cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.7916441
title: Supplementary Material for: Silencing MicroRNA-155 Attenuates Kainic Acid-Induced Seizure by Inhibiting Microglia Activation

description: <b><i>Objective(s):</i></b> Neuroinflammation is an important contributor to the development of seizures and epilepsy. Micro-RNA-155 (miR-155) plays a critical role in immunity and ­inflammation. This study aims to explore the function of miR-155 and miR-155-mediated inflammation in epilepsy. <b><i>Methods:</i></b> About 8-week-old male C57BL/6 mice were administered an intraperitoneal injection (i.p.) of kainic acid (KA) (15 mg/kg) or saline. The mice in the KA group developing acute seizure were further subjected to intracerebroventricular injection (i.c.v.) of antagomir negative control (NC) or miR-155 antagomir. Animal behavior was observed according to Racine’s scale, and electroencephalographs were recorded. Primary microglia were cultured and treated with antagomir NC or antagomir. Whole-cell electrophysiological recording was conducted to detect the spontaneous EPSCs and IPSCs in the neurons treated with different conditioned medium from those microglia. miR-155 were detected by qRT-PCR in those models, as well as in the brain or blood from epileptic patients and healthy controls. <b><i>Results:</i></b> miR-155 was abundantly expressed in glial cells compared with neurons, and its expression was markedly elevated in the brain of epilepsy patients and KA-induced seizure mice. Silencing miR-155 attenuated KA-induced seizure, abnormal electroencephalography, proinflammatory cytokine expression, and microglia morphology change. Moreover, conditioned media from KA-treated microglia impaired neuron excitability, whereas conditioned media from KA and miR-155 antagomir co-treated microglia had no such effects. Finally, miR-155 levels were significantly higher in the blood of epilepsy patients than those of healthy controls. <b><i>Conclusion(s):</i></b> These findings demonstrate that aberrant upregulation of miR-155 contributes to epileptogenesis through inducing microglia neuroinflammation.
DOI: 10.6084/m9.figshare.7916402
title: Supplementary Material for: <b><i>Anopheles stephensi</i></b> Dual Oxidase Silencing Activates the Thioester-Containing Protein 1 Pathway to Suppress <b><i>Plasmodium</i></b> Development

description: We characterized the dual oxidase (Duox) gene in the major Indian malaria vector <i>Anopheles stephensi</i>, which regulates the generation of reactive oxygen species. The AsDuox gene encodes for a 1,475-amino-acid transmembrane protein that contains an N-terminal noncytoplasmic heme peroxidase domain, a calcium-binding domain, seven transmembrane domains, and a C-terminal cytoplasmic NADPH domain. Phylogenetic analyses revealed that <i>A. stephensi</i> Duox protein is highly conserved and shares 97–100% amino acid identity with other anopheline Duoxes. AsDuox is expressed in all the developmental stages of <i>A. stephensi</i> and the pupal stages revealed relatively higher expressions. The Duox gene is induced in <i>Plasmodium</i>-infected mosquito midguts, and RNA interference-mediated silencing of this gene suppressed parasite development through activation of the thioester-containing protein 1 pathway. We propose that this highly conserved anopheline Duox, being a <i>Plasmodium</i> agonist, is an excellent target to control malaria parasite development inside the insect host.
DOI: 10.6084/m9.figshare.7916405
title: gVCF_HG03717

description: 1000 Genomes gVCF mapped to hs37d5 for HG03717. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916399
title: gVCF_NA19085

description: 1000 Genomes gVCF mapped to hs37d5 for NA19085. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916417.v1
title: Supplementary Material for: Disseminated Mycosis by <b><i>Arthrocladium</i></b> <b><i>fulminans</i></b> Jeopardizing a Patient with GATA2 Deficiency

description: GATA2 deficiency is characterized by monocytopenia, deficiency of dendritic cells, and a variable degree of lymphocytopenia affecting B cells and NK cells, leading to an enhanced risk of mycobacterial, viral, and fungal infections. Here we present a patient with a heterozygous intronic GATA2 mutation who acquired a fatal disseminated mycosis due to the black yeast-like fungus <i>Arthrocladium fulminans</i> following an infection with <i>Mycobacterium sherrisii</i>. This case illustrates that in patients with severe uncommon infections, immunodeficiency syndromes must be ruled out.
DOI: 10.6084/m9.figshare.7916381
title: Supplementary Material for: Tollip Inhibits ST2 Signaling in Airway Epithelial Cells Exposed to Type 2 Cytokines and Rhinovirus

description: The negative immune regulator Tollip inhibits the proinflammatory response to rhinovirus (RV) infection, a contributor to airway neutrophilic inflammation and asthma exacerbations, but the underlying molecular mechanisms are poorly understood. Tollip may inhibit IRAK1, a signaling molecule downstream of ST2, the receptor of IL-33. This study was carried out to determine whether Tollip downregulates ST2 signaling via inhibition of IRAK1, but promotes soluble ST2 (sST2) production, thereby limiting excessive IL-8 production in human airway epithelial cells during RV infection in a type 2 cytokine milieu (e.g., IL-13 and IL-33 stimulation). Tollip- and IRAK1-deficient primary human tracheobronchial epithelial (HTBE) cells and Tollip knockout (KO) HTBE cells were generated using the shRNA knockdown and CRISPR/Cas9 approaches, respectively. Cells were stimulated with IL-13, IL-33, and/or RV16. sST2, activated IRAK1, and IL-8 were measured. A Tollip KO mouse model was utilized to test if Tollip regulates the airway inflammatory response to RV infection in vivo under IL-13 and IL-33 treatment. Following IL-13, IL-33, and RV treatment, Tollip-deficient (vs. -sufficient) HTBE cells produced excessive IL-8, accompanied by decreased sST2 production but increased IRAK1 activation. IL-8 production following IL-13/IL-33/RV exposure was markedly attenuated in IRAK1-deficient HTBE cells, as well as in Tollip KO HTBE cells treated with an IRAK1 inhibitor or a recombinant sST2 protein. Tollip KO (vs. wild-type) mice developed exaggerated airway neutrophilic responses to RV in the context of IL-13 and IL-33 treatment. Collectively, these data demonstrate that Tollip restricts excessive IL-8 production in type 2 cytokine-exposed human airways during RV infection by promoting sST2 production and inhibiting IRAK1 activation. sST2 and IRAK1 may be therapeutic targets for attenuating excessive neutrophilic airway inflammation in asthma, especially during RV infection.
DOI: 10.6084/m9.figshare.7916390
title: Database of primers of genes in Escherichia coli K-12 without recognition sequence of NdeI and BamHI

description: Polymerase chain reaction (PCR) remains a critical tool for molecular biologists whether in amplifying small quantities of DNA from the environment or single cell, or in cloning of genes from one species into another. The process requires short stretches of nucleotides known as primers to help identify the region of the template DNA for polymerase amplification. Primers designed for amplification of target genes from environmental DNA differs from those designed for molecular cloning. In the case of molecular cloning, key characteristics of the primer include (i) the need for both forward and reverse primers for targeting a specific stretch of template DNA for amplification, (ii) the primers must also be able to form complementary base pairing with a short stretch of template DNA (18 to 25 nucleotide) with melting temperature of about 55 <sup>o</sup>C, (iii) recognition sequence for specific restriction enzymes selected for molecular cloning should also be appended to the start of the primer sequence, and (iv) a flanking sequence is also needed to be appended upstream of the restriction enzyme recognition sequence to help hinge the polymerase to the DNA-primer construct. Using an in-house MATLAB software, a primer database was created for all genes in <i>Escherichia coli</i> K-12 strain MG1655 (Genbank accession number, NC_000913.3) not having recognition sequence of restriction enzymes, NdeI and BamHI, which otherwise would result in the digestion of the gene by the restriction enzyme used and the failure of the cloning effort. Primers designed by the MATLAB algorithm fulfilled the requirements described above for primers to be used in molecular cloning. For each gene in the genome of <i>E. coli</i> K-12 MG1655 without recognition sequence of NdeI and BamHI, one forward and reverse primer was designed for cloning the gene using the restriction enzyme set, NdeI and BamHI. Collectively, a primer database was created for all genes in <i>E. coli</i> K-12 strain MG1655 not having recognition sequence of NdeI and BamHI. Primers designed could be used for cloning the respective genes using NdeI and BamHI as recognition sequences for the two restriction enzymes have been appended to the primer sequence. Overall, the primer database should find use as a reference for researchers in molecular cloning and plasmid construction applications involving <i>E. coli </i>K-12 MG1655.<br>
DOI: 10.6084/m9.figshare.7916378
title: rda.xlsx

description: Moment of abortion of unilateral and bilateral twins<br>
DOI: 10.6084/m9.figshare.7916399.v1
title: gVCF_NA19085

description: 1000 Genomes gVCF mapped to hs37d5 for NA19085. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916372
title: gVCF_HG02025

description: 1000 Genomes gVCF mapped to hs37d5 for HG02025. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916378.v1
title: rda.xlsx

description: Moment of abortion of unilateral and bilateral twins<br>
DOI: 10.6084/m9.figshare.7916360
title: FarmCPU.T3.M.GWAS.Results

description: FarmCPU.GWAS.T3 Results
DOI: 10.6084/m9.figshare.7916366
title: FarmCPU.T4.M.GWAS.Results

description: FarmCPU.GWAS. T4 Results
DOI: 10.6084/m9.figshare.7916354
title: gVCF_HG03716

description: 1000 Genomes gVCF mapped to hs37d5 for HG03716. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916372.v1
title: gVCF_HG02025

description: 1000 Genomes gVCF mapped to hs37d5 for HG02025. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916366.v1
title: FarmCPU.T4.M.GWAS.Results

description: FarmCPU.GWAS. T4 Results
DOI: 10.6084/m9.figshare.7916330
title: Ins result

description: FarmCPU INS result
DOI: 10.6084/m9.figshare.7916333
title: gVCF_NA19084

description: 1000 Genomes gVCF mapped to hs37d5 for NA19084. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916354.v1
title: gVCF_HG03716

description: 1000 Genomes gVCF mapped to hs37d5 for HG03716. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916324
title: Supplementary Material for: Switching from Secukinumab to Ustekinumab in Psoriasis Patients: Results from a Multicenter Experience

description: <b><i>Background:</i></b> Switching between biologics is commonly performed for the management of plaque psoriasis. However, no evidence about switching from secukinumab to ustekinumab has been reported. <b><i>Methods:</i></b> This retrospective observational multicenter study aimed to describe efficacy and safety of ustekinumab in secukinumab nonresponder patients. <b><i>Results:</i></b> A total of 21 patients unresponsive to secukinumab were treated with ustekinumab for a mean period of 53.3 weeks. Ustekinumab was effective in reducing disease severity, with significant improvements of both psoriasis area severity index (PASI) and dermatology quality of life index (DLQI) scores. PASI score improvements of 31.8, 44, 77.8, 80.3, 80.5, and 89.6%, at week 4, 12, 24, 36, 48, and above 60 weeks, respectively, were detected (<i>p</i> &lt; 0.05), achieving PASI 50, 75, and &gt; 90 responses in 93.8, 87.5, and 50% of patients at week 48. Four patients withdrew from ustekinumab treatment because of inefficacy, and failure of multiple biologic agents (&gt; 2) seemed to affect ustekinumab drug survival. No serious adverse events (AEs) were reported while 38.1% of patients experienced mild AEs. <b><i>Conclusion:</i></b> Ustekinumab was safe and effective in treating patients unresponsive to secukinumab.
DOI: 10.6084/m9.figshare.7916327
title: FarmCPU CV

description: FarmCPU CV
DOI: 10.6084/m9.figshare.7916330.v1
title: Ins result

description: FarmCPU INS result
DOI: 10.6084/m9.figshare.7916321
title: 2018.07 FarmCPU SNP

description: FarmCPU SNP
DOI: 10.6084/m9.figshare.7916324.v1
title: Supplementary Material for: Switching from Secukinumab to Ustekinumab in Psoriasis Patients: Results from a Multicenter Experience

description: <b><i>Background:</i></b> Switching between biologics is commonly performed for the management of plaque psoriasis. However, no evidence about switching from secukinumab to ustekinumab has been reported. <b><i>Methods:</i></b> This retrospective observational multicenter study aimed to describe efficacy and safety of ustekinumab in secukinumab nonresponder patients. <b><i>Results:</i></b> A total of 21 patients unresponsive to secukinumab were treated with ustekinumab for a mean period of 53.3 weeks. Ustekinumab was effective in reducing disease severity, with significant improvements of both psoriasis area severity index (PASI) and dermatology quality of life index (DLQI) scores. PASI score improvements of 31.8, 44, 77.8, 80.3, 80.5, and 89.6%, at week 4, 12, 24, 36, 48, and above 60 weeks, respectively, were detected (<i>p</i> &lt; 0.05), achieving PASI 50, 75, and &gt; 90 responses in 93.8, 87.5, and 50% of patients at week 48. Four patients withdrew from ustekinumab treatment because of inefficacy, and failure of multiple biologic agents (&gt; 2) seemed to affect ustekinumab drug survival. No serious adverse events (AEs) were reported while 38.1% of patients experienced mild AEs. <b><i>Conclusion:</i></b> Ustekinumab was safe and effective in treating patients unresponsive to secukinumab.
DOI: 10.6084/m9.figshare.7916312
title: Supplementary Material for: IL-33/ST2 Axis Regulates Vasculogenic Mimicry via ERK1/2-MMP-2/9 Pathway in Melanoma

description: <b><i>Background:</i></b> Melanoma, an extremely malignant form of cancer, poses a significant health risk. Vasculogenic mimicry (VM), blood vessels formed by tumor cells instead of endothelial cells, is an important factor for the rapid progression of melanoma. Interleukin (IL)-33 is an inflammatory factor commonly found in the tumor microenvironment and plays an important role in the progression of many tumors. IL-33 acts on immune cells and tumor cells through its receptor ST2. This study hypothesized that IL-33 directly affects the progression of melanoma. <b><i>Objectives:</i></b> This study was designed to investigate the effect of IL-33 on VM of melanoma and its potential mechanism of action. <b><i>Methods:</i></b> The expression of ST2 was evaluated in 66 cases of melanoma collected from human patients, and the differences were analyzed. In vitro experiments were conducted to study the effects of the IL-33/ST2 axis on cell migration and invasion and to elucidate possible mechanisms. <b><i>Results:</i></b> ST2 expression is associated with that of matrix metalloproteinase (MMP)-2 and VM in melanoma of patients. IL-33 increases the abilities of proliferation, migration and invasion of melanoma cells and VM tube formation through ST2. IL-33 induces the production of MMP-2/9 via ERK1/2 phosphorylation. <b><i>Conclusion:</i></b> IL-33 can directly act on melanoma cells and promote its development.
DOI: 10.6084/m9.figshare.7916333.v1
title: gVCF_NA19084

description: 1000 Genomes gVCF mapped to hs37d5 for NA19084. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916306
title: Hormonal phenotypic data

description: phenotypic data
DOI: 10.6084/m9.figshare.7916315
title: 2018.07 FarmCPU MAP

description: FarmCPU MAP
DOI: 10.6084/m9.figshare.7916306.v2
title: Hormonal phenotypic data

description: phenotypic data
DOI: 10.6084/m9.figshare.7916315.v1
title: 2018.07 FarmCPU MAP

description: FarmCPU MAP
DOI: 10.6084/m9.figshare.7916297
title: gVCF_HG03715

description: 1000 Genomes gVCF mapped to hs37d5 for HG03715. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916300
title: gVCF_HG02024

description: 1000 Genomes gVCF mapped to hs37d5 for HG02024. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916294
title: gVCF_HG03714

description: 1000 Genomes gVCF mapped to hs37d5 for HG03714. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916300.v1
title: gVCF_HG02024

description: 1000 Genomes gVCF mapped to hs37d5 for HG02024. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916306.v1
title: Genome-Wide Association studies for the concentrations of Insulin, Triiodothyronine and Thyroxine in Chinese Holstein cattle

description: phenotypic data
DOI: 10.6084/m9.figshare.7916285
title: A 3D grain-based model for simulating the micro-mechanical behavior of salt rock

description: This data set includes the main original data generated by the 3D-GBM and source code of three-dimensional Particle Flow Code (PFC3D) for verifying the authenticity of the model. The code should be run at the PFC3D with the version of 5.00.39.
DOI: 10.6084/m9.figshare.7916267
title: gVCF_NA19083

description: 1000 Genomes gVCF mapped to hs37d5 for NA19083. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916264
title: gVCF_HG02023

description: 1000 Genomes gVCF mapped to hs37d5 for HG02023. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916267.v1
title: gVCF_NA19083

description: 1000 Genomes gVCF mapped to hs37d5 for NA19083. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916252
title: gVCF_NA19082

description: 1000 Genomes gVCF mapped to hs37d5 for NA19082. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916255
title: gVCF_HG03713

description: 1000 Genomes gVCF mapped to hs37d5 for HG03713. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916264.v1
title: gVCF_HG02023

description: 1000 Genomes gVCF mapped to hs37d5 for HG02023. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916192
title: gVCF_HG02020

description: 1000 Genomes gVCF mapped to hs37d5 for HG02020. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916255.v1
title: gVCF_HG03713

description: 1000 Genomes gVCF mapped to hs37d5 for HG03713. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916174
title: gVCF_NA19081

description: 1000 Genomes gVCF mapped to hs37d5 for NA19081. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916177
title: gVCF_HG03711

description: 1000 Genomes gVCF mapped to hs37d5 for HG03711. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916192.v1
title: gVCF_HG02020

description: 1000 Genomes gVCF mapped to hs37d5 for HG02020. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916252.v1
title: gVCF_NA19082

description: 1000 Genomes gVCF mapped to hs37d5 for NA19082. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916174.v1
title: gVCF_NA19081

description: 1000 Genomes gVCF mapped to hs37d5 for NA19081. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916129
title: gVCF_HG03709

description: 1000 Genomes gVCF mapped to hs37d5 for HG03709. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916144
title: End-to-end deep image reconstruction from human brain activity

description: Shen, Dwivedi, Majima, Horikawa, and Kamitani (2019) End-to-end deep image reconstruction from human brain activity. Front. Comput. Neurosci. (bioRxiv preprint). <br><br>Here we provide pre-trained deep artificial neural networks (DNN) for reconstructing images from human brain activity. The pre-trained DNNs are composed of generator networks and discriminator networks. The generator networks were trained to reconstruct the stimulus images from human brain fMRI activity. The discriminator networks were trained to distinguish between the reconstructed images and the original stimulus images. The pre-trained DNNs of 3 human subjects are shared here:<br><br>- trainedmodel_sub-01.zip<br>- trainedmodel_sub-02.zip<br>- trainedmodel_sub-03.zip<br><br>These pre-trained DNNs were trained for 500,000 mini-batch iterations, with batch size of 64. In each of the zip files, there are 4 files:<br><br>- generator.caffemodel: the Caffe caffemodel file for the trained generator<br>- generator_test.prototxt: the Caffe prototxt file for the generator<br>- discriminator.caffemodel: the Caffe caffemodel file for the trained discriminator<br>- discriminator.prototxt: the Caffe prototxt file for the discriminator<br><br>Demo code: GitHub<br>
DOI: 10.6084/m9.figshare.7916150
title: gVCF_HG02019

description: 1000 Genomes gVCF mapped to hs37d5 for HG02019. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916129.v1
title: gVCF_HG03709

description: 1000 Genomes gVCF mapped to hs37d5 for HG03709. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916150.v1
title: gVCF_HG02019

description: 1000 Genomes gVCF mapped to hs37d5 for HG02019. Complete collection: https://doi.org/10.6084/m9.figshare.c.4414307
DOI: 10.6084/m9.figshare.7916144.v1
title: End-to-end deep image reconstruction from human brain activity

description: Shen, Dwivedi, Majima, Horikawa, and Kamitani (2019) End-to-end deep image reconstruction from human brain activity. Front. Comput. Neurosci. (bioRxiv preprint). <br><br>Here we provide pre-trained deep artificial neural networks (DNN) for reconstructing images from human brain activity. The shared pre-trained DNNs are the generator networks, which were trained to reconstruct the stimulus images from human brain fMRI activity. The pre-trained DNNs of 3 human subjects are shared here:<br><br>- trainedmodel_sub-01.zip<br>- trainedmodel_sub-02.zip<br>- trainedmodel_sub-03.zip<br><br>These pre-trained DNNs were trained for 500,000 mini-batch iterations, with batch size of 64. In each of the zip files, there are 2 files:<br><br>- generator.caffemodel: the Caffe caffemodel file for the trained generator<br>- generator_test.prototxt: the Caffe prototxt file for the generator<br><br>Demo code: GitHub
DOI: 10.6084/m9.figshare.7916108
title: MOESM5 of Ribosomal/nucleolar stress induction regulates tert-Butyl hydroperoxide (tBHP) mediated oxidative stress in Anopheles gambiae midguts

description: Additional file 5. Proteomic data on differential expression between control and high treatment groups.
DOI: 10.6084/m9.figshare.7916114
title: MOESM6 of Ribosomal/nucleolar stress induction regulates tert-Butyl hydroperoxide (tBHP) mediated oxidative stress in Anopheles gambiae midguts

description: Additional file 6. Proteomic data on differential expression between low and high treatment groups.
DOI: 10.6084/m9.figshare.7916108.v1
title: MOESM5 of Ribosomal/nucleolar stress induction regulates tert-Butyl hydroperoxide (tBHP) mediated oxidative stress in Anopheles gambiae midguts

description: Additional file 5. Proteomic data on differential expression between control and high treatment groups.