Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32839920_1.fastq.gz | Fastqsanger.gz | |||
| SRR32839920_2.fastq.gz | Fastqsanger.gz | |||
| SRR32839921_1.fastq.gz | Fastqsanger.gz | |||
| SRR32839921_2.fastq.gz | Fastqsanger.gz | |||
| SRR32839922_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:The primary goal of this project is to monitor host global gene expression patterns in response to viral infection in the shrimp, Litopenaeus stylirostris.
2012-08-09 | GSE39887 | GEO
Project description:The presence of Donor-Specific anti-HLA Antibodies (DSA) is associated with an increased risk of both acute and chronic antibody-mediated rejection (AMR) in kidney allografts. AMR has remained challenging in kidney transplantation and is the major cause of late allograft loss. However, not all patients with DSA develop AMR, leading to the question of whether this represents accommodation, if other protective mechanisms exist or if this is actually a state of pre-rejection. Clinical and histological features, and gene expression profiles of kidney biopsy and blood samples of donor-specific antibody (DSA)+ patients without rejection were compared to antibody-mediated rejection (AMR) patients to elucidate the mechanisms involved in prevention of AMR. Of the 71 DSA+ patients, 46 had diagnosis of AMR and 25 did not show rejection. 50 DSA- patients without rejection were used as control. A subgroup of patients with available biopsy (n=61) and blood samples (n=54) were analyzed by microarrays. Both, DSA+/AMR+ and DSA+/AMR- biopsies showed increased expression of gene transcripts associated with cytotoxic T, natural killer cells, macrophages, interferon-gamma and rejection compared to DSA- biopsies. Regulatory T cell transcripts were up-regulated in DSA+/AMR+ and B cell transcripts in DSA+/AMR- biopsies. Whole blood gene expression analysis showed increased immune activity in only DSA+/AMR+ patients. There were no differentially expressed tolerant genes studied (n=14) in the blood or biopsy specimens of DSA+/AMR- patients. During a median 36 months follow-up, 4 DSA+/AMR- patients developed AMR, 12 continued to have DSAs but 9 lost DSAs. Gene expression profiles did not predict the development of AMR or persistence of DSAs. These results indicate increased immune activity in DSA+/AMR- biopsies despite lack of histologic findings of rejection.
2013-08-23 | GSE50084 | GEO
Project description:The presence of Donor-Specific anti-HLA Antibodies (DSA) is associated with an increased risk of both acute and chronic antibody-mediated rejection (AMR) in kidney allografts. AMR has remained challenging in kidney transplantation and is the major cause of late allograft loss. However, not all patients with DSA develop AMR, leading to the question of whether this represents accommodation, if other protective mechanisms exist or if this is actually a state of pre-rejection. Clinical and histological features, and gene expression profiles of kidney biopsy and blood samples of donor-specific antibody (DSA)+ patients without rejection were compared to antibody-mediated rejection (AMR) patients to elucidate the mechanisms involved in prevention of AMR. Of the 71 DSA+ patients, 46 had diagnosis of AMR and 25 did not show rejection. 50 DSA- patients without rejection were used as control. A subgroup of patients with available biopsy (n=61) and blood samples (n=54) were analyzed by microarrays. Both, DSA+/AMR+ and DSA+/AMR- biopsies showed increased expression of gene transcripts associated with cytotoxic T, natural killer cells, macrophages, interferon-gamma and rejection compared to DSA- biopsies. Regulatory T cell transcripts were up-regulated in DSA+/AMR+ and B cell transcripts in DSA+/AMR- biopsies. Whole blood gene expression analysis showed increased immune activity in only DSA+/AMR+ patients. There were no differentially expressed tolerant genes studied (n=14) in the blood or biopsy specimens of DSA+/AMR- patients. During a median 36 months follow-up, 4 DSA+/AMR- patients developed AMR, 12 continued to have DSAs but 9 lost DSAs. Gene expression profiles did not predict the development of AMR or persistence of DSAs. These results indicate increased immune activity in DSA+/AMR- biopsies despite lack of histologic findings of rejection. All clinically indicated kidney transplant biopsies performed at our institution after January 2009 were reviewed and 263 patients with anti-HLA antibody testing at the time of biopsy were identified. There were 71 DSA+ and 192 DSA- patients (Figure 1). Of the 71 DSA+ patients, 46 had biopsy diagnosis of acute AMR (n=9) or chronic AMR (n=37), and 25 had normal histopathology or minimal non-specific interstitial fibrosis/tubular atrophy (IFTA). Of the 192 DSA- patients, 50 patients with normal histology and/or mild non-specific IFTA were used as a control group. Clinical and histopathological findings of these 3 groups (DSA+/AMR+, DSA+/AMR- and DSA-) were analyzed. A subgroup of patients who were enrolled in the Institutional Review Board-approved âImmune Monitoring Studyâ who had clinically indicated biopsy (n=61) and whole blood samples (n=54) stored were used for genomic analysis. Twenty-eight biopsy and blood samples from DSA+/AMR+ patients, 13 biopsy and 14 blood samples from DSA+/AMR- patients, and 20 biopsy and 12 blood samples from DSA- patients, were available for microarray analysis.
2013-08-23 | E-GEOD-50084 | biostudies-arrayexpress
Project description:The primary goal of this project is to monitor host global gene expression patterns in response to viral infection in the shrimp, Litopenaeus stylirostris. Specific Pathogen Free (SPF) L. stylirostris were obtained from High Health Aquaculture (Honolulu, Hawaii) and kept in environmentally controlled tanks. For control, animals were injected with saline (30 ul) between the second and third tergal plates of the lateral side of the tail using a 1 ml tuberculin syringe. Infected individuals were inoculated with homogenate created from IHHNV infected shrimp tissue. After 24 hours, the shrimp were sacrificed and tissue was collected from the ventral and flash frozen in liquid nitrogen and stored in the -80 ºC freezer. Libraries of sequence tags were generated via the Long-SAGE kit (Invitrogen®, Carlsbad, CA) until the ditag PCR preparation step and directly pyrosequenced by 454 Roche.
2012-08-09 | E-GEOD-39887 | biostudies-arrayexpress
Project description:Antimicrobial resistance (AMR) is one of the major challenges that humans are facing this century. Understanding the mechanisms behind the rise of AMR is crucial to tackle this global threat. Among the triggers of phenotypic antimicrobial resistance, the contribution of transition metals has been understudied in Mycobacterium abscessus (Mabs), a fast-growing non-tuberculous mycobacterium known for its extreme AMR levels. Deeper understanding of the effects of transition metal ions will be beneficial for our knowledge in AMR and the discovery of potential therapeutic targets. Here, we investigated the impact of transition metal ions, nickel, cobalt and copper on the physiology and drug susceptibility of Mabs.
2024-09-13 | GSE243031 | GEO
Project description:Shrimp allergy is the second most common food allergy in the United States. γδ T cells play a regulatory role in peanut immunotherapy, but their role in shrimp allergy remains unclear. We hypothesized γδ T cells play a regulatory role in shrimp allergic disease. We performed single cell RNA sequencing on peripheral cells from shrimp allergic (SA) and healthy control (HC) subjects after stimulation with shrimp tropomyosin. We found significant expansion of γδ T cells and three distinct clusters. One γδ T cell cluster predominated in SA, characterized as CD8+ with a cytotoxic expression profile. We found significant upregulation of TGF-β1 and downregulation of IL-7R in SA-stimulated vs. HC-stimulated γδ T cells, and IL-10 secretion in stimulated SA γδ T cells. γδ T cells play an important role in the pathogenesis of shrimp allergy through lymphocyte-mediated cytotoxin signaling and cytokine-mediated signaling pathways, including TGFβ-1, IL7/TSLP-IL7R, and IL10-IL10R pathways.
2024-07-01 | GSE268436 | GEO