Comprehensive Analysis of Bulk RNA-Seq and Single-Cell RNA-Seq Data Unveils Sevoflurane-Induced Neurotoxicity Through SLC7A11-Associated Ferroptosis.

Sevoflurane's potential impact on cognitive function and neurodevelopment, especially in susceptible populations such as infants and the elderly, has raised widespread concern. This study focuses on how sevoflurane induces ferroptosis in astrocytes and identifies solute carrier family 7 member 11 (SLC7A11) as a mediator of ferroptosis, providing new insights into sevoflurane-related neurotoxic pathways. We analysed single-cell sequencing (scRNA-seq) data from sevoflurane-exposed mice and control mice, supplemented with bulk RNA-seq data, to assess gene expression alterations.

Identification of differential immune cells and related diagnostic genes in patients with diabetic retinopathy.

Background: Diabetic retinopathy (DR) is a frequent microvascular abnormality associated with diabetes mellitus. The loss of retinal immunity is an important underlying mechanism of the DR pathogenesis, including the change in retinal immunosuppressive characteristics and the blood-retinal barrier disturbances. Therefore, this investigation screens immune-associated biomarkers in the retina of DR patients.

SRY-box transcription factor 9 modulates Müller cell gliosis in diabetic retinopathy by upregulating TXNIP transcription.

Diabetic retinopathy (DR), a common complication of diabetes, involves excessive proliferation and inflammation of Muller cells and ultimately leads to vision loss and blindness. SRY-box transcription factor 9 (SOX9) has been reported to be highly expressed in Müller cells in light-induced retinal damage rats, but the functional role of SOX9 in DR remains unclear. To explore this issue, the DR rat model was successfully constructed via injection with streptozotocin (65 mg/kg) and the retinal thicknesses and blood glucose levels were evaluated.

The roles of miRNA, lncRNA and circRNA in the development of osteoporosis.

Osteoporosis is a common metabolic bone disease, influenced by genetic and environmental factors, that increases bone fragility and fracture risk and, therefore, has a serious adverse effect on the quality of life of patients. However, epigenetic mechanisms involved in the development of osteoporosis remain unclear. There is accumulating evidence that epigenetic modifications may represent mechanisms underlying the links of genetic and environmental factors with increased risk of osteoporosis and bone fracture.

Citrate pretreatment attenuates hypoxia/reoxygenation-induced cardiomyocyte injury via regulating microRNA-142-3p/Rac1 aix.

Citrate has a positive effect on improving the pathophysiological changes of cardiomyocytes such as cardiac failure and auricular fibrillation. However, the underlying mechanism remains still unclear. Rat cardiomyocytes were used to establish hypoxia/reoxygenation (H/R) cell model.

Long non‑coding RNA H19 protects H9c2 cells against hypoxia‑induced injury by activating the PI3K/AKT and ERK/p38 pathways.

Myocardial ischemia/reperfusion injury often leads to adverse cardiovascular outcomes due to severe hypoxia. The present study aimed to evaluate the effects and mechanism of long non‑coding RNA H19 (H19) on rat H9c2 cells with hypoxia‑induced injury. H9c2 cells were infected with lentiviruses to express H19 or H19‑targeting short hairpin RNA (shRNA), or their respective controls, at a multiplicity of infection of 1:100.

CCR7/p-ERK1/2/VEGF signaling promotes retinal neovascularization in a mouse model of oxygen-induced retinopathy.

Aim: To investigate the role of CCR7/p-ERK1/2/VEGF signaling in the mouse model of oxygen-induced retinopathy (OIR).

Methods: Neonatal C57BL/6J mice were evenly randomized into four groups: normoxia, OIR, OIR control (treated with scramble siRNA), and OIR treated (treated with CCR7 siRNA). Normoxia group was not specially handled.

Efficacy and safety of vitamin C for atrial fibrillation after cardiac surgery: A meta-analysis with trial sequential analysis of randomized controlled trials.

Objectives: Antioxidant supplement is an option in preventing postoperative atrial fibrillation (AF) after cardiac surgery. However, the benefits and adverse effects of vitamin C have not been well assessed. We aimed to systematically evaluate the efficacy and safety of vitamin C in preventing postoperative AF in adult patients after cardiac surgery.

Intrathecal Administration of Flavopiridol Promotes Regeneration in Experimental Model of Spinal Cord Injury.

Aim: Spinal cord injury (SCI) is a serious condition of the central nervous system and it affects the quality of life and even hampers the day-to-day activity of the patient. In the current study, we investigated the efficacy of intrathecal administration of flavopiridol in an experimental animal model of SCI. The study also aimed at exploring the physiological effects of flavopiridol on neurons, astrocytes and cell cycle regulatory proteins.

Protective Effect of Sevoflurane Postconditioning against Cardiac Ischemia/Reperfusion Injury via Ameliorating Mitochondrial Impairment, Oxidative Stress and Rescuing Autophagic Clearance.

Background And Purpose: Myocardial infarction leads to heart failure. Autophagy is excessively activated in myocardial ischemia/reperfusion (I/R) in rats. The aim of this study is to investigate whether the protection of sevoflurane postconditioning (SPC) in myocardial I/R is through restored impaired autophagic flux.

Potential therapeutic effects of neurotrophins for acute and chronic neurological diseases.

The neurotrophins (NTs) nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), NT-3, and NT-4/5 are proteins that regulate cell proliferation, differentiation, and survival in both the developing and mature central nervous system (CNS) by binding to two receptor classes, Trk receptors and p75 NTR. Motivated by the broad growth- and survival-promoting effects of these proteins, numerous studies have attempted to use exogenous NTs to prevent the death of cells that are associated with neurological disease or promote the regeneration of severed axons caused by mechanical injury. Indeed, such neurotrophic effects have been repeatedly demonstrated in animal models of stroke, nerve injury, and neurodegenerative disease.