bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cognitive profiles in persons with depressive disorder and Alzheimer’s disease
Authors: Lanza Claudia , Sejunaite Karolina , Steindel Charlotte , Scholz Ingo , Riepe Matthias W 
Published: November 2020

AbstractAlzheimer’s disease and depressive disorder are frequent in old age. Both may be associated with depressed mood and cognitive impairment. Therefore, finding a strategy to clarify the diagnosis underlying subjective complaints of impaired cognition and depressed mood in older persons is of utmost interest. We conducted a cross-sectional retrospective observational clinical cohort study using patient records from 2014 to 2018. From 3758 patients, we included patients aged 60 years and older with a Mini-Mental-Status Examination score of 24 and above. Final analysis included all patients in whom Alzheimer’s disease biomarker analysis was performed (cerebrospinal fluid markers of Alzheimer’s disease or positron emission tomography imaging; n = 179) and patients with depressive disorder in whom Alzheimer’s disease was ruled out by analysis of biomarkers suggestive of Alzheimer’s disease (n = 70). With case–control matching for age, education and gender, performance of patients with Alzheimer’s disease was worse in acquisition, consolidation and recall of verbal information and false-positive answers. None of the results, however, sufficed to differentially diagnose individual patients with Alzheimer’s disease or depressive disorder. With more severe symptoms of depression, patients with biomarker-verified Alzheimer’s disease performed worse in executive testing but were not additionally impaired in verbal episodic memory performance. We conclude that distinguishing between Alzheimer’s disease and depressive disorder is unreliable on clinical grounds and behavioural testing alone. Diagnosing the cause of subjective complaints about deteriorating cognitive function or depressed mood requires additional biomarker assessment, whereas cognitive assessment is needed to define appropriate targets of symptomatic treatment in patients with Alzheimer’s disease and depressive disorder.
Extended antibiotic therapy for the prevention of relapsing and recurrent peritonitis in peritoneal dialysis patients: a randomized controlled trial
Authors: Szeto Cheuk-Chun , Ng Jack Kit-Chung , Wing-Shing Fung Winston , Chan Gordon Chun-Kau , Cheng Phyllis Mei-Shan , Lai Ka-Bik , Pang Wing-Fai , Chow Kai-Ming , Leung Chi-Bon , Li Philip Kam-Tao 
Published: November 2020

AbstractBackgroundRelapsing and recurrent peritonitis episodes are major causes of technique failure in peritoneal dialysis (PD). We examined the efficacy of extended antibiotic therapy for the prevention of relapsing and recurrent peritonitis.MethodsFrom February 2016 to November 2018 we recruited 254 PD patients who fulfilled the diagnostic criteria for PD peritonitis. They were randomized to a standard group, with the duration of intraperitoneal (IP) antibiotic treatment following the International Society for Peritoneal Dialysis (ISPD) guideline according to the causative microorganisms, and an extended group, with 1 extra week of IP antibiotics. The primary endpoint was relapsing, recurrent or repeat peritonitis episodes within 6 months.ResultsThe primary endpoint developed in 36 and 29 patients of the extended and standard groups, respectively (28.3% versus 22.8%; P = 0.34). The rate of complete cure, without relapsing, recurrent or repeat peritonitis within 6 months, was 63.8 and 69.3% for the extended and standard groups, respectively (P = 0.35). Repeat peritonitis episodes were more common in the extended than the standard group (15.0% versus 5.5%; P = 0.013).ConclusionsIn patients with PD-related peritonitis, extending the antibiotic therapy for 1 extra week beyond the ISPD protocol should not be recommended. Extending the treatment does not reduce the risk of relapsing or recurrent peritonitis episodes but rather is associated with a higher risk of repeat peritonitis episodes.
Role of nodal skip metastasis in patients with mid-thoracic oesophageal squamous cell carcinoma: a propensity score matching study
Authors: Xu Zhi-Jie , Zhuo Ze-Guo , Song Tie-Niu , Alai Gu-Ha , Shen Xu , Yao Peng- , Lin Yi-Dan 
Published: November 2020

Abstract

OBJECTIVES
Nodal skip metastasis (NSM) is a common phenomenon in mid-thoracic oesophageal squamous cell carcinoma (MT-OSCC); however, the prognostic implications of NSM in patients with MT-OSCC remain unclear.

METHODS
This retrospective study enrolled 300 patients with MT-OSCC who underwent radical oesophagectomy and who had pathologically confirmed lymph node metastasis from January 2014 to December 2016. The patients were divided into 2 groups according to the presence or absence of NSM. Propensity score matching was applied to minimize patient selection bias. The impact of NSM on overall survival (OS) was assessed by Kaplan–Meier and multiple Cox proportional hazards analyses. The median follow-up time was 57 months.

RESULTS
The NSM rate in the entire cohort was 22.0% (66/300). Pathological N (pN) stage (P &lt; 0.001) and sex (P = 0.001) were identified as significant independent risk factors for NSM. NSM was more frequent in pN1 compared with pN2 patients (87.9% vs 12.1%, P &lt; 0.001) and no NSM was found in pN3. NSM(+) patients had better prognoses than NSM(−) patients (Kaplan–Meier; 3-year OS, 62.1% vs 34.1%, P &lt; 0.001). Propensity score matching produced 51 matched pairs, and the 3-year OS was still better in the NSM(+) compared with the NSM(−) group (66.7% vs 40.0%, P = 0.025). Multivariable Cox analysis confirmed NSM(+) as an independent factor favouring OS in patients with MT-OSCC.

CONCLUSIONS
NSM usually occurs at pN1 stage in patients with MT-OSCC, and is associated with a favourable prognosis.
Mixed evidence for the compression of morbidity hypothesis for smoking elimination—a systematic literature review
Authors: Dieteren Charlotte M , Faber Timor , van Exel Job , Brouwer Werner B F , Mackenbach Johan P , Nusselder Wilma J 
Published: November 2020

Abstract

Background
There is debate around the composition of life years gained from smoking elimination. The aim of this study was to conduct a systematic review of the literature to synthesize existing evidence on the effect of smoking status on health expectancy and to examine whether smoking elimination leads to compression of morbidity.

Methods
Five databases were systematically searched for peer-reviewed articles. Studies that presented quantitative estimates of health expectancy for smokers and non-/never-smokers were eligible for inclusion. Studies were searched, selected and reviewed by two reviewers who extracted the relevant data and assessed the risk of bias of the included articles independently.

Results
The search identified 2491 unique records, whereof 20 articles were eligible for inclusion (including 26 cohorts). The indicators used to measure health included disability/activity limitations (n=9), health-related quality of life (EQ-5D) (n=2), weighted disabilities (n=1), self-rated health (n=9), chronic diseases (n=6), cardiovascular diseases (n=4) and cognitive impairment (n=1). Available evidence showed consistently that non-/never-smokers experience more healthy life years throughout their lives than smokers. Findings were inconsistent on the effect of smoking on the absolute number of unhealthy life years. Findings concerning the time proportionally spent unhealthy were less heterogeneous: nearly all included articles reported that non-/never-smokers experience relatively less unhealthy life years (e.g. relative compression of morbidity).

Conclusions
Support for the relative compression of morbidity due to smoking elimination was evident. Further research is needed into the absolute compression of morbidity hypothesis since current evidence is mixed, and methodology of studies needs to be harmonized.
Chlamydia pneumoniaeandMycoplasma pneumoniaein children with cystic fibrosis: impact on bacterial respiratory microbiota diversity
Authors: Pittet Laure F , Bertelli Claire , Scherz Valentin , Rochat Isabelle , Mardegan Chiara , Brouillet René , Jaton Katia , Mornand Anne , Kaiser Laurent , Posfay-Barbe Klara , Asner Sandra A , Greub Gilbert 
Published: November 2020

ABSTRACTObjectives: The contribution of intracellular and fastidious bacteria in Cystic fibrosis (CF) pulmonary exacerbations, and progressive lung function decline remains unknown. This project aimed to explore their impact on bacterial microbiota diversity over time in CF children. Methods: Sixty-one children enrolled in the MUCOVIB multicentre prospective cohort provided 746 samples, mostly nasopharyngeal swabs, throat swabs and sputa which were analysed using culture, specific real-time qPCRs and 16S rRNA amplicon metagenomics. Results: Chlamydia pneumoniae (n = 3) and Mycoplasma pneumoniae (n = 1) were prospectively documented in 6.6% of CF children. Microbiota alpha-diversity in children with a documented C. pneumoniae was highly variable, similarly to children infected with Staphylococcus aureus or Pseudomonas aeruginosa. The transition from routine follow-up visits to pulmonary exacerbation (n = 17) yielded variable changes in diversity indexes with some extreme loss of diversity. Conclusions: The high rate of C. pneumoniae detection supports the need for regular screenings in CF patients. A minor impact of C. pneumoniae on the microbial community structure was documented. Although detected in a single patient, M. pneumoniae should also be considered as a possible aetiology of lung infection in CF subjects.
Optimal Contribution Selection in Highly Fecund Species With Overlapping Generations
Authors: Hamilton Matthew G 
Published: November 2020

AbstractOptimal contributions approaches to parental selection in closed breeding populations aim to maximize genetic gains, while restraining long-term inbreeding. The adoption of optimal contribution selection (OCS) in highly fecund outcrossing species presents a number of challenges not applicable to species of low fecundity (e.g., livestock) for which they were developed. This is particularly true if overlapping-generations or rolling-front breeding strategies are applied, in which case the number of individuals per family in juvenile (i.e., sexually immature) age groups is not necessarily known but is likely to be large. In these circumstances, conventional OCS procedures must be modified or a large number of dummy individuals defined, making computations onerous. Here, an approach to OCS is presented that involves the use of “between-family relationship matrices” instead of “between-individual relationship matrices.” The method is applicable to breeding programs involving highly fecund outcrossing species with overlapping generations, including circumstances where the number of juveniles per family is unknown but large.
Factors that mold the nuclear landscape of HIV-1 integration
Authors: Bedwell Gregory J , Engelman Alan N 
Published: November 2020

AbstractThe integration of retroviral reverse transcripts into the chromatin of the cells that they infect is required for virus replication. Retroviral integration has far-reaching consequences, from perpetuating deadly human diseases to molding metazoan evolution. The lentivirus human immunodeficiency virus 1 (HIV-1), which is the causative agent of the AIDS pandemic, efficiently infects interphase cells due to the active nuclear import of its preintegration complex (PIC). To enable integration, the PIC must navigate the densely-packed nuclear environment where the genome is organized into different chromatin states of varying accessibility in accordance with cellular needs. The HIV-1 capsid protein interacts with specific host factors to facilitate PIC nuclear import, while additional interactions of viral integrase, the enzyme responsible for viral DNA integration, with cellular nuclear proteins and nucleobases guide integration to specific chromosomal sites. HIV-1 integration favors transcriptionally active chromatin such as speckle-associated domains and disfavors heterochromatin including lamina-associated domains. In this review, we describe virus-host interactions that facilitate HIV-1 PIC nuclear import and integration site targeting, highlighting commonalities among factors that participate in both of these steps. We moreover discuss how the nuclear landscape influences HIV-1 integration site selection as well as the establishment of active versus latent virus infection.
Tumor edge-to-core transition promotes malignancy in primary-to-recurrent glioblastoma progression in a PLAGL1/CD109-mediated mechanism
Authors: Li Chaoxi , Cho Hee Jin , Yamashita Daisuke , Abdelrashid Moaaz , Chen Qin , Bastola Soniya , Chagoya Gustavo , Elsayed Galal A , Komarova Svetlana , Ozaki Saya , Ohtsuka Yoshihiro , Kunieda Takeharu , Kornblum Harley I , Kondo Toru , Nam Do-Hyun , Nakano Ichiro 
Published: November 2020

Abstract

Background
Glioblastoma remains highly lethal due to its inevitable recurrence. Most of this recurrence is found locally, indicating that postsurgical tumor-initiating cells (TICs) accumulate at the tumor edge. These edge-TICs then generate local recurrence harboring new core lesions. Here, we investigated the clinical significance of the edge-to-core (E-to-C) signature generating glioblastoma recurrence and sought to identify its central mediators.

Methods
First, we examined the association of E-to-C-related expression changes to patient outcome in matched primary and recurrent samples (n = 37). Specifically, we tested whether the combined decrease of the edge-TIC marker PROM1 (CD133) with the increase of the core-TIC marker CD109, representing E-to-C transition during the primary-to-recurrence progression, indicates poorer patient outcome. We then investigated the specific molecular mediators that trigger tumor recurrence driven by the E-to-C progression. Subsequently, the functional and translational significance of the identified molecule was validated with our patient-derived edge-TIC models in vitro and in vivo.

Results
Patients exhibiting the CD133low/CD109high signature upon recurrence representing E-to-C transition displayed a strong association with poorer progression-free survival and overall survival among all tested patients. Differential gene expression identified that PLAGL1 was tightly correlated with the core TIC marker CD109 and was linked to shorter patient survival. Experimentally, forced PLAGL1 overexpression enhanced, while its knockdown reduced, glioblastoma edge-derived tumor growth in vivo and subsequent mouse survival, suggesting its essential role in the E-to-C-mediated glioblastoma progression.

Conclusions
E-to-C axis represents an ongoing lethal process in primary glioblastoma contributing to its recurrence, partly in a PLAGL1/CD109-mediated mechanism.
Associations Between Tenofovir Diphosphate in Dried Blood Spots, Impaired Physical Function, and Fracture Risk
Authors: Abdo Mona , Coyle Ryan P , Seifert Sharon M , Castillo-Mancilla Jose R , Jankowski Catherine M , Mawhinney Samantha , Anderson Peter L , Erlandson Kristine M 
Published: November 2020

Abstract

Background
In this study, we evaluate associations between cumulative antiretroviral adherence/exposure, quantified using tenofovir diphosphate (TFV-DP) in dried blood spots (DBS), and human immunodeficiency virus (HIV)-related aging factors.

Methods
This is a cross-sectional analysis of younger (ages 18–35) and older (ages ≥60) persons with HIV (PWH) taking TFV disoproxil fumarate. Tenofovir diphosphate concentrations were quantified in DBS. Linear and logistic regression models were used to evaluate associations between TFV-DP and bone mineral density (BMD), physical function, frailty, and falls.

Results
Forty-five PWH were enrolled (23 younger, 22 older). Every 500 fmol/punch (equivalent to an increase in ~2 doses/week) increase in TFV-DP was associated with decreased hip BMD (−0.021 g/cm2; 95% confidence interval [CI], −0.040 to −0.002; P = .03). Adjusting for total fat mass, every 500 fmol/punch increase in TFV-DP was associated with higher odds of Short Physical Performance Battery impairment (score ≤10; adjusted odds ratio [OR], 1.6; 95% CI, 1.0–2.5; P = .04). Every 500 fmol/punch increase in TFV-DP was associated with slower 400-meter walk time (14.8 seconds; 95% CI, 3.8–25.8; P = .01) and remained significant after adjusting for age, lean body mass, body mass index (BMI), and fat mass (all P ≤ .01). Every 500 fmol/punch increase in TFV-DP was associated with higher odds of reporting a fall in the prior 6 months (OR, 1.8; 95% CI, 1.1–2.8; P = .02); this remained significant after adjusting for age, lean body mass, BMI, and total fat mass (all P &lt; .05).

Conclusions
Higher TFV-DP levels were associated with lower hip BMD, poorer physical function, and greater risk for falls, a concerning combination for increased fracture risk.
Mycobacterium Mucogenicum Bacteremia and Nodular Soft Tissue Infection in a Person Who Uses Tap Water to Inject Drugs
Authors: Boodman Carl , Smith Catherine , von Kuster Ken , Lagacé-Wiens Philippe , Wuerz Terence 
Published: November 2020

Abstract
The ongoing North American epidemic of intravenous opioid and methamphetamine use increases the occurrence of bacteremia from environmental organisms. In this study, we report a case of Mycobacterium mucogenicum bacteremia and associated nodular soft tissue infection in a person who uses tap water to inject drugs.
Having a co-morbidity predicts worse outcome in early rheumatoid arthritis despite intensive treatment: a post hoc evaluation of the pragmatic randomized controlled CareRA trial
Authors: Stouten Veerle , Westhovens René , De Cock Diederik , Van der Elst Kristien , Pazmino Sofia , Bertrand Delphine , Joly Johan , Verschueren Patrick 
Published: November 2020

Abstract

Objectives
To quantify the prevalence of co-morbidities in patients with early RA and determine their prognostic value for effectiveness outcomes in a randomized trial.

Methods
We included patients from the 2-year pragmatic randomized CareRA trial, who had early RA (diagnosis &lt; 1 year), were DMARD naïve and then treated-to-target with different remission induction schemes. Prevalence of co-morbidities was registered at baseline and the Rheumatic Diseases Comorbidity Index (RDCI; range 0–9) was calculated. We tested the relation between baseline RDCI and outcomes including disease activity (DAS28-CRP), physical function (HAQ index), quality of life (SF-36 domains) and hospitalizations over 2 years, using linear mixed models or generalized estimating equations models.

Results
Of 379 included patients, 167 (44%) had a RDCI of minimum 1. RDCI scores of 1, 2 or ≥3 were obtained in 65 (17%), 70 (19%), and 32 (8%) participants, respectively. The most frequent co-morbidity was hypertension (22%). Patients with co-morbidities had significantly higher HAQ (β = 0.215; 95% CI: 0.071, 0.358), DAS28-CRP (β = 0.225; 95% CI: 0.132, 0.319) and lower SF-36 physical component summary scores (β =−3.195; 95% CI: −4.844, −1.546) over 2 years than patients without co-morbidities, after adjusting for possible confounders including disease activity and randomized treatment. Patients with co-morbidities had over time lower chances of achieving remission (OR = 0.724; 95% CI: 0.604, 0.867) and a higher risk of hospitalization (OR = 3.725; 95% CI: 2.136, 6.494).

Conclusion
At disease onset, almost half of RA patients had at least one clinically important co-morbidity. Having co-morbidities was associated with worse functionality and disease activity outcomes over 2 years, despite intensive remission induction treatment.

Trial registration
Clinical trials NCT01172639.
Testing the contiguity of the sleep and fatigue relationship: a daily diary study
Authors: Harris Andrea L , Carmona Nicole E , Moss Taryn G , Carney Colleen E 
Published: November 2020

Abstract

Study Objectives
There is mixed evidence for the relationship between poor sleep and daytime fatigue, and some have suggested that fatigue is simply caused by lack of sleep. Although retrospective measures of insomnia and fatigue tend to correlate, other studies fail to demonstrate a link between objectively disturbed sleep and fatigue. The current study prospectively explored the relationship between sleep and fatigue among those with and without insomnia disorder.

Methods
Participants meeting Research Diagnostic Criteria for insomnia disorder (n = 33) or normal sleepers (n = 32) completed the Consensus Sleep Diary (CSD) and daily fatigue ratings for 2 weeks. Baseline questionnaires evaluated cognitive factors including unhelpful beliefs about sleep and rumination about fatigue. Hierarchical linear modeling tested the within- and between-participant relationships between sleep quality, total sleep time, and daily fatigue ratings. Mediation analyses tested if cognitive factors mediated the relationship between insomnia and fatigue.

Results
Self-reported nightly sleep quality significantly predicted subsequent daily fatigue ratings. Total sleep time was a significant predictor of fatigue within, but not between, participants. Unhelpful sleep beliefs and rumination about fatigue mediated the relationship between insomnia and fatigue reporting.

Conclusions
The results suggest that perception of sleep plays an important role in predicting reports of daytime fatigue. These findings could be used in treatment to help shift the focus away from total sleep times, and instead, focus on challenging maladaptive sleep-related cognitions to change fatigue perception.
Exploring utility of genomic epidemiology to trace origins of highly pathogenic influenza A/H7N9 in Guangdong
Authors: Bai Ru , Sikkema Reina S , Munnink Bas B Oude , Li Cong Rong , Wu Jie , Zou Lirong , Jing Yi , Lu Jing , Yuan Run Yu , Liao Ming , Koopmans Marion , Ke Chang-Wen 
Published: November 2020

AbstractThe first highly pathogenic (HP) influenza A/H7N9 was reported in Guangdong in January 2017. To investigate the emergence and spread of HP A/H7N9 in Guangdong province, we sequenced 297 viruses (58 HP A/H7N9, 19 low pathogenic (LP) A/H7N9, and 220 A/H9N2) during 2016–2017. Our analysis showed that during the fifth wave, three A/H7N9 lineages were co-circulating in Guangdong: the local LP Pearl River Delta (PRD) lineage (13%), the newly imported LP Yangtze River Delta (YRD) lineage (23%), and the HP YRD lineage (64%). Previously circulating YRD-lineage LP during the third wave evolved to the YRD-lineage HP A/H7N9 in Guangdong. All YRD-lineage LP detected during the fifth wave most likely originated from newly imported viruses into Guangdong. Genotype comparison of HP A/H7N9 suggests limited outward spread of HP A/H7N9 to other provinces. The distribution of HP A/H7N9 cleavage site variants on live poultry markets differed from that found in humans, suggesting a V1-type cleavage site may facilitate human infections.