bluuebunny/crossref_metadata_2025_split huggingface dataset:
Central Sensitization in Chronic Musculoskeletal Pain Disorders in Different Populations: A Cross-Sectional Study
Authors: Roldán-Jiménez Cristina , Pérez-Cruzado David , Neblett Randy , Gatchel Robert , Cuesta-Vargas Antonio 
Published: February 2020

AbstractObjectiveChronic musculoskeletal pain disorders (CMPDs) are among the leading causes of disabilities across populations, resulting in high social and financial burden. This persistent pain condition may include the central sensitization (CS) phenomenon, which implies a wide range of symptoms and that may be taken into account in CMPD treatment. CS symptoms can be measured by the Central Sensitization Inventory (CSI). The aims of the study were to describe CS symptoms in patients suffering from several CMPDs and to analyze differences due to gender, age, and body mass index (BMI).DesignThis cross-sectional study recruited a total of 395 Spanish participants suffering from several CMPDs.SettingCS symptoms were measured with the Spanish Version of the CSI. The total score (0–100) and a cutoff score of 40 were recorded.SubjectsA total of 395 participants were included.ResultsThe mean CSI total score for the whole sample was 24.6 ± 12.0 points. CSI total score had subclinical values in the whole sample, whereas participants with scores &gt;40 were found across different CMPDs, such as low back pain (37.8%) and neck pain (32.4%); 14.6% of females and 1.7% of males presented CSI scores &gt;40. Patients showed significant differences in CSI cutoff point by gender (P = 0.010) and CSI total score by age (P = 0.014).ConclusionsGiven the high prevalence of clinically relevant CSI scores (&gt;40) in people with a CMPD, especially low back pain and neck pain, we recommend that clinicians supplement their assessment with the CSI for improved decision-making during treatment.
Factor Timing
Authors: Haddad Valentin , Kozak Serhiy , Santosh Shrihari 
Published: February 2020

Abstract
The optimal factor timing portfolio is equivalent to the stochastic discount factor. We propose and implement a method to characterize both empirically. Our approach imposes restrictions on the dynamics of expected returns, leading to an economically plausible SDF. Market-neutral equity factors are strongly and robustly predictable. Exploiting this predictability leads to substantial improvement in portfolio performance relative to static factor investing. The variance of the corresponding SDF is larger, is more variable over time, and exhibits different cyclical behavior than estimates ignoring this fact. These results pose new challenges for theories that aim to match the cross-section of stock returns.
Authors have furnished an Internet Appendix, which is available on the Oxford University Press Web site next to the link to the final published paper online.
A ‘forgettable minority’? Psychiatric Institutions and the Intellectually Disabled in Ireland, 1965–84
Authors: Kilgannon David 
Published: February 2020

Abstract
This article investigates the admission of the intellectually disabled to institutional psychiatric facilities in the Republic of Ireland between 1965 and 1984, using this as a way to explore disability provision and the later years of the state’s congregate mental hospital network. Drawing on institutional documents and news media, it argues that ‘handicap admissions’ continued along an established pattern, while demonstrating how these facilities remained ill-equipped to meet the needs of disabled residents. In doing so, this article begins to address the broader lacuna surrounding intellectual disability within Irish historiography, while complicating an emergent body of work on the ‘deinstitutionalisation’ of the state’s psychiatric hospitals during the late twentieth century. It suggests ways in which institutional records can be used to access patient experiences and highlights the need for further research on intellectual disability, examinations of which can contribute towards the histories of institutionalisation and social policy in post-war Ireland.
Seasonal senescence of leaves and roots of Populus trichocarpa—is the scenario the same or different?
Authors: Wojciechowska Natalia , Marzec-Schmidt Katarzyna , Kalemba Ewa M , Ludwików Agnieszka , Bagniewska-Zadworna Agnieszka 
Published: February 2020

Abstract
The remobilization and resorption of plant nutrients is considered as a crucial aspect of the seasonal senescence of plant organs. In leaves, the mechanisms responsible for the relocation of valuable compounds are well understood while the related processes in roots are still being debated. Some research indicates that remobilization in roots occurs, while other studies have not found evidence of this process. Considering that the total biomass of fine roots is equal to or greater than that of leaves, clarifying the conflicting reports and ambiguities may provide critical information on the circulation of chemical elements in forest ecosystems. This study provides new information concerning the basis for remobilization processes in roots by combining physiological data with gene expression and protein levels. We suggest that, as in leaves, molecular mechanisms involved in nitrogen (N) resorption are also activated in senescent roots. An analysis of N concentration indicated that N levels decreased during the senescence of both organs. The decrease was associated with an increase in the expression of a glutamine synthetase (GS) gene and a concomitant elevation in the amount of GS—one of the most important enzymes in N metabolism. In addition, significant accumulation of carbohydrates was observed in fine roots, which may represent an adaptation to unfavorable weather conditions that would allow remobilization to occur rather than a rapid death in response to ground frost or cold. Our results provide new insights into the senescence of plant organs and clarify contentious topics related to the remobilization process in fine roots
Relationship between serum C3/C4 ratio and prognosis of immunoglobulin A nephropathy based on propensity score matching
Authors: Zhang Yan , Duan Shu-Wei , Chen Pu , Yin Zhong , Wang Yong , Cai Guang-Yan , Chen Xiang-Mei 
Published: February 2020

Abstract

Background
Aberrant activation of the complement system plays an important role in the pathogenesis and development of immunoglobulin A nephropathy (IgAN). The relationship between serum complement and the clinical-histopathological features and outcomes of IgAN is controversial. This retrospective study aimed to examine the relationship between the complement 3/4 (C3/C4) ratio and the clinicopathologic changes and prognosis of patients with IgAN.

Methods
A total of 397 patients with primary IgAN from January 2007 to December 2012 at the Chinese People's Liberation Army General Hospital were included in this study. The correlation test and Chi-square test or one-way analysis of variance test were performed to evaluate the relationship between the C3/C4 ratio and other clinical-pathological factors. Propensity score matching and a multivariate Cox regression model were used to calculate the risk factors of renal outcome.

Results
The median follow-up period was 75 months. During the follow-up period, 62 patients (15.6%) developed into the end-stage renal disease (ESRD). The C3/C4 ratio at baseline was associated with the level of serum creatinine (SCr), 24 h urinary protein excretion (24 h Upre), global glomerular sclerosis, and tubulointerstitial lesion. The level of SCr and 24 h Upre and the degree of chronic kidney injury were statistically different among groups defined by different C3/C4 ratio levels. The survival rates of patients among groups with different C3/C4 ratio levels were different. After propensity score matching, eighty-eight pairs of patients were successfully matched, and the C3/C4 ratio was an influencing factor for the patients’ outcome (hazard ratio 0.587, 95% confidence interval 0.329–0.880). Patients with a C3/C4 ratio <3.6 had a poorer outcome compared with the others (P = 0.002).

Conclusions
IgAN patients with decreased C3/C4 ratio displayed significantly more severe clinical symptoms and chronic renal injury than patients with higher ratios. A low C3/C4 ratio could be a risk factor for patients developing to ESRD.
Estimating long-term pollution exposure effects through inverse probability weighting methods with Cox proportional hazards models
Authors: Higbee Joshua D. , Lefler Jacob S. , Burnett Richard T. , Ezzati Majid , Marshall Julian D. , Kim Sun-Young , Bechle Matthew , Robinson Allen L. , Pope C. Arden 
Published: February 2020

Background:
Fine particulate matter (PM2.5) is associated with negative health outcomes in both the short and long term. However, the cohort studies that have produced many of the estimates of long-term exposure associations may fail to account for selection bias in pollution exposure as well as covariate imbalance in the study population; therefore, causal modeling techniques may be beneficial.

Methods:
Twenty-nine years of data from the National Health Interview Survey (NHIS) was compiled and linked to modeled annual average outdoor PM2.5 concentration and restricted-use mortality data. A series of Cox proportional hazards models, adjusted using inverse probability weights, yielded causal risk estimates of long-term exposure to ambient PM2.5 on all-cause and cardiopulmonary mortality.

Results:
Covariate-adjusted estimated relative risks per 10 μg/m3 increase in PM2.5 exposure were estimated to be 1.117 (1.083, 1.152) for all-cause mortality and 1.232 (1.174, 1.292) for cardiopulmonary mortality. Inverse probability weighted Cox models provide relatively consistent and robust estimates similar to those in the unweighted baseline multivariate Cox model, though they have marginally lower point estimates and higher standard errors.

Conclusions:
These results provide evidence that long-term exposure to PM2.5 contributes to increased mortality risk in US adults and that the estimated effects are generally robust to modeling choices. The size and robustness of estimated associations highlight the importance of clean air as a matter of public health. Estimated confounding due to measured covariates appears minimal in the NHIS cohort, and various distributional assumptions have little bearing on the magnitude or standard errors of estimated causal associations.
Sevoflurane sedation attenuates early cerebral oedema formation through stabilisation of the adherens junction protein beta catenin in a model of subarachnoid haemorrhage
Authors: Beck-Schimmer Beatrice , Restin Tanja , Muroi Carl , Roth Z’Graggen Birgit , Keller Emanuela , Schläpfer Martin 
Published: February 2020

BACKGROUND
Severe neurological impairment is a problem after subarachnoid haemorrhage (SAH). Although volatile anaesthetics, such as sevoflurane, have demonstrated protective properties in many organs, their use in cerebral injury is controversial. Cerebral vasodilation may lead to increased intracranial pressure (ICP), but at the same time volatile anaesthetics are known to stabilise the SAH-injured endothelial barrier.

OBJECTIVE
To test the effect of sevoflurane on ICP and blood–brain barrier function.

DESIGN
Randomised study.

PARTICIPANTS
One hundred male Wistar rats included, 96 analysed.

INTERVENTIONS
SAH was induced by the endoluminal filament method under ketamine/xylazine anaesthesia. Fifteen minutes after sham surgery or induction of SAH, adult male Wistar rats were randomised to 4 h sedation with either propofol or sevoflurane.

MAIN OUTCOME MEASURES
Mean arterial pressure (MAP), ICP, extravasation of water (small), Evan's blue (intermediate) and IgG (large molecule) were measured. Zonula occludens-1 (ZO-1) and beta-catenin (β-catenin), as important representatives of tight and adherens junction proteins, were determined by western blot.

RESULTS
Propofol and sevoflurane sedation did not affect MAP or ICP in SAH animals. Extravasation of small molecules was higher in SAH-propofol compared with SAH-sevoflurane animals (79.1 ± 0.9 vs. 78.0 ± 0.7%, P = 0.04). For intermediate and large molecules, no difference was detected (P = 0.6 and P = 0.2). Both membrane and cytosolic fractions of ZO-1 as well as membrane β-catenin remained unaffected by the injury and type of sedation. Decreased cytosolic fraction of β-catenin in propofol-SAH animals (59 ± 15%) was found to reach values of sham animals (100%) in the presence of sevoflurane in SAH animals (89 ± 21%; P = 0.04).

CONCLUSION
This experiment demonstrates that low-dose short-term sevoflurane sedation after SAH in vivo did not affect ICP and MAP and at the same time may attenuate early brain oedema formation, potentially by preserving adherens junctions.

TRIAL REGISTRATION
No 115/2014 Veterinäramt Zürich.
From screening chromosomal anomalies to early diagnosis of fetal malformations
Authors: Achiron Reuven , Adamo Laura , Kassif Eran 
Published: February 2020

Purpose of review
The aim of this review is to understand why and how to improve the detection rate of the fetal anomalies in the first trimester.

Recent findings
The role of the first trimester is evolving from aneuploid and basic anatomical screening to a necessary tool to identifying early fetal malformations. In the past 20 years, several studies were conducted to assess the detection rate of anomalies in the first trimester, and despite the improvement in the diagnoses of spina bifida and cleft lip, many anomalies detectable in the first trimester are still being diagnosed in the second trimester scan. Analyzing the factors that improve the detection rate can show the reason why, even in recent years, only 50% of the anomalies are diagnosed in the first trimester.

Summary
Thanks to the improvement in the ultrasound technology, the fetus can be thoroughly studied even in early gestation and it is, therefore, indispensable to increase the detection rate of the anomalies diagnosable from the first trimester. The sonographer's utmost attention should be applied to all pregnancies, not only in high-risk patients, and new protocols based on the mid trimester scan are needed to spread the concept of first trimester anatomical scan.
The European Vulvovaginal Epidemiological Survey (EVES): impact on sexual function of vulvovaginal atrophy of menopause
Authors: Particco Martire , Djumaeva Stora , Nappi Rossella E. , Panay Nick , Palacios Santiago 
Published: February 2020

Abstract

Objective:
To estimate the impact of vulvovaginal atrophy (VVA) on sexual function in a clinical population of postmenopausal women.

Methods:
Women 45 to 75 years old and more than 12 months after the last menstruation, who attended menopausal/gynecological centers in Italy and Spain, were included. Women with at least one VVA symptom completed the following questionnaires: Day-to-Day Impact of Vaginal Aging (DIVA), Female Sexual Function Index (FSFI), and Female Sexual Distress Scale revised (FSDS-R). A physical gynecological examination was performed to confirm the VVA diagnosis. Data were analyzed by chi-square and Student's t tests.

Results:
In all, 2,160 evaluable women were included in the study. VVA was confirmed in 90% of the included participants. The negative impact on sexual function was significantly higher in women with than in women without confirmed VVA, as evaluated with the sexual function component (DIVA-C) of the DIVA questionnaire (P = 0.013). Statistically significant differences (P < 0.0005) were also detected in the scores of overall FSDS-R, the overall FSFI, and of all the FSFI subdomains (desire, arousal, lubrication, orgasm, satisfaction, and pain).

Conclusion:
For postmenopausal women with at least one VVA symptom, the presence of physician-confirmed VVA is associated with significant impaired sexual function, as shown by unadjusted analyses. Given the impact on quality of life and the prevalence of VVA, further research to improve and reduce VVA is warranted.
Effects of NT-814, a dual neurokinin 1 and 3 receptor antagonist, on vasomotor symptoms in postmenopausal women: a placebo-controlled, randomized trial
Authors: Trower Mike , Anderson Richard A. , Ballantyne Elizabeth , Joffe Hadine , Kerr Mary , Pawsey Steve 
Published: February 2020

Abstract

Objectives:
To evaluate the safety, pharmacokinetics, and preliminary efficacy of NT-814, a dual neurokinin 1,3 antagonist, in postmenopausal women with vasomotor symptoms (hot flashes).

Methods:
We completed a double-blind, randomized, placebo-controlled trial in three US clinical research units in 76 postmenopausal women with moderate/severe hot flashes. Participants were randomized to 14 days of once-daily NT-814 or placebo within each of four sequential dose cohorts; 50, 100, 150, and 300 mg. Participants completed diaries of hot flash frequency and severity and waking due to night sweats before (baseline) and during treatment.

Results:
All prespecified efficacy parameters (24-h hot flash frequency and severity, frequency of waking due to night sweats) decreased in all groups (including placebo). Mean reduction from baseline at week 2 in moderate/severe hot flash frequency was 37% in the placebo group and, respectively, 24% (P = 0.048 vs placebo), 59% (P = 0.155), 84% (P < 0.001) and 66% (P = 0.022) in the 50 mg, 100 mg, 150 mg, and 300 mg NT-814 groups; in waking due to night sweats reduction was 20% (P = 0.059), 55% (P = 0.135), 81% (P < 0.001), and 63% (P = 0.031) in the NT-814 groups and 32% in the placebo group. The improvement with NT-814 ≥150 mg was also evident in the first week of treatment. The most common treatment-related adverse events were mild somnolence and headache, more frequently in the 300 mg group. Safety monitoring identified no concerns.

Conclusions:
Once-daily NT-814 (≥150 mg/d) resulted in a rapid, marked improvement in hot flashes and waking due to night sweats. No safety concerns were identified. Doses up to 300 mg were well tolerated.
Molecular genetics of human hypertension
Authors: Luft Friedrich C. 
Published: February 2020

Purpose of review
Genetic variance on blood pressure was shown about 100 years ago; a Mendelian inheritance was initially presumed. Platt and Pickering conducted a lively debate, whether blood pressure was inherited in a Mendelian fashion or whether the condition was polygenic. Genetic-hypertension research has appropriately followed both pathways.

Recent findings
Genome-wide association studies, Pickering model, have identified more than 500 blood-pressure loci, the targets of which are waiting to be evaluated. Then, come the ‘dark-horses’ of hypertension, namely ‘secondary’ causes. These conditions have been remarkably elucidative including pheochromocytoma, primary aldosteronism, Cushing's syndrome, and even renovascular hypertension. All these conditions feature genetic causes. Finally, arrive the Platt followers. A plethora of Mendelian conditions located within the kidney are established. These syndromes involve increased sodium (as chloride) absorption in the distal nephron. Finally, nonsalt-dependent Mendelian forms involving the vascular directly have been described. Mechanistically, Mendelian forms have large effects on blood pressure and offer effective treatment targets.

Summary
Which genetic models will bring us improved therapies? Ongoing studies will answer that question. It behooves the clinician to follow this dynamic area of research.
Role of Matrix Metalloproteinase 9 in Ocular Surface Disorders
Authors: Jamerson Emery C. , Elhusseiny Abdelrahman M. , ElSheikh Reem H. , Eleiwa Taher K. , El Sayed Yasmine M. 
Published: February 2020

Objectives:(1) To explore the role and significance of Matrix Metalloproteinase 9 (MMP-9), a proteolytic enzyme, in various ocular surface diseases of inflammatory, infectious, and traumatic etiology (2), to further elucidate the molecular mechanisms responsible for its overexpression in ocular surface disease states, and (3) to discuss possible targets of therapeutic intervention.Methods:A literature review was conducted of primary sources from 1995 onward using search results populated from the US National Library of Medicine search database.Results:MMP-9 overexpression has been found in in vitro and in vivo models of dry eye disease (DED), corneal ulceration, microbial keratitis, corneal neovascularization, ultraviolet light-induced radiation, and a host of additional surface pathologies. MMP-9 is involved in an intricate signal transduction cascade that includes induction by many proinflammatory molecules including interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-a), nuclear factor kappa light chain enhancer of activated B cells (NF-kB), platelet-activating factor, activator protein 1 (AP-1), and transforming growth factor beta (TGF-B). MMP-9 expression is blunted by a diverse array of molecular factors, such as tissue inhibitors of metalloproteinases, cyclosporine A (CyA), PES_103, epigalloccatechin-3-gallate (EGCG), N-acetylcysteine (NaC), ascorbate, tetracyclines, and corticosteroids. Inhibition of MMP-9 frequently led to improvement of ocular surface disease.Conclusions:Novel insights into the mechanistic action of MMP-9 provide potential for new therapeutic modulations of ocular surface diseases mediated by its overexpression.
Brain perfusion patterns are altered in chronic knee pain: a spatial covariance analysis of arterial spin labelling MRI
Authors: Iwabuchi Sarina J. , Xing Yue , Cottam William J. , Drabek Marianne M. , Tadjibaev Arman , Fernandes Gwen S. , Petersen Kristian K. , Arendt-Nielsen Lars , Graven-Nielsen Thomas , Valdes Ana M. , Zhang Weiya , Doherty Michael , Walsh David , Auer Dorothee P. 
Published: February 2020

Abstract
Chronic musculoskeletal pain is a common problem globally. Current evidence suggests that maladapted central pain pathways are associated with pain chronicity, for example, in postoperative pain after knee replacement. Other factors such as low mood, anxiety, and tendency to catastrophize are also important contributors. We aimed to investigate brain imaging features that underpin pain chronicity based on multivariate pattern analysis of cerebral blood flow (CBF), as a marker of maladaptive brain changes. This was achieved by identifying CBF patterns that discriminate chronic pain from pain-free conditions and by exploring their explanatory power for factors thought to drive pain chronification. In 44 chronic knee pain and 29 pain-free participants, we acquired both CBF and T1-weighted data. Participants completed questionnaires related to affective processes and pressure and cuff algometry to assess pain sensitization. Two factor scores were extracted from these scores representing negative affect and pain sensitization. A spatial covariance principal component analysis of CBF identified 5 components that significantly discriminated chronic pain participants from controls, with the unified network achieving 0.83 discriminatory accuracy (area under the curve). In chronic knee pain, significant patterns of relative hypoperfusion were evident in anterior default-mode and salience network hubs, while hyperperfusion was seen in posterior default mode, thalamus, and sensory regions. One component correlated positively with the pain sensitization score (r = 0.43, P = 0.006), suggesting that this CBF pattern reflects neural activity changes encoding pain sensitization. Here, we report a distinct chronic knee pain-related representation of CBF, pointing toward a brain signature underpinning central aspects of pain sensitization.