Based on the theory of "three regions and sanjiao" in traditional Chinese medicine (TCM), the acupuncture-moxibustion differentiation and treatment system is explored and constructed for spasm syndrome, so as to provide a clearer guiding framework for TCM treatment of spasm syndrome. This disorder is caused essentially by the invasion of pathogenic wind, and located in brain marrow. The key regions of illness cover five zang organs and five tissues, and the core pathogenesis is associated with wind disturbance in brain marrow. In differentiation, spasm syndrome refers to overall transmission (from the upper to the lower) and local transmission (from exterior to interior). This disorder can be classified into sanjiao spasm (heart-lung spasm of the upper jiao, liver-spleen spasm of the middle jiao, and liver-kidney spasm of the lower jiao) and three-region spasm (skin-vessel spasm of the upper region, tendon-muscle spasm of the middle region, and tendon-bone spasm of the lower region). Based on "three regions and sanjiao" theory of acupuncture and moxibustion, 7 "expelling-wind" points can be selected in terms of the etiology of this disease. Baihui (GV20)-toward-Taiyang (EX-HN5) needling is applied to regulate the brain marrow, focusing on the core location of illness; and regarding the key location of illness, the combination of back-shu and front-mu points and that of jing-well and xing-spring points are adopted to regulate five zang organs. The five needling techniques (half needling, leopard-spot needling, joint needling, Hegu needling and shu needling) are used to regulate five tissues.
Humans ; Acupuncture Therapy ; Spasm/diagnosis* ; Moxibustion ; Acupuncture Points ; Medicine, Chinese Traditional ; Diagnosis, Differential

Objective:To analyze the diagnosis and treatment of children with rare diseases in the pediatric intensive care unit (PICU), the distribution of disease types and populations, clinical characteristics, and the use of orphan drugs.Methods:A retrospective case summary was conducted. Data were collected from 105 children aged 29 days to <18 years with a confirmed diagnosis of rare diseases according to the "First Batch of Rare Disease Catalogue in China" who were admitted to the PICU of Beijing Children′s Hospital, Capital Medical University from January 2020 to December 2022. Data including general information, auxiliary examinations, and treatment details for each patient were collected from the hospital′s electronic medical record system. Patients were divided into age groups: infancy (29 days to<1 year), early childhood (1 to <3 years), preschool age (3 to<7 years), school age (7 to<13 years), and adolescence (13 to<18 years) . The chi-square test was used to compare gender distribution differences among various rare diseases. Results:A total of 105 patients with 130 cases meeting the diagnostic criteria were included, accounting for 4.7% (130/2 754) of the total admissions to the PICU. The age at PICU admission was 5.3 (0.8, 9.5) years and there were 81 cases in male. The 3 most common types of diseases were endocrine, nutritional, and metabolic diseases (37 cases); followed by neurological disorders(32 cases); and congenital malformations, deformities, and chromosomal abnormalities(17 cases). The 5 most common rare diseases were methylmalonic acidemia (14 cases), mitochondrial encephalomyopathy (14 cases), atypical hemolytic uremic syndrome (12 cases), autoimmune encephalitis (12 cases), and idiopathic cardiomyopathy (9 cases). The distributions of common rare diseases varied among different age groups. In infants, atypical hemolytic uremic syndrome was most common (6 children). There was no statistically significant difference regarding gender among children with mitochondrial encephalomyopathy (13.6% (11/81) vs. 6.1% (3/49), χ2=1.77, P=0.184). Respiratory failure (36 cases) was the primary reason for rare diseases children to be admitted to the PICU. A total of 95 cases underwent mechanical ventilation, 39 cases received multidisciplinary collaborative diagnosis and treatment, and only 6 children received orphan drug therapy during their stay in the PICU. Conclusions:Rare diseases are not uncommon in PICU. Endocrine, nutritional and metabolic disorders, neurological disorders, congenital malformations, deformities, and chromosomal abnormalities were common. Methylmalonic acidemia, mitochondrial encephalomyopathy, atypical hemolytic uremic syndrome and autoimmune encephalitis have higher cases. Many children with rare diseases in the PICU have complex conditions those are challenging to treat, requiring multidisciplinary collaboration. The utilization rate of orphan drugs among children with rare diseases in PICU needs to be improved.

Objective:To summarize and analyze the clinical characteristics, treatment and prognosis of glycogen storage disease type Ⅱ(GSD Ⅱ) patients admitted to pediatric intensive care units(PICU), and to improve the pediatricians' understanding of children with severe GSD Ⅱ.Methods:Children with GSD Ⅱ admitted to PICU at Beijing Children's Hospital of Capital Medical University between January 2010 and December 2021 were included. Patient's data were collected through the electronic medical record system.After the patient was discharged,telephone follow-ups were conducted regularly for over a year.Results:A total of eight patients with a median age of 30.5 months were included. There were four patients with infantile GSD Ⅱ, whose median age of onset was 5.5 months. There were four patients with late-onset GSD Ⅱ, whose median age of onset was 36.0 months. Eight patients required continuous noninvasive/invasive respiratory support. Three patients with infantile GSD Ⅱ required respiratory support within one month of onset, and three patients with late onset GSD Ⅱ required respiratory support within one year of onset. A total of six patients had cardiac arrest during the course of the disease. One patient was regularly treated with enzyme replacement therapy during hospitalization but his condition did not improve significantly. Three patients were discharged following medical advice,including one patient continuing noninvasive respiratory support after discharge, and two patients requiring onging invasive respiratory support.A total of four children died,including one being an in-hospital death,and three occuring within one year after hospital discharge. A total of 14 genotypes were detected in eight patients, of which three were newly discovered gene mutations.Conclusion:The children with GSD Ⅱ admitted to PICU have severe respiratory dysfunction and need continuous respiratory support during the early stage of the disease. The incidence of cardiopulmonary arrest caused by infection and respiratory muscle weakness is high. It is recommended to closely monitor the lung function and cardiac function of such children, and actively give the prevention and treatment of infectious diseases. Whether enzyme replacement therapy can benefit patients with severe GSD Ⅱ and whether the newly identified mutations correlate with disease severity needs to be further evaluated.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective To investigate the effect of combination of rope-assisted proprioceptive neuromuscular facilitation(PNF)training and rope-assisted brain-computer interface(BCI)training on upper limb function in stroke patients with hemiplegia. Methods From March,2022 to February,2023,96 inpatients with stroke hemiplegia from the Second Affiliated Hospital of Guangxi Medical University were randomly divided into conventional group(n=32),PNF group(n=32)and combined group(n=32).All the groups received routine rehabilitation treatment.The conventional group re-ceived upper limb PNF training,the PNF group received upper limb rope-assisted PNF training,and the com-bined group received both upper limb rope-assisted PNF training and upper limb rope-assisted BCI training,for four weeks.They were assessed with Functiongal Test for the Hemiplegic Upper Extremity-Hong Kong version(FTHUE-HK),Fugl-Meyer Assessment-Upper Extremities(FMA-UE)and modified Barthel Index(MBI)before and after treatment. Results The intra-group effect(F>341.219,P<0.001),inter-group effect(F>21.705,P<0.001)and interaction effect(F>3.171,P<0.05)were significant in the scores of FTHUE-HK and MBI.The intra-group effect(F=520.472,P<0.001)and inter-group effect(F=41.939,P<0.001)were significant in the scores of FMA-UE,and the interaction effect was not(P>0.05).After treatment,the FTHUE-HK,FMA-UE and MBI scores were the best in the combined group(P<0.05). Conclusion The combination of rope-assisted PNF training with rope-assisted BCI device training could further improve the motor function of the upper limbs in stroke patients with hemiplegia,and enhance their activities of daily liv-ing.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.

Objective:To explore the mechanism of Anemarrhenae Rhizoma in treatment of Alzheimer's Disease(AD).Methods:The active ingredients and targets of Anemarrhenae Rhizoma for treatment of AD were screened with network pharmacology methods,the protein-protein interaction(PPI)network was constructed and the core targets were analyzed.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways enriching analysis was performed.The peripheral blood lymphocytes were extracted and lymphoblastoid cell lines(LCL)were constructed and an in vitro cell model of LCL-SKNMC was established.MTT and CCK-8 methods were used to quantify SKNMC/LCL cells,2′,7′-dichlorodihydrofluorescein diacetate(DCFH-DA)probe was used to detect reactive oxygen species(ROS),and immunofluorescence staining was used to detect the generation of Aβ1-42 in a co-cultured model.Western blotting was used to detect protein expression in the co-culture model.The lifespan of N2 nematodes was observed under oxidative stress,normal state,and heat stress;ROS generated by N2 nematodes was detected by DCFH-DA probes.The paralysis time of CL4176 N2 nematodes was evaluated by paralysis assay,and Aβ deposition in the pharynx was detected by Thioflavin S staining.Results:Through network pharmacology,15 potential active ingredients and 103 drug-disease targets were identified.PPI analysis showed that the Anemarrhenae Rhizoma might play anti-AD roles through albumin,Akt1,tumor necrosis factor,epidermal growth factor receptor(EGFR),vascular endothelial growth factor A(VEGFA),mammalian target of rapamycin(mTOR),amyloid precursor protein(APP)and other related targets.KEGG analysis showed that the pharmacological effects of Anemarrhenae Rhizoma might involve the biological processes of Alzheimer's disease,endocrine resistance,insulin resistance;and neuroactive ligand-receptor interaction,phosphatidylinositol 3-kinase(PI3K)-Akt signaling pathway,calcium signaling pathway,AGE-RAGE signaling pathway in diabetes complications,neurotrophic factor signaling pathway and others.The in vitro cell experiments showed that Anemarrhenae Rhizoma was able to reduce the production of ROS and Aβ1-42(both P<0.01),inhibit the expression of β-secretase 1(BACE1),APP and Aβ1-42 proteins(all P<0.05),up-regulate the expression of p-PI3K/PI3K,p-AKT/AKT,p-GSK3β/GSK3β in SKNMC cells(all P<0.05).The in vivo studies further confirmed that Anemarrhenae Rhizoma prolonged the lifespan of C.elegans under stress and normal conditions,reduced the accumulation of ROS and the toxicity of Aβ deposition.Conclusion:Anemarrhenae Rhizoma may reduce the production of Aβ in AD and inhibit its induced oxidative stress,which may be achieved by regulating the PI3K/Akt/GSK-3β pathway.