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The utilization of perovskites as photocatalysts to convert CO2 into fuels and chemicals has received wide attention recently. However, their instability in water hinders their long-term application for overall photocatalytic CO2 reduction. Herein, we integrate the water-stable perovskite-like organolead iodide crystalline material [Pb8I8(H2O)3]8+[−O2C(CH2)4CO2−]4 (TJU-16) with Au co-catalyst for photocatalytic CO2 reduction in aqueous solution without sacrificial reagent. Under the AM 1.5 G simulated illumination, the TJU-16 with 0.19 wt.‰ Au co-catalyst steadily generated electrons for CO2 reduction reaction, which was 2.2 times of pure TJU-16. The Au0.19/TJU-16 catalyzed CO2 reduction at a rate of 84.2 µmol·g−1·h−1, and achieved a solar-to-fuel (STF) conversion efficiency of 0.034%. Our work will motivate the rational design of water-stable perovskite-like materials for photocatalytic applications. [ABSTRACT FROM AUTHOR]

10.3892/or.2011.1489 2 Li Y, Zhang J, Zhao M. Single-wall carbon nanohorns (SWNHs) inhibited proliferation of human glioma cells and promoted its apoptosis. B Retraction Note: Nanoscale Research Letters 2013, 8:100 b https://doi.org/10.1186/1556-276X-8-100 The Editors-in-Chief have retracted this article. [Extracted from the article]

Traumatic brain injury (TBI) triggers the activation of the endogenous coagulation mechanism, and a large amount of thrombin is released to curb uncontrollable bleeding through thrombin receptors, also known as protease-activated receptors (PARs). However, thrombin is one of the most critical factors in secondary brain injury. Thus, the PARs may be effective targets against hemorrhagic brain injury. Since the PAR1 antagonist has an increased bleeding risk in clinical practice, PAR4 blockade has been suggested as a more promising treatment. Here, we explored the expression pattern of PAR4 in the brain of mice after TBI, and explored the effect and possible mechanism of BMS-986120 (BMS), a novel selective and reversible PAR4 antagonist on secondary brain injury. Treatment with BMS protected against TBI in mice. mRNA-seq analysis, Western blot, and qRT-PCR verification in vitro showed that BMS significantly inhibited thrombin-induced inflammation in astrocytes, and suggested that the Tab2/ERK/NF-κB signaling pathway plays a key role in this process. Our findings provide reliable evidence that blocking PAR4 is a safe and effective intervention for TBI, and suggest that BMS has a potential clinical application in the management of TBI. [ABSTRACT FROM AUTHOR]

Reed-type valve is widely used in refrigeration compressor; its dynamic performance directly affects the energy efficiency of compressors. In order to reveal the motion law of the reed-type valve of refrigeration compressor, a dynamic model based on vibration theory is established. According to the actual movement characteristics of the reed valve, the motion process of the reed is divided into two stages (i.e. before the reed bending to the limiter and after the reed bending to the limiter). The one-degree-of-freedom system is used to model before the valve reed bending to the limiter, and the vibration theory of Euler–Bernoulli beam is used to model after the reed bending to the limiter. The fourth-order Runge–Kutta method is applied to solve the new model in the MATLAB environment. In order to verify the validity of the new model, dynamic performance experiments of discharge reed valve at various operating conditions were carried out. The predicted results of the new model, the basic valve theory model and the cantilever beam model are compared with the experimental results. The analysis of error band and root mean square error shows that the calculation results of the new model can more accurately reveal the motion law of reed valve than that of other two models. Then, the effects of valve lift, reed stiffness and compressor speed on the valve dynamics and pressure loss are analyzed. This research can provide a reference for optimizing the structure parameters of reed-type valve and improving the energy efficiency of compressors. [ABSTRACT FROM AUTHOR]

Background: In light of the controversies regarding the surgical treatment of adult Chiari malformation type I (CM-I) with syringomyelia, a retrospective study was conducted to evaluate the safety and efficacy of tonsillectomy followed by modified reconstruction of the cisterna magna with or without craniectomy. Methods: Between 2008 and 2017, 78 adult CM-I patients (36 males and 42 females, mean age 40.6 years old) with syringomyelia were treated with posterior fossa decompression (PFD) with tonsillectomy and modified reconstruction of the cisterna magna. Patients were divided into two study groups: group A (n = 40) underwent cranioplasty with replacement of the bone flap; group B (n = 38) underwent suboccipital craniectomy. Neurological outcomes were evaluated by traditional physician assessment (improved, unchanged, and worsened) and the Chicago Chiari Outcome Scale (CCOS). Syringomyelia outcomes were assessed radiologically. Results: The procedure was successfully performed in all patients, and restoration of normal cerebrospinal fluid (CSF) flow was confirmed by intraoperative ultrasonography. The median postoperative follow-up was 20.3 months (range 18–60 months). Clinical improvement was evident in 66 (84.6%) patients, with no significant differences between the two groups (85.0% vs. 84.2%, P = 0.897). According to the CCOS, 36 patients (90.0%) in group A were labeled as "good" outcome, compared with that of 34 (86.8%) in group B (P = 0.734). Improvement of syringomyelia was also comparable between the groups, which was observed in 35 (87.5%) vs. 33 (86.8%) patients (P = 0.887). The postoperative overall (7.5% vs. 23.7%, P = 0.048) and CSF-related (2.5% vs. 18.4%, P = 0.027) complication rates were significantly lower in group A than group B. Conclusions: Tonsillectomy with modified reconstruction of the cisterna magna without craniectomy seems to be a safe and effective surgical option to treat adult CM-I patients with syringomyelia, though future well-powered prospective randomized studies are warranted to validate these findings. [ABSTRACT FROM AUTHOR]

Introduction: A novel neurosurgical enhanced recovery after surgery (ERAS) program shortens postoperative hospital stay and accelerates functional recovery in elective craniotomy patients. There is a need to evaluate the impact of ERAS program on patients' health-related quality of life (HRQOL). Methods: In a single-center randomized controlled trial, patients were randomized 1:1 to receive perioperative ERAS or conventional care. As a secondary outcome, HRQOL was measured with the EORTC QLQ-C30/BN20 prior to randomization (baseline), at discharge, and at 3- and 6-month follow-up. Results: A total of 65 patients (ERAS: n = 36, conventional care: n = 29) with pathologically confirmed glioma (WHO grade 2–4) were included in the analysis. Progression-free survival at 6 months and HRQOL at baseline were similar between the two groups. Changes of scores did not vary significantly over time, but differed significantly between intervention groups. A clinically relevant better QoL (at 3-month follow-up), physical functioning (at 6-month follow-up) and role functioning (at discharge) was observed in patients in the ERAS group. Symptom scores of constipation (at discharge), motor dysfunction (at discharge, 3- and 6-month follow-up), drowsiness (at 3- and 6-month follow-up), weakness of legs (at 3-month follow-up), and nausea/vomiting (at discharge and 6-month follow-up) were significantly lower in the ERAS group. Conclusions: The neurosurgical ERAS program seems to improve functioning and symptoms scores in glioma patients within 6-month follow-up compared with conventional care. The intervention has a significant main effect HRQOL changes without significant interaction with time. Future well-powered multicenter studies are warranted to confirm this result and address long-term benefits. This study has been registered in the Chinese Clinical Trial Registry (http://www.chictr.org.cn/showproj.aspx?proj=16480) with registration number ChiCTR-INR-16009662. [ABSTRACT FROM AUTHOR]

Endoscopic endonasal transsphenoidal resection has been accepted as a routine therapy for pituitary adenoma, but the postoperative hospital stay is typically several days long. With the advantages of reduced cost and improved patient satisfaction, the application of ambulatory surgery (AS) has developed rapidly. However, AS was still rarely adopted in neurosurgery. Here we designed an AS treatment protocol for pituitary adenoma with the endoscopic endonasal approach (EEA), and reported our initial experiences regarding the safety and efficacy of the AS protocol. 63 patients who presented with pituitary adenoma were screened at the Department of Neurosurgery, Tangdu Hospital from July to September, 2017. A total of 20 pituitary adenoma patients who met the inclusion criteria underwent EEA surgery using this evidence-based AS protocol, which emphasized adequate assessment for eligibility, full preparation to minimize invasiveness, enhanced recovery, and active perioperative patient education. Of the 20 patients enrolled, 18 were discharged on the afternoon of the operation day with a median total length of stay (LOS) of 31 hours (range, 29–32) hours. The median LOS after surgery was 6.5 (range, 5–8) hours. Two patients were transferred from the AS protocol to conventional care due to intraoperative cerebrospinal fluid leakage (one case) and an unsatisfying post-anesthetic discharge score (one case). Complications included transient and reversible mild postoperative nausea and vomiting [visual analog scale (VAS) score <3], headache (VAS score <3) after the operation or early after discharge. No patient was readmitted. Our results supported the safety and efficacy of the AS protocol for pituitary adenoma patients undergoing EEA resection among eligible patients, and further evaluation of this protocol in controlled studies with a larger sample size is warranted. [ABSTRACT FROM AUTHOR]

The healthcare system is undergoing a fundamental transformation fueled by regulatory shifts that reward value over volume, coupled with unprecedented advances in technological capabilities. To address the processes involved in defining, measuring, and delivering value in this shifting landscape, we develop the framework of value-centered marketing (VCM). Building on existing approaches in both healthcare and marketing, we propose three core dimensions of value in VCM: preferences, precision, and process. We also provide an overview of a trifecta of technological advances including the digital capture of health data, improvements in methodologies for data analysis, and exponential increases in processing power and storage capacity, which have created a perfect storm of opportunity for VCM. We describe how these emerging technologies can be combined with insights from marketing science to develop successful VCM strategy and highlight critical research questions. Finally, we discuss potential unintended consequences in the use of tech- and analytics-enabled healthcare. [ABSTRACT FROM AUTHOR]

In this study, we designed a special stress concentration specimen. We studied the stress, strain, craze density, and the change trend in the rate of acoustic emission events in the area with the most intense craze damage. We also examined the evolution of crazing damage under continuous loading. We determined the one-to-one correspondence between crazing and the degree of triaxial stress, and used the finite element method to validate this correspondence. In addition, we analyzed the viscoelasticity area of the specimen and proposed the fracture criteria for crazes and microcracks. [ABSTRACT FROM AUTHOR]

The piriform cortex (PC) is highly susceptible to chemical and electrical seizure induction. Epileptiform activity is associated with an acid shift in extracellular pH, suggesting that acid-sensing ion channels (ASICs) expressed by PC neurons may contribute to this enhanced epileptogenic potential. In epileptic rats and surgical samples from patients with medial temporal lobe epilepsy (TLE), PC layer II ASIC1a-immunopositive neurons appeared swollen with dendritic elongation, and there was loss of ASIC1a-positive neurons in layer III, consistent with enhanced vulnerability to TLE-induced plasticity and cell death. In rats, pilocarpine-induced seizures led to transient downregulation of ASIC1a and concomitant upregulation of ASIC2a in the first few days post-seizure. These changes in expression may be due to seizure-induced oxidative stress as a similar reciprocal change in ASIC1a, and ASIC2a expression was observed in PC12 cells following HO application. The proportion of ASIC1a/ASIC2a heteromers was reduced in the acute phase following status epilepticus (SE) but increased during the latent phase when rats developed spontaneous seizures. Knockdown of ASIC2a by RNAi reduced dendritic length and spine density in primary neurons, suggesting that seizure-induced upregulation of ASIC2a contributes to dendritic lengthening in PC layer II in rats. Administration of the ASIC inhibitor amiloride before pilocarpine reduced the proportion of rats reaching Racine level IV seizures, protected layer II and III neurons, and prolonged survival in the acute phase following SE. Our findings suggest that ASICs may enhance susceptibility to epileptogenesis in the PC. Inhibition of ASICs, particularly ASIC2a, may suppress seizures originating in the PC. [ABSTRACT FROM AUTHOR]

Noxious stimuli applied at doses close to but below the threshold of cell injury induce adaptive responses that provide a defense against additional stress. Epileptic preconditioning protects neurons against status epilepticus and ischemia; however, it is not known if the converse is true. During hypoxia/ischemia (H/I), lactate released from astrocytes is taken up by neurons and is stored for energy, a process mediated by monocarboxylate transporter 4 (MCT4) in astroglia. The present study investigated whether H/I preconditioning can provide protection to neurons against epilepsy through upregulation of MCT4 expression in astrocytes in vitro and in vivo. An oxygen/glucose deprivation protocol was used in primary astrocyte cultures, while rats were subjected to an intermittent hypoxia preconditioning (IHP) paradigm followed by lithium-pilocarpine-induced epilepsy as well as lactate transportation inhibitor injection, with a subsequent evaluation of protein expression as well as behavior. H/I induced an upregulation of MCT4 expression, while an IHP time course of 5 days provided the greatest protection against epileptic seizures, which was most apparent by 3 days after IHP. However, lactate transport function disturbances can block the protective effect induced by IHP. These findings provide a potential basis for the clinical treatment of epilepsy. [ABSTRACT FROM AUTHOR]

Deep brain stimulation is an alternate treatment strategy for intractable epilepsy. The effects of low- and high-frequency electrical stimulation to the substantia nigra pars reticulata (SNr) of different sides on chemically induced neocortical seizure were investigated in the present study. After neocortical seizure was induced by ferric chloride injection into the left sensorimotor cortex, SNr was stimulated ipsilaterally, contralaterally, or bilaterally at frequencies of 130 or 20 Hz in rats. Unilateral and bilateral stimulation at 130 Hz reduced significantly the number of seizures but not their duration. Ipsilateral, contralateral as well as bilateral stimulations at 130 Hz were all equally effective, producing reductions in seizures of 63.62, 77.84, and 68.74 % compared with the control group, respectively. Electrical stimulation at 20 Hz did not reduce the number or duration of seizures regardless of the side stimulated. Both unilateral and bilateral stimulations of SNr at 130 Hz can suppress ictogenesis in the cortex, but electrical stimulation at 130 or 20 Hz does not reduce the severity of individual seizures. The frequency of stimulation is paramount in suppressing neocortical seizures in which DBS at least targets SNr. [ABSTRACT FROM AUTHOR]

microRNA-9 (miR-9) has been found to be upregulated along with tumor progression of gliomas by microarray-based expression profiling, and also be strongly linked to glioblastoma subtypes. However, its prognostic value in glioma is still elusive. miR-9 expression in human gliomas and nonneoplastic brain tissues was measured by real-time quantitative RT-PCR assay. miR-9 expression in glioma tissues was significantly higher than that in corresponding nonneoplastic brain tissues ( P < 0.001). The increased expression of miR-9 was more frequently observed in glioma tissues with high WHO grade than those with low WHO grade tissues ( P = 0.001). The expression levels of miR-9 in glioma tissues with low Karnofsky performance score (KPS) were also significantly higher than those with high KPS ( P = 0.008). Moreover, the overall survival of glioma patients with high miR-9 expression was obviously lower than that with low miR-9 expression ( P < 0.001). Multivariate analysis further showed that high miR-9 expression was an independent prognostic factor for overall survival in glioma patients ( P = 0.01). More importantly, the subgroup analyses indicated that the overall survival of glioma patients with high WHO grade (III-IV) was significantly worse for high miR-9 expression group than for low miR-9 expression group ( P < 0.001), but no significant difference was found for patients with low WHO grade (I-II). These findings suggest for the first time that the increased expression of miR-9 may play an important role in tumor progression in human gliomas. miR-9 might be a useful marker for predicting the clinical outcome of glioma patients, especially for advanced subtypes. [ABSTRACT FROM AUTHOR]

CD147, also known as extracellular matrix metalloproteinase inducer, is a widely distributed cell surface glycoprotein that belongs to the immunoglobulin superfamily. CD147 has been proved to be enriched on the surface of many tumor cells, promoting tumor growth, invasion and metastasis by its stimulation effect on adjacent fibroblasts to produce matrix metalloproteinases. In this study, we aimed to explore the expression pattern of CD147 in glioblastoma (GBM) and investigate whether it could be used to assess subsequent prognosis of patients. For that, we recruited a total of 206 patients with pathologically confirmed GBM and 36 normal control brain tissue specimens. The expression of CD147 in GBM and normal tissues was investigated by immunohistochemistry assay. Genetic factors including MGMT and IDH1 mutation were also investigated to justify the prognostic significance of CD147. Results showed that CD147 expression was increased in GBM compared with that in normal tissues. Kaplan-Meier analysis showed that increased CD147 expression was associated with poor overall survival of patients with GBM. Moreover, Cox's proportional hazards model revealed that CD147 expression was an independent and significant prognostic marker of overall survival in GBM patients. These results proved that CD147 expression was relatively abundant in GBM and can be potentially used to predict prognosis and treatment response in GBM patients. [ABSTRACT FROM AUTHOR]

Single-wall carbon nanohorns (SWNHs) have been demonstrated to accumulate in cytotoxic levels within organs of various animal models and cell types, which emerge as a wide range of promising biomedical imaging. Septic encephalopathy (SE) is an early sign of sepsis and associated with an increased rate of morbidity and mortality. Microglia activation plays an important role in neuroinflammation, which contributes to neuronal damage. Inhibition of microglia activation may have therapeutic benefits, which can alleviate the progression of neurodegeneration. Therefore, we investigated the functional changes of mice microglia cell lines pre-treated with or without lipopolysaccharide (LPS) induced by SWNHs. To address this question, the research about direct role of SWNHs on the growth, proliferation, and apoptosis of microglia cell lines in mice (N9 and BV2) pre-treated with or without LPS had been performed. Our results indicate that the particle diameter of SWNHs in water is between 342 to 712 nm. The images in scanning electron microscope showed that SWNHs on polystyrene surface are individual particles. LPS induced activation of mice microglia, promoted its growth and proliferation, and inhibited its apoptosis. SWNHs inhibited proliferation, delayed mitotic entry, and promoted apoptosis of mice microglia cells. The effects followed gradually increasing cultured time and concentrations of SWNHs, especially in cells pre-treated with LPS. SWNHs induced a significantly increase in G1 phase and inhibition of S phase of mice microglia cells in a dose-manner dependent of SWNHs, especially in cells pre-treated with LPS. The transmission electron microscope images showed that individual spherical SWNH particles smaller than 100 nm in diameters were localized inside lysosomes of mice microglia cells. SWNHs inhibited mitotic entry, growth and proliferation of mice microglia cells, and promoted its apoptosis, especially in cells pre-treated with LPS. SWNHs inhibited expression of Sirt3 and energy metabolism related with Sirt3 in mice microglia cells in a dose-dependent manner, especially in cells pre-treated with LPS. The role of SWNHs on mice microglia was implicating Sirt3 and energy metabolism associated with it. [ABSTRACT FROM AUTHOR]

Recent studies have demonstrated that the chemokine CCL20 and its receptor CCR6 may be involved in tumorigenesis, tumor progression and metastatic spread of various human malignancies. The aim of this study was to investigate the clinicopathological significance and prognostic value of CCL20 and CCR6 expression in human malignant glioma. CCL20 and CCR6 expression in human gliomas and nonneoplastic brain tissues was measured by immunohistochemistry. The association of CCL20 and CCR6 expression with clinicopathological factors or prognosis in glioma patients was statistically analyzed. The expression levels of CCL20 and CCR6 proteins were both up-regulated in glioma tissues. There was a significantly positive correlation between the expression of the two markers ( r = 0.88; P < 0.001). In addition, the overexpressions of CCL20 and CCR6 were both detected in high-grade glioma tissues compared with those in low-grade tissues and increased with ascending tumor World Health Organization (WHO) grades ( P = 0.006 and 0.008, respectively). The increased expressions of CCL20 and CCR6 proteins were also significantly correlated with low Karnofsky performance score (both P = 0.01). Moreover, univariate analysis found that CCL20 expression ( P = 0.002), CCR6 expression ( P = 0.002) and CCL20/CCR6 co-expression ( P < 0.001) were all significantly associated with poor prognosis. In particular, glioma patients with CCL20/CCR6 co-expression have the shortest overall survival. Multivariate analysis further identified the expression levels of CCL20 and CCR6 to be independent prognostic factors. Our data suggest for the first time that CCL20 and CCR6 might play an important role in the regulation of aggressiveness in human gliomas. The up-regulation of CCL20 and CCR6 might be closely associated with poor clinical outcome of patients with gliomas. [ABSTRACT FROM AUTHOR]

Cerium has been demonstrated to damage liver of mice, but very little is known about the molecular mechanisms underlying the mouse liver apoptosis. In order to understand the liver injury induced by intragastric administration of cerium chloride (CeCl) for 60 consecutive days, the hepatocyte ultrasrtucture, various oxidative stress parameters, and the stress-related gene expression levels were investigated for the mouse liver. The results demonstrated that CeCl had an obvious accumulation in the mouse liver, leading to a classical laddering cleavage of DNA and hepatocyte apoptosis. CeCl significantly promoted the accumulation of reactive oxygen species and inhibited the stress-related gene expression of superoxide dismutase, catalase, glutathione peroxidase, metallothionein, heat-shock protein 70, glutathione- S-transferase, P53, and transferring, and it effectively activated the cytochrome p450 1A. It implied that CeCl resulted in apoptosis and alteration of expression levels of the genes related with metal detoxification/metabolism regulation and radical scavenging action in mice. [ABSTRACT FROM AUTHOR]

It has been known that GnRH, LH and their receptors exist in hippocampal neurons. However, whether FSH and its receptor also exist in hippocampal neurons remained unknown yet. In situ hybridization, double-labeled immunofluorescence stain and double-labeled immunohistochemistry stain in adjacent sections were used in our research to study the distribution, co-localization of FSH and its receptor and co-localization of FSH and GnRH receptor in rat hippocampus. The result found that pyramidal neurons from CA1 to CA4 region and granule neurons in dentate gyrus could express FSH and its receptor, majority of hippocampal neurons co-expressed FSH and its receptor, FSH and GnRH receptor. These suggested that hippocampal neurons not only express FSH but also act as FSH target cells. FSH may regulate the function of hippocampal neurons by ways of paracrine or autocrine. At the same time, GnRH may regulate the function of FSH neuron in hippocampus through GnRH receptor. [ABSTRACT FROM AUTHOR]