Ethnopharmacological relevanceSaiga antelope horn (SAH), derived from the male Saiga tatarica Linnaeus, has been used in China for millennia to treat hyperpyretic convulsions and hypertension-related diseases. Clarifying its effectiveness and mechanism of action are essential because of its limited availability. This study will guide the investigation of alternative resources.Aim of the studyThis study aims to illustrate the acute and long-term antihypertensive effects of SAH on spontaneously hypertensive rat (SHR), and further explore its mechanism related to hydrogen sulfide (H2S), other reactive sulfur species (RSS), renin-angiotensin-aldosterone system (RAAS).Materials and methodsThe effectiveness of SAH was investigated in the SHR model. Blood pressure was monitored independently by the tail-cuff method and carotid artery intubation. Hypertension was scored weekly by assessment of physical signs, including facial temperature, water consumption, irritability, pain, and rotation time. The effects of SAH on the RAAS, vasoactive substances, and sympathetic neurotransmitters were measured by enzyme-linked immunosorbent assay (ELISA) and colorimetry on completion of the study. Transcriptomics detected differentially expressed mRNAs and enriched signaling pathways in thoracic aorta tissue. H2 was measured in the mesenteric arteries and thoracic aorta by probe staining and lead sulfide detection. H2S and other RSS were measured in intestinal tissue by liquid chromatography-mass spectrometry. The correlation of the antihypertensive activity of SAH with H2S was tested with DL-propargylglycine (PAG), a cystathionine-γ-lyase (CSE) inhibitor. SAH organ protection was evaluated by histopathologic staining of artery, heart, and kidney tissue.
Abstract Background This study aimed to explored the effects of the Cardiac Rhythm Identification for Simple People (CRISP) method with flipped classroom approach for arrhythmia interpretation in electrocardiogram (ECG) by trainee nurses. Methods A total of 120 trainee nurses were enrolled and randomly divided into the experimental group and the control group using lecture-based learning method. We observed the effects of the two methods in ECG interpretation training and investigated the students’ attitudes toward the teaching practices. Results After training, the ECG test scores in the experimental group were significantly higher than that of the control group. Six months later, the ECG test scores of the experimental group was still higher. Self-learning enthusiasm, understanding of teaching content, satisfaction of teaching mode, satisfaction of teaching effectiveness, and interest in learning ECG were significantly higher in the experimental group. Conclusion CRISP method with flipped classroom approach is a new and effective mode worth trying in ECG teaching for trainee nurses.
Upregulation of Forkhead box G1 (FOXG1) has recently been observed in many cancers, while its effect on radiosensitivity in glioma is still unclear. In this study, we hypothesized that FOXG1 be a major player in radioresistance of glioma as well as the underlying mechanism.Immunohistochemistry (IHC) was conducted to assess FOXG1 expression in glioma tissues and glioma-adjacent tissues. Western Blot was implemented to detect the expression of autophagy-related proteins. CCK-8, colony formation and flow cytometry assays were implemented to assess cell viability, proliferation and apoptosis, respectively. Transmission electron microscope (TEM) was used to observe autophagic vesicles. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) assay was applied to detect the expression of FOXG1.The present study demonstrated that FOXG1 was highly expressed in glioma tissues. FOXG1 expression level was up-regulated in glioma cells following exposure to X-ray irradiation. FOXG1 can attenuate radiosensitivity of glioma cells. Moreover, it revealed that FOXG1 attenuate radiosensitivity of glioma cells by promoting autophagy.The present study suggests that FOXG1 is a pivotal molecule for circumventing radiation-induced cell death in malignant glioma cells through the regulation of autophagy, and it may be a target for the treatment of human brain glioma.
Abstract Atopic dermatitis (AD) is a common chronic pruritic inflammatory skin disorder characterized by recurrent eczematous lesions. Interleukin (IL)−33, a cytokine of the IL-1 family, was found to play an important role in the pathogenesis of AD. As a key component of the inflammasome, NLRP3 has been mostly described in myeloid cells that to mediate inflammasome activation conducted proinflammatory cytokine production of the IL-1 family. However, the role of NLRP3 inflammasome in the pathogenesis of AD, as well as IL-33 processing are highly controversial. Whether NLRP3 can mediate IL-33 expression and secretion independently of the inflammasome in the epithelium of AD has remained unclear. In this article, we found the mRNA expression of Il33 and Nlrp3 were notably increased in the lesional skin of AD patients compared to healthy controls. We then found a significant positive correlation between the expression of Nlrp3 and Il33 in the epithelium of MC903-mediated AD mice model, but no changes were observed for Il36α , Il36γ , Il1β , or Il18 mRNA expression, as well as IL-1β or IL-18 production. Overexpression of NLRP3 in human immortalized epithelial cells increased IL-33 expression, whereas siRNA targeting NLRP3 abolished IL-33 expression. In addition, inhibition of NLRP3 inflammasome activation or caspase-1 activity with MCC950 or VX-765 showed no effect on the expression and secretion of IL-33 in AD mice. Unlike myeloid cells, NLRP3 predominantly located in the nucleus of epithelial cells, which could directly bind to Il33 specific-promoters and transactivate it through an interaction with transcription factor IRF4. Furthermore, NLRP3 deficient mice exhibited a significant alleviated epidermis inflammation and decreased mRNA expression and secretion of IL-33 in MC903-mediated AD mice without interfering with TSLP and IL-1β production. Our results demonstrate a novel ability of NLRP3 to function as a crucial transcription factor of IL-33 in epithelium independently of inflammasome that to mediate the pathological process of AD.
Summary Patients with chronic mucocutaneous candidiasis (CMC) suffer persistent infections with the yeast Candida. CMC includes patients with autoimmune regulator (AIRE) gene mutations who have autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED), and patients without known mutations. CMC patients have dysregulated cytokine production, and dendritic cells (DCs), as central orchestrators, may underlie pathogenic disease mechanisms. In 29 patients with CMC (13 with APECED) and controls, we generated monocyte-derived DCs, stimulated them with Candida albicans, Toll-like receptor-2/6 ligand and lipopolysaccharide to assess cytokine production [interleukin (IL)-12p70, IL-23, interferon (IFN)-γ, IL-2, tumour necrosis factor (TNF)-α, IL-6, transforming growth factor-β, IL-10, IL-5, IL-13] and cell-surface maturation marker expression (CD83, CD86, human leucocyte antigen D-related). In both APECED and non-APECED CMC patients, we demonstrate impairment of DC function as evidenced by altered cytokine expression profiles and DC maturation/activation: (1) both groups over-produce IL-2, IFN-γ, TNF-α and IL-13 and demonstrate impaired DC maturation. (2) Only non-APECED patients showed markedly decreased Candida-stimulated production of IL-23 and markedly increased production of IL-6, suggesting impairment of the IL-6/IL-23/T helper type 17 axis. (3) In contrast, only APECED patients showed DC hyperactivation, which may underlie altered T cell responsiveness, autoimmunity and impaired response to Candida. We demonstrate different pathogenic mechanisms on the same immune response pathway underlying increased susceptibility to Candida infection in these patients.
Calycosin is a bioactive component of Astragali Radix, a Chinese herb for treating allergy. We have previously demonstrated that calycosin effectively inhibited allergic inflammation efficiently. The aim of this study was to explore the mechanism of calycosin on epithelial cells in allergic inflammation.An initial stage of atopic dermatitis (AD) model in which mice were just sensitized with FITC, was established in vivo and immortalized human keratinocytes (HaCaT cells) were utilized in vitro. Initiative key cytokines, TSLP and IL-33, were measured by ELISA, qPCR, immunofluorescence and Western blot. The junctions in epithelial cells were observed by electron microscopy and tight junctions (TJs) (Occludin and ZO-1) were assessed by Western blot and immunofluorescence. TLR4, MyD88, TAK1, TIRAP and NF-κB were measured by qPCR or Western blot.The results showed that TSLP and IL-33 were inhibited significantly by calycosin in the initial stage of AD model. Simultaneously, calycosin attenuated the separated gap among the epithelial cells and increased the expression of TJs. TSLP/IL-33 and TJs were similarly affected in LPS-stimulated HaCaT cells in vitro. Meanwhile, calycosin not only inhibited the expressions of TLR4, MyD88, TAK1 and TIRAP, but also reduced NF-κB activation in vitro and in vivo. An NF-κB inhibitor enhanced the expressions of TJs and reduced that of TSLP/IL-33 in LPS-stimulated HaCaT cells.These results indicated that calycosin reduced the secretion of TSLP/IL-33 and attenuated the disruption of epithelial TJs by inhibiting TLR4 mediated NF-κB signaling pathway. These findings help to understand the beneficial effects of calycosin on AD, and to develop effective preventive or therapeutic strategies to combat this disease and other epithelial barrier deletion-mediated allergic diseases.
Background Healthcare-associated infections (HAI) are infections acquired by patients during treatment in various healthcare institutions. These infections significantly increase morbidity, mortality, and healthcare costs. Enhancing HAI education for nurses can improve patient safety and medical quality. Aim The study aimed to assess the effectiveness of the new conceive-design-implement-operate (CDIO) teaching model on nursing students’ HAI learning outcomes and compare it with the traditional LBL model, providing valuable insights for future HAI education in nursing. Methods A total of 110 nursing students were randomly assigned to one of two groups for HAI training during the 2022–2023 academic year: a group that engaged in the CDIO model and another that received traditional lecture-based learning (LBL). The effectiveness of these pedagogical approaches was evaluated by comparing pre-and post-training test scores, and we used the Course Experience Questionnaire (CEQ) to collect students’ feedback on the course and teaching. Results Compared to traditional LBL method, the CDIO model significantly improved the overall scores and practical application scores of nursing students in the HAI course, with these advantages still retained after 24 weeks. Additionally, preliminary results show that students in the CDIO model scored higher on CEQ categories such as good teaching, clear goals and standards, appropriate assessment, generic skills, and independence, but they also reported an increased workload. Conclusion Our research is the first to apply the CDIO framework to nursing education in HAI courses, enhancing nursing students’ practical application skills, particularly in the sustained retention in this area. Our study indicates that the CDIO teaching model has significant advantages in enhancing course experience and teaching effectiveness.
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