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The E4 allele of the Apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset Alzheimer's disease (AD), and affects clinical outcomes of chronic and acute brain damages. The mechanisms by which apoE affect diverse diseases and disorders may involve modulation of the glial response to various types of brain damages. We examined glial activation in a mouse model where each of the human APOE alleles are expressed under the endogenous mouse APOE promoter, as well as in APOE knock-out mice. APOE4 mice displayed increased glial activation in response to intracerebroventricular lipopolysaccharide (LPS) compared to APOE2 and APOE3 mice by several measures. There were higher levels of microglia/macrophage, astrocytes, and invading T-cells after LPS injection in APOE4 mice. APOE4 mice also displayed greater and more prolonged increases of cytokines (IL-1β, IL-6, TNF-α) than APOE2 and APOE3 mice. We found that APOE4 mice had greater synaptic protein loss after LPS injection, as measured by three different markers: PSD-95, Drebin, and synaptophysin. In all assays, APOE knock-out mice responded similar to APOE4 mice, suggesting that the apoE4 protein may lack anti-inflammatory characteristics of apoE2 and apoE3. Together, these findings demonstrate that APOE4 predisposes to inflammation, which could contribute to its association with Alzheimer's disease and other disorders.

During biomass combustion, the SO2 emission would still be a problem in some cases, although the average sulfur content is relatively lower than that of coal and other fossil fuels. In this work, the characteristics of self-desulfurization during sugarcane leaf combustion in a circulating fluidized bed were experimentally investigated. First, a laboratory fixed-bed reactor was used to study how the char particles take part in the self-desulfurization process. It was observed that SO2 can be largely captured by char in the temperature range of 700–900 °C. Most of the captured sulfur was incorporated with organic char matrix rather than directly retained by inherent alkali and alkaline-earth matters in the form of inorganic salts. During char combustion, substantial amounts of the captured sulfur could be retained in the ash, which was mainly limited by the alkali and alkali-earth matters available. At higher temperatures (>800 °C), the sulfur retention reduced, mainly because the alkali and alkali-earth ma...

This paper presents the experimental results of CaO sorption enhanced anaerobic gasification of biomass in a self-design bubbling fluidized bed reactor, aiming to investigate the influences of operation variables such as CaO to carbon mole ratio (CaO/C), H 2 O to carbon mole ratio (H 2 O/C) and reaction temperature ( T ) on hydrogen (H 2 ) production. Results showed that, over the ranges examined in this study (CaO/C: 0–2; H 2 O/C: 1.2–2.18, T : 489–740 °C), the increase of CaO/C, H 2 O/C and T were all favorable for promoting the H 2 production. The investigated operation variables presented different influences on the H 2 production under fluidized bed conditions from those obtained in thermodynamic equilibrium analysis or fixed bed experiments. The comparison with previous studies on fluidized bed biomass gasification reveals that this method has the advantage of being capable to produce a syngas with high H 2 concentration and low CO 2 concentration.

Amyloid plaques composed of the 42 amino acid form of amyloid-β peptide (Aβ42) are a pathological hallmark of Alzheimer's disease (AD), but soluble and intraneuronal Aβ42 are the more proximal causes of synaptic dysfunction and neurotoxicity. Apolipoprotein E (apoE) modulates this disease process, as inheritance of the ɛ4 allele of the apoE gene is the primary genetic risk factor for AD. To address the solubility of Aβ42 and apoE, the 5xFAD-specific extraction profile for Aβ42 was optimized, a protein extraction protocol was optimized in the presence of minimal to extensive Aβ42 pathology. Sequential extractions with TBS, TBS + Triton X-100 (TBSX), and guanidine-HCl (GuHCl) or formic acid (FA) were used with tissue from young and old wild type or mice expressing 5 familial AD mutations (5xFAD), in disease-susceptible or -resistant brain regions. In older 5xFAD mice, the extraction of insoluble Aβ42 and m-apoE protein was increased with FA compared to GuHCl. The 5 FAD mutations significantly increase production of Aβ42, recapitulating AD-like pathology at a greatly accelerated rate. Consistent protein extraction and the specificity of extractions for soluble or membrane-associated proteins were demonstrated. Age-dependent increases in Aβ42 were observed in all extraction fractions, particularly in the cortex and hippocampus. In both young and old 5xFAD mice, Aβ42 is TBS- or GuHCl-soluble. While in WT mice m-apoE is TBSX-soluble, in 5xFAD mice m-apoE is TBS- or GuHCl-soluble. Thus, the 5xFAD-specific extraction profile of Aβ42 paralleled that of m-apoE. As now characterized, this method identifies the extraction profile for disease relevant apoE and Aβ in the brain, both normal or modified due to neuropathological processes.

Acyl-coenzyme A:cholesterol acyltransferase 1 (ACAT1) is a membrane bound enzyme utilizing long-chain fatty acyl-coenzyme A and cholesterol to form cholesteryl esters and coenzyme A. Previously, we had expressed tagged human ACAT1 (hACAT1) in CHO cells and purified it to homogeneity; however, only a sparse amount of purified protein could be obtained. Here we report that the hACAT1 expression level in H293 cells is 18-fold higher than that in CHO cells. We have developed a milder purification procedure to purify the enzyme to homogeneity. The abundance of the purified protein enabled us to conduct difference intrinsic fluorescence spectroscopy to study the binding between the enzyme and its substrates in CHAPS/phospholipid mixed micelles. The results show that oleoyl CoA binds to ACAT1 with Kd=1.9 μM, and elicits significant structural changes of the protein as manifested by the significantly positive changes in its fluorescence spectrum; stearoyl CoA elicits a similar spectrum change with much lower in magnitude. Previously, kinetic studies had shown that cholesterol is an efficient substrate and an allosteric activator of ACAT1, while its diastereomer epicholesterol is neither a substrate nor an activator. Here we show that both cholesterol and epicholesterol induce positive changes in the ACAT1 fluorescence spectrum; however, the magnitude of spectrum changes induced by cholesterol is much larger than epicholesterol. These results show that stereospecificity, governed by the 3beta-OH moiety in steroid ring A, plays an important role in the binding of cholesterol to ACAT1.

Lipoprotein remodelling in the periphery has been extensively studied. For example, the processing of nascent apoAI particles to cholesterol-loaded HDL lipoproteins during reverse cholesterol transport involves a series of enzymes, transporters in peripheral tissue, as well as other apolipoproteins and lipoproteins. These extensive modifications and interconversions are well defined. Here, we present the hypothesis that a similar process occurs within the blood brain barrier (BBB) via glia-secreted lipid-poor apoE particles undergoing remodelling to become mature central nervous system (CNS) lipoproteins. We further pose several pressing issues and future directions for the study of lipoproteins in the brain.

The interest in utilization of biomass by CO2 sorbent enhanced gasification is increasing due to the concerns about global warming and the wish to produce high purity hydrogen. Pyrolysis in the presence of abundant CaO additives is a fundamental step which determines primary product distribution, composition and properties. In this paper, pure wheat-straw pyrolysis and CaO catalyzed pyrolysis (loading various amounts of CaO additives) at different heating rates were compared using the thermogravimetric Fourier transform infrared (TG-FTIR) analysis. Results showed that CaO additives affected pyrolysis. In the main mass loss stage, the mass loss and maximum mass loss rate decreased with increasing amount of CaO additives. The temperature at the maximum mass loss rate shifted to lower value. CaO additives could not only absorb the released CO2 but also restrain the CO and CH4 yields and meanwhile catalyze the tar reduction reactions. Calculated activation energies at different heating rates were generally in close agreement with that of a previous study and the average activation energy was lowered. Unlike pure wheat-straw pyrolysis, a second mass loss stage mainly caused by calcium carbonate decomposition appeared in CaO catalyzed pyrolysis. The evolution of CO was found to be enhanced by CaO additives in this stage. The total mass loss decreased in the presence of CaO additives. CaO additives can play the roles of both CO2 sorbent and tar reduction catalyst in sorbent enhanced biomass gasification.

With the widespread implementation of next-generation sequencing (NGS) technologies, millions of sequences have been produced. A lot of databases were created to store and organize the high-throughput sequencing data. Numerous analysis software programs and tools have been developed over the past years. Most of them use specific formats for data representation and storage. Data interoperability becomes a crucial challenge and many tools have been developed to convert NGS data from one format to another. However, most of them were developed for specific and limited formats. Here, we present NGS-FC (Next-Generation Sequencing Format Converter), which provides a framework to support the conversion between several formats. It supports 14 formats now and provides interfaces to enable users to improve the existing converters and add new ones. Moreover, NGS-FC achieved the overall competitive performance in comparison with some existing converters in terms of RAM usage and running time. The software is written in Java and can be executed standalone. The source code and documentation are freely available at http://sysbio.suda.edu.cn/NGS-FC .

Recent research has focused on soluble oligomeric assemblies of the 42 amino acid isoform of the amyloid-beta peptide (A beta 42) as the proximal cause of neuronal injury, synaptic loss, and the eventual dementia associated with Alzheimer's disease (AD). While neurotoxicity, neuroinflammation, and deficits in behavior and memory have all been attributed to oligomeric A beta 42, the specific roles for this assembly in the cellular neuropathology of AD remain poorly understood. In particular, lack of reliable and well-characterized forms of easily detectable A beta 42 oligomers has hindered study of the cellular trafficking of exogenous A beta 42 by neurons in vitro and in vivo. Therefore, the objective of this study is to fluorescently label soluble oligomeric A beta 42 without altering the structure or function of this assembly. Previous studies have demonstrated the advantages of using tapping mode atomic force microscopy (AFM) to characterize the structural assemblies formed by synthetic A beta 42 under specific solution conditions (e.g., oligomers, protofibrils, and fibrils). Here, we extend these methods to establish a strategy for fluorescent labeling of oligomeric A beta 42 assemblies that are structurally comparable to unlabeled oligomeric A beta 42. To compare function, we demonstrate that the uptake of labeled and unlabeled oligomeric A beta 42 by neurons in vitro is similar. AFM-characterized fluorophore-A beta 42 oligomers are an exciting new reagent for use in a variety of studies designed to elucidate critical cellular and molecular mechanisms underlying the functions of this A beta 42 assembly form in AD.

By synthesizing reactive powders via a self-sustaining combustion synthesis, the glycine-nitrate process, the gadolinium-doped ceria (GDC) with the chemical formula Ce0.8Gd0.2O1.9 was prepared. The resultant powders were dispersed with the terpineol as the dispersant through different methods such as ball milling and high-shear dispersing. Coagulation factor (CF) was used to mark the degree of agglomeration on the nano-scale GDC in this work. The effect of agglomeration on the densification behavior at different sintering temperatures was investigated. The studies indicated that agglomeration retarded the densification at the sintering stage. The powders with better dispersion exhibited a higher sintered density at the same temperature. After effective dispersion treatment, GDC could be fully densified at the sintering temperature of 1300 °C. The densification temperature was significantly lower than those reported previously. The high sintering kinetics of the ceramics was obtained based on the agglomeration control.

MicroRNAs (miRNAs) are small non-coding RNAs frequently dysregulated in human malignancies. In this study, we found that miR-181c was down-regulated both in glioblastoma tissues and cell lines. We also annotated 566 TCGA miRNA expression profiles and found that patients with high microRNA-181c (miR-181c)-expressing tumors had significantly longer OS and PFS. Overexpression of miR-181c evidently inhibited glioblastoma cell line T98G migration and invasion. Further, the expression of E-cadherin was significantly upregulated and that of N-cadherin and vimentin was significantly down-regulated. We also found that miR-181c overexpression inhibited TGF-β signaling by down-regulating TGFBR1, TGFBR2 and TGFBRAP1 expression. Overall, our study found that miR-181c plays a key role in glioblastoma cell invasion, migration and mesenchymal transition suggesting potential therapeutic applications.

The overall survival remains undesirable in clinical glioma treatment. Inhibition of DNA-PKcs activity by its inhibitors suppresses tumor growth and enhances chemosensitivity of several tumors to chemotherapy. However, whether DNA-PKcs could be a potential target in glioma therapy remains unknown. In this study, we reported that the hyperactivated DNA-PKcs was profoundly correlated with glioma malignancy and observe a significant association between DNA-PKcs activation and survival of the glioma patients. Our data also found that inhibition of DNA-PKcs by its inhibitor KU0060648 sensitized glioma cells to TMZ in vitro. Specifically, we demonstrated that KU0060648 interrupted the formation of DNA-PKcs/AKT complex, leading to suppression of AKT signaling and resultantly enhanced TMZ efficacy. Combination of KU0060648 and TMZ substantially inhibited downstream effectors of AKT. The in vivo results were similar to those obtained in vitro. In conclusion, this study indicated that inhibition of DNA-PKcs activity could suppress glioma malignancies and increase TMZ efficacy, which was mainly through regulation of the of AKT signaling. Therefore, DNA-PKcs/AKT axis may be a promising target for improving current glioma therapy.

Pyrolysis and combustion of wood under different oxygen concentrations were studied by using TG-FTIR analysis in this paper. Effects of oxygen concentration on TGA of wood and evolved gas analysis were thoroughly analyzed, and then the process of pyrolysis and combustion of wood was divided into four steps. The apparent activation energy of pyrolysis and combustion varied linearly with oxygen concentration. The effects of oxygen concentration on the mechanism of two stages of combustion of wood were also studied.

Biomass utilization could relieve the pressure caused by conventional energy shortage and environmental pollution. Advantage should be taken of the abundant biomass in China as clean energy source to substitute for traditional fossil fuels. At present, flash pyrolysis appears to be an efficient method to produce high yields of liquids that could either be directly used as fuel or converted to other valuable chemicals. Experiments were carried out of pyrolyzing biomass particles in a hot dense fluidized bed of sand to obtain high-quality bio-oil. Among four kinds of biomass species adopted in our experiment, Padauk Wood had the best characteristics in producing bio-oil. GC-MS analysis showed bio-oil to be a complex mixture consisting of many compounds. Furthermore, an integrated model was proposed to reveal how temperature influences biomass pyrolysis. Computation indicated that biomass particles underwent rapid heating before pyrolysis.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a member of the tumor necrosis factor alpha family of cytokines that preferentially induces apoptosis in transformed cells, making it a promising cancer therapy. However, many neoplasms are resistant to TRAIL-induced apoptosis by mechanisms that are poorly understood. We demonstrate that the expression of the small heat shock protein alpha B-crystallin (but not other heat shock proteins or apoptosis-regulating proteins) correlates with TRAIL resistance in a panel of human cancer cell lines. Stable expression of wild-type alpha B-crystallin, but not a pseudophosphorylation mutant impaired in its assembly and chaperone function, protects cancer cells from TRAIL-induced caspase-3 activation and apoptosis in vitro. Furthermore, selective inhibition of alpha B-crystallin expression by RNA interference sensitizes cancer cells to TRAIL. In addition, wild-type alpha B-crystallin promotes xenograft tumor growth and inhibits TRAIL-induced apoptosis in vivo in nude mice, whereas a pseudophosphorylation alpha B-crystallin mutant impaired in its anti-apoptotic function inhibits xenograft tumor growth. Collectively, these findings indicate that alpha B-crystallin is a novel regulator of TRAIL-induced apoptosis and tumor growth. Moreover, these results demonstrate that targeted inhibition of alpha B-crystallin promotes TRAIL-induced apoptosis, thereby suggesting a novel strategy to overcome TRAIL resistance in cancer.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising cancer therapy that preferentially induces apoptosis in cancer cells. However, many neoplasms are resistant to TRAIL by mechanisms that are poorly understood. Here we demonstrate that human breast cancer cells, but not normal mammary epithelial cells, are dramatically sensitized to TRAIL-induced apoptosis and caspase activation by peroxisome proliferator-activated receptor gamma (PPARgamma) agonists of the thiazolidinedione (TZD) class. Although TZDs do not significantly alter the expression of components of the TRAIL signaling pathway, they profoundly reduce protein levels of cyclin D3, but not other D-type cyclins, by decreasing cyclin D3 mRNA levels and by inducing its proteasomal degradation. Importantly, both TRAIL sensitization and reduction in cyclin D3 protein levels induced by TZDs are likely PPARgamma-independent because a dominant negative mutant of PPARgamma did not antagonize these effects of TZDs, nor were they affected by the expression levels of PPARgamma. TZDs also inhibit G(1) to S cell cycle progression. Furthermore, silencing cyclin D3 by RNA interference inhibits S phase entry and sensitizes breast cancer cells to TRAIL, indicating a key role for cyclin D3 repression in these events. G(1) cell cycle arrest sensitizes breast cancer cells to TRAIL at least in part by reducing levels of the anti-apoptotic protein survivin: ectopic expression of survivin partially suppresses apoptosis induced by TRAIL and TZDs. We also demonstrate for the first time that TZDs promote TRAIL-induced apoptosis of breast cancer in vivo, suggesting that this combination may be an effective therapy for cancer.

Intramembranous "gamma-secretase" processing of beta-amyloid precursor protein (APP) and other transmembrane proteins, including Notch, is mediated by a macromolecular complex consisting of presenilins (PSs), nicastrin (NCT), APH-1, and PEN-2. We now demonstrate that in cells coexpressing PS1, APH-1, and NCT, full-length PS1 accumulates to high levels and is fairly stable. Upon expression of PEN-2, the levels of PS1 holoprotein are significantly reduced, commensurate with an elevation in levels of PS1 fragments. These findings suggest that APH-1 and NCT are necessary for stabilization of full-length PS1 and that PEN-2 is critical for the proteolysis of stabilized PS1. In N2a and 293 cell lines that stably overexpress PS1, APH-1, NCT, and PEN-2, PS1 fragment levels are elevated by up to 10-fold over endogenous levels. In these cells, we find a marked accumulation of the APP-CTF gamma (AICD) fragment and a concomitant reduction in levels of both APP-CTF beta and CTF alpha. Moreover, the production of the gamma-secretase-generated Notch S3/NICD derivative is modestly elevated. However, we failed to observe a corresponding increase in levels of secreted A beta peptides in the medium of these cells. These results lead us to conclude that, although the PS1, APH-1, NCT, and PEN-2 are essential for gamma-secretase activity, the proteolysis of APP-CTF and Notch S2/NEXT are differentially regulated and require the activity of additional cofactors that promote production of AICD, NICD, and A beta.

A twin fluidized bed solid circulation system, in which two adjacent fluidized beds exchange solids, was developed for coal gasification to produce middle heating value gas. The effects of bed material, operation velocity, and bed structure on the solid circulating rate were tested at a small-scale test facility. Experimental results showed that the solid circulation rate of the system could be adjusted by changing gas velocities of two beds and could attain 30–40 times of the fuel feed rate, which would meet the demands of heat supply to an endothermic process of a gasifier. On the basis of experiments, reasonable operation and design parameters were put forward, which can be used to as a reference for the commercial gasifier design. A mathematical model was erected to calculate the solid circulation rate of the system, and it could predict well the solid flow rate through a horizontal orifice by comparison with experimental data.

We describe surgical treatment of a hemangiopericytoma in the anterior skull base and nasal cavity. The patient underwent a novel method of anterior skull base reconstruction, using the superior turbinate and cerebral falx, which was successful. The patient did not develop a cerebrospinal fluid leak or intracranial infection.

Rationale Pituitary adenomas secreting two or more hormones were referred to the plurihormonal tumors. The management of this type of the tumor was tumor resection and amelioration of the unbalanced hormones. However, it washard to cure the plurihormonal adenomas, as they were usually refractory to the traditional treatment. New therapeutic methods were needed in dealing this tumor. Patient concerns In this report, we described a patient who suffered from plurihormonal pituitary adenomas, with concomitant prolactin (PRL) and growth hormone (GH) secretion. The adenomas showed aggressive behaviors, which was giant, invasive, and refractory to bromocriptine treatments. Interventions The patient underwent a surgical treatment. Diagnosis The pathology together with clinical presentation and blood hormone test confirmed that it was PRL-GH secreting tumors. Outcomes Although a gross resection was achieved, the postoperative hormones were not normalized. There were also abundant programmed death ligand-1 proteins and CD8 lymphocyte infiltration in the tumor tissues. Lessons Our results indicated immunotherapy as a promising treatment for this tumor. More studies were needed to investigate the possibility of the immunotherapy in pituitary adenomas.

BACKGROUND: Medulloblastoma (MB) is the most common malignant brain tumor in children. Although accumulated research suggests that cancer stem-like cells may play a key role in medulloblastoma tumorigenesis, the molecular mechanisms of proliferation still remain elusive and further investigation can provide a novel application for therapeutic target in MB patients. METHODS: The expression of MELK and EZH2 was detected by tissue microarray analysis with 88 MBs and its association with prognosis was identified. Co-location of MELK and EZH2 in MB CSCs and tissues was studied by using confocal and immunostaining. Immunoblotting analysis following co-immunoprecipitation was performed to check the interaction between MELK and EZH2. Through the loss-of-function study by siRNA, CSCs-drived tumor growth was detected. Then we studied the targeted treatment of MB with MELK and EZH2 inhibitor in vivo to confirm the molecular basis of MELK and EZH2. RESULTS: MELK and EZH2 co-located in the nuclei of MB CSCs and MB with extensive nodularity and large cell/anaplastic differed the staining levels as measured using microarray analysis when compared with the other two subgroups. The proportion of MELK positive staining cells was the potential indicator for the survival. MELK bound and phosphorylated EZH2 and its methylation was induced by EZH2 in MB, which regulated the proliferation of CSCs. MELK and EZH2 depletion by siRNA or treatment of inhibitors attenuated the MB CSCs-derived tumor growth in vivo. CONCLUSION: Interaction between MELK and EZH2 is essential for MB CSCs-drived tumor proliferation, thereby identifying a potential therapeutic strategy for MB patients.

Detection of brain gliomas at the earliest stage is of great importance to improve outcomes, but it remains a most challenging task. In this study, oleic acid capped manganese oxide (MnO) nanoparticles (NPs) were prepared by the thermal decomposition of manganese oleate precursors and then transformed to water-dispersible MnO NPs by replacing oleic acid with N-(trimethoxysilylpropyl) ethylene diamine triacetic acid (TETT) silane. The covalently bonded TETT silane offers MnO NPs colloidal stability and abundant carboxylic functional groups allowing the further conjugation of the glioma-specific moiety, folic acid (FA). Moreover, the thin layer of TETT silane ensures a short distance between external Mn ion and water proton, which endows the FA-conjugated, TETT modified MnO (MnO-TETT-FA) NPs a longitudinal relaxivity as high as 4.83 mM(-1) s(-1). Accordingly, the in vivo magnetic resonance (MR) images demonstrated that MnO-TETT-FA NPs could efficiently enhance the MRI contrast for tiny brain gliomas. More importantly, due to the specificity of FA, MnO-TETT-FA NPs led to a clearer margin of the tiny glioma. This together with the good biocompatibility discloses the great potential of MnO-TETT-FA NPs as effective MRI contrast agents for the early diagnosis of brain gliomas.

To study the expression level of folate receptor α (FR-α) in glioma tissue and its clinical significance.Forty-eight human glioma specimens were collected from patients who underwent surgery from March 2012 to March 2013. These specimens were as follows:12 cases of glioblastoma (WHO IV), 6 cases of astrocytoma of each malignancy grade(WHO II, III), 6 cases of oligodendroastrocytoma of each malignancy grade (WHO II, III), 6 cases of oligodendroglioma of each malignancy grade (WHO II, III ). In addition, 6 cases of normal brain tissue resected from brain traumatic patients were taken as negative control, and one case of placental tissue (had got the consent of the parents and their families) was taken as positive control. The expression level of FR-α in tumor tissues was evaluated by Western blot analysis. The results of Western blot analysis were analyzed by t-test. The expression level of FR-α and Ki-67 in tumor tissues was evaluated immunohistochemistry, the results were analyzed by Kruskal-Wallis test and Nemenyi test. The correlation between the expression level of FR-α and cell proliferation index Ki-67 was analyzed by Pearson correlation analysis.Western blot analysis showed that the FR-α was not expressed in normal brain tissue and oligodendroglioma tissue, but highly expressed in astrocytoma, oligodendroastrocytoma and gliomablastoma. The expression level in WHO III astrocytoma was significantly higher than in WHO II (t = 4.497, P0.05). FR-α was also highly expressed in oligodendroastrocytoma and its expression level in WHO III was also significantly higher than in the WHO II (t = 2.876, P0.05). Foremore, immunohistochemistry analysis also showed that FR-α was not expressed in oligodendroglioma, but expressed in astrocytoma, oligodendroastrocytoma and gliomablastoma. The positive rate of FR-α of WHO III was significantly higher than the WHO II astrocytoma(57.8% ± 2.2% vs. 45.7% ± 2.3%,χ(2) = 3.871, P = 0.034). In oligodendroastrocytoma, the positive rate of FR-α of WHO III was significantly higher than the WHO II(56.5% ± 5.4% vs. 37.1% ± 5.2%,χ(2) = 4.454, P = 0.021). Moreover, the expression level of FR-α in gliomablastoma was highest in all histological types of gliomas, the positive rate of FR-α was up to 65.0% ± 4.5%. Pearson correlation analysis showed that the positive rate of FR-α was positively correlated with Ki-67 index (r = 0.903, P0.05).FR-α is expressed in astrocytoma, oligodendroastrocytoma and glioblastoma, and the expression level of FR-α is positively correlated with malignancy grade and Ki-67 index. Therefore, FR-α may be applied as a special target for diagnosis and treatment of glioma.

The advent of brain stimulation techniques to treat movement disorders and psychiatric diseases has shown potential to decode the neural mechanism that underlies the cognitive process by modulating the interrupted circuit. Here, the present investigation aimed at evaluating the influence of deep brain stimulation of the anterior nucleus thalamus (ANT-DBS) on memory.Thirty-two rats were randomized into phosphate buffer saline (PBS) group (n = 8, rats received PBS injections without implantation of electrodes into the ANT), Alzheimer's dementia (AD) group (n = 8, rats received Aβ1-40 injections without implantation of electrodes into the ANT), ANT sham stimulation group (n = 8, rats received Aβ1-40 injections with implantation of electrodes into the ANT but without stimulation) and ANT stimulation group (n = 8, rats received Aβ1-40 injections with implantation of electrodes into the ANT and stimulation). A Morris maze test was used for determining the effect of electrical stimulation on cognitive function in rats. The data were assessed statistically with one-way analysis of variance (ANOVA) followed by Tukey's tests for multiple post hoc comparisons.The data showed that in the training test, PBS group and AD group managed to learn the hidden-platform faster and faster while AD group needed a significantly longer time to reach the platform than PBS group (P0.05). Meanwhile, ANT stimulation group demonstrated a significantly shorter time to reach the platform (P0.05) compared to the AD group, while there was no significant difference between the ANT sham stimulation group and the AD group (P0.05). On the probe test, the AD group spent less time ((10.15 ± 2.34) seconds) in the target quadrant than the PBS group ((28.20 ± 2.75) seconds) (P0.05). And the times of platform-traversing of the AD group (3.35 ± 1.12) significantly decreased compared with the PBS group (8.69 ± 2.87) (P0.05). However, the times of platform-traversing and the time spent in the target quadrant of the ANT stimulation group significantly increased compared to the AD group (P0.05), while times of platform-traversing or the time spent in the target quadrant was not significantly different between the ANT sham stimulation group and the AD group (P0.05).Bilateral high-frequency stimulation of the ANT may be useful as a potential therapeutic modality for cognitive dysfunction in AD.

The basalt-borne peridotite xenoliths from Jiangsu-Anhui provinces were analyzed for whole rock Os isotopic compositions in two laboratories of USTC, China and CRPG, France, respectively. The 187 Os/ 188 Os ratio of the sample set ranges from 0.119 to 0.129 (25 samples, USTC) and from 0.117 to 0.131 (17 samples, CRPG). The Os isotopic compositions of most samples are less than 0.129 and depleted relatively to the primitive mantle, showing a good correlation with the major element compositions. With the 187 Os/ 188 Os-Al 2 O 3 alumichron, the samples yield a model age of 2.5 ± 0.1 Ga (data of USTC) and 1.9 ± 0.1 Ga (data of CRPG), late Archean to early Proterozoic. The two samples with the lowest 187 Os/ 188 Os ratio (0.119 and 0.117) have the T RD (Re depleted age) of 1.1 Ga (USTC) and 1.4 Ga (CRPG), mid-Proterozoic. The Os isotope model age shows that the peridotite xenoliths from Cenozoic alkali basalt in Jiangsu-Anhui provinces have an old formation age (early- to mid- Proterozoic). They are not newly produced mantle after the Phanerozoic replacement of the lithosphere mantle, but residual fractions of Proterozoic mantle.

A variety of investigations have led to the conclusion that presenilins (PS) play a critical role in intramembranous, gamma-secretase proteolysis of selected type I membrane proteins, including Notch1 and amyloid precursor protein (APP). We now show that the generation of the S3/Notch intracellular domain and APP-carboxyl-terminal fragment gamma (CTFgamma) derivatives are dependent on PS expression and inhibited by a highly selective and potent gamma-secretase inhibitor. Unexpectedly, the APP-CTFgamma derivative is generated by processing between Leu-645 and Val-646 (of APP(695)), several amino acids carboxyl-terminal to the scissile bonds for production of amyloid beta protein peptides. Although the relationship of APP-CTFgamma to the production of amyloid beta protein peptides is not known, we conclude that in contrast to the highly selective PS-dependent processing of Notch, the PS-dependent gamma-secretase processing of APP is largely nonselective and occurs at multiple sites within the APP transmembrane domain.

In the yeast Saccharomyces cerevisiae, two acyl-CoA:sterol acyltransferases (ASATs) that catalyze the synthesis of steryl esters have been identified, namely Are2p (Sat1p) and Are1p (Sat2p). Deletion of either ARE1 or ARE2 has no effect on cell viability, and are1are2 double mutants grow in a similar manner to wild-type despite the complete lack of cellular ASAT activity and steryl ester formation [Yang, H., Bard, M., Bruner, D. A., Gleeson, A., Deckelbaum, R. J., Aljinovic, G., Pohl, T. M., Rothstein, R. & Sturley, S. L. (1996) Science 272, 1353-1356; Yu, C., Kennedy, J., Chang, C. C. Y. & Rothblatt, J. A. (1996) J. Biol. Chem. 271, 24157-24163]. Here we show that both Are2p and Are1p reside in the endoplasmic reticulum as demonstrated by measuring ASAT activity in subcellular fractions of are1 and are2 deletion strains. This localization was confirmed by fluorescence microscopy using hybrid proteins of Are2p and Are1p fused to green fluorescent protein (GFP). Lipid analysis of are1 and are2 deletion strains revealed that Are2p and Are1p utilize sterol substrates in vivo with different efficiency; Are2p has a significant preference for ergosterol as a substrate, whereas Are1p esterifies sterol precursors, mainly lanosterol, as well as ergosterol. The specificity towards fatty acids is similar for both isoenzymes. The lack of steryl esters in are1are2 mutant cells is largely compensated by an increased level of free sterols. Nevertheless, terbinafine, an inhibitor of ergosterol biosynthesis, inhibits growth of are1are2 cells more efficiently than growth of wild-type. In a growth competition experiment are1are2 cells grow more slowly than wild-type after several rounds of cultivation, suggesting that Are1p and Are2p or steryl esters, the product formed by these two enzymes, are more important in the natural environment than under laboratory conditions.

Acyl-CoA:cholesterol acyltransferase (ACAT) is a key enzyme in cellular cholesterol homeostasis and in atherosclerosis. ACAT-1 may function as an allosteric enzyme. We took a multifaceted approach to investigate the subunit composition of ACAT-1. When ACAT-1 with two different tags were co-expressed in the same Chinese hamster ovary cells, antibody specific to one tag caused co-immunoprecipitation of both types of ACAT-1 proteins. Radioimmunoprecipitations of cells expressing the untagged ACAT-1 or the 6-histidine-tagged ACAT-1 yielded a single radiolabeled band of predicted size on SDS-polyacrylamide gel electrophoresis. These results show that ACAT-1 exists as homo-oligomers in intact Chinese hamster ovary cells. We solubilized HisACAT-1 with the detergent deoxycholate or CHAPS (3-[(3-cholamidopropyl)-dimethylammonio]-1-propanesulfonic acid), performed gel filtration chromatography and sucrose density gradient centrifugations in H(2)O and D(2)O, and determined the Stokes radii and sedimentation coefficients of the HisACAT1-detergent complexes. The estimated molecular mass of HisACAT-1 is 263 kDa, which is 4 times that of the HisACAT-1 monomer (69 kDa). Finally, cross-linking experiments in intact cells and in vitro show that the increase in cross-linker concentrations causes an increase in size of the HisACAT-1-positive signals, forming material(s) 4 times the size of the monomer, supporting the conclusion that ACAT-1 is a homotetrameric enzyme.

The ε4 allele of the gene that encodes apolipoprotein E (APOE4) is the greatest genetic risk factor for Alzheimer's disease (AD), while APOE2 reduces AD risk, compared to APOE3. The mechanism(s) underlying the effects of APOE on AD pathology remains unclear. In vivo, dendritic spine density is lower in APOE4-targeted replacement (APOE-TR) mice compared with APOE2- and APOE3-TR mice. To investigate whether this apoE4-induced decrease in spine density results from alterations in the formation or the loss of dendritic spines, the effects of neuron age and apoE isoform on the total number and subclasses of spines were examined in long-term wild-type neurons co-cultured with glia from APOE2-, APOE3- and APOE4-TR mice. Dendritic spine density and maturation were evaluated by immunocytochemistry via the presence of drebrin (an actin-binding protein) with GluN1 (NMDA receptor subunit) and GluA2 (AMPA receptor subunit) clusters. ApoE isoform effects were analyzed via a method previously established that identifies phases of spine formation (day-in-vitro, DIV10–18), maintenance (DIV18–21) and loss (DIV21–26). In the formation phase, apoE4 delayed total spine formation. During the maintenance phase, the density of GluN1 + GluA2 spines did not change with apoE2, while the density of these spines decreased with apoE4 compared to apoE3, primarily due to the loss of GluA2 in spines. During the loss phase, total spine density was lower in neurons with apoE4 compared to apoE3. Thus, apoE4 delays total spine formation and may induce early synaptic dysfunction via impaired regulation of GluA2 in spines.

The post-menopausal loss of estrogen is key in the increased incidence of Alzheimer's disease (AD) in women. However, estrogen therapy (ET) clinical trials have produced conflicting results. The APOE gene of apolipoprotein E (apoE) likely modulates the effects of ET in AD. APOE4 is the greatest genetic risk factor for AD, increasing risk up to 15-fold compared with APOE3, and the negative effect of APOE4 on AD risk and neuropathology is greater in women than men. The interactive effects of APOE and ET may converge on modulation of amyloid-beta (Aβ) levels, as independently both the loss of estrogen and APOE4 increases Aβ accumulation. Thus, in this study, 3-month old female EFAD mice (5XFAD mice crossed with apoE-targeted replacement mice), which express increased levels of Aβ42 and human APOE were ovariectomized and treated for 3 months with either 17-β estradiol (OVX(ET+), 0.25mg total) or vehicle control (OVX(ET-)) and the effects on Aβ accumulation were determined. Compared to the OVX(ET-) cohort, in the OVX(ET+) cohort, extracellular amyloid and Aβ deposition in the hippocampus and cortex were decreased with APOE2 and APOE3, but were increased with APOE4 by IHC. Biochemical analysis demonstrated increased total and insoluble Aβ levels with APOE4, and decreased soluble Aβ42 levels with both APOE3 and APOE4, after ET. These data suggest that ET administered at menopause may benefit APOE4 negative women by decreasing extracellular and soluble Aβ42. However, for APOE4 carriers, the efficacy of ET will be dependent on the relative impact of extracellular and soluble Aβ on AD-induced neurodegeneration.

The aim of this study was to evaluate the clinical results and surgical outcomes of cystic vestibular schwannomas (VSs) with fluid-fluid levels.Forty-five patients with cystic VSs and 86 with solid VSs were enrolled in the study. The patients in the cystic VSs were further divided into those with and without fluid-fluid levels. The clinical and neuroimaging features, intraoperative findings, and surgical outcomes of the 3 groups were retrospectively compared.Peritumoral adhesion was significantly greater in the fluid-level group (70.8%) than in the nonfluid-level group (28.6%) and the solid group (25.6%; p0.0001). Complete removal of the VS occurred significantly less in the fluid-level group (45.8%, 11/24) than in the nonfluid-level group (76.2%, 16/21) and the solid group (75.6%, 65/86; p = 0.015). Postoperative facial nerve function in the fluid-level group was less favorable than in the other 2 groups; good/satisfactory facial nerve function 1 year after surgery was noted in 50.0% cases in the fluid-level group compared with 83.3% cases in the nonfluid-level group (p = 0.038).Cystic VSs with fluid-fluid levels more frequently adhered to surrounding neurovascular structures and had a less favorable surgical outcome. A possible mechanism of peritumoral adhesion is intratumoral hemorrhage and consequent inflammatory reactions that lead to destruction of the tumor-nerve barrier. These findings may be useful in predicting surgical outcome and planning surgical strategy preoperatively.

Background The medial wall of the cavernous sinus is believed to play a significant role in determining the direction of growth of pituitary adenomas and in planning pituitary surgery. However, it remains unclear whether there is a dural wall between the pituitary gland and the cavernous sinus. Objective To identify and trace the membranelike structures medial to the cavernous sinus and around the pituitary gland and their relationships with surrounding structures. Methods Sixteen cadavers (7 females and 9 males; age range, 54-89 years; mean age, 77 years) were used in this study and prepared as 16 sets of transverse (5 sets), coronal (2 sets), and sagittal (9 sets) plastinated sections that were examined at both macro- and microscopic levels. Results The pituitary gland was fully enclosed in a fibrous capsule, but the components and thickness of the capsule varied on different aspects of the gland. The meningeal dural layer was sandwiched between the anterosuperior aspect of the gland capsule and the cavernous sinus. Posteroinferiorly, however, this dural layer disappeared as it fused with the capsule. A weblike loose fibrous network connected the capsule, carotid artery, venous plexus, and the dura of the middle cranial fossa. Conclusion The medial wall of the cavernous sinus consists of both the meningeal dura and weblike loose fibrous network, which are located at the anterosuperior and posteroinferior aspects, respectively.

The transcriptional regulator PRDM1 controls cell-fate decisions and has been implicated in human tumorigenesis as a tumor suppressor. However, its pathological role in glioma remains elusive. In this study, we showed that PRDM1 protein levels were inversely correlated with the pathological grade of gliomas and were predictive of patient survival in a retrospective analysis. Restored expression of PRDM1 inhibited proliferation and suppressed invasion by glioma cells. Mechanistic investigation revealed that PRDM1 attenuated glioma malignancy by negatively modulating Wnt/β-catenin signaling and this modulation was dependent on the Wnt inhibitor Dkk1. Using bioinformatics and biological approaches, we found that PRDM1 was a direct target of miR-30a-5p, and PRDM1 dysfunction was attributable to miR-30a-5p-mediated repression. Our results provide evidence that PRDM1 deficiency contributes to the phenotype maintenance and pathogenesis of gliomas.

APOE4 is the greatest risk factor for Alzheimer disease (AD) and synergistic effects with amyloid-β peptide (Aβ) suggest interactions among apoE isoforms and different forms of Aβ accumulation. However, it remains unclear how the APOE genotype affects plaque morphology, intraneuronal Aβ, soluble Aβ42, and oligomeric Aβ (oAβ), particularly in vivo. As the introduction of human APOE significantly delays amyloid deposition in transgenic mice expressing familial AD (FAD) mutations (FAD-Tg), 5xFAD-Tg mice, which exhibit amyloid deposition by age 2 months, were crossed with apoE-targeted replacement mice to produce the new EFAD-Tg mice. Compared with 5xFAD mice, Aβ deposition was delayed by ∼4 months in the EFAD mice, allowing detection of early changes in Aβ accumulation from 2–6 months. Although plaque deposition is generally greater in E4FAD mice, E2/E3FAD mice have significantly more diffuse and E4FAD more compact plaques. As a first report in FAD-Tg mice, the APOE genotypes had no effect on intraneuronal Aβ accumulation in EFAD mice. In E4FAD mice, total apoE levels were lower and total Aβ levels higher than in E2FAD and E3FAD mice. Profiles from sequential three-step extractions (TBS, detergent, and formic acid) demonstrated that the lower level of total apoE4 is reflected only in the detergent-soluble fraction, indicating that less apoE4 is lipoprotein-associated, and perhaps less lipidated, compared with apoE2 and apoE3. Soluble Aβ42 and oAβ levels were highest in E4FAD mice, although soluble apoE2, apoE3, and apoE4 levels were comparable, suggesting that the differences in soluble Aβ42 and oAβ result from functional differences among the apoE isoforms. Thus, APOE differentially regulates multiple aspects of Aβ accumulation.

Background The form(s) of amyloid-β peptide (Aβ) associated with the pathology characteristic of Alzheimer's disease (AD) remains unclear. In particular, the neurotoxicity of intraneuronal Aβ accumulation is an issue of considerable controversy; even the existence of Aβ deposits within neurons has recently been challenged by Winton and co-workers. These authors purport that it is actually intraneuronal APP that is being detected by antibodies thought to be specific for Aβ. To further address this issue, an anti-Aβ antibody was developed (MOAB-2) that specifically detects Aβ, but not APP. This antibody allows for the further evaluation of the early accumulation of intraneuronal Aβ in transgenic mice with increased levels of human Aβ in 5xFAD and 3xTg mice. Results MOAB-2 (mouse IgG2b) is a pan-specific, high-titer antibody to Aβ residues 1-4 as demonstrated by biochemical and immunohistochemical analyses (IHC), particularly compared to 6E10 (a commonly used commercial antibody to Aβ residues 3-8). MOAB-2 did not detect APP or APP-CTFs in cell culture media/lysates (HEK-APPSwe or HEK-APPSwe/BACE1) or in brain homogenates from transgenic mice expressing 5 familial AD (FAD) mutation (5xFAD mice). Using IHC on 5xFAD brain tissue, MOAB-2 immunoreactivity co-localized with C-terminal antibodies specific for Aβ40 and Aβ42. MOAB-2 did not co-localize with either N- or C-terminal antibodies to APP. In addition, no MOAB-2-immunreactivity was observed in the brains of 5xFAD/BACE-/- mice, although significant amounts of APP were detected by N- and C-terminal antibodies to APP, as well as by 6E10. In both 5xFAD and 3xTg mouse brain tissue, MOAB-2 co-localized with cathepsin-D, a marker for acidic organelles, further evidence for intraneuronal Aβ, distinct from Aβ associated with the cell membrane. MOAB-2 demonstrated strong intraneuronal and extra-cellular immunoreactivity in 5xFAD and 3xTg mouse brain tissues. Conclusions Both intraneuronal Aβ accumulation and extracellular Aβ deposition was demonstrated in 5xFAD mice and 3xTg mice with MOAB-2, an antibody that will help differentiate intracellular Aβ from APP. However, further investigation is required to determine whether a molecular mechanism links the presence of intraneuronal Aβ with neurotoxicity. As well, understanding the relevance of these observations to human AD patients is critical.

Although the direct combustion of biomass for energy that applies circulating fluidized bed (CFB) technology is steadily expanding worldwide, only few studies have conducted an environmental assessment of biomass ash thus far. Therefore, this study aims to integrate information on the environmental effects of biomass ash. We investigated the concentration of heavy metal in biomass ash samples (bottom ash, cyclone ash, and filter ash) derived from a CFB boiler that combusted agricultural and forest residues at a biomass power plant (2×12 MW) in China. Ash samples were gathered for the digestion and leaching test. The heavy metal content in the solution and the leachate was studied via an inductively coupled plasma-mass spectrometer and a Malvern Mastersizer 2000 mercury analyzer. Measurements for the chemical composition, particle size distribution, and the surface morphology were carried out. Most of the metals in cyclone ash particles were enriched, whereas Ti and Hg were enriched in filter ash. Residence time contributed most to heavy metal enrichment. Under HJ/T 300 conditions, the heavy metals showed serious leaching characteristics. Under EN 12457-2 conditions, leaching behavior was hardly detected.

Apolipoprotein E (apoE) and apoE/amyloid-β(Aβ) transgenic (Tg) mouse models are critical to understanding apoE-isoform effects on Alzheimer's disease risk. Compared to wild type,apoE−/−mice exhibit neuronal deficits, similar to apoE4-Tg compared to apoE3-Tg mice, providing a model for Aβ-independent apoE effects on neurodegeneration. To determine the effects of apoE on Aβ-induced neuropathology,apoE−/−mice were crossed with Aβ-Tg mice, resulting in a significant delay in plaque deposition. Surprisingly, crossing human-apoE-Tg mice withapoE−/−/Aβ-Tg mice further delayed plaque deposition, which eventually developed in apoE4/Aβ-Tg mice prior to apoE3/Aβ-Tg. One approach to address hAPOE-induced temporal delay in Aβpathology is an additional insult, like head injury. Another is crossing human-apoE-Tg mice with Aβ-Tg mice that have rapid-onset Aβpathology. For example, because 5xFAD mice develop plaques by 2 months, the prediction is that human-apoE/5xFAD-Tg mice develop plaques around 6 months and 12 months before other human-apoE/Aβ-Tg mice. Thus, tractable models for human-apoE/Aβ-Tg mice continue to evolve.

The rheological characteristics of granular pseudo-fluid are studied using conventional method from continuous-flow theory. Quartz sand particle systems in different sizes, spherical glass particles and alumina particles are focused in this work for their low-velocity shearing movements in a small gap between two concentric rotating cylinders. The accurate rheological equations of those granular systems were obtained and it was found that the shear stress all decreases with the increasing shear rate, it is a totally different trend comparing with normal fluid. Detailed analyzing was carried out on the effects of particle size, shape and surface property on this very special rheological phenomenon. It can be concluded that those physical characteristics of particle and the bearing capacity of tangential force on the particle contact surface are key factors to the distribution and strength of the force chains in the granular systems, and the appearance of force chains is the fundamental reason to the specificity of those granular pseudo-fluid.

The combustion of biomass was studied experimentally in a 0.5MW circulating fluidized bed combustor. Sugarcane, bark and sawdust were used as feeding materials. During the combustion process, the bed temperature was kept at a low level (750 °C) to inhibit ash melting and overcome agglomeration. The temperature distributions along the height of furnace and combustion efficiency were analyzed. In addition, the influence of air staging on NO emission has been investigated. The results showed that most part of biomass combustion occurs in the freeboard. The combustion efficiency can be high even at low temperature, and the value reaches 99.07% in the sugarcane run. Moreover, the adoption of secondary air not only reduces the flue gas CO concentration, but also suppress the NO formation to some extent. The results of this study can provide guidance for industrial practice.

This chapter outlines protocols that produce homogenous preparations of oligomeric and fibrillar amyloid -β peptide (Aβ). While there are several isoforms of this peptide, the 42 amino acid form is the focus because of its genetic and pathological link to Alzheimer’s disease (AD). Past decades of AD research highlight the dependence of Aβ42 function on its structural assembly state. Biochemical, cellular and in vivo studies of Aβ42 usually begin with purified peptide obtained by chemical synthesis or recombinant expression. The initial steps to solubilize and prepare these purified dry peptide stocks are critical to controlling the structural assembly of Aβ. To develop homogenous Aβ42 assemblies, we initially monomerize the peptide, erasing any “structural history” that could seed aggregation, by using a strong solvent. It is this starting material that has allowed us to define and optimize conditions that consistently produce homogenous solutions of soluble oligomeric and fibrillar Aβ42 assemblies. These preparations have been developed and characterized by using atomic force microscopy (AFM) to identify the structurally discrete species formed by Aβ42 under specific solution conditions. These preparations have been used extensively to demonstrate a variety of functional differences between oligomeric and fibrillar Aβ42. We also present a protocol for fluorescently labeling oligomeric Aβ42 that does not affect structure, as measured by AFM, or function, as measured by a cellular uptake assay. These reagents are critical experimental tools that allow for defining specific structure/function connections.

The geometric constraint solving can transform into the numerical optimization solving. In the paper introduce a hybrid approach that simultaneously applies Genetic Algorithm (GA), and tabu search (TS) to create a generally well-performing search heuristics, and combat the problem of premature convergence. This algorithm uses GA to search the area where the best solution may exist in the whole space, and then. When the algorithm approaches to the best solution and the search speed is too slow, we can change to the effective local search strategy—TS in order to enhance the ability of the GA on fine searching. It makes the algorithm get rid off the prematurity convergence situation. We apply this algorithm into the geometric constraint solving. The experiment shows that the hybrid algorithm has the effective convergence property and it can find the global best solution.

Potassium in straw is relatively high and exists mainly as readily available potassium (K(r)). The release and transformation of the K(r) during biomass combustion mean a decrease or loss of potash fertiliser value. The purpose of this work is to quantify the transformation and the distribution of the K(r) under conditions that can obviously reduce the loss of it, and then to try to offer some suggestions for new biomass projects. A pilot-scale circulating fluidized bed (CFB) combustor (0.5 MW(th)) has been applied to combust rice straw. The combustion temperature was kept at a low level (lower than 700 degrees C) to reduce the transformation of potassium. The K(r) and the total potassium (K(t)) in the rice straw, the bottom ash, and the flyash were determined after chemical fractionation and wet acid digestion, respectively. The mass balance of the biomass ash, the K(r) and the K(t) in stable operation were quantified. The experimental results showed that the flyash accounted for more than 95% of the total straw ash. The flyash contained around 92% of the K(t) and 86% of the K(r) of the straw. In the flyash about 3% of the K(r) of straw was transformed to unavailable potassium (K(u)) during combustion. On the basis of the obtained results, four suggestions that reduce the loss of the K(r) are given for the better development of biomass-fired power plants.

Soluble forms of amyloid-β peptide (Aβ) are a molecular focus in Alzheimer's disease research. Soluble Aβ dimers (≈ 8 kDa), timers (≈ 12 kDa), tetramers (≈ 16 kDa) and Aβ*56 (≈ 56 kDa) have shown biological activity. These Aβ molecules have been derived from diverse sources, including chemical synthesis, transfected cells, and mouse and human brain, leading to uncertainty about toxicity and potency. Herein, synthetic Aβ peptide-derived oligomers, cell- and brain-derived low-n oligomers, and Aβ*56, were injected intracerebroventricularly (icv) into rats assayed under the Alternating Lever Cyclic Ratio (ALCR) cognitive assay. Cognitive deficits were detected at 1.3μM of synthetic Aβ oligomers and at low nanomolar concentrations of cell-secreted Aβ oligomers. Trimers, from transgenic mouse brain (Tg2576), did not cause cognitive impairment at any dose tested, whereas Aβ*56 induced concentration-dependent cognitive impairment at 0.9μM and 1.3μM. Thus, while multiple forms of Aβ have cognition impairing activity, there are significant differences in effective concentration and potency.

Restenosis is one of several complications following carotid endarterectomy (CEA). The pathogenesis of restenosis may be related to postsurgery inflammation and leukocyte recruitment mediated by cellular adhesion molecules. In this study, we examine the role of vascular cell adhesion molecule-1 (VCAM-1) in carotid neointimal hyperplasia following carotid surgical mechanical de-endothelialization (CSMDE) in a rat model of CEA.The inhibition of siRNA on VCAM-1 protein expression was determined by using the methods of immunostaining and Western blot. Ultrasound imaging and morphometric analysis were applied to measure the degree of CSMDE-induced carotid artery neointimal hyperplasia of rats.We found that a lentivirus-based construct expressing a small interfering RNA (siRNA) against VCAM-1 could effectively (P.05, n = 10 per group) reduce VCAM-1 protein expression in the carotid arteries of rats undergoing CSMDE (CSMDE+RNAi: 135.0 +/- 27.6%) when compared that of CSMDE with scrambled siRNA (CSMDE+CON: 182.7 +/- 36.4%). Doppler ultrasonography revealed that CSMDE+RNAi was accompanied by a significant reduction in the extent of stenosis demonstrated by increased blood velocity (665.85 +/- 48.37 mm/s) and linear diameter (0.59 +/- 0.77 mm) compared to CSMDE+CON (46.72 +/- 28.67 mm/s with undetectable linear diameter, P.05, n = 10 per group). In addition, morphometric analysis of hematoxylin and eosin (HE)-stained sections indicated that the intima (innermost layer of media at lesion site)/media area ratio (I/M) was significantly increased (P.05, n = 10 per group) both in the CSMDE (3.99 +/- 0.65) and CSMDE+CON (4.33 +/- 0.59) groups compared with the SHAM group (0.35 +/- 0.13). However, CSMDE+RNAi resulted in a significant (P.05, n = 10 per group) decrease in the I/M ratio (1.79 +/- 0.43) compared to CSMDE+CON, whereas there were no significant differences in the total arterial area and medial areas among the groups.These results suggest that perivascular events mediated by VCAM-1 are likely to play an important role in the pathogenesis of carotid artery neointimal hyperplasia in rats after CSMDE.