Publications by authors named "Foozhan Tahmasebinia"

Spinal cord injury (SCI) often results in severe neurological deficits and secondary complications, including disruptions in female reproductive health. Current treatment options are limited in addressing both neurological recovery and reproductive outcomes. This study investigated the impact of photobiomodulation therapy (PBMT) on spinal cord healing and ovarian health in a female rat model of SCI.

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Ribosome recycling is a fundamental biological process crucial for cellular health. Defective recycling disrupts ribosome biogenesis and organelle function, particularly in mitochondria, contributing to ribosomopathies, neurodegenerative diseases, and cancer. While not directly linked to human diseases via known genetic mutations, emerging evidence suggests a critical interplay between ribosome recycling and organelle quality control.

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Spinal cord injury (SCI) is a severe condition often leading to lasting neurological impairment and associated reproductive health issues in males. The aim of this study was to investigate the therapeutic potential of photobiomodulation therapy (PBMT) during the inflammatory phase of SCI to prevent oxidative damage, reduce inflammation, and mitigate potential damage to testicular function. Eighteen male rats were randomly divided into three groups: Group A (laminectomy only), group B (contusion), and group C (contusion+PBMT).

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The 40S ribosomal subunit recycling pathway is an integral link in the cellular quality control network, occurring after translational errors have been corrected by the ribosome-associated quality control (RQC) machinery. Despite our understanding of its role, the impact of translation quality control on cellular metabolism remains poorly understood. Here, we reveal a conserved role of the 40S ribosomal subunit recycling (USP10-G3BP1) complex in regulating mitochondrial dynamics and function.

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Article Synopsis
  • Huntington's disease is a genetic disorder characterized by the progressive degeneration of brain nerve cells, leading to motor and cognitive issues, with no definitive cure available yet.
  • A study tested the drug Apelin-13 on male Wistar rats with a Huntington’s disease model to see if it could help improve symptoms and reduce inflammation.
  • Results showed that Apelin-13 treatment enhanced motor function, increased neuronal density, reduced inflammation, and improved overall brain health in the rats.
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  • * Chronic use of METH disrupts the normal function of neurotransmitters like dopamine, leading to various stress responses and cell death processes in the brain.
  • * The article reviews the detrimental effects of METH on neuronal activities and discusses the need for new treatment strategies to combat its neurotoxic impact.
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  • - Diabetes can cause serious complications like diabetic foot ulcers (DFUs), which can lead to infections and amputations, highlighting the need for better treatments.
  • - The study explored the effectiveness of photobiomodulation therapy (PBT) and autologous platelet gel (APG) on healing DFUs, analyzing data from various reputable medical databases and selecting 57 relevant studies.
  • - Results indicated that both APG and PBT can significantly improve healing times, reduce pain, and decrease the need for surgeries, marking them as promising treatments for managing DFUs.
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  • - Methamphetamine (METH) disrupts neurotransmitter activity in the central nervous system, leading to neurotoxicity through various pathways, including increased reactive nitrogen and oxygen species and mitochondrial apoptosis.
  • - This study analyzed structural changes in the amygdala of ten male postmortem brains, comparing chronic METH users to control subjects using various scientific techniques like immunohistochemistry and real-time PCR.
  • - Results showed METH addiction led to decreased levels of protective proteins and increased inflammation and neurodegeneration in the amygdala, with reactive oxygen species production linked to specific signaling pathways.
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Stimulator of IFN genes type I (STING-Type I) IFN signaling in myeloid cells plays a critical role in effective antitumor immune responses, but STING agonists as monotherapy have shown limited efficacy in clinical trials. The mechanisms that downregulate STING signaling are not fully understood. Here, we report that protein phosphatase 2A (PP2A), with its specific B regulatory subunit Striatin 4 (STRN4), negatively regulated STING-Type I IFN in macrophages.

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Drosophila melanogaster (Drosophila, fruit fly, or fly) is an important model organism in the studies of molecular genetic analysis and mechanism of Parkinson's disease (PD), benefiting from its powerful genetic tools and massive available genetic mutants. People have generated different fly models to mimic the inherited PDs and most of them have obvious mitochondrial abnormalities. Here, we describe some common approaches to analyze mitochondrial functions and morphological changes in Drosophila PD models.

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Methamphetamine (Meth) is a neuro-stimulator substrate which might lead to neural cell death and the activation of several interconnected cellular pathways as well. However, the precise molecular mechanisms underlying Meth-induced neural cell death remained unclear yet. The current study aimed to assess the specific relationship between long-term Meth exposure and several endoplasmic reticulum stress, autophagy, and apoptosis associated markers including C/EBP homologous protein (CHOP), Tribbles homolog 3(Trib3), Nuclear protein 1(NUPR1), and Beclin-1 expression in postmortem human striatum.

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Parkinson's disease (PD) is one of the most common neurodegenerative disorders. The neuroinflammation in the brain of PD patients is one of the critical processes in the immune pathogenesis of PD leading to the neural loss in the substantia nigra. Due to the anti-inflammatory effects of curcumin (CU) and low-level laser therapy (LLLT), we examined the protective effect of CU and LLLT on PC12 cells treated with 6-hydroxydopamine (6-OHDA) as a Parkinson model.

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Methamphetamine (METH) abuse is accompanied by oxidative stress, METH-induced neurotoxicity, and apoptosis. Oxidative stress has devastating effects on the structure of proteins and cells. Autophagy is an evolutionarily conserved intracellular regulated mechanism for orderly degradation of dysfunctional proteins or removing damaged organelles.

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Bone marrow stromal stem cells (BMSCs), a type of adult stem cells, secrete bioactive molecules such as trophic factors, growth factors, chemokine and cytokines that may be effective against oxidative stress in neurodegenerative diseases. In this study, we examined the protective effect of BMSCs conditioned media (CM) and photobiomodulation therapy (PBMT) on PC12 cells exposed to H2O2 as an oxidative injury model. BMSCs were cultured and confirmed by flow cytometry analysis and underwent osteogenic and adipogenic differentiation.

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Many studies have shown the positive effect of laser radiation and application of the mesenchymal stem cells (MSCs) and their secretion in stimulating bone regeneration. The aim of this study was determining effects of MSC conditioned media (CM) and low-level laser (LLL) on healing bone defects in the hypothyroid male rat. We assigned 30 male Wistar rats randomly to 3 groups: control, hypothyroidism, CM+LLL.

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The role of T helper 17 (Th17) cells in auto-inflammatory neurological disorders such as Multiple Sclerosis (MS), Alzheimer's disease (AD), Parkinson's disease (PD) and schizophrenia has not been clarified completely. Th17-derived pro-inflammatory cytokines including IL-17, IL-21, IL-22, IL-23, GM-CSF, and IFN-γ have a critical role in the pathogenesis of these disorders. In this review, we demonstrate the role of Th17 cells and their related cytokines in the immunopathology of above-mentioned disorders to get a better understanding of neuroinflammatory mechanisms mediated by Th17 cells associated with events leading to neurodegeneration.

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Amyloid β (Aβ) fibrils and amorphous aggregates are found in the brain of patients with Alzheimer's disease (AD), and are implicated in the etiology of AD. The metal imbalance is also among leading causes of AD, owing to the fact that Aβ aggregation takes place in the synaptic cleft where Aβ, Cu(II) and Fe(III) are found in abnormally high concentrations. Aβ40 and Aβ42 are the main components of plaques found in afflicted brains.

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