bluuebunny/crossref_metadata_2025_split huggingface dataset:
Atrial fibrillation prevalence, awareness and management in a nationwide survey of adults in China
Authors: Du Xin , Guo Lizhu , Xia Shijun , Du Jing , Anderson Craig , Arima Hisatomi , Huffman Mark , Yuan Yiqiang , Zheng Yang , Wu Shulin , Guang Xuefeng , Zhou Xianhui , Lin Hongbo , Cheng Xiaoshu , Dong Jianzeng , Ma Changsheng 
Published: January 2021

ObjectiveTo determine AF prevalence and gaps in atrial fibrillation (AF) awareness and management in China.MethodsWe conducted a community-based survey of 47 841 adults (age ≥45 years) in seven geographic regions of China between 2014 and 2016. Participants underwent a structured questionnaire, a standard 12-lead ECG, physical examination and blood sampling. AF prevalence, defined by either ECG detection or self-report, was estimated according to sampling weights, non-response and age and sex distribution of the population. We used multivariable logistic regression to estimate associations among sociodemographic, clinical and geographic factors with the AF prevalence, awareness and treatment.ResultsThe weighted AF prevalence was 1.8% (95% CI 1.7% to 1.9%), but varied from 0.9% to 2.4% across geographical regions and equates to being present in an estimated 7.9 (95% CI 7.4 to 8.4) million people in China. Among men and women, the AF prevalence increased from 0.8% and 0.6% in the age group 45–54 years to 5.4% and 4.9% in the age group ≥75 years, respectively. Proportions of people who were aware of having AF decreased overall from 65.3% in 45–54 year-olds to 53.9% in ≥75 year-olds and varied between sex (men 58.5%, women 68.8%) and residency status (urban 78.3%, rural 35.3%). Only 6.0% of patients with high-risk AF received anticoagulation therapy.ConclusionsAF prevalence is higher than previously reported in China, with low awareness and large treatment gaps. Large-scale efforts are urgently needed to reduce AF adverse consequences.
Levels of economic growth and cross-province spread of the COVID-19 in China
Authors: Mo Qiqing , Chen Xinguang , Yu Bin , Ma Zhenyu 
Published: January 2021

BackgroundAfter the first COVID-19 case detected on 8 December 2019 in Wuhan, the Provincial Capital of Hubei, the epidemic quickly spread throughout the whole country of China. Low developmental levels are often associated with infectious disease epidemic, this study attempted to test this notion with COVID-19 data.MethodsData by province from 8 December 2019 to 16 February 2020 were analysed using regression method. Outcomes were days from the first COVID-19 case in the origin of Hubei Province to the date when case was first detected in a destination province, and cumulative number of confirmed cases. Provincial gross domestic products (GDPs) were used to predict the outcomes while considering spatial distance and population density.ResultsOf the total 70 548 COVID-19 cases in all 31 provinces, 58 182 (82.5%) were detected in Hubei and 12 366 (17.5%) in other destination provinces. Regression analysis of data from the 30 provinces indicated that GDP was negatively associated with days of virus spreading (β=−0.2950, p<0.10) and positively associated with cumulative cases (β=97.8709, p<0.01) after controlling for spatial distance. The relationships were reversed with β=0.1287 (p<0.01) for days and β=−54.3756 (p<0.01) for cumulative cases after weighing in population density and controlling for spatial distance.ConclusionHigher levels of developmental is a risk factor for cross-province spread of COVID-19. This study adds new data to literature regarding the role of economic growth in facilitating spatial spreading of infectious diseases, and provides timely data informing antiepidemic strategies and developmental plan to balance economic growth and people’s health.
Effect of ambient temperature on stroke onset: a time-series analysis between 2003 and 2014 in Shenzhen, China
Authors: Li Lei , Huang Suli , Duan Yanran , Liu Peiyi , Lei Lin , Tian Yuchen , Xiang Ming , Peng Ji , Cheng Jinquan , Yin Ping 
Published: January 2021

ObjectiveEvidence on the relationship between ambient temperature and morbidity of different stroke subtypes in China is limited. This study aimed to assess the influence of ambient temperature on stroke risk in Shenzhen, China.MethodsFrom 1 January 2003 to 31 December 2014, 114 552 stroke cases in Shenzhen were collected. A generalised additive model with quasi-Poisson regression combined with a distributed lag non-linear model was applied to evaluate the temperature effects on stroke subtypes. Furthermore, this study explored the variability of the effects across sex, age and education.ResultsThe immediate heat effects on ischaemic stroke (IS) and the persistent effects of ambient temperature on intracerebral haemorrhage (ICH) were significant. Overall, the cold-related relative risks (RRs) of IS, ICH and subarachnoid haemorrhage (SAH) were 1.02 (0.97–1.07), 1.16 (1.04–1.30) and 1.12 (0.61–2.04), whereas the heat-related RRs were 1.00 (0.97–1.04), 0.80 (0.73–0.88) and 1.05 (0.63–1.78), respectively. For IS, a weakly beneficial cold effect was found among men while a detrimental heat effect among both men and women, the elderly and higher-educated population at lag0. However, regarding ICH, the temperature effects in men, the young and higher-educated population are stronger at lag0–4, lag0–7 as cold reveals threat and heat reveals protection.ConclusionResponses of diverse stroke subtypes to ambient temperature varied. Effective measures should be taken to increase public awareness about the effects of ambient temperature on stroke attack and to educate the public about self-protection.
Normal salivary gland ultrasonography could rule out the diagnosis of Sjögren’s syndrome in anti-SSA-negative patients with sicca syndrome
Authors: Al Tabaa Omar , Gouze Hélène , Hamroun Sabrina , Bergé Elisabeth , Belkhir Rakiba , Pavy Stephan , Jousse-Joulin Sandrine , Mariette Xavier 
Published: January 2021

ObjectiveTo evaluate the relevance of salivary gland ultrasound (SGUS) and its place in the diagnostic algorithm in patients referred with dry syndrome (DS) for a suspicion of Sjögren’s syndrome (SS).MethodsWe included all patients assessed at our dedicated DS clinic from June 2015 to September 2019 for which a SGUS has been carried out. Images were read blindly and the worst salivary gland was scored according to OMERACT classification. Clinical features, disease activity and treatments were collected.Results337 patients were seen from June 2015 to September 2019. 269 patients underwent SGUS. 77 patients were diagnosed with SS and 192 did not meet the ACR/EULAR criteria for SS: non-Sjögren’s DS (NSDS). Of these 192 patients, 60 had another possible cause of DS, and 132 patients were diagnosed with SAPS (sicca, asthenia, polyalgia syndrome).SGUS abnormalities were significantly higher in patients with SS versus NSDS: 51% vs 8% for a score ≥2 (p<0.0001), and 43% vs 3% for a score ≥3 (p<0.0001). SGUS score ≥2 had a specificity (Sp) of 91%, sensitivity (Se) of 57%, positive predictive value (PPV) of 72% and negative predictive value (NPV) of 82% for SS diagnosis. SGUS’s characteristics in SSA-negative patients were similar to the whole population (Se=42%, Sp=91%, PPV=42%, NPV=92%). The high specificity and NPV in this population could avoid labial salivary gland biopsy (LSGB) in SSA-negative patients with normal SGUS (186 patients, 69%).ConclusionSGUS is useful for SS diagnosis. If anti-SSA antibodies are negative and SGUS score <2, the diagnosis of SS is very improbable and LSGB could be avoided.
Analysis of the $$ \varvec{e^+ e^- \rightarrow J/\psi D{\bar{D}}}$$ reaction close to the threshold concerning claims of a $$\chi _{c0}(2P)$$ state
Authors: Wang En , Liang Wei-Hong , Oset Eulogio 
Published: January 2021

AbstractWe analyze the $$D{\bar{D}}$$

D

D

¯

mass distribution from a recent Belle experiment on the $$e^+e^- \rightarrow J/\psi D{\bar{D}}$$

e
+

e
-

→
J
/
ψ
D

D

¯

reaction, and show that the mass distribution divided by phase space does not have a clear peak above the $$D{\bar{D}}$$

D

D

¯

threshold that justifies the experimental claim of a $$\chi _{c0}(2P)$$

χ

c
0

(
2
P
)

state from those data. Then we use a unitary formalism with coupled channels $$D^+D^-$$

D
+

D
-

, $$D^0{\bar{D}}^0$$

D
0

D

¯

0

, $$D_s{\bar{D}}_s$$

D
s

D

¯

s

, and $$\eta \eta $$

η
η

, with some of the interactions taken from a theoretical model, and use the data to fix other parameters. We then show that, given the poor quality of the data, we can get different fits leading to very different $$D{\bar{D}}$$

D

D

¯

amplitudes, some of them supporting a $$D{\bar{D}}$$

D

D

¯

bound state and others not. The main conclusion is that the claim for the $$\chi _{c0}(2P)$$

χ

c
0

(
2
P
)

state, already included in the PDG, is premature, but refined data can provide very valuable information on the $$D{\bar{D}}$$

D

D

¯

scattering amplitude. As side effects, we warn about the use of a Breit-Wigner amplitude parameterization close to threshold, and show that the $$D_s{\bar{D}}_s$$

D
s

D

¯

s

channel plays an important role in this reaction.
Therapy-Induced Transdifferentiation Promotes Glioma Growth Independent of EGFR Signaling
Authors: Oh Hwanhee , Hwang Inah , Jang Ja-Young , Wu Lingxiang , Cao Dongqing , Yao Jun , Ying Haoqiang , Li Jian Yi , Yao Yu , Hu Baoli , Wang Qianghu , Zheng Hongwu , Paik Jihye 
Published: January 2021

Abstract

EGFR is frequently amplified, mutated, and overexpressed in malignant gliomas. Yet the EGFR-targeted therapies have thus far produced only marginal clinical responses, and the underlying mechanism remains poorly understood. Using an inducible oncogenic EGFR-driven glioma mouse model system, our current study reveals that a small population of glioma cells can evade therapy-initiated apoptosis and potentiate relapse development by adopting a mesenchymal-like phenotypic state that no longer depends on oncogenic EGFR signaling. Transcriptome analyses of proximal and distal treatment responses identified TGFβ/YAP/Slug signaling cascade activation as a major regulatory mechanism that promotes therapy-induced glioma mesenchymal lineage transdifferentiation. Following anti-EGFR treatment, TGFβ secreted from stressed glioma cells acted to promote YAP nuclear translocation that stimulated upregulation of the pro-mesenchymal transcriptional factor SLUG and subsequent glioma lineage transdifferentiation toward a stable therapy-refractory state. Blockade of this adaptive response through suppression of TGFβ-mediated YAP activation significantly delayed anti-EGFR relapse and prolonged animal survival. Together, our findings shed new insight into EGFR-targeted therapy resistance and suggest that combinatorial therapies of targeting both EGFR and mechanisms underlying glioma lineage transdifferentiation could ultimately lead to deeper and more durable responses.

Significance:
This study demonstrates that molecular reprogramming and lineage transdifferentiation underlie anti-EGFR therapy resistance and are clinically relevant to the development of new combinatorial targeting strategies against malignant gliomas with aberrant EGFR signaling.
Targeting IGF Perturbs Global Replication through Ribonucleotide Reductase Dysfunction
Authors: Rieunier Guillaume , Wu Xiaoning , Harris Letitia E. , Mills Jack V. , Nandakumar Ashwin , Colling Laura , Seraia Elena , Hatch Stephanie B. , Ebner Daniel V. , Folkes Lisa K. , Weyer-Czernilofsky Ulrike , Bogenrieder Thomas , Ryan Anderson J. , Macaulay Valentine M. 
Published: January 2021

Abstract

Inhibition of IGF receptor (IGF1R) delays repair of radiation-induced DNA double-strand breaks (DSB), prompting us to investigate whether IGF1R influences endogenous DNA damage. Here we demonstrate that IGF1R inhibition generates endogenous DNA lesions protected by 53BP1 bodies, indicating under-replicated DNA. In cancer cells, inhibition or depletion of IGF1R delayed replication fork progression accompanied by activation of ATR–CHK1 signaling and the intra-S-phase checkpoint. This phenotype reflected unanticipated regulation of global replication by IGF1 mediated via AKT, MEK/ERK, and JUN to influence expression of ribonucleotide reductase (RNR) subunit RRM2. Consequently, inhibition or depletion of IGF1R downregulated RRM2, compromising RNR function and perturbing dNTP supply. The resulting delay in fork progression and hallmarks of replication stress were rescued by RRM2 overexpression, confirming RRM2 as the critical factor through which IGF1 regulates replication. Suspecting existence of a backup pathway protecting from toxic sequelae of replication stress, targeted compound screens in breast cancer cells identified synergy between IGF inhibition and ATM loss. Reciprocal screens of ATM-proficient/deficient fibroblasts identified an IGF1R inhibitor as the top hit. IGF inhibition selectively compromised growth of ATM-null cells and spheroids and caused regression of ATM-null xenografts. This synthetic-lethal effect reflected conversion of single-stranded lesions in IGF-inhibited cells into toxic DSBs upon ATM inhibition. Overall, these data implicate IGF1R in alleviating replication stress, and the reciprocal IGF:ATM codependence we identify provides an approach to exploit this effect in ATM-deficient cancers.

Significance:
This study identifies regulation of ribonucleotide reductase function and dNTP supply by IGFs and demonstrates that IGF axis blockade induces replication stress and reciprocal codependence on ATM.
CanRisk Tool—A Web Interface for the Prediction of Breast and Ovarian Cancer Risk and the Likelihood of Carrying Genetic Pathogenic Variants
Authors: Carver Tim , Hartley Simon , Lee Andrew , Cunningham Alex P. , Archer Stephanie , Babb de Villiers Chantal , Roberts Jonathan , Ruston Rod , Walter Fiona M. , Tischkowitz Marc , Easton Douglas F. , Antoniou Antonis C. 
Published: January 2021

Abstract

Background:
The CanRisk Tool (https://canrisk.org) is the next-generation web interface for the latest version of the BOADICEA (Breast and Ovarian Analysis of Disease Incidence and Carrier Estimation Algorithm) state-of-the-art risk model and a forthcoming ovarian cancer risk model.

Methods:
The tool captures information on family history, rare pathogenic variants in cancer susceptibility genes, polygenic risk scores, lifestyle/hormonal/clinical features, and imaging risk factors to predict breast and ovarian cancer risks and estimate the probabilities of carrying pathogenic variants in certain genes. It was implemented using modern web frameworks, technologies, and web services to make it extensible and increase accessibility to researchers and third-party applications. The design of the graphical user interface was informed by feedback from health care professionals and a formal evaluation.

Results:
This freely accessible tool was designed to be user friendly for clinicians and to boost acceptability in clinical settings. The tool incorporates a novel graphical pedigree builder to facilitate collection of the family history data required by risk calculations.

Conclusions:
The CanRisk Tool provides health care professionals and researchers with a user-friendly interface to carry out multifactorial breast and ovarian cancer risk predictions. It is the first freely accessible cancer risk prediction program to carry the CE marking.

Impact:
There have been over 3,100 account registrations, and 98,000 breast and ovarian cancer risk calculations have been run within the first 9 months of the CanRisk Tool launch.
Perivascular Adipose Tissue Inflammation in Ischemic Heart Disease
Authors: Mazzotta Celestina , Basu Sanchita , Gower Adam C. , Karki Shakun , Farb Melissa G. , Sroczynski Emily , Zizza Elaina , Sarhan Anas , Pande Ashvin N. , Walsh Kenneth , Dobrilovic Nikola , Gokce Noyan 
Published: January 2021

Objective:
There is growing recognition that adipose tissue–derived proatherogenic mediators contribute to obesity-related cardiovascular disease. We sought to characterize regional differences in perivascular adipose tissue (PVAT) phenotype in relation to atherosclerosis susceptibility.

Approach and Results:

We examined thoracic PVAT samples in 34 subjects (body mass index 32±6 kg/m
2
, age 59±11 years) undergoing valvular, aortic, or coronary artery bypass graft surgeries and performed transcriptomic characterization using whole-genome expression profiling and quantitative polymerase chain reaction analyses. We identified a highly inflamed region of PVAT surrounding the human aortic root in close proximity to coronary takeoff and adjoining epicardial fat. In subjects undergoing coronary artery bypass graft, we found 300 genes significantly upregulated (false discovery rate
Q
<0.1) in paired samples of PVAT surrounding the aortic root compared with nonatherosclerotic left internal mammary artery. Genes encoding proteins mechanistically implicated in atherogenesis were enriched in aortic PVAT consisting of signaling pathways linked to inflammation,
WNT
(wingless-related integration site) signaling, matrix remodeling, coagulation, and angiogenesis. Overexpression of several proatherogenic transcripts, including
IL1β
,
CCL2
(
MCP-1
), and
IL6
, were confirmed by quantitative polymerase chain reaction and significantly bolstered in coronary artery disease subjects. Angiographic coronary artery disease burden quantified by the Gensini score positively correlated with the expression of inflammatory genes in PVAT. Moreover, periaortic adipose inflammation was markedly higher in obese subjects with striking upregulation (≈8-fold) of
IL1β
expression compared to nonobese individuals.

Conclusions:
Proatherogenic mediators that originate from dysfunctional PVAT may contribute to vascular disease mechanisms in human vessels. Moreover, PVAT may adopt detrimental properties under obese conditions that play a key role in the pathophysiology of ischemic heart disease.

Graphic Abstract:
A graphic abstract is available for this article.
Improvement of Maximal Exercise Performance After Catheter‐Ablation of Atrial Fibrillation and Its Prognostic Significance for Long‐Term Rhythm Outcome
Authors: Mujović Nebojša M. , Marinković Milan M. , Nedeljković Ivana , Marković Nebojša , Banović Marko , Vučićević Vera , Stanković Goran , Potpara Tatjana S. 
Published: January 2021

Background
Rhythm control may improve functional capacity in patients with atrial fibrillation (AF). Long‐term exercise tolerance improvement and its prognostic implications following catheter‐ablation (CA) of paroxysmal and nonparoxysmal AF are underreported.

Methods and Results

Consecutive patients underwent cardiopulmonary exercise testing just before and 12 months after their index CA of AF. Follow‐up 24‐hour Holter recordings were obtained at 6‐month intervals post‐CA, and any atrial arrhythmia >30 seconds detected after 3 months postprocedure was considered AF recurrence. Of 110 patients (mean age 57.5±10.6 years, 77.2% males) with paroxysmal AF (n=66) or nonparoxysmal AF (n=44), the 12‐month exercise tolerance improved significantly in those who maintained sinus rhythm during the first 12 months post‐CA (n=96), but not in patients with AF recurrence (n=14). After CA, the 12‐month respiratory exchange ratio at maximal workload significantly increased in patients with paroxysmal AF, whereas those with nonparoxysmal AF significantly reduced their heart rate during the 12‐month cardiopulmonary exercise testing (all
P
≤0.001). During the follow‐up of 42.8±7.8 months, a total of 29 patients (26.3%) experienced recurrent AF. On multivariate analysis including patients without recurrent AF at 12 months after CA, the extent of work time improvement at follow‐up cardiopulmonary exercise testing was independently associated with the rhythm outcome beyond 12 months postprocedure (hazard ratio of 0.936 [95% CI, 0.894–0.979] for each 10 seconds increase in the work time following ablation,
P
=0.004).

Conclusions
CA of AF was associated with recovery of exercise intolerance in patients with paroxysmal AF or nonparoxysmal AF. Inability to improve exercise capacity at 12 months post‐CA was an independent risk factor for later AF recurrence.
Liver Fibrosis Scoring Systems as Novel Tools for Predicting Cardiovascular Outcomes in Patients Following Elective Percutaneous Coronary Intervention
Authors: Liu Hui‐Hui , Cao Ye‐Xuan , Jin Jing‐Lu , Hua Qi , Li Yan‐Fang , Guo Yuan‐Lin , Zhu Cheng‐Gang , Wu Na‐Qiong , Gao Run‐Lin , Li Jian‐Jun 
Published: January 2021

Background
Previous studies have suggested a strong association of liver fibrosis scores (LFSs) with cardiovascular outcomes in patients with different cardiovascular diseases. Nonetheless, it is basically blank regarding the prognostic significance of LFSs in patients following percutaneous coronary intervention (PCI). This study sought to examine the potential role of LFSs in predicting long‐term outcomes in a large cohort of patients with stable coronary artery disease after elective PCI.

Methods and Results
In this multicenter, prospective study, we consecutively enrolled 4003 patients with stable coronary artery disease undergoing PCI. Eight currently available noninvasive LFSs were assessed for each subject. All patients were followed up for the occurrence of cardiovascular events including cardiovascular death, nonfatal myocardial infarction, and stroke. During an average follow‐up of 5.0±1.6 years, 315 (7.87%) major cardiovascular events were recorded. Subjects who developed cardiovascular events were more likely to have intermediate or high LFSs, including nonalcoholic fatty liver disease fibrosis score; fibrosis‐4 score; body mass index, aspartate aminotransferase/alanine aminotransferase ratio, diabetes mellitus score (BARD); and aspartate aminotransferase/alanine aminotransferase ratio. Furthermore, compared with subjects with low scores, those with intermediate plus high score levels had significantly increased risk of cardiovascular events (adjusted hazard ratios ranging 1.57–1.92). Moreover, the addition of non‐alcoholic fatty liver disease fibrosis score; fibrosis‐4 score; or body mass index, aspartate aminotransferase/alanine aminotransferase ratio, diabetes mellitus score into a model with established cardiovascular risk factors significantly improved the prediction ability.

Conclusions
High LFSs levels might be useful for predicting adverse prognosis in patients with stable coronary artery disease following PCI, suggesting the possibility of the application of LFSs in the risk stratification before elective PCI.
Challenging Western Legal Orientalism
Authors: Infantino Marta , Wang Weiwei 
Published: January 2021

Abstract
In 2014 the Chinese State Council announced the establishment of a nationwide comprehensive social credit system. Western narratives often describe the initiative as a technologically enhanced tool of autocratic control for scoring people. Yet, as the paper aims to show, similar accounts are tainted by several misunderstandings which perpetuate Western orientalist postures towards Chinese law.
For the purpose of comparatively assessing the Chinese social credit system, the paper analyses the pilot programs set up to monitor people and enterprises’ behaviour by twenty-eight Chinese cities. The analysis will demonstrate that these pilot programs rely on low-tech methodologies, have limited strings attached, and are based on a relatively transparent legal framework. From a comparative perspective, our findings suggest that Chinese cities’ experiments raise problems that are similar to those posed by measurement practices widely employed in the West.