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Original images associated with MOLECULAR-CELL-D-16-01448R2.

Additional file 3: Supplementary Table 2. List of the primers used for pyrosequencing and amplicon sequencing (Illumina MiSeq system).

An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures. Related Article: G.Schatte, S.Labiuk, B.Li, P.-G.Burnett, M.Reaney, P.Grochulski, M.Fodje, J.Yang, R.Sammynaiken|2012|Acta Crystallogr.,Sect.E:Struct.Rep.Online|68|o50|doi:10.1107/S1600536811051488

Regionally DE genes list. (XLSX 282Â kb)

Additional file 3: Table S2. Annotation of the M. Tuberculosis genes and clusters. M. tuberculosis genes are represented by gene symbols and the protein RefSeq ID and COG category eggNOG.

Efficiency of D-B primers in detecting SARS-COV-2 virus in nasopharyngeal swabs. cDNA of reverse-transcribed RNA extracted from nasopharyngeal swabs of patient S1 underwent 3 decimal dilutions and subjected to qPCR with SYBR green kit+ UDG and D-B primer mix #8. (A) amplification plot and insert efficiency plot of Ct vs log dilution. Slope= -3.2942 representing 101.27% amplification efficiency and R2= 0.9934. (B) melt curve of the amplicons depicted in panel A. Ct dilution values: 100- 25.55, 10-1- 28.38, 10-2- 32.14, NTC- 39.48. qPCR was performed under standard conditions.

Provincial and territorial policy documents and indicator scores; table contains all CHARPP indicator scores from 13 provincial and territorial harm reduction policy report cards. (XLSX 57Â kb)

Library construction chemistry comparison using tumor samples. Two NEB workflows were evaluated. The first has bead clean up after each of the library construction steps (A); the second has the bead cleanup after A-tail removed (B). Input gDNA was from three different clinical samples (Source 1â 3). (JPEG 27Â kb)

Amodiaquine (AQ) is associated with a relatively high incidence of idiosyncratic drug-induced liver injury (IDILI) and agranulocytosis. A previous study reported that a combination of high dose AQ and glutathione (GSH) depletion led to liver injury. However, the characteristics of this toxicity were very different from AQ-induced liver injury in humans. We developed a model of AQ-induced liver injury with characteristics similar to the injury in humans by treating mice with lower doses of AQ for several weeks. In this study we found that not only did GSH depletion not increase AQ covalent binding to hepatic proteins at this lower dose, but also it paradoxically prevented the liver injury. We extended the model to rats and found AQ treatment led to a mild delayed onset liver injury that resolved despite continued treatment with AQ. Immunohistochemistry indicated the presence of Kupffer cell activation, apoptosis and hepatocyte proliferation in the liver. There was also an increase in serum IL-2, IL-5, IL-9, IL-12, MCP-1 and TGFβ, but a decrease in leptin. Coincident with the elevated serum ALT, the number of liver CD4+ T-cells, IL-17 secreting cells and TH17/Treg cells increased at Week 3 and decreased during continued treatment. Increases in NK1.1+ cells and activated M2 macrophages were also observed during liver injury. These results suggest that the outcome of the liver injury was determined by the balance between effector and regulatory cells. Co-treatment with cyclosporin prevented AQ-induced liver injury, which supports an immune mechanism. Retinoic acid (RA), which has been reported to enhance natural killer (NK) cell activity, exacerbated AQ-induced liver injury. These results suggest that AQ-induced IDILI is immune mediated and the subsequent adaptation appears to represent immune tolerance.

Supplementary tables for "A comprehensive, flexible collection of SARS-CoV-2 coding regions"