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Karimpour, M.

Publications and source records attributed to Karimpour, M..

5 recordsLinked to original sources

Evaluating Single-Cell Perturbation Response Models Is Far from Straightforward

Predicting cellular responses to genetic and chemical perturbations remains a central challenge in single-cell biology and a key step toward building in silico virtual cells. The rapid growth of perturbation datasets and advances in deep-learning models have raised expectations for accurate and generalizable prediction. We show that these expectations are overly optimistic, largely due to the failure modes of existing evaluation metrics. In this study, using cross-splitting, controlled noise experiments, and synthetic data, we systematically evaluate both prediction models and evaluation metrics. We demonstrate that widely used metrics, including correlation-based measures and common distributional distances, are strongly influenced by scale, sparsity, and dimensionality, often misrepresenting model performance. In particular, the Wasserstein distance fails in high-dimensional gene expression spaces under variance scaling, while the Energy distance can overlook disruptions in gene-gene dependencies. Our analyses further reveal that complex deep learning models often underperform simple baselines and remain far from empirical performance bounds across multiple chemical perturbation datasets. Together, our framework exposes critical pitfalls, establishes robust evaluation guidelines, and provides a foundation for trustworthy benchmarking toward reliable virtual-cell models.

bioinformatics↗

Olfactory receptor 2 drives abdominal aortic aneurysm by promoting CX3CR1-mediated monocyte recruitment

BackgroundAbdominal aortic aneurysms (AAA) are characterized by an intricate interplay of extracellular matrix degradation and inflammation. Macrophages are centrally involved in these processes. The mechanisms underlying macrophage activation in AAA remain incompletely understood. Vascular macrophages have been shown to express olfactory receptor 2 (Olfr2), a G-protein coupled receptor involved in mediating the sense of smelling and regulating inflammatory activity in macrophages. Whether Olfr2 plays a role in modulating macrophage responses in AAA formation remains unknown. Methods & ResultsIn silico micro-array analysis showed increased expression of the human Olfr2 orthologue OR6A2 in AAA tissue compared to healthy aorta. Flow cytometric analysis revealed increased expression of OR6A2 on classical, non-classical, and intermediate monocytes of patients with a large AAA (> 5cm) in comparison to patients with smaller AAA (< 5cm). Up to 30% of vascular macrophages expressed OR6A2 in human AAA and Olfr2 in mouse AAA tissue. Olfr2 expression peaked on major histocompatibility complex II-high (MHCIIhigh) and C-C chemokine receptor type 2-low (CCR2low) aortic monocytes and macrophages on day 7 following experimental AAA initiation and decreased to baseline expression on day 28. Olfr2 gene (Olfr2-/-) deficiency protected mice from AAA formation, which was accompanied by lowered ECM degradation, reduced macrophage infiltration and increased smooth muscle cell content. Conversely, treatment with the Olfr2 agonist octanal exacerbated AAA formation and inflammation, while the antagonist citral reduced AAA formation in comparison to vehicle treated mice. Bulk transcriptome analysis of aortic tissue revealed reduced inflammatory gene expression in Olfr2-/- mice at day 7 following AAA initiation. Spectral flow cytometry resolved 20 aortic immune cell populations, which were largely reduced in quantity by Olfr2-deficiency at day 7 and day 28 post experimental AAA formation, while circulating leukocyte counts and monocyte subset distribution were not altered between Olfr2+/+ and Olfr2-/- mice. Circulating Ly6Chigh-monocytes exhibited reduced expression of the CX3C motif chemokine receptor 1 (CX3CR1) and CCR2 during AAA formation. Transcriptional analysis of monocytes confirmed downregulation of pathways associated with cell adhesion, motility and migration. In vitro, Olfr2-/- monocytes showed impaired migration towards the CX3CR1 ligand CX3CL1. Competitive transfer of Olfr2+/+ and Olfr2-/- monocytes confirmed reduced migratory capacity of Olfr2-/- monocytes into the developing AAA. ConclusionWe demonstrate a critical relevance for Olfr2 in the modulation of the inflammatory response underlying AAA, which is mediated by enhanced monocyte recruitment.

immunology↗

Gene expression adaptation of metastases to their host tissue

The adaptation of metastatic cells to their host tissue critically determines the pathogenicity of a cancer and therefore patient survival. Yet, it remains elusive to what extent the host environment drives gene expression programs in metastatic cells. Here we identify adaptive mechanisms that enable metastases to establish themselves in a novel tissue context. We performed single-cell RNA-sequencing on malignant and benign tissue samples from untreated donors with colorectal adenocarcinoma and liver metastasis to deduce tissue adaptive expression patterns. A novel computational approach identified genes and pathways that consistently adapted to the host tissue at the transition from the primary tumor to the paired metastasis across donors. This analysis revealed that the majority of expression changes in the metastasis reflect an expression signature reminiscent of benign liver epithelial cells. Cellular processes adapting to the liver environment include basic cellular functions such as energy metabolism, as well as tissue-specific pathways such as the regulation of lipid metabolism by PPAR-. These adaptations potentially increase the pathogenicity of the metastatic cells and may provide new therapeutic strategies.

cancer biology↗

The Influence of Knee Varus Deformity on the Kinematic and Dynamic Characteristics of Musculoskeletal Models During Gait

BackgroundMusculoskeletal modeling has paved the way of measuring kinematic and kinetic variables during motions. Nonetheless, since the commonly-used generic models are created based on averaged data; thus, they cannot accurately mimic subjects with skeletal deformities. To overcome this obstacle, one can build personalized models based on subjects MRI or CT scan data, which is both time and money consuming. The other promising way is to manipulate generic models and create semi-personalized models to match with the individuals skeletal system at the joint of interest. Research QuestionCan a semi-personalized model reduce marker error in gait analysis? How a semi-personalized model differentiates the ROM of the lower limb joints and muscle activation pattern while having varus deformity? MethodWe developed the varus-valgus tool (freely available on: https://simtk.org/projects/var-val-tool) in MATLAB using OpenSim Application Programming Interface (API) to incorporate varus-valgus deformity in the generic OpenSim models. A 36-year-old female subject with a complaint of knee pain participated in our study. The subject had 6.5 and 11.9 degrees of varus in the right and left leg, respectively. A semi-personalized model of the subject was first created using generic OpenSim models. Then, markers error during Inverse Kinematic (IK), joints Range of Motion (ROM) and the activation of Tensor Fasciae Latae (TFL), a knee adductor, and Gracilis, a knee abductor, were calculated and compared between a semi-personalized model and a generic model. ResultsSignificant difference was observed in markers error during IK between generic and semipersonalized models (p<0.05). Substantial alterations were found in the ROM of the hip, knee and ankle joints while using semi-personalized model. Moreover, the activation pattern of TFL experienced a dramatic rise whereas Gracilis saw a fall during each gait cycle in semi-personalized models. SignificanceImplementing varus-valgus deformity in the generic models substantially reduces markers error which leads to more accurate results. It was observed that semi-personalized models showed different ROM compared to generic ones.

bioengineering↗

Effects of Reduced Achilles Subtendons Relative Displacement on Healthy Elderly Walking: A Simulation Study

Walking in healthy elderly people is characterized by lower performance. Since conventional training programs have had limited success in improving gait performance, it is essential to identify underlying causes of walking deficits in healthy elderly adults. Recent studies have qualitatively shown that the decreased relative displacement of Achilles subtendons is likely the primary contributor to lower propulsion in the elderlys walking by creating a higher dependency on their triceps-surae muscle functions. Due to the invasive nature of experimental investigations, in this study, we developed a computational model and analyzed the effects of reduced Achilles subtendons relative displacement on the total metabolic rate and muscles force profiles during normal walking. Our musculoskeletal simulations revealed a 17% increase in the total metabolic rate in elderly adults whose Achilles subtendons were restricted to have no relative displacement. Changing the restriction level resulted in significant changes in the force distribution of the plantar flexor muscles, notably, a 40% reduction in the Medial Gastrocnemius and a 124% increase in the Soleus forces during the propulsion phase of walking. Also, we quantitatively presented the higher dependency of triceps-surae muscle functions regarding the limitation on their corresponding Achilles subtendons relative displacement. The results of this study confirm the experimental observations and can be used as initial insight into devising novel rehabilitation training programs with the focus on improving Achilles subtendons relative displacement.

bioengineering↗