2970 results for "愛の戦士完全破壊2-re-imagination-version-鞭首絞め・電撃・ヘソか"

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• RNA-seq of CML074 Tumor tissue; Timpepoint 1

  Dataset EGAD00001001259

• MT alignment

  Alignement including 83 MT AA sequences and 2 reference sequences, rCRS and RSRS

  Dataset EGAD00010001574

• Patient WGS for #198

  Whole genome sequencing of patient tumour and blood

  Dataset EGAD50000000217

• Broad Utility of Ultrasensitive Analysis of ctDNA Dynamics Across Solid Tumors Treated with Immunotherapy

  https://vhio.net/privacy-policy-2/

  Dac EGAC50000000723

• SF7003

  Oligodendroglioma (WHO gr. 2)

  Dataset EGAD00001008297

• BiSeqS

  Runs that contain data for the sensitivity and specificity experiments for BiSeqS.

  Dataset EGAD00001003323

• HCA Organoids | Colon - Cancer, Nanopore Sequencing Data

  Nanopore Sequencing Data

  Dataset EGAD00001015536

• Multimodal Immune Profiling to Determine Mechanisms of COVID-19 Clinical Trajectory in Uganda

  We conducted a prospective cohort study of adults (RESERVE-U-C19) admitted to Entebbe Regional Referral Hospital (ERRH), a national COVID-19 referral center, across three viral variant-driven phases of the pandemic in Uganda. In this cohort, which reflects the entire spectrum of SARS-CoV-2 infection, we integrated clinical data with serum proteomics (N=306) and whole-blood transcriptomics (N=100) to determine a range of host responses associated with COVID-19 severity, SARS-CoV-2/HIV co-infection, and circulating viral variants. Beyond the prognostic importance of myeloid cell-driven immune activation and lymphopenia, we show that multifaceted impairment of host protein synthesis and extensive redox imbalance define core metabolic signatures of severe COVID-19, with central roles for IL-7, IL-15, and lymphotoxin-α in COVID-19 respiratory failure. While prognostic signatures were generally consistent in SARS-CoV-2/HIV-coinfection, type I interferon responses uniquely scaled with COVID-19 severity in persons living with HIV. Throughout the pandemic, COVID-19 severity peaked during phases dominated by A.23/A.23.1 and Delta B.1.617.2/AY variants, with Delta phase COVID-19 distinguished by exaggerated pro-inflammatory myeloid cell and inflammasome activation, NK and CD8+ T-cell depletion, impaired host protein synthesis, and upregulation of viral cell entry and trafficking pathways. Data from this study available through dbGaP include raw RNA-Seq data from whole-blood of adult participants (N=100).

  Study phs003246

• Field studies of Cryptosporidiosis and Enteropathogens in Bangladesh

  Cryptosporidiosis causes severe diarrhea in infants in the developing world. There is no vaccine to prevent it, and little in the way of treatment. This study on Bangladeshi urban slum children aims to support the design of a vaccine, both by determining how the immune system protects from infection and by identifying the genotypes of the parasite that should be included in a vaccine, as well as aid in development of therapies by identifying human genes that control infection. The primary objective of the study was to determine the incidence and contribution to disease of the different species and genotypes of cryptosporidia. Secondary objectives were designed to determine acquired immune response to cryptosporidiosis and identify human genes that influence susceptibility to cryptosporidiosis. This is an observational study. Children were recruited from Mirpur Dhaka slum (Cohort 1) and rural Mirzapur (Cohort 2) and followed for cryptosporidium infection longitudinally from birth through age 4 years in Cohort 1 and birth through age 2 years in Cohort 2. Biweekly household visits for diarrheal surveillance were made in addition to anthropometric measurements of mother and child, blood samples collected two times each year from the child, a work-up of diarrheal stools and non-diarrheal surveillance stools for cryptosporidium and other enteropathogens, and blood and breast milk samples from the mother. A detailed description of the study design and procedures can be obtained from publication: Kevin L Steiner, et al., 2018, PMID: 29897482.

  Study phs001665

• DNA polymerase and mismatch repair deficient cancers exert distinct genome-wide microsatellite signatures 2

  Study EGAS00001004816