dataesr/scientific-paragraphs-categorization huggingface dataset:
Strengths and limitations To the best of our knowledge, this is the first large-scale interventional controlled study evaluating the impact of selective reporting for UTIs in the outpatient setting. Our sample was large (more than 21 000 E. coliepositive urine cultures with AST per year), as data were collected from the health insurance databases, which cover 99% of the population living in France. We obtained a high matching rate (87. 4%) due to the quality of data collected by laboratories and the number of variables we selected for the indirect data linkage method. Among the secondary objectives, we intended to evaluate the potential unintended clinical consequences, as data are scarce in the literature on this topic. However, even if our findings were reassuring, no causal relationship could be established between antibiotic prescriptions and medical consultations or hospitalizations.
Second, we used prescription proportions instead of rates. We made that choice to fit our objective of a decrease in the proportion of broad-spectrum antibiotics. Third, information on clinical indications is not available in the databases used. It prevented us from identifying which indication the antibiotic was prescribed for (e. g. cystitis, pyelonephritis, and indication other than UTI) and precisely measuring compliance with guidelines. The guidelines apply indiscriminately to all male patients but are different for female patients' cystitis and pyelonephritis. Thus, we estimated compliance with guidelines by sex, and for female patients, we chose to present an estimation compliance by differentiating between cystitis and pyelonephritis, the exact proportion of urine cultures prescribed for each situation is impossible to evaluate.
Ethics statement This cross-trial analysis is a secondary analysis of data that have already been individually published. Ethics approval was granted for the respective four trials from the relevant ethics committees. Consent procedures are detailed in the primary trial publications. Ethical approval for the PopART trial was granted by ethics committees of the London School of Hygiene & Tropical Medicine, the University of Zambia and Stellenbosch University. The trial was registered on ClinicalTrials. gov: NCT01900977. The SEARCH trial protocol was approved by the ethics committees at the.
Study settings Each trial has published its own protocol  [8] [9] [10] [11]  as well as its primary outcome results  [13] [14] [15] [16]. In total, the trials enrolled 105 communities (clusters) and delivered interventions reaching almost 1. 5 million people  [17]. The trials implemented different interventions (Table  1 ), data collection tools and methods (Table  2 ). All trials included a comprehensive set of interventions to provide universal access to HIV testing and facilitate linkage to HIV care  [17]. PopART, TasP, and Ya Tsie implemented doorto-door home-based services provided by community health workers. SEARCH used a hybrid model of multi-disease community-based health fairs and mobile outreach. Whilst PopART and Ya Tsie implemented universal testing only in their intervention arm, such interventions were also implemented in the control arm for SEARCH and TasP at baseline, and repeated every six months for TasP.
Measures To enumerate the population, SEARCH and TasP conducted population-wide household census. TasP updated residency data every six months at each intervention round, whilst SEARCH conducted a census prior to intervention delivery at baseline and endline. PopART randomly selected �2 000 adults per community at baseline to constitute a population cohort surveyed annually, and enrolled new individuals at months 12 and 24. In Ya Tsie, a 20% random sample of household-like structures identified by satellite imagery was selected for enumeration, enrolment, and constitution of a population cohort. HIV prevalence and the prevalence of non-suppression among PLHIV were estimated at a community level for each of the 105 communities enrolled in the four trials. Due to differences in data availability, HIV prevalence was estimated at baseline for PopART and Ya Tsie, and at or around midpoint for TasP and SEARCH (Tables  2  and S1 ).
We then estimated the expected HIV incidence reduction associated with the observed reduction in the prevalence of non-suppression among PLHIV for each trial arm of each study. Specifically, for each trial-arm in each study, we calculated the predicted change in HIV incidence from baseline to endline, summarising this change both as a difference and as a ratio. For both analyses, a bootstrap approach, in which each cluster was sampled with replacement, was applied to compute 95% confidence intervals and p-values  [19]. All analyses were performed using R version 4. 3. 0. A dedicated dataset and an R script are provided for replication (S1 File).
University of California, San Francisco; the Kenya Medical Research Institute; and the Makerere University School of Medicine in Uganda; and registered on ClinicalTrials. gov: NCT01864603. The ANRS 12249 TasP trial was approved by the Biomedical Research Ethics Committee of the University of KwaZulu-Natal, South Africa (BFC 104/11) and the Medicines Control Council of South Africa; and registered on ClinicalTrials. gov: NCT01509508 and in the South African National Clinical Trials Register: DOH-27-0512-3974. The Ya Tsie trial was approved by institutional review boards at the US Centers for Disease Control and Prevention and the Botswana Ministry of Health and Wellness; and registered on ClinicalTrials. gov: NCT01965470.
Acknowledgments The  Universal Test and Treat Trial Consortium  ( UT3C ) is composed of the teams of five trials: the Ya Tsie BCPP trial (ClinicalTrials. govNCT01965470), the MaxART trial (ClinicalTrials. gov  NCT02909218 ), the HPNT 071 PopART trial (ClinicalTrials. govNCT01900977,), the SEARCH trial (ClinicalTrials. govNCT01864603) and the  ANRS 12249 TasP trial (Clinical-Trials. govNCT01509508). The authors thank all members of the study teams including the  Universal Testing and Treatment Trials Consortium  ( UT3C ), the communities where we work, our sponsors, and all the policy makers, organizations and community members around the world engaging in efforts of HIV epidemic control. The views expressed here represent those of the authors only and do not necessarily represent the official position of the funding agencies.
Grant Ref:  MR/R010161/1. The SEARCH trial was supported by the  Division of AIDS, National Institute of Allergy and Infectious Diseases of the National Institutes of Health  (awards  U01AI099959 ,  UM1AI068636 , and  R01 AI074345-06A1 ); the  President's Emergency Plan for AIDS Relief ; and  Gilead Sciences , which provided tenofovir-emtricitabine (Truvada) in kind. The ANRS 12249 TasP trial was sponsored by the  French National Agency for AIDS and Viral Hepatitis Research (ANRS ; grant number,  2011-375 ), and funded by the  ANRS , the  Deutsche Gesellschaft fu ¨r Internationale Zusammenarbeit (GIZ ; grant number,  81151938 ), and the  Bill & Melinda Gates Foundation  through the  3ie Initiative. The Ya Tsie trial was supported by the  President's Emergency Plan for AIDS Relief  through the  Centers for Disease Control and Prevention (CDC)  (cooperative agreements  U01 GH000447  and  U2G GH001911 ); the  National Institutes of Health ; the  Oak Foundation ; and the  Sub-Saharan African Network for TB/HIV Research Excellence (SANTHE) , a  Developing Excellence in Leadership , Training, and  Science (DELTAS) Africa initiative  (grant  DEL-15-006 , through  Wellcome Trust   107752/Z/15/Z ).
Lower Fluorescence in situ hybridization of mouse chromosomes using the human ALOX15 cDNA as probe. Pro-metaphase chromosomes were prepared as described in Section 4. (A) A Metaphase spread prepared from hepatocytes of a heterozygous founder animal is shown after the M-FISH set using all 21 murine whole chromosomes. In the white frame, the inverted 4 ,6-diamidino-2phenylindole counter-staining of the same metaphase is shown with the signal of the ALOX15 cDNA (red signal) from the first round of FISH (for details see Section 4). Accordingly, the human ALOX15 cDNA was inserted in one of the two murine chromosomes 2 (#2), more exactly into subband 2E1~E2. (B) FISH result of a homozygous aP2-ALOX15 individual. These data indicate that the human ALOX15 transgene was inserted in both homologous murine chromosomes 2.
Fluorescence in situ hybridization of mouse chromosomes using the human ALOX15 cDNA as probe. Pro-metaphase chromosomes were prepared as described in Section 4. (A) A Met aphase spread prepared from hepatocytes of a heterozygous founder animal is shown after the M FISH set using all 21 murine whole chromosomes. In the white frame, the inverted 4′,6-diamidino 2-phenylindole counter-staining of the same metaphase is shown with the signal of the ALOX15 cDNA (red signal) from the first round of FISH (for details see Section 4). Accordingly, the human ALOX15 cDNA was inserted in one of the two murine chromosomes 2 (#2), more exactly into sub band 2E1~E2. (B) FISH result of a homozygous aP2-ALOX15 individual. These data indicate tha the human ALOX15 transgene was inserted in both homologous murine chromosomes 2.
Assuming a similar specific activity of mouse and human ALOX15, more endogenous Alox15 should be present in these cells when compared with the transgenic human ALOX15. Representative chromatograms are shown; the statistical evaluation of the data is given in Table  1. Table  1. Ex vivo activity assays of peritoneal lavage cells prepared from mice of different genotype. Representative chromatograms are shown; the statistical evaluation of the data is given in Table  1. Table  1. Ex vivo activity assays of peritoneal lavage cells prepared from mice of different genotype. 10 7 peritoneal lavage cells prepared from mice of different genotypes (n = 3 of each genotype) were incubated with exogenously added arachidonic acid as described in Section 4. The arachidonicacid-derived oxygenation products were prepared and further analyzed by RP-HPLC.
The arachidonic-acidderived oxygenation products were prepared and further analyzed by RP-HPLC (see Section 4). Statistical evaluation of the experimental raw data was performed using the Student's t-test function of the Microsoft Excel software package. # wildtype vs. aP2-ALOX15, p < 0. 01; § aP2-ALOX15 vs. aP2-ALOX15 + ALOX15 -/-, p < 0. 01.
As negative controls, we also quantified the plasma concentrations of other oxylipins that are not formed from arachidonic acid, eicosapentaenoic acid, docosahexaenoic acid, nor 8,11,14-eicosatrienoic acid by human ALOX15 (8-HETE, 8-HEPE, 10-HDHA, 8-HETrE). First, we quantified the sum of all oxygenated polyenoic fatty acids present in the blood plasma of the two genotypes (Figure  5A ). Here, we did not find a significant difference between the two genotypes. These data indicate that the degree of oxidative challenge is similar in both genotypes. In other words, overexpression of human ALOX15 did not lead to an increased oxidative stress in the aP2-ALOX15 mice. When we analyzed the major arachidonic acid oxygenation products, we found that the plasma concentrations of 15-HETE in transgenic aP2-ALOX15 mice were almost five-fold higher than those in wildtype control animals (C57BL/6).
In contrast, there were no significant differences between the two genotypes when the plasma levels of 8-HETE (not an ALOX15 product) were compared. These data can be interpreted as an indication of the in vivo activity of the transgenic human ALOX15. Next, we analyzed the oxygenation products of three other polyenoic fatty acids. Human ALOX15 converts 5,8,11,14-eicosapentaenoic acid predominantly to 15-HEPE  [83]. We found that the 15-HEPE plasma concentrations were more than five-fold higher in aP2-ALOX15 mice when compared with wildtype controls. Here again, we did not find any difference between the two genotypes for 8-HEPE, which is not formed by human ALOX15 (Figure  6C ). Similar results were obtained for the major oxygenation products formed from 4,7,10,13,16,19-docosahexaenoic acid (Figure  6D ) and 8,11,14-eicosatrienoic acid (Figure  6E ).
Then, 20 metaphases were acquired on a Zeiss Axioplan microscope (Carl Zeiss, Jena, Germany) equipped with corresponding filters and ISIS software (MetaSystems, Altlussheim, Germany). The positions of the acquired metaphases were registered; thus, the same 20 metaphases could be evaluated again after a second FISH was conducted on the same slide using a commercial multicolor FISH probe (M-FISH) set staining all 21 different murine chromosomes in specific color combinations ("SkyPaintTM DNA Kit M-10 for Mouse Chromosomes", Applied Spectral Imaging, Edingen-Neckarhausen, Germany). Accordingly, the chromosome in which the human ALOX15 cDNA was inserted could be identified.
Whole-Genome Sequencing Genomic DNA was prepared from 58 mg of liver tissue using the Invisorb ® Spin Tissue Mini Kit (Invitek Molecular GmbH, Berlin, Germany). An additional RNAse treatment was performed, and the RNA-free DNA preparation was quality-checked with agarose gel electrophoresis. The DNA was sequenced using the shot-gun technology (ATLAS Biolabs GmbH, Berlin, Germany). The whole genome sequence data can be obtained by interested scientists upon request from Dr. K. R. Kakularam.
4. 9. LC-MS/MS Analysis of the Blood Plasma Oxylipidomes Mouse Alox15 is an arachidonic acid 12-lipoxygenating enzyme  [82] , whereas the human ortholog oxygenates the same substrate predominantly to 15-H(p)ETE  [78]. If aP2-ALOX15 transgenic mice have significantly elevated 15-HETE plasma levels, these data may be interpreted as an indication of the in vivo activity of the transgenic enzyme. To explore whether the pattern of the plasma oxylipins was impacted by in vivo expression of the transgenic human ALOX15, we quantified the amounts of more than 40 different freeoxygenated PUFAs in the blood plasma  [117]. For this purpose, EDTA blood was drawn from sacrificed mice, and after a 15 min incubation period, the blood plasma was prepared by centrifugation. Then, 10 µL of blood plasma was mixed with 450 µL of water and 10 µL of a mixture of internal standards (LTB4-d4, 20-HETE-d6, 15-HETE-d8, 13-HODE-d4, 14,15-DHET-d11, 9,10-DiHOME-d4, 12,13-EpOME-d4, 8,9-EET-d11, PGE2-d4; 10 ng/mL each).
Stock A: water containing 0. 05% acetic acid. Stock B: 1:1 mixture (by vol. ) of methanol: acetonitrile. The HPLC system was connected to a triple-quadrupole MS system (Agilent 6495 System, Agilent Technologies, Santa Clara, CA, USA). Negative electrospray ionization was carried out. The mass spectrometer was run in dynamic MRM mode, and each metabolite was detected simultaneously by two independent mass transitions that are characteristic for the different analytes. Experimental raw data were evaluated with the Agilent Mass-Hunter software package, version B10. 0. For all metabolites analyzed in this study, individual calibration curves were established, and the lower detection limits were also determined. More detailed information on this analytical procedure is given in  [117].
10 7 peritoneal lavage cells prepared from mice of different genotypes (n = 3 of each genotype) were incubated with exogenously added arachidonic acid as described in Section 4. The arachidonic-acidderived oxygenation products were prepared and further analyzed by RP-HPLC. The statistical evaluation of the experimental raw data was performed using the Student's t-test function of the Microsoft Excel software package. # wildtype mice vs. aP2-ALOX15 animals, p < 0. 01, § aP2-ALOX15 mice vs. aP2-ALOX15 + ALOX15 -/-animals p < 0. 01.
Active screening was targeted at villages previously identified as being at greatest risk in each area based on historical, epidemiological and geographical data as defined by the socalled "identification of villages at risk" (IVR) strategy  [20]. This strategy was mainly applied in the HDs at risk. During IVR activities, clinical and epidemiological suspects were tested with a simplified algorithm (Fig  2b ). Serology was based on CATTb or a rapid diagnostic test (RDT SD1, Abbott Diagnostics, South Korea)  [21]  and parasitology was based only on LNA if enlarged lymph nodes were present. A sample of blood dried on filter paper was then collected to perform a trypanolysis (TL) test in the laboratory  [22]. When the TL was positive, the village concerned was automatically selected for exhaustive active screening and the TL-positive subject was tested using mAECT BC.
Tsetse are explicitly included in the model to capture human-tsetse-human transmission cycles and, furthermore, it is assumed that there is differential risk in exposure to tsetse bites between different people. As described in the vector control section, from 2016 and 2017, vector control was implemented in Bonon (Bouaflé HD) and Sinfra, respectively, and the corresponding reduction in tsetse populations is included in the transmission model for these foci. Tsetse trap data were used to inform the parameters associated with observed tsetse population reduction by fitting the tsetse population dynamic sub-model to these data via maximum likelihood estimation (see S1 Text). To fit the full deterministic epidemiological model to data we use a Markov chain Monte Carlo (MCMC) methodology (see S1 Text) which compares annual active and passive case reporting simulated in the model to those observed in the data for each year for each HD.
Acknowledgements The authors wish to thank their institutions, and all contributors to the control of gHAT in Côte d'Ivoire, whatever their status. The PNETHA and partners thank  WHO  for their support to collect and consolidate data on reported gHAT cases in the frame of the WHO Atlas. The authors wish to pay tribute to  Pierre Cattand  who significantly contributed to the HAT control in Côte d'Ivoire.
Surface Plasmon Resonance Analysis The NECL2 EC was captured on a Biacore CM5 sensor chip (GE Healthcare) to a nal immobilization density of ~ 1600 resonance units (RUs). All kinects experiments were performed at 25°C at a ow rate of 30 µl/min. Two-fold serial dilutions of CRTAM EC , CRTAM IgV-Stalk in HBS-P + buffer (GE Healthcare) was injected over the CM5 chip. Sensograms were t with BIAcore T200 software using 1:1 Langmuir binding (GE Healthcare). Other binding analyses were done by a gradient of 30-1. 87 µM of CRTAM IgC-Stalk that were injected over the CM5 chip with NECL2 EC immobilized at the same conditions described above.
Cell-cell interaction assay Cos7 transfected cells with NECL2 full were co-cultured with Jurkat expressing the CRTAM EC , CRTAM IgV or CRTAM IgC. Jurkat transfected with the empty plasmid pYpet-N1 was used as a negative control. The cells were allowed to interact for 16 hours. The cell-cell interactions were examined with Planapo 40x/1. 0 objective in an inverted Olympus IX 50 epi uorescence microscopy. The images were acquired with a digital camera, Olympus DP70HD, coupled to the microscope. Quantitative image analysis of CRTAM-polarization to cell-cell interaction site. In order to quantify the recruitment of CRTAM to the cell-cell interaction site, the polarization coe cient was calculated using ImageJ software. Boxes were drawn around the cell-cell interface and on the rest of the cells -where the cells were not in contact.
Funding This work was supported by  INSERM , the " Investments for the Future" Labex Signalife  ( ANR-11-LABX-0028-01 ), ITMO cancer ( 2019-2023 ), the  ARC Foundation. EK is supported by a fellowship from  Ligue Nationale Contre le Cancer. PA team is also supported by grants from  ARC Foundation  (Equipe labelliseé  2022-2025 ), the  ALF association  ( 2021-2022 ), and  INCA  ( PLBIO-2019-133 ). PA, AJ and GR are member of the  OPALE Carnot institute.
Risk of WNVD in individuals with auto-Abs against type I IFNs We estimated the risk of WNVD conferred by the presence and nature of neutralizing auto-Abs by comparing the proportions of subjects with various types or combinations of auto-Abs with the proportions of individuals carrying the corresponding neutralizing auto-Abs in the general population after adjustment for age and sex. General population data were obtained by systematically performing neutralization assays on samples from 34,159 healthy men and women aged 18-100 yr  (Bastard et al. , 2021a). We found no significant difference between WNVIC and the general population, regardless of the type or combination of auto-Abs considered (Fig. 4 A ). Conversely, the prevalence of auto-Abs and of various combinations of these antibodies was significantly higher in all disease groups than in the general population, and it increased with disease severity (Fig.
Acknowledgments We thank the patients and their families for participating in our research. We thank all members of both branches of the  Laboratory of Human Genetics of Infectious Diseases  for discussions and technical and administrative support. We thank  Lazaro Lorenzo Diaz, Laboratory of Human Genetics of Infectious Diseases ,  Necker Branch ,  Institut National de la Santé et de la Recherche Médicale (INSERM)   U1163 , and  Necker Hospital for Sick Children, Paris, France ,  EU. A. Borghesi  wishes to thank  Giampaolo Merlini  for thoughtful discussions on the methods for anti-cytokine auto-Ab discovery. The  Laboratory of Human Genetics of Infectious Diseases  is supported by the  Howard Hughes Medical Institute , The  Rockefeller University , the  St. Giles Foundation , the  National Institutes of Health (NIH ; grants  R01AI088364 ,  R01AI127564 ,  R01AI163029 , and  R21AI160576 ), the  National Center for Advancing Translational Sciences (NCATS) , the  NIH Clinical and Translational Science Award (CTSA) program  ( UL1TR001866 ), the  Fisher Center for Alzheimer's Research Foundation , the  Meyer Foundation , the  JPB Foundation , the " Investissement d'Avenir" program  launched by the  French Government  and implemented by the  Agence Nationale de la Recherche  ( ANR ; grant  ANR-10-IAHU-01 ), the  Integrative Biology of Emerging Infectious Diseases Laboratory of Excellence  (grant  ANR-10-LABX-62-IBEID ), the  French Foundation for Medical Research (FRM ; grant  EQU201903007798 ),  ANR   GENVIR  ( ANR-20-CE93-003 ),  ANR AI2D  ( ANR-22-CE15-0046 ), and  ANR AAILC  ( ANR-21-LIBA-0002 ) projects, the  HORIZON-HLTH-2021-DISEASE-04 program  under grant agreement  01057100  ( UNDINE) , the  ANR-RHU   COVIFERON Program  ( ANR-21-RHUS-08 ), the  Square Foundation, Grandir -Fonds de solidarité pour l'enfance , the  Fondation du Souffle , the  SCOR Corporate Foundation for Science , the  Battersea & Bowery Advisory Group , The  French Ministry of Higher Education, Research, and Innovation  ( MESRI-COVID-19 ),  INSERM ,  REACTing-INSERM , and the  University of Paris.
The  Laboratory of Virology and Infectious Disease  ( M. R. MacDonald  and  C. M. Rice ) is supported by  NIH  grants  R01AI124690  and  R01AI091707. Open Access funding provided by  Rockefeller University. Author contributions:  A. Gervais ,  F. Rovida ,  M. A. Avanzini ,  S. Croce ,  S. -C. Lin ,  A. Ferrari ,  C. W. Thorball ,  O. Constant ,  T. Le Voyer ,  Q. Philippot ,  J. Rosain ,  M. Angelini ,  M. Pérez Lorenzo ,  L. Bizien ,  C. Achille ,  F. Trespidi ,  I. Cassaniti ,  D. Lilleri ,  C. Fornara , Gervais et al. Journal of Experimental Medicine 16 of 18 Anti-type I IFNs auto-Abs in WNV encephalitis https://doi. org/10. 1084/jem. 20230661.