Each layer of sewer sediments from combined and storm sewers
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA542070 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9039970_1.fastq.gz | Fastqsanger.gz | |||
| SRR9039970_2.fastq.gz | Fastqsanger.gz | |||
| SRR9039980_1.fastq.gz | Fastqsanger.gz | |||
| SRR9039980_2.fastq.gz | Fastqsanger.gz | |||
| SRR9039990_1.fastq.gz | Fastqsanger.gz |
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Project description:Here we introduce STORM-seq, a standardized and generally available approach to profiling total RNA in single cells by miniaturization of the Takara SMART-seq Stranded (SSS) kit. The use of nanoliter-scale reaction volumes allows STORM-seq to efficiently scale to hundreds of high-complexity single cell libraries per run, from dissociated tissues and non-adherent cells, with greater than 99% per cell/library success. The use of ribosomal RNA depletion and random hexamer priming, rather than oligo-dT (poly-A) selection, allows comprehensive, whole-transcriptome analysis in each individual cell. STORM-seq recovers both coding and non-coding transcripts at an equal or greater rate to full volume reactions. Applying the method to cultured K562 cells and primary human fallopian tube epithelial (FTE) cells results in equivalent or better gene detection than manual preparation. Across all transcript biotypes, additional mRNA and lncRNA transcripts are detected beyond SSS or SMART-seq2. STORM-seq libraries from primary human FTE reveal intermediate cell types not observed by other technologies, with clear transitional significance visible upon data integration. STORM-seq provides a scalable, efficient protocol to recover deep whole transcriptomes from individual cells while minimizing costs.
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Project description:An H5N1 virus-encoded microRNA directly targets mammalian poly(rC) binding protein 2 and is a major contributor to H5N1-associated ‘cytokine storm’ and mortality.
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Project description:Human survival from injury requires an appropriate inflammatory and immune response. We describe the circulating leukocyte transcriptome after severe trauma and show that the severe stress produce a global reprioritization affecting >80% of the cellular functions and pathways, a truly unexpected “genomic storm.” In severe blunt trauma, the early leukocyte genomic response is consistent with simultaneously increased expression of genes involved in the systemic inflammatory, innate immune, and compensatory antiinflammatory responses, as well as in the suppression of genes involved in adaptive immunity. Furthermore, complications like nosocomial infections and organ failure are not associated with any genomic evidence of a second hit and differ only in the magnitude and duration of this genomic reprioritization. Blood was sampled from 167 severe blunt trauma patients under the age of 55 yr who consented to blood sampling. The first blood sample was taken within 12 h of the injury and 1, 4, 7, 14, 21, and 28 d after injury. Study subjects were treated under the guidance of standard operating procedures developed, implemented, and audited across all participating centers to minimize treatment variation. In addition, 37 healthy control subjects were sampled. Total blood leukocytes were isolated according to protocols published previously. Total cellular RNA was extracted and hybridized onto an HU133 Plus 2.0 GeneChip (Affymetrix) according to the manufacturer’s recommendations.
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Project description:Human survival from injury requires an appropriate inflammatory and immune response. We describe the circulating leukocyte transcriptome after severe trauma and show that the severe stress produce a global reprioritization affecting >80% of the cellular functions and pathways, a truly unexpected “genomic storm.” In severe blunt trauma, the early leukocyte genomic response is consistent with simultaneously increased expression of genes involved in the systemic inflammatory, innate immune, and compensatory antiinflammatory responses, as well as in the suppression of genes involved in adaptive immunity. Furthermore, complications like nosocomial infections and organ failure are not associated with any genomic evidence of a second hit and differ only in the magnitude and duration of this genomic reprioritization.
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