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Biology subjects

Abdullah, L.

Publications and source records attributed to Abdullah, L..

3 recordsLinked to original sources

RAD: A Read-structure Agnostic Demultiplexer for Single-Cell Long-Read Sequencing and Analysis

Single-cell long-read sequencing (LRS) techniques enable the analysis of full transcript sequences within a cell. However, the high error rate inherent to LRS introduces computational challenges for parsing information like cell barcode, and custom workflows are often required to handle complex read layouts, such as split combinatorial barcodes. We introduce an error-robust, read-structure agnostic demultiplexer (RAD). In RAD, users can easily specify read structure, such as adapter sequence and barcode relative position, and can rapidly extract these elements for each read. In addition to finding the barcode, RAD implements efficient barcode correction strategies for scenarios of knowing or not knowing the full barcode whitelist or having paired short-read single-cell sequencing data for a short whitelist. In synthetic and real-world benchmarks, RAD is faster and achieves significantly higher sensitivity than existing pipelines while having comparable precision. We show RAD can be applied to high-definition long-read spatial transcriptomic data and demonstrate single cell and spatial analysis of B cell isotype and secretion states.

bioinformatics↗

Hierarchal single-cell lineage tracing reveals differential fate commitment of CD8 T-cell clones in response to acute infection.

Generating balanced populations of CD8 effector and memory T cells is necessary for immediate and durable immunity to infections and cancer. Yet, a definitive understanding of CD8 differentiation remains unclear. We used CARLIN, a processive lineage recording mouse model with single-cell RNA-seq and TCR-seq to track endogenous antigen-specific CD8 T cells during acute viral infection. We identified a diverse repertoire of expanded T-cell clones represented by seven transcriptional states. TCR enrichment analysis revealed differential memory- or effector-fate biases within clonal populations. Shared Vb segments and amino acid motifs were found within biased categories despite high TCR diversity. Using single-cell CARLIN barcode-seq we tracked multi-generational clones and found that unlike unbiased or memory-biased clones, which stably retain their fate profiles, effector-biased clones could adopt memory- or effector-bias within subclones. Collectively, our study demonstrates that a heterogenous T-cell repertoire specific for a shared antigen is composed of clones with distinct TCR-intrinsic fate-biases.

immunology↗

Exploratory analyses suggest less cognitive decline on nilvadipine treatment in very mild Alzheimer’s disease subjects

BackgroundWe explored whether the effects of nilvadipine on cognition were influenced by baseline Alzheimers disease (AD) severity.\n\nMethodsExploratory analyses were performed on the modified intention-to-treat (mITT) dataset (n = 497) of a phase III randomized placebo-controlled trial to examine the response to nilvadipine in very mild, mild and moderate AD subjects. The outcome measures included total and subscale scores of the Alzheimers Disease Assessment Scale Cognitive 12 (ADAS-Cog 12), the Clinical Dementia Rating Scale sum of boxes (CDR-sb) and the AD composite score (ADCOMS), an outcome measure recently developed to detect treatment responses in subjects with prodromal AD. Cerebrospinal fluid (CSF) biomarkers A{beta}38, A{beta}40, A{beta}42, total tau and P181 tau were measured in a subset of samples (n = 55). Regression analyses were adjusted for potential confounders and effect modifiers in order to examine the interactive effects of nilvadipine and AD severity on cognitive outcomes over 78-weeks.\n\nResultsCompared to their respective placebo-controls, nilvadipine-treated, very mild AD subjects showed less decline, whereas moderate AD subjects showed greater decline on the ADAS-Cog 12. Also in very mild AD, a beneficial effect (as measured by ADCOMS), was detected in the nilvadipine treated group. Therapeutic effects of nilvadipine were also observed for a composite memory trait in very mild AD subjects and a composite language trait in mild AD subjects. CSF A{beta}42/A{beta}40 ratios were increased in mild AD and decreased in moderate AD patients treated with nilvadipine, compared to their respective controls.\n\nConclusionThese data suggest that very mild AD subjects benefited from nilvadipine and that future clinical trials of nilvadipine in this population are required to confirm these findings.\n\nTrial RegistrationNCT02017340 Registered 20 December 2013, https://clinicaltrials.gov/ct2/show/NCT02017340\n\nEUDRACT Reference Number 2012-002764-27 Registered 04 February 2013, https://www.clinicaltrialsregister.eu/ctr-search/search?query=2012-002764-27

clinical trials↗