Echocardiography, Three-Dimensional ; Heart Defects, Congenital ; diagnostic imaging ; therapy ; Humans

Child ; Child, Preschool ; Humans ; Vestibulocochlear Nerve Diseases ; diagnosis ; prevention & control

AIM: To explore the effect and the corresponding mechanism of medium chain triglyceride (MCT) on CYP7A1 gene expression in mice. METHODS: C57BL/6J mice (15/group) were respectively received mash as AIN-93G formula (basic control BC), or 1% cholesterol supplemented AIN-93G formula (Chol), or 1% cholesterol and 14% long chain triglyceride (LCT) rich in myristic acid supplemented AIN-93G formula (Chol+LCT), or 1%cholesterol and 14% MCT (caprylic acid/capric acid: 3/1) supplemented AIN-93G formula (Chol+MCT) for 6 weeks. The change of serum total cholesterol (TC), the content of cholesterol in liver, the bile acid pool of mice and the expression of cholesterol 7-hydroxylase (CYP7A 1) gene were investigated. RESULTS: Compared to mice fed Chol diet, the mice fed Chol+MCT diet had the lower serum TC (P

Objective To explore the key points of perioperative nursing patients with planted soft tissue expander after breast cancer surgery.Method The clinical data of 55 patients with planted soft tissue expander after breast cancer surgery were reviewed to summarize the nursing measures.Result Operative process in 55 pattents were succesful,surgery time ranged from 3 to 5 hours.16 of 55 patients developed with complications and all of them were recovered and discharged.Conclusions Perioperative nursing intervention for the patients with planted soft tissue expander after breast cancer surgery can reduce the incidence of complications,improve the life quality and help them build up their confidence in social and family life.

https://www.cjrtponline.com/CN/abstract/abstract1669.shtml

This paper describes a calibration phantom system for QCT bone mineral density determination, which consists of 4-standard-solid-sample calibration phantom, a quality assurance (QA) phantom and the bone mineral density analysis software. The system adds to the new applications of CT systems, and provides a new method with a good accuracy and reliability for the examination, diagnosis, prevention, treatment of osteoporosis diseases and the observation of curative effect of drugs.
Absorptiometry, Photon ; instrumentation ; methods ; Algorithms ; Animals ; Bone Density ; Calibration ; Equipment Design ; Humans ; Image Processing, Computer-Assisted ; methods ; Imaging, Three-Dimensional ; methods ; Osteoporosis ; diagnostic imaging ; Phantoms, Imaging ; Software ; Tomography, X-Ray Computed ; instrumentation ; methods

AIM: To investigate effects of OX-LDL and VitE on the levels of IL-6,IL-8 and TNF-? in human umbilical vein endothelial cells(HUVEC). METHODS: Human umbilical vein endothelial cells were obtained by in vitro culture. HUVEC treated with or without Vit E was incubated with OX-LDL, and the levels of IL-6, IL-8 and TNF-? were determined by enzyme-linked immunosorbent assy technique. RESULTS:50 ?g/L,100 ?g/L, 200 ?g/L OX-LDL induced the release of IL-6,IL-8 and TNF-? by HUVEC in a dose-dependent manner. Compared with the control group , the levels of IL-6 and IL-8 were significantly increased at 6-12 h of stimulation with OX-LDL . Maximal levels of IL-6 and IL-8 occurred after 24-36 h, reaching a plateau maintained for at least 48 h. TNF-? rose after 2-6 h in HUVEC, and reached a maximum after 12 h. In contrast to IL-6 and IL-8, TNF-? declined after 48 h. However, when VitE (50 mg/L,100 mg/L,200 mg/L)was added, it can significant inhibited the release of IL-6, IL-8 and TNF-? in a dose-dependent manner, and after 48 h these cytokines have no diference between OX-LDL+VitE groups and OX-LDL groups. CONCLUSION: OX-LDL can obviously stimulate the production of IL-6,IL-8 and TNF-? in vascular endothelial cells, which can significantly be inhibited by VitE in a short time.

AMI: To clarify whether OX-LDL and simvastatin can induce the changes of PKC activity and cytosolic free Ca 2+ in rat aortic smooth muscle cells (ASMC). METHODS: PKC activity and cytosolic free Ca 2+ were measured by its ability to transfer phosphate from ATP to lysine-rich histone and flow cytometric analysis after loading with the Ca 2+ dye fluo 3/Am, respectively. RESULTS: OX-LDL increased PKC total activity in a dose-dependent manner and induced translocation of PKC from the cytosolic to membrane, while OX-LDL induced biphasic [Ca 2+ ]i responses including the rapid initial transient phase and the sustained phase. When simvastatin was added, the translocation of PKC was markedly decreased and simvastatin did not impair the initial peak response to OX-LDL but significantly reduced the subsequent plateau phase. CONCLUSSION: OX-LDL can induce dynamic changes of signal transduction of PKC and cytosolic free Ca 2+ in ASMC and these two events are closely linked.

AIM To investigate the effect of OX- LDL and HMG-CoA reductase inhibitors simvastatin on PKC activity and cytosolic free Ca2+ in cultured human monocytes. METHOD The activity of PKC was determined by its ability to transfer phosphate fm [32P] ATP to lysine-rich histone and cytosolic free calcium[Ca2+]i was measured by flow cytometric analysis loading with the Ca2+ dye fluo3/Am.RE- SULTS OX-LDL increased PKC total activity in a dose-dependent manner with phase peaking at 12 min, then decreased slowly and maintained for at least 20 min, while OX-LDL induced biphasic [Ca2+ ], responses including the rapid initial transient phase and the sustained phase. Removal of extracellular Ca2+ did not inhibit the rapid initial transient phase of OX-LDL-induced rise. in [ Ca2+ ]i, but abol- abolished the sustained phase of [ Ca2+ ] i response to OX LDL. When simvastatin was added, the activity of PKC was markedly decreased and simvastatin did not impair the initial peak response to OX-LDL but sig- nificantly reduced the subsequent plateau phase. CONCLUSION OX-LDL can significantly activate the activity of PKC and elevate [Ca2+ ]i in monocytes. The rapid initial transient phase was the result of mobilization of [Ca2+ ], fm intracellular pool and sustained phase resulted from the influx of extracellular Ca2+. The inhibition of PKC activity induced by simvastatin may be contribute to the changes of intracellular Ca2+.