bluuebunny/crossref_metadata_2025_split huggingface dataset:
Detecting Cyberbullying and Cyberaggression in Social Media
Authors: Chatzakou Despoina , Leontiadis Ilias , Blackburn Jeremy , Cristofaro Emiliano De , Stringhini Gianluca , Vakali Athena , Kourtellis Nicolas 
Published: October 2019

Cyberbullying and cyberaggression are increasingly worrisome phenomena affecting people across all demographics. More than half of young social media users worldwide have been exposed to such prolonged and/or coordinated digital harassment. Victims can experience a wide range of emotions, with negative consequences such as embarrassment, depression, isolation from other community members, which embed the risk to lead to even more critical consequences, such as suicide attempts.
In this work, we take the first concrete steps to understand the characteristics of abusive behavior in Twitter, one of today’s largest social media platforms. We analyze 1.2 million users and 2.1 million tweets, comparing users participating in discussions around seemingly normal topics like the NBA, to those more likely to be hate-related, such as the Gamergate controversy, or the gender pay inequality at the BBC station. We also explore specific manifestations of abusive behavior, i.e., cyberbullying and cyberaggression, in one of the hate-related communities (Gamergate). We present a robust methodology to distinguish bullies and aggressors from normal Twitter users by considering text, user, and network-based attributes. Using various state-of-the-art machine-learning algorithms, we classify these accounts with over 90% accuracy and AUC. Finally, we discuss the current status of Twitter user accounts marked as abusive by our methodology and study the performance of potential mechanisms that can be used by Twitter to suspend users in the future.
The Mobile Server Problem
Authors: Feldkord Björn , Der Heide Friedhelm Meyer Auf 
Published: October 2019

We introduce the Mobile Server problem, inspired by current trends to move computational tasks from cloud structures to multiple devices close to the end user. An example of this is embedded systems in autonomous cars that communicate to coordinate their actions.

Our model is a variant of the classical Page Migration problem. More formally, we consider a mobile server holding a data page. The server can move in the Euclidean space (of arbitrary dimension). In every round, requests for data items from the page pop up at arbitrary points in the space. The requests are served, each at a cost of the distance from the requesting point and the server, and the mobile server may move, at a cost
D
times the distance traveled for some constant
D
. We assume a maximum distance
m
that the server is allowed to move per round.

We show that no online algorithm can achieve a competitive ratio independent of the length of the input sequence in this setting. Hence, we augment the maximum movement distance of the online algorithms to (1+&delta) times the maximum distance of the offline solution. We provide a deterministic algorithm that is simple to describe and works for multiple variants of our problem. The algorithm achieves almost tight competitive ratios independent of the length of the input sequence.
Our algorithm also achieves a constant competitive ratio without resource augmentation in a variant where the movement of clients is also restricted.
Effect of General Anaesthesia versus Conscious Sedation on Clinical and Procedural Outcome in Patients Undergoing Endovascular Stroke Treatment: A Matched-Pair Analysis
Authors: Rohde Stefan , Schwarz Stephan , Alexandrou Maria , Reimann Gernot , Ellerkmann Richard Klaus , Politi Maria , Kastrup Andreas , Papanagiotou Panagiotis 
Published: October 2019

<b><i>Introduction:</i></b> General anaesthesia (GA) during mechanical thrombectomy (MT) might lead to an inferior clinical outcome compared to conscious sedation (CS). It was hypothesised that using CS might avoid a critical drop in cerebral perfusion, shorten the time of the intervention and therefore might result in better clinical outcome. In this study, we compared the procedural and clinical results of patients who underwent MT under GA or CS at two tertiary neuro-vascular centres on the basis of a matched-pair analysis. <b><i>Methods:</i></b> Using a matched-pair approach, we compared the data of 56 patients that were treated under CS at centre A (<i>n</i> = 28) with selected patients who were treated under GA at the centre B (<i>n</i> = 28). Patients were matched for age, sex, site of vessel occlusion, NIHSS at admission (±3 points), time from symptom onset to initial stroke imaging, intravenous-lysis and co-morbidities. All patients had an ASPECT-score of ≥8. To exclude the effect of technical failures, only patients with successful recanalization of the occluded vessel (TICI 2b and 3) were included into the study. The primary endpoint was the proportion of patients with early good clinical outcome after MT, defined by a modified Ranking Scale (mRS)-score ≤2 at discharge. Secondary endpoints were the time from symptom onset to the start of the procedure, the duration of the procedure and the rate of procedural complications. <b><i>Results:</i></b> There were no differences concerning gender, age, the site of vessel occlusion and the degree of stroke severity at baseline. The proportion of patients with an early good clinical outcome (mRS ≤2 at discharge) was 60.4% (17/28) in both groups. The time from symptom onset to the start of the procedure was shorter at centre B, while the duration of the procedure was significantly faster at A, resulting in an overall time from symptom onset to complete recanalization of 152.2 ± 68.0 min for patients treated at centre A and 171.1 ± 43.5 min for patients at centre B (ns). <b><i>Conclusion:</i></b> Our study revealed no differences in the investigated clinical outcome for patients undergoing endovascular stroke treatment under GA versus CS.
Atrial Fibrillation in Long QT Syndrome by Genotype
Authors: Platonov Pyotr G. , McNitt Scott , Polonsky Bronislava , Rosero Spencer Z. , Zareba Wojciech 
Published: October 2019

Background:
Long QT syndrome (LQTS) is caused by the abnormal function of ion channels, which may also affect atrial electrophysiology and be associated with the risk of atrial fibrillation (AF). However, large-scale studies of AF risk among patients with LQTS and its relation to LQTS manifestations are lacking. We aimed to assess the risk of AF and its relationship to the LQTS genotype and the long-term prognosis in patients with LQTS.

Methods:
Genotype-positive patients with LQTS (784 LQT1, 746 LQT2, and 233 LQT3) were compared with 2043 genotype-negative family members. Information on the occurrence of AF was based on physician-reported ECG-verified events. Multivariate Cox proportional hazards regression analyses were performed for ages 0 to 60 and after 60 years (reflecting an early and late-onset of AF) to assess the risk of incident AF by genotype and the relationship of AF to the risk of cardiac events defined as syncope, documented torsades de pointes, and aborted cardiac arrest or sudden cardiac death.

Results:

In patients followed from birth to 60 years of age, patients with LQT3 had an increased risk of AF compared with genotype-negative family members (hazard ratio=6.62; 95% CI, 2.04–21.49;
P
<0.001), while neither LQT1 nor LQT2 demonstrated increased AF risk. After the age of 60 years, patients with LQT2 had significantly lower risk of AF compared with genotype-negative controls (hazard ratio=0.07; 95% CI, 0.01–0.53,
P
=0.011). AF was a significant predictor of cardiac events in patients with LQT3 through the age of 60 (hazard ratio=5.38; 95% CI, 1.17–24.82;
P
=0.031).

Conclusions:
Our data demonstrate an increased risk of early age AF in patients with LQT3 and also indicate a protective effect of the LQT2 genotype in it’s association with a decreased risk of AF after the age of 60.
Impaired Autophagy in CD11b
+
Dendritic Cells Expands CD4
+
Regulatory T Cells and Limits Atherosclerosis in Mice
Authors: Clement Marc , Raffort Juliette , Lareyre Fabien , Tsiantoulas Dimitrios , Newland Stephen , Lu Yuning , Masters Leanne , Harrison James , Saveljeva Svetlana , Ma Marcella K.L. , Ozsvar-Kozma Maria , Lam Brian Y.H. , Yeo Giles S.H. , Binder Christoph J. , Kaser Arthur , Mallat Ziad 
Published: October 2019

Rationale:
Atherosclerosis is a chronic inflammatory disease. Recent studies have shown that dysfunctional autophagy in endothelial cells, smooth muscle cells, and macrophages, plays a detrimental role during atherogenesis, leading to the suggestion that autophagy-stimulating approaches may provide benefit.

Objective:
Dendritic cells (DCs) are at the crossroad of innate and adaptive immune responses and profoundly modulate the development of atherosclerosis. Intriguingly, the role of autophagy in DC function during atherosclerosis and how the autophagy process would impact disease development has not been addressed.

Methods and Results:

Here, we show that the autophagic flux in atherosclerosis-susceptible
Ldlr
−/−
(low-density lipoprotein receptor–deficient) mice is substantially higher in splenic and aortic DCs compared with macrophages and is further activated under hypercholesterolemic conditions. RNA sequencing and functional studies on selective cell populations reveal that disruption of autophagy through deletion of
Atg16l1
differentially affects the biology and functions of DC subsets in
Ldlr
−/−
mice under high-fat diet.
Atg16
l1
deficient CD11b
+
DCs develop a TGF (transforming growth factor)-β–dependent tolerogenic phenotype and promote the expansion of regulatory T cells, whereas no such effects are seen with
Atg16l1
deficient CD8α
+
DCs.
Atg16l1
deletion in DCs (all CD11c-expressing cells) expands aortic regulatory T cells in vivo, limits the accumulation of T helper cells type 1, and reduces the development of atherosclerosis in
Ldlr
−/−
mice. In contrast, no such effects are seen when
Atg16l1
is deleted selectively in conventional CD8α
+
DCs and CD103
+
DCs. Total T-cell or selective regulatory T-cell depletion abrogates the atheroprotective effect of
Atg16l1
deficient DCs.

Conclusions:

In contrast to its proatherogenic role in macrophages, autophagy disruption in DCs induces a counter-regulatory response that maintains immune homeostasis in
Ldlr
−/−
mice under high-fat diet and limits atherogenesis. Selective modulation of autophagy in DCs could constitute an interesting therapeutic target in atherosclerosis.
Impact of Neck Disability on Health‐Related Quality of Life among Head and Neck Cancer Survivors
Authors: Nilsen Marci L. , Lyu Lingyun , Belsky Michael A. , Mady Leila J. , Zandberg Dan P. , Clump David A. , Skinner Heath D. , Peddada Shyamal Das , George Susan , Johnson Jonas T. 
Published: October 2019

ObjectiveAlthough neck impairment has been described following surgical resection, limited studies have investigated its prevalence in nonsurgical treatment. The purpose of this study is to determine the prevalence and predictors of neck disability following head and neck cancer (HNC) treatment and to explore its association with quality of life (QOL).Study DesignCross‐sectional study.SettingHNC survivorship clinic.Subjects and MethodsWe identified 214 survivors who completed treatment ≥1 year prior to evaluation in the clinic. Self‐reported neck impairment was measured using the Neck Disability Index. QOL was measured using the University of Washington QOL Questionnaire, with physical and social subscale scores calculated. Regression analysis and trend tests were employed to explore associations.ResultsOver half of survivors (54.2%) reported neck disability. The odds of neck disability in survivors who received nonsurgical treatment and those who received surgery plus adjuvant treatment were 3.46 and 4.98 times higher compared to surgery alone (P =. 008, P =. 004). Survivors who underwent surgery only had higher physical and social QOL than those who received nonsurgical treatment (physical QOL: P <. 001, social QOL: P =. 023) and those who received surgery plus adjuvant treatment (physical QOL: P <. 001, social QOL: P =. 039).ConclusionThis study revealed a high prevalence of neck disability following nonsurgical treatment. While neck disability is an established sequela of surgical resection, the impact of nonsurgical treatment has gone unrecognized. Early identification and intervention to prevent progression of neck disability are crucial to optimize QOL.
A Model for the Prediction of Survival in Patients With Upper Tract Urothelial Carcinoma After Surgery
Authors: Zhang Guang-lin , Zhou Wei 
Published: October 2019

Objective: We aimed to formulate and validate prognostic nomograms that can be used to predict the prognosis of patients with upper tract urothelial carcinoma (UTUC). Methods: By consulting the Surveillance, Epidemiology, and End Results (SEER) database, we identified patients who were surgically treated for UTUC between 2004 and 2013. Variables were analyzed in both univariate and multivariate analyses. Nomograms were constructed based on independent prognostic factors. The prognostic nomogram models were established and validated internally and externally to determine their ability to predict the survival of patients with UTUC. Results: A total of 4990 patients were collected and enrolled in our analyses. Of these, 3327 patients were assigned to the training set and 1663 to the validation set. Nomograms were effectively applied to predict the 3- and 5-year survivals of patients with UTUC after surgery. The nomograms exhibited better accuracy for predicting overall survival (OS) and cancer-specific survival (CSS) than the tumor-node-metastasis (TNM) staging system and the SEER stage in both the training and validation sets. Calibration curves indicated that the nomograms exhibited high correlation to actual observed results for both OS and CSS. Conclusions: The nomogram models showed stronger predictive ability than the TNM staging system and the SEER stage. Precise estimates of the prognosis of UTUC might help doctors to make better treatment decisions.
HDL-cholesterol elevation associated with fingolimod and dimethyl fumarate therapies in multiple sclerosis
Authors: Blumenfeld Kan S , Staun-Ram E , Golan D , Miller A 
Published: October 2019

Background Patients with Multiple Sclerosis (PwMS) display altered lipoproteins levels and function, which seem to affect disease risk and progress. Whether disease-modifying therapies affect the lipoprotein profile in PwMS has scarcely been studied. Objective The study aims to assess whether fingolimod and dimethyl fumarate (DMF) affect lipoproteins in PwMS. Methods We compared retrospectively the blood lipoprotein levels of 29 fingolimod-treated and 41 DMF-treated patients before and after 3 and 12 months of therapy. Patients treated with cholesterol-reducing medications were not included. Data on weight change and disease activity during 1-year follow-up were obtained. Results HDL level, HDL/LDL ratio and HDL/total cholesterol ratio were increased in both treatment groups after 3 months’ therapy and sustained, with no change in LDL or triglycerides. While at baseline only 26% of patients met the recommended minimum of HDL 60 mg/dl, after 3 months’ therapy, 43% of fingolimod-treated and 47% of DMF-treated patients reached the recommended level. The majority of patients had no weight reduction. Conclusions Fingolimod and DMF therapies are associated with a specific increase in HDL in PwMS. Further studies are required to validate these findings and their potential implication as biomarker of reduced inflammatory state and/or reduced risk of neurodegeneration or cardiovascular comorbidity.
Targeted next generation sequencing identifies a genetic spectrum of DNA variants in patients with hemiplegic migraine
Authors: Maksemous Neven , Smith Robert A , Sutherland Heidi G , Maher Bridget H , Ibrahim Omar , Nicholson Garth A , Carpenter Elisabeth P , Lea Rod A , Cader M Zameel , Griffiths Lyn R 
Published: October 2019

Objective: Hemiplegic migraine in both familial (FHM) and sporadic (SHM) forms is a rare subtype of migraine with aura that can be traced to mutations in the CACNA1A, ATP1A2 and SCN1A genes. It is characterised by severe attacks of typical migraine accompanied by hemiparesis, as well as episodes of complex aura that vary significantly between individuals. Methods: Using a targeted next generation sequencing (NGS) multigene panel, we have sequenced the genomic DNA of 172 suspected hemiplegic migraine cases, in whom no mutation had previously been found by Sanger sequencing (SS) of a limited number of exons with high mutation frequency in FHM genes. Results: Genetic screening identified 29 variants, 10 of which were novel, in 35 cases in the three FHM genes ( CACNA1A, ATP1A2 and SCN1A). Interestingly, in this suspected HM cohort, the ATP1A2 gene harboured the highest number of variants with 24/35 cases (68.6%), while CACNA1A ranked the second gene, with 5 variants identified in 7/35 cases (20%). All detected variants were confirmed by SS and were absent in 100 non-migraine healthy control individuals. Assessment of variants with the American College of Medical Genetics and Genomics guidelines classified 8 variants as pathogenic, 3 as likely pathogenic and 18 as variants of unknown significance. Targeted NGS gene panel increased the diagnostic yield by fourfold over iterative SS in our diagnostics facility. Conclusion: We have identified 29 potentially causative variants in an Australian and New Zealand cohort of suspected HM cases and found that the ATP1A2 gene was the most commonly mutated gene. Our results suggest that screening using NGS multigene panels to investigate ATP1A2 alongside CACNA1A and SCN1A is a clinically useful and efficient method.
Development of Hematopoietic Stem Cells in the Human Embryo
Authors: Medvinsky Alexander 
Published: October 2019

Abstract
Haematopoietic stem cells (HSCs) develop intra-embryonically in the aorta-gonad-mesonephros (AGM) region, more specifically in the ventral domain of the embryonic dorsal aorta. This process is highly conserved across vertebrate species. Key transcription factors and signalling pathways involved in HSC development have been identified using various model organisms. As a mammal, the mouse represents an excellent model for understanding HSC development in the human embryo. However, in utero development significantly reduces accessibility of the embryo for experimentation, which hampers analysis of dynamic developmental processes.
We have overcome this hurdle by establishing AGM in vitro systems that can recapitulate in vivo HSC development. The generation of HSCs during embryonic development is a highly specific process. So far any significant expansion of HSCs from adult sources using solely external molecular cues have been largely unsuccessful. This is despite the fact that there is a pressing need to supply clinically relevant HSCs to some groups of patients. The generation of HSCs from pluripotent stem cells (ES/iPS cells) holds great hopes for regenerative medicine, however, this goal has not been achieved without genetic manipulations due to poor understanding of mechanisms acting in the embryo.
Using a dissociation-reaggregation AGM culture system enabled developmental hierarchy of developing mouse HSCs to be reconstructed. On co-aggregation with AGM stroma or OP9 cells, embryonic precursors mature into adult definitive HSCs, which can provide multi-lineage long-term repopulation upon transplantation into adult irradiated recipients. We have established that during development, mouse HSCs mature through upregulation CD41, CD43 and CD45 haematopoietic markers. The analysis of the AGM niche revealed a highly heterogeneous signalling landscape that can regulate HSC development in a concerted manner.
During human development, HSCs also emerge first in the ventral domain of the embryonic dorsal aorta and reside in a population, which express markers known from mouse HSC development. These first HSCs emerge in small numbers, possess an enormous regenerative/ self-renewing potential and can generate hundreds of fully functional daughter HSCs. However, it appears that establishing human AGM cultures, which recapitulate HSC development because of yet unclear reasons, is problematic. This makes it difficult to study the developing human HSC hierarchy and AGM stromal factors driving HSC development.
In this talk, commonalities and differences in mouse and human development as well as routes to the solution of this hurdle will be discussed.

Disclosures
No relevant conflicts of interest to declare.
Weight-Based Enoxaparin Dosing for Venous Thromboembolism (VTE) >100kg Gives Similar Anti-Xa Levels to Patients <100kg, with No Increase in Bleeding
Authors: Maclachlan Kylee H , Stevens Hannah P , Chunilal Sanjeev D , Tran Huyen A 
Published: October 2019

Abstract
Background: In clinical trials assessing venous thromboemobolism (VTE) management, patients with obesity are under-represented or specifically excluded. The International Society on Thrombosis and Haemostasis advises against direct-acting oral anticoagulants in patients >120kg(1). Therefore, low-molecular weight heparin and warfarin remain the standard of care in this population.
Objective : To assess weight-based enoxaparin dosing in VTE, with no capping of prescribed doses, comparing patients weighing >100kg with those weighing <100kg. The primary outcome was anti-Xa activity levels, as a surrogate marker of bleeding and recurrence risk, with the secondary outcome measures of major bleeding and VTE recurrence at 30 days.
Methods: A 5-year retrospective audit of patients with acute VTE who were prescribed enoxaparin at 1mg/kg BD, with an anti-Xa level taken 2-6 hours post-dose. Patients with an eGFR <30 were excluded.
Results: 166 patients weighing >100kg with acute VTE were identified, and 63 were excluded for not fulfilling all criteria. 64 patients weighing <100kg were assessed for comparison. Table 1 describes the patient characteristics, anti-Xa levels and clinical outcomes for patient above and below 100kg. Figure 1 demonstrates the anti-Xa levels in group 1 according to weight, and the distribution of anti-Xa levels below, within and above the therapeutic range (0.5-1.0U/mL).
Discussion: Patients above and below 100kg dosed with 1mg/kg enoxaparin BD showed no significant difference in either median anti-Xa levels, or distribution of anti-Xa activity. Regardless of weight, the majority of patients with an eGFR of 30-59 mL/min had anti-Xa levels >1.0U/mL. The obese patients did not suffer any major bleeding or VTE recurrence within 30 days. In comparison, the patients weighing <100kg, despite similar levels of anticoagulation, had higher rates of bleeding and recurrence. This was likely due to their older age and comorbidities, particularly renal impairment and concurrent cancer. These findings are consistent with the observation that bleeding risk is primarily determined by clinical characteristics rather than the anti-Xa activity alone.
Conclusion: These data support a weight-based dosing strategy for enoxaparin in obese patients with VTE, with no dose-capping, to ensure therapeutic drug levels. Routine anti-Xa levels in patients weighing >100kg, particularly in those with moderate renal impairment, allow tailoring of doses to the therapeutic anti-Xa range.
Reference:
(1) Martin K et al. Use of the direct oral anticoagulants in obese patients: guidance from the SSC of the ISTH. Journal of thrombosis and haemostasis 2016; 14: 1308-13.

Disclosures
No relevant conflicts of interest to declare.