Selenium inhibits ferroptosis in hyperglycemic cerebral ischemia/reperfusion injury by stimulating the Hippo pathway.

Hyperglycemia can exacerbate cerebral ischemia/reperfusion (I/R) injury, and the mechanism involves oxidative stress, apoptosis, autophagy and mitochondrial function. Our previous research showed that selenium (Se) could alleviate this injury. The aim of this study was to examine how selenium alleviates hyperglycemia-mediated exacerbation of cerebral I/R injury by regulating ferroptosis.

Glutamine potentiates gentamicin to kill lab-evolved gentamicin-resistant and clinically isolated multidrug-resistant .

Introduction: Gentamicin is a conventional antibiotic in clinic. However, with the wide use of antibiotics, gentamicin-resistant (E. coli) is an ever-increasing problem that causes infection in both humans and animals.

Oxymatrine Alleviates Hyperglycemic Cerebral Ischemia/Reperfusion Injury via Protecting Microvessel.

Hyperglycemia aggravates cerebral ischemia/reperfusion (I/R) injury via vascular injury. There is still a lack of effective pharmaceutical preparations for cerebral I/R injury under hyperglycemia. This study aimed to investigate the effects of oxymatrine (OMT) on hyperglycemia-exacerbated cerebral I/R injury in vitro and in vivo.

Effect of hyperglycemia on microglial polarization after cerebral ischemia-reperfusion injury in rats.

Hyperglycemia has been shown to aggravate ischemic brain damage, in which the inflammatory reaction induced by hyperglycemia is involved in the worsening of cerebral ischemia-reperfusion injury. However, the role of microglial polarization in hyperglycemia-aggravating cerebral ischemia-reperfusion injury remains unknown. The present study investigated whether diabetic hyperglycemia inhibited or activated microglia, as well as microglial subtypes 1 and 2.

Region-specific changes in aquaporin 4 induced by hyperglycemia underlie the differences in cell swelling in the cortex and striatum after cerebral ischemia-reperfusion.

Brain edema is a major cause of death in patients who suffer an ischemic stroke. Diabetes has been shown to aggravate brain edema after cerebral ischemia-reperfusion, but few studies have focused on the heterogeneity of this response across different brain regions. Aquaporin 4 plays an important role in the formation and regression of brain edema.

The Involvement of Mitochondrial Biogenesis in Selenium Reduced Hyperglycemia-Aggravated Cerebral Ischemia Injury.

Selenium has been shown to possess antioxidant and neuroprotective effects by modulating mitochondrial function and activating mitochondrial biogenesis. Our previous study has also suggested that selenium protected neurons against glutamate toxicity and hyperglycemia-induced damage by regulating mitochondrial fission and fusion. However, it is still not known whether the mitochondrial biogenesis is involved in selenium alleviating hyperglycemia-aggravated cerebral ischemia reperfusion (I/R) injury.

Synaptic remodeling and reduced expression of the transcription factors, HES1 and HES5, in the cortex neurons of cognitively impaired hyperhomocysteinemic mice.

Hyperhomocysteinemia (HHcy) is associated with cognitive impairment and neurodegenerative diseases. The synaptic ultrastructure and the expression of hairy enhancer of split (HES) genes are involved in cognitive impairment induced by HHcy, but their precise role remains unclear. The present study aimed to measure synaptic remodeling and the expression of HES1 and HES5 in the cortex neurons of mice with HHcy to clarify their role in cognitive impairment.

Coenzyme Q10 Protects Astrocytes from Ultraviolet B-Induced Damage Through Inhibition of ERK 1/2 Pathway Overexpression.

Overexpression of extracellular signal-regulated kinase ½ (ERK ½) signaling pathway leads to overproduction of reactive oxygen species (ROS) which induces oxidative stress. Coenzyme Q10 (CoQ10) scavenges ROS and protects cells against oxidative stress. The present study was designed to examine whether the protection of Coenzyme Q10 against oxidative damage in astrocytes is through regulating ERK 1/2 pathway.

Overexpression of selenoprotein H prevents mitochondrial dynamic imbalance induced by glutamate exposure.

Selenium and selenoproteins play important roles in neuroprotection against glutamate‑induced cell damage, in which mitochondrial dysfunction is considered a major pathogenic feature. Recent studies have revealed that mitochondrial fission could activates mitochondrial initiated cell death pathway. The objectives of the study are to determine whether glutamate induced cell death is mediated through mitochondrial initiated cell death pathway and activation of autophagy, and whether overexpression of selenoprotein H can protect cells from glutamate toxicity by preserving mitochondrial morphology and suppressing autophagy.

Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells.

Background: Previous studies have indicated that selenium supplementation may be beneficial in neuroprotection against glutamate-induced cell damage, in which mitochondrial dysfunction is considered a major pathogenic feature. However, the exact mechanisms by which selenium protects against glutamate-provoked mitochondrial perturbation remain ambiguous. In this study glutamate exposed murine hippocampal neuronal HT22 cell was used as a model to investigate the underlying mechanisms of selenium-dependent protection against mitochondria damage.

Interleukin-17A promotes the formation of inflammation in the lung tissues of rats with pulmonary fibrosis.

The aim of the present study was to investigate the effects of interleukin (IL)-17A in a rat model of pulmonary fibrosis. In total, 20 female Wistar rats were randomly divided into a normal saline (NS group) and a bleomycin group (BLM group). The BLM group rats were intratracheally instilled with BLM, while the NS group rats were intratracheally instilled with saline.

Metabolome strategy against Edwardsiella tarda infection through glucose-enhanced metabolic modulation in tilapias.

Edwardsiella tarda causes fish disease and great economic loss. However, metabolic strategy against the pathogen remains unexplored. In the present study, GC-MS based metabolomics was used to investigate the metabolic profile from tilapias infected by sublethal dose of E.

Liver functional metabolomics discloses an action of L-leucine against Streptococcus iniae infection in tilapias.

Streptococcus iniae seriously affects the intensive farming of tilapias. Much work has been conducted on prevention and control of S. iniae infection, but little published information on the metabolic response is available in tilapias against the bacterial infection, and no metabolic modulation way may be adopted to control this disease.

One-Pot Synthesis of Mesoporous TiO₂ Micropheres and Its Application for High-Efficiency Dye-Sensitized Solar Cells.

TiO2 microspheres are of great interest for a great deal of applications, especially in the solar cell field. Because of their unique microstructure and light-scattering effect, TiO2 microsphere-based solar cells often exhibit superior photovoltaic performance. Hence, exploring new suitable TiO2 microspheres for high-efficiency solar cells is essential.

L-proline increases survival of tilapias infected by Streptococcus agalactiae in higher water temperature.

Streptococcosis causes massive tilapia kills, which results in heavy economic losses of tilapia farming industry. Out of the Streptococcosis, Streptococcus agalactiae is the major pathogen. The bacterium causes higher mortality of tilapias in higher than lower temperatures.

N-acetylglucosamine enhances survival ability of tilapias infected by Streptococcus iniae.

Streptococcus iniae infection has emerged as a serious fish health and economic problem in the global aquaculture operations. Current antibiotic options are few and possess severe practical limitations and potential adverse environmental impacts. The major factor contributing to the large burden of S.

Effect of matrine on transforming growth factor β1 and hepatocyte growth factor in rat liver fibrosis model.

Objective: To observe the preventive and control effect of matrine on transforming growth factor (TGF-β1) and hepatocyte growth factor (HGF) of liver fibrosis tissue in rats.

Methods: A total of 48 SD rats were randomly divided into A, B, C, D groups with 12 in each, group A as the normal control group and groups B, C, D as liver fibrosis models using composite modulus method with carbon tetrachloride (CCL4). Group B was the model group, group C adopted γ-interferon lavage therapy in the second day of modeling, and group D adopted matrine lavage treatment, at 4 and 8 weeks after treatment.

Analysis of factors affecting the life quality of the patients with late stomach cancer.

Aims And Objectives: To provide a theoretical basis for the clinical care of patients with late stomach cancer, we investigated the life quality and analysed its related factor in the patients with late stomach cancer.

Background: Due to the lack of effective screening methods, stomach cancer usually has been in the advanced stage when patients are diagnosed. However, the treatment for late stomach cancer is a tough problem in today's medicine.

[Raman characterization of high-pressure phase transition in AlN nanowires].

High-pressure phase transition of AlN nanowires was investigated in the range of 0-33.1 GPa by in situ Raman spectrum method in diamond anvil cell (DAC). The A1 (LO) vibration mode exhibits considerably asymmetry and broadening, indicating the occurrence of wurtzite-to-rocksalt phase transition.

[Relationship between millimeter wave irradiation in pregnant mice and c-Fos protein expression in hippocampus and learning and memory functions in their offsprings].

Objective: To determine the threshold of millimeter wave irradiation for fetal injury in mice and the mechanism of decrease of learning and memory function in their offsprings and to verify whether the millimeter wave has the non-thermal effect.

Methods: Pregnant mice were irradiated by millimeter wave with frequencies of 37.4, 42.

Iron loading inhibits ferroportin1 expression in PC12 cells.

Ferroportin1 (FP1 or MTP1/IREG1), the product of the SLC40A1 gene, is a main iron export protein in mammals. Its mRNA contains an iron response element (IRE) in its 5' untranslated region, but the way this gene is regulated by iron is still unclear. The existence of FP1 in the brain has been recently confirmed.