dataesr/scientific-paragraphs-categorization huggingface dataset:
Results We were surprised to identify the 16S rDNA of B. quintana in two Demodex mites from the same patient. Amplification of spacer 894 7 matched with B. quintana Toulouse strain (coverage 100% and identity 100%, GenBank accession number AY660712). with this system and found three mites to be positive: the two already identified by 16S rDNA and another from the same patient. B. quintana was finally identified in three out of the six Demodex mites collected from that patient. The patient was a 63-year-old woman from Schenefeld/ Hamburg (Germany) who presented with erythematotelangiectatic rosacea defined by a mild telangiectasia and moderate flushing, but neither non-transient erythema nor papules and pustules. To our knowledge, she was not homeless, infested with lice, or in contact with lice-infested homeless people.
Acknowledgments We thank  Stephen White  and  Wytze van der Veer  ( UC Irvine ) for the use of the circular dichroism spectrophotometers and  Fabrice Giusti  ( IBPC ) for the synthesis of amphipol A8-35. We also thank  Cambridge Isotopes  for the gift of insect cell media for pilot expression studies. This work was supported by grant  R01AI092129  from the  National Institute of Allergy and Infectious Diseases , by the  Centre National de la Recherche Scientifique , by University Paris-7, and by the " Initiative d'Excellence" program  from the  French State  (Grant " DYNAMO ",  ANR-11-LABX-0011-01 ).
After incubation, 250-μl aliquots were filtrated using a cell harvester, over glass fiber filters (Whatman, GF/B) pre-soaked in 0. 3% polyethylenimine. The aliquots were rapidly washed three times with 4 ml of the same buffer. The radioactivity retained by the filters was counted in a beta scintillation analyzer (Packard, Meriden, CT, USA). Curves were fit to the data with Prism non-linear least squares curve-fitting program (GraphPad Software, San Diego, CA, USA). One-site fits were tested.
DATA QUANTIFICATION H 3 receptor binding measurement The brainstem and posterior hypothalamic nuclei were identified with Berman's stereotaxic atlas  (Berman, 1968; Berman and Jones, 1982). The analysis of IO binding to H 3 Rs has been completed in greater detail using  Brodal and Kawamura's (1980)  monograph. The autoradiograms of the binding to H 3 Rs were analyzed and quantified using NIH Image software. [ 3 H] Plastic standards (Amersham) were used to calibrate 3 H concentrations. Receptor density was expressed in fmol/mg of protein and evaluated for both the brainstem structures and the TMN. A mean receptor density value was calculated for each nucleus from 60 serial sections. The specific binding value was determined as the difference between total and non-specific binding components for a given area and was evaluated as the mean ± SEM.
Statistical analysis Analysis of variance (Super Anova) was used to test the effects of the vestibular lesion (intact versus UVN cats), the survival period (1 week versus 3 weeks), the side (deafferented versus intact), and the structure (VN, the IO and SN subdivisions, the PH, and the posterior hypothalamic nuclei) on H 3 R binding density, and to determine the interactions between these variables. Super ANOVA was followed by post hoc analysis with the Scheffé test and multicomparison Fisher's test (stateview II software).
Acknowledgments We are grateful to  Prof. E. Pick  for the plasmids, to  Dr. L. Baciou  for helpful discussions and to  Dr. F. Lederer  for the preparation of neutrophiles. We acknowledge the financial support of the  COSTCM1201 Action  ( Biomimetic models ) and of  ANR2010-blan-1536-01. We are indebted to EDF for financial support (contract  RB 2013-15 ).
Statistics The number of studied animals (20 animals per group) was calculated based on a mortality reduction from 80% in the NT group infected with PAO1 to an expected mortality rate of 50% in the treated groups, with 90% statistical power and a two-sided alpha value of 0. 05. The data were expressed as the means 6 standard deviation (SD) or median [inter-quartile range, IQR] according to the distribution of the data. Student's t-test or the Mann-Whitney rank-sum test were used for inter-group comparisons. Kaplan-Meier analysis was performed to evaluate 48-h mortality. Intergroup differences were evaluated using the log rank test. The data analysis was performed with SPSS for Windows (Chicago, IL), version 12. 0. A value of p#0. 05 was considered statistically significant.
Patients A prospective cohort study was conducted on 26 consecutive kidney transplant patients at the Transplant Unit of the University Hospital of Poitiers between December 1, 2009 and October 30, 2010. Adult recipients (18-70 years) of a first (n = 22) or second kidney transplant (n = 5) were eligible for enrollment. Among these, 7 patients (31%) were pre-emptively transplanted (Table  1 ). Analysis of HMGB1, IL-33 and sST2 serum levels before kidney transplantation showed no difference between pre-emptively and non-pre-emptively transplanted patients (data not shown). All recipients received immunosuppressive treatment based on an induction therapy (either basiliximab or Thymoglobulin), a calcineurin inhibitor (either cyclosporine or tacrolimus) and a secondary agent (either mycophenolate mofetil or enteric-coated mycophenolate sodium).
Flow Cytometry Cells were stained with membrane antibodies diluted in PBS containing 2% FBS and fixed. For in vitro experiments, cell viability was evaluated by the LIVE/DEADH Fixable Near-IR Dead Stain Kit (Invitrogen). Membrane antibodies FITC mouse anti-human CD3, PE mouse anti-human iNKT cell (clone 6B11) and PerCP/Cy5. 5 mouse anti-human CD69 were provided by BD Biosciences (San Jose, CA). Appropriate isotype control was used for each marker. Cells were analysed by FACS Canto II TM and FacsDiva TM software (BD, Franklin Lakes, NJ) and data were analysed using FlowJo TM software (version 7. 5. 5 Treestar, Ashland, OR). CD69 expression was analysed gating on CD3(+ )6B11(+) cells, defined as iNKT cells.
0%), we found a significant correlation between these serum levels and cold ischemia time from H0. 5 to POD3, which was not the case for HMGB1 (Table  2 ). Inasmuch as severity of tissue injury can be considered a reliable indicator of cold ischemia, these data support a close relationship between IL- 33 release and kidney IRI. Postulating that renal inflammatory injury might be concomitant with local release of alarmins, we further assessed urinary excretion of HMGB1 and IL-33, expressed as alarmin/creatinine ratios to correct for dilution. As shown in Figure  1B  and E , urinary levels of both HMGB1 and IL-33 were significantly higher at H3 than before transplantation (702. 4627,6 vs 272. 2698,7 pg/ml, p,0. 001 and 16. 2610. 0 vs 0 pg/ml, p,0. 05, respectively). The similar expression profiles, whether alarmin levels were normalized against urinary creatinine or not (Figure  1C , F), point to renal endothelial and/or tubular epithelial cells as main cellular origin of HMGB1 and IL-33, as the increase cannot be explained simply by changes in glomerular filtration rate.
The captured rats were transported to the laboratory and immediately anaesthetized using isoflurane. A blood sample was obtained by cardiac puncture. Subsequently, the rats were sacrificed by cervical dislocation. The rats that succumbed to capture were frozen at -20 °C and thawed on the day of dissection. Data were recorded on weight, size, sex, sexual maturity (i. e. the presence of seminal vesicles in males and a developed uterus in females) and pregnancy. Lung and liver lobe fragments weighing between 50 and 100 mg were collected, and the kidney was removed. The heart was incorporated in an antibiotic solution with 1•2 × 10 -5 g/ml amoxicillin (Amoxicilline Panpharma, France), 120 UI/ml penicillin and 120 μg/ml streptomycin (Pen-Strep Liq 10 000, Gibco, USA). Faecal samples were collected from the rectum, and all tissue and faecal samples were stored at -80 °C immediately following collection.
Variables Two categories of explanatory covariates were considered: rat-related and socioeconomic covariates. Rat survival during the trapping was also considered, as death and freeze-thaw cycles before dissection could alter the sample quality and underestimate the prevalence. The rat data included the species (determined by external morphology and macroscopic observations), sex, weight, size, and approximate age, based on sexual maturity and pregnancy. A body mass metric was constructed from the residuals that resulted from the regression of weight on size  [22]. The capture success, a proxy of the population size, was accurately defined in five sites by capture success = n i t i × d i , where n i is the number of rats captured, t i the number of traps set and d i the number of days of trapping at the site i.
The extent and features of urbanization were characterized using the socioeconomic data. Eleven candidate variables were extracted from the 2009 national census data provided by the Institut National de la Statistique et des Etudes Economiques. Remotely sensed data were obtained at the smallest geographical unit, which is the Ilot Regroupé pour l'Information Statistique (IRIS). Each IRIS contains 2000 inhabitants. The socioeconomic variables are displayed in Table  1.
Spatial analysis The location and number of rats in each trapping area that tested positive and negative were mapped using ArcGIS version 9. 3 (ESRI, USA). Spatial clusters of high and low pathogen prevalence were identified using the Getis-Ord Gi* statistic. The local sum for features and the feature's neighbours were compared proportionally to the sum of all features. When the local sum was statistically significantly different from the expectation, the region was denoted as having low or high prevalence. To identify the potential socioeconomic proxies of RBZ, the candidate variables from the census data sets were extracted from the IRIS units with trapping locations. An approach using various boundaries for the quadrats when extracting data was implemented to verify the effects of different spatial scales on the risk factors  [23].
The socioeconomic data were extracted using four quadrat sizes: 100 m × 100 m, 200 m × 200 m, 400 m × 400 m, and 800 m × 800 m. The socioeconomic metrics for each quadrat were calculated by weighting the remotely sensed data by the percentage of the IRIS surface that was included in the quadrat. For each spatial level of analysis, a new data set was obtained by spatial query using the software R project version 3. 0. 1 (R Development Core Team, Austria) and ArcGIS version 9. 3 (ESRI, Redland, CA, USA).
All remotely sensed data were transformed to be normally distributed when they were incorporated into the models, and missing data were not considered. Simple logistic regression (SLR) was used to examine the relationship between each pathogen's prevalence and the explanatory variables. Covariates that were significantly associated with pathogen infection or exposure at an α-level of 0•10 were considered for further analysis. To select independent variables, rat-related covariates were tested for multicollinearity using Spearman's rank correlation (ρ > 0•7) with the Hmisc package in R, whereas socioeconomic covariates were described with a principal component analysis (PCA) using the FactoMineR package in R. From the PCA result, one variable per main axis was chosen based on the comprehensiveness of the data.
Test of the spatial extents of remotely sensed extracted data The new datasets extracted from the four quadrats were incorporated into the final models selected for L. interrogans infection status (see Supplementary online material). The P values associated with the relationship between infection status and the covariates decreased with increasing quadrat size. Larger quadrats displayed a better goodness-of-fit model (Table  4 ). Spatial distributions of the covariates are shown in Figure  2 ; areas of higher and lower levels of L. interrogans infection were mainly located in densely populated and low-income areas.
Spatial analysis methodology The risk analysis demonstrated an overlap of densely populated, low-income urbanized areas and Norway rats with L. interrogans, SEOV, and HEV infections. Socioeconomic data collected by the INSEE census are most commonly aggregated at the administrative boundary or census areal unit level. Spatial scale can affect the strength and significance of statistical associations, which is known as the modifiable areal unit problem (MAUP)  [23]. To minimize the MAUP effect in statistical inference, the covariates can be analysed at hierarchical levels of areal units from the finest to the coarsest resolution to confirm consistent model results  [24]. Five hierarchical levels of census units were used in this study. Only the smallest unit failed to confirm the relationship between socioeconomic data and L.
ACKNOWLEDGEMENTS We thank the  city of Lyon and its 'Service d'hygiène'  ( Dr. Gilbert Gault ), the waste plant  UIOM de Lyon (M Joël Baud) , the  Parc de la Tête  d'Or managers ( Dr. David Gomis  and  Dr. Guillaume Douay ), and the  Agence d'urbanisation  for assisting with rat and census data collection. We thank  Philippe Berny  and  Joffrey Goullois  for assisting with rat collections,  Emmanuelle Gilot-Fromont  for assisting with diagnosis and analysis,  Zorée Djelouadji  and  Lorraine McElhinney  ( AHVLA ) for assisting with screening for Leptospira and Seoul virus, respectively, and the  Institut National Geographique et Forestière (IGN)  for providing census data. The hantavirus identification was funded by the  Defra Surveillance  Project  SV3037. This project was supported by the  European Commission  under the  Food, Agriculture and Fisheries and the Biotechnology theme of the Seventh Framework Programme for Research and Technological Development  (grant no.
Protein bands were detected using ECL reagent or ECL Plus reagent (Thermo Fisher Scientific). Images of immunoblots were acquired using the FluorChem E & M imager from Protein Simple (number FM0418), a digital darkroom technology. Densitometric analysis of immunoblots was performed using Alpha View software (Protein Simple). Immunoprecipitation Analysis-For each immunoprecipitation conducted with lens tissue study, 100 E10 lenses were microdissected into four regions of differentiation as described above and extracted with OG/T buffer. To determine the association of p-IGF-1R with ␣6 integrin, the entire EC, EQ, FP, and FC fractions were incubated with antibody to ␣6 integrin (4 °C overnight), followed by incubation with TrueBlot immunoprecipitation beads (eBiosciences) for 1 h as described previously  (2).
TUNEL and TO-PRO-3 staining was imaged by confocal microscopy. Quantification for the TUNEL assay in lens cell cultures was performed by analyzing four randomly selected fields from each sample over three independent studies, represented as the percent of total nuclei (stained with TO-PRO-3) that were TUNEL-positive. Image Analysis-The Nikon Eclipse TE2000-U microscope (Optical Apparatus) was used to obtain phase images that were acquired using the Cool Snap HQ 2 camera (Photometrics) with Image-Pro Plus software (Phase 3 Imaging Systems). Confocal microscopy was performed using the Zeiss LSM510 META confocal microscope. Single optical planes were selected from z-stacks, each 1 m thick, unless otherwise indicated, using the LSM5 Image Browser. Statistical Analysis-Statistical data analysis was performed with the t test on three or more independent experiments using.
Note that nuclear localization of active ERK observed in the ␣6 ϩ/ϩ mouse lens at E18. 5 is distinct from that which occurs at E12. 5, when it localized to the nuclei of differentiating primary lens fiber cells  (42). All images were obtained by confocal microscopy. Images in A (ii and iii)-F, are single optical slices of 1-m thickness selected from an acquired z-stack; B-E, scale bar ϭ 20 m. F, scale bar ϭ 100 m. Results show that in the absence of ␣6 integrin there was diminished activation of IGF-1R, moderate reduction in phosphotyrosine, and inhibition of ERK activation, a downstream effector of IGF-1R, whereas the lens capsule remained intact. Labeling of the lens capsule with the 4G10 antibody is nonspecific. Data are representative of three independent studies where lenses from 3 different ␣6 ϩ/ϩ or ␣6 Ϫ/Ϫ mice embryos were examined.
F, immunoblot for the caspase-3 target cl-PARP-1. Immunoblot analysis was also performed for the lens differentiation specific proteins filensin (G) and CP49 (H). The results show that ␣6 integrin is necessary to maintain low levels of caspase-3 activity and inducing lens epithelial cell differentiation initiation. Densitometric analyses of immunoblots for ␣6 integrin, filensin, and CP49 were plotted as a ratio to actin; cl-PARP-1 as a ratio to GAPDH; and p-IGF-1R against total IGF-1R. For confocal imaging, z-stacks were collected and analyzed, and the data are presented as a single optical plane of 0. 5 m. Results are representative of at least three or more independent studies. Error bars represent S. E. *, p Ͻ 0. 05, t test. Scale bar, 20 m.
5 is distinct from that which occurs at E12. 5, when it localized to the nuclei of differentiating primary lens fiber cells (42). All images were obtained by confocal microscopy. Images in A (ii and iii)-F, are single optical slices of 1-m thickness selected from an acquired z-stack; B-E, scale bar ϭ 20 m. F, scale bar ϭ 100 m. Results show that in the absence of ␣6 integrin there was diminished activation of IGF-1R, moderate reduction in phosphotyrosine, and inhibition of ERK activation, a downstream effector of IGF-1R, whereas the lens capsule remained intact. Labeling of the lens capsule with the 4G10 antibody is nonspecific. Data are representative of three independent studies where lenses from 3 different ␣6 ϩ/ϩ or ␣6 Ϫ/Ϫ mice embryos were examined.
Fluorescence intensity of cl-caspase-3 was quantified by creating line scans (panels iii and iv, quantified below) across the field of cells using LSM Image Examiner, confirming increased caspase-3 activation in response to ␣6 integrin knockdown. F, immunoblot for the caspase-3 target cl-PARP-1. Immunoblot analysis was also performed for the lens differentiation specific proteins filensin (G) and CP49 (H). The results show that ␣6 integrin is necessary to maintain low levels of caspase-3 activity and inducing lens epithelial cell differentiation initiation. Densitometric analyses of immunoblots for ␣6 integrin, filensin, and CP49 were plotted as a ratio to actin; cl-PARP-1 as a ratio to GAPDH; and p-IGF-1R against total IGF-1R. For confocal imaging, z-stacks were collected and analyzed, and the data are presented as a single optical plane of 0.
Results show that ␣6 integrin is an essential upstream signal of NFB-mediated expression of survival proteins in the Bcl-2 and IAP families in lens epithelial cells. Densitometric analyses of immunoblots for Bcl-2, Bcl-X L , ch-IAP-1, X-IAP, and survivin were plotted as a ratio to GAPDH; and p-NFB p65 against total NFB p65. For confocal imaging, z-stacks were collected and analyzed, and the data are presented as a single optical plane of 0. 5 m. Results are representative of at least three studies. Error bars represent S. E. *, p Ͻ 0. 05, t test. Scale bar, 20 m.
Most prevalent is mass spectrometry, however this lacks well-established reference databases and is biased toward detecting high-concentration compounds, which are major limitations for assessment of the plasma proteome by this technology  [1, 6]. So-called "transcriptomic reporter assays" provide an alternate means to assess perturbations in plasma on a system-wide scale  [7]. This strategy consists of measuring whole genome transcriptional responses elicited in reporter cells exposed in vitro to patient plasma. This type of approach has already proven useful in studies of several immunologically mediated diseases. It was employed to help unravel the pathogenesis of systemic onset juvenile idiopathic arthritis, eventually leading to the adoption of a novel therapeutic modality for treatment of this disease  [7, 8].
Plasma collection Septic patients were enrolled from Khon Kaen Regional Hospital, Khon Kaen, Thailand. Patients who met at least two of the criteria for severe inflammatory response syndrome (SIRS) were enrolled in the study  [3, 15]. As part of the routine investigations, clinical specimens were collected for bacterial culture within 24 h following SIRS diagnosis. Only blood samples obtained from patients who were retrospectively diagnosed with cultureproven sepsis were retained for further analyses. Patients with negative blood cultures were excluded. Severe sepsis was defined according to the current guidelines from the Surviving Sepsis Campaign  [15]. These criteria include several clinical and laboratory findings of sepsisinduced tissue hypoperfusion or organ dysfunction. We used the subset of these criteria for which the necessary data had been collected for our patient cohort: elevation in creatinine to >2.
0 mg/dl, elevation in bilirubin to > 2. 0 mg/dl, platelet count <100,000/μL, and sepsis induced hypotension (septic shock). In hospital death was also counted as severe sepsis. Demographic and clinical data were recorded for all subjects (Additional files 1, 2, and 3). Uninfected healthy controls were selected as individuals who had no signs of acute infectious diseases during the previous 3 months or at the time of the study. Uninfected controls also had to have normal blood counts, normal fasting blood glucose, and normal glycosylated hemoglobin. Three milliliters of whole blood was collected from each patient and healthy control into heparinized tubes (BD Biosciences). For sepsis patients, samples were grouped as drawn either in the first 48 h of admission, or at >48 h after admission. To separate plasma, blood samples were centrifuged at 2,000 rpm for 10 minutes and the plasma component was transferred into a cryogenic vial and stored at -80°C until used.
Data normalization All data analyses were performed using R (version 2. 14. 0; http://cran. r-project. org/bin/windows/base/old/2. 14. 0/). Data pre-processing of background subtracted data was performed by using the preprocessCore package from Bioconductor. Pre-processing included rescaling intensity by quantile normalization. After normalization, expressions were floored with intensities <10 set to 10. Transcripts with detection p-value of less than or equal to 0. 01 in at least one sample (PALO) were selected for further analysis. Samples from the same cell type and batch were normalized to the average intensity of samples cultured in medium alone. A filter was set to include only transcripts that had at least two-fold changes and 100 intensity differences compared to medium control. Background subtracted and processed data from these experiments have been deposited at NCBI's Gene Expression Omnibus database (http://www.
Unsupervised analysis Principle component analysis (PCA) was performed using the R function "prcomp". The first two principal components, PC1 and PC2, were plotted against each other. Each colored dot represents an individual sample. Euclidean distances were calculated by measuring the distance from each sample to the average of samples stimulated with uninfected plasma. The comparison between severe and non-severe sepsis was performed using the Mann-Whitney U-test. Hierarchical clustering analysis was performed using the function "heatmap. 2" from the R package "gplots". Euclidean distance and complete linkage methods were used by default.
Class prediction To determine the performance of our predictive signature, class prediction of binary variables was carried out by support vector machine (SVM; package "e1071") and random forest (RF; package "randomForest") algorithms. These machine learning methods are robust, well-accepted and commonly used methods for class prediction. Receiver operating characteristic (ROC) curves were constructed using the R package "ROCR". Area under the curve (AUC) and confidence intervals were calculated using the R package "Hmisc".