To evaluate the design and implementation effects of the "Rapid Recognition and Management of Critically Ill Patients" course, and to provide a reference for the improvement of situational simulation teaching in emergency and critical care settings.

Traditional Chinese medicine (TCM) is a well-accepted therapy for atopic dermatitis (AD). However, there are currently no evidence-based guidelines integrating TCM and Western medicine for the treatment of AD, limiting the clinical application of such combined approaches. Therefore, the China Association of Chinese Medicine initiated the development of the current guideline, focusing on key issues related to the use of TCM in the treatment of AD. This guideline was developed in accordance with the principles of the guideline formulation manual published by the World Health Organization. A comprehensive review of the literature on the combined use of TCM and Western medicine to treat AD was conducted. The findings were extensively discussed by experts in dermatology and pharmacy with expertise in both TCM and Western medicine. This guideline comprises 23 recommendations across seven major areas, including TCM syndrome differentiation and classification of AD, principles and application scenarios of TCM combined with Western medicine for treating AD, outcome indicators for evaluating clinical efficacy of AD treatment, integration of TCM pattern classification and Western medicine across disease stages, daily management of AD, the use of internal TCM therapies and proprietary Chinese medicines, and TCM external treatments. Please cite this article as: Du XR, Wu MY, Tao MC, Lin Y, Gu CY, Wu MF, Cao Y, Chen DC, Li W, Wang HW, Wang Y, Wang Y, Lu HZ, Liu X, Su XF, Li FL. Clinical practice guidelines for the diagnosis and treatment of atopic dermatitis with integrative traditional Chinese and Western medicine. J Integr Med. 2025; 23(6):641-653.
Dermatitis, Atopic/drug therapy* ; Humans ; Medicine, Chinese Traditional/methods* ; Integrative Medicine ; Drugs, Chinese Herbal/therapeutic use* ; Practice Guidelines as Topic

Objective To investigate the role of circular RNAs(circRNA)in Alzheimer's disease(AD)and its potential mechanism.Methods Six-month-old APP/PS1 mouse model of AD and wild type(WT)mice were subjected and then randomly divided into WT group,WT+circ-Olfm1 knockout group,AD group(transgenic APP/PS1 mice),AD+circ-Olfm1 knockout group,AD+FOXO3a knockout group,with 3 mice in each group.① The total RNA of mouse brain was extracted,and the differential expression of circRNAs and mRNAs between the AD mice and WT mice was detected,and the obtained circRNAs and mRNAs were analyzed with gene ontology(GO)analysis.② RT-qPCR was used to detect the expression of the top 10 up-regulated and down-regulated circRNAs,as well as the expression of circ-Olfm1 and miR-330-5p.③ Lentiviral vectors were prepared and stereotaxically injected into the cortex or hippocampus of WT and AD mice to knock out circ-Olfm1 gene.Water maze test was used to evaluate the effect of circ-Olfm1 knockout on cognitive function,and immunofluorescence assay was employed to observe the deposition of amyloid β(Aβ)plaque in the brain.④ The interaction between circ-Olfm1 and miR-330-5p was verified by double luciferase reporter gene analysis.⑤ The protein levels of AMPK and FOXO3a were detected by Western blotting.⑥ Transmission electron microscopy was utilized to observe the mitochondria of the hippocampus.⑦ The levels of inflammatory factors IL-6,IL-1β and TNF-α were detected by ELISA.Results There were totally 52 differentially expressed circRNAs identified between the AD and WT mice,including 28 up-regulated and 24 down-regulated(fold change>1.5,P<0.05).These differentially expressed genes are mainly involved in signal transduction,learning and memory and other functions.circ-Olfm1 was identified as the most significantly differentially expressed circRNA,which is highly expressed in the neurons and up-regulated in the cerebral cortex and hippocampus of the AD mice.Knockout of circ-Olfm1 reduced the number of Aβ plaques in the cerebral cortex and hippocampus of AD mice(P<0.01).In starBase database,there are complementary sequences observed between circ-Olfm1 and miR-330-5p.Western blotting showed that the addition of Aβ42 significantly increased the expression of AMPK and FOXO3a in the neuronal cells(P<0.01).And silencing circ-Olfm1 led to decreased expression of AMPK and FOXO3a in neuronal cells+Aβ42(P<0.01).ELISA revealed that knockout of FOXO3a significantly increased the levels of inflammatory factors IL-6,IL-1β,and TNF-α(P<0.01).Transmission electron microscopy displayed that knocking FOXO3a out significantly aggravated mitochondrial damage(P<0.01).Conclusion circ-Olfm1 is up-regulated in the brain tissue and neurons+Aβ42 of AD rats,and the mechanism of cognitive impairment in AD rats may be through its regulating FOXO3a protein.

Objective To investigate the effect of pramlintide,a pancreatic amyloid peptide analog,on learning and memory of Alzheimer's disease(AD)mice through antioxidant stress,and to determine the expression of phosphatidylinositol 3-kinase/protein kinase B(PI3K/Akt)signaling pathway.Methods The APP/PS1 mice were divided into a pramlintide treatment group(intraperitoneal injection of 0.5 μmol/L per day for 10 weeks)and an AD group(same dose of PBS),with 5 mice in each group.The learning and memory abilities were detected with water maze test,the pathological changes of the hippocampus were observed with HE staining and immunohistochemistry,the morphological characteristics of dendritic spines in hippocampus were observed after Golgi staining,and the ultrastructure of hippocampal neurons was observed through transmission electron microscopy(TEM).The content of malondialdehyde(MDA)and the level of superoxide dismutase(SOD)in the hippocampal tissue were detected by biochemical assay,and the levels of inflammatory factors IL-6,TNF-α and IL-1β were determined with ELISA.Western blotting was applied to measure the expression of PI3K/Akt signaling pathway related proteins in the hippocampus.In the cell experiment,SH-SY5Y cells were added with Aβ 1-42 to establish a cell model of AD.After the cells were treated with pramlintide,the levels of oxidative stress and inflammatory response were detected,and cell apoptosis was detected by immunofluorescence.Results The animal experiments showed that pramlintide treatment resulted in significantly shortened escape latency(P<0.01),increased platform crossings(P<0.01),and prolonged time to exploring hidden platform(P<0.01).In the hippocampal tissue of the pramlintide treatment group,HE staining displayed hippocampal neurons in high density and neat arrangement(P<0.05),immunohistochemical results showed significantly reduced Aβ protein(P<0.01),Golgi staining results demonstrated more dendritic spines(P<0.05),TEM revealed almost intact neuronal mitochondrial structure,with reduced vacuolization and clear and identifiable morphology.When compared with the AD group,the levels of oxidative stress and inflammatory response were decreased(P<0.01),and the relative expression of p-PI3K/PI3K and p-Akt/Akt proteins was increased(P<0.01)in the treatment group.In cell experiments,the levels of oxidative stress and inflammatory response were decreased in AD cell model after pramlintide treatment(P<0.01),and the results of immunofluorescence showed that cell apoptosis was declined(P<0.01).Conclusion Pramlintide can improve the cognitive function,reduce the hippocampal deposition of Aβ,reduce oxidative stress and inflammatory response,alleviate the pathological changes of neuronal ultrastructure,and enhance the expression of PI3K/Akt signaling pathway in AD mice.

Objective To investigate the expression level of circular RNA circ-Tns3 in Alzheimer's disease(AD)mice and its role in Aβ-induced neuronal damage.Methods Five APP/PS1 transgenic AD mice and 5 wild-type(WT)mice,weighting of 23～26 g and aged 6 months were subjected in the study.Morris water maze test was used to assess learning and memory abilities,and immunohistochemical staining was performed to observe the number of Aβ plaques in the hippocampal tissue.Subsequently,total RNA was extracted from the brains to detect the differential expression of circRNAs between AD and WT mice,and the results were further analyzed with Gene Ontology(GO)analysis and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis.The top 6 differentially expressed circRNAs were validated by real-time quantitative PCR(RT-qPCR).In in vitro experiments,Aβ1-42 was used to treat neuronal cells to establish AD cell model,and si-circ-Tns3 was transfected into Aβ1-42-treated neuronal cells to knock down circ-Tns3.RT-qPCR was used to determine the expression levels of circ-Tns3 and miR-671-5p.Cell viability and apoptotic rate were detected by CCK-8 assay and TUNEL staining,respectively.The levels of superoxide dismutase(SOD)and malondialdehyde(MDA)were measured using corresponding kits,and the levels of inflammatory factors IL-6,IL-1β,and TNF-α were detected with ELISA.The interaction between circ-Tns3 and miR-671-5p was verified by dual-luciferase reporter assay and RNA-binding protein immunoprecipitation(RIP)assay.The expression level of Sirt1 protein was detected by Western blotting.Results The 6-month-old AD mice exhibited significant cognitive impairment and Aβ deposition(P<0.01).There were 269 differentially expressed circRNAs identified between AD and WT mice,of which 159 were up-regulated and 110 down-regulated.GO and KEGG enrichment analyses showed that these differentially expressed circRNAs were mainly involved in synaptic transmission,memory,and cholinergic synapse signaling pathways.The expression of circ-Tns3 was significantly increased not only in the brain tissue of AD mice but also in neuronal cells after Aβ1-42 treatment.In cellular experiments,knockdown of circ-Tns3 significantly reduced cell viability and number of apoptotic cells in Aβ1-42-treated neuronal cells,decreased MDA content,increased SOD activity,and reduced the levels of IL-6,IL-1β,and TNF-α(P<0.01).The starBase database predicted that circ-Tns3 and miR-671-5p have complementary sequences,and dual-luciferase reporter and RIP assays confirmed their interaction.The bioinformatics database predicted that miR-671-5p and sirt1 have complementary sequences.Western blotting indicated that in neuronal cells treated with Aβ1-42,the expression of sirt1 was increased after knockdown of circ-Tns3(P<0.01).In Aβ1-42-treated neuronal cells,after knockdown of circ-Tns3,addition of miR-671-5p inhibitor significantly decreased the expression level of sirt1 protein(P<0.01).Conclusions circ-Tns3 is highly expressed in AD mice and cell model of AD.Knocking circ-Tns3 down improves neuronal damage.circ-Tns3 may be involved in the neuronal damage through regulating sirt 1 protein by binding to miR-671-5p.

Objective To investigate the effects of amylin,also known as islet amyloid polypeptide(IAPP),on learning and memory abilities and the phosphatidylinositol 3-kinase/protein kinase B(PI3K/Akt)signaling pathway in APP/PS1 mice.Methods A total of 20 APP/PS1 mice were randomly divided into Alzheimer's disease(AD)group and IAPP group,with 10 mice in each group.The mice in the latter group were given an intraperitoneal injection of 0.5 μmol/L IAPP,and those of the former group received same dose of PBS.Both interventions were given once per day,for 10 weeks.Morris water maze test was used to measure the learning and memory abilities;HE staining was employed to observe the pathological changes in the hippocampus;Transmission electron microscopy was utilized to observe the ultrastructure of hippocampal neurons;Biochemical assay were conducted to detect the contents of glutathione peroxidase(GSH-Px),malondialdehyde(MDA)and superoxide dismutase(SOD)in hippocampal tissues;ELISA was applied to measure the levels of inflammatory factors such as IL-1β,IL-6,and TNF-α as well as content of Aβ42 in hippocampal tissues;And Western blotting was conducted to detect the expression of PI3K/Akt proteins.Results Compared with the AD group,significantly shorter platform latency(P＜0.01),increased number of traversing the platform and longer time to explore the hidden platform(P＜0.01)were observed in the IAPP group,but no such difference was seen in the swimming speed of the mice.HE staining displayed that the IAPP group had more and well-arranged nerve cells in the hippocampal tissue when compared with the AD group(P＜0.05).Lower Aβ protein expression(P＜0.01),reduced oxidative stress and decreased contents of inflammatory factors(P＜0.01)in hippocampal tissue were observed in the IAPP group than the AD group.The IAPP group showed clearer structure of neuronal mitochondria,reduced vacuolization,and better arranged microtubules and microfilaments,and elevated expression of p-PI3K/PI3K and p-Akt/Akt proteins when compared with the AD group(P＜0.01).Conclusion Amylin can reduce oxidative stress and inflammatory responses,improve learning and memory abilities in AD mice,and promote the activity of PI3K/Akt signaling pathway.

We report a case of a male patient who developed persistent fever and central nervous system symptoms after eating raw snails for 10 days. The patient was diagnosed with Angiostrongyliasis depended on the clinical presentation, epidemiological history, and etiological results. The patient recovered after receiving albendazole anthelmintic and dexamethasone anti-inflammatory therapy. This article incorporates literature review to sort out the diagnosis and treatment of this patient, in order to provide feasible reference for clinicians.

We report a case of a male patient who developed persistent fever and central nervous system symptoms after eating raw snails for 10 days. The patient was diagnosed with Angiostrongyliasis depended on the clinical presentation, epidemiological history, and etiological results. The patient recovered after receiving albendazole anthelmintic and dexamethasone anti-inflammatory therapy. This article incorporates literature review to sort out the diagnosis and treatment of this patient, in order to provide feasible reference for clinicians.

Objective:To summarize the genetic and phenotypic features of MORC family CW-type zinc finger 2 (MORC2) gene-related neuropathy in Chinese patients. Methods:The clinical and whole exome sequencing data of MORC2 gene-related neuropathy families with a definitive genetic diagnosis were collected from the Third Xiangya Hospital of Central South University between 2010 and 2023. Literature involving Chinese families with MORC2 gene-related neuropathy was extensively reviewed to provide a comprehensive summary of the genetic and phenotypic spectrum of the disease. Results:A total of 10 families with MORC2 gene-related neuropathy were identified and analyzed. Six different heterozygous pathogenic variants in the MORC2 gene were observed among these families, including the novel variant c.1330G>C (p.G444R) that had not been previously reported. Six families presented as axonal Charcot-Marie-Tooth disease caused by variants in the MORC2 gene (CMT2Z) phenotype with childhood or adult onset, and carried variants c.754C>T (p.R252W), c.1199A>G (p.Q400R), c.1330G>C (p.G444R), or c.1396G>A (p. D466N); 3 families manifested as severe spinal muscular atrophy (SMA)-like phenotype with infantile onset, all carried c.260C>T (p.S87L); 1 family carried c.1181A>G (p.Y394C), presented as DIGFAN syndrome phenotype with infantile onset combined with mental and motor retardation. Systematic review showed 8 Chinese families carried pathogenic variants of the MORC2 gene, among which 5 families were associated with the CMT2Z phenotype, carrying c.754C>T (p.R252W), c.1079A>G (p.E360G), c.1220G>A (p.C407Y), or c.1397A>G (p.D466G); 1 family was associated with SMA-like phenotype, carrying c.260C>T (p.S87L); and 2 families were associated with DIGFAN syndrome, carrying c.79G>A (p.E27K) and c.292G>A (p.G98R). Conclusions:A novel pathogenic variant c.1330G>C (p.G444R) of the MORC2 gene associated with the CMT2 phenotype is reported. Eleven pathogenic variants of the MORC2 gene have been reported in the Chinese patients to date, and c.754C>T(p.R252W) may be the most common. Patients with MORC2 gene-related neuropathy carrying different variants present with significant clinical heterogeneity, manifesting as CMT2Z, early-onset severe SMA-like myasthenia, or DIGFAN syndrome.

Purpose To investigate the expression of fork-head box protein A1(FOXA1)in esophageal squamous cell car-cinoma(ESCC)and its association with clinicopathologic char-acteristics and prognosis.Methods Immunohistochemistry was used to detect FOXA1 protein expression in 532 cases of esopha-geal squamous cell carcinoma.The correlation between FOXA1 protein expression and clinicopathologic features and prognosis of patients was analyzed.Results In 532 cases of esophageal squamous cell carcinoma,183 cases overexpressed FOXA1 pro-tein(34.4％).FOXA1 overexpression was associated with ES-CC vascular infiltration(P=0.032),poorly differentiation(P=0.032),and tumor size(P＜0.001).The overall survival(OS)and disease free survival(DFS)of patients with stage Ⅰ+Ⅱ esophageal squamous cell carcinoma with high FOXA1 ex-pression tended to be poor(OS:P=0.094;DFS:P=0.107).In ESCC patients with survival longer than 24 months,the high FOXA1 expression group had significantly shorter OS and DFS(OS:P=0.048;DFS:P=0.047).Multivariate survival anal-ysis showed that the depth of tumor invasion was an independent prognostic factor affecting the prognosis of esophageal squamous cell carcinoma.Conclusion FOXA1 is overexpressed in e-sophageal squamous cell carcinoma,and its high expression is related to tumor size,vascular infiltration and poorly differentia-tion.Patients with high FOXA1 expression tended to have poor prognosis in OS and DFS.When OS and DFS≥24 months,high FOXA1 expression may be used as a reference indicator for poor prognosis in ESCC patients.