Diabetic neuropathy(DN)is a prevalent chronic complication of diabetes,characterized by a com-plex pathogenesis involving various cell types and molecular pathways.Research indicates that microglia,serving as the innate immune cells of the central nervous system,are pivotal in the development of DN.In recent years,with the in-depth understanding of the pathogenesis of DN,targeting microglia polarization has become a new research hotspot.This article provides an overview of current research on the regulatory mechanisms of microglia polarization,the impact of mi-croglia polarization on DN,and treatment strategies that target microglia polarization to improve DN.The objective is to elucidate the pivotal role of microglia in the pathogenesis of DN,and assess the efficacy and constraints of existing and emerging treatment methods targeting microglia,in order to offer a fresh perspective for future research and clinical treat-ment of DN.

In order to explore the role of signal transducer and activator of transcription 3(STAT3)in the infection process of porcine hemagglutinating encephalomyelitis virus(PHEV),Western blot,qRT-PCR and indirect immunofluorescence experiments were used to detect the phosphoryla-tion level and subcellular localization changes of STAT3 after PHEV infection.The replication of PHEV were examined in cells with STAT3 knockdown or overexpression,respectively.The results showed the phosphorylation level of STAT3 at tyrosine 705 was significantly increased after PHEV infection,and the expression of STAT3 in the nucleus increased.In addition,STAT3 knock-down in cells can significantly inhibit PHEV replication.The above results further reveal the path-ogenic mechanism of PHEV and provide a theoretical basis for the research of anti-PHEV drugs.

In order to explore the role of signal transducer and activator of transcription 3(STAT3)in the infection process of porcine hemagglutinating encephalomyelitis virus(PHEV),Western blot,qRT-PCR and indirect immunofluorescence experiments were used to detect the phosphoryla-tion level and subcellular localization changes of STAT3 after PHEV infection.The replication of PHEV were examined in cells with STAT3 knockdown or overexpression,respectively.The results showed the phosphorylation level of STAT3 at tyrosine 705 was significantly increased after PHEV infection,and the expression of STAT3 in the nucleus increased.In addition,STAT3 knock-down in cells can significantly inhibit PHEV replication.The above results further reveal the path-ogenic mechanism of PHEV and provide a theoretical basis for the research of anti-PHEV drugs.

Diabetic neuropathy(DN)is a prevalent chronic complication of diabetes,characterized by a com-plex pathogenesis involving various cell types and molecular pathways.Research indicates that microglia,serving as the innate immune cells of the central nervous system,are pivotal in the development of DN.In recent years,with the in-depth understanding of the pathogenesis of DN,targeting microglia polarization has become a new research hotspot.This article provides an overview of current research on the regulatory mechanisms of microglia polarization,the impact of mi-croglia polarization on DN,and treatment strategies that target microglia polarization to improve DN.The objective is to elucidate the pivotal role of microglia in the pathogenesis of DN,and assess the efficacy and constraints of existing and emerging treatment methods targeting microglia,in order to offer a fresh perspective for future research and clinical treat-ment of DN.

Objective To study the effects of 5-HT1A receptor in hippocampal dentate gyrus on anxiety behavior of adult rats with Parkinson's disease (PD).Methods PD model in rats was constructed by using 6-hydroxydopamine (6-OHDA) to lesion the medial forebrain bundle (MFB).In lesioned rats and sham-operated rats,we examined the changes of the number of TFH-positive neurons in the SNc and VTA.We also examined how 5-HT1A receptor of hippocampal dentate gyrus (DG) modulates the anxiety-related behavior using open field test and elevated plus-maze test,and examined monoamine neurotransmitter changes in the striatum,medial prefrontal cortex (mPFC),amygdale and ventral hippocampus using reverse-phase high performance liquid chromatography with electrochemical detection.Results In 6-OHDA-lesioned rats,the SNc of the injected side showed a total loss of TH-ir neurons compared with the unlesioned side,and the number of TH-ir neurons in the VTA on the lesioned side decreased significantly to (34± 2)％.The locomotor activity in 6-OHDA-lesioned rats decreased compared with that in sham-operated rats.Unilaterally lesioning the MFB decreased the percentage of time spent in the center in the open-field test and percentages of open arm entries and open arm time of elevated plus maze test when compared with sham-operated rats.In the sham-operated rats,intra-DG injection of 8-OH-DPAT did not affect anxiety-like behavior.In 6-OHDA-lesioned rats,intra-DG injection of 8-OH-DPAT significantly increased the percentage of time spent in the center at a dose of 100 ng and 500 ng when compared with saline injection into the DG.Injection of WAY-100635 did not affect rats in the two groups.Unilateral 6-OHDA lesions of the MFB in rats significantly decreased DA levels in the ipsilateral striatum,mPFC,amygdale and ventral hippocampus compared with those in sham-operated rats,but had no effect on 5-HT or NA levels in those structures.Conclusion Unilateral 6-OHDA lesion of the MFB not only totally damaged DA neurons in SNc and partly damaged DA neurons in VTA,but also decreased DA level in the ipsilateral striatum,mPFC,amygdale and ventral hippocampus.Unilateral 6-OHDA lesion of the MFB induces anxiety-related behavior,and activation of 5-HT1A receptor in the hippocampal dentate gyrus has anxiolytic effect in the rat model of Parkinson's disease.

Objective: To screen and identify the mutations in Kawasaki disease by targeted enrichment of genomic region sequencing technique and investigate susceptibility genes associated with coronary artery lesion. Method: This was a case-control study.A total of 114 patients diagnosed as Kawasaki disease treated in Shanghai Children′s Hospital between December 2015 and November 2016 were studied and another 45 healthy children who were physically examined in outpatient department were enrolled as control group. Patients were divided into two groups based on the results of echocardiogram. Peripheral venous blood was obtained from patients and controls. Genomic DNA was extracted. SeqCap EZ Choice libraries were prepared by targeted enrichment of genomic region technology. Then the libraries were sequenced to identify susceptibility genes associated with coronary artery lesion in patients diagnosed as Kawasaki disease.Susceptible genes were identified by Burden test, Pearson chi-square test or Fisher′s exact probability test. Result: There was statistically significant difference in TNFRSF11B(rs2073618)G>C(p.N3K)mutation and GG/GC/CC genotype between Kawasaki disease group and control group(χ²=15.52, P=0.00). There was statistically significant difference in TNFRSF13B(rs34562254)C>T(p.P251L)mutation(χ²=10.40, P=0.01)and LEFTY1(rs360057)T>G(p.D322A)mutation(χ²=8.505, P=0.01)between patients with coronary artery lesions and those without. Conclusion Targeted enrichment of genomic region sequencing technology can be used to do primary screening for the susceptible genes associated with coronary artery lesions in Chinese Kawasaki patients and may provide theoretical basis for larger sample investigation of risk prediction score standard in Kawasaki disease.