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A comparative study was conducted on the soil C and N pools in a 19-year-old broadleaf plantation and a Chinese fir (Cunninghamia lanceolata) plantation in subtropical China, aimed to understand the effects of tree species on the soil C and N pools. In the broadleaf plantation, the C and N stocks in 0-40 cm soil layer were 99.41 Mg.hm-2 and 6. 18 Mg.hm-2, being 33.1 % and 22. 6 % larger than those in Chinese fir plantation, respectively. The standing biomass and the C and N stocks of forest floor in the broadleaf plantation were 1.60, 1.49, and 1.52 times of those in Chinese fir plantation, respectively, and the differences were statistically significant. There was a significant negative relationship between the forest floor C/N ratio and the soil C and N stocks. In the broadleaf plantation, the fine root biomass in 0-80 cm soil layer was 1.28 times of that in the Chinese fir plantation, and the fine root biomass in 0-10 cm soil layer accounted for 48. 2 % of the total fine root biomass. The C and N stocks in the fine roots in the broadleaf plantation were also higher than those in the Chinese fir plantation. In 0-10 cm soil layer, its C stock had a significant positive relationship with the fine root C stock. It was suggested that as compared with Chinese fir plantation, the soil in broadleaf plantation had a greater potential to accumulate organic carbon.

Recent studies have shown that oligomeric amyloid-β (oAβ) peptide can potentially activate microglia in addition to inducing more potent neurotoxicity compared with fibrillar Aβ (fAβ); however, its mechanisms of action remain unclear. This study was designed to investigate the possible mechanisms involved in the microglial activation induced by oAβ in BV-2 microglial cells. The results showed that oAβ induced activated properties of microglia, including higher proliferative capacity as well as increased production of reactive oxygen species, nitric oxide (NO), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β). NADPH oxidase inhibitors [diphenylene iodonium (DPI) and apocynin (4-hydroxy-3-methoxy-acetophenone)] prevented the microglial activation induced by oAβ, suggesting that NADPH oxidase activation was involved in microglial activation. In addition, TNF-α and IL-1β, which are massively released by activated microglia, significantly induced the activation of microglia, thereby resulting in the production of NO and proliferation of microglia, respectively. These effects could be inhibited by diphenylene iodonium and apocynin, indicating a self-cycle regulated by NADPH oxidase in microglial activation in response to oAβ. In conclusion, microglial activation induced by oAβ is possibly mediated by NADPH oxidase, suggesting that oAβ, which is normally considered a neurotoxin, may also lead to indirect neuronal damage through the pro-inflammation activation of microglia in Alzheimer's disease and that NADPH oxidase could be a potential target to prevent oAβ-induced inflammatory neurodegeneration.

Pseudoginsenoside-F11 (PF11), a component of Panax quinquefolism (American ginseng), plays a lot of beneficial effects on disorders of central nervous system. In this paper, the neuroprotective effect of PF11 on Parkinson's disease (PD) and the possible mechanism were investigated in a rat PD model. PF11 was orally administered at 3, 6, and 12 mg/kg once daily for a period of 2 weeks before and 1 week after the unilateral lesion of left medial forebrain bundle (MFB) induced by 6-hydroxydopamine (6-OHDA). The results showed that PF11 markedly improved the locomotor, motor balance, coordination, and apomorphine-induced rotations in 6-OHDA-lesioned rats. The expression of tyrosine hydroxylase (TH) in substantia nigra (SN) and the content of extracellular dopamine (DA) in striatum were also significantly increased after PF11 treatment. Moreover, significant reduction in the levels of striatal extracellular hydroxyl radical ( (∙) OH), detected as 2,3- and 2,5-dihydroxy benzoic acid (2,3- and 2,5-DHBA), and increase in the level of striatal extracellular ascorbic acid (AA) were observed in the PF11-treated groups compared with 6-OHDA-lesioned rats. Taken together, we propose that PF11 has potent anti-Parkinson property possibly through inhibiting free radical formation and stimulating endogenous antioxidant release.

Objective: To evaluate systematically the effect of n-3 long-chain polyunsaturated fatty acid (n-3 LC-PUFA) supplementation of pregnant women on head circumference of newborn infants., Methods: A thorough literature search was done for full texts which studied the effect of n-3 LC-PUFA supplementation of pregnant women on head circumference of newborn infants among PubMed, Cochrane Library, Chinese periodical full text database and Wanfang database using the mesh terms as n-3, long chain polyunsaturated fatty acids, DHA, EPA, docosahexaenoic acid, eicosapentaenoic acid, fish oil, pregnancy, infant. Only randomized controlled trials were chosen for analysis. A total of 74 relevant articles were selected. RevMan 5.0 software was used to perform the Meta analysis on those valid studies. Weighted mean difference was calculated with inverse variance method. The sensitivity analysis was also performed., Results: Eight articles met the inclusion criteria, among which 6 literatures were from developing countries and the other 2 from developed countries. All of them were written in English. These studies were reported from 2001 to 2011. Intervention group included 871 objects with n-3 LC-PUFA supplementation, whereas control group included 894 objects with placebo or no supplementation. Supplementation was associated with significantly greater head circumference of the infants in the intervention group than that of the control group (weighted mean difference was 0.17 cm, 95%confidence interval (CI) was 0.01 - 0.32 cm, P < 0.05). But the difference was no long significant according to the sensitivity analysis (weighted mean difference was 0.16 cm, 95%CI was -0.01 - 0.34 cm, P = 0.07). The funnel plot was symmetrical, indicating there was no publication bias between the eight studies., Conclusion: It can't be confirmed whether supplementation with n-3 LC-PUFA of pregnant women can increase the infants' head circumference at birth from present data acquired.

The involvement of microglial activation in metal neurotoxicity is becoming increasingly recognized. Some metal ions, such as zinc (II) and manganese (II), have been recently reported as microglial activators to induce the release of inflammatory mediators including cytokines, chemokines and nitric oxide (NO) which are involved in the pathogenesis of neurological diseases. Cobalt is essential for human life. However, excessive cobalt is cytotoxic and neurotoxic. In the present study, we determined cobalt-induced production of NO and cytokines/chemokines in N9 cells, a murine microglial cell line. High levels of cobalt significantly up-regulated iNOS mRNA and protein expression, which resulted in the release of NO. Cobalt induced the production of tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) in a concentration- and time-dependent manner in both N9 cells and primary mouse microglia and increased lipopolysaccharides (LPS)-induced cytokine production. Further study showed that cobalt induced cytokine production by a mechanism involving both nuclear factor kappa B (NF-κB) and p38 mitogen-activated protein kinase (MAPK) signaling pathways. The involvement of reactive oxygen species (ROS) in microglial activation was also confirmed. These findings suggested that cobalt neurotoxicity should be attributed not only directly to neuronal damage but also indirectly to microglial activation which might potentiate neuronal injury via elevation of proinflammatory mediator levels., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Previous studies have shown that ethanol induces oxidative DNA damage in human peripheral lymphocytes. In the present study, protective effect of resveratrol and ascorbic acid on ethanol-induced oxidative DNA damage in human peripheral lymphocytes in vitro were comparatively investigated. Pretreatments with resveratrol at 5, 25, and 50μM, which were in the concentration range of in vitro research, significantly inhibited ethanol-induced oxidative DNA damage in 24h, whereas ascorbic acid showed such DNA protective activity only in 1h. Further study showed that both compounds could directly scavenge hydroxyl radical produced during ethanol metabolism. Resveratrol significantly inhibited ethanol metabolism by regulating alcohol dehydrogenase 1B (ADH1B) and acetaldehyde dehydrogenase 2 (ALDH2) mRNA expressions. Moreover, resveratrol also activated the base excision repair (BER) system in mRNA and protein levels in DNA auto-repair process. However, ascorbic acid showed no effect on ethanol metabolic pathway and BER system. Thus, the present study provided the first evidence that even though both resveratrol and ascorbic acid are anti-oxidants, they possessed differential mechanisms of action in protection against ethanol-induced oxidative DNA damage in human peripheral lymphocytes., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Background: To characterize the human humoral immune response against enterovirus 71 (EV71) infection and map human epitopes on the viral capsid proteins., Methods: A series of 256 peptides spanning the capsid proteins (VP1, VP2, VP3) of BJ08 strain (genomic C4) were synthesized. An indirect enzyme-linked immunosorbent assay (ELISA) was carried out to detect anti-EV71 IgM and IgG in sera of infected children in acute or recovery phase. The partially overlapped peptides contained 12 amino acids and were coated in the plate as antigen (0.1 μg/μl). Sera from rabbits immunized with inactivated BJ08 virus were also used to screen the peptide panel., Results: A total of 10 human anti-EV71 IgM epitopes (vp1-14 in VP1; vp2-6, 21, 40 and 50 in VP2 and vp3-10, 12, 15, 24 and 75 in VP3) were identified in acute phase sera. In contrast, only one anti-EV71 IgG epitope in VP1 (vp1-15) was identified in sera of recovery stage. Four rabbit anti-EV71 IgG epitopes (vp1-14, 31, 54 and 71) were identified and mapped to VP1., Conclusion: These data suggested that human IgM epitopes were mainly mapped to VP2 and VP3 with multi-epitope responses occurred at acute infection, while the only IgG epitope located on protein VP1 was activated in recovery phase sera. The dynamic changes of humoral immune response at different stages of infection may have public health significance in evaluation of EV71 vaccine immunogenicity and the clinical application of diagnostic reagents.

When extracting discriminative features from multimodal data, current methods rarely concern themselves with the data distribution. In this paper, we present an assumption that is consistent with the viewpoint of discrimination, that is, a person's overall biometric data should be regarded as one class in the input space, and his different biometric data can form different Gaussians distributions, i.e., different subclasses. Hence, we propose a novel multimodal feature extraction and recognition approach based on subclass discriminant analysis (SDA). Specifically, one person's different bio-data are treated as different subclasses of one class, and a transformed space is calculated, where the difference among subclasses belonging to different persons is maximized, and the difference within each subclass is minimized. Then, the obtained multimodal features are used for classification. Two solutions are presented to overcome the singularity problem encountered in calculation, which are using PCA preprocessing, and employing the generalized singular value decomposition (GSVD) technique, respectively. Further, we provide nonlinear extensions of SDA based multimodal feature extraction, that is, the feature fusion based on KPCA-SDA and KSDA-GSVD. In KPCA-SDA, we first apply Kernel PCA on each single modal before performing SDA. While in KSDA-GSVD, we directly perform Kernel SDA to fuse multimodal data by applying GSVD to avoid the singular problem. For simplicity two typical types of biometric data are considered in this paper, i.e., palmprint data and face data. Compared with several representative multimodal biometrics recognition methods, experimental results show that our approaches outperform related multimodal recognition methods and KSDA-GSVD achieves the best recognition performance.

Conventional gene selection methods based on principal component analysis (PCA) use only the first principal component (PC) of PCA or sparse PCA to select characteristic genes. These methods indeed assume that the first PC plays a dominant role in gene selection. However, in a number of cases this assumption is not satisfied, so the conventional PCA-based methods usually provide poor selection results. In order to improve the performance of the PCA-based gene selection method, we put forward the gene selection method via weighting PCs by singular values (WPCS). Because different PCs have different importance, the singular values are exploited as the weights to represent the influence on gene selection of different PCs. The ROC curves and AUC statistics on artificial data show that our method outperforms the state-of-the-art methods. Moreover, experimental results on real gene expression data sets show that our method can extract more characteristic genes in response to abiotic stresses than conventional gene selection methods.

Local perfusion of morphine produces increased levels of extracellular ascorbic acid (AA) in the nucleus accumbens (NAc) of freely moving rats. However, the pathways that regulate morphine-induced AA release in the NAc are unclear. In the present study, we used high performance liquid chromatography with electrochemical detection (HPLC-ECD) to examine the effects of intra-ventral tegmental area (VTA) administration of a GABA(A) agonist and antagonist on morphine-induced increases in AA of the NAc. Also, using high performance liquid chromatography with fluorescent detection (HPLC-FD) and HPLC-ECD, the releases of γ-aminobutyric acid (GABA) and dopamine (DA) in the NAc induced by intra-VTA administration of a GABA(A) agonist and antagonist were also investigated. The results obtained showed that morphine (1 mM), locally perfused into the NAc, significantly increased AA release in the NAc and also GABA release. Intra-VTA infusion of bicuculline (150 ng/rat), a GABA receptor antagonist, not only abolished the enhanced extracellular AA and GABA levels produced by local perfusion of morphine but also decreased the basal release of extracellular GABA and increased the basal release of extracellular DA in the NAc. Muscimol (100 ng/rat), a GABA receptor agonist, affected the basal release of GABA and DA, but not the basal AA levels, or the morphine-induced changes in AA and GABA levels. These findings suggest that the GABA(A) receptors in the VTA play an important role in the modulation of morphine-induced AA release in the NAc, and the effect of morphine on AA release in the NAc is partially regulated by the GABA(A) receptor-mediated action of DA afferents from the VTA., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Seed oil of Brucea javanica (BJO) is extracted from the seeds of herb medicine Brucea javanica (L.), and its emulsion formulation (BJOE) has been used clinically to treat carcinomas for many years in China. The antileukemia potential of BJO was investigated in human acute myeloid leukemia cell lines (AML) U937 and HL-60 in vitro and in a mouse U937 xenograft tumor model. BJO induced AML cell apoptosis through activation of caspase-8 and modulation of apoptosis-related proteins. Meanwhile, the inhibition of survivin and XIAP increased the cytotoxicity of BJO. Consistent with these findings, BJO also increased subG(1) phase cells and cause PARP cleavage in AML patients' leukemia cells. In contrast, only weak cytotoxicity of BJO was found in peripheral blood lymphocytes (PBLs) of healthy volunteers. Moreover, oleic acid and linoleic acid were found to be the active components of BJO. Our study provided strong evidence for the first time that BJO induced apoptosis of both cultured and primary AML cells. Furthermore, intravenous injection of BJO significantly inhibited U937 tumor growth in the xenograft mouse model. These results suggest that BJO may have a therapeutic role in the treatment of human leukemia.

Psychostimulants are frequently abused as a result of their stimulatory effects on several neurotransmitter systems within the central nervous system. Both dopaminergic and glutaminergic neurotransmissions have been closely associated with psychostimulant dependence. In addition to its classical endocrine function in the periphery, oxytocin, an important neurohypophyseal neuropeptide in the central nervous system, has a wide range of behavioral effects, including regulating drug abuse. The present paper reviews the progress of research into the role of oxytocin in reducing psychostimulant-induced psychological dependence and the mechanisms by which oxytocin mediates its effects.

Context: We recently reported that F2, an oligomer procyanidin fraction isolated from grape seeds, triggered an original form of cell death in U-87 human glioblastoma cells with a phenotype resembling morphological characteristics of paraptosis. However, the specific death mode induced by F2 and the mechanism of its action have not been assessed so far., Objective: In the present work, we therefore further investigated the death mode of human glioblastoma cells induced by F2 and gained insight into the nature of the signaling pathways activated by F2 in glioblastoma cells., Materials and Methods: Cell viability assay using MTT, (AO/EB) double staining, Western blot analysis, and Ca2+ assay using fura-2., Results: Morphology studies revealed extensive cytoplasmic vacuolization in dying cells and no apoptotic body formation, membrane bleb formation, or nuclear fragmentation, though some was accompanied by MAPK activation and new protein synthesis, and was independent of caspase activation. Moreover, we demonstrated the involvement of calcium mobilization in F2-induced U-87 cell signaling., Discussion and Conclusion: Altogether we showed that F2 induced a kind of cell death resembling paraptosis in U-87 cells. The current report complements previous studies on the characterization of F2-induced U-87 cell death, enhances our understanding of the action mechanism of F2 on glioma, and helps in the development of novel antitumor therapeutics.

Eleven new monoterpenes, paeonidangenin (1), paeonidanin A (2), paeonidanin B (3), paeonidanin C (4), paeonidanin D (5), paeonidanin E (6), paeoniflorone (7), 4-O-methylbenzoylpaeoniflorin (8), 4-O-methylgalloylpaeoniflorin (9), 4-O-methyldebenzoylpaeoniflorin (10), and 4-O-methylalbiflorin (11), were isolated from the 60% ethanol extract of the roots of Paeonia albiflora. Their structures were determined primarily on the basis of 1D and 2D NMR techniques and MS studies. Paeonidanins D (5) and E (6) are unprecedented examples of "cage-like" monoterpene dimers. The inhibitory effects of the isolated compounds on nitric oxide production by lipopolysaccharide (LPS)-activated N9 microglia were evaluated.

Gliomas are the most common and lethal tumor type in the brain. The present study investigated the effect of oligomer procyanidins (F2) (F2, degree of polymerization 2-15), a natural fraction isolated from grape seeds on the biological behavior of glioblastoma cells. We found that F2 significantly inhibited the glioblastoma growth, with little cytotoxicity on normal cells, induced G2/M arrest and decreased mitochondrial membrane potential in U-87 cells. It also induced a non-apoptotic cell death phenotype resembling paraptosis in U-87 cells. In addition, it was found for the first time that F2 in non-cytotoxic concentrations selectively inhibited U-87 cell chemotaxis mediated by a G-protein coupled receptor formyl peptide receptor FPR, which is implicated in tumor cell invasion and metastasis. Further experiments indicated that F2 inhibited fMLF-induced U-87 cell calcium mobilization and MAP kinases ERK1/2 phosphorylation. Moreover, F2 attenuated the glioblastoma FPR expression, a new molecular target for glioma therapeutics, which has been shown to play important roles in glioma cells chemotaxis, proliferation and angiogenesis in addition to its promotion to tumor progression, but did not affect FPR mRNA expression in U-87 cells. Taken together, our results suggest that F2 may be a promising candidate for the development of novel anti-tumor therapeutics.

Aim: To find a rapid and efficient analysis method of gastrointestinal microflora in Pi-deficient (spleen-deficient) rats and to evaluate traditional Chinese drugs., Methods: Enterobacterial repetitive intergenic consensus-PCR (ERIC-PCR) based assay was performed to examine changes of intestinal microflora in two Pi-deficienct animal models and to evaluate the efficacy of four traditional Chinese drugs as well as a probiotic recipe and another therapy in Pi-deficient rats., Results: A molecular marker was identified for Pi-deficiency in rats. The pharmacodynamic evaluation system, including identified molecular markers (net integral area and abundance of DNA bands), Shannon's index for diversity of intestinal microflora, and Sorenson's pairwise similarity coefficient, was established. The four major clinical recipes of traditional Chinese drugs for Pi-deficiency in rats, especially at their medium dose (equivalence to the clinical dose), produced more pronounced recovery activities in Pi-deficient rats, while higher doses of these recipes did not show a better therapeutic effect but some toxic effects such as perturbation deterioration of intestinal microflora., Conclusion: Both fingerprint analysis and identified marker can show Pi-deficiency in rats and its difference after treatment. The identified molecular marker may be applied in screening for the active compounds both in relative traditional Chinese drugs and in pharmacodynamic study of Pi-deficiency in rats.

The present study investigated the protective effects of ginsenoside Rb(1) (GRb(1)) against genotoxicity induced by cyclophosphamide (CP). Single cell gel electrophoresis, flow cytometry assay with annexin V-FITC/propidine iodide (PI) and acridine orange (AO)/ethidium bromide (EB) staining assay were employed to measure DNA damage and cell apoptosis, respectively. The activities of total superoxide dismutase (T-SOD) and glutathione peroxidase (GPx) and the malondialdehyde (MDA) content were also investigated by a number of colormetric methods. The results showed that the CP produced significant DNA damage and cell apoptosis in mouse bone marrow cells or peripheral blood leukocytes, markedly inhibited the activities of T-SOD and GPx, and markedly increased the MDA content. GRb(1) significantly inhibited DNA damages and cell apoptosis in mouse bone marrow cells or peripheral blood leukocytes induced by CP and antagonized the reduction of CP-induced T-SOD and GPx activities, and inhibited the increase in MDA content induced by CP. The anti-tumor study of GRb(1) showed that GRb(1) did not affect the anti-tumor activities of CP. In conclusion, GRb(1) had significant protective effects against DNA damage and apoptosis induced by CP., (Copyright © 2009 Elsevier B.V. All rights reserved.)

Accumulating evidence has shown the neuroactive properties of oxytocin (OT), a neurohypophyseal neuropeptide, and its ability to reduce the abuse potential of drugs. The present study investigated the effects of OT on the conditioned place preference (CPP) induced by methamphetamine (MAP, 2.0 mg/kg, i.p.) in mice and the possible role of glutamatergic neurotransmission in the reinstatement of CPP. The results showed that OT (0.1, 0.5, 2.5 microg, i.c.v.) significantly inhibited the acquisition and facilitated the extinction of MAP-induced CPP and abolished the reinstatement of CPP induced by restraint stress. This effect of OT could be attenuated by atosiban (Ato, 2.0 microg, i.c.v.), a selective OT-receptor antagonist. OT failed to block the expression and the reinstatement of CPP induced by MAP challenge. Extracellular glutamate (Glu) levels in the medial prefrontal cortex (mPFC) were determined using microdialysis coupled to a high-performance liquid chromatography (HPLC) with a fluorescence detection system. The results indicated that OT markedly inhibited extracellular Glu levels induced by restraint stress in CPP mice, but not those induced by MAP priming. Ato also attenuated the effects of OT on the changes in Glu levels. Therefore, these findings suggest that OT inhibits drug reward-related behaviors induced by MAP via the OT receptor, and OT blocks the reinstatement of CPP, at least partially, by interfering with the glutamatergic system in the mPFC.

Objective: To determine the effect of three Jianpi Buqi recipes on intestinal microflora of Pi-qi-deficiency rat with molecular biology methods and attempt to clarify the mechanisms of therapy., Method: Rat model of Pi-qi-deficiency was induced by exercise fatigue simultaneously diet incontinence and then administrated with the decoctions of Si-jun-zi-tang (including crude drug) (10.8, 3.6, 1.2 g x kg(-1)), Li-zhong-tang (16.2, 5.4, 1.8 g x kg(-1)) and Buzhong Yiqi-tang (14.4, 4.8, 1.6 g x kg(-1)) recipes which were in common use of clinic of traditional Chinese medicine (TCM). With application of ERIC-PCR (enterobacterial repetitive intergenic consensus-PCR) fingerprint analysis, the efficacy on Pi-qi-deficiency and perturbation of intestinal mircoflora of these recipes were examined and evaluated., Result: Remarkable differences of ERIC-PCR profile were found between Pi-qi-deficiency state rats and normal rats. The Shannon's Index (H') was increased when treated with all doses of three Jianpibuqi recipes decoctions and Sorenson's pairwise similarity coefficient (Cs) was also increased significantly after treatment., Conclusion: ERIC-PCR fingerprint can be utilized as an initial screening of changes of the composition of bacterial communities that are associated with the development of intestinal disease. It can also be used to build a better understanding of Pi-qi-deficiency and to investigate the pharmacodynamic effect of TCM on Pi-qi-deficiency. Three Jianpi Buqi recipes are demonstrated to produce pronounced recovery activities on intestinal microflora of Pi-qi-deficient rats, which may be considered one of mechanisms of their performances.

It is suggested that reactive oxygen species produced during ethanol intake may induce oxidative DNA damage. The present study, by the use of single cell gel electrophoresis (comet assay), investigated the potential genotoxicity of acute and long-term ethanol administration in mouse peripheral leucocytes. Urinary 8-hydroxy-2'-deoxyguanosine and total antioxidant capacity and reactive oxygen species in whole blood were also detected. Acute or long-term administration of ethanol, at the dose of 2.5 or 5.0 g/kg intraperitoneally, for 30 days, could induce significant DNA damage in peripheral leucocytes, which could be repaired at least 3 days after ethanol withdrawal in long-term ethanol treatment. A significant increase of urinary 8-hydroxy-2'-deoxyguanosine and generations of reactive oxygen species in whole blood after ethanol administration were observed, which demonstrated the ethanol-induced oxidative DNA damage. Interestingly, it was found that the total antioxidant capacity was significantly increased in whole blood after long-term ethanol administration compared to the control group, which suggested enhancement in the activities of the antioxidative defence system against oxidative tissue damage caused by excessive ethanol consumption. Thus, the present studies provide a clear evidence that ethanol induced DNA damage in peripheral leucocytes, which might result from ethanol-induced oxidative stress in the body.

Excessive activation of microglial cells has been implicated in various neurodegenerative diseases. Resveratrol, a polyphenolic compound found in grapes and wine, has been reported to reduce the activation of microglia. In the present study, 5-[2-(4-bromothiophen-2-yl)vinyl]benzene-1,3-diol (RV09), a novel resveratrol analogue, was found to suppress NO production by LPS-activated N9 microglial cell line and/or cultured rat cortical microglia. RV09 appeared to have a slight NO-scavenging activity in sodium nitroprusside (SNP) solution. The inhibition of iNOS was also observed, suggesting the blockage of transcriptional levels. Moreover, RV09 attenuated the expression of mRNA and protein of tumor necrosis factor-alpha (TNF-alpha) in a concentration-dependent manner. Further studies revealed that RV09 blocked IkappaBalpha phosphorylation and degradation, as well as reactive oxygen species (ROS) production in N9 microglial cells. It was also found that RV09 is a effective scavenger for 2,2-diphenyl-1-picrylhydrazyl (DPPH) used as a general free radical model. In the summary, these data suggest that, by blocking IkappaBalpha phosphorylation and degradation, RV09 acts to suppress the LPS-induced NO and TNF-alpha production in microglia, and this effect was mediated, at least in part, by inhibiting the generation of ROS. Our results suggested that RV09 is a novel anti-inflammatory agent which can inhibit proinflammatory responses of microglia.

The inhibitory effects of 21 resveratrol derivatives on lipopolysaccharide (LPS)-induced nitric oxide (NO) production in microglia and their structure-activity relationships were studied. It was found, for the first time, that certain resveratrol derivatives that have 3,5-dimethoxyl groups in the A-ring, such as (E)-4-(3,5-dimethoxystyryl)phenol (pterostilbene, compound 2), or have substituted the B-ring of resveratrol with quinolyl, such as (E)-5-[2-(quinolin-4-yl)vinyl]benzene-1,3-diol (compound 18) and (E)-4-(3,5-dimethoxystyryl)quinoline (compound 19), strongly inhibited NO production. Compounds 2, 18, and 19 reduced LPS-induced protein and mRNA expression of inducible NO synthase (iNOS), but did not display direct NO-scavenging activity up to 30 microM in sodium nitroprusside (SNP) solution. Moreover, compounds 2, 18, and 19 could also significantly inhibit the production of TNF-alpha by LPS-activated microglia. Further studies revealed that compounds 2, 18, and 19 inhibited LPS-induced NO and TNF-alpha production in microglia by blocking IkappaBalpha phosphorylation and degradation. The potent inhibitory effects of compounds 2, 18, and 19 on microglial activation suggest their potential for treatment of neurodegenerative diseases accompanied by microglial activation.

The promyelocytic leukemia (PML) gene is a tumor suppressor gene associated with cell apoptosis, cell proliferation, and senescence. However, the role of PML in the ethanol-induced apoptosis is not fully-known. In this study, using wild-type mouse embryo fibroblasts (MEF) and PML null MEF cells, we found that (1) ethanol (100 mM and 200 mM) could obviously induce apoptosis of wild-type MEF cells, whereas, in PML null MEF cells, the pro-apoptotic function of ethanol was partially blocked; (2) the expression levels of phosphorylated p53 and two of its target genes, p21 and Bax, could be significantly up-regulated by ethanol (200 mM) in wild-type MEF cells in a time-dependent manner, but not in PML null MEF cells. These results indicate that PML plays an important role in ethanol-induced apoptosis, and p53-dependent apoptotic pathway may be involved in this process.

Making textual research on Bencao and documents, this article inquires to the origin and development of genuine medicinal herbs of Shanyao (Rhizoma Dioscoreae) on the points of change of the growing areas and the development of cultivating and processing techniques and clinical uses. The study indicates that the medicinal use of Dioscorea oposita went through several periods: the period of the use of wild D. oposita before Tang dynasty, the period of the mixed use of wild and cultivating D. oposita from Song to the middle of Qing dynasty, and the period of the main use of cultivating D. oposita after the latter stage of Qing dynasty (18th century). It considers that the growing area of genuine medicinal herbs of Shanyao appeared in Ming dynasty and finally formed "Huaishanyao" on the early of 20th century. The acknowledgement of Huaishanyao as genuine medicinal herbs is related closely to its cultivating and processing techniques and clinical uses. The development of cultivating techniques provided the resource of Shanyao, the invention of processing techniques improved its appearance and quality, and the clinical uses and practices by modern and contemporary famous medical men played an important role to the social approval and development of Huaishanyao.

Unlabelled: To explore the dynamic change of paeoniflorin content in root of Paeonia lactiflora., Method: The samples were collected and paeoniflorin content was determined by HPLC., Result: The results showed that the average content of paeoniflorin was the lowest at 3.05% in the roots collected in May, and during the fruit time it was rather high in August at 4.72%, and in September at 4.58%. The average content showed no significant differences during June to October., Conclusion: Wild plant of P. lactiflora might be collected for medical use during blooming stage until wilting stage.

Despite the significant anti-tumor activities, cyclophosphamide (CP) also shows cytotoxicity to normal cells. In order to explore the protective effects of drugs against CP-induced adverse effects, 20(S)-ginsenoside Rg(3) was tested for its possibly protective activities on CP-induced DNA damage and cell apoptosis in mouse bone marrow cells or peripheral lymphocyte cells. In the current study, the alkaline single cell gel electrophoresis (comet assay), flow cytometry assay with annexin V-FITC/PI and AO/EB staining assay were employed to measure DNA strand breakage and cell apoptosis, respectively. The activities of SOD and GPx and the contents of MDA were also tested by the various colormetric methods. The results showed that CP at a dose of 100 mg/kg, i.p. significantly caused DNA damages in both mouse bone marrow cells and peripheral lymphocyte cells, and markedly inhibited the activities of GPx and SOD and increased MDA contents in mouse blood. Moreover, CP at a dose of 200 mg/kg, i.p. triggered apoptosis in mouse bone marrow cells. On the other hand, 20(S)-ginsenoside Rg(3) orally administered at a dose of 20 mg/kg to the animals once a day for 2 days significantly inhibited CP-induced DNA damages in mouse bone marrow cells and peripheral lymphocyte cells, decrease the apoptotic numbers of bone marrow cells, antagonized the reduction of the activities of SOD and GPx, and the increase in MDA contents. In conclusion, 20(S)-ginsenoside Rg(3) showed the significant protective effects on CP-induced cell DNA damage and apoptosis. These effects might be partially attributed to its protective actions against CP-induced oxidative stress.

A new steroidal alkaloid ( 1), together with three known steroidal alkaloids ( 2 - 4), has been isolated from the roots and rhizomes of Veratrum japonicum (Baker) Loes. f.., their structures were established as neogermine ( 1), germine ( 2), germerine ( 3), and neogermbudine ( 4) by means of physicochemical properties and spectroscopic analysis. Compounds 1 - 4 exhibited genotoxicity on brain cells in mice by using single-cell gel electrophoresis (Comet assay).

Oleamide (cis-9,10-octadecenoamide) is an endogenous sleep-inducing lipid and prototypic member of a new class of biological signaling molecules identified in recent years. In the present study, the anxiolytic-like effect of oleamide was studied in several experimental models of anxiety in group-housed and socially isolated mice. As the results show, socially isolated mice exhibited an anxiogenic-like profile in the elevated plus-maze test, the light/dark test, and the hole-board test, which could be significantly reversed by oleamide (10 or 20 mg/kg, i.p.). Moreover, oleamide significantly reduced the anxiety levels in grouped-housed mice. In the isolation-induced aggressive test, oleamide markedly reduced the attacking duration and increased the attacking latency. It is concluded that oleamide has an anxiolytic-like effect in socially isolated or group-housed mice, which suggests that fatty acid amides might be involved in the regulation of anxiety-related behavior in mice.

Ethanol is a principle ingredient of alcoholic beverages with potential neurotoxicity and carcinogenicity, and the ethanol-associated oxidative DNA damage in the central nervous system is well documented. The present work studied the possible protective effects of grape seed oligomer and polymer procyanidin fractions against ethanol-induced toxicity and compared these with resveratrol and other well-known antioxidants (ascorbic acid and vitamin E). By using the single cell gel electrophoresis (comet assay), a simple and sensitive technique for genotoxicity studies, the potential genotoxicity of acute and chronic ethanol administration in the different brain regions was investigated. Acute ethanol administration, at the dose of 2.5 or 5.0 g kg(-1) i.p., could induce significant DNA damage in cerebellum and hippocampus. Chronic administration of ethanol at the dose of 2.5 or 5.0 g kg-1 p.o. for 30 days could induce significant DNA damage in cerebellum, hippocampus, hypothalamus, and cortex, which could be auto-repaired at least 3 days after ethanol withdrawal. Oral administration of grape seed oligomer and polymer procyanidins and resveratrol (25, 50, and 100 mg kg(-1)) for 3 days before acute ethanol (5.0 g kg(-1), i.p.) or repeated administration of these substances together with ethanol (5.0 g kg(-1), p.o.) for 30 consecutive days could significantly inhibit DNA damage in brain cells induced by ethanol. As compared, ascorbic acid (50, 100, and 200 mg kg(-1)) and vitamin E (100, 200, and 400 mg kg(-1)) could also present protective effects on ethanol-induced DNA damage. Furthermore, the concentrations of ethanol and acetaldehyde in brain regions of the mice were detected by gas chromatography after administration of ethanol plus antioxidants. All of the results indicated that ethanol could induce region-specific oxidative DNA damage in which the cerebellum and hippocampus were more vulnerable, but intake of grape seed procyanidins or other natural antioxidants could protect the brain against ethanol-induced genotoxicity.

The anxiolytic effect of the saponins from Aniliaeea Panax quinquefolium L. (PQS) was studied in male mice by using a number of experimental paradigms of anxiety and compared with that of the known anxiolytic compound diazepam. Use of the elevated plus-maze test revealed that PQS (50 mg/kg, p.o.) and diazepam (2.5 mg/kg, p.o.) increased the percentage of time and entries spent in open arms. In the light/dark test, PQS (50 and 100 mg/kg, p.o.) and diazepam (2.5 mg/kg, p.o.) prolonged the time spent in the light area. In the hole-board test, PQS (50 and 100 mg/kg, p.o.) and diazepam (2.5 mg/kg, p.o.) significantly increased both head-dip counts and head-dip duration. Both PQS (50 and 100 mg/kg, p.o.) and diazepam (2.5 mg/kg, p.o.) decreased the total fighting time in the isolation-induced aggressive test. Since PQS, in contrast to diazepam, had no effect on locomotion in these tests, its side-effect profile might be considered superior to the benzodiazepines. Thus, the present findings suggest that PQS might be a potential candidate for use as an anxiolytic drug.

Morphine produces a variety of behavioral and biochemical changes related to its abuse. Our previous studies showed that Pseudoginsenoside-F11 (PF11), an ocotillol-type saponin existing in American ginseng, can antagonize pharmacological effects of morphine. To further investigate the effects of PF11 on morphine abuse and the underlying mechanisms, we tested the effects of PF11 on morphine-induced development of behavioral sensitization and alterations in glutamate levels in the medial prefrontal cortex (mPFC) in freely moving mice by using in vivo microdialysis. As the results shown, PF11 antagonized the development of behavioral sensitization and decrease of glutamate in the mPFC induced by morphine. Therefore, these findings suggest that PF11 may block the development of morphine-induced behavioral sensitization via its effect, at least partially, on the glutamatergic system in the mPFC.

This paper develops an unsupervised discriminant projection (UDP) technique for dimensionality reduction of high-dimensional data in small sample size cases. UDP can be seen as a linear approximation of a multimanifolds-based learning framework which takes into account both the local and nonlocal quantities. UDP characterizes the local scatter as well as the nonlocal scatter, seeking to find a projection that simultaneously maximizes the nonlocal scatter and minimizes the local scatter. This characteristic makes UDP more intuitive and more powerful than the most up-to-date method, Locality Preserving Projection (LPP), which considers only the local scatter for clustering or classification tasks. The proposed method is applied to face and palm biometrics and is examined using the Yale, FERET, and AR face image databases and the PolyU palmprint database. The experimental results show that UDP consistently outperforms LPP and PCA and outperforms LDA when the training sample size per class is small. This demonstrates that UDP is a good choice for real-world biometrics applications.

It is controversial regarding to the roles of acetaldehyde and ethanol in the central nervous system. In the present study, the effects of acetaldehyde and ethanol on extracellular levels of glutamate, taurine and GABA in the anterior cingulate cortex (ACC) of freely moving rats were investigated by using the microdialysis technique coupled to high performance liquid chromatography (HPLC) with fluorescent detection. The result showed that glutamate levels were significantly decreased after acute administration of acetaldehyde (AcH, 20 and 100 mg/kg, i.p.), while taurine levels were significantly increased after the higher dose of acetaldehyde (100 mg/kg, i.p.). GABA levels had no changes at any doses of acetaldehyde tested. Interestingly, similar changes of these amino acids were induced by ethanol (EtOH, 3 g/kg, i.p.) when sodium azide (NaN3, 10 mg/kg, i.p.), a catalase inhibitor that can reduce brain ethanol metabolism, was used simultaneously. These findings suggest that acetaldehyde and ethanol have the similar effects on the extracellular output of glutamate, taurine and GABA in the ACC.

Previous studies have shown that acute systemic administration of ethanol induced ascorbic acid (AA) release in mouse striatum and prefrontal cortex. Clozapine and olanzapine showed similar effects on ethanol-induced AA release in mouse striatum. However, their effects on ethanol-induced AA release in mouse prefrontal cortex have not been reported. Thus, their effects on this neurochemical event were further investigated in the present study. The results showed that ethanol (4.0 gkg i.p.) significantly stimulated AA release in the prefrontal cortex by about 200 of baseline in mice. Clozapine and olanzapine, at the dose of 1.0 mgkg s.c., had no effect on basal AA or ethanol-induced AA release. However, both drugs, at the dose of 10 mgkg s.c., significantly inhibited ethanol-induced AA release. The present study demonstrated for the first time that similar actions were exhibited by clozapine and olanzapine for the regulation of ethanol-induced AA release in the mouse prefrontal cortex.

The mechanism of ethanol, morphine, methamphetamine (MAP), and nicotine-induced ascorbic acid (AA) release in striatum, and nucleus accumbens (NAc) is not well understood. Our previous study showed that the glutamatergic system was involved in the addictive drug-induced AA release in NAc and striatum. Furthermore, frontal decortication eliminates drug-induced ascorbic acid release in the striatum but not in the NAc. In the present study, the roles of the hippocampus in drug-induced AA release in the striatum and NAc were studied by using microdialysis coupled to high performance liquid chromatography with electrochemical detection (HPLC-ECD). Ethanol (3.0 g/kg, i.p.), methamphetamine (3.0 mg/kg, i.p.), and nicotine (1.5 mg/kg, i.p.) significantly stimulated AA release in the striatum and NAc, respectively. Morphine (20 mg/kg, i.p.) significantly stimulated AA release in the striatum, but not in the NAc. After hippocampal lesion by kainic acid, AA release induced by ethanol, methamphetamine, and nicotine could be eliminated in NAc, but not in the striatum. These results suggest that the hippocampus might be a common and necessary area in addictive drug-induced AA release in the NAc, which also imply that different pathways might be involved in drug-induced AA release in the striatum and the NAc of the rats.

The topologies of data distributions are very important for data description. Usually, it is not easy to find a description that can give us an intuitional understanding of the topologies for general distributions. In this paper, a novel concept, a topology graph, is proposed as a description for the principal topology of data distribution. The topology graph builds a one-to-one correspondence between the principal topology of the distribution and the topology itself: annularity features of the principal topology correspond to the loops of the graph, and the divarication features correspond to the branches of the graph. In general, the topology graph can be considered as the skeleton of the data distribution. A divide-and-combine learning strategy is developed to find the topology graphs for general data distributions. The learning strategy is focused on the constrained local description learning and automatic topology generation. Following the learning strategy, a cluster growing algorithm is developed. Experimental results on both artificial datasets and real-world applications show good performance of the proposed algorithm.

Upon activation, brain macrophages, the microglia, release proinflammatory mediators that play important roles in eliciting neuroinflammatory responses associated with neurodegenerative diseases. As resveratrol, an antioxidant component of grape, has been reported to exert anti-inflammatory activities on macrophages, we investigated its effects on the production of TNF-alpha (TNF-alpha) and nitric oxide (NO) by lipopolysaccharide (LPS)-activated microglia. Exposure of cultured rat cortical microglia and a mouse microglial cell line N9 to LPS increased their release of TNF-alpha and NO, which was significantly inhibited by resveratrol. Further studies revealed that resveratrol suppressed LPS-induced degradation of IkappaBalpha, expression of iNOS and phosphorylation of p38 mitogen-activated protein kinases (MAPKs) in N9 microglial cells. These results demonstrate a potent suppressive effect of resveratrol on proinflammatory responses of microglia, suggesting a therapeutic potential for this compound in neurodegenerative diseases accompanied by microglial activation.

The effects of clozapine, olanzapine and haloperidol on ethanol-induced striatal ascorbic acid (AA) release in mice were compared by using microdialysis coupled to high performance liquid chromatography with electrochemical detection. Ethanol (4.0 g/kg i.p.) significantly stimulated striatal AA release by about 200% of baseline in mice. Clozapine and olanzapine, two atypical neuroleptic drugs, at the dose of 1.0 mg/kg s.c., had no effect on basal AA or ethanol-induced AA release. However, both drugs, at the dose of 10 mg/kg s.c., significantly inhibited ethanol-induced AA release. In contrast, haloperidol, a typical neuroleptic drug, at the doses of 0.1-2.0 mg/kg, had no effect on both basal and ethanol-induced AA release. The present study demonstrated that similar actions were exhibited by clozapine and olanzapine, but not by haloperidol, for the regulation of ethanol-induced AA release in the mouse striatum.

In this paper, a new technique coined two-dimensional principal component analysis (2DPCA) is developed for image representation. As opposed to PCA, 2DPCA is based on 2D image matrices rather than 1D vectors so the image matrix does not need to be transformed into a vector prior to feature extraction. Instead, an image covariance matrix is constructed directly using the original image matrices, and its eigenvectors are derived for image feature extraction. To test 2DPCA and evaluate its performance, a series of experiments were performed on three face image databases: ORL, AR, and Yale face databases. The recognition rate across all trials was higher using 2DPCA than PCA. The experimental results also indicated that the extraction of image features is computationally more efficient using 2DPCA than PCA.

In the present study, pseudoginsenoside-F(11) (PF(11)), a saponin that existed in American ginseng, was studied on its protective effect on methamphetamine (MA)-induced behavioral and neurochemical toxicities in mice. MA was intraperitoneally administered at the dose of 10 mg/kg four times at 2-h intervals, and PF(11) was orally administered at the doses of 4 and 8 mg/kg two times at 4-h intervals, 60 min prior to MA administration. The results showed that PF(11) did not significantly influence, but greatly ameliorated, the anxiety-like behavior induced by MA in the light-dark box task. In the forced swimming task, PF(11) significantly shortened the prolonged immobility time induced by MA. In the appetitively motivated T-maze task, PF(11) greatly shortened MA-induced prolonged latency and decreased the error counts. Similar results were also observed in the Morris water maze task. PF(11) significantly shortened the escape latency prolonged by MA. There were significant decreases in the contents of dopamine (DA), 3,4-dihydroxyphenacetic acid (DOPAC), homovanillic acid (HVA), and 5-hydroxyindoacetic acid (5-HIAA) in the brain of MA-treated mice. PF(11) could partially, but significantly, antagonize MA-induced decreases of DA. The above results demonstrate that PF(11) is effective in protection of MA-induced neurotoxicity and also suggest that natural products, such as ginseng, might be potential candidates for the prevention and treatment of the neurological disorders induced by MA abuse.

The anti-seizure effect of oleamide, an endogenous sleep-inducing fatty acid amide, was studied in mice. Oleamide, in the dose range 43.7-700.0 mg kg(-1), significantly and dose-dependently inhibited the seizures induced by pentylenetetrazole. However, oleamide showed no inhibitory action on the seizures induced by picrotoxin, strychnine, caffeine or semicarbazide. These results provide the first evidence for the anti-seizure effect of oleamide, and suggest that this effect may be selective to the seizure model induced by pentylenetetrazole.

Aim: To assess the effect of semicarbazide hydrochloride (SCZ), the blocker of synthetic enzyme for GABA, on the hypnotic activity of melatonin., Methods: Righting reflex method in mice and electroencephalography (EEG) in rats were used to determine effects of SCZ on sleep and hypnotic activity of melatonin., Results: Melatonin displayed a marked hypnotic activity both in righting reflex experiment and EEG recording. SCZ had no influence on sleep parameters in mice and rats when it was used alone. However, it blocked the sleep-potentiation effect of melatonin in mice. SCZ also inhibited melatonin-induced increase in total sleep time, slow wave sleep time, and paradoxical sleep time, and prevented melatonin-induced decrease in awake time in rats., Conclusion: SCZ antagonized the hypnotic activity of melatonin. It is thought that the hypnotic activity of melatonin is mediated by GABAergic system.

Objective: To describe the difference between native and nonative herbs by determining contents of seven kinds of flavone for twenty-five samples from seventeen areas., Methods: HPLC. Fluid phase: MEOH-H2O-CH3COOH(ICE) (41:59:0.2) and (50:50:0.2). Detection wavelength: 275., Results: The contents of baicalin are 6%-9%, wogenin are 2%-8%, baicalein are 0.1%-1.6%, neobaicalein are 0.01%-0.2%, wogonin are 0.01%-0.3%, visidulin and oroxylin are trace amounts or undetected., Conclusion: The native and nonative herbs have no distinct differce in absolute component ratio. The ratio of baicalin and wogenin is under three. The ratio of baicalin and baicalein, baicalin and wogonin is between twenty and fifty.