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

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

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.

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

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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

Objective: To investigate the effects of oxLDL and HMG-CoA reductase inhibitor simvastatin on PKC activity, and level of cytosol ic free Ca 2+ in cultured human umbilical vein endothelial cells. Methods: Th e activity of PKC was determined by its ability to transfer phosphate from 32P-ATP to lysine-rich histone and level of cytosolic free calcium［Ca2+ ］i was measured by flow cytometric analysis loading with the Ca2+ dye F luo-3/Am. Results: oxLDL increased PKC total activity in a dose-de pendent manner and peaked after 12 min, then decreased slowly and maintained for at least 30 min, while oxLDL induced biphasic ［Ca2+］i responses includ ing the rapid initial transient phase and the sustained phase. Removal of extrac ellular Ca2+ did not inhibit the rapid transient phase, but abolished the sustained phase. When simvastatin was added, the activity of PKC wasmarkedly dec reased with no impairment to the initial peak response, but significantly reduce d the sustained phase. Conclusion: oxLDL can induced dynamic changes of signal transduction of PKC and level of cytosolic free Ca2+ in HUVEC, these 2 events are closely linked. The change of rapid initial transient phase i s the result of mobilization of Ca2+ from intracellular pool and the chang e of sustained phase is from the influx of extracellular Ca2+. The inhibit ion of PKC activity induced by simvastatin may contribute to the changes of ［Ca 2+］i.

AIM　To investigate the effect of OX-LDL and HMG- CoA reductase inhibitors simvastatin on PKC activity and cytosolic free Ca2+ in cultured human monocy tes. METHOD　The activity of PKC was determined by its ability to tr ansfer phosphate from ［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. RESULTS　OX-LDL increased PKC tot al activity in a dose-dependent manner with phase peaking at 12 min, then decre ased slowly and maintained for at least 20 min, while OX-LDL induced biphasic ［Ca2+］i responses including the rapid initial transient phase and the sustained phase. Removal of extracellular Ca2+ did not inhibit the rapid i nitial transient phase of OX-LDL-induced rise in ［Ca2+］i,but abolish ed the sustained phase of ［Ca2+］i response to OX-LDL. When simvastati n was added, the activity of PKC was markedly decreased and simvastatin did not impair the initial peak response to OX-LDL but significantly reduced the subseq uent plateau phase. CONCLUSION OX-LDL can significantly activate t he activity of PKC and elevate ［Ca2+］i in monocytes. The rapid initial transient phase was the result of mobilization of ［Ca2+］i from intrac ellular pool and sustained phase resulted from the influx of extracellular Ca 2+. The inhibition of PKC activity induced by simvastatin may be contribute to the changes of intracellular Ca2+.

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+.