white‐nose syndrome, an emerging infectious disease in bats
Authors: Wilder Aryn P. , Kunz Thomas H. , Sorenson Michael D. 
Published: September 2015

AbstractLandscape complexity influences patterns of animal dispersal, which in turn may affect both gene flow and the spread of pathogens. White‐nose syndrome (WNS) is an introduced fungal disease that has spread rapidly throughout eastern North America, causing massive mortality in bat populations. We tested for a relationship between the population genetic structure of the most common host, the little brown myotis (Myotis lucifugus), and the geographic spread of WNS to date by evaluating logistic regression models of WNS risk among hibernating colonies in eastern North America. We hypothesized that risk of WNS to susceptible host colonies should increase with both geographic proximity and genetic similarity, reflecting historical connectivity, to infected colonies. Consistent with this hypothesis, inclusion of genetic distance between infected and susceptible colonies significantly improved models of disease spread, capturing heterogeneity in the spatial expansion of WNS despite low levels of genetic differentiation among eastern populations. Expanding our genetic analysis to the continental range of little brown myotis reveals strongly contrasting patterns of population structure between eastern and western North America. Genetic structure increases markedly moving westward into the northern Great Plains, beyond the current distribution of WNS. In western North America, genetic differentiation of geographically proximate populations often exceeds levels observed across the entire eastern region, suggesting infrequent and/or locally restricted dispersal, and thus relatively limited opportunities for pathogen introduction in western North America. Taken together, our analyses suggest a possibly slower future rate of spread of the WNS pathogen, at least as mediated by little brown myotis.
Candida and cardiovascular implantable electronic devices: a case of lead and native aortic valve endocarditis and literature review
Authors: Glavis‐Bloom Justin , Vasher Scott , Marmor Meghan , Fine Antonella B. , Chan Philip A. , Tashima Karen T. , Lonks John R. , Kojic Erna M. 
Published: September 2015

SummaryUse of cardiovascular implantable electronic devices (CIED), including permanent pacemakers (PPM) and implantable cardioverter defibrillators (ICD), has increased dramatically over the past two decades. Most CIED infections are caused by staphylococci. Fungal causes are rare and their prognosis is poor. To our knowledge, there has not been a previously reported case of multifocal Candida endocarditis involving both a native left‐sided heart valve and a CIED lead. Here, we report the case of a 70‐year‐old patient who presented with nausea, vomiting, and generalised fatigue, and was found to have Candida glabrata endocarditis involving both a native aortic valve and right atrial ICD lead. We review the literature and summarise four additional cases of CIED‐associated Candida endocarditis published from 2009 to 2014, updating a previously published review of cases prior to 2009. We additionally review treatment guidelines and discuss management of CIED‐associated Candida endocarditis.
Molecular types of Cryptococcus gattii/Cryptococcus neoformans species complex from clinical and environmental sources in Nairobi, Kenya
Authors: Kangogo Mourine , Bader Oliver , Boga Hamadi , Wanyoike Wanjiru , Folba Claudia , Worasilchai Navaporn , Weig Michael , Groß Uwe , Bii Christine C. 
Published: September 2015

SummaryCryptococcal meningitis infections cause high mortality rates among HIV‐infected patients in Sub‐Saharan Africa. The high incidences of cryptococcal infections may be attributed to common environmental sources which, if identified, could lead to institution of appropriate control strategies. To determine the genotypes of Cryptococcus gattii/C. neoformans‐ species complex from Nairobi, Kenya, 123 clinical and environmental isolates were characterised. Typing was done using orotidine monophosphate pyrophosphorylase (URA5) gene restriction fragment length polymorphism (URA5‐RFLP). The majority of the isolates [105/123; 85.4%] were C. neoformans genotype (AFLPI/VNI) and 1.6% AFLP1A/VNB/VNII, whereas (13%) were C. gattii (AFLP4/VGI). This is the first report on the genotypes of C. gattii/C. neoformans species complex from clinical and environmental sources in Nairobi, Kenya and the isolation of C. gattii genotype AFLP4/VGI from the environment in Kenya.
Abnormal regional homogeneity in patients with irritable bowel syndrome: A resting‐state functional MRI study
Authors: Ke J. , Qi R. , Liu C. , Xu Q. , Wang F. , Zhang L. , Lu G. 
Published: September 2015

AbstractBackgroundTask‐related brain imaging research has implicated abnormal central processing of visceral sensation in irritable bowel syndrome (IBS). However, how brain function of IBS patients is altered during resting‐state remains to be determined. We investigated spontaneous brain activity of patients with IBS using regional homogeneity (ReHo) analysis in resting‐state functional magnetic resonance imaging (rs‐fMRI).MethodsThirty‐one patients with diarrhea‐predominant IBS and 32 age‐ and sex‐ matched healthy controls underwent clinical assessments and rs‐fMRI scanning. ReHo maps were acquired by calculating the Kendall's coefficient of concordance and compared between the IBS group and the control group. The effects of psychological disturbance on group differences were assessed by including anxiety and depression levels as covariates in the statistical analyses. Multiple regression analyses were conducted to examine the relationship between ReHo values and disease duration, symptom severity, and pain intensity.Key ResultsCompared with controls, IBS patients showed increased ReHo in the postcentral gyrus and thalamus and decreased ReHo in the anterior cingulate cortex and prefrontal cortex. The inclusion of anxiety and depression as covariates did not alter ReHo differences between the two groups. Furthermore, significant correlations were found between clinical indices and ReHo values in some brain regions in the IBS group.Conclusions & InferencesIBS patients have abnormal local synchronization of spontaneous brain activity in regions involved in visceral afferent processing, emotional arousal, and cognitive modulation. Combining rs‐fMRI and ReHo analysis seems to be a valuable approach to investigate the neural basis of IBS.
Peroxisome proliferator‐activated receptor δ inhibits Porphyromonas gingivalis lipopolysaccharide‐induced activation of matrix metalloproteinase‐2 by downregulating NADPH oxidase 4 in human gingival fibroblasts
Authors: Yoo T. , Ham S.A. , Hwang J.S. , Lee W.J. , Paek K.S. , Oh J.W. , Kim J.H. , Do J.T. , Han C.W. , Kim J.H. , Seo H.G. 
Published: September 2015

SummaryWe investigated the roles of peroxisome proliferator‐activated receptor δ (PPARδ) in Porphyromonas gingivalis‐derived lipopolysaccharide (Pg‐LPS)‐induced activation of matrix metalloproteinase 2 (MMP‐2). In human gingival fibroblasts (HGFs), activation of PPARδ by GW501516, a specific ligand of PPARδ, inhibited Pg‐LPS‐induced activation of MMP‐2 and generation of reactive oxygen species (ROS), which was associated with reduced expression of NADPH oxidase 4 (Nox4). These effects were significantly smaller in the presence of small interfering RNA targeting PPARδ or the specific PPARδ inhibitor GSK0660, indicating that PPARδ is involved in these events. In addition, modulation of Nox4 expression by small interfering RNA influenced the effect of PPARδ on MMP‐2 activity, suggesting a mechanism in which Nox4‐derived ROS modulates MMP‐2 activity. Furthermore, c‐Jun N‐terminal kinase and p38, but not extracellular signal‐regulated kinase, mediated PPARδ‐dependent inhibition of MMP‐2 activity in HGFs treated with Pg‐LPS. Concomitantly, PPARδ‐mediated inhibition of MMP‐2 activity was associated with the restoration of types I and III collagen to levels approaching those in HGFs not treated with Pg‐LPS. These results indicate that PPARδ‐mediated downregulation of Nox4 modulates cellular redox status, which in turn plays a critical role in extracellular matrix homeostasis through ROS‐dependent regulation of MMP‐2 activity.
Association mapping and resistant alleles’ analysis for japonica rice blast resistance
Authors: Guo Liying , Guo Wei , Zhao Hongwei , Wang Jingguo , Liu Hualong , Sun Jian , Zheng Hongliang , Sha Hanjing , Zou Detang 
Published: September 2015

AbstractRice blast is one of the major fungal diseases that badly reduce rice production in China and worldwide. Association mapping for blast resistance was performed on 226 japonica rice cultivars with 118 pairs of SSR markers. The blast resistance was evaluated by inoculating with two isolates, DB22 and DB77, at the tillering stage in 2013 and 2014, separately. A total of 31 associations with 17 different SSRs were significantly (P < 0.05) associated with blast resistance based on the mixed linear model (MLM), of which nine markers could be detected in both 2013 and 2014, including two markers that were simultaneously associated with the two isolates. Five of the nine stable markers were consistent with the genome regions identified by linkage mapping in previous reports. Phenotypic effects of each allele of the nine stable markers were compared, and 18 favourable alleles were identified. Five elite parental combinations were designed for improving blast resistance in rice. Our results demonstrate that association mapping can complement and enhance previous QTL information for marker‐assisted selection and breeding by design.
Clostridium difficile infection in the pediatric transplant patient
Authors: Nicholson Maribeth R. , Osgood Christy L. , Acra Sari A. , Edwards Kathryn M. 
Published: September 2015

AbstractCDIs are on the rise in both hospital and community settings in adults and children. Children with cancer or a history of HSCT or SOT appear to be at higher risk for primary disease, recurrent disease, and severe outcomes when compared to children with other comorbidities. The reasons for this are not clear and no studies to date have analyzed risk factors for CDI in pediatric transplant patients. Colonization rates in children with cancer and a transplant history are also high. Determining which children are colonized with Clostridium difficile and symptomatic from another source vs. symptomatic from CDI is difficult and a clinical conundrum for the transplant physician. The use of fecal transplantation for severe or rCDI is likely safe and effective in the immunosuppressed pediatric cancer or transplant patient, but this will need to be more thoroughly studied in this patient population.