MiR-106a-5p targets PFKFB3 and improves sepsis through regulating macrophage pyroptosis and inflammatory response.

The enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase isoform 3 (PFKFB3) is a critical regulator of glycolysis and plays a key role in modulating the inflammatory response, thereby contributing to the development of inflammatory diseases such as sepsis. Despite its importance, the development of strategies to target PFKFB3 in the context of sepsis remains challenging. In this study, we employed a microRNA-based approach to decrease PFKFB3 expression. Through multiple meta-analyses, we observed a downregulation of miR-106a-5p expression and an upregulation of PFKFB3 expression in clinical sepsis samples. These changes were also confirmed in blood monocytes from patients with early sepsis and from a mouse model of lipopolysaccharide (LPS)-induced sepsis. Overexpression of miR-106a-5p significantly decreased the LPS-induced increase in glycolytic capacity, inflammatory response, and pyroptosis in macrophages. Mechanistically, we identified PFKFB3 as a direct target protein of miR-106a-5p and demonstrated its essential role in LPS-induced pyroptosis and inflammatory response in macrophages. Furthermore, treatment with agomir-miR-106a-5p conferred a protective effect in an LPS mouse model of sepsis, but this effect was attenuated in myeloid-specific Pfkfb3 knockout mice. These findings indicate that miR-106a-5p inhibits macrophage pyroptosis and inflammatory response in sepsis by regulating PFKFB3-mediated glucose metabolism, representing a potential therapeutic option for the treatment of sepsis.

Highly-sensitive optical thermometer developed based on an intervalence charge transfer mashup.

Optical thermometers based on lanthanide thermal-coupled levels have attracted great attention owing to its fundamental importance in the fields of public health, biology, and integrated circuit. However, the inherent structural properties (shielded effect on 4f configurations, intense non-radiation relaxation) strictly suppress the sensing performance, limiting the relative temperature sensitivity (SR). To circumvent these limitations, we propose an intervalence charge transfer mashup strategy by inducing d0 electron configured transition metals. Specifically, transition metals Ta5+ is incorporated in Tm3+/Eu3+:LiNbO3, which improves the SR from 5.30 to 11.16% K-1. The validity of this component-modulation behavior is observed on other oxide crystals (NaY(Mo1-zWzO4)2) as well. Furthermore, the observed regulation is well explained by DFT calculation that indicates the d-orbit component at valence band minimum remains the core factor governing the electron transfer process. We successfully relate the SR to the band structure of luminescence carrier, offering a novel perspective for the collocation design of lanthanide configurations.

Chromium immobilization from wastewater via iron-modified hydrochar: Different iron fabricants and practicality assessment.

The recycling of industrial solid by-products such as red mud (RM) has become an urgent priority, due to their large quantities and lack of reutilization methods can lead to resource wastage. In this work, RM was employed to fabricate green hydrochar (HC) to prepare zero-valent iron (ZVI) modified carbonous materials, and conventional iron salts (IS, FeCl3) was applied as comparison, fabricated HC labeled as RM/HC and IS/HC, respectively. The physicochemical properties of these HC were comprehensively characterized. Further, hexavalent chromium (Cr(VI)) removal performance was assessed (375.66 and 337.19 mg/g for RM/HC and IS/HC, respectively). The influence of dosage and initial pH were evaluated, while isotherms, kinetics, and thermodynamics analysis were also conducted, to mimic the surface interactions. The stability and recyclability of adsorbents also verified, while the practical feasibility was assessed by bok choy-planting experiment. This work revealed that RM can be used as a high value and green fabricant for HC the effective removal of chromium contaminants from the wastewater.

Comparisons of procedural characteristics and clinical outcomes between SMARTTOUCH SURROUNDFLOW catheter and other catheters for atrial fibrillation radiofrequency catheter ablation: a systematic literature review.

BACKGROUND: SMARTTOUCH SURROUNDFLOW (STSF) catheter is the new generation of SMARTTOUCH (ST) catheter with an upgraded irrigation system for radiofrequency catheter ablation (RFCA) in patients with atrial fibrillation (AF). METHODS: This systematic literature review searched the major English and Chinese bibliographic databases from 2016 to 2022 for any original clinical studies assessing the STSF catheter for RFCA in AF patients. Meta-analysis with a random effects model was used for evidence synthesis. RESULTS: Pooled outcomes from 19 included studies indicated that STSF catheter was associated with a significantly shorter procedure time (weighted mean difference (WMD): -17.4 min, p<0.001), shorter ablation time (WMD: -6.6 min, p<0.001) and lower catheter irrigation fluid volume (WMD: -492.7 mL, p<0.001) than ST catheter. Pooled outcomes from four included studies with paroxysmal AF patients reported that using the STSF catheter for RFCA was associated with a significantly shorter ablation time (WMD: -5.7 min, p<0.001) and a lower risk of 1-year postablation arrhythmia recurrence (rate ratio: 0.504, p<0.001) than the SURROUNDFLOW (SF) catheter. Significant reductions in procedure time and ablation time associated with the STSF catheter were also reported in the other four studies using non-ST/SF catheters as the control. Overall complications of STSF catheter and control catheters were comparable. CONCLUSIONS: Using the STSF catheter was superior to using the ST catheter to conduct RFCA for AF by significantly reducing procedure time, ablation time, fluoroscopy time and irrigation fluid volume. The superiority of the STSF catheter over the SF catheter and other non-ST/SF catheters for RFCA needs further confirmation.

Puerarin prevents sepsis-associated encephalopathy by regulating the AKT1 pathway in microglia.

BACKGROUND: Previous studies have reported that puerarin possesses cardioprotective, vasodilatory, anti-inflammatory, anti-apoptotic, and hypoglycemic properties. However, the impact of puerarin on sepsis-associated encephalopathy (SAE) remains unexplored. In this study, we explored whether puerarin can modulate microglia-mediated neuroinflammation for the treatment of SAE and delved into the underlying mechanisms. METHODS: We established a murine model of SAE through intraperitoneal injection of lipopolysaccharide (LPS). The puerarin treatment group received pretreatment with puerarin. For in vitro experiments, BV2 cells were pre-incubated with puerarin for 2 h before LPS exposure. We employed network pharmacology, the Morris Water Maze (MWM) test, Novel Object Recognition (NOR) test, immunofluorescence staining, enzyme-linked immunosorbent assay (ELISA), Western blotting, and quantitative real-time PCR (qRT-PCR) to elucidate the molecular mechanism of underlying puerarin's effects in SAE treatment. RESULTS: Our findings demonstrate that puerarin significantly reduced the production of inflammatory cytokines (TNF-α and IL-6) in the peripheral blood of LPS-treated mice. Moreover, puerarin treatment markedly ameliorated sepsis-associated cognitive impairment. Puerarin also exhibited inhibitory effects on the release of TNF-α and IL-6 from microglia, thereby preventing hippocampal neuronal cell death. Network pharmacology analysis identified AKT1 as a potential therapeutic target for puerarin in SAE treatment. Subsequently, we validated these results in both in vitro and in vitro experiments. Our study conclusively demonstrated that puerarin reduced LPS-induced phosphorylation of AKT1, with the AKT activator SC79 reversing puerarin's anti-inflammatory effects through the activation of the AKT1 signaling pathway. CONCLUSION: Puerarin exerts an anti-neuroinflammatory effect against SAE by modulating the AKT1 pathway in microglia.

Field investigation of the heat stress in outdoor of healthcare workers wearing personal protective equipment in South China.

Since the advent of coronavirus disease 2019 (COVID-19), healthcare workers (HCWs) wearing personal protective equipment (PPE) has become a common phenomenon. COVID-19 outbreaks overlap with heat waves, and healthcare workers must unfortunately wear PPE during hot weather and experience excessive heat stress. Healthcare workers are at risk of developing heat-related health problems during hot periods in South China. The investigation of thermal response to heat stress among HCWs when they do not wear PPE and when they finish work wearing PPE, and the impact of PPE use on HCWs' physical health were conducted. The field survey were conducted in Guangzhou, including 11 districts. In this survey, HCWs were invited to answer a questionnaire about their heat perception in the thermal environment around them. Most HCWs experienced discomfort in their back, head, face, etc., and nearly 80% of HCWs experienced "profuse sweating." Up to 96.81% of HCWs felt "hot" or "very hot." The air temperature had a significant impact on thermal comfort. Healthcare workers' whole thermal sensation and local thermal sensation were increased significantly by wearing PPE and their thermal sensation vote (TSV) tended towards "very hot." The adaptive ability of the healthcare workers would decreased while wearing PPE. In addition, the accept range of the air temperature (T a) were determined in this investigation. Graphical Abstract.

Individuals with T-786C and G894T genotypes of eNOS in Chinese Han population have an increased risk of developing rheumatoid arthritis.

Several genetic polymorphisms in endothelial nitric oxide synthase (eNOS) are associated with the pathogenesis of rheumatoid arthritis (RA). This study explored the effect of eNOS gene polymorphism on genetic susceptibility of RA in Chinese Han population. Patients with RA (n=236) and healthy volunteers (n=240) were enrolled in this study. Genotyping of eNOS T-786C and G894T polymorphisms was performed by polymerase chain reaction-restriction fragment length polymorphism. Genotyping and gene frequency distribution of eNOS T-786C and G894T polymorphisms were evaluated. RA patients showed higher frequencies of mutated TC and CC genotypes of eNOS T-786C polymorphism and mutated GT and TT genotypes of G894T polymorphism than healthy controls. More specifically, the genotype frequencies of eNOS T-786C polymorphism were significantly different between RA patients and controls. The expression of eNOS was enhanced in RA patients compared with controls. Further, eNOS expression was enhanced after C was replaced with T in T-786C polymorphism in the promoter. Overall, the individuals with mutations in T-786C and G894T of eNOS may have an increased risk of RA, and T-786C and G894T polymorphisms of eNOS are associated with genetic susceptibility of RA in Chinese Han population.

Activated AMPK-mediated glucose uptake and mitochondrial dysfunction is critically involved in the glutamate-induced oxidative injury in HT22 cell.

BACKGROUND: Accumulation of glutamate damages neurons via the reactive oxygen species (ROS) injury, which was involved in the development of neurodegenerative diseases. However, the mechanism of neuronal oxidative stress damage caused by glutamate and the intervention targets still needs to be further studied. This study explored whether 5' adenosine monophosphate-activated protein kinase (AMPK)-induced glucose metabolic and mitochondrial dysfunction were related to glutamate-dependent ROS injury of the neuron. METHODS: Neuronal oxidative stress injury was induced by glutamate treatment in HT-22 cells. Western blotting was used to evaluate the phosphorylation of the AMPK. The XF24 Flux Analyzer was used to measure the effect of glutamate and Compound C (a well-known pharmacological inhibitor of AMPK phosphorylation) on the cellular oxygen consumption rate (OCR) of HT-22 cells. Glucose uptake, intracellular ROS, mitochondrial potential, apoptosis and cell viability were quantified using biochemical assays. RESULTS: Glutamate caused the phosphorylation of AMPK and subsequently promoted the glucose uptake. Furthermore, AMPK-mediated glucose uptake enhanced OCR and increased the intracellular ROS levels in neurons. The pharmacological inhibition of AMPK phosphorylation by Compound C attenuated glutamate-induced toxicity in HT22 cells by regulating the glucose uptake/mitochondrial respiration/ROS pathway. CONCLUSIONS: The AMPK phosphorylation/glucose uptake/mitochondrial respiration/ROS pathway was involved in glutamate-induced excitotoxic injury in HT22 cells. The inhibition of AMPK phosphorylation may be a potential target for the development of therapeutic agents for treating the glutamate-induced neurotoxicity.

Ionizing radiation-induced DNA damage responses affect cell compressibility.

Radiotherapy is an important treatment modality for cancer patients. Ionizing radiation kills cancer cells by inducing DNA damage. However, it remains unclear how this process affects the biomechanical properties of cells and how cellular mechanics affect DNA damage and repair. In this study, the effects of ionizing radiation on cell mechanics were investigated by precisely measuring the compressibility of cells in suspension using an in-house developed microfluidic device. We found that cell compressibility significantly increased after irradiation, depending on cell type and radiation dose. Radiation-induced DNA damage response (DDR) is an important process that alters cell mechanics, and this association was confirmed experimentally by inhibiting the DDR process. Furthermore, the mechanisms involved in changes in cell compressibility were investigated from the perspective of the nucleus and cytoplasm. Experiments showed that radiation reduced H3K9me3 staining intensity but had no effect on F-actin. This suggested that chromatin decondensation caused by radiation-induced DDR is the primary cause of changes in cell compressibility after radiation. The effects of cell mechanics on radiation-induced DNA damage were also investigated. The addition of blebbistatin reduced cytoskeletal forces on the nucleus, which resulted in a reduction in radiation-induced DNA damage. Collectively, this study elucidated reciprocal mechanisms of radiation-induced DNA damage and cell mechanics.

N-acetylcysteine for chronic kidney disease: a systematic review and meta-analysis.

OBJECTIVE: The present study aimed to evaluate the safety and benefits of N-acetylcysteine (NAC) for chronic kidney disease (CKD) through a systematic review and meta-analysis. METHODS AND MATERIALS: We performed a literature search until 5 May 2020 in the CENTRAL, MEDLINE, EMBASE, CINAHL, Clinical Trials Registry Platform and CBM. Two reviewers independently identified eligible articles and extract data. The risk of bias and publication bias were evaluated in all included trials and Cochrane Collaboration's RevMan5.3 software was used for data analysis. Fifteen trials (20 articles) involving a total of 768 patients were included. RESULTS: The summary results of the studies showed that NAC did reduce cardiovascular events among people with CKD, the RR was 0.60, and the number that needs to be treated (NNT) was 5.29. Pooled date of estimated glomerular filtration rate (eGFR) and serum creatinine (Scr) in the NAC group were better than those in the placebo group. No patients in all studies were terminated due to side effect. Subgroup analysis also showed that inflammatory cytokines and homocysteine were significantly lower in NAC group. CONCLUSION: These results suggested that NAC appears to be safe without obvious adverse events, which can also benefit kidney function, relieve inflammation and reduce cardiovascular events among people with CKD.

Artemisinin improves neurocognitive deficits associated with sepsis by activating the AMPK axis in microglia.

Sepsis is life-threatening organ dysfunction due to dysregulated systemic inflammatory and immune response to infection, often leading to cognitive impairments. Growing evidence shows that artemisinin, an antimalarial drug, possesses potent anti-inflammatory and immunoregulatory activities. In this study we investigated whether artemisinin exerted protective effect against neurocognitive deficits associated with sepsis and explored the underlying mechanisms. Mice were injected with LPS (750 µg · kg-1 · d-1, ip, for 7 days) to establish an animal model of sepsis. Artemisinin (30 mg · kg-1 · d-1, ip) was administered starting 4 days prior LPS injection and lasting to the end of LPS injection. We showed that artemisinin administration significantly improved LPS-induced cognitive impairments assessed in Morris water maze and Y maze tests, attenuated neuronal damage and microglial activation in the hippocampus. In BV2 microglial cells treated with LPS (100 ng/mL), pre-application of artemisinin (40 µΜ) significantly reduced the production of proinflammatory cytokines (i.e., TNF-α, IL-6) and suppressed microglial migration. Furthermore, we revealed that artemisinin significantly suppressed the nuclear translocation of NF-κB and the expression of proinflammatory cytokines by activating the AMPKα1 pathway; knockdown of AMPKα1 markedly abolished the anti-inflammatory effects of artemisinin in BV2 microglial cells. In conclusion, atemisinin is a potential therapeutic agent for sepsis-associated neuroinflammation and cognitive impairment, and its effect is probably mediated by activation of the AMPKα1 signaling pathway in microglia.

A novel versatile instrument for combined studies of persistent luminescence, thermoluminescence, and mechanoluminescence in micro-scale.

This paper presents a new method for combined measurements of persistent luminescence (PersL), thermoluminescence (TL), and mechanoluminescence (ML) of luminescent materials in the micrometer scale. Both the hardware and software designs have been illustrated in detail, and the experimental procedures to execute the emission map, PersL, TL, and ML measurements have been demonstrated. The PersL, TL, and ML properties of the SrAl2O4:Eu2+, Dy3+ micropowder, as well as the corresponding temperature variable emission spectra, have been measured. The results show good agreement with published investigations, indicating the accomplishment of designed functions. The instrument would be a powerful tool for exploring phosphorescent materials in the micrometer and smaller scales.

Silencing of circFoxO3 Protects HT22 Cells from Glutamate-Induced Oxidative Injury via Regulating the Mitochondrial Apoptosis Pathway.

Recent studies demonstrated that FoxO3 circular RNA (circFoxO3) plays an important regulatory role in tumourigenesis and cardiomyopathy. However, the role of circFoxO3 in neurodegenerative diseases remains unknown. The aim of this study was to examine the possible role of circFoxO3 in neurodegenerative diseases and the underlying mechanisms. To model human neurodegenerative conditions, hippocampus-derived neurons were treated with glutamate. Using molecular and cellular biology approaches, we found that circFoxO3 expression was significantly higher in the glutamate treatment group than that in the control group. Furthermore, silencing of circFoxO3 protected HT22 cells from glutamate-induced oxidative injury through the inhibition of the mitochondrial apoptotic pathway. Collectively, our study demonstrates that endogenous circFoxO3 plays a key role in inducing apoptosis and neuronal cell death and may act as a novel therapeutic target for neurodegenerative diseases.

Acute-phase serum superoxide dismutase level as a predictive biomarker for stroke-associated infection.

Background and Purpose: Oxidative stress is involved in the development of infections. However, whether oxidative stress indicators can be used as markers of stroke-associated infection (SAI) is still unclear. The purpose of this study was to test the predictive values of superoxide dismutase (SOD) and malondialdehyde (MDA) levels for SAI incidence.Methods: A total of 45 consecutive patients with ischemic stroke who were admitted to our hospital were enrolled. A prospective study was carried out to observe the occurrence of SAI during the first 7 days after stroke. Accordingly, the patients were divided into SAI and non-SAI groups. The relationship between SOD and MDA serum levels and SAI was analyzed.Results: The patients in the SAI group had significantly higher serum SOD levels than those in the non-SAI group (41.638 ± 3.428 U/ml vs. 36.542 ± 9.114 U/ml, p = 0.033). However, there were no significant differences in MDA levels between the SAI and non-SAI group (p > 0.05). The discriminating ability of serum SOD level for SAI was measured using an ROC curve. Serum level of SOD >38.16 U/ml was useful in diagnosing SAI with a sensitivity of 88% and a specificity of 61%. Kaplan-Meier curves showed that the group with serum SOD level >38.16 U/ml had higher rates of SAI incidence (χ2 = 9.688, p = 0.002; log rank test). Furthermore, Cox regression analysis indicated that a serum SOD level >38.16 U/ml was an independent risk factor for SAI (hazard ratio = 5.836; 95% CI, 1.298-26.244; p = 0.021).Conclusions: Acute-phase serum SOD level could be a predictor of SAI.

Astrocytic damage in glial fibrillary acidic protein astrocytopathy during initial attack.

OBJECTIVE: Determination of glial fibrillary acidic protein (GFAP), aquaporin 4 (AQP4), and myelin oligodendrocyte glycoprotein (MOG) levels in cerebrospinal fluid (CSF), and astrocytic damage analysis in patients with GFAP astrocytopathy (GFAP-A) and other conditions. METHODS: GFAP, AQP4, and MOG levels in CSF were detected via enzyme-linked immunosorbent assays. Anti-GFAP, anti-AQP4, and anti-MOG IgGs were detected via indirect immunofluorescence assays. RESULTS: In 32 GFAP-Astrocytopathy patients, CSF GFAP was significantly higher during acute exacerbation than it was in patients with MOG encephalomyelitis, multiple sclerosis, autoimmune encephalitis, and an "other inflammatory neurological disorders" group (all p < 0.0001). CSF GFAP levels were slightly higher in the GFAP-A group than in an anti-AQP4 IgG-positive neuromyelitis optica spectrum disorder group (p = 0.012). There were no significant differences between the CSF MOG and AQP4 levels in the GFAP-A group and those of other groups. CSF GFAP levels were significantly reduced after steroid treatment (p = 0.011). CSF GFAP levels differed significantly in GFAP-Astrocytopathy patients with and without encephalitis (p = 0.016). In GFAP-Astrocytopathy patients, CSF GFAP was correlated with Expanded Disability Status Scale (EDSS) score during attack (r = 0.545, p = 0.001). In follow-up examinations however, in GFAP-Astrocytopathy patients CSF GFAP level was not correlated with EDSS score 6 months later. CONCLUSIONS: CSF GFAP level and pathological examination of GFAP-Astrocytopathy patients revealed astrocyte damage. CSF GFAP level was associated with steroid treatment at the acute stage, therefore CSF GFAP may be a sensitive biomarker with respect to the effects of therapy during the acute stage.

Derivation of a Prediction Rule for Unfavorable Outcome after Ischemic Stroke in the Chinese Population.

BACKGROUND: Efficient assessment of patients after ischemic stroke has important reference value for doctors to choose appropriate treatment for patients. Our study aimed to develop a new prognostic model for predicting outcomes 3 months after ischemic stroke among Chinese Population. METHODS: A prospective observational cohort study among ischemic stroke patients presenting to Emergency Department in the Second Affiliated Hospital of Guangzhou Medical University was conducted from May 2012 to June 2013. Demographic data of ischemic stroke patients, assessment of NIHSS and laboratory results were collected. Based on 3-month modified Rankin Scale (mRS) ischemic stroke patients were divided into either favorable outcome (mRS: 0-2) or unfavorable outcome groups (mRS: 3-6). The variables closely associated with prognosis of ischemic stroke were selected to develop the new prognostic model (NAAP) consisted of 4 parameters: NIHSS, age, atrial fibrillation, and prealbumin. The prognostic value of the modified prognostic model was then compared with NIHSS alone. RESULTS: A total of 454 patients with suspected stroke were recruited. One hundred eighty-six patients with ischemic stroke were included in the final analysis. A new prognostic model, NAAP was developed. The area under curve (AUC) of NAAP was .861 (95%confidence interval: .803-.907), whilst the AUC of NIHSS was .783 (95%CI: .717-.840), (P = .0048). Decision curve analysis showed that NAAP had a higher net benefit for threshold probabilities of 65% for predictive risk of poor outcomes. CONCLUSIONS: The modified prognostic model, NAAP may be a better prognostic tool for predicting 3-month unfavorable outcomes for ischemic stroke than NIHSS alone.

Serum PPARγ level and PPARγ gene polymorphism as well as severity and prognosis of brain injury in patients with arteriosclotic cerebral infarction.

The aim of the study was to study the serum peroxisome proliferator-activated receptor gamma (PPARγ) level and PPARγ gene polymorphism as well as the severity and prognosis of brain injury in patients with arteriosclotic cerebral infarction (ACI). A total of 246 ACI patients presenting at the Department of Neurology of Zengcheng District People's Hospital of Guangzhou between April 2009 and July 2015 were selected as the case group, and 382 control subjects were enrolled as the control group. The hepatic and renal functions and homocysteine (Hcy) expression levels were measured. Enzyme-linked immunosorbent assay (ELISA) kit was used to detect the serum PPARγ levels of the ACI patients. Polymerase chain reaction-restriction fragment length polymorphism method was applied to measure the PPARγ gene polymorphism. The proportions of hypertension patients, diabetes patients and smoking people in the case group were significantly higher than those in the control group. The levels of cholesterol and fasting blood glucose in the case group were elevated obviously compared with those in the control group. The levels of indexes related to the hepatic function and renal function in the case group were remarkably higher than those in the control group. The serum PPARγ levels were increased progressively at acute stage. The distribution frequencies of PPARγ genotypes CC, CT and TT in the case group were higher than those in the control group; compared with that in the control group, the proportion of C allele in the case group was raised obviously, while that of T allele was significantly decreased. The serum PPARγ level has a close correlation with the PPARγ gene polymorphism in ACI patients, and PPARγ is also remarkably related to the severity of brain injury; therefore, PPARγ has great significance in the diagnosis and treatment of cerebral infarction.

Temperature-Dependent and Threshold Behavior of Sm3+ Ions on Fluorescence Properties of Lithium Niobate Single Crystals.

Temperature-dependent and threshold behavior of Sm3+ ions on fluorescence properties of lithium niobate (LiNbO3, LN) single crystals were systematically investigated. The test materials, congruent LiNbO3 single crystals (Sm:LN), with various concentrations of doped Sm3+ ions from 0.2 to 2.0 mol.%, were grown using the Czochralski technique. Absorption spectra were obtained at room temperature, and photoluminescence spectra were measured at various temperatures in the range from 73 K to 423 K. Judd⁻Ofelt theory was applied to calculate the intensity parameters Ωt (t = 2, 4, 6) for 1.0 mol.% Sm3+-doped LiNbO3, as well as the radiative transition rate, Ar, branching ratio, ß, and radiative lifetime, τr, of the fluorescent 4G5/2 level. Under 409 nm laser excitation, the photoluminescence spectra of the visible fluorescence of Sm3+ mainly contains 568, 610, and 651 nm emission spectra, corresponding to the energy level transitions of 4G5/2→6H5/2, 4G5/2→6H7/2, and 4G5/2→6H9/2, respectively. The concentration of Sm3+ ions has great impact on the fluorescence intensity. The luminescence intensity of Sm (1.0 mol.%):LN is about ten times as against Sm (0.2 mol.%):LN at 610 nm. The intensity of the fluorescence spectra were found to be highly depend on temperature, as well as the concentration of Sm3+ ions in LiNbO3 single crystals, as predicted; however, the lifetime changed little with the temperature, indicating that the temperature has little effect on it, in Sm:LN single crystals. Sm:LN single crystals, with orange-red emission spectra, can be used as the active material in new light sources, fluorescent display devices, UV-sensors, and visible lasers.

Artemisinin Prevents Glutamate-Induced Neuronal Cell Death Via Akt Pathway Activation.

Artemisinin is an anti-malarial drug that has been in use for almost half century. Recently, novel biological effects of artemisinin on cancer, inflammation-related disorders and cardiovascular disease were reported. However, neuroprotective actions of artemisinin against glutamate-induced oxidative stress have not been investigated. In the current study, we determined the effect of artemisinin against oxidative insult in HT-22 mouse hippocampal cell line. We found that pretreatment of artemisinin declined reactive oxygen species (ROS) production, attenuated the collapse of mitochondrial membrane potential induced by glutamate and rescued HT-22 cells from glutamate-induced cell death. Furthermore, our study demonstrated that artemisinin activated Akt/Bcl-2 signaling and that neuroprotective effect of artemisinin was blocked by Akt-specific inhibitor, MK2206. Taken together, our study indicated that artemisinin prevented neuronal HT-22 cell from glutamate-induced oxidative injury by activation of Akt signaling pathway.

IL-17A Enhances Microglial Response to OGD by Regulating p53 and PI3K/Akt Pathways with Involvement of ROS/HMGB1.

Cerebral ischemia-reperfusion injury (IRI) has a complex pathogenesis, and interleukin-17 (IL-17) is a newly identified class of the cytokine family that plays an important role in ischemic inflammation. An oxygen-glucose deprivation (OGD) model showed that IL-17A expression was significantly up-regulated in microglial cells. After IL-17A siRNA transfection, the inhibition of proliferation, and the increased apoptosis in microglial cells, induced by OGD/reperfusion, was improved, and the elevation of Caspase-3, Caspase-8, Caspase-9, and poly ADP ribose polymerase (PARP) activities was inhibited. Mass spectrometry demonstrated that IL-17A functioned through a series of factors associated with oxidative stress and apoptosis and regulated Caspase-3 activity and apoptosis in microglial cells via the p53 and PI3K/Akt signaling pathways. IL-17A, HMGB1, and ROS were regulated mutually to exhibit a synergistic effect in the OGD model of microglial cells, but the down-regulation of IL-17A or HMGB1 expression did not completely inhibit the production of ROS. These findings demonstrated that ROS might be located upstream of IL-17A and HMGB1 so that ROS can regulate HMGB1/IL-17A expression to affect the p53 and PI3K/Akt signaling pathways and therefore promote the occurrence of apoptosis in microglial cells. These findings provide a novel evidence for the role of IL-17A in ischemic cerebral diseases.