Protease-activated receptor-2 (PAR-2) belongs to the receptor family which is coupled with G-protein. The N-terminus of PAR-2 is cleaved by some proteases to generate a new N-terminus. The new N-terminus can interact with and activate the receptor itself. The update research reported that PAR-2 could be expressed on some cancers as well as tumor cell lines. There are some relationships between the PAR-2 expression and the behaviors of tumor cell, such as proliferation, angiogenesis, migration and invasion.

D-amino acids were believed to have no function in higher organisms several years ago. Recently, D-serine was proved to be synthesized by astrocytes in vivo and be released to work as an effective coagonist at the “glycine-binding” site of the N-methyl-D-aspartate (NMDA) glutamate receptors in central nervous system. In this paper, the synthesis, metabolism and function of D-serine were reviewed briefly.

Vesicular glutamate transporters(VGLUTs)package specifically glutamate into synaptic vesicles in the presynaptic terminal for subsequent release into the synaptic cleft.VGLUT1 and VGLUT2 together label all glutamatergic neurons,are highly specific markers of glutamatergic neurons and their axon terminals.VGLUT1 and VGLUT2 are respectively the neurochemical marker of cortico-cortical projection and thalamo-cortical projection.VGLUT3 is also expressed in cholinergic interneurons,serotoninergic neurons,subsets of GABAergic interneurons in the hippocampus and cerebral cortex.The disfunction of VGLUTs can lead to the abnormal excitatory neurotransmitter glutamate,resulting in many nervous system disease.In order to give a clue for prevention and therapy of these diseases,this paper reviews the disfunction of VGLUTs effects on Alzheimer's disease(AD),Parkinson's disease(PD),schizophrenia,depressive disorder,epilepsy and deafness.

Alzheimer′s disease(AD)is one of the neurodegenerative diseases.Now it seriously threatens the life of the elderly.The pathogenesis of AD is not clear,thus there is no cure for this disease.The current treatment can′t reverse the pathological change of the disease or prevent the development of the disease,and the symptoms of the AD patients can only be partly improved.In recent years,the application of RNAi technology to the inhibition of the expression of the AD-related genes provides a new method for the treatment of AD.This article mainly introduces the application of the RNAi technology to AD.

Aim To disclose the molecular mechanism of Liuwei Dihuang decoction(LW)enhances the cognitive function of central nervous system, the effects of Liuwei Dihuang decoction on the differential expression genes in the hippocampus of senescence-accelerated mouse was studied. Methods There were 8 gene expression patterns, such as SAMP8 and SAMR1, SAMP8 as negative control and SAMR1 as positive control, huperzine A-treated SAMP8 and SAMP8 as negative control, LW-treated SAMP8 and SAMP8 as negative control, were compared and assessed by use of the differential expression cDNA microarray of the hippocampus of SAMP8 and SAMR1. The response genes of LW were compared. Results LW had significant modulating effects on some of the gene expressions. Expressions of genes, such as DUSP12, NSF, STUB1, CaMKⅡ?, AMFR, UQCRFS1 and other 11 novel genes without any functional clues changed significantly. These genes involved in the protein-tyrosine phosphatase family, the AAA(ATPases associated with diverse cellular activities)gene family, the serine/threonine protein kinases family, ubiquitin ligase, mitochondrial function and so on. Conclusions These results suggested LW effects on the cognitive impairments might be multi-mechanism and these genes might be the potential gene targets for LW effects on the impairments.

Chemical warfare agents and chemical terrorism agents have been identified as one of the major threats to human survival and national security currently. The key to dealing with these threats is the effective medical countermeasures of which specific antidotes take center stage. In the past decade,real or potential chemical threats which has sparked regional conflicts,terrorist activities or chemical accidents intentionally or unintentionally have increased the investment in antidotes research and development worldwide. Here,we introduced the research status on medical countermeasures against chemical threat by giving an overview of the United States ″Countermeasures Against Chemi?cal Threats(CounterACT)Program″,and then the recent research progress in antidotes against nerve agents,sulfur mustard and cyanide toxicities were reviewed.

AimThe aim of this study was to establish a rodent model with similar characters of human metabolic syndrome(MS).Methods Three species mice and Wistar rats were fed with high energy chows(HEC)for 6 to 23 weeks.Animals were weighted every week.Fasting blood glucose(FBG)together with total cholesterol(TC)and low density lipoprotein-cholesterol(LDL-C)were investigated by oxidase test every two week.And fasting blood insulin(FINS)was determined by radioimmunoassay.Homeostasis model assessment of insulin resistance(HOMA-IR)was calculated as FBG×FINS/22.5.At the end of the experiment,oral glucose tolerance test(OGTT)was performed.Then animals were decapitated,and coel-fat and orchio-fat were collected and weighted to calculate the visceral fat coefficient(VFC).Results FBG,serum TC and LDL-C significantly increased(P<0.01)after 6 weeks feed of HEC in KM mice.The mice also formed abdominal obesity and insulin resistant together with impairment of glucose tolerance(P<0.05 or P<0.01).Though similar to the KM mice,C57BL/6 and BALB/c mice couldn't form abdominal obesity while the latter had increased body weight(P<0.05 or P<0.01).Wistar rats formed hyperlipidemia from 1 to 10 week and hyperglycemia from 10 to 23 week together with insulin resistance and impaired glucose tolerance(P<0.05 or P<0.01).Conclusion KM mice feed with HEC for 6 weeks could successfully establish metabolic syndrome mice model which might be suitable for drug-screening,the major characters includes the formation of abdominal obesity(increase of VFC),the increase of serum TC,LDL-C,FBG and HOMA-IR,and the decrease of OGTT.

Autocrine motility factor (AMF) plays an important role in the stimulation of the migration and motility of cells, especially the generation, migration and angiogenesis of tumor. Recently, it has been found that AMF has three isoforms, ATX-t, ATX-m and PD-I alpha. The PD-I alpha isoform is specifically expressed in the brain, which plays extensive functions in nervous system, such as regulating neural development and differentiation, promoting neurotrauma repair, inducing neuropathic pain, even contributing neurodegeneration under some circumstances. This indicates the close relationship of AMF/AMFR and the pathophysiology of the nervous system. This paper mainly reviews the function of AMF and AMFR and its possible mechanism in the nervous system.

Luteinizing hormone(LH)is a gonadotropin of hypothalamic-pituitary-gonadal axis(HPG),secreted by the anteri?or pituitary. The secretion of LH is directly controlled by the release of gonadotropin releasing hormone(GnRH),acts at the ovaries and testes to stimulate the production of gonadal hormones. Aging leads to increases in LH,and higher serum levels of LH has been ob?served in Alzheimer′s disease(AD)patients when compared to age-matched controls. Evidences from basic research and epidemiologi?cal investigation support the critical role of elevated LH in pathogenic process of AD and deteriorating cognitive decline. Here we sum?marize the recent discoveries containing human AD epidemiological evidence for LH,cognitive impairments resulting from LH activi?ty,LH in AD pathology and LH receptor signaling mechanisms.

Alzheimer′s disease(AD)is a degenerative metabolic disease,whose exact pathological mechanism still remains unknown. Currently,studies have found that patients in AD accompany with insulin signaling pathway impairment and cerebral glu?cose metabolism dysfunction. As insulin signaling pathway and cerebral glucose metabolism homeostasis play a key role in AD ,some researches consider AD as“typeⅢdiabetes”. This review aims to discuss the alteration of cerebral insulin signaling pathway and glu?cose metabolism in AD,as well as their relationship with AD. We will also elaborate the advance in anti-AD drugs based on cerebral insulin signaling pathway.