Cell Journal (Yakhteh)
Volume:26 Issue: 5, May 2024

Trimethyltin (TMT) chloride is an organotin compound used in industry. It has been linked to generatingreactive oxygen species (ROS), inflammatory processes, and neuronal death. Carvacrol is a monoterpene phenolfound in the Lamiaceae plant family, modulating inflammatory conditions and necroptosis in neural tissue. This studyaimed to investigate the neuroprotective effects of carvacrol in a rat model of hippocampal neuronal injury inducedby TMT. In this experimental study, sixty male Wistar rats were randomly divided into five groups(n=12): group 1 receiving saline, group 2 received dimethyl sulfoxide (DMSO) as a vehicle for 21 days, group 3 receivinga single dose of TMT (8 mg/kg) and groups 4 and 5 receiving carvacrol 40 and 70 mg/kg daily for 21 days after a singledose of TMT. All injections were intraperitoneal (I.P.). Caspase-3, Bax, Bcl-2, and Bdnf gene expression and the numberof pyknotic neurons in the hippocampus were quantified. Spatial memory was assessed with a radial arm maze. Statistical analysis of histological data revealed the carvacrol significantly attenuated cognitive dysfunction andthe number of pyknotic neurons in the hippocampal CA1 region of rats treated with TMT. Based on real-time polymerasechain reaction (PCR), carvacrol modulated the expression of genes involved in apoptosis (Bax and Caspase-3) andupregulated anti-apoptotic (Bcl-2) and brain derived neurotrophic factor (Bdnf) genes in the hippocampal tissue. These findings revealed neuroprotective effects of carvacrol which might be mediated by apoptotic andanti-apopetotic factors.

In Parkinson's disease (PD), mitochondrial defects and oxidative stress cause an increase in free radicalsand the death of dopaminergic neurons in the substantia nigra. By preventing lipid peroxidation and protecting againstperoxide radicals, vitamin E is the most important antioxidant of biological membranes that can neutralize free radicals.Also, the improvement of the functional status of mitochondria can be influenced by exercise, which can be partially theresult of changes in the mitochondrial mitophagy and dynamics system. This study aimed to investigate the interactiveeffects of six weeks of vitamin E (VE) consumption and training on the mitochondrial function [Cytochrome C (Cyt-C),Adenosine triphosphate (Atp) synthase, optical atrophy1 mitochondrial dynamics like guanosine triphosphatase(GTPase), 8-Oxodequanosin and Pten induced kinase 1 (Pink1) is a protein coding gene] in the hippocampus tissueof PD rats. In this experimental study, 4-6-month-old Sprague-Dawley rats (mean weight 250 ± 30 g)were given parkinsonism with reserpine (2 mg/kg) and were categorized into different groups, including healthy (H),PD, VE solvent+PD (Sham), aerobic exercise+PD (AE+PD), VE+PD, AE+VE+PD. The aerobic training program wascarried out for six weeks and 5 sessions per week and each session lasted 15-22 minutes. VE was also taken orallyat 30 mg/kg daily. A six-week regimen of VE supplement along with the AE significantly reduced the Cyt-C gene expression level,also we observed a significant increase in gene expression level of the Pink1, Atp synthase and Opa1 (P<0.05). There is nosignificant difference was found in the level of 8-Oxog detected in hippocampal tissue samples (P>0.05). The consumption of VE along with AE may provide therapeutic effects on mitochondrial damage in PD rats.

Despite the advances in treatment, breast cancer (BC) remains a major cause of death in women. Thisstudy aims to evaluate the prognostic significance of detecting circulating tumor cells (CTCs) and disseminated tumorcells (DTCs) in paired peripheral blood (PB) and bone marrow (BM) samples obtained both before and after adjuvantchemotherapy from patients with operable BC. In this experimental study, from 160 patients with primary BC, we collected 160 PB and BM samplesbefore and we could be able to collect PB and BM samples from 100 of them after adjuvant chemotherapy. The expressionlevel of cytokeratin 19 (CK19), carcinoembryonic antigen (CEA), mammaglobin 1 (MGB1), mucin 2 (MUC2) and trefoil factor1 (TFF1) mRNAs in the PB/BM samples were analyzed by quantitative real-time polymerase chain reaction (PCR). Multivariate Cox regression analyses indicated that the detection of CK19 mRNA-positive CTCs/DTCs eitherbefore or after adjuvant chemotherapy was an independent factor for prognosis associated with decreased diseasefreesurvival (DFS). Patients with tumor cells detected in both PB and BM and patients with persistent detection oftumor cells before and after chemotherapy had worse outcomes compared to those with tumor cells detected in one orneither of the compartments. This study suggests that the detection of CK19 mRNA-positive CTCs/DTCs either before or after adjuvantchemotherapy could be an independent predictor of DFS in operable BC patients.

The objective of this study was to assess whether Spen paralogue and orthologue C-terminal domaincontaining 1 (SPOCD1) gene expression could serve as a valuable prognostic and diagnostic biomarker in commoncancers, drawing from insights in recent literature. We sought to verify this concept by utilizing data sourced from TheCancer Genome Atlas (TCGA) alongside clinical samples. In this bioinformatics and experimental study, SPOCD1 RNA-seq data from 12 commoncancers were collected from TCGA Pan-Cancer Atlas using the R package "TCGA BIOLINKS" and normalized foranalysis. Various analytical tools, including receiver operating characteristic (ROC) curves, Kaplan-Meier and Coxregressionanalyses, and pathway enrichment analysis via the molecular signatures database (MSigDB), were applied.Drug resistance/sensitivity correlations with SPOCD1 expression were explored using the Gene Expression Omnibus(GEO) database. Clinical colorectal cancer (CRC) samples, including both colon and rectal malignant samples, werealso evaluated. The results showed elevated SPOCD1 expression in most cancers (9/12), with notable prognostic valuein COAD, HNSC, KICH, and LIHC, and a correlation with poor prognosis in COAD for disease-free survival. ROCcurve analysis suggested SPOCD1 as a diagnostic biomarker in the majority of cases (7/12), although this patternwas inconsistent in clinical CRC samples. Pathway enrichment analysis revealed a strong correlation betweenSPOCD1 expression and critical molecular pathways. Unlike former results, we found that SPOCD1 upregulatedwhen interacting with PD-0325901. However, treating with Panobinostat led to downregulation. Both are as anticancerreagents. This study confirms the potential of SPOCD1 as a diagnostic and prognostic biomarker in prevalentcancers. However, extensive clinical data, particularly for CRC, are required to validate its reliability. DifferentCOAD subtypes may exhibit varying correlations with SPOCD1 expression levels, underscoring the need for furtherinvestigation to fully understand its diagnostic and prognostic value.

The prevalence of neurological disorders often varies by sex, with conditions such as Alzheimer’s diseaseand autism spectrum disorder (ASD) demonstrating notable differences in incidence. The aim of this study is tounderstand the molecular basis for these divergences in order to facilitate the creation of sex-specific therapeuticstrategies. This study is a bioinformatic analysis of publicly available RNA sequencing datasets involvingautism patients. The study utilized RNA sequencing data from postmortem human brains’ prefrontal cortex, including38 neurotypical controls and 34 individuals with ASD. The sequencing data was obtained from previously publishedpapers, and we downloaded the raw data from SRA. We investigated the molecular basis of sex-biased presentationin ASD through comprehensive transcriptomic analysis. Comparative analysis of gene expression between male and female subjects, both autistic and unaffected,was conducted, using a significance level of ≤0.01. In autistic individuals, 136 genes demonstrated differentialexpression between sexes, predominantly upregulated in males, indicating a bias in male gene expression. Amongthese, 12 genes were identified as risk factors in the SFARI dataset. While most sex-biased genes were autosomal,expression differences on sex chromosomes were also observed in neurotypical subjects. Notable genes includedTCF7L2, collagen family genes, and solute carrier family genes. In ASD males, extracellular matrix (ECM) organizationemerged as a significant pathway, while immune-related processes were prominent in unaffected individuals. Our study highlights the impact of the ECM pathway in ASD, with notable differences between sexes,particularly in males. MIR424 shows promise as a potential biomarker for ASD in males. Recognizing the importanceof sex differences in ASD transcriptomic research is crucial, as these variances provide insights into the disorder’spathophysiology and may guide the development of more personalized treatments for both sexes.

Despite a lower estimated rate of cancer incidence in Iran compared to the global average, the trend is unfortunatelyincreasing. This necessitates the implementation of early detection of cancer and targeted therapies to effectively treatvarious types of cancer. Therefore, the 5th “International Royan Cancer Conference: From Bench to Bedside" washeld to focus on critical cancer-related aspects such as gene- and cell therapy, immunotherapy, oligonucleotides incancer treatment, biosensors for detection, and drug delivery. The 2-day conference took place in February 2024 at theRoyan Institute, Tehran. This collaborative effort brought together experts from both basic and clinical research fields.The primary objective of the conference was to address clinical challenges and harness the potential of basic sciencesfor early cancer diagnosis and treatment, with a robust emphasis on ethical considerations. The conference aimedto ensure optimal patient care while advancing scientific understanding in the field and facilitating effective researchcollaborations among researchers and enthusiasts dedicated to combating cancer.

In this article published in Cell J, Vol 24, No 12, 2022, on pages 741-747, the authors found that there was somemistakes in the Table 1 and we have corrected them in the following table.The authors would like to apologize for any inconvenience.

In this article published in Cell J, Vol 17, No 1, 2015, on pages 159-162, the authors found that the affiliation of secondauthor in address 2 was missed during the formatting of the paper. Therefore, we corrected it.The authors would like to apologize for any inconvenience.