Alzheimer's disease(AD)is a highly destructive neurodegenerative disorder,and due to its complex pathology and insuffi-cient treatment,it is urgent to explore new targets that can directly address the root cause of the disease.In recent years,numerous stud-ies have shown that triggering receptor expressed on myeloid cells 2(TREM2)in microglial cells has the function of delaying the pro-gression of AD,and its abnormality plays a key role in the development and progression of AD,with a potential of being used as a target for the treatment of AD.This article reviews the biological characteristics of TREM2 and discusses its important role in the three major pathological features of AD and its potential as a target for AD treatment,in order to deepen the understanding of the role of TREM2 in AD and provide a theoretical reference for exploring new targets for AD treatment in the future.

ObjectiveTo investigate the impact of early intervention with Yishen Huazhuo prescription （YHP） on the learning and memory of accelerated aging model mice， as well as its underlying mechanism. MethodForty-eight 3-month-old male SAMP8 mice were randomly assigned into four groups， including the model group， low-dose YHP group， high-dose YHP group， and donepezil group. Additionally， 24 SAMR1 mice of the same age were divided into a control group and a YHP treatment control group， each consisting of 12 mice. The YHP groups received YHP at doses of 6.24 g·kg^-1 and 12.48 g·kg^-1， while the donepezil group was treated with donepezil at a dose of 0.65 mg·kg^-1. The model group and control groups were given physiological saline. The mice were gavaged once daily for a duration of four weeks. Spatial learning and memory abilities of mice were assessed using the Morris water maze test. Immunofluorescence staining was employed to evaluate neuronal density as well as expression levels of M1 microglial （MG） polarization marker inducible nitric oxide synthase （iNOS） and M2 MG polarization marker arginase-1 （Arg-1） in the hippocampus region. Enzyme-linked immunosorbent assay （ELISA） was used to measure serum levels of pro-inflammatory factor interleukin 1β （IL-1β） and anti-inflammatory factor transforming growth factor-β₁ （TGF-β₁）. Furthermore， Western blot analysis was conducted to determine expressions of amyloid β peptide1-42 （Aβ_1-42） along with triggering receptor expressed on myeloid cells 2 （TREM2）/nuclear factor kappa B （NF-κB） signaling pathway-related proteins TREM2， phospho （p）-NF-κB p65， and phospho-inhibitory kappa B kinase β （IKKβ） in the hippocampus. ResultCompared with the control group， the model group exhibited a significantly prolonged escape latency （P<0.01）， a significant reduction in neuron-specific nuclear protein （NeuN） expression in the hippocampus， a significant increase in iNOS expression in MG， and a significant decrease in Arg-1 expression. The serum IL-1β content was significantly increased， while the TGF-β₁ content was significantly decreased. Additionally， there was a significant decrease in TREM2 expression in the hippocampus and significant increases in p-NF-κB p65， p-IKKβ， and Aβ_1-42 expressions （P<0.05， P<0.01）. However， no significant changes were observed in escape latency， times of crossing the platform， and hippocampal NeuN expression in the YHP treatment control group. Conversely， iNOS expression in MG as well as the hippocampal p-NF-κB p65， p-IKKβ， and Aβ_1-42 expressions were significantly decreased. Furthermore， TREM2 expression was significantly increased （P<0.05， P<0.01）. In comparison to the model group， the low-dose YHP group showed a significantly shortened escape latency and an increased number of crossing the platform （P<0.05， P<0.01）. In the high-dose YHP group， the escape latency was significantly shortened （P<0.05）. In the low-dose YHP group， high-dose YHP group， the expression of NeuN in the hippocampus was significantly increased， the expression of iNOS in MG was significantly decreased， and the expression of Arg-l was significantly increased. The serum IL-1β content was significantly decreased， while the TGF-β₁ content was significantly increased. Furthermore， the expression of TREM2 in the hippocampus was significantly increased， and the expressions of p-NF-κB p65， p-IKKβ， and Aβ_1-42 were significantly decreased （P<0.01）. ConclusionEarly YHP intervention may promote the transformation of hippocampal MG from M1 to M2 by regulating the TREM2/NF-κB signaling pathway， reduce the release of neuroinflammatory factors， protect hippocampal neurons， and reduce the deposition of Aβ_1-42， and finally delay the occurrence of learning and memory decline in SAMP8 mice.

This study explores the application of animation in medical teaching. On the one hand, the status quo of the application of animation in medical teaching was analyzed by conducting questionnaire survey for the effect of animation-enhanced teaching of the biology course; on the other hand, new animations were made by the researchers to analyze its effect on the students' self-study. The results showed that the scores of the students receiving text and teaching animation resources were significantly higher than that of students receiving only textual information in the learning process (P<0.01), and the same goes for the number of the students that complete the >75％ of the learning content. The results showed that the teaching animation can improve the students' self-study performance and raise their interest in self-study.

Objective To analyze the molecular characteristic and trace the resource of dengue virus in Zhuhaidistrict of Guangzhou during 2012-2015.Methods Collected the cases data of dengue fever in Zhuhai district from 2012-2015 and analyzed the epidemical characteristic.DENV strains were isolated by C6/36 cells,the E gene was amplified from the positive specimen by RT-PCR.The PCR products were sequenced and then analyzed by bio-information software.Results Total of 6 260 DENV infection cases were reported,and the cases happened in every age group;57.78％ of the cases occurred in October.16 virus strains were isolated from 48 samples and the whole E genes were successfully amplified,the virus strains from 2013 and 2014 were the same one and the nucleotide sequence 99.93％ identify with DENV-1 in 2009.Phylogenetic analysis showed that DENV-1 belonged to the G1 genotype,genetically close to the strains from Thailand;strains from 2015 were the same one and belonged to the Cosmopolitan genotype of DENV-2,most similar with the strains from India.Conclusions The DENV-1 outbreak in Haizhu district of Guangzhou during 2012-2015 were belonged to G1 that originated from Thailand and might indigenous in 2009;DENV-2 was belonged to Cosmopolitan genotype which was imported.

Objective To investigate the protection of agmatine on blood brain barrier (BBB) permeability and the effect on the expression of aquaporin 4 (AQP4) and matrix metalloproteinase 9 (MMP9) in ischemic reperfusion injury rats.Methods Sixty healthy male Sprague-Dawley rats were randomly divided into normal control group (NC),model group and agmatine group,and there were 20 rats in each group.Normal control group was treated with intraperitoneal injection of saline in 2 hours after incision and suture of skin.Model group was treated with intraperitoneal injection of saline in 2 hours after the establishment of middle cerebral artery occulation (MCAO) model.Agmatine group was treated with intraperitoneal injection of agmatine (AGM) in 2 hours after the establishment of MCAO model.The damage of blood brain barrier was detected by measuring the permeability of blood brain barrier.The infarct size of brain was observed with TTC staining.The morphological changes of neurons were observed with electron microscope.The expressions of AQP4 and MMP9 were detected using immunohistochemical method.Results The permeability of BBB of agmatine treatment group (0.31±0.10) decreased significantly compared with the model group (0.46±0.09) (P＜0.05),but was still significantly higher than the normal control group (0.24±0.12) (P＜0.05).There was no infarction area in normal control group and the infarction areas of agmatine group decreased obviously compared with the model group.Compared with model group,the number of neurons with morphological changes reduced significantly and the degree of pathological changes of neurons was obviously improved in agmatine group.Compared with normal control group,the expression of AQP4 and MMP9 in ischemic penumbra of left cerebral hemisphere parietal cortex in the rats of model group and agmatine group increased significantly(P＜0.05).And the expression of AQP4 and MMP9 in model group was significantly higher than that of agmatine group(P＜0.05).Conclusion Agmatine has a protective effect on BBB with ischemia-reperfusion injury due to its down-regulation the expression of AQP-4 and MMP-9.