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Rahmani, S.

Publications and source records attributed to Rahmani, S..

9 recordsLinked to original sources

A Cohort-Based Global Sensitivity Benchmark of MRI-Derived Whole-Heart Electromechanical Models in Healthy Hearts

Patient-specific four-chamber electromechanical models provide a physics-constrained framework for investigating whole-heart cardiac physiology and disease mechanisms. Identifying which model parameters impact whole-heart function is important for understanding cellular-, tissue-, and organ-scale determinants of cardiac performance and for calibrating patient-specific models. However, previous global sensitivity analyses of cardiac electromechanical models have typically been performed on a single heart, and systematic evaluation of how parameter influence compares across anatomically different subjects remains limited. We created four-chamber electromechanical models using cardiac MRI from five healthy subjects (n = 5). The models simulated atrial and ventricular cellular electrophysiology, calcium dynamics, and active contraction, with heterogeneous fibre orientation, transversely isotropic tissue mechanics, pericardial constraint, and a closed-loop cardiovascular system providing physiological boundary conditions. In total, 46 parameters described the integrated model. Using Gaussian process emulators, we performed multi-scale global sensitivity analysis to evaluate the relative contribution of model parameters to left and right atrial and ventricular function. Across all anatomies, the most influential parameters were systemic and pulmonary resistances, ventricular end-diastolic pressures, and the venous reference pressure, highlighting the dominant role of haemodynamic loading conditions in governing pressure- and volume-based outputs. A chamber-level analysis of atrioventricular coupling revealed a phase-dependent pattern. Atrial pressures were predominantly governed by global haemodynamic parameters (> 90% of total sensitivity), atrial filling volumes showed substantial ventricular influence ({approx}40-55% across anatomies), and atrial end-systolic volumes were primarily determined by intrinsic atrial parameters ({approx}60-65%). These patterns were consistent across subjects despite differences in anatomy. We show that, in healthy male subjects, inter-individual anatomical variation does not substantially change the ranking of dominant parameters. This work provides a repeatable modelling and sensitivity analysis framework and establishes a benchmark reference for whole-heart electromechanical modelling in healthy hearts. Author summaryComputational models of the heart can simulate cardiac physiology in unprecedented detail, but these models contain many parameters whose influence on predicted function is not fully understood. We built patient-specific four-chamber heart models from MRI scans of five healthy subjects and used statistical methods to systematically test how 46 model parameters affect simulated cardiac performance. Across all five subjects, we found that the haemodynamic loading parameters, including systemic and pulmonary vascular resistance, ventricular filling pressures, and the venous reference pressure, consistently had the greatest influence on the model outputs, regardless of differences in individual heart anatomy. This finding suggests that in healthy resting conditions, the boundary conditions of the cardiovascular system, rather than individual differences in heart geometry or electrical properties, are the primary drivers of whole-heart function. We also found a structured coupling pattern between the upper and lower heart chambers, where global haemodynamic parameters dominate atrial pressure regulation, ventricular mechanics shape atrial filling, and intrinsic atrial properties control atrial emptying. This work provides a benchmark dataset of five anatomically detailed heart models and a sensitivity analysis framework to guide calibration of future cardiac digital twin models.

systems biology↗

Differences in intrinsic cellular O-GlcNAcylation impact response to metabolic stress

The cellular response to metabolic stress is complex and involves various signals and pathways leading to cellular adaptation. AMP-activated Protein Kinase (AMPK) senses nutrient insufficiency reflected in the ratio of ATP to AMP/ADP and/or glucose availability. In addition, the dynamic modification of proteins with O-linked {beta}-N-Acetylglucosamine (O-GlcNAc) by O-GlcNAc transferase (OGT) is also nutrient sensitive, given that the substrate for this modification is the product of the hexosamine biosynthetic pathway. AMPK can also regulate the hexosamine biosynthetic pathway, and O-GlcNAc may reciprocally regulate AMPK activity under some contexts. However, it remains unclear which parameters establish the extent of reciprocal regulation of AMPK and protein O-GlcNAc modification and whether these signals can be orthogonal under some circumstances. Here, we used ARPE-19 and MDA-MB-231 cells to examine how nutrient limitation or pharmacological activation combined with inhibition of AMPK and O-GlcNAcylation impacts the activation of the reciprocal pathway. We found that the intrinsic level of global protein O-GlcNAc modification may impact how AMPK and metabolic stress regulate global O-GlcNAcylation, and that both signaling systems could be orthogonal in some contexts. These results contribute to understanding the complexity of cellular signaling in response to nutrient availability.

cell biology↗

Cargo-selective regulation of clathrin-mediated endocytosis by AMP-activated protein kinase

The cell surface abundance of many proteins is controlled by clathrin-mediated endocytosis (CME). CME is driven by the assembly of clathrin and other proteins on the inner leaflet of the plasma membrane into clathrin-coated pits (CCPs). Regulation of CCP dynamics allows for control of the function of specific cell surface proteins, impacting a range of cellular outcomes. AMP-activated protein kinase (AMPK) becomes activated upon metabolic insufficiency and facilitates cellular adaptation to nutrient stress. Here, we examined how AMPK regulates CME and the cell surface membrane traffic of {beta}1-integrin. We find that AMPK controls CCP dynamics and regulates the abundance of the endocytic adaptor protein Dab2 within CCPs in a manner that requires the GTPase Arf6, thus selectively promoting the CCP recruitment and internalization of {beta}1-integrin. This reveals a novel signaling pathway for cargo-selective metabolic regulation of CME by AMPK, impacting the function of cell surface proteins such as integrins.

cell biology↗

Vasculature segmentation in 3D hierarchical phase-contrast tomography images of human kidneys

Efficient algorithms are needed to segment vasculature in new three-dimensional (3D) medical imaging datasets at scale for a wide range of research and clinical applications. Manual segmentation of vessels in images is time-consuming and expensive. Computational approaches are more scalable but have limitations in accuracy. We organized a global machine learning competition, engaging 1,401 participants, to help develop new deep learning methods for 3D blood vessel segmentation. This paper presents a detailed analysis of the top-performing solutions using manually curated 3D Hierarchical Phase-Contrast Tomography datasets of the human kidney, focusing on the segmentation accuracy and morphological analysis, thereby establishing a benchmark for future studies in blood vessel segmentation within phase-contrast tomography imaging.

bioinformatics↗

Transplanted Autologous Neural Stem Cells Show Promise in Restoring Motor Function in Monkey Spinal Cord Injury

Spinal cord injury (SCI) is a devastating condition that can result in permanent loss of motor and sensory function. In recent years, transplantation of neural stem cells (NSCs) has emerged as a promising therapeutic approach for SCI. However, adult NSCs residing in the central nervous system (CNS) show promise for cell-replacement therapy in neurodegenerative disorders. In this study, we aimed to investigate the efficacy of transplanting autologous NSCs isolated from the subventricular zone (SVZ-NSCs) into a spinal cord injury model in Rhesus monkeys. We induced SCI in eight Rhesus monkeys and then transplanted SVZ-NSCs into the injury site. Behavioral assessments and magnetic resonance imaging (MRI) were performed to evaluate the functional and structural recovery of the spinal cord. Histological analyses were also performed to assess the survival and differentiation of the transplanted cells. SVZ-NSCs were capable of expressing SOX2, Nestin, and GFAP in addition to self-renewing and spontaneous differentiation in vitro. The monkeys showed sensory and motor function recovery, spinal tract regeneration, and partial reconstruction of the spinal cord. Positive Reinforcement Training confirmed no adverse effects from the isolation procedure. Our findings suggest that NSCs transplantation could be a promising therapeutic approach for SCI in humans, and further studies are warranted to investigate its potential for clinical translation. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=159 SRC="FIGDIR/small/539673v1_ufig1.gif" ALT="Figure 1"> View larger version (69K): org.highwire.dtl.DTLVardef@1f9257forg.highwire.dtl.DTLVardef@cbd0aorg.highwire.dtl.DTLVardef@4ef324org.highwire.dtl.DTLVardef@13ce48b_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

InterOpt: Improved gene expression quantification in qPCR experiments using weighted aggregation of reference genes

Quantification of gene expression is a crucial task in biomedical studies. Although high-throughput methods enable rapid and simultaneous expression quantification of coding or non-coding regions, qPCR is still vastly used due to its high availability, sensitivity, specificity, reproducibility, low cost, and ease of use. A limitation of qPCR has been the need of internal controls or reference genes (RGs) with stable expression in different conditions, to normalize the expression level of the other target genes. So far, several stability criteria and numerous methods for selecting a group of RGs have been proposed, however, important challenges must be addressed. Here we introduce a mathematical basis for precise modeling of qPCR expression normalization and justify widely used stability measures of RGs. We then propose a family of scale-invariant functions, as an alternative to the geometric mean, to optimize aggregated expression of RGs. We provide closed-form optimizations for several scale-invariant aggregation functions. Among them, we show the superiority of weighted geometric mean, whose parameters optimize standard deviation as the stability measure of aggregated RGs expression. We provide experimental support for this finding using real data of solid tumors and liquid biopsies of different sample sizes. The proposed methods can be easily integrated in the existing qPCR expression normalization pipelines of genes and non-coding RNAs. We also provide an implementation of the proposed methods as an R package, with GPU acceleration. Availability and implementationhttps://github.com/asalimih/InterOpt Contactasalimih@gmail.com

bioinformatics↗

Micro to macro scale analysis of the intact human renal arterial tree with Synchrotron Tomography

The architecture of the kidney vasculature is essential for its function. Although structural profiling of the intact rodent kidney vasculature has been performed, it is challenging to map vascular architecture of larger human organs. We hypothesised that hierarchical phase-contrast tomography (HiP-CT) would enable quantitative analysis of the entire human kidney vasculature. Combining label-free HiP-CT imaging of an intact kidney from a 63-year-old male with topology network analysis, we quantitated vasculature architecture in the human kidney down to the scale of arterioles. Although human and rat kidney vascular topologies are comparable, vascular radius decreases at a significantly faster rate in humans as vessels branch from artery towards the cortex. At branching points of large vessels, radii are theoretically optimised to minimise flow resistance, an observation not found for smaller arterioles. Structural differences in the vasculature were found in different spatial zones of the kidney reflecting their unique functional roles. Overall, this represents the first time the entire arterial vasculature of a human kidney has been mapped providing essential inputs for computational models of kidney vascular flow and synthetic vascular architectures, with implications for understanding how the structure of individual blood vessels collectively scales to facilitate organ function.

bioengineering↗

O-GlcNAc transferase modulates formation of clathrin-coated pits

Clathrin-mediated endocytosis (CME) controls the internalization and function of a wide range of cell surface proteins. CME occurs by the assembly of clathrin and many other proteins on the inner leaflet of the plasma membrane into clathrin-coated pits (CCPs). These structures recruit specific membrane protein cargo destined for internalization and trigger the generation of membrane curvature that precedes eventual scission of CCPs from the plasma membrane to yield intracellular vesicles. The diversity of cell surface protein cargo thus controlled by CME indicates that CCP formation is regulated to allow cellular adaptation under different contexts. Of interest is how cues derived from cellular metabolism may regulate CME, given the reciprocal role of CME in controlling cellular metabolism. The modification of proteins with O-linked {beta}-N-acetylglucosamine (O-GlcNAc) is sensitive to nutrient availability and may allow cellular adaptation to different metabolic conditions. We examined how the modification of proteins with O-GlcNAc may control CCP formation and thus CME. We used perturbation of key enzymes responsible for protein O-GlcNAc modification, as well as specific mutants of the endocytic regulator AAK1 predicted to be impaired for O-GlcNAc modification. We identify that CCP initiation and the assembly of clathrin and other proteins within CCPs is controlled by O-GlcNAc protein modification. This reveals a new dimension of regulation of CME and highlights the important reciprocal regulation of cellular metabolism and endocytosis.

cell biology↗

Graph Theoretical Design of Biomimetic Aramid Nanofiber Nanocomposites as Insulation Coatings for Implantable Bioelectronics

An insulation material combining crack and delamination resistance, flexibility, strong adhesion, and biocompatibility is vital for implantable bioelectronic devices of all types. Creating a material with the combination of all these properties is a particularly distinct challenge for implantable electrodes. Here we describe a nanocomposite material addressing these technological challenges based on aramid nanofibers (ANFs) whose unique mechanical properties are complemented by the epoxy resins with strong adhesion to various surfaces. The nanoscale structure of the ANF/epoxy nanocomposite coating replicates the nanofibrous organization of human cartilage, which is known for its exceptional toughness and longevity. The structural analogy between percolating networks of cartilage and ANF was demonstrated using Graph Theory (GT) analysis. The match of multiple GT indexes indicated the near identical organization pattern of cartilage and ANF/epoxy nanocomposite. When compared with the standard insulating material for bioelectronics, Parylene C, the ANF/epoxy nanocomposite demonstrates excellent interfacial adhesion, biocompatibility, and low inflammatory response. This study opens the possibility for the development of insulation materials suitable for different types of electronics for neural engineering and other biomedical applications. Also important, GT analysis makes possible structural characterization of complex biological and biomimetic materials.

bioengineering↗