Exosomes are extracellular vesicles secreted by cells with lipid bilayer structure.As an important carrier of intercel-lular communication,exosomes are involved in regulating various pathological and physiological processes of the body.Exosomes can be used by immune cells to enhance or suppress immune response,and exosomes play an important role in allergic sensitization and in-flammation,in which mast cell-derived exosomes can absorb IgE and down-regulate IgE levels in the whole body.Tolerogenic exo-somes can inhibit allergic immune response by inducing regulatory T cells.Exosomes promote Th1 response to allergens;exosomes can also regulate IgE to promote antigen presentation,so exosomes are one of the development directions of immunotherapy.This article reviews the relationship between exosomes and allergic diseases and the progress in allergen specific immunotherapy.

Objective To explore the effect of phloretin on the proliferation,apoptosis,and tumorigenicity of ovarian cancer cells by regu-lating the Rac1/Akt/NF-κB signaling pathway.Methods The ovarian cancer cell line SKOV3 and the human normal ovarian epithelial cell line IOSE-80 were divided into the following groups:control,low-dose phloretin,medium-dose phloretin,high-dose phloretin,PM A,and high-dose phloretin+PMA.Morphological changes were observed under a microscope.Cell viability and apoptosis were assessed using the CCK-8 assay,colony formation assay,and flow cytometry.Western blotting was performed to detect the expression of proteins related to the Rac1/Akt/NF-κB signaling pathway.Tumor-bearing nude mice were established,tumor weights were measured,and the expres-sion levels of Rae1 and Akt in tumor tissues were analyzed.Results Compared with the control group,SKOV3 cells treated with low-,medium-,and high-dose phloretin showed reduced survival rate,colony formation,and expression of p-NF-κB p65/NF-κB p65,p-Akt/Akt,and Rac 1 in a dose-dependent manner.However,PM A reversed the inhibitory effects of high-dose phloretin on the malignant progression of ovarian cancer.In vivo experiments demonstrated that phloretin significantly inhibited tumor growth and reduced Akt and Rae1 expres-sion in tumor tissues(P＜0.05).Conclusion Phloretin suppresses the malignant progression of ovarian cancer by inhibiting the Rae1/Akt/NF-κB signaling pathway.

Objective To explore the effect of phloretin on the proliferation,apoptosis,and tumorigenicity of ovarian cancer cells by regu-lating the Rac1/Akt/NF-κB signaling pathway.Methods The ovarian cancer cell line SKOV3 and the human normal ovarian epithelial cell line IOSE-80 were divided into the following groups:control,low-dose phloretin,medium-dose phloretin,high-dose phloretin,PM A,and high-dose phloretin+PMA.Morphological changes were observed under a microscope.Cell viability and apoptosis were assessed using the CCK-8 assay,colony formation assay,and flow cytometry.Western blotting was performed to detect the expression of proteins related to the Rac1/Akt/NF-κB signaling pathway.Tumor-bearing nude mice were established,tumor weights were measured,and the expres-sion levels of Rae1 and Akt in tumor tissues were analyzed.Results Compared with the control group,SKOV3 cells treated with low-,medium-,and high-dose phloretin showed reduced survival rate,colony formation,and expression of p-NF-κB p65/NF-κB p65,p-Akt/Akt,and Rac 1 in a dose-dependent manner.However,PM A reversed the inhibitory effects of high-dose phloretin on the malignant progression of ovarian cancer.In vivo experiments demonstrated that phloretin significantly inhibited tumor growth and reduced Akt and Rae1 expres-sion in tumor tissues(P＜0.05).Conclusion Phloretin suppresses the malignant progression of ovarian cancer by inhibiting the Rae1/Akt/NF-κB signaling pathway.

Exosomes are extracellular vesicles secreted by cells with lipid bilayer structure.As an important carrier of intercel-lular communication,exosomes are involved in regulating various pathological and physiological processes of the body.Exosomes can be used by immune cells to enhance or suppress immune response,and exosomes play an important role in allergic sensitization and in-flammation,in which mast cell-derived exosomes can absorb IgE and down-regulate IgE levels in the whole body.Tolerogenic exo-somes can inhibit allergic immune response by inducing regulatory T cells.Exosomes promote Th1 response to allergens;exosomes can also regulate IgE to promote antigen presentation,so exosomes are one of the development directions of immunotherapy.This article reviews the relationship between exosomes and allergic diseases and the progress in allergen specific immunotherapy.

ObjectiveTo investigate the effect of kinesin family member 15 （KIF15） on the proliferation of hepatocellular carcinoma （HCC） cells and its mechanism of action. MethodsTCGA and GEPIA datasets were analyzed to determine the expression of KIF15 in HCC and its effect on tumor stage and survival. Quantitative real-time PCR and Western blot were used to measure the expression level of KIF15 in human-derived HCC cell lines （HepG2， Hep3B， MHCC-97H， and LM3） and human normal liver cell line L02 cultured in vitro， and Hep3B and HepG2 were selected for subsequent studies. CCK-8 assay， plate colony formation assay， and EdU staining were performed for Hep3B cells transfected with shRNA-NC or shRNA-KIF15 and HepG2 cells transfected with LV-vector or LV-KIF15 to evaluate the viability and proliferative capacity of these cells. GSEA was used to analyze the potential signaling pathways associated with KIF15 in HCC， and Western blot was used for detection. The independent-samples t test was used for comparison of continuous data between two groups； a one-way analysis of variance was used for comparison between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsThe analysis of TCGA and GEPIA datasets showed that in HCC patients， the expression of KIF15 in HCC tissue was significantly higher than that in normal tissue， and the HCC patients with high KIF15 expression tended to have a poorer prognosis. Compared with sh-NC-Hep3B， sh3-Hep3B showed significant reductions in the mRNA and protein levels of KIF15 （P<0.05）， cell viability， clone formation number， and EdU positive rate （all P<0.05）. Compared with vector-HepG2， LV-KIF15-HepG2 showed significant increases in the mRNA and protein levels of KIF15 （P<0.05）， cell viability， clone formation number， and EdU positive rate （all P<0.05）. Subcutaneous tumor assay showed that compared with sh-NC-Hep3B， sh3-Hep3B showed reductions in tumor volume and tumor weight， as well as a significant reduction in the immunohistochemical score of Ki67 and a significant increase in the immunohistochemical score of TUNEL （P<0.05）. GSEA analysis showed that the PI3K/AKT/mTOR pathway was positively correlated with KIF15 in HCC （NES=1.59， P<0.001）. Western blot showed that LY294002 could inhibit the PI3K/AKT/mTOR pathway upregulated in LV-KIF15-HepG2， and compared with LV-KIF15-HepG2， LY294002+LV-KIF15-HepG2 showed significant reductions in cell viability， clone formation number， and EdU positive rate （all P<0.05）. ConclusionKIF15 enhances the viability and proliferative capacity of HCC cells by upregulating the PI3K/AKT/mTOR signaling pathway.

Central nervous system idiopathic inflammatory demyelinating diseases (CNS-IIDD) is an autoimmune disorder characterized by inflammatory demyelination. The disease follows a course of recurrent attacks and remission, with some cases displaying continuous progression, often resulting in disability. The incidence of CNS-IIDD has been increasing, imposing a substantial burden on both patients′ families and society in recent years. A promising strategy for disease management involves the identification of humoral biomarkers to diagnose CNS-IIDD and predict disease attack and progression. Such biomarkers could aid in identifying individuals at high risk of disability, enabling targeted preventive interventions. This study summarizes advancements in the identification of humoral biomarkers and their potential for predicting disease activity and progression to offer novel insights into the management of CNS-IIDD.

Central nervous system idiopathic inflammatory demyelinating diseases (CNS-IIDD) is an autoimmune disorder characterized by inflammatory demyelination. The disease follows a course of recurrent attacks and remission, with some cases displaying continuous progression, often resulting in disability. The incidence of CNS-IIDD has been increasing, imposing a substantial burden on both patients′ families and society in recent years. A promising strategy for disease management involves the identification of humoral biomarkers to diagnose CNS-IIDD and predict disease attack and progression. Such biomarkers could aid in identifying individuals at high risk of disability, enabling targeted preventive interventions. This study summarizes advancements in the identification of humoral biomarkers and their potential for predicting disease activity and progression to offer novel insights into the management of CNS-IIDD.

Since there is a lack of obvious clinical symptoms in the early stage of hepatocellular carcinoma (HCC), most patients have progressed to the advanced stage at the time of confirmed diagnosis. There are limited treatment options for HCC patients who miss the opportunity for surgery, so it is of great importance to find new therapeutic targets. Tumor-associated macrophages (TAMs) are a group of macrophages existing in the tumor immune microenvironment and affect the malignant behaviors of HCC cells and the state of immune escape within the tumor. This article introduces the origin and classification of TAM, summarizes the role and mechanism of TAMs in vascular proliferation, invasion and metastasis, formation and maintenance of stemness, and anti-tumor immunity in HCC, and briefly describes the current research advances in therapeutic targets for TAM, and it is pointed out that targeting TAM may be a promising direction for clinical treatment.

Objective: To determine the first dengue fever case in Taizhou and trace probable transmission sources. Methods: Collected serum of three patients for antigen, antibody and nucleic acid detection. Dengue viruses were isolated and cultured in C6/36 cell. The whole length of E gene was amplified by reverse transcriptase-polymerase chain reaction(RT-PCR) and then sequenced. The phylogenetic tree was drawn. Results: Three cases were positive in nucleic acid detection. Two cases were IgM positive. One case was NSI antigen postive. Three strains of type I dengue virus were isolated from samples. The phylogenetic trees shown that the three strains were on the same branch. The identities of nucleotide were 99.87%. The identities of amino acid were 99.6%-99.8%. Conclusions The dengue virus strains isolated in Taizhou was imported from Guangdong or Southeast Asia and caused location infection.

Objective: To analyze characteristics of virus infections in patients with acute exacerbations of chronic obstructive pulmonary disease (COPD), and to analyze the role of virus infection in acute exacerbations of COPD. Methods: Totally 193 patients of COPD with acute exacerbations admitted to the Hospital of Sichuan Provincial Armed Police Force from April 2015 to March 2016 were enrolled as group A, and 50 patients of COPD in stable stage in the same period were enrolled as group B. IgM antibodies to respiratory syncytial virus, adenovirus, parainfluenza virus, influenza A virus, and influenza B virus in two groups were detected. General conditions and total virus infection rate were analyzed. Infection rates of each virus in group A were calculated. Proportion of single virus infection, two virus infections and several virus infections in group A with virus infection were calculated. Virus infection rates in different seasons in group A were also analyzed. Results: There was no significant difference in age, sex, and course of disease between the two groups(P>0.05). The virus infection rate of group A was 13.47%, which was higher than that of group B(χ²=5.29, P<0.05). The most common virus found in group A was influenza B virus(infection rate 12.44%), followed by influenza A virus(infection rate 7.78%), parainfluenza virus(infection rate 7.25%), adenovirus(infection rate 2.63%), respiratory syncytial virus(infection rate 1.32%). Single virus infection accounted for 34.6% of acute exacerbation COPD patients with virus infection, and two virus infections accounted for 15.4%, and three or more virus infections accounted for 50%. Virus infection rate in summer and autumn were higher than that in winter and spring, but the differences were not statistically significant(P>0.05). Conclusions This study showed that 14.37% of patients with acute exacerbations of COPD had viral infections, and most of them were infected with two or more viruses. Virus infection may play an important role in the acute exacerbation of COPD, and we need to pay attention to the prevention and treatment of virus infection in patients with COPD.