dataesr/scientific-paragraphs-categorization huggingface dataset:
24 h following infection the number of internalized bacteria had decreased from 100% to 9. 6% in normoxia and from 13. 8% to 1. 5% in hypoxia (Figure  1D ). Next, we investigated the consequence of decreased bacterial uptake in hypoxia for host cell survival. P. aeruginosa is cytotoxic and capable of inducing death in epithelial cells  [30]. To assess cytotoxicity in our model, we measured Lactate dehydrogenase (LDH) release following bacterial infection. 24 hours following infection, normoxic P. aeruginosa infected cells released significantly more LDH than hypoxic P. aeruginosa infected cells indicating decreased induction of cell death by P. aeruginosa infection under hypoxic conditions (Figure  1E ). These data support a protective role for hypoxia in reducing epithelial cell infection by P.
C: Uptake of P. aeruginosa over time in normoxia and hypoxia. D: Internalization of P. aeruginosa directly after infection (day 1) or 24 h after infection (day 2). E: Cell toxicity of uninfected and P. aeruginosa infected cells was measured by LDH release directly after infection (day 1) or 24 h after infection (day 2). Data represent mean 6 SEM of 3 independent experiments throughout (*,p 0. 05; *** p,0. 0001). doi:10. 1371/journal. pone. 0056491. g001 colonic epithelial cells resulting in increased expression of the NF-kB target cyclooxygenase 2 (COX-2) (Figure  3A+S2 ). To investigate whether hypoxia elicited increased NF-kB activity is equally mediated by all three major toll like receptors (TLRs), NF-kB-dependent luciferase reporter assays with selective TLR 2, 4 and 5 agonists were performed.
5 mg/ml) and TLR5 (flagellin, 0. 5 mg/ml). Data represent mean 6 SEM of 6 independent experiments (*** p,0. 0001). C: Intracellular P. aeruginosa in A549 cells in normoxia or hypoxia in the presence or absence of the NF-kB inhibitor BAY 11-7082 (10 mM) or its solvent DMSO were determined in an antibiotic protection assay. Data represent mean 6 SEM of 4 independent experiments (* p,0. 05, *** p,0. 0001). D: Antibiotic protection assay with P. aeruginosa in MEF wt and IKK2/2cells under normoxic and hypoxic conditions. Data represent mean 6 SEM of 2 independent experiments (* p,0. 05). doi:10. 1371/journal. pone. 0056491. g003.
Figure1. Hypoxia prevents internalization of P. aeruginosa into epithelial cells. A549 cells were infected with P. aeruginosa under normoxic (N) and hypoxic (H) conditions, after pre-incubation for 24 h in the respective environment for all experiments (A-E). A: Internalization of P. aeruginosa in normoxia, hypoxia and in normoxia after pre-incubation in hypoxia. B: Adhesion of P. aeruginosa in normoxia and hypoxia. C: Uptake of P. aeruginosa over time in normoxia and hypoxia. D: Internalization of P. aeruginosa directly after infection (day 1) or 24 h after infection (day 2). E: Cell toxicity of uninfected and P. aeruginosa infected cells was measured by LDH release directly after infection (day 1) or 24 h after infection (day 2). Data represent mean 6 SEM of 3 independent experiments throughout (*,p 0.
Annexin V staining Phosphatidyl-serine (PS) exposure in ex-vivo treated PELderived cells was assessed using Annexin V-FITC kit (Immunotech/Beckman Coulter) according to manufacturer instructions. Approximately 10000 cells per sample were acquired and analyzed using the CellQuest software (Becton Dickinson). Similar experiments were performed on BL-41 and BC-1 cells, using Fixable Viability Stain 450 (BD Biosciences) and PE Annexin V (BD Biosciences) according to manufacturer instructions. Approximately 20000 cells per sample were acquired and analyzed using the FACSDiva software (BD Biosciences).
PCR and qRT-PCR Tissues were harvested from PEL NOD/SCID mice having developed solid tumor mass. Regular PCR and real-time RT-PCR were used to quantitate the absolute LANA1, v-FLIP and v-Cyclin DNA content and mRNA expression, using a 2X PCR (Master Mix, Fermentas), and Light Cycler RNA Master kit (Roche Diagnostics), respectively. We also used the Lightcycler 4. 05 software version. Primers sequences were designed by TIB-MOLBIOL (Germany): V-FLIP (Forward, 5'-gTgTTCATACCTCAACCCACAC; Reverse, 5'-CACACAgCTCCCCgTCTAC); V-cyclin (Forwad, 5'-TCAgTTTgCCAggAATACAACCTAg; Reverse, 5'-AAgAAggAAgTTACgTCCgTCg); LANA-1 (Forwad, 5'-CCgAggACgAAATggAAgTg; Reverse, 5'-ggTgATgTTCTgAgTACATAgCgg); ORF50/RTA (Forward: CgCAATgCgTTACgTTgTTg; Reverse: gCCCggACTgTTgAATCg). Normalization of the transcript levels was done with the G6PDH or beta actin housekeeping gene internal levels.
Statistical Analysis SPSS Version 16. 0 and Microsoft Office Excel 2010 were used for statistical analyses. Except for survival analyses, mean values were reported and compared using ANOVA with associated post-hoc tests: Dunnettt, Tukey, and Student-Newman-Keuls (SNK). When applicable, SPSS syntaxtool was used to perform multiple comparisons within interaction groups in multi-Way ANOVA. In survival analyses, median values were reported and compared using Log Rank, Breslow, and Tarone-Ware tests, with similar results. Statistical significance was reported when the p-value was ≤ 0. 05. The symbol *was used to compare treatment groups to control, while the symbol ‡was used to compare combination treatments to single treatments.
Patients We analyzed data from three retrospective studies of HIV-negative patients with Pneumocystis jiroveci pneumonia. The first study  [9]  included HIV-negative patients admitted to two ICUs between 1988 and 1996 for PCP and compared patients who did (n=23) and did not (n=8) receive HDS in addition to standard treatment. The second study described HIV-negative patients with PCP managed in the ICU between 1989 and 1990 and looked for predictors of mortality; 33 of the 39 patients received HDS  [10]. Finally, the third study compared 56 cancer patients with PCP to 56 cancer patients with bacterial pneumonia admitted to the ICU between 2001 and 2006; of the patients with PCP, 21 received HDS  [5]. Only patients from theses studies who were admitted in ICU were included in the present study.
In addition to the data from these three studies, we included data from patients admitted for PCP to the ICU of the Saint Louis Teaching Hospital, Paris, France, between 2006 and 2011. The IRB from Clermont Ferrand approved data collection for the addition of patients from St Louis hospital in this non interventional study. Medical chart were reviewed by the investigators (VL or AD) for all included patients. For all four sources of patients, inclusion criteria were age over 18 years, ICU admission, and PCP. Only definite case of PCP were considered (positive IF for pneumocystis or MGG coloration in BAL). Exclusion criteria were patients with HIV infection and patients who were not admitted to the ICU. Moreover, colonized patients defined with positive P. jiroveci PCR only, without any pulmonary symptom or treatment of P.
Data collection The following data were collected for each patient at ICU admission: age, sex, underlying disease, exposure to immunosuppressants, steroid therapy before PCP, prophylactic treatments, time from symptom onset to ICU admission, oxygen requirements, P/F ratio, and underlying disease (as two categories, namely hematological or other malignancy and solid organ transplantation or immunological disease). During the ICU stay, the following were recorded: organ failures, use of mechanical ventilation, use of vasoactive agents, pneumothorax, ICU-acquired infections, and vital status. The P/F ratio was computed in the patients on endotracheal mechanical ventilation and estimated in the other patients. PCP was classified as severe when the P/F ratio at ICU admission was ≤100 and mild when it was >100.
Nevertheless, our study is the largest in this field  [8, 16]  and showed that HDS was independently associated with mortality. Third, we did not have complete data collected on the day of steroid therapy initiation. Fourth, some patients were included many years ago, at a time when the proportion of patients given HDS was higher than in recent years. In this early period, few tests were available for detecting viral infections. Viral co-infection may increase ICU mortality and the risk of ICU-acquired infections  [2, 18]. Moreover, ICU mortality of immunocompromised patient improved over time  [17, 21]. Fifth, we separate patients in three groups according the steroids dose, resulting in a limited number of patients in each group. Particularly, in LDS group mortality was the lowest but not significantly different from other group due to the small number of patients.
50 ng/ml, whereas a few follicles (approximately 1%) contained less sST2 than was detectable in the plasma (minimum value 8. 41 ng/ml which was four times lower than in the plasma). No correlation was detected between plasma and FF levels of sST2. Peripheral blood plasma and FF levels of IL-33 were also analysed. IL-33 was detected in the plasma of seven of the twentyone women analysed, levels were similar in the FF, figure  1B. IL-33 was not detected in the FF of any of the women who did not have detectable IL-33 in the plasma. In patients where IL-33 was detectable FF levels did not correlate with sST2 (data not shown). Mean plasma or FF sST2 and IL-33 levels do not correlate with the number of follicles nor oocytes retrieved per patient (data not shown). We compared mean FF sST2 and IL-33 levels between women who had a successful or failed IVF/ICSI cycle (clinical pregnancy and live birth -33% of patients), shown in table  1.
Plasma or FF sST2 levels did not correlate with plasma FSH, LH or E2 levels (data not shown). G-CSF levels were not different between the groups (figure  4B ). As levels of sST2 were different between good and average embryo grades, we next asked if the levels of sST2 in the FF predict pregnancy success. The embryos were returned to the patients, either as a single or double embryo transfer, and the outcome of pregnancy ''live birth'' or ''no pregnancy'' was recorded. When two embryos were transferred only ''live twin births'' or ''no pregnancy'' were included. sST2 levels did not differ between ICSI cycles that did or did not result in a live birth (figure  4C ). G-CSF levels were higher in the follicles of women who had live births (p,0. 001; figure  4D  and table 2 ). Next we looked at each embryo grade and compared the live birth rate.
The proposed ECG compression algorithm is tested upon a set of ECG records extracted from the MIT-BIH Arrhythmia Data Base including different cardiac anomalies as well as the normal ECG signal. The obtained results are evaluated in terms of compression ratio and mean square error which are, respectively, around 1:8 and 7%. Besides the numerical evaluation, the visual perception demonstrates the high quality of ECG signal restitution where the different ECG waves are recovered correctly.
e. the number of bits that we were earning when transmitting the compressed ECG signal. As the MIT-BIH ARRYTHMIA database records have a resolution of 11 bits and the ECG signal was transmitted with a resolution of almost 1. 5 bits (Avglen: average length of words: Avglen = 1. 5083 bits), so we have a significant gain on the number of transmitted bits. The number of bits to be transmitted is equal to 12403 bits, so the compression ratio is 1:7. 2653. The mean square error MSE = 0. 0741 and the percentage of the difference of the mean square error (Percentage of Root mean square Difference, PRD) is 19. 35%. The PRD is most important, when receiving the ECG signal, the set of waves {P, T, Q and S} are well restored while the R waves are attenuated. However, this distortion of the ECG signal does not destroy the useful information carried by that signal as it does not reveal non-existent pathological cases.
Comparative study The ECG signal compression algorithms are several. In order to promote our algorithm it is indispensable to compare it to works, already realized, and that the results are satisfactory. Among these algorithms for which the sampling rate is 360 Hz, 11-bit resolution and the MIT-BIH ARRHYTHMIA database records are used, we quote: Djohan algorithm used the discrete wavelet transform  [27]. It carried a value of PRD 3. 9% with a compression ratio of 12. 5% for the MIT-BIH ARRHYTHMIA database 117. dat record. The algorithm developed by Robert S. H. Istepanian et al. is based on the wavelet transform and using two methods of encoding; the first named Optimal Zonal Wavelet Coding (OZWC) and the other one is called wavelet transform Higher Order Statistics based Coding (WHOSC)  [43].
They carried out a compression ratio of 1:8. 16 and 1:17. 51 for OZWC and WHOSC, respectively, applied to the 100. dat of the MIT-BIH ARRHYTHMIA database record. The algorithm based on the combination of wavelet transform and Set Partitioning in Hiearchical Tree (SPIHT)  [45] ; it provided a PRD value of 1. 31% and a compression ratio of 45% applied to the 117. dat record of the MIT-BIH ARRHYTHMIA database. The set of the results are shown in table  2. The comparative study, illustrated by the table above, shows, that even though our algorithm does not outperform the most of the compared algorithms, the obtained results are acceptable and encouraging. Examining the table of the comparative study shows, in other hands, as examples, that the proposed algorithm outperforms Djohan's and Istepanian based on OZWC algorithms in sense of compression ratio.
24th IUPAP Conference on Computational Physics (IUPAP-CCP 2012) IOP Publishing Journal of Physics: Conference Series 454 (2013) 012086 doi:10. 1088/1742-6596/454/1/012086 Figure 10. Reconstruction error (red line) in superposition with the original ECG signal (black line). Table 1 lists the rate of compression CR values, root mean square error RMS, average length of words (Avglen: Averagelength) corresponding to a set, chosen arbitrarily, of pathological case extracted from the MIT-BIH ARRHYTHMIA database records. Assessment of the ECG compression algorithm applied to the MIT-BIH ARRYTHMIA records exhibited pathological cases. Despite the interest of the numerical evaluation of the ECG signal compression algorithm, the quantitative one based upon the visual perception is essential for clinical cases.
SELECTION OF STUDIES AND EXCLUSION CRITERIA A systematic search of the literature was conducted using Pubmed and Sciencedirect databases until March 2013. The article identification was based on various combinations of the following keywords: ("NAA" OR "N -acetylaspartate" OR "N -Acetylaspartic acid") AND ("at-risk" OR "vulnerability" OR "liability" OR "ARMS") AND ("schizophrenia" OR "psychosis" OR "schizotypy") AND ("spectroscopy" OR "MRS"). The search was limited to original English-written articles related to research in human subjects. This primary search yielded 11 articles and was completed by a manual search from references cited in primarily found articles. This secondary search yielded 20 articles. 1 H-MRS studies require selection of a voxel for spectrum acquisition. Many studies in HRS acquire spectra from different brain regions or subregions and with different voxel sizes, leading to difficulties in comparing findings.
In order to tabulate NAA levels in a way that would enable us to compare between studies, only studies expressing or allowing to compute NAA concentrations as a ratio to creatine (Cr) were included. Cr represents components of the cell's energy metabolism and is assumed to remain relatively constant. Moreover, only studies investigating at least HRS and healthy control groups matched for gender and age were included. Among the selected articles, nine studies were excluded for not reporting original data in HRS (n = 6) and/or for not reporting NAA/Cr in our region of interest, the PFC (n = 3). Two studies were excluded because the group of HRS and the group of healthy controls were not matched for age. A final total of nine articles were retained for analysis. Characteristics of studies are described in Table  1  (participants demographical characteristics and volume of the voxel placed in the PFC for 1 H-MRS acquisition).
A 406objective mounted on a LEICA DM6000 microscope was used for manual counting. Surface area was calculated on corresponding Hoechst images using ImageJ software. 7 sections (each 192 mm apart) per animal were analyzed in a blind manner. The density of caspase-3 positive cells was calculated by dividing their number by the corresponding area. Average densities per animal were estimated and compared between groups with a Student t-test using the GraphPrism software. A panel of different neural precursor marker antibodies were used: rat anti-Pdgfra (1/800, BD biosciences #558774) as an oligodendrocyte precursor marker, rabbit anti-GFAP (1/1000, Dako #Z0334) and rabbit anti-Ndrg2 (1/500; kind gift from T. Miyata, ref  [43] ) as astrocyte markers, rabbit anti-Pax6 (1/500, Abcam, #ab5790), rabbit anti-Sox2 (1/500, Millipore AB5603) and mouse anti-Nestin (1/500, Millipore MAB353) as more immature precursor markers.
For each animal, the entire dorsal hippocampal CA3 structure (bilateral) was excised from 60 sections and pooled. Total RNA was isolated using a picopure RNA isolation kit (Arcturus) according to manufacturer's instructions. RNA quantity and quality were assessed using a Nanodrop ND-1000 spectrophotometer (ThermoScientific) and Agilent 2100 Bioanalyzer (Agilent Technologies, USA) respectively. To generate cDNA for qPCR experiments, RNA reverse transcription and amplification was performed using a Nugen Ovation Pico WTA system following manufacturer's instructions. Real time qPCR assays using the SYBRgreen method followed MIQE guidelines  [44]. Gene-specific primers for Olig1 (forward CGTCTTGGCTTGTGACTAGCG and reverse GCCAGT-TAAATTCGGCTACTGTC), for Npy (forward GCTCTGCGA-CACTACATCAATCTC, reverse AGGGCTG-GATCTCTTGCCATA) and for Sst (forward GGAAGACATTCACATCCTGTTAGCTT reverse AGAGGTCTGGCTAGGACAACAATATTA) were designed using Primer Express Software (PE Applied Biosystems).
Electron microscopy (EM) and morphometry Semi-thin sections (0. 5 mm) were stained with toluidine blue and images were acquired with a Coolsnap CCD camera mounted on a Provis Olympus Microscope. Ultra-thin sections (40 nm) were mounted on either 200 mesh or one slot grids, cut and double stained with uranyl acetate and lead citrate prior to observation with a Philips (CM-100) electron microscope. Digital images from the CA3 region were obtained with a CCD camera (Gatan Orius). Morphometric analysis was performed with the software Digital Micrograph. For each nucleus, its widest diameter was measured, and the mean calculated from 50 neuronal nuclei from two mice per genotype. Only neurons displaying a clearly visible nucleolus were taken into account. Golgi apparatuses (GA) were analyzed in 50 cells from two WT animals and two KO animals.
Acknowledgments We thank  Nicolas Narboux-Neme  for in situ hybridization advice,  Sylvie Dumont  and  Dominique Wendum  at the IFR 65 for laser microdissection,  Benoit Albaud  and  David Gentien  for help with picochip analyses,  Virginie Lavilla  for help with quantitative PCRs. We thank  R. Belvindrah ,  A. Sobel  and  F. Phan Dinh Tuy  for constructive comments on the manuscript. The team of FF is part of the  Bio-Psy Labex  and the  Ecole des Neurosciences de Paris Ile-de-France network.
The authors thank the  Inserm Avenir program , the  French Agence National de la Recherche  ( ANR-08-MNP-013 ), the  Bettencourt Schueller Foundation  and the  Jerome Lejeune Foundation  for grant support to FF, and Paris 6 and  An-Najah  universities for support to RKN. The authors thank the  Ile de France region through the Neuropole (Nerf)  for support of EBJ and animal house facilities, and the  FRC Rotary  for confocal microscope equipment. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competitive ELISA assay (cELISA) Serological evidence of avian influenza virus was detected using a Competitive Enzyme-Linked Immunosorbent Assay (cELISA) (ID-screenH Influenza A Antibody Competition ELISA Kit, ID-Vet, Montpellier, France) specific to influenza A nucleoprotein (NP) as described by Zhou et al  [15]. The results were expressed as the percentage of competition value according to the following formula: (OD samples/OD negative)6100. Poultry flocks were considered positive for antibodies to influenza A NP if the average percentage of competition (mean value of 20 tested sera) is lower than 45. Statistical analyses. Statistical analyses were carried out with the R software and the flock was considered as an epidemiological unit. Between-flock prevalence and confidence intervals were estimated using the epiR package.
Among the available data collected in the questionnaire, seven categorical variables were selected to study the risk of AI infection such as: area (geographical location of the farms), bird species, nearby poultry farms -including backyard -within a radius of 500 m around the farmhouse, nearby humid zone (proximity to river, lakes, swamps), biosecurity measures (building infrastructure, equipments, farm management), owner/workers circulating between farms and contacts with migratory birds (wild birds observed or not in the neighboring areas). These variables were first entered in univariate logistic regression models, with flock status (infected/not infected) as dependent variable. An initial multivariate model was built based on all the predictors with p#0. 25 (LR test) in the univariate screening.
Variable selection for the final model was carried out through a backward elimination process based on the log-likelihood ratio test as recommended by  Hosmer and Lemeshow (2000)   [16]. Spatial autocorrelation between flocks was taken into account by including governorate as a random effect in the regression models. Between-flock seroprevalence was mapped using a geographical information system software (ArcGIS v. 9. 2 ß ESRI Inc. ). To ascertain the effect of age upon the susceptibility to influenza virus infection, univariate logistic regression was also performed for long cycle poultry systems (layers, broiler breeders, and turkeys). Age was categorized into three categories based on the laying phase (before 18 weeks, from 18 to 32 weeks, after 32 weeks).
Viral HA and NA gene's sequencing and phylogenetic analysis The DNA templates were purified and sequenced by the Big Dye TerminatorH v1. 1 sequencing kit (Applied Biosystems, CA, USA). Post sequencing products were purified prior to running on 3730 XL DNA (ABI Prism 377, DNA sequencer, Applied Biosystem Inc. , CA, USA) Analyzer. Sequences were aligned using the Bioedit 5. 0. 6 program. The two segments were phylogenetically analyzed on the basis of their protein sequences. The MEGA5. 01 version 3. 65 program was used for tree building using the neighbor-joining method. The number of bootstrap replications was set to 1000. All branches supported by more than 50% bootstrap values were considered to be in the same group in the trees. Abbreviations used and GenBank accession numbers of different H9N2 viruses included in the phylogenetic analysis are listed in supplementary Table  S2.
The detection limit of rRT-PCR was 3. 7610 25 ng/ml (while by RT-PCR, the limit was 3. 7610 22 ng/ml) or 1 TCID 50 /ml, respectively. The correlation coefficient R 2 value was 0. 99, indicating linear regression between the standard curve line and the individual Ct data points. It seems that the confirmation of Ag EIA positive results was high by rRT-PCR, but low as compared to Cell culture and egg inoculation. In addition, conventional RT-PCR detected a 1500 bp and a 410 bp products specific to the H9 and N2 genes respectively. Four isolates from areas with the highest seroprevalence (Nabeul, Sfax and Tunis) were selected for HA and NA gene sequencing to discuss molecular evolution during H9N2 AIV outbreaks. Mixed speculations were chosen: broiler, layer, broiler breeder and turkey within the AIV isolates correspond to several seasons.