BackgroundAllergic rhinitis (AR) and chronic spontaneous urticaria (CSU) are often concurrent in patients. Changes in DNA methylation affect T cell biological processes, which may explain the occurrence and progression of comorbidity. However, downstream regulatory pathways of DNA methylation in two diseases and the underlying mechanisms have not been fully elucidated.MethodsThe GSE50101, GSE72541, GSE50222 and OEP002482 were mined for the identification of differentially expressed genes (DEGs) or co-expressed genes and differentially methylated genes (DMGs) in AR and CSU patients. We applied GO analysis and consensus clustering to study the potential functions and signal pathways of selected genes in two diseases. GSVA and logistic regression analysis were used to find the regulatory pathway between DNA methylation and activation patterns of CD4+ T cells. Besides, we used the Illumina 850k chip to detect DNA methylation expression profiles and recognize the differentially methylated CpG positions (DMPs) on corresponding genes. Finally, we annotated the biological process of these genes using GO and KEGG pathway analysis.ResultThe AR-related DEGs were found closely related to the differentiation and activation of CD4+ T cells. The DEGs or co-expressed genes of CD4+ T cells in AR and CSU patients were also clustered using GO and KEGG analysis and we got 57 co-regulatory pathways. Furthermore, logistic regression analysis showed that the regulation of cellular component size was closely related to the activation of CD4+ T cells regulated by DNA methylation. We got self-tested data using the Illumina 850k chip and identified 98 CpGs that were differentially methylated in patients. Finally, we mapped the DMPs to 15 genes and found that they were mainly enriched in the same CD4+T cell regulating pathway.ConclusionOur study indicated that DNA methylation affected by pollen participated in the activation patterns of CD4 + T cells, providing a novel direction for the symptomatic treatment of the co-occurrence of AR and CSU.

Inconsistent training programs for public health emergency (PHE) have been criticized as a contributing factor in PHE's managerial weak points. In response, to analyze the relevant discrepancies among the medical students in the class of 2021 from Xiangya School of Medicine of Central South University, the present study conducted an online questionnaire survey using convenience sampling. The questionnaire comprised four sections, including the basic information, the subjective cognition in PHE, the rescue knowledge and capabilities of PHE, and the mastery of PHE regulations and psychological intervention abilities. To compare the abovementioned aspects, related data were collected from 235 medical students divided into two groups, namely, clinical medical students (Group A) and preventive medical students (Group B). We found a more positive attitude in PHE (P = 0.014) and a better grasp of the PHE classification (P = 0.027) and the reporting system in group B compared with group A. In addition, even if group B showed the same response capability in communicable diseases as group A, the former had less access to clinical practice, resulting in poorer performance in the noncommunicable diseases during a fire, flood, and traffic accidents (P = 0.002, P = 0.018, P = 0.002). The different emphasis of each training program contributed to the uneven distribution of abilities and cognition. Meanwhile, the lack of an integrated PHE curriculum led to unsystematic expertise. Hence, to optimize the PHE management system, equal attention should be paid to medical students with diverse majors along with a complete integrated PHE curriculum.

Homeobox B2 (HOXB2) is a transcription factor that belongs to the homeobox family. Previous investigations have demonstrated that tumor prognosis was strongly linked to aberrant HOXB2 expression. However, the mechanism linking HOXB2 to the tumor microenvironment (TME) and prognosis has not been explored in detail. Three cohorts at different stages of colorectal cancer (GSE17536, GSE17537, GSE14333) demonstrated that elevated HOXB2 expression had significantly association with poorer overall survival (OS), disease-specific survival (DSS), and disease-free survival (DFS). Additionally, the poor prognosis in low grade glioma (LGG) (OS HR = 1.8, P-value = 0.00084; DFS HR = 1.5, P-value = 0.014) was associated with increased HOXB2 expression. Moreover, we also demonstrated that the correlation between HOXB2 expression with prognosis of gastric cancer, breast cancer, and liver cancer. What’s more, the results analyzed by TIMER further showed that HOXB2 expression was associated with immune infiltration level of colon adenocarcinoma (COAD), rectum adenocarcinoma (READ) and LGG, particularly B cells, CD4+ T cells, CD8+ cells. macrophages, neutrophils, and dendritic cells (DCs). The positive correlation between HOXB2 expression and the expression of immune maker genes was also observed. The results of RT-qPCR were reliable and we supposed that HOXB2 expressing validation provided strong evidence for HOXB2 functioning as a novel prognosis biomarker. These findings suggested that poor prognosis and increased immune infiltration levels were found to be correlated with increased HOXB2 expression in multiple cancers, especially in COAD, READ and LGG. Furthermore, in COAD, LGG and READ, HOXB2 potentially regulates TAMs, DCs, T cell exhaustion, and Tregs. Therefore, HOXB2 can serve as a biomarker with special prognostic value and may be involved in the regulation of immune cell infiltration in patients with COAD, READ and LGG.