Anticipatory anxiety is a negative emotion that arises when individuals encounter potential threats or uncertainties in the future. It is the core symptom of a variety of anxiety disorders, and is closely associated with the occurrence, severity, treatment outcome, and prognosis of anxiety disorders, which has garnered a growing amount of focus in clinical practice. Nevertheless, scientific research on anticipatory anxiety continues to face obstacles such as unclear pathological mechanisms, the absence of simple and consistent self-assessment tools, and effective interventions. To improve understanding of the role of anticipatory anxiety in the diagnosis and treatment of anxiety disorders, this study reviews pertinent domestic and international literature, and briefly introduces the concept, assessment and measurement, activation paradigm, pathological mechanisms, and interventions of anticipatory anxiety.

Anticipatory anxiety is a negative emotion that arises when individuals encounter potential threats or uncertainties in the future. It is the core symptom of a variety of anxiety disorders, and is closely associated with the occurrence, severity, treatment outcome, and prognosis of anxiety disorders, which has garnered a growing amount of focus in clinical practice. Nevertheless, scientific research on anticipatory anxiety continues to face obstacles such as unclear pathological mechanisms, the absence of simple and consistent self-assessment tools, and effective interventions. To improve understanding of the role of anticipatory anxiety in the diagnosis and treatment of anxiety disorders, this study reviews pertinent domestic and international literature, and briefly introduces the concept, assessment and measurement, activation paradigm, pathological mechanisms, and interventions of anticipatory anxiety.

Objective To investigate the effect and mechanism of Tiaobu Xinshen Prescription(Codonopsis Radix,Polygoni Multiflori Radix Praeparata,Lycii Fructus,Astragali Radix,etc.)on synaptic plasticity in 5xFAD transgenic mice with Alzheimer's disease(AD).Methods Eighteen 5-month-old male wild-type(WT)mice and 18 5xFAD transgenic mice were randomly divided into control group(0.9％NaCl),Tiaobu Xinshen Prescription group(granules,4.18 g·kg-1)and Aricept group(Donepezil Hydrochloride,0.625 mg·kg-1),with six mice in each group.According to the above groups,the rats were given intragastric administration once a day for 60 days.The ultrastructure of hippocampus in mice was observed by transmission electron microscopy.Western Blot was used to detect the protein expression levels of Synaptophsin,PSD-95,p-NMDAR1,NMDAR1,p-CaMKⅡa,CaMKⅡa,PI3K,p-Akt,Akt,p-mTOR and mTOR in mouse cortical tissue.Results Compared with the WT mice control group,the ultrastructure of synapses in the hippocampal CA1 region of the 5xFAD control group was irregular,the mitochondria was atrophied and reduced,the mitochondrial cristae was broken and disappeared,the synaptic membrane was irregularly and curved,the synaptic vesicles were reduced,and the postsynaptic density(PDS)was thinned or even broken.The protein expressions of Synaptophsin,PSD-95,p-NMDAR1/NMDAR1,p-CaMKⅡa/CaMKⅡa,PI3K,p-Akt/Akt and p-mTOR/mTOR in the cortex were significantly down-regulated(P<0.05).Compared with the mice in the 5xFAD control group,the ultrastructure of synapses in the hippocampal CA1 region of the mice in the Tiaobu Xinshen Prescription 5xFAD group was significantly changed,the number of mitochondria was increased,the number of synaptic vesicles was increased,the synaptic membrane was intact,and the postsynaptic density was thickened.The protein expressions of Synaptophsin,PSD-95,p-NMDAR1/NMDAR1,p-CaMKⅡa/CaMKⅡa,PI3K,p-Akt/Akt and p-mTOR/mTOR in the cortex were significantly up-regulated(P<0.05).Conclusion Tiaobu Xinshen Prescription may promote the synthesis of synaptic plasticity-related proteins by activating the PI3K/Akt/mTOR pathway,thereby improving the cognitive dysfunction of AD.

Abstract: Objective To screen and validate the differentially expressed microRNAs (miRNAs) in peripheral blood Methods - mononuclearcells(PBMCs)ofpatientswithsilicosis. Forty eightpatientswithoccupationalsilicosisatstageⅠ(case group)and45healthycontrols(controlgroup)wereselectedasresearchsubjectsbyrandomnumbertablemethod.PBMCswere-separatedbyFicollPaquegradientcentrifugationfromperipheralblood.Threepeoplefromeachgroupwererandomlyselected for miRNAs transcriptome sequencing. R Studio software was used to screen differentially expressed miRNAs, and FunRich software was used to predict the upstream transcription factors related to the differentially expressed miRNAs in PBMCs. The - Results differentially expressed miRNAs were verified by real time quantitative polymerase chain reaction. A total of 124 - - differentiallyexpressedmiRNAswerescreened,amongthem,97miRNAswereupregulatedand27miRNAswere down regulated.- The 67 targetgenes predicted by differentialmiRNAs were mainly involved in intracellularprocesses and nucleic acid binding transcriptionfactoractivities,includingcelladhesionmolecules,ratsarcoma,osteoclastdifferentiationandotherpathways.The-------------topfivemiRNAsdifferentiallyupregulatedwerehsamiR1373p,hsamiR500b3p,hsamiR190a5p,hsamiR1413pand------------hsamiR223p.ThetopfivedifferentiallydownregulatedmiRNAswerehsamiR2025p,hsamiR548ai,hsamiR55873p,------hsamiR5705pandhsamiR103983p.ThechangeofthesemiRNAswereconsistentwiththeresultspredictedaccordingto the miRNAs transcriptome sequencing. The transcription factors including specificity protein 1, early growth response 1, zinc Conclusion finger protein 161, etc., were obtained according to the differentially expressed miRNAs. The differentially

Objective To investigate the relationship between activation of gliacytes , mitogen-activated protein kinase (p38MAPK) and neuronal apoptosis after microinjecting aggregated Aβ25-35 into hippocampus.Methods The model was established by using stereotaxic technique to inject 10μg aggregated Aβ25-35 into dorsal hippocampus in rats .The rats were grouped as the control , vehicle and model groups .Immunohistochemistry and Western blotting were used for detection of activation of microglia(MG), atrocytes (AS) and expression of p-p38MAPK in the hippocampus.ELISA was used to evaluate the level of TNF-αand IL-1β.The survival neurons were observed by Nissl staining and the apoptotic neurons were identified by tunnel staining .Results Expression of ox-42, GFAP, p-p38MAPK were up-regulated in hippocampus, as well as TNF-α、IL-1β, which reached a highest value on the 7th day after injection of Aβ25-35.However, the number of neuron with Nissl positive decreased gradually , and the tunnel positive neurons increased highly and reached a peak value on the 7th day.There were significant differences between the control and vehicle group ( P <0.01). Conclusion Apoptosis of the neuron caused by Aβ25-35 injection may result from activation of gliacytes , p38 MAPK and increase of TNF-αand IL-1βlevel.

This study is to observe the effect of ilexonin A (IA) on the expression of basic fibroblast growth factor (bFGF) and growth associated protein-43 (GAP-43), and neurogenesis after cerebral ischemia-reperfusion in rats and explore its possible mechanism of protecting neuronal injury. Models of middle cerebral artery occlusion (MCAO) were established in SD rats. Before and after two hours ischemia-reperfusion, IA (20 and 40 mg x kg(-1)) was injected immediately and on 3, 7, 14, and 28 d once a day. The neurological severity was evaluated by neurological severity scores (NSS); neuronal injury in the boundary zone of the infarction area was evaluated by TUNEL and Niss1 staining. The expressions of bFGF and GAP-43 and neurogenesis were evaluated by Western blotting and 5-bromodeoxyuridine (Brdu) fluorescence staining, respectively. After treatment with IA, the NSS of treatment groups were lower than that of the models (3 and 7 d). The number of TUNEL positive neurons decreased and Nissl positive neurons increased at the same time (3 d). The expressions of bFGF and GAP-43 increased significantly in the boundary zone of the infarction area when compared to model group. Moreover, IA markedly enhanced the neurogenesis in the brain after ischemia-reperfusion, which revealed an increase of Brdu/NeuN positive cells in the boundary zone of the infarction area. The possible mechanism of protecting neuronal injury of IA may be related to inhibition on neuronal apoptosis, upregulation of bFGF and GAP-43, and neurogenesis in boundary zone of infarction after cerebral ischemia-reperfusion.

The probable mechanism of the reduction of rat cerebral ischemic-reperfusion injury by propyl gallate was studied. Intraluminal suture middle cerebral artery occlusion model of rat was employed. Propyl gallate was injected immediately after the ischemia was happened. The activity of NF-kappaB, and the expression of COX-2 and HSP70 on the peripheral ischemia were determined by Western blotting. The expression of TNF-alpha was determined by ELISA assay. RT-PCR and immunofluorescence staining were employed to detect the transcription and expression of TLR-4. Results showed that propyl gallate could inhibit the activity of NF-kappaB in the peripheral ischemia, and reduce the expression of COX-2 and TNF-alpha. As the upstream of NF-kappaB, the transcription and expression of TLR-4 decreased, as well as HSP70, the endogenic ligand of TLR-4. As an antioxidant, propyl gallate could reduce the cerebral ischemic-reperfusion injury through inhibiting the activity of NF-kappaB and decreasing the COX-2 and TNF-alpha in the peripheral ischemia. It also could influence HSP70 and TLR-4.