超线性Hammerstein型积分方程组的特征值与特征函数

在一定条件下讨论了超线性Hammerstein积分方程组的特征值与特征函数及其性质，对已有结果做了本质上的推广.

关于单纯逼近的定义与Croom商榷

将 Croom 关于多面体之间的连续映射的单纯逼近的定义与一般通常采用的定义进行比较,指出这2种定义是不等价的,由于 Croom 的定义减弱了条件,不要求满足星形性质,因而不能反映“逼近”的程度,致使应用该定义时不得不补足条件.

Effect of lead on ERK activity and the protective function of bFGF in rat primary culture astroglia

Objective： To observe the effects of lead on levels ofphosphorylated extracellular signal regulated kinase （p-ERK） in the cytoplasm of primary cultures of rat astroglial cells and the possible protective effect of basic fibroblast growth factor （bFGF） on lead-induced effects. Methods： The primary astroglia cells from 1-6 d old Wistar rats were cultured. The cells pretreated with the MEK1 （mitogen-activated protein kinase kinase 1） inhibitor PD98059 and bFGF, respectively, were exposed to Pb acetate of different concentrations for different times. Western blotting and reverse transcription polymerase chain reaction （RT-PCR） methods were used to detect the protein and mRNA expressions of ERK. Results： mRNA expression for ERK peaked 15 min after initiation of lead exposure （P〈0.05） and protein expression of p-ERK peaked at 30 min （P〈0.05）. ERK mRNA levels and p-ERK protein levels returned to baseline after 60 and 120 min of lead exposure, respectively （P〉0.05）. The increase in p-ERK levels in lead-treated cells could be inhibited by PD098059. Activation of ERK in the cells by lead was prevented by pretreatment with bFGF. Total ERK protein levels did not change under the same experimental conditions （P〉0.05）. Conclusion： Low-level lead exposure resulted in transient activation of ERK through the MEK pathway, which then returned to basal levels in the continued presence of lead. Exogenous bFGF protected ERK signaling components in astroglia from lead poisoning.

Hub Genes of Astrocyte Involved in Glaucoma with Ocular Hypertension by Integrated Bioinformatics Analysis

This study was conducted to elucidate the potential key candidate genes and pathways in role of astrocyte involved in glaucoma with ocular hypertension.Methods Expression profiles GSE2378 and GSE758 including 27 reactive optic nerve head astrocytes(ONHAs)by hypertensions and 26 normal controls,were integrated and deeply analyzed.Differentially expressed genes(DEGs)were sorted and candidate genes and pathways enrichment were analyzed.DEGs-associated protein-protein interaction network(PPI)was performed.Results A total of 119 consistently expressed genes were identified from 281 commonly changed DEGs,including 68 up-regulated genes and 51 down-regulated genes.PPI network complex filtered 75 DEGs(43 up-regulated and 32 down-regulated genes)of the 119 consistently altered DEGs and developed 117 edges,and 10 hub genes were identified.The most significant 3 modules were filtered from PPI,pathway enrichment analysis showed that module 1 was associated with extracellular exosome.Module 2 was mainly associated with antibody-dependent cellular cytotoxicity(ADCC)and module 3 was mainly associated with Hippo signaling pathway.Conclusion Taken above,using integrated bioinformatical analysis,we have identified DEGs candidate genes and pathways in role of astrocyte involved in glaucoma with ocular hypertension,which could improve our understanding of the cause and underlying molecular events,and these candidate genes and pathways could be therapeutic targets for glaucoma.

On the nature of X-ray “unobscured” Seyfert 2 galaxies

We present a systematic study to reveal the effect of host galaxy contamination to the identification of X-ray "unobscured" Seyfert 2 galaxies.We compiled a sample of 14 X-ray "unobscured" Seyfert 2 galaxies and 29 X-ray obscured Seyfert 2s,with infrared [Ne II] and [O IV] emission line flux measurements.In this work we classify Seyfert 2s as "unobscured" or obscured in X-ray simply based on X-ray spectral fitting.We find that our X-ay "unobscured" Seyfert 2s have statistically higher [Ne II]/[O IV] line ratios,compared with obscured ones.Since the [Ne II]/[O IV] line ratio reflects the relative strength of star formation activity comparing with the SMBH accretion,the observed differences in [Ne II]/[O IV] line ratios clearly indicate relatively stronger X-ray contamination from star formation in the host galaxies in X-ray "unobscured" Seyfert 2s.Therefore we could attribute the X-ray "unobscured" appearance to host galaxy contamination for most(if not all) of our X-ray "unobscured" Seyfert 2s.Further analysis indicates that "unobscured" Seyfert 2s have intrinsically lower AGN luminosity but similar star formation rates,compared with obscured ones.This is also consistent with previous studies showing most X-ray "unobscured" Seyfert 2s are at lower luminosities,and relatively stronger contaminations from the host galaxies are thus expected.Finally we develop a screening criterion to distinguish potential pure Seyfert 2s from X-ray "unobscured" appearances which could be caused by strong host galaxy contamination.

Targeting Wnt signaling at the neuroimmune interface for dopaminergic neuroprotectionJrepair in Parkinson＇s disease

During the past three decades, the Wingless-type MMTV integration site （Wnt） signaling cascade has emerged as an essential system regulating multiple processes in developing and adult brain. Accumulating evidence points to a dysregulation of Wnt signaling in major neurodegenerative pathologies including Parkinson＇s disease （PD）, a common neurodegenerative disorder characterized by the pro- gressive loss of midbrain dopaminergic （mDA） neurons and deregulated activation of astrocytes and microglia. This review highlights the emerging link between Wnt signaling and key inflammatory pathways during mDA neuron damage/repair in PD progression. In particular, we summarize recent evidence documenting that aging and neurotoxicant exposure strongly antagonize Wnt/β-catenin signaling in mDA neurons and subventricular zone （SVZ） neuroprogenitors via astrocyte-microglial interactions. Dysregulation of the crosstalk between Wnt/β-catenin signaling and anti-oxidant/anti-inflammatory pathways delineate novel mechanisms driving the decline of SVZ plasticity with age and the limited nigrostriatal dopaminergic self-repair in PD. These findings hold a promise in devetoping therapies that target Wnt/β-catenin signaling to enhance endogenous restoration and neuronal outcome in age-dependent diseases, such as PD.

Protective effect of astrocyte-conditioned medium on neurons following hypoxia and mechanical injury

Objective： To investigate the protective effect of mouse astrocyte-conditioned medium （ACM） on hypoxic and mechanically injured neurons by a cell model in vitro, and to explore the possible mechanism. Methods： The model of hypoxic neuronal injury was caused by 3% 02 in three-gas incubator. Neurons were cultured with ordinary medium or 20% ACM respectively and randomly divided into hypoxic group （hypoxia for 4, 8, 24 h and marked as H4R0, H8R0, H24R0） and hypoxia reoxygenation group （H4R24, H8R24, H24R24）. Mechanical injury model was developed by scratching neurons cultured in 20% ACM or ordinary medium to different degrees. Neu- rons in both medium were divided into normal control group, mild, moderate and severe injury groups. The 20% ACM was added 24 h before hypoxia/reoxygenation or mechanical injury. The morphology and survival of neurons were observed and counted by trypan blue staining. The concentration of NO, lactic dehydrogenase （LDH） and membrane ATPase activity were detected by corresponding kits. Results： It was showed that 20% ACM can obviously promote the survival rate of hypoxia/reoxygenated neurons and scratched neurons as well. The morphology and num- ber of neurons exposed to hypoxia or scratch injury showed great difference between groups with or without ACM treatment. Compared with control group, the concentration of NO and LDH was much lower in hypoxic/reoxygenated neurons treated with 20% ACM, and the ATPase activity was higher. For the mechanical injury model, neurons with moderate injury also revealed a lower NO and LDH concen- tration than the control group. All the differences were sta- tistically significant （P〈0.05）. Conclusion： ACM can promote the survival and func- tional recovery of neurons following hypoxia or scratching to a certain degree. The mechanism may be associated with reducing the synthesis and release of NO and LDH as well as increasing the activity of membrane ATPase.