Objective: To investigate the mechanism of in alleviating colonic mucosal inflammation in ten-eleven translocation (TET) protein 2 gene knockout (TET2-/-) mice with ulcerative colitis (UC) by regulating DNA methyltransferase (DNMT) and DNA hydroxymethylase. Methods: Male specific pathogen-free (SPF) grade C57BL/6J wild-type (WT) mice (n = 8) and TET2-/- mice (n = 20) were used to establish UC models by freely drinking 3% dextran sulfate sodium solution for 7 d. After UC model validation through histopathological examination in two mice from each type, the remaining mice were divided into four groups (n = 6 in each group): WT model (WT + UC), TET2-/- model (TET2-/- + UC), TET2-/- mild moxibustion (TET2-/- + MM), and TET2-/- electroacupuncture (TET2-/- + EA) groups. TET2-/- + MM group received mild moxibustion on Tianshu (ST25) and Qihai (CV6) for 10 min daily for 7 d. The TET2-/- + EA group also applied electroacupuncture (1 mA, 2/100 Hz) at the same acupoints for 10 min daily for 7 d. The disease activity index (DAI) scores of each group of mice were accessed daily. The colon lengths of mice in groups were measured following intervention. The pathological changes in the colon tissues were observed with hematoxylin and eosin (HE) staining. The concentrations of interleukin (IL)-6, C-C motif chemokine 17 (CCL17), and C-X-C motif chemokine ligand 10 (CXCL10) in serum were detected by enzyme-linked immunosorbent assay (ELISA). The expression of DNMT proteins (DNMT1, DNMT3A, and DNMT3B) in the colon tissues was detected by immunohistochemistry. The expression of 5-methylcytosine (5-mC), 5-hydroxymethylcytosine (5-hmC), histone deacetylase 2 (HDAC2), and DNA hydroxymethylase family proteins (TET 1 and TET3) was detected using immunofluorescence, which also determined the co-localization of TET1 and IL-6 protein. Results: Compared with WT + UC group, TET2-/- + UC group exhibited significantly higher DAI scores and shorter colon lengths (P < 0.01). Both mild moxibustion and electroacupuncture significantly decreased DAI scores and ameliorated colon shortening in TET2-/- mice (P < 0.001). Histopathological scores of TET2-/- + UC mice were significantly higher than those of WT + UC group (P < 0.001) and were significantly reduced after both mild moxibustion and electroacupuncture interventions (P < 0.001). Serum levels of IL-6, CCL17, and CXCL10 were significantly elevated in TET2-/- + UC group compared with WT + UC group (P < 0.001). Mild moxibustion significantly reduced IL-6, CCL17, and CXCL10 levels (P < 0.001, P < 0.001, and P < 0.01, respectively), while electroacupuncture also significantly reduced IL-6, CCL17, and CXCL10 levels (P < 0.05, P < 0.01, and P < 0.01, respectively). TET2-/- + UC mice showed increased expression levels of DNMT1, DNMT3A , DNMT3B, and 5-mC (P < 0.05, P < 0.01 and P < 0.001, respectively), with decreased expression levels of TET1, TET3, 5-hmC, and HDAC2 (P < 0.001). Mild moxibustion significantly reduced DNMT1, DNMT3B, and 5-mC levels (P < 0.05, P < 0.01, and P < 0.001, respectively), while increasing expression levels of TET1, TET3, 5-hmC, and HDAC2 (P < 0.001, P < 0.001, P < 0.05, and P < 0.001, respectively). Electroacupuncture significantly decreased 5-mC and DNMT3B levels (P < 0.001 and P < 0.01, respectively) and increased 5-hmC and HDAC2 levels (P < 0.05 and P < 0.001, respectively), but did not significantly affect TET1 and TET3 expression (P > 0.05). Compared with TET2-/- + MM group, TET2-/- + EA group showed significantly higher 5-mC expression (P < 0.001). TET2-/- + UC group exhibited markedly increased IL-6 expression and higher co-localization of TET1 and IL-6 in mucosal epithelium, whereas minimal IL-6 expression was observed in the other groups. Conclusion Mild moxibustion and electroacupuncture significantly ameliorate colonic inflammation exacerbated by TET2 deficiency in UC mice via epigenetic modulation. Distinct mechanisms exist between the two interventions: mild moxibustion regulates both DNMT and hydroxymethylase, whereas electroacupuncture primarily affects DNMT.

Allergen-associated proteases, pollutants, viral and fungal pathogens disrupted epithelial barrier integrity and promoted airway epithelial release of alarmins.Epithelial-derived Alarmins include thymic stromal lymphopoietin (TSLP), interleukin 33 (IL-33), and interleukin 25 (IL-25), which acted on a variety of effector cells such as dendritic cells (DCs), T-lymphocytes, innate lymphocyte cells (ILC2), B-lymphocytes, eosinophils, mast cells, basophils, and macrophages. T-lymphocytes, innate lymphocyte cell type 2 (ILC2), B-lymphocytes, eosinophils, mast cells, basophils and macrophages are the effector cells. By affecting the physiological and biochemical functions of target cells, such as proliferation and differentiation, survival and recruitment, and material metabolism, the alarmins had activated the intrinsic and adaptive immunity, and played a key role in allergic diseases such as bronchial asthma, atopic dermatitis, allergic rhinitis, and urticaria. A variety of monoclonal antibodies targeting epithelial-derived alarm factors have been developed for the above allergic diseases, and some of these products are already put into clinical use. As epidemiological studies showed that skin allergy closely related to airway allergy, allergic co-morbidities has imposed a heavy economic and psychological burden to patients. In-depth understanding the mechanism of alarmins will help to understand the developing and progression of allergic diseases, and develop more effective diagnostic and therapeutic strategies for allergic co-morbidities. This article reviews the mechanism and recent research advances of epithelial-derived alarmins in a variety of allergic diseases.

Allergen-associated proteases, pollutants, viral and fungal pathogens disrupted epithelial barrier integrity and promoted airway epithelial release of alarmins.Epithelial-derived Alarmins include thymic stromal lymphopoietin (TSLP), interleukin 33 (IL-33), and interleukin 25 (IL-25), which acted on a variety of effector cells such as dendritic cells (DCs), T-lymphocytes, innate lymphocyte cells (ILC2), B-lymphocytes, eosinophils, mast cells, basophils, and macrophages. T-lymphocytes, innate lymphocyte cell type 2 (ILC2), B-lymphocytes, eosinophils, mast cells, basophils and macrophages are the effector cells. By affecting the physiological and biochemical functions of target cells, such as proliferation and differentiation, survival and recruitment, and material metabolism, the alarmins had activated the intrinsic and adaptive immunity, and played a key role in allergic diseases such as bronchial asthma, atopic dermatitis, allergic rhinitis, and urticaria. A variety of monoclonal antibodies targeting epithelial-derived alarm factors have been developed for the above allergic diseases, and some of these products are already put into clinical use. As epidemiological studies showed that skin allergy closely related to airway allergy, allergic co-morbidities has imposed a heavy economic and psychological burden to patients. In-depth understanding the mechanism of alarmins will help to understand the developing and progression of allergic diseases, and develop more effective diagnostic and therapeutic strategies for allergic co-morbidities. This article reviews the mechanism and recent research advances of epithelial-derived alarmins in a variety of allergic diseases.

Objective To analyze the cunent situation and latent profiles of nurses'perceived organizational support,and explore the influencing factors of different types.Methods Through convenience sampling,a total of 1,860 nurses from the Pearl River Delta,Northern Guangdong,Eastern Guangdong and Western Guangdong regions of Guangdong Province were selected for the survey between October and December 2023.The demographic questionnaire,the Perceived Organizational Support Scale,and the Psychological Resilience Scale were used for investigation.The latent profiles of the nurses'perceived organizational support,the influencing factors of latent profiles were identified by single-factor analysis and multivariate Logistic regression.Results The score of the items of the perceived organizational support in l,819 nurses is(3.47±0.88)scores.Nurses perceived organizational support is divided into 3 latent classes,namely"poor group"(10.1％),"balanced group"(44.4％),and"rich group"(45.5％).The influencing factors include recruitment type,hospital level,and psychological resilience(all P＜0.05).Conclusion The perceived organizational support among nurses is moderately high and heterogeneous,which could be divided into 3 latent profiles.Nursing managers should focus on nurses from the poor group and balanced group and intervene with nurses according to the influencing factors of the different latent profiles to improve the level of nurses perceived organizational support.

Objective To analyze the cunent situation and latent profiles of nurses'perceived organizational support,and explore the influencing factors of different types.Methods Through convenience sampling,a total of 1,860 nurses from the Pearl River Delta,Northern Guangdong,Eastern Guangdong and Western Guangdong regions of Guangdong Province were selected for the survey between October and December 2023.The demographic questionnaire,the Perceived Organizational Support Scale,and the Psychological Resilience Scale were used for investigation.The latent profiles of the nurses'perceived organizational support,the influencing factors of latent profiles were identified by single-factor analysis and multivariate Logistic regression.Results The score of the items of the perceived organizational support in l,819 nurses is(3.47±0.88)scores.Nurses perceived organizational support is divided into 3 latent classes,namely"poor group"(10.1％),"balanced group"(44.4％),and"rich group"(45.5％).The influencing factors include recruitment type,hospital level,and psychological resilience(all P＜0.05).Conclusion The perceived organizational support among nurses is moderately high and heterogeneous,which could be divided into 3 latent profiles.Nursing managers should focus on nurses from the poor group and balanced group and intervene with nurses according to the influencing factors of the different latent profiles to improve the level of nurses perceived organizational support.

Epilepsy is a kind of brain dysfunction syndrome characterized by paroxysmal,transient,repetitive and rigid characteristics caused by abnormal discharge of highly synchronized neurons in the brain.Epilepsy is often accompanied by cognitive dysfunction.At present,anti-seizure medications are the most important methods of clinical treatment.Most of the traditional anti-seizure medications can cause cognitive dysfunction,and the influence of new anti-seizure medications on cognitive function is not completely clear.This paper reviews the influence of new anti-seizure medications on cognitive function and the possible related mechanisms of action based on relevant literature at home and abroad.It is expected that clinicians should pay attention to cognitive function in the process of diagnosis and treatment of epilepsy,and help clinicians realize the influence of anti-seizure medications on cognitive function,and rationally choose anti-seizure medications for patients.

【Objective:】 To study the application and effect of peer education mode in the nursing of patients with urinary tumor, and explore the ways to improve the quality of clinical care and the humanistic significance of this mode in clinical nursing. 【Methods:】 84 patients with urological tumors who received surgical treatment in urology department of a third-class hospital from March 2021 to December 2021 were randomly divided into the control group and the experimental group, with 42 patients in each group. The subjects in control group adopted routine intervention mode.The subjects in experimental group integrated the peer education program into the routine nursing mode.SAS and SDS scales were used to evaluate patients’ state of anxiety and depression, and the degree of nursing satisfaction. 【Results:】 The scores of SAS and SDS in the experimental group were significantly lower than that of the experimental group before intervention and the control group after intervention (P<0.05).The number of very satisfied, moderately satisfied and dissatisfied cases in the control group was 12, 29 and 1 respectively, and in the experimental group was 19, 23 and 0 respectively. The difference was statistically significant (P<0.05). 【Conclusion:】 Adopting peer education with humanistic care significance can effectively alleviate patients’ preoperative anxiety, depression and other adverse mental state, reduce preoperative stress, and provide a new way for nursing quality.

ObjectiveTo explore the action mechanism of Linggan Wuwei Jiangxintang on the treatment of lipopolysaccharide （LPS）-induced acute lung injury （ALI） in mice. MethodTraditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）， GeneCards， DisGeNET， and Herb databases were combined with clinical data from Gene Expression Omnibus （GEO） to screen the key targets of Linggan Wuwei Jiangxintang in the treatment of ALI. The protein-protein interaction （PPI） network was constructed to screen the core targets， and gene ontology （GO） and Kyoto encyclopedia of genes and genomes （KEGG） pathway enrichment analyses were performed. The mouse ALI model was established by LPS induction to verify the effect and key targets of Linggan Wuwei Jiangxintang on the treatment of ALI. The expression levels of Toll-like receptor 4 （TLR4）， nuclear transcription factor-κB p65 （NF-κB p65）， and phosphorylated NF-κB p65 （NF-κB p-p65） in lung tissue were detected by Western blot. ResultThe analysis showed that the treatment of ALI with Linggan Wuwei Jiangxintang was related to 10 core targets such as interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， and JUN， involving TNF signaling pathway， Toll-like receptor signaling pathway， NF-κB signaling pathway， etc. The animal experimental results show that Linggan Wuwei Jiangxintang can reduce lung injury， improve the pathological state of ALI mice， significantly reduce the expression of TNF-α and IL-6 in serum， increase the activity of total superoxide dismutase （T-SOD） and catalase （CAT） in lung tissue， and reduce the expression levels of JUN， TLR4， NF-κB p65， and NF-κB p-p65 proteins in lung tissue. ConclusionLinggan Wuwei Jiangxintang can inhibit LPS-induced inflammation and oxidative damage in ALI mice， and its mechanism may be related to the inhibition of TLR4/NF-κB signaling pathway and the reduction of inflammatory factors such as TNF-α and IL-6.