Biology subjects

Kazemi, S.

Publications and source records attributed to Kazemi, S..

3 recordsLinked to original sources

bioRxiv2024

Cycles in Seizure Duration and Their Underlying Dynamics in the Tetanus Toxin Rat Model

Seizure duration, a characteristic of epilepsy that is understudied in relation in its relationship with rhythmic cycles, provides critical insights into the severity and temporal dynamics of seizures. This study investigates the rhythmic patterns of seizure duration in the Tetanus Toxin (TT) rat model of epilepsy, which is a well-established platform enabling long-term, stable recordings and observation of seizure emergence and remission. Our analysis shows significant cyclical patterns in seizure durations, with periods ranging from 4 to 8 days across rats. The synchronization index and circular-linear correlations revealed phase-locked relationships between seizure durations and cycles, suggesting non-random, predictable temporal dynamics. Further analyses examined the relationship between seizure durations, inter-seizure intervals, and dominant EEG power. The relationship between inter-seizure intervals and seizure duration was modest, suggesting little to no temporal dependency. In contrast, seizure duration showed stronger associations with EEG power in dominant frequency bands, potentially reflecting fluctuations in neural excitability. The findings highlight that seizure durations exhibit predictable rhythms, which could transform seizure prediction and enable time-based intervention strategies, ultimately improving epilepsy management and patient outcomes. These insights lay the groundwork for personalized, rhythm-aware therapeutic approaches.

neuroscience↗

bioRxiv2023

Criticality and partial synchronization analysis in Wilson-Cowan and Jansen-Rit neural mass models

Synchronization is a phenomenon observed in neuronal networks involved in diverse brain activities. Neural mass models such as Wilson-Cowan (WC) and Jansen-Rit (JR) manifest synchronized states. Although they have been studied for decades, their ability to demonstrate second-order phase transition (SOPT) and criticality has not received enough attention, which serves as candidates for the development of healthy brain networks. In this study, two networks of coupled WC and JR nodes with small-world topologies were constructed and Kuramoto order parameter (KOP) was used to quantify the amount of synchronization. In addition, we investigated the presence of SOPT using the synchronization coefficient of variation. Both networks reached high synchrony by changing the coupling weight between their nodes. Moreover, they exhibited abrupt changes in the synchronization at certain values of the control parameter not necessarily related to a phase transition. While SOPT was observed only in JR model, neither WC nor JR model showed power-law behavior. Our study further investigated the global synchronization phenomenon that is known to exist in pathological brain states, such as seizure. JR model showed global synchronization, while WC model seemed to be more suitable in producing partially synchronized patterns. Corresponding author summaryYousef Jamali received his M.Sc. degree in physics from Sharif University, Tehran, Iran, in 2004, and his Ph.D. degree in physics from Sharif University, Tehran, Iran, in 2009. After finishing his Ph.D. thesis, in 2009, he got two years postdoctoral research associate position at the University of California at Berkeley, Department of Bioengineering. He is currently an Associate Professor in the Applied Mathematics Department (Biomathematics division), at Tarbiat Modares University, Tehran, Iran. His current research interests include the interdisciplinary area of the complex system especially on the modeling of brain. In fact, his interests are how the brain works at the critical state and how this complex system synchronized under different conditions.

neuroscience↗

bioRxiv2021

Variations in cell-surface ACE2 levels alter direct binding of SARS-CoV-2 Spike protein and viral infectivity: Implications for measuring Spike protein interactions with animal ACE2 orthologs

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of COVID-19, the most severe pandemic in a century. The virus gains access to host cells when the viral Spike protein (S-protein) binds to the host cell-surface receptor angiotensin-converting enzyme 2 (ACE2). Studies have attempted to understand SARS-CoV-2 S-protein interaction with vertebrate orthologs of ACE2 by expressing ACE2 orthologs in mammalian cells and measuring viral infection or S-protein binding. Often these cells only transiently express ACE2 proteins and levels of ACE2 at the cell surface are not quantified. Here, we describe a cell-based assay that uses stably transfected cells expressing ACE2 proteins in a bi-cistronic vector with an easy to quantify reporter protein to normalize ACE2 expression. We found that both binding of the S-protein receptor-binding domain (RBD) and infection with a SARS-CoV-2 pseudovirus is proportional to the amount of human ACE2 expressed at the cell surface, which can be inferred by quantifying the level of reporter protein, Thy1.1. We also compared different ACE2 orthologs which were expressed in stably transfected cells expressing equivalent levels of Thy1.1. When ranked for either viral infectivity or RBD binding, mouse ACE2 had a weak to undetectable affinity for S-protein while human ACE2 was the highest level detected and feline ACE2 had an intermediate phenotype. The generation of stably transfected cells whose ACE2 level can be normalized for cross-ortholog comparisons allows us to create a reusable cellular library useful for measuring emerging SARS-CoV-2 variants ability to potentially infect different animals. ImportanceSARS-CoV-2 is a zoonotic virus responsible for the worst global pandemic in a century. An understanding of how the virus can infect other vertebrate species is important for controlling viral spread and understanding the natural history of the virus. Here we describe a method to generate cells stably expressing equivalent levels of different ACE2 orthologs, the receptor for SARS-CoV-2, on the surface of a human cell line. We find that both binding of the viral Spike protein receptor binding domain (RBD) and infection of cells with a SARS-CoV-2 pseudovirus are proportional to ACE2 levels at the cell surface. Adaptation of this method will allow for the creation of a library of stable transfected cells expressing equivalent levels of different vertebrate ACE2 orthologs which can be repeatedly used for identifying vertebrate species which may be susceptible to infection with SARS-CoV-2 and its many variants.

microbiology↗