Extract of Ginkgo biloba promotes neuronal regeneration in the hippocampus after exposure to acrylamide

Previous studies have demonstrated a neuroprotective effect of extract of Ginkgo biloba against neuronal damage, but have mainly focused on antioxidation of extract of Ginkgo biloba. To date, limited studies have determined whether extrasct of Ginkgo biloba has a protective effect on neuronal damage. In the present study, acrylamide and 30, 60, and 120 mg/kg extract of Ginkgo biloba were administered for 4 weeks by gavage to establish mouse models. Our results showed that 30, 60, and 120 mg/kg extract of Ginkgo biloba effectively alleviated the abnormal gait of poisoned mice, and up-regulated protein expression levels of doublecortin（DCX）, brain-derived neurotrophic factor, and growth associated protein-43（GAP-43） in the hippocampus. Simultaneously, DCX-and GAP-43-immunoreactive cells increased. These findings suggest that extract of Ginkgo biloba can mitigate neurotoxicity induced by acrylamide, and thereby promote neuronal regeneration in the hippocampus of acrylamide-treated mice.

Acrylamide neurotoxicity on the cerebrum of weaning rats

The mechanism underlying acrylamide-induced neurotoxicity remains controversial. Previous studies have focused on acrylamide-induced toxicity in adult rodents, but neurotoxicity in weaning rats has not been investigated. To explore the neurotoxic effect of acrylamide on the developing brain, weaning rats were gavaged with 0, 5, 15, and 30 mg/kg acrylamide for 4 consecutive weeks. No obvious neurotoxicity was observed in weaning rats in the low-dose acrylamide group （5 mg/kg）. However, rats from the moderateand high-dose acrylamide groups （15 and 30 mg/kg） had an abnormal gait. Furthermore, biochemical tests in these rats demonstrated that glutamate concentration was significantly reduced, and ^-aminobutyric acid content was significantly increased and was dependent on acrylamide dose. Immunohis- tochemical staining showed that in the cerebral cortex, γ-aminobutyric acid, glutamic acid decarboxylase and glial fibrillary acidic protein expression increased remarkably in the moderate- and high-dose acrylamide groups. These results indicate that in weaning rats, acrylamide is positively associated with neurotoxicity in a dose-dependent manner, which may correlate with upregulation of γ-aminobutyric acid and subsequent neuronal degeneration after the initial acrylamide exposure.

Toxic effect of acrylamide on the development of hippocampal neurons of weaning rats

Although numerous studies have examined the neurotoxicity of acrylamide in adult animals,the effects on neuronal development in the embryonic and lactational periods are largely unknown.Thus,we examined the toxicity of acrylamide on neuronal development in the hippocampus of fetal rats during pregnancy.Sprague-Dawley rats were mated with male rats at a 1：1 ratio.Rats were administered 0,5,10 or 20 mg/kg acrylamide intragastrically from embryonic days 6–21.The gait scores were examined in pregnant rats in each group to analyze maternal toxicity.Eight weaning rats from each group were also euthanized on postnatal day 21 for follow-up studies.Nissl staining was used to observe histological change in the hippocampus.Immunohistochemistry was conducted to observe the condition of neurites,including dendrites and axons.Western blot assay was used to measure the expression levels of the specific nerve axon membrane protein,growth associated protein 43,and the presynaptic vesicle membrane specific protein,synaptophysin.The gait scores of gravid rats significantly increased,suggesting that acrylamide induced maternal motor dysfunction.The number of neurons,as well as expression of growth associated protein 43 and synaptophysin,was reduced with increasing acrylamide dose in postnatal day 21 weaning rats.These data suggest that acrylamide exerts dose-dependent toxic effects on the growth and development of hippocampal neurons of weaning rats.

Cortical regulation of striatal projection neurons and interneurons in a Parkinson's disease rat model

Striatal neurons can be either projection neurons or interneurons, with each type exhibiting distinct susceptibility to various types of brain damage. In this study, 6-hydroxydopamine was injected into the right medial forebrain bundle to induce dopamine depletion, and/or ibotenic acid was injected into the M1 cortex to induce motor cortex lesions. Immunohistochemistry and western blot assay showed that dopaminergic depletion results in significant loss of striatal projection neurons marked by dopamine- and cyclic adenosine monophosphate-regulated phosphoprotein, molecular weight 32 k Da, calbindin, and μ-opioid receptor, while cortical lesions reversed these pathological changes. After dopaminergic deletion, the number of neuropeptide Y-positive striatal interneurons markedly increased, which was also inhibited by cortical lesioning. No noticeable change in the number of parvalbumin-positive interneurons was found in 6-hydroxydopamine-treated rats. Striatal projection neurons and interneurons show different susceptibility to dopaminergic depletion. Further, cortical lesions inhibit striatal dysfunction and damage induced by 6-hydroxydopamine, which provides a new possibility for clinical treatment of Parkinson＇s disease.

A Survey of Visual Analytic Pipelines

Visual analytics has been widely studied in the past decade. One key to make visual analytics practical for both research and industrial applications is the appropriate definition and implementation of the visual analytics pipeline which provides effective abstractions for designing and implementing visual analytics systems. In this paper we review the previous work on visual analytics pipelines and individual modules from multiple perspectives： data, visualization, model and knowledge. In each module we discuss various representations and descriptions of pipelines inside the module, and compare the commonalities and the differences among them.

Statistical process monitoring based on improved principal component analysis and its application to chemical processes

In this paper, a novel criterion is proposed to determine the retained principal components (PCs) that capture the dominant variability of online monitored data. The variations of PCs were calculated according to their mean and covariance changes between the modeling sample and the online monitored data. The retained PCs containing dominant variations were selected and defined as correlative PCs (CPCs). The new Hotelling's T2 statistic based on CPCs was then employed to monitor the process. Case studies on the simulated continuous stirred tank reactor and the well-known Tennessee Eastman process demonstrated the feasibility and effectiveness of the CPCs-based fault detection methods.

Orthogonality of Redesigned tRNA Molecules with Three Stop Codons

The ability to expand genetic code in living cells has emerged as a powerful method with diverse applications.Here,we design re-placement of the anticodons of E.coli tRNAs that recognize codons for 20 natural amino acids,with three anti-stop codons,resulting in a total of 60 engineered tRNA constructs.We test these constructs one by one in E.coli,and found that six tRNAsCUA(tyrV,serX,hisR,trpT,glnV and leuX),two tRNAsUCA(trpT and leuX)and one tRNAUUA(tyrV)allowed efficient expression of Red Fluorescence Protein(RFP)with the presence of a corresponding stop codon in frame.Furthermore,we exploit the mutual orthogonality of tRNASer CUA,tRNATrpUCA and tRNATyrUUA with corresponding stop codons and demonstrated that the tRNASer CUA and the tRNATrp UCA can provide dynamic range and low crosstalk.Finally,we show the TAG and TGA can not only be used as an"AND gate"circuit to control the translation of target gene,but also be used to control the translation of a prodeoxyviolacein(PDV)pathway and a reporter in parallel.Overall,this work provides flexible tools for translational control and holds great potential to promote synthetic biology studies.