Objective: Study on the mechanism of Tongfengning in reducing serum uric acid from the perspective of renal urate transporter. Method: The human renal tubular epithelial cells(HK-2)was randomly divided into normal group, model group, Tongfengning low, medium and high dose group (7.65,15.3,30.6 g·kg^-1) and benzbromarone group (50 μmo1·L^-1),different culture media were given for intervention.HK-2 and cell supernatant were collected after 24 h of intervention. The expressions of urate transporter 1 (URAT1), glucose transporter 9 (GLUT9), organic anion transporter 1(OAT1), organic anion transporter 3(OAT3), and ATP-binding cassette superfamily G member 2 (ABCG2) protein and mRNA were detected in HK-2 of all groups by Western blot and Real-time PCR. Result: Compared with normal group, the expression of URAT1, GLUT9 protein and mRNA was significantly increased(P<0.01), while the expression of ABCG2 protein and mRNA was significantly decreased in model group (P<0.01). Compared with model group, the expression of URAT1, GLUT9 protein and mRNA in each dose of Tongfengning group and benzbromarone group were decreased (P<0.01), and each doses of Tongfengning group was superior to the benzbromarone group. The expression of ABCG2 protein and mRNA was increased in each dose of Tongfengning group (P<0.01). Compared with Tongfengning medium dose group, the expression of URAT1,GLUT9 protein and mRNA increased, while the expression of ABCG2 protein and mRNA decreased in the low and Tongfengning high dose groups (P<0.01). OAT1 and OAT3 were not expressed in all groups. Conclusion: Tongfengning can regulate the reabsorption and secretion of uric acid in renal tubules, promote the excretion of uric acid in kidney and reduce the level of serum uric acid by down-regulating the expression of URAT1, GLUT9 protein and mRNA in HK-2 and up-regulating the expression of ABCG2 protein and mRNA. It is suggested that the regulation of renal uric acid transporter protein may be one of the specific mechanisms of Tongfengning to reduce serum uric acid by promoting dampness and turbid removal. OAT1, OAT3 protein and mRNA were not expressed in HK-2 cultured in vitro.

OBJECTIVE: To investigate the composition of gut microbiota and its correlation with the severity of behavior symptoms in children with autism spectrum disorder (ASD). METHODS: A total of 30 children with ASD were enrolled as the ASD group, and 20 healthy children matched for age and sex were enrolled as the healthy control group. Related clinical data were analyzed. The V3-V4 hypervariable regions of the bacterial 16S rRNA gene in fecal samples were sequenced. The severity of behavior symptoms in children with ASD was assessed using the autism behavior checklist. The Spearman's correlation analysis was used to investigate the correlation between gut microbiota and the severity of behavior symptoms in children with ASD. RESULTS: There was a significant difference in the composition of gut microbiota between the two groups. Compared with the healthy control group, the ASD group had significant reductions in Shannon index and Shannoneven index (P<0.05), as well as a significant reduction in the percentage of Firmicutes and a significant increase in the percentage of Acidobacteria in feces (P<0.05). In the ASD group, the dominant bacteria were Megamonas, Megasphaera, and Barnesiella, while in the healthy control group, the dominant bacteria were Eubacterium_rectale_group, Ezakiella, and Streptococcus. In the children with ASD, the abundance of Megamonas was positively correlated with the scores of health/physical/behavior and language communication (P<0.05). CONCLUSIONS The development of ASD and the severity of behavior symptoms are closely associated with the composition of gut microbiota.
Autism Spectrum Disorder ; Bacteria ; Child ; Feces ; Gastrointestinal Microbiome ; Humans ; RNA, Ribosomal, 16S

Objective: To study the effect of individualized treatment of prominent ears using mattress suture combined tubed cartilage method. Methods: A total of 21 patients (28 ears) with prominent ear deformity were retrospectively analyzed from January 2013 to December 2015. Horizontal mattress suture and tubed cartilage were used to correct the deformed ears. The patients were followed up for 6 months to 1 year (mean: 9 months). Results: Hematoma occurred in 3 cases after operation, but the wounds were healed after removal of hematoma. No infection, flap necrosis, cartilage absorption or deformation, or other complications occurred. 28 ears were corrected. The shape of the antihelix was smooth and the auriculocephalic angle and scapha-conchal angle were significantly reduced, compared with preoperative. No obvious scar hypertrophy was left on incision. Conclusions The method of horizontal mattress suture combined with tubed cartilage is simple to use for prominent ear, result in satisfactory and stable outcomes.

Brain magnetic resonance imaging (MRI) of the elderly often reveals white matter changes (WMCs) with substantial variability across individuals.Our study was designed to explore MRI features and site-specific factors of ischemic WMCs.Clinical data of consecutive patients diagnosed with ischemic cerebral vascular disease who had undergone brain MRI were collected and analyzed.Multi-logistic regression analysis comparing patients with mild versus severe WMCs was performed to detect independent associations.Analyses of variance (ANOVAs) were used to detect regionally specific differences in lesions.We found that lesion distribution differed significantly across five cerebral areas,with lesions being predominant in the frontal lobe and parieto-occipital area.To explore WMCs risk factors,after adjusting for gender,diabetes mellitus,and hypertension,only age (P＜0.01),creatinine (P=0.01),alkaline phosphatase (ALP) (P=0.01) and low-density lipoprotein cholesterol (LDL-C) (P=0.03) were found to be independently associated with severe WMCs.Age (P＜0.001) was strongly associated with WMCs in the frontal lobe while hypertension was independently related to lesions in the basal ganglia (P=0.048) or infratentorial area (P=0.016).In conclusion,MRI of WMCs showed that ischemic WMCs occurred mostly in the frontal lobe and parieto-occipital area.The infratentorial area was least affected by WMCs.Typically,age-related WMCs were observed in the frontal lobes,while hypertension-related WMCs tended to occur in the basal ganglia and infratentorial area.

Objective To establish a model of acute gouty arthritis( AGA) in rats and observe its maintenance time. Methods The AGA model of rats was established by injecting monosodium urate ( MSU) at the concentration of 25 mg/mL into the ankle joint cavity. The rats were observed for 8 d at different time points. Skin temperature, degree of joint swelling, gait, inflammatory cells in synovial fluid, histopathological changes of synovial tissue and other indicators were observed to determine whether the modeling and maintenance time were successful. Results At 3 h after modeling, differ-ences in the swelling of ankle joint, increase of skin temperature, abnormal gait, the number of inflammatory cells in syno-vial fluid, synovial hyperplasia, capillary congestion, and disarrangement of synovial cells in the rats were observed in the saline group and the model group (P <0. 01). At 4 hours after modeling, the above mentioned inflammatory changes in the saline group were significantly reduced, compared with that at 3 h, showing a significant difference (P<0. 01), while the inflammatory changes of the model group were increased significantly compared with that at 3 hours ( P<0. 01 ) , and showed significant difference compared with the saline group (P<0. 01). At 24 h after modeling, the indexes in the rats of saline group returned to normal, but the inflammation of the model group was increased. At 48-72 h after modeling, the local inflammation such as ankle swelling, skin temperature, and abnormal gait of the rats in the model group reached a peak. The inflammation of the ankle joint in the model group was gradually reduced from 96 to 168 h after the model was established, but there were still significant differences in the indexes compared with the blank group (P<0. 01). At 192 h after modeling, the joint swelling, skin temperature and abnormal gait of the rats in the model group returned to normal, however, there were significant differences in the number of inflammatory cells and the pathological changes of synovial membrane compared with the blank group ( P<0. 01 ) . Conclusions A rat model of AGA can be successfully prepared and identified at 4 h after modeling by injection of MSU crystal suspension into the ankle joint cavity. This rat model of AGA can be maintained at least 168 hours after modeling.

Objective To investigate whether atractylenolide (ATL-) has protective effect on lipopolysaccharide (LPS)-induced disseminated intravascular coagulation (DIC) in vivo and in vitro, and explore whether NF-κB signaling pathway is involved in ATL- treatment. Methods New Zealand white rabbits were injected with LPS through marginal ear vein over a period of 6 h at a rate of 600 μg/kg (10 mL/h). Similarly, in the treatment groups, 1.0, 2.0, or 5.0 mg/kg ATL- were given. Both survival rate and organ function were tested, including the level of alanine aminotransferase (ALT), blood urine nitrogen (BUN), and TNF-α were examined by ELISA. Also hemostatic and fibrinolytic parameters in serum were measured. RAW 264.7 macrophage cells were administered with control, LPS, LPS + ATL- and ATL- alone, and TNF-α, phosphorylation (P)-IκBα, phosphorylation (P)-NF-κB (P65) and NF-κB (P65) were determined by Western blot. Results The administration of LPS resulted in 73.3% mortality rate, and the increase of serum TNF-α, BUN and ALT levels. When ATL- treatment significantly increased the survival rate of LPS-induced DIC model, also improved the function of blood coagulation. And protein analysis indicated that ATL-I remarkably protected liver and renal as decreasing TNF-α expression. In vitro, ATL-I obviously decreased LPS-induced TNF-α production and the expression of P-NF-κB (P65), with the decrease of P-IκBα. Conclusions ATL- has protective effect on LPS-induced DIC, which can elevate the survival rate, reduce organ damage, improve the function of blood coagulation and suppress TNF-α expression by inhibiting the activation of NF-κB signaling pathway.