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The solution absorption system has great potential for recovery of water and latent heat from industrial gas. However, few investigations have been conducted on the synergistic removal of SO2 and the treatment of the associated precipitation when the method is applied for flue gas from coal-fired power plants. To solve this problem, a falling-film reaction platform was established and the CaCl2 solution was chosen as the liquid desiccant. The effects of solution temperature and concentration, solution pH, O2 content and catalyst concentration on the efficiency of SO2 removal were investigated. The solubility of the CaSO4·2H2O precipitates in the CaCl2 solution was measured. The results revealed that the precipitated component was influenced by the O2 content. The decrease in solution pH was responsible for the decrease in the efficiency of SO2 removal. The highest SO2 removal efficiency of 95.6% was obtained during the operation of solution circulation in this experiment. In addition, the solubility test showed that a higher temperature, a lower concentration and the addition of Ca(OH)2 were conducive to reducing the solubility of the CaSO4·2H2O precipitate in CaCl2 solution.

Purpose To assess the present evidence regarding the efficiency, safety, and potential risks of pharmacotherapy used for Parkinson's disease psychosis (PDPsy) treatment. Patients and methods We searched the following databases: PubMed, the Cochrane Library, ISI Web of Science, and Embase using the following terms: atypical antipsychotics, pimavanserin, olanzapine, quetiapine, clozapine, Parkinson's disease and psychosis. We systematically reviewed all randomized placebo-controlled trials comparing an atypical antipsychotic with a placebo. Results A total of 13 randomized placebo-controlled trials for a total 1142 cases were identified involving pimavanserin (n=4), clozapine (n=2), olanzapine (n=3), and quetiapine (n=4). For each atypical antipsychotic, a descriptive synthesis and meta-analyses was presented. Pimavanserin was associated with a significant improvement in psychotic symptoms compared to a placebo without worsening motor function. Clozapine was efficacious in alleviating psychotic symptoms and did not exacerbate motor function either. Quetiapine and Olanzapine did not demonstrate significant differences in reducing psychotic symptoms but may aggravate motor function. Conclusions There is strong evidence that pimavanserin is effective for the treatment of PDPsy. Clozapine is also recommended but should be used with caution due to its side effects. In the future, more well-designed randomized controlled trials (RCTs) are needed to confirm and update the findings reported in this meta-analysis.

In this work, the effects of oxygen plasma treatment by inductive coupled plasma on current transport of AlInN/GaN Schottky diodes were investigated. The current-voltage (I-V) results show that oxygen plasma treatment can significantly suppress reverse leakage current of the Schottky diodes by over three orders of magnitude, and meanwhile can enhance remarkably the effective barrier height and improve the ideality factor of the Schottky contact by forming a thin oxidation layer at the AlInN surface. However, I-V curve occurs a transient and recoverable reduction in current response at low forward bias. The further analysis indicates that donor-like traps related to nitrogen vacancies or their complexes induced by oxygen plasma treatment are responsible for this transient current reduction.

We systematically synthesized mixed-halide hybrid perovskite CH3NH3Pb(BrxI1−x)3 (0 ≤ x ≤ 1) crystals in the full composition range by a solvothermal method. The as-synthesized crystals retained cuboid shapes, and the crystalline structure transitioned from the tetragonal phase to the cubic phase with an increasing Br-ion content. The photoluminescence (PL) of CH3NH3Pb(BrxI1−x)3 crystals exhibited a continuous variation from red (768 nm) to green (549 nm) with increasing the volume ratio of HBr (VHBr%), corresponding to a variation in the bandgap from 1.61 eV to 2.26 eV. Moreover, the bandgap of the crystals changed nonlinearly as a quadratic function of x with a bowing parameter of 0.53 eV. Notably, the CH3NH3Pb(BrxI1−x)3 (0.4 ≤ x ≤ 0.6) crystals exhibited obvious phase separation by prolonged illumination. The cause for the phase separation was attributed to the formation of small clusters enriched in lower-band-gap, iodide-rich and higher-band-gap, bromide-rich domains, which induced localized strain to promote halide phase separation. We also clarified the relationship between the PL features and the band structures of the crystals.

Our previous research revealed that rifampicin could protect PC12 (pheochromocytoma 12) cells from rotenone-induced cytotoxicity by reversing the aggregation of α-synuclein. Furthermore, increasing evidence indicated that the misfolded α-synuclein with SUMOylation, an important protein posttranslational modification, was easier to solubilize and was less toxic. Here, we investigated whether rifampicin could stabilize α-synuclein and prevent rotenone-induced PC12 cells from undergoing apoptosis by enhancing SUMOylation of α-synuclein. The expression of SUMO1 and SUMO2/3, the two main proteins responsible for the SUMOylation modification in PC12 cells, were detected by western blotting. Co-immunoprecipitation was performed to compare qualitatively the SUMOylation modification of α-synuclein. The cell viability and apoptosis rate were measured by a CCK-8 assay kit and flow cytometry, respectively. We targeted Ubc9 as a key enzyme in the SUMOylation modification pathway and knocked down the UBC9 gene using a short interfering RNA. Treatment with 150 μmol/L rifampicin, increased the expressions of SUMO1 and SUMO2/3 in cells by 1.5 times compared with the control group; meanwhile, the cell viability of rotenone-induced cells increased from 20 to 80% (P

We systematically synthesized CH 3 NH 3 PbI 3 crystals using solvothermal process, and the reaction conditions such as concentration of the precursor, temperature, time, and lead source have been comprehensively investigated to obtain shape-controlled CH 3 NH 3 PbI 3 crystals. The results showed that the CH 3 NH 3 PbI 3 crystals exhibit tetragonal phase and the crystals change from nanoparticles to hopper-faced cuboids. Photoluminescence spectra of the crystals obtained with different lead sources show a blue shift due to the presence of defects in the crystals, and the peak intensity is very sensitive to the lead sources. Moreover, impurities (undesirable byproducts and excess components like HI or CH 3 NH 2 ) presented during crystal growth can result in hopper growth.

To mitigate strain relaxation of AlGaN barrier in AlGaN/GaN heterostructures, a new method is proposed by inducing an additional biaxial compressive pre-stress. Here, MgO dielectric with a twice larger thermal-expansion coefficient than AlGaN was deposited on the surface of Si3N4-passivated AlGaN/GaN heterostructures at high temperature to demonstrate this idea. The ultraviolet Raman results verify that MgO dielectric introduced a temperature-dependent biaxial compressive stress to the AlGaN barrier. The calculated variations of two-dimensional-electron-gas concentration before and after depositing the MgO dielectric according to piezoelectric polarization theory are in good agreement with those from Hall effect measurements in the temperature range of 80–600 K, which further confirms the presence of the additional compressive pre-stress to AlGaN.

Radiotherapy (RT) is the most effective treatment for nasopharyngeal carcinoma (NPC) but may cause stenosis of the carotid arteries. This meta-analysis evaluates the prevalence of carotid stenosis after radiation therapy.Online search for studies reporting carotid stenosis in patients with NPC who received radiation therapy (RT) compared to NPC patients who did not receive RT and compared to healthy controls.Twelve studies were included for a total analysis of 1928 patients (837 received RT and 1091 were controls). RT patients showed a statistically significant higher incidence of overall stenosis (pooled risk ratio = 4.17 [2.44, 7.10], p 0.00001) and an even greater incidence of significant stenosis (50% or more) (pooled risk ratio = 8.72 [3.53, 21.55], p 0.00001). Analyzing by individual blood vessels showed that the RT patients had significantly higher incidence of stenosis in common carotid artery (CCA), external carotid artery (ECA), carotid bulb, CCA and internal carotid artery (ICA), and CCA/ICA/carotid bulb.NPC patients who receive RT have increased risk of developing carotid stenosis, and should be screened after treatment.

The brain is the major dose-limiting organ in patients undergoing radiotherapy for assorted conditions. Radiation-induced brain injury is common and mainly occurs in patients receiving radiotherapy for malignant head and neck tumors, arteriovenous malformations, or lung cancer-derived brain metastases. Nevertheless, the underlying mechanisms of radiation-induced brain injury are largely unknown. Although many treatment strategies are employed for affected individuals, the effects remain suboptimal. Accordingly, animal models are extremely important for elucidating pathogenic radiation-associated mechanisms and for developing more efficacious therapies. So far, models employing various animal species with different radiation dosages and fractions have been introduced to investigate the prevention, mechanisms, early detection, and management of radiation-induced brain injury. However, these models all have limitations, and none are widely accepted. This review summarizes the animal models currently set forth for studies of radiation-induced brain injury, especially rat and mouse, as well as radiation dosages, dose fractionation, and secondary pathophysiological responses.

We report on improved electrical properties of Schottky contacts to InGaN alloys by introducing a photoelectrochemical treatment. The Schottky barrier height determined by a thermionic-field emission model, a dominating forward-current-transport mechanism, increased by 0.15 eV from 1.02 eV for conventional contacts to 1.17 eV for those with photoelectrochemical treatment at room temperature, while the ideality factors is closer to 1 after photoelectrochemical treatment. Furthermore, the reverse leakage mechanism varies from an ohmic transport mechanism at relatively low voltage and space charge-limited current mechanism at relatively high voltage for conventional contacts to Frenkel–Poole emission for improved Schottky contacts, which is attributed to partly removing surface states by the photoelectrochemical treatment.

A growing body of evidence has supported that environmental factors, such as exposure to heavy metal and pesticides, play an important role in the pathogenesis of Parkinson׳s disease (PD). Rotenone, the active ingredient in various pesticides, has been identified as an inducer of PD. It has been revealed that rotenone induces activation of microglia and generation of pro-inflammatory factors in PD. Our previous studies demonstrated that rifampicin possessed neural protective effect in PD. In this study, we aimed to study the effect of rifampicin on the inflammation induced by rotenone in microglia and the underlying mechanisms. Results demonstrated that rifampicin pretreatment significantly reduced rotenone-induced cytotoxicity and gene expression of IL-1β in BV2 microglia. Moreover, western blot analysis verified that rifampicin pretreatment suppressed NLRP3 inflammasome activation via inhibiting caspase-1 cleavage and protein expression of NLRP3. As it is indicated that reactive oxidative stress (ROS) is one of the activators for NLRP3 inflammasome, we further employed 2′,7′-Dichlorodihydrofluorescein diacetate (DCFH-DA) staining and Rhodamine123 staining to detect intracellular ROS and mitochondrial membrane potential (MMP), respectively. Results confirmed that rifampicin obviously reduced intracellular ROS and reversed loss of MMP in BV2 cells treated by rotenone. Taken together, our data indicate that rifampicin pretreatment inhibits maturation of IL-1β and neuroinflammation induced by rotenone via attenuating NLRP3 inflammasome activation. Rifampicin might emerge as a promising candidate for modulating neuroinflammation in PD.

The visible and ultraviolet (UV) Raman scattering of an AlInN/AlN/GaN heterostructure were measured under z ( x , _ ) z ¯ configuration at room temperature. Compared with the visible Raman spectrum, three new peaks at 609, 700, and 840 cm −1 occurred in the UV Raman spectrum and were verified to result from the resonance enhanced Raman effect. The near-resonance Raman scattering is stimulated by the electron transition process between the valence band and subband of triangular quantum well located at the interface of AlN/GaN because this transition process has a near equal energy with the 325 nm excitation light. According to the calculated dispersion relations of interface phonon modes in the AlInN/AlN/GaN heterostructure and the 2DEG-related resonance enhanced effect, these new Raman peaks were mainly attributed to the interface phonon modes and disorder-activated mode. The contributions from the bulk phonon modes of AlN and AlInN layers play a very minor role.

Mitochondrial and autophagic dysfunction, as well as neuroinflammation, are associated with the pathophysiology of Parkinson's disease (PD). Rotenone, an inhibitor of mitochondrial complex I, has been associated as an environmental neurotoxin related to PD. Our previous studies reported that rifampicin inhibited microglia activation and production of proinflammatory mediators induced by rotenone, but the precise mechanism has not been completely elucidated. BV2 cells were pretreated for 2h with rifampicin followed by 0.1μM rotenone, alone or in combination with chloroquine. Here, we demonstrate that rifampicin pretreatment alleviated rotenone induced release of IL-1β and IL-6, and its effects were suppressed when autophagy was inhibited by chloroquine. Moreover, preconditioning with 50μM rifampicin significantly increased viability of SH-SY5Y cells cocultured with rotenone-treated BV2 cells in the transwell coculture system. Chloroquine partially abolished the neuroprotective effects of rifampicin pretreatment. Rifampicin pretreatment significantly reversed rotenone-induced mitochondrial membrane potential reduction and reactive oxygen species accumulation. We suggest that the mechanism for rifampicin-mediated anti-inflammatory and antioxidant effects is the enhancement of autophagy. Indeed, the ratio of LC3-II/LC3-I in rifampicin-pretreated BV2 cells was significantly higher than that in cells without pretreatment. Fluorescence and electron microscopy analyses indicate an increase of lysosomes colocalized with mitochondria in cells pretreated with rifampicin, which confirms that the damaged mitochondria were cleared through autophagy (mitophagy). Taken together, the data provide further evidence that rifampicin exerts neuroprotection against rotenone-induced microglia inflammation, partially through the autophagy pathway. Modulation of autophagy by rifampicin is a novel therapeutic strategy for PD.

Lead sulfide (PbS) with multi-morphologies were synthesized via solvothermal route under the assistance of l -cysteine. Reaction conditions such as concentration of l -cysteine, reacting temperature, reacting time and solvents have been systemically investigated in order to obtain shape-controlled PbS micro-crystals. A series of morphologies, such as cubic, Dendritic Hierarchical, Octagonal Hierarchical flowerlike and Vertebration shapes were obtained successfully. Self-assembly and a hypothesis based on Boltzmann distribution were introduced for illustration of morphology evolution obtained under different reacting temperatures, and the effect of the solvents and the role of l -cysteine were also discussed in detail. To testify the effects of different morphologies on the optical properties of PbS, the absorption spectra of some samples were measured. These results demonstrated that our work offers an effective way to develop the tunable synthesis of multi-shaped PbS for various applications.

Objective: Radiation-induced brachial plexus injury is a devastating complication that occurs after radiotherapy in the vicinity of the brachial plexus. Nasopharyngeal carcinoma, the most common type of cancer in Guangdong Province, is primarily treated with radiotherapy with subsequent side effects. However, radiation-induced brachial plexus injury is rarely reported in nasopharyngeal carcinoma. To draw attention to this correlation, we analyzed the clinical characteristics including the imaging findings of 10 patients suffering from radiation-induced brachial plexus injury for nasopharyngeal carcinoma. Methods: We considered the patients’ medical histories, analyzed their clinical characteristics, and monitored the long-term efficacy of treatment. Results: The total irradiation dose of the nasopharynx ranged from 66.6 to 74 Gy, and that of the supraclavicular fossa ranged from 60 to 70 Gy. The mean latency was 8.2+5.5 years. Seven patients initially complained of bilateral weakness, and three patients complained of isolated pain. The injuries of eight patients reached Grade 3 or worse. Magnetic resonance imaging showed a low signal on T1-weighted images and a high signal on short tau inversion recovery sequences in all cases. Swollen nerve fibers were clearly displayed in magnetic resonance diffusion tensor imaging. Electromyography showed myokymia in three patients. With conservative therapy, only one patient was temporarily relieved of pain, while the conditions of others were not ameliorated. Conclusions: Radiation-induced brachial plexus injury is a late but catastrophic complication in patients with nasopharyngeal carcinoma. Clinicians should be aware of radiation-induced brachial plexus injury when deciding on treatment and should give them regular follow-up post radiotherapy.

In order to solve the serious backup roll spalling of roughing mill during ultra-wide stainless steel rolling process, a 3D elastic deformation finite element model of 4-high roll stacks was established for simulating the mechanical behavior during the hot rolling process. The asymmetric contact pressure between backup and work rolls is the key factor for the frequent roll spalling accidents. Based on the principle of homogenizing contact pressure between rolls, minimizing harmful contact zone in different strip widths and considering roll wearing as a whole, SCR (Smart Contact Backup Rolls) was developed. The simulation reveals when using the SMS200 backup roll contour, the peak position of contact pressure keeps consistent with the practical spalling position. Instead, the peak value of the roll contact pressure with SCR technology decreases significantly with various strip widths. The unevenness coefficients of roll contact pressure with SCR technology decline sharply from 1.36 and more to less than 1....

Alzheimer disease (AD) is a neurodegenerative disorder and the most common form of dementia. Histopathologically is characterized by the presence extracellular neuritic plaques and with a large number of neurons lost. In this paper, we design a new nanomaterial, graphene quantum dots (GQDs) conjugated neuroprotective peptide glycine-proline-glutamate (GQDG) and administer it to APP/PS1 transgenic mice. The in vitro assays including ThT and CD proved that GQDs and GQDG could inhibit the aggregation of Aβ1-42 fibrils. Morris water maze was performed to exanimate learning and memory capacity of APP/PS1 transgenic mice. The surface area of Aβ plaque deposits reduced in the GQDG group compared to the Tg Ctrl groups. Furthermore, newly generated neuronal precursor cell and neuron were test by immunohistochemical. Besides, neurons were impregnated by DiI using gene gun to show dendritic spine. Results indicated enhancement of learning and memory capacity and increased amounts of dendritic spine were observed. Inflammation factors and amyloid-β (Aβ) were tested with suspension array and ELISA, respectively. Several pro-inflammatory cytokines (IL-1α, IL-1β, IL-6, IL-33, IL-17α, MIP-1β and TNF-α) had decreased in GQDG group compared with Control group. Reversely, anti-inflammatory cytokines (IL-4, IL-10) had increased in GQDG group compared with Control group. Thus, we demonstrate that the GQDG is a promising drug in treatment of neurodegenerative diseases such as AD.

Summary Aims To establish a radiation-induced neural injury model using C17.2 neural stem cells (NSCs) and to investigate whether basic fibroblast growth factor (bFGF) can protect the radiation-induced injury of C17.2 NSCs. Furthermore, we aim to identify the possible mechanisms involved in this model. Methods C17.2 NSCs received a single exposure (3, 6, and 9 Gy, respectively) at a dose rate of 300 cGy/min with a control group receiving 0 Gy. Different concentrations of bFGF were added for 24 h, 5 min postirradiation. The MTS assay and flow cytometry were used to detect cytotoxicity and apoptosis. Expression of FGFR1, ERK1/2, and p-ERK1/2 proteins was detected with or without U0126 was pretreated prior to C17.2 NSCs receiving irradiation. Results C17.2 NSCs showed a dose-dependent cell death as the dose of radiation was increased. Additionally, the rate of apoptosis in the C17.2 NSCs reached 31.2 ± 1.23% in the 6 Gy irradiation group, which was the most significant when compared to the other irradiation treated groups. bFGF showed protective effect on cell apoptosis in a dose-dependent manner. The mean percentage of apoptotic cells decreased to 7.83 ± 1.75% when 100 ng/mL bFGF was given. Furthermore, U0126 could block the protective effect of bFGF by inhibiting the phosphorylation of ERK1/2. Conclusions An in vitro cellular model of radiation-induced apoptosis of NSCs, in C17.2 NSCs, was developed successfully. Additionally, bFGF can protect neurons from radiation injury in vitro via the ERK1/2 signal transduction pathway.

SUMMARY Aims: The aims of this study were to find out whether kallikrein could induce angiogenesis and affect the cerebral blood flow (rCBF) in the early period after cerebral ischemia/reperfusion (CI/R). Methods: The adenovirus carried human tissue kallikrein (HTK) gene was administrated into the periinfarction region after CI/R. At 12, 24, and 72 h after treatments, neurological deficits were evaluated; expression of HTK and vascular endothelial growth factor (VEGF) were detected by immunohistochemistry staining; the infarction volume was measured; and rCBF was examined by( 14)C‐iodoantipyrine microtracing technique. Results: The expression of VEGF was enhanced significantly in pAdCMV‐HTK group than controls over all time points (P < 0.05). Furthermore, the rCBF in pAdCMV‐HTK group increased markedly than controls at 24 and 72 h after treatment (P < 0.05), and the improved neurological deficit was accompanied by reduced infarction volume in pAdCMV‐HTK group 24 and 72 h posttreatment. Conclusion: In the early period after CI/R, kallikrein could induce the angiogenesis and improve rCBF in periinfarction region, and further reduce the infarction volume and improve the neurological deficits.

Let W and V be centrally symmetric sets in a normed space X. The relative Kolmogorov n-width of W relative to V in X is defined by Kn(W,V,X):=infLnsupf∈Winfg∈V∩Ln‖f−g‖X, where the infimum is taken over all n-dimensional subspaces Ln of X. Let Pr(t)=tσ∏j=1l(t2−tj2), tj⩾0, j=1,2,…,l, l⩾1, σ=0 or 1, r=2l+σ. Denote by Pr(D) (D=ddt) the self-conjugate differential operator induced by Pr(t), and by Kq(Pr) the generalized Sobolev class of 2π-periodic smooth functions defined by Kq(Pr)={f∈L˜q,2π(r):‖Pr(D)f‖q⩽1}, where L˜q,2π(r)={f∈Lq(T):f(r−1) is absolutely continuous on T=[0,2π] and f(r)∈Lq(T)}. In this paper, we consider the relative Kolmogorov n-width of Kp(Pr) relative to Kp(Pr) in the space Lq(T), and obtain the asymptotic orders of relative widths Kn(K∞(Pr),K∞(Pr),Lq(T)) and Kn(K1(Pr),K1(Pr),Lq(T)) for 1⩽q⩽∞.

For two subsets W and V of a Banach space X , let K n ( W, V, X ) denote the relative Kolmogorov n -width of W relative to V defined by K n ( W , V , X ) = inf L n sup f ∈ W inf g ∈ V ∩ L n ∥ f - g ∥ x , where the infimum is taken over all n -dimensional linear subspaces L n of X . Let W 2 (Δ r ) denote the class of 2π-periodic functions f with d -variables satisfying ∫ [ - π , π ] d | Δ r f ( x ) | 2 d x ≤ 1 , while Δ r is the r -iterate of Laplace operator Δ. This article discusses the relative Kolmogorov n -width of W 2 (Δ r ) relative to W 2 (Δ r ) in L q ([−π, π] d ) (1 ≤ q ≤ ∞), and obtain its weak asymptotic result.

Background Neurology is complex, abstract, and difficult for students to learn. However, a good learning method for neurology clerkship training is required to help students quickly develop strong clinical thinking as well as problem-solving skills. Both the traditional lecture-based learning (LBL) and the relatively new team-based learning (TBL) methods have inherent strengths and weaknesses when applied to neurology clerkship education. However, the strengths of each method may complement the weaknesses of the other. Combining TBL with LBL may produce better learning outcomes than TBL or LBL alone. We propose a hybrid method (TBL + LBL) and designed an experiment to compare the learning outcomes with those of pure LBL and pure TBL. Methods One hundred twenty-seven fourth-year medical students attended a two-week neurology clerkship program organized by the Department of Neurology, Sun Yat-Sen Memorial Hospital. All of the students were from Grade 2007, Department of Clinical Medicine, Zhongshan School of Medicine, Sun Yat-Sen University. These students were assigned to one of three groups randomly: Group A (TBL + LBL, with 41 students), Group B (LBL, with 43 students), and Group C (TBL, with 43 students). The learning outcomes were evaluated by a questionnaire and two tests covering basic knowledge of neurology and clinical practice. Results The practice test scores of Group A were similar to those of Group B, but significantly higher than those of Group C. The theoretical test scores and the total scores of Group A were significantly higher than those of Groups B and C. In addition, 100% of the students in Group A were satisfied with the combination of TBL + LBL. Conclusions Our results support our proposal that the combination of TBL + LBL is acceptable to students and produces better learning outcomes than either method alone in neurology clerkships. In addition, the proposed hybrid method may also be suited for other medical clerkships that require students to absorb a large amount of abstract and complex course materials in a short period, such as pediatrics and internal medicine clerkships.

Background & objectives: The gut contains some endogenous and exogenous microorganisms that can become potential pathogens of sepsis under certain circumstances. Therefore, the integrity and normal function of gut barrier is important for preventing the development of sepsis. The present study was designed to assess the effects of ulinastatin, a urinary trypsin inhibitor on gut barrier function and mortality in experimental sepsis. Methods: Male Sprague-Dawley rats were subjected to ceacal ligation and puncture (CLP) or sham procedure. Rats were then treated with ulinastatin 50,000 U/kg/day or saline. The mortality rate was determined. Histology, apoptosis assays, and PCR were performed using ileum specimens at 3, 6, and 12 h following CLP. Serum levels of tumour necrosis factor α (TNF-α) and interleukin-6 (IL-6) were also measured at 0, 3, 6, and 12 h following CLP. Results: Compared with the saline-treated CLP rats, the ulinastatin CLP rats had significantly increased survival time (P

Amyloid protein can damage nerve cells through a variety of biological mechanisms including oxidative stress, alterations in calcium homeostasis, and proapoptosis. Edaravone, a potent free radical scavenger possessing antioxidant effects, has been proved neuroprotective effect in stroke patients. The current study aimed to investigate the effects of EDA in an Aβ-induced rat model of AD, by studying Aβ1–40-induced voltage-gated calcium channel currents in hippocampal CA1 pyramidal neurons, learning and memory behavioral tests, the number of surviving cholinergic neurons in the basal forebrain, and the acetylcholine level in the hippocampus in this rat model of AD. The results showed that the Aβ1–40-induced increase ofICacan be inhibited by EDA in a dose-dependent manner. Treatment with EDA significantly improved Aβ1–40-induced learning and memory performance. Choline acetyltransferase positive cells in basal forebrain and acetylcholine content in the hippocampus were increased by the administration of EDA as compared with the non-EDA treated Aβ1–40group. These results demonstrate that EDA can inhibit the neurotoxic effect of Aβtoxicity. Collectively, these findings suggest that EDA may serve as a potential complemental treatment strategy for AD.

Agents inhibiting microglial activation are attracting attention as candidate drugs for neuroprotection in neurodegenerative diseases. Recently, researchers have focused on the immunosuppression induced by rifampicin. Our previous study showed that rifampicin inhibits the production of lipopolysaccharide (LPS)-induced pro-inflammatory mediators and improves neuron survival in inflammation; however, the mechanism through which rifampicin inhibits microglial inflammation and its neuroprotective effects are not completely understood. In this study, we examined the effects of rifampicin on morphological changes induced by LPS in murine microglial BV2 cells. Then we investigated, in BV2 microglia, the effects of rifampicin on two signaling pathway componentss stimulated by LPS, the Toll-like receptor-4 (TLR-4) and the nuclear factor-κB (NF-κB). In addition, we co-cultured BV2 microglia and neurons to observe the indirect neuroprotective effects of rifampicin. Rifampicin inhibited LPS-stimulated expression of the TLR-4 gene. When neurons were co-cultured with LPS-stimulated BV2 microglia, pre-treatment with rifampicin increased neuronal viability and reduced the number of apoptotic cells. Taken together, these findings suggest that rifampicin, with its anti-inflammatory properties, may be a promising agent for the treatment of neurodegenerative diseases.

To enhance the avalanche ionization, we designed a new separate absorption and multiplication AlGaN solar-blind avalanche photodiode (APD) by using a high/low-Al-content AlGaN heterostructure as the multiplication region instead of the conventional AlGaN homogeneous layer. The calculated results show that the designed APD with Al0.3Ga0.7N/Al0.45Ga0.55N heterostructure multiplication region exhibits a 60% higher gain than the conventional APD and a smaller avalanche breakdown voltage due to the use of the low-Al-content Al0.3Ga0.7N which has about a six times higher hole ionization coefficient than the high-Al-content Al0.45Ga0.55N. Meanwhile, the designed APD still remains a good solar-blind characteristic by introducing a quarter-wave AlGaN/AlN distributed Bragg reflectors structure at the bottom of the device.

It is well known that -nitride semiconductors can generate the magnitude of MV/cm polarization electric field which is comparable with their ionization electric fields. To take full advantage of the polarization electric field, we design an N-face AlGaN solar-blind avalanche photodiode (APD) with an Al0.45Ga0.55N/Al0.3Ga0.7N heterostructure as separate absorption and multiplication (SAM) regions. The simulation results show that the N-face APDs are more beneficial to improving the avalanche gain and reducing the avalanche breakdown voltage compared with the Ga-face APDs due to the effect of the polarization electric field. Furthermore, the Al0.45Ga0.55N/Al0.3Ga0.7N heterostructure SAM regions used in APDs instead of homogeneous Al0.45Ga0.55N SAM structure can increase significantly avalanche gain because of the increased hole ionization coefficient by using the relatively low Al-content AlGaN in the multiplication region. Meanwhile, a quarter-wave AlGaN/AlN distributed Bragg reflector structure at the bottom of the device is designed to remain a solar-blind characteristic of the heterostructure SAM-APDs.

Patients suffering from epilepsy need long-term medication. However, after the epilepsy is completely under control, the recurrence rate is high once the drug dose is reduced gradually. The present study investigated the possible correlation between the changes shown by ambulatory electroencephalography (EEG) and epilepsy recurrence after medication withdrawal, and assessed the value of ambulatory EEG findings in predicting the recurrence of epilepsy after medication withdrawal, in 265 patients from Southern China followed up for 5 years. Anticonvulsants were withdrawn until onset had been controlled thoroughly for over 3 years and ambulatory EEG detected no abnormalities. Ambulatory EEG was performed at least once per year, and findings at the first visit, during treatment, and before and after medication withdrawal were compared and analyzed. There were 47 patients with recurrent epilepsy in this study. Patients with normal ambulatory EEG findings at the first visit and during treatment had lower recurrence rate (about 8.1%) compared to patients with epileptic waves (25.0%), and patients with focal epileptic waves in the temporal, occipital, frontal, and parietal lobes, or in multiple areas was even higher. Patients with epileptic waves also showed higher clinical recurrence rate during the follow-up period. Abnormal ambulatory EEG findings are an important indicator of epileptic recurrence, and is of great value in predicting the recurrence of epilepsy after medication withdrawal.

Neurotoxic homocysteine (Hcy) is thought to be an independent risk factor for neurodegenerative diseases, including Alzheimer's disease. This study is to determine whether HT22 cells, a murine hippocampal neuronal model, can be used as an in vitro model, besides the primary neuronal cultures, to investigate the effects of Hcy.MTS assay and Hoechst 33342/propidium iodide discrimination were used to assess the cell viability and cell death on undifferentiated and differentiated HT22 cells. Semi-quantitative reverse transcription polymerase chain reaction and western blot were used to determine the expression of N-methyl D-aspartate (NMDA) receptor.We found that undifferentiated and differentiated HT22 cells responded to Hcy toxicity differentially, with the undifferentiated cells resistant while the differentiated cells sensitive. The underlying mechanism appeared to be the differential expression levels of NMDA glutamate receptor between the undifferentiated and differentiated cells. Similar to what have been observed in primary neuronal cultures, the Hcy toxicity in the differentiated HT22 cells was largely attenuated by NMDA receptor antagonists, MK-801 and memantine.These results suggest for the first time that the differentiation of HT22 cells could induce the expression of NMDA receptors, which lead to Hcy mediate concentration-dependent apoptosis-necrotic continuum of HT22 cell death. The differentiation status of the HT22 cells is important for modeling neurons in vitro, with the differentiated HT22 neurons resembling more characteristics of primary hippocampal neurons while the undifferentiated HT22 cells being proliferating neuronal precursor cells. The differentiated HT22 neurons can be used as a platform to study Hcy toxicity.