dataesr/scientific-paragraphs-categorization huggingface dataset:
Included Studies The European Eye Epidemiology (E3) consortium is a collaborative network across Europe with the overarching aim of developing and analyzing large pooled datasets to increase understanding of eye diseases and vision loss. [33]  For this meta-analysis, we included 14 and Tromsø Eye Study) were harmonized in advance as described previously. [7]  The other seven included studies were the AugUR (Age-related diseases: understanding genetic and non-genetic influences -a study at the University of Regensburg) -Study  [34] , population the Coimbra Eye Study (CES)  [35] , the EPIC-Norfolk (European Prospective Investigation into Cancer-Norfolk) -Study  [36] , the Gutenberg Health Study (GHS)  [37] , the LIFE (Leipzig Research Centre for Civilization Diseases) -Adult Study (LIFE-Adult)  [38] , the NICOLA (Northern Ireland Cohort for the Longitudinal Study of Ageing) -Study  [39] , and the UEMS (Ural Eye and Medical study).
RESULTS Mean age of 38,694 participants (with available data on AMD, age, sex, and at least one medication) ranged from 61. 5 ± 7. 1 years in the GHS to 82. 6 ± 3. 8 years in the Crescendo-3C Study. Prevalence of any AMD ranged from 12. 1% in the GHS to 64. 5% in MARS and prevalence of late AMD ranged from 0. 5% in the EPIC-Norfolk Study to 35. 5% in MARS, with 9332 and 951 cases for any and late AMD, respectively. Table  1  presents further population characteristics and use of systemic medications. In our random-effects meta-analysis, we found LLD intake and use of anti-diabetic drugs to be associated with lower AMD prevalence in both the basic model 1 (supplemental figures 1 and 2) and the fully adjusted model 2 (OR 0. 85; 95% CI 0. 79 -0. 91; p<0. 001, I²=0%; and OR 0. 78; 95% CI 0. 66 -0.
91, p=0. 002, I²=57%, respectively; Figures  1  and 2 ). We observed no association of LLD and anti-diabetic drugs with late AMD (OR 0. 87; 95% CI 0. 71 -1. 06; p=0. 16, I²=0%; and OR 1. 12; 95% CI 0. 87 -1. 44, p=0. 37, I²=0%, for model 2 respectively; supplemental figures 3 and 4) and no association of NSAID and L-dopa with any form of AMD (supplemental figures 5-8). Additional sensitivity analyses, excluding LIFE-Adult data, showed similar results (data not shown).
[64]  Suggested mechanisms include different pathways of biological aging. Metformin is considered to have anti-oxidative and anti-inflammatory properties and to reduce oxidative stress within the RPE, which is an important part of AMD pathophysiology. [21, 64]  Rodent models indicated an influence on the adenosine triphosphate (ATP) levels, restoring cellular energy homeostasis  [65]  and an increased autophagy needed for the clearance of dysfunctional cell components. [64, 66]  Previous results, however, are not easily transferable to the general population, given that the included patients suffered from diabetes, which may interfere with AMD pathogenesis. A clinical trial investigating the safety and efficacy of metformin use to decrease GA progression in nondiabetic patients with dry AMD is being conducted at the moment (METforMIN, ClinicalTrials.
gov: NCT02684578). [67]  We found no association of NSAIDs with prevalence of any or late AMD in our population. Similarly, previous literature on NSAIDs and AMD reported inconsistent results. A recent study on female teachers reported a reduced risk of AMD in a subset of low-dose acetylsalicylic acid (ASA) and cyclooxygenase-2 (COX-2) inhibitor users using longitudinal data  [19]  and another large scale study found small effects of NSAID use on AMD incidence. [18]  In contrast, results from a randomized controlled trial (RCT) did not show an effect of ASA use on progression to late AMD  [17]. Particularly ASA, which is part of the group of NSAID and anti-thrombotic drugs has been subject to various inhomogeneous studies and has even been reported to increase the risk of AMD  [68, 69]. Yet, OTC drugs are often used as needed and not regularly and as such may underlie a recall bias more than frequently used drugs.
AMD status was objectively assessed based on color fundus photography in all studies using very similar and comparable classification systems. Image grading protocols differed slightly between studies but were either harmonized prior to our analysis or used comparable classification systems. Because a meta-analysis of all participating studies was conducted, results are not limited to one single study population only. However, several limitations need to be considered. Firstly, our study included crosssectional data only. Thus, our findings display statistical association between drug use and AMD prevalence only and do not allow for the assessment of causality or risk. Assessments of systemic medication intake differed between studies and may be subject to re-call bias, misclassification or incomplete records.
Moreover, duration of intake was not comprehensively assessed and we combined classes of drugs and did not differentiate between specific subtypes (e. g. LLD included statins and fibrates, and anti-diabetic drugs included oral drugs and insulin). Lastly, the prescription of any medication does not confirm the actual intake, which would be better represented by blood levels of the specific agent. These methodological differences may have introduced noise, reduced statistical precision and did not allow for assessments of drug-dose-relationship. As expected, when combining different large-scale (population) studies, we observed between-study heterogeneity for different variables, which was addressed by using random-effect meta-analysis. Moreover, LIFE-Adult only provided data on early AMD, different to all other studies.
M. H. , BR 6028/2-1 to CB), and by the National Institutes of Health (NIH R01 EY RES 511967 to I. M. H. ). MARS (Münster Aging and Retina Study) was supported by Deutsche Forschungsgemeinschaft (DFG) Grants HE 2293/5-1, 5-2, 5-3, and PA 357/7-1, the Intramural International Monetary Fund of the University of Muenster, the Pro Retina Foundation and the Jackstaedt Foundation (DP, HWH). The EPIC-Norfolk study (DOI 10. 22025/2019. 10. 105. 00004) has received funding from the Medical Research Council (MR/N003284/1 and MC-UU_12015/1) and Cancer Research UK (C864/A14136). The clinic for the third health examination was funded by Research into Ageing (262). We are grateful to all the participants who have been part of the project and to the many members of the study teams at the University of Cambridge who have enabled this research.
Data collection All data were collected online from patients' medical files after being screened using MTBM working lists. All data from patients diagnosed from September 1, 2019 to April 15, 2020 were collected retrospectively. Data from patients included after April 15, 2020 were collected both prospectively and consecutively. Three periods were defined according to French COVID-19 governmental containment measures. The first period (P0), prior to COVID-19, was defined from before the onset of the epidemic until February 29, 2020. From this date, French government instituted a first lockdown  [16]. The second period (P1) was defined as the first epidemic wave and lasted from March 1 to  May 11, 2020 , when the first lockdown ended. A third period (P2) was defined from May 12, 2020 to the end of the study.
Data collection included patient characteristics such as age, gender, weight, body mass index, ECOG performance status (PS) and distance between home and care centre. We also collected primary tumour location, histological type, date and type of first symptom, disease stage at diagnosis (resectable, borderline, locally advanced or metastatic according NCCN classification), and CA19-9 levels  [1, 17]. Diagnostic management was described using dates of the first specialist care consultation or admission, imaging technique, biopsy, and MTBM. Times from symptoms onset to first imaging, to diagnosis and to treatment, time from diagnosis to MTBM, and time from first imaging to treatment were calculated according to existing standards  [18]. The first therapeutic strategy (upfront surgery, preoperative (neoadjuvant or induction) chemotherapy, palliative chemotherapy or exclusive best supportive care) was defined using date of application, modalities, and justification (COVID-19 guidelines or usual guidelines)  [1, 12].
Ethical approval As this study was non-interventional, approval by an independent ethical committee was not required. The institutional review board at Reims University Hospital approved the study. All analysed patients were informed and did not express their opposition to the study. It was registered on ClinicalTrials. gov (NCT04406571). The database was built in accordance with the MR004 protocol of the Commission Nationale de l'Informatique et des Liberte´s (CNIL).
Data analysis Before analysis, each escape percentage was adjusted based on the number of paired control escape responses using Abbott's formula  26. The Kaplan-Meier survival analysis method was used to analyze and interpret mosquito behavioral response data. Multiple log-rank tests were used to compare two Kaplan-Meier survival curves for escape response data of mosquitoes exposed to contact and non-contact chambers, control and treatment, concentrations, substances and species, using the SAS version 9 software package (SAS Institute, Cary, NC)  17. Survival curve comparison patterns were considered signi cantly different at P < 0. 05. Escape times (ETs) in minutes were recorded from the beginning of the test for 25% (ET 25 ), 50% (ET 50 ) and 75% (ET 75 ) of the test mosquitoes to escape from the test chamber.
SUPPLEMENTARY INFORMATION A. Qubit mapping and gate decomposition In order to express the ansatz in terms of a qubit circuit, one needs to map the fermionic operators onto qubit operators. Among the different existing mappings, we choose the Jordan-Wigner transformation. To implement this, one first needs to choose an ordering for the different one-body states. For a Hubbard chain of length N , we choose to index the states by site index, the N first being attributed to spin-up, the N second for spin-down states, so that c † i↑ = c † i and c † i↓ = c † i+N. We express the creation and annihilation operators as follows: c † i = ⊗ j<i Z j ⊗ 0 1 0 0 = ⊗ j<i Z j ⊗ X i -iY i 2 (5) c i = ⊗ j<i Z j ⊗ 0 0 1 0 = ⊗ j<i Z j ⊗ X i + iY i 2 (6) Having express fermionic operators into Pauli strings, one can rewrite the operator contained in the ansatz: In order to prepare one-body states as initial states, we use a method based on QR decomposition  [34, 35]  implemented in the OpenFermion package  [36]  that decompose a basis transformation into a set of Givens rotations, that can be expressed as: e -i(c † i ci+1+c † i+1 ci)θ = e -i(XiXi+1+YiYi+1)θ/2 =    1 0 0 0 0 cos(θ) -i sin(θ) 0 0 i sin(θ) cos(θ) 0 0 0 0 1    , (7) G(ϕ) = e i(c † i ci+1-c † i+1 ci)ϕ = e i(XiYi+1-Xi+1Yi)ϕ/2 =    1 0 0 0 0 cos(ϕ) -sin(ϕ) 0 0 sin(ϕ) cos(ϕ) 0 0 0 0 1    (9) The last step is to find a gate decomposition that suits one's hardware specification.
Study design and oversight The RIVA-SVT 100 study was an international, single group assignment, open-label, prospective cohort study aiming to treat portal, mesenteric, and splenic vein thrombosis with rivaroxaban. The study was sponsored by the University of Insubria in Varese, Italy, and partially financed by Bayer AG, Germany, and the Canadian Venous Thromboembolism Research Network (CanVECTOR). A steering committee was responsible for the design and conduct of the study and analysis of the data. A total of 18 centers from Italy, Canada, France, and Germany participated in the study. The coordinating center in Varese collected the data. Local data managers and a member of the steering committee (N. R. ) regularly monitored and reviewed the data for completeness and generated queries sent to all participating centers in case of inconsistencies or missing information.
Laboratory tests included complete blood count, PT/INR, aPTT, renal function test, and liver function test. The decision on the need for thrombophilia testing and the timing of the tests was entirely left to the discretion of the attending physician. If available, data were collected for the following thrombophilia types: factor V Leiden and prothrombin G20210A gene mutations; antithrombin, protein C, and protein S levels; antiphospholipid antibodies; and homocysteinemia. The same applied for the presence of the JAK2 V617F mutation.
Statistical analysis Continuous variables are expressed as mean plus or minus the standard deviation (SD) or as median with interquartile range (IQR) when data do not have a normal distribution, according to the Wilk-Shapiro test; categorical variables as absolute values and relative frequencies. According to the distribution and the number of detected events, the Student's t test or Wilcoxon rank-sum (Mann-Whitney U test) test and the x 2 or Fisher's exact tests were used to compare groups of quantitative and qualitative variables, respectively. Independent predictive factors for bleeding events (including major and clinically relevant, nonmajor bleeding) were assessed with Cox model regression. Follow-up was considered from the beginning of rivaroxaban treatment (day 0). The occurrence of outcomes during the 3-month follow-up was expressed as cumulative incidence (with 95% Wilson confidence interval [CI]).
Three-month follow-up Three patients (3%) were lost to follow-up at 3 months. After reviewing administrative databases, survival of these patients at 6 months could be confirmed. Of the 97 evaluable patients at 3 months, 90 completed study treatment with rivaroxaban according to the protocol. Of the remaining 7 patients, 6 were switched to parenteral therapy and 1 permanently stopped anticoagulation because of deterioration of clinical conditions. Mean duration of rivaroxaban treatment before interruption was 1. 4 months (SD, 0. 8 months). Reasons for switching to parenteral therapy included newly started chemotherapy (n 5 1), decision of the treating physician (n 5 1), need for surgical procedure (n 5 1), recurrent thrombosis (n 5 2), and bleeding (n 5 1). Four of these 6 patients were subsequently restarted on rivaroxaban after a minimum of 32 and a maximum of 53 days.
However, we collected this information from 8 centers, which enrolled a total of 58 patients (58%) in the study. In these centers, the total number of patients with SVT evaluated for inclusion in the study was 264; therefore, the number of excluded patients was 242 (80. 7% of the screened population). The most common reasons for exclusion were parenteral treatment duration of. 7 days in 38. 0% of cases, known liver cirrhosis in 16. 9%, ongoing treatment with VKAs in 11. 6%, and low platelet count in 10. 7%. These data suggest that for a substantial proportion of patients, the exclusion was due to a delay in the referral to participating centers and not to clinical exclusion criteria. Indeed, selection bias due to referral of selected patients to participating centers cannot be excluded, which may have influenced the prevalence of provoking factors in our population.
Acknowledgments The authors wish to thank  Dr. Giovanna Colombo  and  Dr. Lorenza Bert  u for their active role as data managers for this study. Gualtiero Palareti ,  Paolo Prandoni , and  Franco Piovella  are the central independent adjudication committee for clinical outcomes. This research was sponsored by the  University of Insubria, Varese, Italy , and partially financed by  Bayer AG, Germany  and  CanVECTOR. The  CanVECTOR Network  holds grant funding from the  Canadian Institutes of Health Research  ( CDT-142654 ) and from the  Fonds de recherche du Qu  ebec -Sant e (File #  309911 ). M. C. , A. D. , and A. L. -L. are members of the  CanVECTOR Network. W. A. , N. R. , J. B. W. , M. D. N. , V. D. S. , and M. S. are members of the steering committee. The following list of investigators were involved in patient enrollment:  Samuela Pegoraro ,  Lucia Maria Caiano , and  Giulia Conte ,  University of Insubria, Varese, Italy ;  Luise Tittl ,  Sandra Marten , and  Christiane Naue ,  Dresden University Hospital, Dresden, Germany ;  Roberto Santi ,  Luca Albertin , and  Patrizia Sciancalepore, "A.
V. , Almelo, The Netherlands) with a scan range from 10 • to 100 • 2θ. Cu-Kα was the source of the radiation; step size was fixed at 0. 003 • (2θ) and a time per step at 340 s. The High Score Plus software (version: 4. 8, Malvern Panalytical B. V. , Almelo, The Netherlands) and the ICDD (International Center for Diffraction Data, PDF4+) crystallographic database (Newtown Square, PA, USA) were used to identify the XRD diffractograms. The water absorption test (ASTM C1585) was carried out for the samples (250 mm × 250 mm × 50 mm) immersed in the distilled water to 1 /4 of their height for 30 min, 1 /2 of their height for 1 h, 3 /4 of their height for 1 h, and above the height for 24 h. At each time point, the samples were weighed. Water absorption (n) was calculated according to the formula: n = m s -m d m d * 100%, (1) where m s -the mass of the sample in a saturated state; m d -the mass of the sample in the dry state.
The compressive strength test was carried out on the MATEST 3000 kM device. The linear rate of force increase was 1. 25 kN per second. The test for each material composition was made at least three times. Measurement of thermal conductivity at 50 • C, 30 • C, 10 • C, and -10 • C was made using the HZM 446 Lambda Smal plate apparatus (NEZTSCH, Selb, Germany). The accuracy of the temperature stabilization was ±0. 2 • C. All tests were carried out after 28 days of sample curing. All data are the average of three to six repetitions. The standard deviation was calculated and presented.
EBV genome sequence reads were mapped with the Burrows-Wheeler aligner (BWA) reference-based assembly method to type 1 or type 2 EBV genomes (GenBank accession numbers NC007605 or DQ279927 [strain AG876]), allowing the resulting EBV genome sequences to be classified as type 1 or type 2 EBV based on the similarity of their Epstein-Barr nuclear antigen 2 (EBNA2) and EBNA3 genes to the reference sequences (Table  2 ). As in previous studies  (20, 21) , SPAdes de novo assemblies of the sequence reads were also made, and the major EBV contigs were then substituted into the relevant BWA sequence to produce consensus EBV genome sequences (GenBank accession numbers MT648642 to MT648662). The regions of the genomes derived from the de novo assembly contigs are underlined in Fig. 1  and in Fig. S1  in the supplemental material.
Some of the samples contained mixtures of both full-length viral genome and a viral contig with a unique deletion. Selected examples of this can be seen in Fig. 1 , in which sample 2 has the standard read depth pattern with no deletion. In sample 19, the virus genome deletion is almost complete (marked in red), and sample 21 has a partial deletion with some full-length genome also present. The complete set of read maps is shown in Fig. S1 , which shows samples 3, 6, 12, 13, and 21 to have localized partial reductions in sequence read depth. Because the deletion in sample 19 was almost complete, its GenBank sequence (GenBank accession number MT648660) lacks the deleted nucleotides, but the other samples had sufficient wild-type EBV reads present to give a complete genome in the sequence deposited in GenBank (accession numbers are listed in Table  2 ).
1 ; also see Fig. S1 ). Examination of the sequence reads in the BWA assemblies suggested boundaries of the deletions, and PCR primers that would amplify across each deletion   41 ) current (C) and new (T/NK) EBV genome sequences from patients 1 to 21 reported in this study (Table  1 ), showing that the new sequences are distributed according to their geographic origins. Current sequences were analyzed previously  (21). The cluster of type 2 EBV genomes is indicated. An enlarged version of the same data (in which the strain names can be read) is shown in Fig. S2  in the supplemental material. point were designed (primer sequences are listed in Fig. S4 ). Specific PCR products unique to each deletion that spanned the deletion points in each virus tested were obtained (Fig. 3 ). These were sequenced and confirmed the precise deletion points, also identifying any novel sequence that might be inserted at the breakpoint.
This also confirmed that the discontinuities in the EBV sequence were internal deletions in the viral genome and did not represent points of integration into the cell chromosome. Cases 3, 6, 13, and 19 had single unique deletions (coordinates are listed in Table  2 ). Case 12 had two adjacent deletions, about 1. 6 kb apart (Table  2 ). Sample 21 had a large deletion but also had a separate inversion junction, joining two parts of the EBV genome. The deletions are summarized in Fig. 4 , relative to the reference EBV genome (GenBank accession number NC007605) scale. As reported previously for the Asian CAEBV and NK/T cell lymphomas (6-8), the BART locus was frequently affected by the deletions. Our data support and extend those observations with examples of T cell infections in HV, IBD, and HLH.
MATERIALS AND METHODS Patient samples and DNA analysis. DNA was extracted from patient blood samples using the QIAamp DNA blood maxikit (Qiagen). Written informed consent was obtained from all human participants in this study in accordance with the Helsinki Declaration, local legislation, and ethical guidelines from the Comité de Protection des Personnes de l'Ile de France II, Hôpital Necker-Enfants-Malades (Paris, France). PCR analysis of EBV deletions used the Q5 Hot Start High-Fidelity DNA polymerase kit (New England Biolabs). EBV DNA target enrichment and sequencing were as described previously  (20). The reference-based sequence assembly used BWA version 0. 7. 17-r1188, and de novo assembly was with SPAdes version 3. 13. 0-Linux. BAC-cloned EBV strains. The B95-8 type 1 EBV BAC clone p2089 (35) was a kind gift from H.
J. Delecluse and W. Hammerschmidt. T2T2 B95-8 EBV, in which the EBNA2 and EBNA3 loci have been replaced by corresponding sequences from AG876 type 2 EBV, was created by sequentially recombining the EBNA3 sequence and then the EBNA2 sequence into a version of p2089 lacking the EBNA3 locus called E3KO (36), using a RecA-based bacterial recombineering strategy  (37). A 22. 1-kb region of the AG876 type 2 EBV genome containing the EBNA3 locus was captured in a hybrid yeast artificial chromosome (YAC)/BAC vector by transformation-associated recombination (TAR) cloning in yeast spheroids, and then a SalI restriction fragment excised from this clone (positions 77328 to 93838 of the AG876 sequence [GenBank accession number DQ279927]) spanning the EBNA3 region was cloned into a recombineering vector and recombined with E3KO.
The resulting EBV recombinant genome was validated by restriction digestion and sequenced after EBV hybrid enrichment  (20)  of the DNA from the virus producer cell line. This confirmed that the type 2 EBNA3 region DNA sequence replaced positions 78020 to 91439 of the type 1 EBV (numbering as in GenBank accession number NC007605). Then, plasmid p121 containing the type 2 EBNA2 gene was recombined as described previously  (38)  to give a B95-8 virus backbone with type 2 EBNA2 and EBNA3 genes. The type 2 EBNA3 region in this virus includes the sections of gp350 and gp42 that differ between type 1 EBV and type 2 EBV (21) and the Zp V3 promoter  (21)  found in type 2 EBVs (Fig. 6A ). EBNA2 was the only gene replaced by the recombination at the EBNA2 locus. The type 2 Jijoye EBV genome was cloned into a BAC vector that contained GFP and hygromycin expression cassettes inserted between the BVRF1 and BVLF1 open reading frames, adapting a published procedure  (25, 39).