dataesr/scientific-paragraphs-categorization huggingface dataset:
Gene selection from databases OMIM is a comprehensive, daily-updated human phenotype database, containing more than  Using the CTD database, 11, 142 and 813 genes were retrieved using the CF, Pancreatic diseases and Liver Disease key words, respectively. Fig  4 presents  a Venn diagram showing the shared genes between these key words. Only 3 genes were found to be shared among the 3 used key words: TGFB1 (NCBI Accession ID: 7040), TNFRSF1A (NCBI Accession ID: 7132), CFM1 (NCBI Accession ID: 10167). Surprisingly, among some differences with the OMIM search, the CFTR gene was not found to be present in the list of genes retrieved using the Liver Disease key word in CTD. HuGE Navigator database is an integrated, searchable, Web-based knowledge base which mines the scientific literature on human genetic associations and human genome epidemiology  [29, 30].
Differential gene expressions retrieved from bibliographic analysis Differentially expressed genes in CF were retrieved from PubMed. First, a small-scale microarray study performed with human native nasal epithelial cells (F508del homozygous patients vs. controls) was used  [31]. We also retrieved genes from other papers aimed to compare gene expression in CF vs normal cells  [32]. Another work using non-CF and F508del-CFTR homozygote samples, showed significant changes in the expression in 24 genes (two-sample t-test, p < 0. 00001). A three-filter comparative analysis showed that 18 genes were significantly increased and 6 genes were decreased in CF relative to and non-CF samples, respectively  [33]. We also retrieved genes from a microarray study in which results from 12 CF and 11 non-CF participants were used  [34] , and from data in which functional CFTR was absent of the plasma membrane  [35].
Therefore, we used this list of 15 genes (Table  2 ). Finally, a study with normal, steatotis, NASH with fatty liver, and NASH without fatty liver samples was analyzed. Among 11,633 genes with altered expression out of 33,252 genes, 39 genes were changed in expression, between normal and NASH  [21]. Thus, a list of 84 differentially expressed genes from 4 different studies was used in the present study (Table  2 ). For pancreatic disease, a study with normal and Chronic Pancreatitis specimens was used  [43]. Comparison of the expression of 5,600 genes between the normal and Chronic Pancreatitis was performed. GenBank accession numbers of 152 genes with increased expression (  [43] , Footnote 1) and 34 with decreased genes levels in Chronic Pancreatitis (  [43] , Footnote 2) were retrieved.
We analyzed those genes one by one and removed non human genes and pseudo genes. This led us to list 129 increased genes and 23 decreased genes in Chronic Pancreatitis (Table  3 ). Because 152 genes were simultaneously increased in pancreatic cancer, only 5 of 5,600 genes were significantly over expressed in Chronic Pancreatitis compared with normal pancreas: Mucin-6 (GenBank Accession Number: L07517), COMP (GenBank Accession Number: L32137), TPSB1 (GenBank Accession Number: M33493), Rearranged Ig-lambda light chain (GenBank Accession Number: X57809) and CRISP-3 (GenBank Accession Number: X95240). An analysis of 6,800 different genes expressed in samples of normal pancreas and Chronic Pancreatitis was studied  [44]. 107 genes were predicted to be expressed within cells with Chronic Pancreatitis  ([44] , Table  1 ).
Gene name NASH vs. controls Reference Aldehyde oxidase (AOX1, OMIM: 602841) -2. 4 Cu/Zn SOD (SOD1, OMIM: 147450) -3. 7 Catalase (CAT, OMIM: 115500) -2. 4 Glucose-6 phosphatase (G6PC, OMIM: 613742) -4. 9 Alcohol   nasal epithelial cells from F508del-CFTR homozygous patients and non-CF controls. GSE48452  [48]  is an expression profiling performed with samples of control human liver, healthy obese, steatosis and NASH). Only controls and NASH groups were re-analyzed here. ): SLC12A2 SLC39A14 SLC17A2 SLC44A1 SLC34A2 SLCO3A1 SLC25A36 SLCO2A1 SLC13A5 SLC22A15 SLC35B1 SLC4A2 SLC1A4 SLC31A1 SLC2A3 SLC2A10 SLC24A3 SLC33A1 SLC4A7 SLC5A1 SLC28A3 SLC25A24 SLC17A4 SLC44A3 SLC35F2 SLC38A10 SLC43A1 SLCO4C1 SLC22A3 SLC5A6 SLC35A2 SLC25A38 SLC6A11 SLC39A7 SLC1A1 SLC39A9 SLC2A14 SLC16A10 SLC22A23 SLC4A4 SLC41A2 SLC25A39 SLC38A11 SLC11A2 SLC16A4 SLC13A3 SLC6A6 SLC12A6 SLC24A6 SLC9A3R1 SLC23A1 SLC12A8 SLC46A1 SLCO1B3 SLC2A13 SLC5A4 SLC2A9 SLC38A6 SLC39A8 SLC43A3 SLC25A13 SLC35E1 SLC25A11 SLC25A12 SLC39A1 SLC39A6 SLC35C1 SLC35B4 SLC3A2 SLC30A5 SLC46A3 SLC25A34 SLC25A46 SLC10A7 SLC6A7 SLC9A8 SLC45A2 SLC25A17 SLC25A6 SLC45A1 SLC10A4 SLC22A2 SLC17A5 SLC26A6 SLC2A12 SLC39A3 SLC5A5 SLC20A1 SLC8A1 SLC26A1 SLC38A4 SLC25A33 SLC25A43 SLC6A9 SLC25A31 SLC37A3 SLC1A3 SLC27A2 SLC25A28 SLC24A2 SLC13A2 SLC1A5 SLC7A6 SLC39A10 SLC25A27 SLC5A12 SLC9A11 SLC29A4 SLC38A7 SLC25A37 SLC34A1 SLC6A15 SLC29A2 SLC17A7 SLC20A2 SLC18A3 SLC25A37 SLC9A9 LST-3TM12 SLC38A8 SLC22A8 SLC35B3 SLC16A13 SLC43A2 SLC25A20 SLC22A6 SLC22A13 SLC14A2 SLC25A41 SLC35F1 SLC37A1 SLC4A5 SLC27A6 SLC32A1 SLC44A2 SLC5A10 SLC26A5 SLC7A9 SLC9A1 SLC22A11 SLC25A23 SLC25A44 SLC30A1 SLC7A3 SLC17A8 SLC6A5 SLC25A42 SLC25A2 SLC39A4 SLC25A35 SLC36A3 SLC45A4 SLC9A3R2 SLC6A3 SLC25A18 SLC9A7 SLC2A6 SLC45A3 SLCO6A1 For PI, we failed to find any array analysis.
Therefore, we used a gene expression of type 1 diabetes-vs-classical type 1A diabetes-vs-healthy controls array (GSE44314)  [49]. We solely reanalyzed classical type 1A diabetes-vs-healthy controls. 246, 211 and 145 genes were retrieved from our GSE40445, GSE48452 and GSE44314 re-analysis, respectively (Table  5 ). A Venn diagram was drawn (not shown) but no common genes among the genes selected from the 3 studies were found. Therefore, if there are some common genes in the 3 studies, they do not appear among the most highly regulated genes of each study.
Common genes in CF, retrieved from bibliography and microarray studies We then search for common genes between the genes which were obtained by the bibliographic search for CF genes (Table  1 ), Liver Disease (Table  2 ) and Chronic Pancreatitis (Tables  3  and 4 ) and the genes which were retrieved by the re-analyzing of GSE40445, GSE48452 and GSE44314. The result is summarized in Table  6. Only 4 genes were found to be common to both groups of genes retrieved from the bibliographic analysis and the GEO database analysis, regarding CF. These genes were IFRD1 (Interferon-related developmental regulator 1, OMIM Accession ID: 603502), IFI16 (Interferon gamma inducible protein 16, OMIM Accession ID: 147586), CCNE2 (Cyclin E2, OMIM Accession ID: 603775) and IGFBP2 (Insulin-like growth factor-binding protein 2, OMIM Accession ID: 146731).
Genes expressed at increased levels in Chronic Pancreatitis OMIM ID Reference LGALS4 (Lectin, Galactoside-Binding, Soluble We failed to find published works from PubMed, showing that IFI16, CCNE2 and IGFBP2 are also possibly involved in CF. Therefore, we searched in previously published works some lines of evidence to link these genes to CF. IFI16 has a possible role in chronic inflammatory autoimmune disorders. The IFI16 protein is normally expressed in nuclei but may be mislocalized in the cytoplasm and secreted. Indeed, significant levels of extracellular IFI16 protein have been identified in the sera of patients with autoimmune diseases  [52]. These data provide evidence for a function of IFI16 upon inflammation and tissue damage, as it is also observed in CF. The human CCNE2 gene encodes a 404-amino-acid protein, related to cyclin E.
Because chronic inflammation is an important modulator of the IGF/ IGFBP system in CF and because IGF2 promotes development of pancreatic beta cells, related to some forms of diabetes mellitus, we also propose that IGFBP-2 is a modifier gene in CF. Candidate genes in CF were selected due to their involvement in CF-related diseases or in similar diseases. Published studies have mostly examined genes involved in immune or inflammatory response (for review:  [59] ). These genes are: ACE, ADRβ2, ATB, CAPN10, ClCN2, DEFβ4, ENaC, FcβRII, GCLC, GSTM1, GSTM3, GSTP1, GSTT1, HFE, HLA-I, HLA-II, HLA-III, HSP70, IFN-γ, IL1-β, IL6, IL10, IL18, KCNJ11, MBL2, MIF, NOS1, NOS3, MASP-2, PPARβ, SERPINA1, SERPINA3, SFTPA1, SFTPA2, TLR4, TGFB1, TNFα, TNFα-receptor, and TNFβ  [59]. Among the published modifier genes  [59] , we found using databases that TGFB1, SERPINA1, TNFα-receptor, GSTP1, ADRβ2, GSTM1, GSTT1 and TNFα are also involved in pancreatic and liver diseases (Figs  3  and 4 ).
Among candidate gene modifiers of clinical phenotypes in CF, we also retrieved MBL2, EDNRA, TGFB1, IFRD1, IL8, MSRA, ADIPOR2, TCF7L2 and SERPINA1 (for review:  [60] ). When compared to our database search, we found that TGFB1 was present in OMIM and CTD and that IFRD1 and SERPINA1 were only present in OMIM, indicating that they are also possibly involved in pancreatic and liver diseases. IFRD1 was also found in our CF-vs-non CF re-analysis of SE40445 (Table  6 ). In conclusion, we propose here that IFI16, CCNE2 and IGFBP2 are new candidates of modifiers genes in CF. Common genes in CF and Chronic Pancreatitis and in CF and Liver Disease retrieved from bibliography and microarray studies. Common genes in CF-vs-non CF re-analysis of SE40445 and bibliographic search for Chronic Pancreatitis and Liver Disease were EPHX1 (Epoxide Hydrolase 1 Microsomal, OMIM Accession ID: 132810) and SLC33A1 (Solute carrier family 33 (Acetyl-CoA Transporter), member 1, OMIM Accession ID: 603690), respectively.
EPHX1 gene encodes a ubiquitous enzyme (α/β hydrolases), localized in the ER. Mutations in the EPHX1 gene contribute to several diseases  [61]  in link with tobacco exposure and lung Table  6. Genes involved in CF, Chronic Pancreatitis and Liver Disease. Common genes present in our re-analyzed data of the GEO database and in our bibliographic analysis. Common genes in CF and in pancreatic and in liver affections are underlined.
CF-vs-non CF re-analysis of SE40445 IFRD1*  [32] [33] [34] [35] 37 ] IFI16  [32] [33] [34] [35] 37 ] CCNE2  [32]  IGFBP2  [33, 35]  EPHX1  [38]  SLC33A1  [41]  Diabetes-vs-healthy reanalysis of GSE44314 HLA-DRB1**  [32] [33] [34] [35] 37 ] DSP  [32] [33] [34] [35] 37 ] HLA-DQA1  [34]  HLA-DRB1**  [43, 44]  CTSA  [43]  PKM  [43]  SLC25A36  [41]  TGFB1***  [40]  NASH-vs-healthy re-analysis of GSE48452 HLA-DRA  [32] [33] [34] [35] 37 ] GPNMB  [32] [33] [34] [35] 37 ] NCF2  [32] [33] [34] [35] 37 ] RASGRP1  [32] [33] [34] [35] 37]  LGALS3  [32] [33] [34] [35] 37]  PTPN13  [32] [33] [34] [35] 37]  LYZ  [43]  PECAM1  [43, 44]  HLA-DRA  [43]  DPYSL2  [44]  GPNMB  [43, 44]  HLA-DMA  [44]  IQGAP1  [43]  ENTPD1  [44]  CD74  [43, 44]  LCP1  [44]  IGKC  [44]  SPARC  [43, 44]  GUCY1B3  [43]  PDGFRB  [44]  CD37  [44]  COL3A1  [43, 44]  HLA-DPB1  [43]  GSN****  [43, 44]  MGMT  [43]  TCF4  [44]  PMP22  [43, 44]  STXBP1  [39]  ABR  [40]  SLC6A6  [41]  SLC39A10  [41]  Underlined: Genes that were found in the bibliographic analysis for CF and Chronic Pancreatitis genes.
Therefore, we propose here that SLC33A1 is likely a strong modulator in CF. Differentially expressed genes in the bibliographic search for CF and in the Diabetes-vshealthy re-analysis of GSE44314 were the Major Histocompatibility Complex Class II genes DRB1 and DQA1 (OMIM Accession ID: 142857 and 146880, respectively) and the Desmoplakin gene (DSP, OMIM Accession ID: 125647) (Table  6 ). HLA-DQA1 and HLA-DQB1 are likely genetic markers of the Celiac Disease  [71]  which was suggested to be a risk factor in CF  [72, 73]. Therefore, together with our present results, we propose HLA-DQA1 and HLA-DQB1 genes, as new modifiers in CF. Desmoplakin is a cytoskeletal linker protein conferring the structural integrity of tissues by linking intermediate filament cytoskeleton from cell to cell (for review:  [74] ).
In remodeled airways, as in CF, abnormalities of the cytokeratins and desmoplakins are observed  [75]. According to the importance of intermediate filaments and cell-to-cell communications in CF  [76, 77] , DSP gene expression is likely involved. Differentially expressed genes in the bibliographic search for CF and in NASH-vs-healthy re-analysis of GSE48452 were: HLA-DRA (OMIM Accession ID: 142860), GPNMB (Glycoprotein NMB, OMIM Accession ID: 604368), NCF2 (Neutrophil Cytosolic Factor 2, OMIM Accession ID: 608515), RASGRP1 (RAS Guanyl Nucleotide-Releasing Protein 1, OMIM Accession ID: 603962), LGALS3 (Lectin, Galactosidase-Binding, Soluble 3, OMIM Accession ID: 153619), PTPN13 (Protein-Tyrosine Phosphatase, Nonreceptor-Type 13; OMIM Accession ID: 600267) (Table  6 ). Involvement of Class II major histocompatibility complex (MHC) genes in CF were discussed above.
1, 1 and 9 pathways were retrieved for IFI16, IGFBP2 and CCNE2, respectively  (Fig 6). No pathway was common between those genes. The 4 common genes in CF and Chronic Pancreatitis and the 6 common genes in CF and Liver Disease were further submitted to the pathway search (Table  7 ). The only common pathway between CF, Chronic Pancreatitis and Liver Disease was "Immune System" (REACTOME: 6900). The implicated genes were IFI16 for CF, HLA-DQB1 for CF plus Chronic Pancreatitis and LGALS3, NCF2 and RASGRP1 for CF plus Liver Disease (Table  7 ). Therefore, genes of the Immune System are likely involved in CF and in its association with Chronic Pancreatitis and Liver Disease. We further search for the diseases that are statistically enriched among our genes. Modifiers candidates in CF (IFI16, CCNE2 and IGFBP2), the common genes in CF and Chronic Pancreatitis (EPHX1, HLA-DQA1 -DQB1, DSP) and in CF in link to Liver Disease (SLC33A1, GPNMB, NCF2, RASGRP1, LGALS3 and PTPN13) were entered as a single data set in CTD.
Nevertheless, further studies are still needed. Therefore, our aim was to depict new candidate genes with modifying activity in CF, in association with liver and pancreatic diseases. Using databases, bibliographic mining and gene expression analysis we found some candidate genes specific to lung, liver and pancreas. Nevertheless, two groups of different genes could be built, depending on the way they were retrieved. Unsurprisingly, databases search led to known genes involved in CF. Therefore, we focused on genes obtained by microarray results re-analysis, compared to those from our bibliographic analysis. We highlighted 3 genes specific to CF, 4 genes specific to CF and Chronic Pancreatitis and 6 genes for CF and Liver Disease. Nevertheless, we failed to find common genes in CF, Chronic Pancreatitis and Liver Disease.
3. 3. Pore Waters. Figure  3  shows the concentrations of natural Zn and 68 Zn en measured for the pore waters; these data reveal direct correlations between Zn concentrations and total dosing levels and incubation times. For example, the pore water with the highest Zn concentration of 11. 5 μg mL -1 was obtained for the soil with the highest Zn 2+ /Zn-NP ratio of 13, and that was incubated for 12 months (Figure  3a ) (Table  S1 ). Essentially identical concentrations of the three Zn forms were determined for the filtered and unfiltered pore water samples. The average 68 Zn en / 64 Zn en ratio for all pore water samples is 1. 08 ± 0. 02 (sd, n = 46) (Figure  1B ). After 3 and 6 months, the pore water pH was slightly higher for all treatments that received DEG than in the water control, but after 12 months the difference was negligible (Table  S3 ).
Search strategy for identifying relevant studies An expert librarian performed a search of PubMed/ MEDLINE, Excerpta Medica Database, African Journals Online and African Index Medicus without any language restriction. The search strategy included the following terms: ' Africa' , 'pulmonary hypertension' , and 'pulmonary arterial hypertension'. Individual country names for the 54 African countries were also used as additional key search terms to identify more abstracts on the subject. References of all relevant original and review articles were scrutinized for additional potential data sources. The main search strategy conducted in PubMed is available in the review protocol  [19].
Data extraction and management Two review authors (JJB and JJN) independently extracted data including: first author name, year of publication, year of participants' inclusion, country, study design, setting, sample size, age distribution, proportion of males, diagnostic criteria for PH, number of cases of PH, and etiologies of PH as classified by international guidelines  [2]. Authors were contacted at least twice to request relevant missing information. A World Health Organization Afro sub-region was assigned to each study based on the country of recruitment.
Data synthesis and analysis A meta-analysis was conducted for data obtained from studies in the same population (patients with chronic obstructive pulmonary disease, with heart failure, on hemodialysis, presenting with cardiac complaints, with HIV infection, with rheumatic heart disease, with sickle cell disease, with systemic lupus erythematous, with cardiac surgery, and with systemic sclerosis). Standard errors for the study-specific estimates were determined from the point estimate and the appropriate denominators. Then, the study-specific estimates were pooled through a random-effects meta-analysis model, to obtain an overall summary estimate of the prevalence across studies, after stabilizing the variance of individual studies using the Freeman-Tukey double arc-sine transformation  [21].
Heterogeneity was evaluated by the χ2 test on Cochrane's Q statistic which is quantified by I 2 values  [22] , assuming that I 2 values of 25%, 50% and 75% respectively represent low, medium and high heterogeneity  [23]. Inter-rater agreement for study inclusion was assessed using Cohen's kappa (κ) coefficient  [24]. Egger's test served to detect publication bias  [25]. A p value <0. 1 was considered indicative of statistically significant publication bias. Data were analyzed using Stata software (Stata Corp. 2013. Stata Statistical Software: Release 13. College Station, TX: StataCorp LP). We conducted a narrative synthesis in the case of limited data for a meta-analysis.
Results The review process Initially, a total of 1611 records were identified. After elimination of duplicates, 1543 records were retained. Titles and abstracts were screened and 1470 records were found irrelevant and excluded. Agreement between review authors on abstract selection was moderate (κ = 0. 69). Full-texts of the remaining 73 papers were scrutinized for eligibility, among which 48 were excluded (Fig. 1 ). Overall, 25 papers were found eligible and were included in the data synthesis; 24 papers reported the prevalence of PH , while one other paper reported PH etiologies  [17]. The inter-rater agreement for final study inclusion between review authors was high (κ = 0. 93).
Methodological quality and characteristics of included studies The characteristics of each included study are presented in Additional file 1. Twelve (48%), seven (28%), and six (24%) papers had respectively a low, moderate and high risk of bias in their methodological quality [See Additional file 2]; all were cross sectional studies. The diagnosis of PH was performed using right heart catheterization in only one study while the rest used echocardiography. The studies included were published from 2003 to 2017 and reported surveys conducted from 2004 to 2015. Eight studies were from Northern, five from Central, four from Eastern, three from Southern, Fig. 1  The review process and three from Western Africa. Two studies included data from different countries. Nineteen studies prospectively collected data and the others, retrospectively.
We also hope that all these efforts will bring to define local and adapted guidelines for the diagnosis and management of PH in Africa, taking into account the specific patterns of the disease across the continent. This review had some limitations. First, although we searched several databases, this review is based on a limited number of original studies published in specific populations. Second, the limited number of studies included in the review did not permit us to perform meaningful subgroup analyses to determine sources of heterogeneity. Third, not all African sub-regions were represented in all the specific populations, making the results of this study particular in terms of generalizability to the entire continent. Nonetheless, this is the first comprehensive review on the prevalence, incidence and etiologies of PH in Africa; it gives a clear overview of the burden of PH in Africa and crucial gaps to fill in future research.
Acknowledgements None. 4  Department of Public Health, Faculty of Medicine and Biomedical Sciences, University of Yaoundé 1, Yaoundé, Cameroon. 5Sickle  Cell Disease Unit, Mother and Child Centre of the Chantal Biya Foundation, Yaoundé, Cameroon. 6Department of  Disease, Epidemics and Pandemics Control, Ministry of Public Health, Yaoundé, Cameroon. 7Clinical  Research Education, Networking and Consultancy (CRENC) ,  Douala, Cameroon. 8School of  Public Health, Faculty of Medicine & Biomedical Sciences, University of Queensland, Brisbane, Australia. Received: 1 June 2017 Accepted: 30 November 2017.
ACKNOWLEDGEMENTS Se convocaron sesiones de formación y luego los participantes completaron por su cuenta el curso. Doscientos veinte profesionales de atención primaria participantes completaron los cuestionarios antes y después de la capacitación. Se observó un progreso promedio de los conocimientos de 8% (intervalo de confianza del 95% 7,0-8,8; P < 0,001). Se demostró que el curso representa una opción aceptable y versátil de formación descentralizada sobre la TB en la niñez, siempre y cuando se puedan cumplir los requisitos tecnológicos.
In the hadronic scenarios pion decays and hadronic synchrotron emission are the processes responsible for the high-energy emission if protons are accelerated to sufficiently high energies  [6]. Blazars are classified as FSRQ or BL Lac (Flat Spectrum Radio Quasars) based on the strength of the emission lines where the latest are characterized by featureless emission lines. Based on the peak of the SED, 1ES 1215+303 is classified as an intermediate (IBL) or high frequency peaked BL Lac (HBL)  [7]   [8]. In this contribution, we present the long-term lightcurve derived using almost nine years of data accumulated by the Fermi-LAT satellite. This study resulted also in the detection of new flaring activities occurring on the time interval from 2015 and 2017. This proceeding is organized as follows: Section 2 describes the Fermi-LAT detector and observations.
Fermi-LAT The Fermi Gamma Ray Space Telescope mission was launched on 2008 June 11, with two instruments on board; the Large Area Telescope (LAT) and the GLAST Burst Monitor (GBM). The Fermi-LAT satellite is studying the high-energy (HE; E > O(MeV )) sky by converting γrays into electron/positron pairs in one of the thin tungsten foils of the detector  [9]. The LAT instrument covers the energy range from ∼ 20 MeV up to few hundreds of GeV and celebrated its 9 th successful operational year in June 2017. The data accumulated by Fermi-LAT is publicly available, released in the form of event (PH) and spacecraft (SC) files containing the lifetime information and spacecraft pointing positions.
Data Analysis For this study we used almost nine years of data taken on survey mode on 1ES 1215+303 since the start of Fermi-LAT. The data analysis is conducted with the likelihood framework provided in the Fermi ScienceTools software package, version v10r0p5. We selected events with energies 100 MeV < E < 500 GeV from a 15 • region of interest (RoI) centered on the position of 1ES 1215+303 (R. A. = 12 h 17 m 52 s , decl. = +30 • 07 00 , J2000). In this analysis, the background model includes the all known γ-ray sources from the third Fermi-LAT catalog (3FGL) within the RoI and the sources located up to 5 • outside the RoI edges. The galactic and isotropic diffuse emissions were modeled with gll_iem_v06 and iso_P8R2_SOURCE_V6_v06 respectively from the Fermi ScienceTools and a set of instrument response functions P8R2_SOURCE_V6 1  were used.