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Rahman, M. R.

Publications and source records attributed to Rahman, M. R..

5 recordsLinked to original sources

Reproducible Zero-Shot Decoding of Conceptual Knowledge from Human fMRI: A Systematic Evaluation of the Semantic Output Code Framework

Zero-shot learning from functional magnetic resonance imaging (fMRI) data offers a principled approach to decoding conceptual knowledge without requiring training examples for every target concept. The Semantic Output Code (SOC) framework, introduced by Palatucci et al. [2009], operationalises this idea through a two-stage pipeline: a regression-based mapping from voxel activations to a semantic feature space (the S map), followed by nearest-neighbour retrieval over a semantic knowledge base (the L map). Despite its foundational role in the field, no fully documented, open-source replication of this framework has been published on the original Mitchell et al. [2008] fMRI dataset. We present such a replication and extend it through a systematic evaluation of every major design choice in the pipeline. Using the official 25-verb co-occurrence feature space from Mitchell et al. [2008] and the correlation-stability voxel selection criterion, our pipeline achieves a mean pairwise 2-way forced-choice accuracy of 76.5% (SD = 4.9%, range: 70.0%-84.1%) across all nine subjects of the Mitchell dataset, within 0.5 percentage points of the published benchmark of 77%. We document and resolve a previously unreported evaluation artefact caused by a degenerate zero-vector knowledge base entry for one stimulus word (skyscraper), which suppressed accuracy by approximately 8 percentage points under the broken configuration. Sensitivity analyses across regularisation strength, voxel count, and knowledge base normalisation demonstrate that the pipeline is robust to hyperparameter choice within a broad operating range, with voxel count being the single most impactful factor. Substantial inter-subject variability is documented, with pairwise accuracy ranging from 70.0% (P9) to 84.1% (P1), a spread of 14.1 percentage points that exceeds the difference between our mean and the Mitchell benchmark. All code, the expanded 60-word knowledge base, and the complete evaluation pipeline are released as open-source software at https://github.com/Rashed525/fmri-zsl-pipeline.

neuroscience↗

Homology modeling and functional characterization of multidrug effluxor Mta protein from Bacillus Atrophaeus: An explanatory insilico approach

Phenotypically similar to B. subtilis, Bacillus atrophaeus is a Gram-positive, aerobic, spore-forming bacteria. It is a black-pigmented bacterial genus. Therefore, it is of interest to study the uncharacterized proteins in the genome. For a detailed computational sequence-structure-function analysis using available data and resources, an uncharacterized protein Mta (AKL87074.1) in the genome was selected. In this study, attempts were made to study the physicochemical properties, predict secondary structure, modeling the 3-D protein, pocket identification, protein-protein interaction and phylogenetic analysis of Mta protein. The predicted active site using CASTp is analyzed for understanding their multidrug resistance function. Because Mta is a MerR family member, these investigations on these functional aspects could lead us for better understanding of antibiotic resistance phenomenon.

bioinformatics↗

Blood-based molecular biomarker signatures in Alzheimer’s disease: Insights from systems biomedicine analyses

Background and objectivesAlzheimers disease (AD) is the progressive neurodegenerative disease characterized by dementia, but no peripheral biomarkers available yet that can detect the AD. This study aimed to identify systems biomarker signatures in the AD through integrative analyses.\n\nMaterials and MethodsWe used two microarray transcriptomics datasets of blood from AD patients to identify differentially expressed genes (DEGs). Geneset and protein overrepresentation analysis, protein-protein interaction (PPI), DEGs-Transcription Factor interactions, DEGs-MicroRNAs interactions, protein-drug interactions, and protein subcellular localizations analyses were done on common DEGs.\n\nResultsTotal 25 DEGs were detected between the two datasets. Integration of DEGs with biomolecular networks revealed hub proteins (TUBB, ATF3, NOL6, UQCRC1, SND1, CASP2, BTF3, INPP5K, VCAM1, and CSTF1), TFs (FOXC1, ZNF3, GEMIN7, and SMG9), miRNAs (mir-20a-5p, mir-93-5p, mir-16-5p, let-7b-5p, mir-708-5p, mir-24-3p, mir-26b-5p, mir-17-5p, mir-4270, and mir-4441). The analyses revealed candidate blood based biomarkers in the AD. We evaluated the histone modifications of the identified biomolecules. The hub genes and transcription factors (TFs) revealed that they possess several histone modification sites associated with Alzheimers disease. The protein-drug interactions revealed 10 candidate drugs consisting of antineoplastic (Vinorelbine, Vincristine, Vinblastine, Epothilone D, Epothilone B, CYT997, and ZEN-012), dermatologicals (Podofilox), and immunosuppressive agents (Colchicine) that may target the candidate systems biomarkers. The subcellular localization analysis revealed the interactions of the DEGs range from nucleus to plasma membrane through cytosol.\n\nConclusionsThis study presents blood based systems molecular biomarker signatures at RNA and protein levels which might be useful as peripheral biomarkers in the AD. The candidate drugs, histone modification sites, and subcellular localizations will be useful in future drug design in the AD.

systems biology↗

Common molecular biomarker signatures in blood and brain of Alzheimers disease

BackgroundAlzheimers disease (AD) is a progressive neurodegenerative disease characterized by memory loss and confusion. Neuroimaging and cerebrospinal fluid-based early detection is limited in sensitivity and specificity as well as by cost. Therefore, detecting AD from blood cell analysis could improve early diagnosis and treatment of the disease. The present study aimed to identify blood cell transcripts that reflect brain expression levels of factors linked to AD progression.\n\nMethodsWe analyzed blood cell and brain microarray gene expression datasets from NCBI-GEO for AD association and expression in blood and brain. We also used eQTL and epigenetics data to identify AD-related genes that were regulated similarly in blood and brain.\n\nResultsWe identified 9 differentially expressed genes (DEG; AD versus controls) common to blood cells and brain (CNBD1, SUCLG2-AS1, CCDC65, PDE4D, MTMR1, C3, SLC6A15, LINC01806, and FRG1JP) and 18 genes (HSD17B1, GAS5, RPS5, VKORC1, GLE1, WDR1, RPL12, MORN1, RAD52, SDR39U1, NPHP4, MT1E, SORD, LINC00638, MCM3AP-AS1, GSDMD, RPS9, and GNL2) that were commonly dysregulated between AD blood and brain tissues using SNP and cis-eQTL data. This data revealed significant neurodegeneration-associated molecular pathways in the ribosomal and complement systems. Integration of these different analyses revealed dys-regulation of hub transcription factors (SREBF2, NR1H2, NR1H3, PRDM1, XBP1) and microRNAs (miR-518e, miR-518a-3p, miR-518b, miR-518c, miR-518d-3p and miR-518f) in AD. Several significant histone modification sites in DEGs were also identified.\n\nConclusionWe have identified new putative links between pathological processes in brain and transcripts in blood cells in AD subjects that may enable the use of blood to diagnose and monitor AD onset and progression.

neuroscience↗

The geography of malaria elimination in Bangladesh: combining data layers to estimate the spatial spread of parasites

Malaria control programs face difficult resource allocation decisions. Of particular concern for countries aiming for malaria elimination, the regular movement of individuals to and from endemic areas undermines local interventions by reintroducing infections and sustaining local transmission. Quantifying this movement of malaria parasites around a country has become a priority for national control programs, but remains methodologically challenging, particularly in areas with highly mobile populations. Here, we combined multiple data sources to measure the geographical spread of malaria parasites, including epidemiological surveillance data, travel surveys, parasite genetic data, and anonymized mobile phone data. We collected parasite genetic barcodes and travel surveys from 2,090 patients residing in 176 unions in southeast Bangladesh. We developed a genetic mixing index to quantify the likelihood of samples being local or imported. We then inferred the direction and intensity of parasite flow between locations using an epidemiological model, and estimated the proportion of imported cases assuming mobility patterns parameterized using the travel survey and mobile phone calling data. Our results show that each data source provided related but different information about the patterns of geographic spread of parasites. We identify a consistent north/south separation of the Chittagong Hill Tracts region in Bangladesh, and found that in addition to imported infections from forested regions, frequent mixing also occurs in low transmission but highly populated areas in the southwest. Thus, unlike risk maps generated from incidence alone, our maps provide evidence that elimination programs must address ongoing movement of parasites around the lower transmission areas in the southwest.

epidemiology↗