dataesr/scientific-paragraphs-categorization huggingface dataset:
Jingtai isolates JT081204 and JT090318 were identical with the corresponding sequence available in GenBank (GQ228818). When the 10 unique cox1 gene sequences were translated into amino acids sequence, 7 unique protein sequences were obtained with sequence variation of 0. 19-0. 56% and a total of 6 amino acid variation sites. Amino acid sequences of isolates JT080526, JT090104, JT090115-2, and YJ100610 were identical to the corresponding sequence available in GenBank (ACK55903) and that of isolate JT081204 was identical to T. multiceps cox1 available in GenBank (ACS37254). When Blast analysis with cox1 gene sequences was performed, more than 20 T. multiceps partial cox1 gene sequences from 346 to 445 bp were also available in GenBank. Partial cox1 gene sequences from the 10 unique sequences in this study could be further grouped into 4 unique sequences with variation rate of 0.
Phylogenetic analysis of taeniid cox1 gene The complete cox1 gene sequences from the other Taenia mt genomes available in GenBank were selected and aligned. Accordingly, a phylogenetic tree was constructed with cox1 gene sequences from this study and previously published mt sequences of related Taenia species, including T. multiceps (GQ228818 and FJ495086), T. saginata (AY684274), T. asiatica (AF445798), T. solium (AB086256), T. hydatigena (GQ228819 and FJ518620), T. crassiceps (AF216699), T. pisiformis (GU569096 and NC013844), and T. taeniaeformis (JQ663994 and FJ597547), with E. granulosus (AF297617) as the outgroup. The cox1 gene sequences were 1,623 bp in length for all T. multiceps isolates, but it was 1,620 bp for T. saginata, T. asiatica, T. solium, T. hydatigena, and T. pisiformis.
Partial sequences of nad1 and cox1 showed differences ranging from 1. 27 to 2. 54% and from 0. 22 to 0. 67%, respectively, and a conclusion was made that Sardinian sheep samples had at least 3 specific genetic variants  [19]. However, comparison between the partial cox1 sequences of the T. multiceps isolates from infected cattle from Erzurum Province, Turkey and other T. multiceps isolates available in GenBank showed nucleotide differences ranging from 0. 2 to 2. 6%  [20]. Although coenurosis in sheep and goats were reported in China, the molecular identification of T. multiceps was rarely conducted. Recently, the complete mt genome of T. multiceps from Chinese isolates was reported and provided useful markers for studying the systematics, population genetics, and molecular epidemiology of Taenia  [13, 21].
ACKNOWLEDGMENTS This work was supported by  National Key Project of Scientific and Technical Supporting Program  (No. 2007BAD40B04 ) and partially supported by  National Beef Cattle and Yak Industrial Technology System, NBCITS, MOA  (No. CARS-38 );  National Nonprofit Institute Research Grant  (No. 1610322012026 );  Gansu Province Agricultural Biotechnology Research and Application Development Project  (No. GNSW-2010-01 );  Gansu Province Scientific and Technical Supporting Program  (No. 1104NKCA082 ).
ACKNOWLEDGMENTS We thank  David Villareal  for assistance with tissue culture. The endothelial cells used in these studies were isolated from human umbilical cords, which were collected by the pediatric, perinatal, and mobile unit of the  UCLA Clinical and Translational Science Institute at LA Biomed/Harbor-UCLA Medical Center  ( UL1TR000124 ). This work was supported in part by grant  R01AI054928  from the  National Institutes of Health , United States. S. G. F. is a cofounder and shareholder of  Novadigm Therapeutics, Inc. None of the other authors has any financial conflicts.
Patient Samples and CLL cell isolation Peripheral blood (PB) samples were obtained after informed consent, from patients with B-CLL that were treatment naïve (untreated) or had received treatment but not in the preceding three months. The studies were approved by Local Ethics Committees (Comité de Protection des Personnes de Brest (France) and West of Scotland Research Ethics Service, NHS Greater Glasgow and Clyde (UK)). Linked clinical data of CLL patients were stored (Table  1 ). CLL lymphocytes were isolated and used freshly or cryopreserved as previously described  (23). After separation, CLL cell purity was > 95% in all cases, determined by flow cytometry. Normal PB mononuclear cells (PBMCs) were isolated from buffy coats by density gradient centrifugation using Histopaque (Sigma-Aldrich) and used freshly or cryopreserved.
Data and statistical analysis Average responses from at least 3 individual donors are shown (mean ± SEM). Statistical analysis was performed using GraphPad Prism 4 (GraphPad Software Inc. , CA), using Students paired or unpaired t-test (*p<0. 05; **p<0. 005; ***p<0. 001). Flow cytometry data were analyzed using FlowJo (Tree Star Inc. , Ashland, OR).
Financial Support: Project grants from Chief Scientists Office Scotland (CZB/4/748) -AMM and LM; Tenovus-Scotland -EC and AMMcC; Kay Kendall Leukaemia Fund (KKL501); Cancérpole Grand-Ouest, the Association pour la Recherche sur le Cancer (ARC-1092), the Ligue Nationale contre le Cancer (Comité Grand-Ouest) -LM; MRC clinical training fellowship -AMMcC.
2% were linked to care within 12 months  [29]. A study in Northern Alberta, Canada, found that 92% of individuals diagnosed with HIV infection accessed care following their diagnosis; 70% within 2 months of diagnosis  [24]. Both Canadian studies also found that time to care varied by race/ethnicity, age, exposure category, and geography. Differences in late diagnosis with HIV disease or linkage to care between countries may be due to differences in individual and system level factors such as health care delivery and access to care. Differences may also result from lack of uniformity in definitions for late diagnosis or linkage to care, or from data based on particular subpopulations. We analyzed data from the national HIV surveillance systems of Australia, Canada, France, Italy, Spain, and the United States and used uniform definitions to determine the percentage of people with HIV who were diagnosed late and the percentage linked into care overall and by demographic and risk characteristics.
Methods HIV surveillance data can be used to monitor stage of disease at HIV diagnosis and care visits by examining CD4 count and viral load data for HIV-infected people. We used data from HIV surveillance systems in Australia, Canada, France, Italy, Spain, and the United States to determine the percentage of people diagnosed late with HIV and who were linked to care after HIV diagnosis as measured by CD4 count and viral load (VL) tests overall and by demographic and risk characteristics. The countries included in the analyses agreed to participate among member countries from Europe, North America, and Australia that participate in an informal annual meeting to discuss HIV surveillance. Each country maintains a national surveillance system with country-specific reporting rules and representation of the population.
In general, people diagnosed with HIV should receive an initial assessment of immune system status and viral load promptly after diagnosis  [35, 36] , and with guidelines now recommending treatment be offered to people with less severe disease (e. g. , WHO guidelines recommend treatment at CD4 count #350 cells/mm 3 )  [40]  prompt linkage to care could improve worldwide. Because not all countries could provide data on stage of disease at diagnosis, we also assessed AIDS diagnosis in relation to the time of HIV diagnosis (Tables  2  and 3 ). This measure reflects people with AIDS who may have been recently diagnosed or people who were diagnosed with HIV years before their AIDS diagnosis and who may or may not have been on treatment. While this measure is not directly comparable to the late diagnosis measure presented in Table  1 , and does not reflect people who may have developed AIDS but were promptly treated, it can indicate a need for earlier detection and prompt treatment.
Acknowledgments Disclaimer: The findings and conclusions in this study are those of the authors and do not necessarily represent the views of the  Centers for Disease Control and Prevention. The Canadian authors acknowledge the provincial and territory surveillance officers who send non-nominal confidential reports for national HIV surveillance, particularly those who customized a data submission in support of this analysis. The authors want to thank  Eboni Bell ,  Orise Fellow ,  Centers for Disease Control and Prevention, Atlanta, GA , for her assistance with the literature review.
0 20-29 12 66. 7 24 45. 8 169 74. 2 30-39 38 65. 8 64 60. 9 449 62. 9 40-49 37 59. 5 88 70. 5 523 58. 0 50 or older 35 68. 6 69 66. 7 458 69. 9 Sex Male 112 64. 3 201 67. 7 1,113 68. 09 Female 11 72. 7 46 47. 8 500 57. 41 Transmission category d MSM 67 59. 7 32 62. 5 477 64 IDU 3 33. 3 59 42. 4 111 28 MSM-IDU 3 0. 0 9 11. 1 2 0 Heterosexual 39 82. 1 33 66. 7 1,001 70 Other 11 63. 6 4 75. 0 21 42 [33]w diagnoses of AIDS in Australia, reported by 31 March 2012. AIDS notifications are accepted as being an incomplete record of AIDS diagnoses in Australia in 2010. bThisdataset is not nationally representative; it includes data from 7 of the 13 provinces and territories. The case definition for AIDS in Canada is based on confirmed HIV diagnosis and presence/diagnosis of an AIDS-defining condition (no criteria for CD4 count are included in Canada's AIDS case definition).
6 80. 0 71. 4 69. 2 71. 3 74. 0 77. 3 0 74. 2 67. 8 72. 7 63. 6 100. 0 68. 3 68. 2 Canada b Total N 976 5 14 208 314 262 172 1 725 236 231 66 8 208 44 $1 CD4 or VL within 3 months of diagnosis % 89. 8 83. 3 81. 3 87. 7 89. 7 91. 2 91. 9 90. 2 89. 4 20. 0 90. 9 100. 0 90. 9 85. 0 74. 0 Australia a Total N 1054 6 16 269 340 262 161 898 151 5 656 23 22 280 73 Total Age, years 0-9 10-19 20-29 30-39 40-49 50 or older Missing Sex Male Female Transgender Transmission category f MSM IDU MSM-IDU Heterosexual Other Missing a Cases of HIV infection newly diagnosed HIV infection in Australia in 2010 including cases previously diagnosed overseas. b This dataset is c HIV surveillance includes the whole country except Sardegna region (coverage 97. 8%). Data reported by 31 December 2010. d Data Source: e Includes cases of HIV infection diagnosed in 14 jurisdictions of the United States and reported by 31 December 2011.
Acknowledgments This work was supported in part by the  Creative Core AHA-MOMENT  grant from  Slovene Ministry of Science and European Fund for Regional Development  and by  Cross-Border Cooperation Programme Italy -Slovenia 2007-2013, (Project  PROTEO ,  Code N. CB166 ). The author wishes to thank  Alicja Gruszka  for her comments. Received: 25 September 2013 Accepted: 30 October 2013 Published: 1 November 2013.
PROPAGAPATH  7  is a dynamic and oriented signaling propagation pathway database, developed by Helios Biosciences (Romainville, France), originally developed, validated, and enriched with immunological and neural cell propagation data. We wanted to evaluate the potency of this model to detect minimal propagation pathways -potentially not already identified by conventional studies -when confronted with data from human skin epidermal keratinocytes. We used a combination of full genome expression studies and PROPAGAPATH analysis  7  to understand which endogenous pathways the keratinocytes trigger in response to VF stimulation.
analysis of quantitative PCr data Fluorescence incorporated in amplified DNA was continuously measured during the PCR cycles. This resulted in a "fluorescence intensity" versus "PCR cycle" plot allowing for the evaluation of a relative expression (RE) value for each marker. The value selected for RE calculations was the "output point" (Ct) of the fluorescence curve. For a given marker, the higher the number of cycles, the lower the mRNA quantity. The RE value was expressed in arbitrary units according to the formula: (1/2 number of cycles ) × 10 6. Abbreviations: DeFB4, defensin, beta 4; s100a7, s100 calcium-binding protein a7; sOD2, superoxide dismutase 2; std, standard; VFB, Vitreoscilla filiformis biomass. Raw data were analyzed with Microsoft Excel ® software (Microsoft Corporation, Redmond, WA, USA).
Morphometric analysis was performed using NIH ImageJ software for data quantification. For immunofluorescence detection of smooth muscle specific protein and GFP expression carotid artery/Matrigel sections were stained for calponin (rabbit anti calponin: 1:200; Epitomics, CA, USA), CX 3 CR1 (rabbit anti CX 3 CR1:1:50; ProSci Incorporated, CA, USA), F4/80 (Rat anti mouse F4/80: 1:100; eBioscience; Hatfield, UK), Laminin (mouse anti laminin: 1:500; Novus Biologicals, Cambridge, UK) and/or CD42b (rat anti CD42b: 1:200; emfret Analytics GmbH & co. KG, Eibelstadt, Germany). Goat anti-rabbit, anti-mouse or anti rat Alexa Fluor 546 or 488 (1:250 or 500; Abcam, Cambridge, UK) was used as secondary antibody and DAPI was used for nuclear staining. Rabbit, mouse or rat IgG (1:50 or 200; Abcam, Cambridge, UK) were used as isotype controls.
No additional labelling was required for GFP. Several thin optical slices (thickness,0. 7 mm) of high-resolution sequential confocal scans (Nikon eC1 plus, TE2000E) of carotid artery sections were acquired to identify single GFP + cells coexpressing smooth muscle marker and to avoid false positive images due to overlapping cells. The acquired images were coded and analysed by two observers blinded to the codes. The 3D reconstruction and analysis of the images was performed using IMARIS software (Bitplane Scientific Software, Zurich, Switzerland). In vitro cell tubulation and tunneling assay in 3D matrix CX 3 CR1 positive cells were FACS sorted from whole bone marrow of CX 3 CR1 gfp/+ and CX 3 CR1 gfp/gfp mice and were sandwiched between DQ-red BSA (Invitrogen; Bio-Sciences, Dublin, Ireland) fortified Matrigel layers with CX 3 CL1 gradient in a 15 m-angiogenesis slide (Ibidi, Munich, Germany).
CX 3 CL1 gradient was created by serially layering two layers of Matrigel consisting of 50 and 100 nM rmCX 3 CL1 respectively. The cells were imaged using high-resolution sequential confocal scans (Nikon eC1 plus, TE2000E) at 3 hrs and every day up to day 7 post seeding. A separate series of experiments were conducted in the absence and presence of Rho inhibitor (10 mM; Y27632; MERCK, Darmstadt, Germany). The acquired confocal images were 3D reconstructed and analysed using IMARIS software.
CX 3 CR1 positive cells (GFP positive; Green) integrated into microvascular wall and were also present in perivascular region and co-expressed smooth muscle marker (Calponin; Red) (Scale bar: 10 mm). In the CX 3 CR1 functionally deficient (CX 3 CR1 gfp/gfp ) mice the number of vascular and perivascular cells (GFP positive; Green) (D) and co-expressing smooth muscle marker (E) were significantly reduced. Data is expressed as mean 6 SEM of 20 carotid artery cross sections/mice (n = 4 independently performed experiments). F, Microvessels in the plaque stained with CX 3 CR1 (Green) and DAPI (nucleus; blue) were 3D reconstructed using IMARIS software to depict signet ring structures and their tubular architecture. G, The number of signet-ring cells was significantly reduced in CX 3 CR1 gfp/gfp mice.
Study design This was a retrospective, multicenter study of renal transplant recipients with aHUS-related ESRD. Sixty-six patients included in the French aHUS registry from 21 French transplantation centers were considered for inclusion. Renal transplant centers were contacted to date and update clinical data regarding graft outcome. Criteria for inclusion in the study were: (1) Patients with adult-onset (=18 years) aHUS who had received a renal transplant between January 1995 and December 2009 and (2) Patients who had undergone a genetic investigation of the complement alternative pathway. Exclusion criteria were: (1) HUS with an identified cause such as STEC-induced HUS, Thrombotic Thrombopenic Purpura (TTP) associated with ADAMST 13 deficiency, malignancy or autoimmune-related HUS. (  2.
Clinical data The following clinical data were obtained from medical records: pretransplant characteristics, the age at the time of aHUS onset, ESRD, renal transplantation and posttransplant recurrence. Meaningful independent variables for all kidney transplants were recorded: deceased or living donor kidney, donor age, number of HLA mismatches, cold ischemia time, induction therapy (anti-thymoglobulin [ATG] or interleukin 2 receptor alpha anti-IL2Ra]), calcineurin inhibitor (CNI) or mTOR-based maintenance regimen, plasmatherapy regimen, delayed graft function and number of acute rejection episodes.
Variables with p values of less than 0. 20 in the univariate analysis were entered into multivariate analysis through a forward subset selection with no switching. Risk ratios (RRs) are shown with their upper and lower 95% confidence limits. For all statistical measures, p < 0. 05 was considered significant. Statistical analysis was performed using the NCSS software (Hintze, J. 2012. NCSS 8. NCSS, LLC. Kaysville, UT, USA).
So far, it remains unclear whether the high incidence of acute rejection results from low exposure to CNI, fueled by the wish to limit CNI-related endothelial toxicity, or from a complementdependent enhanced alloimmune response  (57, 58). Certain considerations need to be taken into account when interpreting the results. The first is that the patients were retrospectively selected from the French registry of aHUS. A second limitation is that the patients were enrolled over a large period of time and the inclusion criterion for previous genetic testing could have introduced selection bias. Such bias may be minimal as we failed to identify a significant difference in the outcome of grafts performed between 1995 and 2002 (before the knowledge of complement associated aHUS) and between 2002 and 2009 (data not shown).
Acknowledgments We are grateful to the clinicians who referred their patients for complement investigations and accepted that patients were included in the study and particularly to  Bruno Hurault De Ligny (Caen) ,  Christophe Legendre  (Necker),  Benoit Barrou  and  Nadia Arzouk  ( Piti é Salp étri ère ),  Antoine Durrbach  ( Bic être ),  Maryvonne Hourmant  (Nantes),  Pierre Francois Weestel (Amiens) ,  Patrick Le Pogamp and C écile Vigneau (Rennes) ,  Marie Essig  (Limoges),  Olivier Toupance  (Reims),  Christophe Mariat  and  Nicolas Maillard  ( Saint Etienne ),  Denis Glotz  ( St Louis ),  Mathias Buchler  (Tours),  Philippe Lang  (Mondor),  St éphane Burtey and Noemie Jourde (Marseille), Isabelle Etienne (Rouen). We thank  Stephanie Ngo ,  Delphine Beury ,  Nelly Poulain ,  Christine Hautreux  and  Jacques Blouin  who provided expert technical support and  Lubka Roumenina  for the discussion about the functional consequences of complement mutations.
Methods The Second Line study is a 96-week, multinational trial of participants virologically failing first-line therapy randomized 1 : 1 to currently recommended second line treatment (2-3N(t)RTI þ LPV/r) or RAL (400 mg b. i. d. ) þ LPV/r (400/100 mg b. i. d. or 800 mg/200 mg q. i. d. ). Eligible participants were HIV-1 positive adults (aged !16 years) who had received first-line cART comprised of a nonnucloeside reverse transcriptase inhibitor (NNRTI)þ2N(t)RTIs for at least 24 weeks with no change within 12 weeks prior to screening; evidence of virological failure defined by two consecutive (!7 days apart) plasma HIV RNA viral load more than 500 copies per ml; no previous exposure to protease inhibitors and/or integrase inhibitors. The study was approved by each site's Ethics Committee and was registered at Clinicaltrials.
gov (NCT00931463). The cohort median (IQR) age was 38. 5  (32. 4-44. 4 ) years, 55% male, 42% Asian and 36% African, 73% heterosexual transmission, with an estimated median duration of HIV infection of six (3. 6-8. 7) years. The primary 48-week results of the Second Line study have been described  [14]. Of the 37 sites that participated in the Second Line study eight sites from five countries (South Africa, India, Malaysia, Thailand and Argentina) participated in the body composition sub-study (clinicaltrials. gov identifier: NCT01513122). These sites had access to a dual energy X-ray absorptiometry (DXA) scanner and recruitment was open to all participants screened at these sites between July 2010 and July 2011. The sub-study was approved by each site's Ethics committee's and all participants gave written, informed consent.
Statistical analysis Analyses included available data from all participants who consented to the sub-study, who underwent randomization, received at least one dose of study medication and who completed both a week 0 and 48 DXA scan. Results were considered statistically significant at a two-sided a ¼ 0. 05. A sample size of 100 per randomized treatment arm was required to achieve 80% power to detect a mean difference of 1. 7% change in BMD. Linear regression was used to compare means of differences (baseline to week 48) between randomized Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. arms. McNemars test for paired proportions was used to compare the categorized BMD variables. The association between BMD changes and the baseline variables was assessed by linear regression, any variable with P < 0.
Discussion The effects of raltegravir on BMD in people living with HIV have not been well defined. The bone sub-study of the Second Line clinical trial was conducted on 210 HIV-positive participants recruited from a range of middle-income countries in which there is a paucity of BMD data. The data generated in this sub-study of participants with confirmed virological failure of an NNRTIþ2N(t)RTI cART regimen, demonstrate that effective second line therapy with either WHO standard of care [ritonavir-boosted protease inhibitor (r/PI) þ 2-3 N(t)RTIs] or the nucleoside sparing regimen (r/LPV þ RAL) reduced BMD over 48 weeks. However, the raltegravir arm was associated with less BMD loss than the N(t)RTI arm. The covariates predicting a greater loss of BMD in both the lumbar spine and proximal femur over the 48 weeks were low baseline BMI and longer duration of TDF on study.
ACKNOWLEDGMENTS We would like to thank  Pablo Flaiszman  for the artistic work on the figures. Jérémie David Goldstein ,  Louis Pérol , and  Audrey Baeyens  were supported by the  Ministère de l'Enseignement Supérieur et de la Recherche  and  Bruno Zaragoza  by the  Université Pierre et Marie Curie ,  Paris 06. This work was supported by the  EFSD/JDRF/NN 2011  and  INSERM/DGOS 2011  (to Eliane Piaggio), and by  ANRS  (to  Gilles Marodon ).
Method Quantifications were performed by real-time PCR on a Light cycler instrument (Roche Diagnostics) using the second-derivative-maximum method provided by the Light Cycler quantification software, version 3. 5 (Roche Diagnostics). Two linkers: Linker 11b and 11TAb (or 11GTb in the virological context; see below) (see Additional file 1: Table  S1A ) were used for the quantification of uDNA L and pDNA L , respectively. These linkers were assembled by annealing two partially complementary unphosphorylated oligonucleotides (to give 34 nM) final concentration) in the presence of 200 mM NaCl. To quantify linear forms of HIV-1 DNA, a ligation reaction mixture was carried out by addition of linkers (final concentration: 30 nM) to DNA, in the presence of 10 units of ligase from the Quick ligation kit (NEB), for 2 hours at room temperature in a final volume of 20 μL, according to the manufacturer's instructions.
Products were separated by in a 16% acrylamide/urea denaturing gel, analyzed with a Typhoon TRIO variable mode imager (GE Healthcare, USA) and quantified with ImageQuant TL software. The susceptibility of IN to RAL, EVG and DTG was determined in vitro by assessing IN activity in the presence of various concentrations of strand transfer inhibitors. 50% inhibitory concentrations (IC50) were determined with Prism 5. 0 software. The HIV-1 ODN substrate sequences were: U5B: 5′-GTGTGGAAAATCTCTAGCAGT-3′; U5A: 5′-ACTGCTAGAGATTTTCCACAC-3′.