Deciphering the enigma of RNA editing in the ATP1_alpha subunit of ATP synthase in Triticum aestivum.

There is evidence that RNA editing is related to plant cellular stress as well as electron transport organelles, such as mitochondria. The mitochondrial atp1 gene encodes the alpha-subunit of Atp synthase. Control as well as two periods of drought stress treatments were analyzed in the cDNAs generated from the mitochondrial atp1 gene of two cultivars of Triticum aestivum [Giza 168 (G168) and Gemmiza 10 (GM10)]. Following RNA-seq data assembly, atp1 cDNAs from the control (acc. no. OQ129415), 2-hour (acc. no. OQ129416), and 12-hour (acc. no. OQ129417) time points of the T. aestivum cultivar G168 were obtained. Control (acc. no. OQ129419), 2-hour (acc. no. OQ129420), and 12-hour (acc. no. OQ129421) samples all included reconstructed atp1 transcripts from Gemmiza 10. Atp1 transcripts were assembled using the wheat atp1 gene (acc. no. NC_036024). RNA-seq raw data was utilized to identify 11 RNA editing sites in atp1 in the tolerant cultivar Giza168 and 6 in the sensitive cultivar Gemmiza10. The significant difference in RNA editing observed between control and drought stress conditions in sites led to synonymous amino acids. This led to no change in tertiary structure between tolerant and sensitive cultivars. But the change was focused between produced protein and its correspondence sequence on DNA.

The Effect of Probiotic Supplementation on the Gut-Brain Axis in Psychiatric Patients.

The pathophysiology of several psychiatric diseases may entail disturbances in the hypothalamic-pituitary-adrenal (HPA) axis and metabolic pathways. Variations in how these effects present themselves may be connected to individual variances in clinical symptoms and treatment responses, such as the observation that a significant fraction of participants do not respond to current antipsychotic drugs. A bidirectional signaling pathway between the central nervous system and the gastrointestinal tract is known as the microbiota-gut-brain axis. The large and small intestines contain more than 100 trillion microbial cells, contributing to the intestinal ecosystem's incredible complexity. Interactions between the microbiota and intestinal epithelium can alter brain physiology and affect mood and behavior. There has recently been a focus on how these relationships impact mental health. According to evidence, intestinal microbiota may play a role in neurological and mental illnesses. Intestinal metabolites of microbial origin, such as short-chain fatty acids, tryptophan metabolites, and bacterial components that might stimulate the host's immune system, are mentioned in this review. We aim to shed some on the growing role of gut microbiota in inducing/manipulating several psychiatric disorders, which may pave the way for novel microbiota-based therapies.

Molecular characterization and phylogenetic analysis of Rhynchophorus ferrugineus (Olivier) in Eastern Province, Saudi Arabia.

Red palm weevil (RPW) is the most aggressive date palm parasite in the Middle East, and especially in the Gulf region. Originated in Southeast Asia, this pest has been detected in the entire Arabian Peninsula, North Africa, Italy, Latin America, and other territories. It is important to local from obtrusive species, which help augmenting the pest control strategies. In the present study we collected 21 RPW samples from 21 different locations in the Eastern Province, Saudi Arabia to genetically characterize them using RAPD- and ISSR-based clustering. Unweighted pair group method with arithmetic mean (UPGMA) for RAPD data categorized the 21 accessions into seven distinct groups, with Al-Oyonn and Juaymah each categorized in solitary group, meanwhile, UPGMA for ISSR indicated six different groups, with Battaliyah, Al-Oyoon, and Juaymah each assigned to a separate group. Combining RAPD and ISSR data revealed two accession; Al-Oyoon and Juaymah that might be considered obtrusive species. Based on distance calculations, we proposed that the potential origins of RPW collected from these locations are Iran and the United Arab Emirates. However, this assumption needs further studies for confirmation.

Vorinostat-loaded titanium oxide nanoparticles (anatase) induce G2/M cell cycle arrest in breast cancer cells via PALB2 upregulation.

Breast cancer is a group of diseases in which cells divide out of controlled, typically resulting in a mass. Erlotinib is targeted cancer drug which functions as an inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase. It is used mainly to treat of non-small cell lung cancer patients and has an action against pancreatic cancer. Vorinostat (aka suberanilohydroxamic acid) is an inhibitor of histone deacetylases (HDAC), which has an epigenetic modulation activity. It is used to treat cutaneous T cell lymphoma. In the present study, the erlotinib (ERL) and vorinostat (SAHA) loaded TiO2 nanoparticles (NPs) were used for the treatment of the breast cancer cells (MDA-MB-231 and MCF-7) and human cancerous amniotic cells (WISH). Cell count and viability were negatively affected in all treatments compared to normal cells and bare TiO2 NPs. Apoptosis results indicated a significant increase in the total apoptosis in all treatments compared with control cells. ERL- and SAHA-loaded TiO2 NPs treatments arrested breast cancer cells at G2/M phase, which indicate the cytotoxic effect of these treatment. Partner and localizer of BRCA2 (PALB2) gene expression was assessed using qPCR. The results indicate that PLAB2 was upregulated in ERL- and SAHA-loaded TiO2 NPs compared with control cells and can be used as nanocarrier for chemotherapy drugs. However, this conclusion necessitates further confirmative investigation.

Metformin Reshapes the Methylation Profile in Breast and Colorectal Cancer Cells

With no sharp cure, breast cancer still be the major and the most serious life-threatening disease worldwide. Colorectal is the third most commonly occurring cancer in men and the second most commonly occurring cancer in women. In the present investigation, colon cancer cells (CaCo-2) and breast cancer cells (MCF-7) were treated with elevated doses of metformin (MET) for 48h. Cell count was assessed using trypan blue test, and the cytotoxicity was evaluated using MTT assay. Methylation-specific PCR was performed on the bisulfite-treated DNA against two tumor suppressor genes; RASSF1A and RB. Results indicated that: in breast cancer, the cell count was decreased significantly (P>0.005) after being treated with 5, 10, 20, 50, and 100 mM of MET. The elevated concentration had increased reduction percentages on the MCF-7 cells, as 5 mM and 100 mM have yielded 35% and 93.3% reduction in cell viability, respectively. Colon cancer cells have responded to the doses of MET differently, as for the 5 mM and the 100 mM, it gave 88% and 60% reduction in cells viability, respectively. Cytotoxicity assay revealed that 5 mM and 100 mM of MET caused breast cancer cells to loss 61.53% and 85.16% of its viability, respectively, whereas colon cancer cells have responded to the 5 mM and 100 mM of MET by reducing the cells viability with 96.91% and 96.24%, respectively. No RB promoter methylation was detected in colon cells, while RASSF1A was partially methylated. In the MCF-7 breast cancer cells, both RASSF1A and RB were partially methylated.

Procaine Induces Epigenetic Changes in HCT116 Colon Cancer Cells.

Colon cancer is the third most commonly diagnosed cancer in the world, and it is the major cause of morbidity and mortality throughout the world. The present study aimed at treating colon cancer cell line (HCT116) with different chemotherapeutic drug/drug combinations (procaine, vorinostat "SAHA," sodium phenylbutyrate, erlotinib, and carboplatin). Two different final concentrations were applied: 3 µM and 5 µM. Trypan blue test was performed to assess the viability of the cell before and after being treated with the drugs. The data obtained showed that there was a significant decrease in the viability of cells after applying the chemotherapeutic drugs/drug combinations. Also, DNA fragmentation assay was carried out to study the effect of these drugs on the activation of apoptosis-mediated DNA degradation process. The results indicated that all the drugs/drug combinations had a severe effect on inducing DNA fragmentation. Global DNA methylation quantification was performed to identify the role of these drugs individually or in combination in hypo- or hypermethylating the CpG dinucleotide all over the genome of the HCT116 colon cancer cell line. Data obtained indicated that different combinations had different effects in reducing or increasing the level of methylation, which might indicate the effectiveness of combining drugs in treating colon cancer cells.