Objective: To observe the effect oftuina plus music therapy on range of motion of ankle joints and muscle spasm of lower limbs in children with spastic cerebral palsy. Method:All of 286 cases that conformed to the diagnostic criteria of infantile cerebral palsy were treated with 7 types of tuina manipulations respectively to unblock the Governor Vessel, reinforce the kidney and strengthen the spleen, pinch along the spine, stimulate specific foot-reflex area and different spinal segments, accelerate recovery of muscle strength and increase joint range of motion, 25-30 rain each treatment, once or twice a day, 30 d constitute a course of treatment.After this, the efficacy on femoral medial adduction and dorsiflexion angle and composite spasticity score (CSS) was evaluated. Result: The statistical analysis showed significant differences in dorsiflexion and femoral medial adduction angle and CCS scores (P<0.01) after the treatments. Conclusion: Tuina plus music therapy can lubricate the joints, relax contraction of tendons, alleviate muscle spasm and improve scissors and toe-walking gaits, thereby benefiting the gross motor function of infants in sitting, kneeling, standing and walking.

Objective To explore effects of atorvastatin on the expressions of cyclooxygenase-2(COX-2) and membrane-associated prostaglandin E2 synthase-1 (mPGES-1) in the carotid atherosclerotic plaques of rabbits.Methods Totally 33 male New Zealand white rabbits(≥ 36months of age ) were assigned into normal control group (n=8) and animal model group with carotid atherosclerotic stenosis (n =25).The rabbit models were randomly divided into non-intervention group,celecoxib treatment group (15 mg · kg-1 · d-1,twice daily) and atorvastatin treatment group (5 mg · kg-1 · d-1,once daily) (n=8 each).Four weeks after treatment,the mRNA and protein expressions of COX-2 and mPGES-1 in carotid plaques were determined by RT-PCR and Western blot,respectively.Results The mRNA expressions of COX-2 (0.97±0.09,0.44±0.05,0.60±0.04vs.0.23±0.04,F=66.77,P＜0.01) and mPGES-1 (0.92±0.07,0.41±0.04,0.61±0.03 vs.0.17±0.03,F=54.87,P＜0.01)in carotid atherosclerotic plaques were significantly higher in non intervention group,celecoxib treatment group and atorvastatin treatment group than in normal control group.The mRNA expressions of COX-2 and mPGES-1 were decreased in celecoxib treatment group and atorvastatin treatment group as compared with non-intervention group ( both P ＜ 0.01 ).The protein expressions of COX-2 (0.89±0.06,0.42±0.07,0.62±0.04 vs.0.18±0.05,F=61.75,P ＜0.01) and mPGES-1(0.91±0.05,0.44±0.05,0.63±0.05 vs.0.21±0.04,F=86.44,P＜0.01)in carotid atherosclerotic plaques in non-intervention group,celecoxib treatment group and atorvastatin treatment group were increased as compared with those in normal control group.The mRNA and protein expressions of COX-2 and mPGES-1 were decreased in celecoxib treatment group and atorvastatin treatment group as compared with non-intervention group(all P＜0.01 ).The expressions of COX-2 and mPGES-1 in carotid atherosclerotic plaques were reduced in celecoxib treatment group as compared with atorvastatin treatment group (P ＜ 0.01).Conclusions As COX-2 inhibitor celecoxib,atorvastatin may inhibit the expressions of COX-2 and mPGES-1,and interfere with the inflammatory response which plays key role in the pathological progress of carotid atherosclerotic plaques,and thus slow the progress of carotid atherosclerosis.

Objectives To investigate the occipital cortex metabolite alterations in repetitive and severe neonatal hypoglycemia rats treated with sodium pyruvate and to reveal the protective role of sodium pyruvate using high resolution 1H nuclear magnetic resonance spectroscopy.Methods Thirty-six 2-dayold Sprague-Dawley rats were randomly divided into hypoglycemia group and pyruvate group with 18 rats in each group.Rats in both groups received intraperitoneal injections of insulin (40 U/kg body weight) at 2,4 and 6 days of age to induce severe hypoglycemia (blood glucose value ≤ 1.4 mmol/L).In the hypoglycemia group,2.5 hours after insulin injection,intraperitoneal injection of 50％ glucose (2 ml/kg) was administered to terminate hypoglycemia,while in the pyruvate group,50％ glucose (2 ml/kg) and sodium pyruvate solution 2.5 ml/kg (500 mg/kg) were injected.Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay was used to observe the status of injured neurons in six neonatal rats,and metabolite changes in occipital cortex of the other 12 rats were detected by 1H nuclear magnetic resonance spectroscopy.The difference between the two groups was compared by independent-samples t test.Results Neonatal rats of both groups reached severe hypoglycemia level 2.5 hours after insulin injection.Compared with hypoglycemia group,pyruvate group had fewer injured neurons (45±5 vs 113 ± 12,t=0.782,P=0.013) and lower injured index in the occipital cortex (0.15 ± 0.03 vs 0.36 ± 0.06,t=l.143,P=0.020).Pyruvate group showed significant decreases in the concentration of taurine [(13.31 ± 2.06) vs (18.44 ± 3.86) mol/kg,t=8.231],glutamine[(1.50 ± 0.24) vs (2.02 ± 0.40) mol/kg,t=3.137],glutamate[(7.04 ± 0.95) vs (9.40 ± 1.73) mol/kg,t=6.449],aspartate[(1.51 ± 0.28) vs (2.15 ± 0.58) mol/kg,t=2.561] and creatine [(6.37±0.99) vs (8.46± 1.77) mol/kg,t =4.226] in the occipital cortex (all P'＜0.017).Conclusions Simultaneous use of glucose and sodium pyruvate to terminate hypoglycemia in repetitive and severe neonatal hypoglycemia rats can effectively alleviate severe hypoglycemia-induced occipital lobe damage via regulating excitatory amino acid neurotransmitters,energy metabolism and other metabolic pathways.

Objective:To establish the bacterial endotoxin test for HSSYO-001-3S. Methods: HSSYO-001-3S was dissolved in dimethylsulfoxide,diluted by BET water and centrifuged,and then the supernatant was used for the bacterial endotoxin test. The ex-periment was carried out according to the gel-clot technique for bacterial endotoxin inspection and the related regulations in Chinese Pharmacopoeia (2015 edition,volumeⅣ,general rule 1443). Results:HSSYO-001-3S was added with cosolvent and diluted by BET water to 1 mg·ml-1,and there was no interference effects to bacterial endotoxin test from the supernatant diluted four times or more. Conclusion:Bacterial endotoxin test can be used to control the quality of HSSYO-001-3S.

Objective To explore the mechanism of action of curcumin in the treatment of silicosis by network pharmacology combined with molecular docking technology. Methods The targets prediction network of curcumin in treating silicosis was established based on the collection of targets of curcumin and silicosis in multiple databases, cross-targets were submitted to the STRING database, and their connectivity was analyzed by Cytoscape software. Gene ontology (GO) function analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed on the top 20 genes. The molecular docking was performed on the key targets to study the mechanism of action of curcumin in treating silicosis. Results A total of 311 targets related to curcumin, 270 targets related to silicosis, and 74 cross-targets were obtained from the databases. GO function analysis revealed 2 665 related pathways, and KEGG pathway enrichment analysis revealed 188 related pathways. Molecular docking results showed that curcumin had good binding ability with the targets of mitogen-activated protein kinase 3 (MAPK3), interleukin (IL) 6, serine/threonine kinase 1 (AKT1), vascular endothelial growth factor A (VEGFA), signal transducer and activator of transcription 3, albumin, Jun proto-oncogene, tumor necrosis factor (TNF), IL1B, tumor protein p53, C-C motif chemokine ligand 2 and fibronectin 1. Conclusion The therapeutical effects of curcumin on silicosis were implemented through multi-targets and multi-pathways. Curcumin may play a role in the treatment of silicosis by binding to the core targets MAPK3, IL6, AKT1, VEGFA and TNF and regulating the MAPK, IL6, TNF, phosphatidylinositol 3-kinase/protein kinase B and VEGF signaling pathways.

Objective:To investigate the relationship between the E2 and E4 alleles of apolipoprotein E (apoE) gene and myocardial infarction (MI) in type 2 diabetes Mellitus (T2DM) patients, and to explore the relationship between apoE polymorphism and blood lipid metabolism.Methods:This case control study was conducted from August 2016 to March 2020 in China-Japan Friendship Hospital, 3 459 inpatients with T2DM were included including 3 044 patients without MI (T2DM group) and 415 patients with MI (T2DM+MI group). Real time fluorescent quantitative PCR was used to detect apoE polymorphism. Automatic biochemical analyzer was used to detect lipid levels. Logistic regression analyses were performed to determine the association of apoE with risk of MI in patients with T2DM.Results:(1) The frequency of E4 allele in T2DM+MI group (12.29%, 102/830) was significantly higher than in T2DM group (9.13%,556/6 088), while the frequency of E2 allele in T2DM+MI group (7.35%,61/830) was significantly lower than that in T2DM group (8.21%,500/6 088), P=0.012. Logistic regression analyses showed that E4 allele carrier (E3/E4+E4/E4) faced a higher risk for MI in T2DM patients ( OR=1.48, 95% CI 1.14-1.92, P=0.003), while E2 allele carrier(E2/E3+E2/E2)did not face a higher risk of MI in T2DM patients ( OR=0.88, P=0.642). (2) The levels of apoE polymorphism and blood lipid: The levels of TC, LDL-C and apoB increased in the order of E4 allele, wild type and E2 allele ( P<0.05). The levels of HDL-C, apoA1 and apoE decreased in the order of E4 allele, Wild type and E2 allele ( P<0.05). Conclusion:The E4 allele is a risk factor for MI in T2DM patients, and apoE polymorphism can affect blood lipid level in this patent cohort.

A patient with SARS-CoV-2 infection was adimitted to Shanghai Shibei hospital of Jing'an District in early 2023. According to the patient's complaits， clinical manifestations， physical symptoms， laboratory examination， radiological image results， plus lumbar puncture， the patient was diagnosed with novel coronavirus encephalitis. The patient was discharged from the hospital after a combined treatment of Chinese and western medicine.

Diabetes have been shown to cause progressive neuronal injury with pain and numbness via advanced glycation end-products (AGEs)-induced neuronal cell apoptosis; however, the valuable drug targets for diabetic neuropathy have been poorly reported so far. In this study, we discovered a natural small-molecule schisandrol A (SolA) with significant protective effect against AGEs-induced neuronal cell apoptosis. ATP6V0D1, a major subunit of vacuolar-type ATPase (V-ATPase) in lysosome was identified as a crucial cellular target of SolA. Moreover, SolA allosterically mediated ATP6V0D1 conformation via targeting a unique cysteine 335 residue to activate V-ATPase-dependent lysosomal acidification. Interestingly, SolA-induced lysosome pH downregulation resulted in a mitochondrial-lysosomal crosstalk by selectively promoting mitochondrial BH3-only protein BIM degradation, thereby preserving mitochondrial homeostasis and neuronal cells survival. Collectively, our findings reveal ATP6V0D1 is a valuable pharmacological target for diabetes-associated neuronal injury via controlling lysosomal acidification, and also provide the first small-molecule template allosterically activating V-ATPase for preventing diabetic neuropathy.

Mitochondrial shape rapidly changes by dynamic balance of fusion and fission to adjust to constantly changing energy demands of cancer cells. Mitochondrial dynamics balance is exactly regulated by molecular motor consisted of myosin and actin cytoskeleton proteins. Thus, targeting myosin-actin molecular motor is considered as a promising strategy for anti-cancer. In this study, we performed a proof-of-concept study with a natural-derived small-molecule J13 to test the feasibility of anti-cancer therapeutics