bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differences in Pelvic Floor Symptoms During Pregnancy Between Hispanic and Non-Hispanic White Women
Authors: Saltzman Hanna M. , Egger Marlene J. , Bardsley Tyler , Ding Qian , Shaw Janet M. , Nygaard Ingrid E. 
Published: May 2018

Objectives
This study aimed to describe and compare pelvic floor symptoms and symptom burden between nulliparous Hispanic and non-Hispanic white women in the third trimester of pregnancy and to determine, in women with stress urinary incontinence (SUI), whether bother differs between groups, adjusted for UI severity.

Methods
In this cross-sectional analysis, participants completed the Epidemiology of Prolapse and Incontinence and Incontinence Severity Index questionnaires. We compared differences in symptom domains between groups using logistic regression and tested the effect of ethnicity on bother in women with SUI using linear regression.

Results
The sample comprised 418 non-Hispanic white and 154 Hispanic women. Prevalence rates of symptom domains ranged from 5.0% and 7.1% for pelvic organ prolapse to 95.2% and 94.2% for overactive bladder in non-Hispanic white and Hispanic women, respectively. After adjusting age, height, weight, education, physical activity, and gestational age, non-Hispanic whites had 2.37-fold increased odds (95% confidence interval, 1.44–3.92) for defecatory dysfunction and had nonsignificant increases in other symptom domains. Non-Hispanic whites were more likely to endorse symptoms in 3 or more domains than Hispanic women (58.9% vs 40.3%, respectively; P = 0.0001). Given the same UI severity (Incontinence Severity Index), Hispanic women with SUI reported 7.5 points greater bother (Epidemiology of Prolapse and Incontinence) than non-Hispanic white women (P = 0.07).

Conclusions
After adjustment, we found few differences in the prevalence of pelvic floor symptom domains between Hispanic and non-Hispanic white women, apart from defecatory dysfunction. If differences by ethnicity in other pelvic floor symptoms exist, they do not seem to originate during the first pregnancy.
Effect of Morbid Obesity on Midurethral Sling Efficacy for the Management of Stress Urinary Incontinence
Authors: Elshatanoufy Solafa , Matthews Alexandra , Yousif Mairy , Jamil Marcus , Gutta Sravanthi , Gill Harmanjit , Galvin Shelley L. , Luck Ali M. 
Published: May 2018

Objectives
The aim of our study was to assess midurethral sling (MUS) failure rate in the morbidly obese (body mass index [BMI] ≥40 kg/m2) population as compared with normal-weight individuals. Our secondary objective was to assess the difference in complication rates.

Methods
This is a retrospective cohort study. We included all patients who underwent a synthetic MUS procedure from January 1, 2008, to December 31, 2015, in our health system. Failure was defined as reported stress urinary incontinence symptoms or treatment for stress urinary incontinence. Variables collected were BMI; smoking status; comorbidities; perioperative (≤24 hours), short-term (≤30 days), and long-term (>30 days) complications; and follow-up time. Statistics include analysis of variance, χ2 test, logistic regression, Kaplan-Meier method, and Cox regression.

Results
There were 431 patients included in our analysis. Forty-nine patients were in class 3 with a BMI mean of 44.9 ± 5.07 kg/m2. Median follow-up time was 52 months (range, 6–119 months). Class 3 obesity (BMI ≥40 kg/m2) was the only group that had an increased risk of failure when compared with the normal-weight group (P = 0.03; odds ratio, 2.47; 95% confidence interval, 1.09–5.59). Obesity was not a significant predictor of perioperative, short-term, or long-term postoperative complications (P = 0.19, P = 0.28, and P = 0.089, respectively) after controlling for other comorbidities.

Conclusions
Patients in the class 3 obesity group who are treated with an MUS are 2 times as likely to fail when compared with those in the normal-weight category on long-term follow-up with similar low complication rates.
Long-Term Cognitive and Psychological Functioning in Post–Electroconvulsive Therapy Patients
Authors: Miller Michelle L. , Luu Hien , Gaasedelen Owen , Hahn-Ketter Amanda E. , Elmore Alexis , Dezhkam Naseem , Bayless John , Moser David J. , Whiteside Douglas M. 
Published: May 2018

Objective
Electroconvulsive therapy (ECT) is associated with positive outcomes for treatment-resistant mood disorders in the short term. However, there is limited research on long-term cognitive or psychological changes beyond 1 year after -ECT. This study evaluated long-term outcomes in cognitive functioning, psychiatric symptoms, and quality of life for individuals who had undergone ECT.

Methods
Eligible participants (N = 294) who completed a brief pre-ECT neuropsychological assessment within the last 14 years were recruited for a follow-up evaluation; a limited sample agreed to follow-up testing (n = 34). At follow-up, participants were administered cognitive measures (Repeatable Battery for the Assessment of Neuropsychological Status [RBANS], Wide Range Achievement Test-4 Word Reading, Trail Making Test, Wechsler Adult Intelligence Scale—Fourth Edition Letter Number Sequence and Digit Span, and Controlled Oral Word Association Test), along with emotional functioning measures (Beck Depression Inventory—Second Edition [BDI-II] and Beck Anxiety Inventory) and the World Health Organization Quality of Life–BREF quality of life measure. Follow-up-testing occurred on average (SD) 6.01 (3.5) years after last ECT treatment.

Results
At follow-up, a paired t test showed a large and robust reduction in mean BDI-II score. Scores in cognitive domains remained largely unchanged. A trend was observed for a mean reduction in RBANS visual spatial scores. Lower BDI-II scores were significantly associated with higher RBANS scores and improved quality of life.

Conclusions
For some ECT patients, memory, cognitive functioning, and decreases in depressive symptoms can remain intact and stable even several years after ECT. However, the selective sampling at follow-up makes these results difficult to generalize to all post-ECT patients. Future research should examine what variables may predict stable cognitive functioning and a decline in psychiatric symptoms after ECT.
PBMC Fixation and Processing for Chromium Single-Cell RNA Sequencing
Authors: Chen Jinguo , Cheung Foo , Shi Rongye , Zhou Huizhi , Wenrui Wenrui , Consortium CHI , Candia Julián , Kotliarov Yuri , Stagliano Katie R. , Tsang John S. 
Published: May 2018

AbstractBackgroundInterest in single-cell transcriptomic analysis is growing rapidly, especially for profiling rare or heterogeneous populations of cells. In almost all reported works investigators have used live cells, which introduces cell stress during preparation and hinders complex study designs. Recent studies have indicated that cells fixed by denaturing fixative can be used in single-cell sequencing, however they did not usually work with most types of primary cells including immune cells.MethodsThe methanol-fixation and new processing method was introduced to preserve human peripheral blood mononuclear cells (PBMCs) for single-cell RNA sequencing (scRNA-Seq) analysis on 10X Chromium platform.ResultsWhen methanol fixation protocol was broken up into three steps: fixation, storage and rehydration, we found that PBMC RNA was degraded during rehydration with PBS, not at cell fixation and up to three-month storage steps. Resuspension but not rehydration in 3X saline sodium citrate (SSC) buffer instead of PBS preserved PBMC RNA integrity and prevented RNA leakage. Diluted SSC buffer did not interfere with full-length cDNA synthesis. The methanol-fixed PBMCs resuspended in 3X SSC were successfully implemented into 10X Chromium standard scRNA-seq workflows with no elevated low quality cells and cell doublets. The fixation process did not alter the single-cell transcriptional profiles and gene expression levels. Major subpopulations classified by marker genes could be identified in fixed PBMCs at a similar proportion as in live PBMCs. This new fixation processing protocol also worked in several other fixed primary cell types and cell lines as in live ones.ConclusionsWe expect that the methanol-based cell fixation procedure presented here will allow better and more effective batching schemes for a complex single cell experimental design with primary cells or tissues.
Structural basis for selective stalling of human ribosome nascent chain complexes by a drug-like molecule
Authors: Li Wenfei , Ward Fred R. , McClure Kim F. , Chang Stacey Tsai-Lan , Montabana Elizabeth , Liras Spiros , Dullea Robert , Cate Jamie H. D. 
Published: May 2018

AbstractSmall molecules that target the ribosome generally have a global impact on protein synthesis. However, the drug-like molecule PF-06446846 (PF846) binds the human ribosome and selectively blocks the translation of a small subset of proteins by an unknown mechanism. In high-resolution cryo-electron microscopy (cryo-EM) structures of human ribosome nascent chain complexes stalled by PF846, PF846 binds in the ribosome exit tunnel in a newly-identified and eukaryotic-specific pocket formed by the 28S ribosomal RNA (rRNA), and redirects the path of the nascent polypeptide chain. PF846 arrests the translating ribosome in the rotated state that precedes mRNA and tRNA translocation, with peptidyl-tRNA occupying a mixture of A/A and hybrid A/P sites, in which the tRNA 3’-CCA end is improperly docked in the peptidyl transferase center. Using mRNA libraries, selections of PF846-dependent translation elongation stalling sequences reveal sequence preferences near the peptidyl transferase center, and uncover a newly-identified mechanism by which PF846 selectively blocks translation termination. These results illuminate how a small molecule selectively stalls the translation of the human ribosome, and provides a structural foundation for developing small molecules that inhibit the production of proteins of therapeutic interest.
Highly Multiplexed Single-Cell RNA-seq for Defining Cell Population and Transcriptional Spaces
Authors: Gehring Jase , Park Jong Hwee , Chen Sisi , Thomson Matthew , Pachter Lior 
Published: May 2018

AbstractWe describe a universal sample multiplexing method for single-cell RNA-seq in which cells are chemically labeled with identifying DNA oligonucleotides. Analysis of a 96-plex perturbation experiment revealed changes in cell population structure and transcriptional states that cannot be discerned from bulk measurements, establishing a cost effective means to survey cell populations from large experiments and clinical samples with the depth and resolution of single-cell RNA-seq.
Decreased mitochondrial metabolic requirements in fasting animals carry an oxidative cost
Authors: Salin Karine , Villasevil Eugenia M. , Anderson Graeme J. , Auer Sonya K. , Selman Colin , Hartley Richard C. , Mullen William , Chinopoulos Christos , Metcalfe Neil B. 
Published: May 2018

Summary

Many animals experience periods of food shortage in their natural environment. It has been hypothesised that the metabolic responses of animals to naturally‐occurring periods of food deprivation may have long‐term negative impacts on their subsequent life‐history.

In particular, reductions in energy requirements in response to fasting may help preserve limited resources but potentially come at a cost of increased oxidative stress. However, little is known about this trade‐off since studies of energy metabolism are generally conducted separately from those of oxidative stress.

Using a novel approach that combines measurements of mitochondrial function with in vivo levels of hydrogen peroxide (H2O2) in brown trout (Salmo trutta), we show here that fasting induces energy savings in a highly metabolically active organ (the liver) but at the cost of a significant increase in H2O2, an important form of reactive oxygen species (ROS).

After a 2‐week period of fasting, brown trout reduced their whole‐liver mitochondrial respiratory capacities (state 3, state 4 and cytochrome c oxidase activity), mainly due to reductions in liver size (and hence the total mitochondrial content). This was compensated for at the level of the mitochondrion, with an increase in state 3 respiration combined with a decrease in state 4 respiration, suggesting a selective increase in the capacity to produce ATP without a concomitant increase in energy dissipated through proton leakage. However, the reduction in total hepatic metabolic capacity in fasted fish was associated with an almost two‐fold increase in in vivo mitochondrial H2O2 levels (as measured by the MitoB probe).

The resulting increase in mitochondrial ROS, and hence potential risk of oxidative damage, provides mechanistic insight into the trade‐off between the short‐term energetic benefits of reducing metabolism in response to fasting and the potential long‐term costs to subsequent life‐history traits.
Maternal density stress and coccidian parasitism: Synergistic effects on overwinter survival in root voles
Authors: Yang Yan‐Bin , Shang Guo‐Zhen , Du Shou‐Yang , Zhang Xin , Wu Yan , Bian Jiang‐Hui 
Published: May 2018

Abstract

Individuals in poor physiological condition are known to be more susceptible to infection that, once it occurs, further deteriorates the individuals' conditions, making them even more susceptible to infection and leading to death. This vicious synergy between the host condition and infection has recently been proposed to be among the key factors determining the oscillation characteristics in natural populations. Field studies that directly test such a hypothesis, however, are currently scarce, and the physiological traits involved remain largely unclear.

In this field study, we systematically examined the synergistic effects of maternal stress and coccidian parasitic interaction on the physiological conditions and overwinter survival of offspring in the root vole (Microtus oeconomus) via repeated live trapping and measurements of faecal corticosterone metabolite (FCM) levels and immunocompetence in captured animals.

We found that maternal density stress significantly increased FCM levels and both the prevalence and intensity of coccidian infection in offspring, significantly suppressed offspring immunocompetence and reduced offspring overwinter survival. Coccidian infection significantly potentiated increases in FCM levels and exacerbated the immune suppression induced by maternal density stress. Coccidian infection also significantly accelerated a decrease in overwinter survival and a population decline in maternal‐density‐stressed populations.

Our findings indicate that both stress and immune systems are involved in the synergistic process through which stressors and parasites interact with the host to influence the fitness of individuals and cause a population decline in the natural environment.

A plain language summary is available for this article.
Acceleration or deceleration of litter decomposition by herbivory depends on nutrient availability through intraspecific differences in induced plant resistance traits
Authors: Burghardt Karin T. , Bradford Mark A. , Schmitz Oswald J. 
Published: May 2018

AbstractHerbivores often induce changes in plant defensive chemistry or nutrient content that may respectively inhibit or promote microbial decomposition of senesced litter. Often the directional impact of herbivores on decomposition is considered to be a property of a species or ecosystem. While rarely explored, plasticity in the induction of defensive strategies across environmental gradients may also result in divergent impacts of herbivores on decomposition (deceleration vs. acceleration).Here, we examined how soil nutrient conditions determine legacy effects of herbivory, using nine goldenrod genotypes grown across four levels of nutrient supply and with or without grasshopper herbivory. In this species, herbivory induces defensive traits in genotypes grown in high nutrient conditions but induces tolerance (compensatory growth) in low nutrient conditions. We combined senesced litter from each treatment with a common soil inoculum in microcosms and measured soil respiration and litter mass loss over 100 days as estimates of decomposition.Plant genotype, nutrient environment, and herbivory each altered decomposition. The legacy effect of herbivory overwhelmed the positive effect of high soil nutrient supply on decomposition. This significant herbivory × nutrient environment interaction meant that herbivore‐induced plants grown in high nutrient environments produced litter that was more resistant to microbial breakdown than litter from the same genotype not exposed to herbivores. But the opposite occurred at low nutrient levels where litter from herbivore‐induced plants was most readily decomposed. Furthermore, we mechanistically tie treatment‐induced changes in leaf traits to decomposition rates. Lastly, we demonstrate a significant correlation between herbivore growth rates on living tissue and decomposition efficiency by the microbial community of senesced tissue, suggesting that herbivores and microbes perceive the “quality” of the induced substrate similarly.Synthesis. Herbivore‐induced changes in leaf palatability and trait expression due to defense induction or compensatory growth can cascade through to either inhibit or promote the decomposability of leaf litter within a single species. Here, the key determinant of which occurs is the soil fertility environment of the goldenrod clone. These findings offer mechanistic understanding of how spatial heterogeneity in ecosystem process rates may be generated by spatial variation in herbivory and nutrient availability.
Reduction in polyamine catabolism leads to spermine‐mediated airway epithelial injury and induces asthma features
Authors: Jain V. , Raina S. , Gheware A. P. , Singh R. , Rehman R. , Negi V. , Murray Stewart T. , Mabalirajan U. , Mishra A. K. , Casero R. A. , Agrawal A. , Ghosh B. 
Published: May 2018

AbstractBackgroundAirway epithelial injury is a crucial component of acute and severe asthma pathogenesis and a promising target for treatment of refractory asthma. However, the underlying mechanism of epithelial injury remains poorly explored. Although high levels of polyamines, mainly spermine, have been found in asthma and comorbidity, their role in airway epithelial injury and the cause of their altered levels in asthma have not been explored.MethodsWe measured key polyamine metabolic enzymes in lung samples from normal and asthmatic subjects and in mice with OVA‐induced allergic airway inflammation (AAI). Polyamine metabolism was modulated using pharmacologic/genetic modulators. Epithelial stress and apoptosis were measured by TSLP levels and TUNEL assay, respectively.ResultsWe found loss of the polyamine catabolic enzymes spermidine/spermine‐N (1)‐acetyltransferase‐1 (SAT1) and spermine oxidase (SMOX) predominantly in bronchial epithelial cells (BECs) of human asthmatic lung samples and mice with AAI. In naïve mice, SAT1 or SMOX knockdown led to airway hyper‐responsiveness, remodeling, and BEC apoptosis. Conversely, in mice with AAI, overexpression of either SAT1 or SMOX alleviated asthmatic features and reduced TSLP levels and BEC apoptosis. Similarly, while pharmacological induction of SAT1 and SMOX using the polyamine analogue bis(ethyl)norspermine (BENSPM) alleviated asthmatic features with reduced TSLP levels and BEC apoptosis, pharmacological inhibition of these enzymes using BERENIL or MDL72527, respectively, worsened them. Spermine accumulation in lungs correlated with BEC apoptosis, and spermine treatment caused apoptosis of human BEAS‐2B cells in vitro.ConclusionsSpermine induces BEC injury. Induction of polyamine catabolism may represent a novel therapeutic approach for asthma via reversing BEC stress.
Atopic asthma after rhinovirus‐induced wheezing is associated with DNA methylation change in the SMAD3 gene promoter
Authors: Lund R. J. , Osmala M. , Malonzo M. , Lukkarinen M. , Leino A. , Salmi J. , Vuorikoski S. , Turunen R. , Vuorinen T. , Akdis C. , Lähdesmäki H. , Lahesmaa R. , Jartti T. 
Published: May 2018

AbstractChildren with rhinovirus‐induced severe early wheezing have an increased risk of developing asthma later in life. The exact molecular mechanisms for this association are still mostly unknown. To identify potential changes in the transcriptional and epigenetic regulation in rhinovirus‐associated atopic or nonatopic asthma, we analyzed a cohort of 5‐year‐old children (n = 45) according to the virus etiology of the first severe wheezing episode at the mean age of 13 months and to 5‐year asthma outcome. The development of atopic asthma in children with early rhinovirus‐induced wheezing was associated with DNA methylation changes at several genomic sites in chromosomal regions previously linked to asthma. The strongest changes in atopic asthma were detected in the promoter region of SMAD3 gene at chr 15q22.33 and introns of DDO/METTL24 genes at 6q21. These changes were validated to be present also at the average age of 8 years.
Initiating transitional care for adolescents with cystic fibrosis at the age of 12 is both feasible and promising
Authors: Skov M , Teilmann G , Damgaard I N , Nielsen K G , Hertz P G , Holgersen M G , Presfeldt M , Dalager A M S , Brask M , Boisen K A 
Published: May 2018

AbstractAimAdolescence is a vulnerable period in cystic fibrosis, associated with declining lung function. This study described, implemented and evaluated a transition programme for adolescents.MethodsWe conducted a single centre, nonrandomised and noncontrolled prospective programme at the cystic fibrosis centre at Copenhagen University Hospital Rigshospitalet from 2010 to 2011, assessing patients aged 12–18 at baseline and after 12 months. Changes implemented included staff training on communication, a more youth‐friendly feel to the outpatient clinic, the introduction of youth consultations partly alone with the adolescent, and a parents’ evening focusing on cystic fibrosis in adolescence. Lung function and body mass index (BMI) were measured monthly and adolescents were assessed for their readiness for transition and quality of life at baseline and 12 months.ResultsWe found that 40 (98%) of the eligible patients participated and youth consultations were successfully implemented with no dropouts. The readiness checklist score increased significantly over the one‐year study period, indicating increased readiness for transfer and self‐care. Overall quality of life, lung function and BMI remained stable during the study period.ConclusionA well‐structured transition programme for cystic fibrosis patients as young as 12 years of age proved to be both feasible and sustainable.