Objective To analyze the curative effect of acupuncture at Gongsun, Sifeng combined with visceral acupoint tapping in children with mesenteric lymphadenitis (type of gastrointestinal heat accumulation), and its influence on serum intestinal fatty acid-binding protein (I-FABP) and vasoactive intestinal peptide (VIP). Methods A total of 60 children with mesenteric lymphadenitis (type of gastrointestinal heat accumulation) were selected, and were divided into control group (n=30, conventional treatment combined with acupuncture at Gongsun and Sifeng acupoints) and study group (n=30, visceral acupoint tapping on the basis of the control group) according to the random number table method. The clinical efficacy, changes of main symptoms and signs were compared, and the expression levels of serum I-FABP and VIP were detected. Results The total effective rate of the study group was higher than that of the control group(P < 0.05). After 2 weeks of treatment, the serum I-FABP levels of the two groups were lower than that before treatment, and the serum I-FABP level of the study group was lower than that of the control group (P < 0.05). After 2 weeks of treatment, the serum VIP levels of the two groups were higher than that before treatment, and the serum VIP level of the study group was higher than that of the control group (P < 0.05). After 2 weeks of treatment, the improvement of main symptoms and signs in the study group was better than that in the control group (P < 0.05). Conclusion Acupuncture at Gongsun and Sifeng combined with visceral acupoint tapping can be used to treat children with mesenteric lymphadytis (gastrointestinal heat accumulation type), regulate and improve gastrointestinal function, adjust the level of serum I-FABP and VI, and relieve the main symptoms and signs of children, and can be used as an effective therapeutic method.

Objective: To analyze effect of fractured file removal from the middle third root canal on root fracture resistance using finite element analysis, which provides a theoretical basis for clinical prognosis evaluation. Methods: Two finite-element models were established, the fractured file removal model (fractured file located in the middle third of root canals, followed by ultrasonic file removal and root canal preparation) and the control model (root canal preparation only), and compressive displacement dependencies on compressive force was computed and compared with experimental data for validation. The validated finite-element models were used to analyze the stress distribution differences during the initiation, propagation and completion of the crack between fractured file removal specimen and control one. Results: The critical breaking force of the fractured file removal specimen was 406 N, and the finite element simulation result was 396 N. The critical breaking force of the control specimen was 502 N, and the finite element simulation result was 483 N. The position of crack initiation in the finite element simulation was basically consistent with that in the experiment. The experimental data of compressive test and the results of finite-element computation were in agreement, thus validating the finite-element model. In the process of continuous pressure, the stress distribution of the control root is relatively uniform, and the location of crack initiation and the direction of propagation have a certain unpredictability. Compared with the control root, the stress concentration on the root with fracture file removal was obvious, especially on edges, and the number of cracks are much more. Because of the thinner radicular wall, the crack propagation rate is faster too. Therefore, the overall root fracture resistant is decreased obviously. Conclusions During the fractured file removal procedure, amount of dentine removed should be minimized, and the edges and corners which caused by fractured file removal should be shaped to smooth in order to reduce the stress concentration and prevent the root from fracture.

OBJECTIVETo investigate the role of miR-199a-3p in cardiac fibrosis and the potential target of miR-199a-3p.

METHODSCardiac fibroblasts were isolated from C57BL/6 mice and cultured. The miR-199a-3p mimic and Smad1 siRNA were transiently transfected into the cardiac fibroblasts via liposome. Dual luciferase reporter assay was performed to confirm the interaction between miR-199a-3p and the 3'-UTR of Smad1. The expressions of Smad1 and fibrosis-related genes at the mRNA and protein levels in the cells after miR-199a-3p mimic transfection were determined using RT-qPCR and Western blotting, respectively. The expressions of Smad1, Smad3 and fibrosis-related genes at the protein level in cells transfected with miR-199a-3p mimic and Smad1 siRNA were detected using Western blotting.

RESULTSOver-expression of miR-199a-3p significantly increased the expression of cardiac fibrosis-related genes in cultured mouse cardiac fibroblasts. Dual luciferase reporter assay revealed the interaction of miR-199a-3p with the 3'-UTR of Smad1. The results of RT-qPCR and Western blotting confirmed that miR-199a-3p inhibited Smad1 expression at the post- transcriptional level. Transfection with miR-199a-3p mimic and siRNA-mediated Smad1 silencing consistently activated the Smad3 signaling pathway and enhanced the expressions of cardiac fibrosis-related genes in the cardiac fibroblasts.

CONCLUSIONSAs the target gene of miR-199a-3p, Smad1 mediates the pro-fibrotic effect of miR-199a-3p by activating the Smad3 signaling in cultured mouse cardiac fibroblasts.

Objective To investigate the effect of human urinary kallidinogenase (HUK) on cerebral ischemia reperfusion injury in mice.Methods One hundred and ten male ICR mice were randomly divided into sham operation,control and HUK groups.A cerebral ischemia-reperfusion model was induced by transient middle cerebral artery occlusion.The infarct volume was detected by triphenyltetrazolium chloride staining.Bcl-2,Bax,and caspase-3 expression levels in the ischemic cortex were detected by Western blot.Bcl-2 and Bax positive cells in the hippocampal CA1 area on the ischemic side were detected using Immunohistochemical staining.Apoptotic cells in the ischemic cortex were detected by TUNEL staining.Results No infarction and neurological deficits were found in the sham operation group.At 24 h after ischemia-reperfusion,the infarction voltne (P ＜0.01) and neurological deficit score (P =0.02) in the HUK group were significantly lower than those in the control group;at 72 h after ischemia-reperfusion,the infarction volume (P ＜ 0.01) and neurologic deficit score (P =0.03) in the HUK group were also significantly lower than those in the control group.Westem blot analysis showed that the expression level of Bcl-2 in the ischemic cortex in the HUK group was significantly higher than that in the control group (P ＜ 0.001),and the expression levels of caspase-3 (P ＜ 0.001) and Bax (P ＜ 0.001) in the cerebral cortex in the HUK group were significantly lower than those in the control group.No apoptotic cells were found in the sham operation group.The number of apoptotic cells in hippocampal CA1 area (P ＜ 0.01) and the number of Bax positive cells (P ＜0.01) in the HUK group were significantly less than those in the control group,while the number of Bcl-2 positive cells was significantly more in the control group (P ＜ 0.01).Conclusions HUK has a certain protective effect on ischemia-reperfusion injury in mice,its mechanism may be associated with the upregulation of Bcl-2 protein expression and downregulation of caspase-3 and Bax protein expression,thus inhibiting cell apoptosis.

Objective To analyze the clinical features,pathogenic factors and sites of thrombus involvement in patients with cerebral venous/venous sinus thrombosis (CVST) complicated with cerebral hemorrhage.Methods Eighty-seven patients with CVST,admitted to our hospital from January 2013 to December 2016,were selected and divided into observation group (n=39) and control group (n=48) according to cerebral hemorrhage.The demographic data,clinical features,pathogenic factors,and location of the involved venous/venous sinus were compared and analyzed between the two groups.The independent influencing factors of CVST combined with intracerebral hemorrhage were assessed using multivariable Logistic regression.Results Percentages of patients with decreased visual acuity (35.9％),epileptic seizure (48.7％),motor/sensory disorders (46.2％),consciousness changes (25.6％) and aphasia (12.8％) of the observation group were significantly higher than those of the control group (12.5％,16.7％,18.8％,8.3％,and 0％,P＜0.05).In the aspect of potential pathogenic factors,the proportion of patients at pregnancy/puerperium in the observation group (20.6％) was significantly higher than that in the control group (6.3％,P＜0.05).In the aspect of involving venous/venous sinus area,the proportion of patients involved in straight sinus in the observation group (30.8％) was significantly higher than that in the control group (12.5％,P＜0.05).Multivariate Logistic analysis showed that pregnancy/puerperium and involvement of straight sinus were the independent influencing factors of CVST combined with cerebral hemorrhage (OR=6.752,P=0.017,95％CI:2.295-16.213;OR=4.573,P=0.029,95％CI:1.316-11.751).Conclusion CVST patients at pregnancy/postpartum or with straight sinus thrombosis are more prone to cerebral hemorrhage,and targeted treatment should be given as soon as possible.

AIM:MicroRNAs ( miRNAs) were recognized to play significant roles in cardiac hypertrophy .But, it remains unknown whether cyclin/Rb pathway is modulated by miRNAs during cardiac hypertrophy .This study investigates the potential roles of microRNA-1 (miR-1) and microRNA-16 (miR-16) in modulating cyclin/Rb pathway during cardiomyocyte hypertrophy .METHODS:An animal model of hypertrophy was established in a rat with abdominal aortic constriction (AAC).In addition, a cell model of hypertrophy was also achieved based on PE-promoted neonatal rat ventricular cardiomyocyte .RESULTS:miR-1 and-16 expression were markedly de-creased in hypertrophic myocardium and hypertrophic cardiomyocytes in rats .Overexpression of miR-1 and -16 suppressed rat cardiac hypertrophy and hypertrophic phenotype of cultured cardiomyocytes .Expression of cyclins D1, D2 and E1, CDK6 and phosphorylated pRb was increased in hypertrophic myocardium and hypertrophic cardiomyocytes , but could be reversed by enforced expression of miR-1 and -16.CDK6 was validated to be modulated post-transcriptionally by miR-1, and cyclins D1, D2 and E1 were further validated to be modulated post-transcriptionally by miR-16.CONCLUSION: Attenuations of miR-1 and -16 provoke cardiomyocyte hypertrophy via derepressing the cyclins D1, D2, E1 and CDK6, and activating cyclin/Rb pathway.

AIM:To investigate the effect of miR-214 on cardiomyocyte hypertrophy and the expression of the potential target genes . METHODS:A cell model of hypertrophy was established based on angiotensin-Ⅱ( Ang-Ⅱ)-induced neonatal mouse ventricular car-diomyocytes (NMVCs).Dual luciferase reporter assay was performed to verify the interaction between miR-214 and the 3’ UTR of MEF2C.The expression of MEF2C and hypertrophy-related genes at mRNA and protein levels was determined by RT-qPCR and Wes-tern blotting, respectively.RESULTS:The expression of ANP, ACTA1,β-MHC and miR-214 was markedly increased in Ang-Ⅱ-in-duced hypertrophic cardiomyocytes .Dual luciferase reporter assay revealed that miR-214 interacted with the 3’ UTR of MEF2C, and miR-214 was verified to inhibit MEF2C expression at the transcriptional level .The protein expression of MEF2C was markedly in-creased in the hypertrophic cardiomyocytes .Moreover, miR-214 mimic, in parallel to MEF2C siRNA, inhibited the expression of hy-pertrophy-related genes in Ang-Ⅱ-induced NMVCs.CONCLUSION:MEF2C is a target gene of miR-214, which mediates the effect of miR-214 on attenuating cardiomyocyte hypertrophy .

AIM:To determine circular RNA (circRNA) profiles in the diabetic mouse myocardium , and to investigate the effect of circRNA_000203 on fibrotic phenotypes in cardiac fibroblasts .METHODS:Masson trichrome stai-ning was performed on the myocardium of the diabetic db /db mice and the non diabetic db/m control mice .circRNA ex-pression profile in the diabetic myocardium was detected by circRNAs microarray .The expression of circRNA_000203 was determined by real time fluorescence quantitative PCR ( RT-qPCR ) .Recombinant circRNA_000203 adenovirus was pre-pared for enforced the expression of circRNA_000203 in mouse cardiac fibroblasts.The expression of Col1a2, Col3a1andα-SMA was determined in circRNA_000203-modified cardiac fibroblasts , respectively .RESULTS:Masson trichrome stai-ning showed that fibrosis was increased in the diabetic mouse myocardium .The results of circRNA array detection revealed that circRNAs were dysregulated in the diabetic myocardium .circRNA_000203 was up-regulated in the diabetic myocardi-um.Significant over-expression of circRNA_000203 was achieved in the cardiac fibroblasts after infection with the recombi-nant circRNA_000203 adenovirus.The mRNA and protein expression of Col1a2, Col3a1 and α-SMA was significantly in-creased in the cardiac fibroblasts with over-expression of circRNA_000203.CONCLUSION:circRNA_000203 is up-regu-lated in the diabetic mouse myocardium .It has pro-fibrotic effect on the cardiac fibroblasts .

AIM:To investigate the effect of microRNA-214 ( miR-214) on cardiomyocyte hypertrophy and the expression of the potential target genes .METHODS:A cell model of hypertrophy was established based on angiotensin-Ⅱ( Ang-Ⅱ)-induced neonatal mouse ventricular cardiomyocytes ( NMVCs) .Dual luciferase reporter assay was performed to verify the interaction between miR-214 and the 3’ UTR of MEF2C.The expression of MEF2C and hypertrophy-related genes at mRNA and protein levels was determined by RT-qPCR and Western blot , respectively .RESULTS:The expression of ANP, ACTA1,β-MHC and miR-214 was markedly increased in Ang-Ⅱ-induced hypertrophic cardiomyocytes .Dual lu-ciferase reporter assay revealed that miR-214 interacted with the 3’ UTR of MEF2C, and miR-214 was verified to inhibit MEF2C expression at the transcriptional level .The protein expression of MEF2C was markedly increased in the hypertro-phic cardiomyocytes .Moreover, miR-214 mimic, in parallel to MEF2C siRNA, inhibited the expression of hypertrophy-re-lated genes in Ang-Ⅱ-induced NMVCs.CONCLUSION:MEF2C is a target gene of miR-214, which mediates the effect of miR-214 on attenuating cardiomyocyte hypertrophy .

Objectives To analyze the clinical features and outcome of typhoid fever complicated with hemophagocytic syndrome (Ty-AHS) in children.Methods The clinical data from one case of Ty-AHS was retrospectively analyzed, and related articles were reviewed.Results A 4-year-old boy suffered from persistent diarrhea, alternating high and low temperature, apathia, hepatosplenomegaly, manifestation of acute peritonitis, and pyoperitoneum. Routine blood examination showed that eosinophil was 0, and hemoglobin and platelet were obviously decreased; CRP and procalcitonin were obviously increased;plasma ifbrinogen was dropped to 0.8 g/L; lactate dehydrogenase was elevated to 3835 U/L; Serum ferritin was 1884 ng/mL;triglyceride was 2.42 mmol/L; EBV-DNA titer was 2.81×104 copies/mL; Blood culture showed salmonella enterica serotype IIIb. Abdominal ultrasonography showed enlargement of mesenteric lymph node and middle volume of pyoperitoneum. Chest X-ray showed pneumonia. Lymphocyte analysis showed that the ratio of CD4+/CD8+ was decreased; CD3-CD16+56+ cell and CD19+ cell were all decreased. Bone marrow cytomorphologic examination revealed that bone marrow hyperplasia was active, there were no obvious abnormalities in granulocyte, macrophage and macrophage and there were a lot of tissue cells and white blood cells. After two weeks of strengthened anti-infection and dexamethasone treatment, the symptoms in patients were disappeared, and signs and laboratory tests gradually returned to normal.Conclusions Ty-AHS is a rare complication in children with acute onset and rapid progression, and combination of antibiotics and hormone therapy is effective.