bluuebunny/crossref_metadata_2025_split huggingface dataset:
Urodynamic findings in women with refractory overactive bladder symptoms
Authors: Al‐Zahrani Ali A , Gajewski Jerzy 
Published: September 2015

ObjectivesTo assess: (i) the correlation between overactive bladder symptoms and urodynamic findings in female patients; and (ii) the association of urinary symptoms with the presence of detrusor overactivity and/or bladder outlet obstruction.MethodsThe present retrospective study included female patients with overactive bladder symptoms who underwent urodynamic evaluation by a single physician. Patients with previous anti‐incontinence surgery or neurogenic bladder were excluded. Spearman's correlation coefficients were calculated to correlate overactive bladder symptoms with the urodynamic findings. Univariate and multivariate logistic regression analyses were used to determine the independent factors for detrusor overactivity and bladder outlet obstruction.ResultsOverall, 1737 reports were analyzed. All patients had urgency with or without urgency urinary incontinence. Urgency, urgency urinary incontinence and nocturia correlated with detrusor overactivity. The severity of frequency, nocturia and slow stream correlated with bladder outlet obstruction. In contrast, stress urinary incontinence showed an inverse, but weak, correlation with bladder outlet obstruction. Stress urinary incontinence correlated moderately with urine leak. Storage symptoms showed an inverse, but weak, correlation with maximum cystometric capacity. Multivariate analysis data showed that age, urgency, urgency urinary incontinence and nocturia were independent predictors of detrusor overactivity, whereas the severity of frequency was a predictor of bladder outlet obstruction.ConclusionAs overactive bladder symptoms increase in severity, female patients tend to have a smaller bladder capacity and a higher incidence of detrusor overactivity. A significant number of these patients have bladder outlet obstruction.
Salvage computed tomography‐guided transhepatic radiofrequency ablation for unresected aldosteronoma of adrenohepatic fusion after adrenalectomy
Authors: Park Jung Jae , Park Byung Kwan , Kim Jae Hyeon , Jeong Byong Chang , Kim Chan Kyo 
Published: September 2015

AbstractAdrenalectomy is a treatment of choice for functioning adrenocortical adenoma. We experienced a case of unresected aldosteronoma after right adrenalectomy. Computed tomography‐guided transhepatic radiofrequency ablation was carried out to treat the unresected functioning adenoma. The purpose of our case report was to show the clinical findings, computed tomography imaging features and computed tomography‐guided transhepatic ablation techniques for adrenocortical adenoma arising from adrenohepatic fusion.
Bronchioalveolar morphogenesis of human bronchial epithelial cells depending upon hepatocyte growth factor
Authors: Kato Takashi , Oka Kiyomasa , Nakamura Toshikazu , Ito Akihiko 
Published: September 2015

AbstractLung alveolar regeneration occurs in adult human lungs as a result of proliferation, differentiation and alveolar morphogenesis of stem cells. It is increasingly being believed that bronchial epithelial cells (BECs) have a potential as stem cells, because they are potent to differentiate into multiple central and peripheral lung cell types in three‐dimensional (3D) cultures, and they develop multiple foci with well‐differentiated histogenesis after transformed into neoplastic cells. In this study, we investigated morphogenic abilities of HBE135 human BECs immortalized by E6/E7 oncogene in 3D cultures. When HBE135 cells were cultured alone or co‐cultured with endothelial cells, the cells formed spherical colonies without branching. However, in co‐culture with lung fibroblast MRC‐9 cells, HBE135 cells formed colonies with bronchioalveolar‐like complex branching, suggesting that MRC‐9‐derived soluble factor(s) are responsible for the branching formation. MRC‐9 cells, not endothelial cells, were found to highly express hepatocyte growth factor (HGF), a soluble molecule involved in liver and kidney regeneration. An anti‐HGF neutralizing antibody severely suppressed the complex branching formation, but addition of HGF could not sufficiently compensate the morphogenic effects of MRC‐9 cells, suggesting that MCR‐9‐derived HGF was necessary but insufficient for the bronchioalveolar structure formation. Immunohistochemistry revealed that Met, a cognate receptor for HGF, was highly expressed and phosphorylated in neoplastic BECs from lung adenocarcinomas with well‐differentiated, not poorly differentiated, histogenesis. These results are consistent with the notion that BECs have an aspect of stem cells. This aspect appears to become manifest through HGF–Met signalling pathway activation.
Human scaphoid non‐unions exhibit increased osteoclast activity compared to adjacent cancellous bone
Authors: Schira Jessica , Schulte Matthias , Döbele Carmen , Wallner Christoph , Abraham Stephanie , Daigeler Adrien , Kneser Ulrich , Lehnhardt Marcus , Behr Björn 
Published: September 2015

AbstractScaphoid bones have a high prevalence for non‐union. Even with adequate treatment, bone regeneration may not occur in certain instances. Although this condition is well described, the molecular pathology of scaphoid non‐unions is still poorly defined. In this study, gene expression of osteogenic and angiogenic growth and transcription factors as well as inflammatory mediators were analysed in human scaphoid non‐unions and intraindividually compared to adjacent autologous cancellous bone from the distal radius. In addition, histology and immunohistochemical stainings were performed to verify qRT‐PCR data. Gene expression analysis revealed a significant up‐regulation of RANKL, ALP, CYCLIN D1, MMP‐13, OPG, NFATc1, TGF‐β and WNT5A in scaphoid non‐unions. Interestingly, RANKL and NFATc1, both markers for osteoclastogenesis, were significantly induced in non‐unions. Moreover, WNT5A was highly up‐regulated in all non‐union samples. TRAP staining confirmed the observation of induced osteoclastogenesis in non‐unions. With respect to genes related to osteogenesis, alkaline phosphatase was significantly up‐regulated in scaphoid non‐unions. No differences were detectable for other osteogenic genes such as RUNX‐2 or BMP‐2. Importantly, we did not detect differences in angiogenesis between scaphoid non‐unions and controls in both gene expression and immunohistochemistry. Summarized, our data indicate increased osteoclast activity in scaphoid non‐unions possibly as a result of the alterations in RANKL, TGF‐β and WNT5A expression levels. These data increase our understanding for the reduced bone regeneration capacity present in scaphoid non‐unions and may translate into the identification of new therapeutic targets to avoid secondary damages and prevent occurrence of non‐unions to scaphoid bones.
Dissecting susceptibility from exogenous triggers: the model of alopecia areata and associated inflammatory skin diseases
Authors: Garzorz N. , Alsisi M. , Todorova A. , Atenhan A. , Thomas J. , Lauffer F. , Ring J. , Schmidt‐Weber C. , Biedermann T. , Eyerich S. , Eyerich K. 
Published: September 2015

AbstractBackgroundAlopecia areata (AA) is a T‐cell‐driven autoimmune disease of the hair follicle and frequently reported to be associated with inflammatory skin diseases (ISD) such as atopic eczema (AE) or psoriasis. Interestingly, AA on the one hand and both AE and psoriasis on the other hand are believed to be driven by mutually antagonistic T‐cell subsets.ObjectiveTo characterize AA‐specific T‐cell profiles and inflammatory pattern by intra‐individual comparison of AA and coexistent ISD.Methods112 patients with AA were recruited and investigated for coexisting ISD. In‐depth analyses were performed in patients with AA and AE (n = 2), AA and psoriasis (n = 1), AA and psoriasis and AE (n = 1) and AA and lichen planus (n = 1), using histology, immunohistochemistry and cytokine staining of T cells isolated from lesional skin.ResultsOf 112 AA patients investigated, 23 suffered from an ISD. The prevalence of AE, vitiligo, psoriasis and lichen planus was higher in the investigated AA cohort than in the normal population. The clinical as well as histological phenotype of AA the coexistent ISD were unequivocal. In line with this, T‐cell infiltrates were found to be disease‐characteristics with AA and lichen planus dominated by CD8+ and IFN‐γ+ TNF‐α+ producing T cells while psoriasis lesions in the same patients were dominated by IL‐17+ and AE by IL‐4+ T cells.ConclusionAA patients have a higher incidence of various T‐cell‐driven inflammatory skin diseases than the normal population, a phenomenon which might relate to over‐activation of skin‐homing T cells and to specific immune triggers as the primary cause of inflammation. More importantly, we showed that by using AA as a model disease, our approach of intra‐individual comparison of distinct inflammatory responses in the same patient is feasible and offers the unique possibility to gain insights into disease pathogenesis independent from genetic susceptibilities.
Changes in Frailty After Kidney Transplantation
Authors: McAdams‐DeMarco Mara A. , Isaacs Kyra , Darko Louisa , Salter Megan L. , Gupta Natasha , King Elizabeth A. , Walston Jeremy , Segev Dorry L. 
Published: September 2015

ObjectivesTo understand the natural history of frailty after an aggressive surgical intervention, kidney transplantation (KT).DesignProspective cohort study (December 2008–March 2014).SettingBaltimore, Maryland.ParticipantsKidney transplantation recipients (N = 349).MeasurementsThe Fried frailty score was measured at the time of KT and during routine clinical follow‐up. Using a Cox proportional hazards model, factors associated with improvements in frailty score after KT were identified. Using a longitudinal analysis, predictors of frailty score changes after KT were identified using a multilevel mixed‐effects Poisson model.ResultsAt KT, 19.8% of recipients were frail; 1 month after KT, 33.3% were frail; at 2 months, 27.7% were frail; and at 3 months, 17.2% were frail. On average, frailty scores had worsened by 1 month (mean change 0.4, P < .001), returned to baseline by 2 months (mean change 0.2, P = .07), and improved by 3 months (mean change −0.3, P = .04) after KT. The only recipient or transplant factor associated with improvement in frailty score after KT was pre‐KT frailty (hazard ratio = 2.55, 95% confidence interval (CI) = 1.71–3.82, P < .001). Pre‐KT frailty status (relative risk (RR) = 1.49, 95% CI = 1.29–1.72, P < .001), recipient diabetes mellitus (RR = 1.26, 95% CI = 1.08–1.46, P = .003), and delayed graft function (RR = 1.22, 95% CI = 1.04–1.43, P = .02) were independently associated with long‐term changes in frailty score.ConclusionAfter KT, in adult recipients of all ages, frailty initially worsens but then improves by 3 months. Although KT recipients who were frail at KT had higher frailty scores over the long term, they were most likely to show improvements in their physiological reserve after KT, supporting the transplantation in these individuals and suggesting that pretransplant frailty is not an irreversible state of low physiological reserve.
Hyperparathyroidism Associated with Long‐Term Proton Pump Inhibitors Independent of Concurrent Bisphosphonate Therapy in Elderly Adults
Authors: Hinson Andrew M. , Wilkerson Bekka M. , Rothman‐Fitts Ivy , Riggs Ann T. , Stack Brendan C. , Bodenner Donald L. 
Published: September 2015

ObjectivesTo measure the effect of proton pump inhibitors (PPIs), with and without concurrent bisphosphonates, on parathyroid hormone (PTH), vitamin D, and calcium.DesignRetrospective chart review of individuals 60 years and older. Subjects with reduced renal function (creatinine >1.3 mg/dL) and low vitamin D (<30 ng/mL) were excluded.SettingAcademic geriatric outpatient center in southern midwest.ParticipantsIndividuals aged 60 and older with concurrent calcium, PTH, vitamin D, and creatinine laboratory measurements (N = 80) meeting labeled criteria.MeasurementsSerum calcium, PTH, vitamin D, and creatinine.ResultsChronic PPI exposure was associated with statistically significantly higher PTH (65.5 vs 30.3 pg/mL, P < .001; normal range 10–55 pg/mL) and lower calcium (9.1 vs 9.4 mg/dL, P = .02; normal range 8.5–10.5 mg/dL) than no PPI exposure. Chronic PPI exposure with concurrent BP therapy was associated with statistically significantly higher PTH (65.2 vs 43.4 pg/mL, P = .05) and lower calcium (9.2 vs 9.6 mg/dL, P = .04) than BP therapy only.ConclusionBased on the present study, chronic PPI exposure in elderly adults is associated with mild hyperparathyroidism regardless of concurrent oral BP administration.
Performance and ideology in speaking tests for adult migrants
Authors: Rydell Maria 
Published: September 2015

Language learning linked to migration is an important issue in many contemporary societies. This article discusses how adult migrants following a L2 Swedish course express beliefs on competence, language learning and language use during a test event. The theoretical framework is based on performance theory and the Bakhtinian notion of addressivity. Drawing on an interactional analysis of 27 video‐recorded paired speaking tests (a candidate‐candidate discussion) in the final national exam in an L2 Swedish course for adult migrants, the article discusses how the speaking tests could be interpreted asinstitutionalized staged performance. It is argued here that institutional performance puts ideologies on display. Stance‐taking, interactional alignment and an orientation to dominant discourses on monolingualism and integration become important resources for keeping the discussion going in front of the examiners. Finally, the study argues that the view of speaking tests as performance provides a deeper understanding of the complexity of language use in test settings.
Stall no more at polyproline stretches with the translation elongation factors EF‐P and IF‐5A
Authors: Lassak Jürgen , Wilson Daniel N. , Jung Kirsten 
Published: September 2015

SummarySynthesis of polyproline proteins leads to translation arrest. To overcome this ribosome stalling effect, bacteria depend on a specialized translation elongation factor P (EF‐P), being orthologous and functionally identical to eukaryotic/archaeal elongation factor e/aIF‐5A (recently renamed ‘EF5’). EF‐P binds to the stalled ribosome between the peptidyl‐tRNA binding and tRNA‐exiting sites, and stimulates peptidyl‐transferase activity, thus allowing translation to resume. In their active form, both EF‐P and e/aIF‐5A are post‐translationally modified at a positively charged residue, which protrudes toward the peptidyl‐transferase center when bound to the ribosome. While archaeal and eukaryotic IF‐5A strictly depend on (deoxy‐) hypusination (hypusinylation) of a conserved lysine, bacteria have evolved diverse analogous modification strategies to activate EF‐P. In Escherichia coli and Salmonella enterica a lysine is extended by β‐lysinylation and subsequently hydroxylated, whereas in Pseudomonas aeruginosa and Shewanella oneidensis an arginine in the equivalent position is rhamnosylated. Inactivation of EF‐P, or the corresponding modification systems, reduces not only bacterial fitness, but also impairs virulence. Here, we review the function of EF‐P and IF‐5A and their unusual posttranslational protein modifications.
Antagonistic within‐host interactions between plant viruses: molecular basis and impact on viral and host fitness
Authors: Syller Jerzy , Grupa Anna 
Published: September 2015

SummaryDouble infections of related or unrelated viruses frequently occur in single plants, the viral agents being inoculated into the host plant simultaneously (co‐infection) or sequentially (super‐infection). Plants attacked by viruses activate sophisticated defence pathways which operate at different levels, often at significant fitness costs, resulting in yield reduction in crop plants. The occurrence and severity of the negative effects depend on the type of within‐host interaction between the infecting viruses. Unrelated viruses generally interact with each other in a synergistic manner, whereas interactions between related viruses are mostly antagonistic. These can incur substantial fitness costs to one or both of the competitors. A relatively well‐known antagonistic interaction is cross‐protection, also referred to as super‐infection exclusion. This type of interaction occurs when a previous infection with one virus prevents or interferes with subsequent infection by a homologous second virus. The current knowledge on why and how one virus variant excludes or restricts another is scant. Super‐infection exclusion between viruses has predominantly been attributed to the induction of RNA silencing, which is a major antiviral defence mechanism in plants. There are, however, presumptions that various mechanisms are involved in this phenomenon. This review outlines the current state of knowledge concerning the molecular mechanisms behind antagonistic interactions between plant viruses. Harmful or beneficial effects of these interactions on viral and host plant fitness are also characterized. Moreover, the review briefly outlines the past and present attempts to utilize antagonistic interactions among viruses to protect crop plants against destructive diseases.
Site and mechanism of the colokinetic action of the ghrelin receptor agonist, HM01
Authors: Naitou K. , Mamerto T. P. , Pustovit R. V. , Callaghan B. , Rivera L. R. , Chan A. J. , Ringuet M. T. , Pietra C. , Furness J. B. 
Published: September 2015

AbstractBackgroundIt has been recently demonstrated that the ghrelin receptor agonist, HM01, caused defecation in rats that were treated to provide a model for the constipation of Parkinson's disease. HM01 significantly increased fecal output and increased Fos activity in neurons of the hypothalamus and hindbrain, but not in the spinal defecation center. Other ghrelin agonists act on the defecation center.MethodsReceptor pharmacology was examined in ghrelin receptor (GHSR1a) transfected cells. Anesthetized rats were used to investigate sites and mechanisms of action.Key ResultsHM01 activated rat GHSR1a at nanomolar concentrations and was antagonized by the GHSR1a antagonist, YIL781. HM01, intravenous, was potent to activate propulsive colorectal contractions. This was prevented by pelvic nerve section and by intravenous YIL781, but not by spinal cord section rostral to the defecation centers. Direct intrathecal application of HM01 to the defecation center at spinal level L6‐S1 initiated propulsive contractions of the colorectum.Conclusions & InferencesHM01 stimulates GHSR1a receptors on neurons in the lumbosacral defecation centers to cause propulsive contractions and emptying of the colorectum. It has greater potency when given systemically, compared with other GHSR1a agonists.
High prevalence of colonization of oral cavity by respiratory pathogens in frail older patients with oropharyngeal dysphagia
Authors: Ortega O. , Sakwinska O. , Combremont S. , Berger B. , Sauser J. , Parra C. , Zarcero S. , Nart J. , Carrión S. , Clavé P. 
Published: September 2015

AbstractBackgroundAspiration pneumonia (AP) is caused by dysfunctional swallowing resulting in aspiration of material colonized by respiratory pathogens. The aim of this study was to assess and compare the swallowing physiology, health status, oral health status, and oral/nasal microbiota in frail older patients (FOP) with oropharyngeal dysphagia (OD) and a control group.MethodsWe studied 47 FOP (>70 year) with OD by videofluoroscopy (17 with acute pneumonia –APN‐, 15 with prior pneumonia–PNP‐ and 15 without) and 14 older controls without OD (H). Oral/nasal colonization by five respiratory pathogens was evaluated by qPCR, whereas commensal microbiota composition was assessed by pyrosequencing.Key Results(i) Frail older patients with OD presented similar comorbidities, poor functionality, polymedication, and prevalent videofluoroscopic signs of impaired safety of swallow (33.3–61.5%). However, patients with OD‐APN also presented malnutrition, delayed laryngeal vestibule closure (409.23 ± 115.6 ms; p < 0.05), and silent aspirations (15.6%). (ii) Oral health was poor in all groups, 90% presented periodontitis and 72%, caries. (iii) Total bacterial load was similar in all groups, but higher in the oropharynx (>108 CFU/mL) than in the nose (<106 CFU/mL) (p < 0.0001). Colonization by respiratory pathogens was very high: 93% in OD patients (p < 0.05 vs H); 93% in OD‐PNP (p < 0.05 vs H); 88% in OD‐APN (p = 0.07 vs H), and lower in controls (67%).Conclusions & InferencesFrail older patients with OD had impaired health status, poor oral health, high oral bacterial load, and prevalence of oral colonization by respiratory pathogens and VFS signs of impaired safety of swallow, and were therefore at risk for contracting AP.
Pure Time Preference: Reply to Johansson and Rosenqvist
Authors: Lowry Rosemary , Peterson Martin 
Published: September 2015

AbstractJohansson and Rosenqvist reject our argument for the rational permissibility of pure time preferences (PTP). Johansson and Rosenqvist's main objection is that where two options, X and Y, have equal intrinsic value, there will be a reason to be indifferent between X and Y, and therefore a reason to not hold a PTP for X or Y. In this reply, we argue that if two options have equal intrinsic value, it does not follow that you have a reason to be indifferent. Rather, the two equally large intrinsic values cancel each other out, like two equal weights on kitchen scales.
Exercise pathophysiology and the role of oxygen therapy in idiopathic interstitial pneumonia
Authors: Troy Lauren K. , Young Iven H. , Lau Edmund M.T. , Corte Tamera J. 
Published: September 2015

AbstractExercise limitation is a common feature in idiopathic interstitial pneumonia (IIP). There are multiple contributing pathophysiological mechanisms, including ventilatory mechanical limitation, impaired gas exchange, pulmonary vascular insufficiency and peripheral muscle dysfunction. Progressive exertional dyspnoea and functional incapacity impact significantly on quality of life. Exercise‐induced desaturation is frequently observed and is predictive of poorer outcomes. Tests to assess the cardiorespiratory system under stress (e.g. cardiopulmonary exercise testing and the 6‐min walk test) can provide important physiologic and prognostic information as adjuncts to resting measurements of lung function. Despite many advances in understanding disease mechanisms, therapies to improve exercise capacity, symptom burden and quality of life are lacking. Exercise training and supplemental oxygen are two potential interventions that require closer evaluation in patients with IIP.