Correlation between coenzyme Q10 content and the nutrient sensors in AKI induced by Hemiscorpius lepturus envenomation.

Introduction: Acute kidney injury (AKI) may have a negative effect on mitochondrial hemostasis and bioenergetics as well as coenzyme Q10 (CoQ10) content. PGC-1α, AMPK, sirtuin 1 (Sirt1), and Sirt3, as the key metabolic regulators under nutritional stress, stimulate energy production via mitochondrial biogenesis during AKI. However, no report is available on the relationship between CoQ10 level and nutrient sensors in the pathophysiology of AKI caused by Hemiscorpius lepturus scorpion envenomation. Methods: Three doses of venoms (1, 5, and 10 mg/kg) were administered by subcutaneous (SC) injection to male albino mice. The animals were sacrificed 1 day or 7 days after administration of venom and their kidneys were collected to analyze gene expression involved in AKI, nutrient sensors, and apoptosis signaling activation by real-time polymerase chain reaction (PCR) and the measurement of CoQ10 level using the High-performance liquid chromatography (HPLC) method. Results: The data indicated a significant decrease in CoQ10 level after the administration of venom in 5 and 10 mg/kg. In addition, 1 day after the treatment, a significant over-expression of Sirt1 (5 and 10 mg/kg) was observed compared with normal mice. Overexpression of Sirt3 occurred 1 day and 7 days after treatment only at the dose of 5.0 mg/kg of venom. Furthermore, over-expression of AMPK as an important mitochondrial energetic sensor happened 1 day and 7 days after the injection of venom (5 mg/kg) (P < 0.01). The significant increase in the gene expression of caspase-9 and 3 after the injection of venom (5 and 10 mg/kg) confirmed the role of cell death signaling. Conclusion: The venom-induced energy-sensing pathways have a key role in gene expression of PGC-1α, AMPK, Sirt3, and CoQ10 content after venom-induced AKI.

Incorporation of Silver Nanoparticles in Hydrogel Matrices for Controlling Wound Infection.

For centuries, silver has been recognized for its antibacterial properties. With the development of nanotechnology, silver nanoparticles (AgNPs) have garnered significant attention for their diverse uses in antimicrobial gel formulations, dressings for wound healing, orthopedic applications, medical catheters and instruments, implants, and contact lens coatings. A major focus has been determining AgNPs' physical, chemical, and biological characteristics and their potential to be incorporated in biocomposite materials, particularly hydrogel scaffolds, for burn and wound healing. Though AgNPs have been rigorously explored and extensively utilized in medical and nonmedical applications, important research is still needed to elucidate their antibacterial activity when incorporated in wound-healing scaffolds. In this review, we provide an up-to-date, 10-yr (2010-2019), comprehensive literature review on advancements in the understanding of AgNP characteristics, including the particles' preparation and mechanisms of activity, and we explore various hydrogel scaffolds for delivering AgNPs.

Evaluation of Cytotoxic Activity of Betanin Against U87MG Human Glioma Cells and Normal Human Lymphocytes and Its Anticancer Potential Through Mitochondrial Pathway.

Recent studies revealed an antioxidant activity and anticancer efficiency of betanin. In this study, we investigated the cytotoxic effects and the possible mechanisms of betanin-induced apoptosis against U87MG human glioma cells and compared the results to those of human normal lymphocytes. MTT assay, caspase-3 activation assays in cells and succinate dehydrogenases (SDH), mitochondrial swelling, reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP), and cytochrome C release assays in isolated mitochondria were obtained from U87MG human glioma cells and noncancerous human lymphocytes The results illustrated the significant cytotoxic effect of betanin on U87MG human glioma cells, with a concentration value that inhibits 50% of the cell growth of 7 µg/ml after 12 h of treatment. MTT assay demonstrated that the betanin is selectively toxic to U87MG human glioma cells, and betanin induced cell apoptosis via activation of caspase-3 along with modulation of apoptosis-related mitochondria. Meanwhile, betanin selectively increased ROS formation, mitochondria swelling, MMP decrease, and cytochrome c release in cancerous mitochondria but in normal mitochondria. Based on the evidence obtained from this study, it is concluded that the betanin is a promising natural compound to fight U87MG human glioma cells via induction of apoptosis through activation of intrinsic pathways.

Multi-drug resistance of Staphylococcus aureus Strains in Baqiyatallah hospital: a Primary Step Towards Digital Health Biomonitoring Systems.

The aim of the study was to evaluate the drug-resistance patterns of Staphylococcus aureus infections in Baqiyatallah hospital within 2010-2019 and to present a novel monitoring and detection system making use of molecular laboratory methods teamed with molecular delimitation analyses. This in turn is a primary step to establishment of a digital health system within Baqiyatallah hospital as a perfect pilot instance for other hospitals to follow upon. Totally, 100 patients of Baqiyatallah hospital suspicious of Staphylococcus aureus infections were sampled. Bacterial identity confirmations were done using routine biochemical test. Antibiograms were made for all the patients in this study. Consequently, bacterial total DNA was extracted and 16S rDNA gene amplified and sequenced for all patients. To uncover any cryptic strain grouping within the samples, a molecular delimitation method, i.e. automated barcode gap discovery (ABGD), was done. Our results showed Ceftaroline to be the most and Erythromycin and Oxacillin the least effective drugs. Delimitation uncovered 19 groups out of which group 19 seemed to have location-specific genetic signals in regards to susceptibility of Erythromycin and Oxacillin. Our results indicate the importance of genetic identification of bacteria with respect to their genetic patterns before antibiotic administration in order to both reduce unnecessary medicine use and to biomonitor the bacterial patterns in respect to their behavior towards general antibiotics.

The effects of Hemiscorpius lepturus induced-acute kidney injury on PGC-1α gene expression: From induction to suppression in mice.

Hemiscorpius lepturus envenomation induces acute kidney injury (AKI) through hemoglubinoria and mitochondrial dysfunction. Mitochondria supports ATP production to promote the regulation of fluid and electrolyte balance. Mitochondrial homeostasis in different metabolic environments can be adjusted by overexpression of PGC-1α. High reactive oxygen species (ROS) production after H. lepturus envenomation and heme oxygenase-1 (HO-1) overexpression causes ATP depletion as well as mitochondrial homeostasis disruption, which lead to progression in renal diseases. The present study aims to evaluate the role of venom induced-AKI in modulating mitochondrial function in cell death and metabolic signaling associated with PPAR-α, PGC-1α, and Nrf-2 as the main transcription factors involved in metabolism. Based on the data, two significant events occurred after envenomation: reduction of gl glutathione level and overexpression of the cytoprotective enzyme HO-1. Apaoptosis induction is associated with a significant decrease in the transcription of PPAR-α, PGC-1α and Nrf-2 after administrating lethal dose of venom (10 mg/kg). Furthermore, at the lower doses of venom (1 and 5 mg/kg), with a significant recovery accompanied with PGC-1α upregulation occurs after AKI. As the findings indicate, PGC-1α has a key role in restoring the mitochondrial function at the recovery phase of mouse model of AKI, which highlights the PGC-1α as a therapeutic target for venom induced-AKI prevention and treatment.