Objective To investigate the quality of life for clinical patients with malignant tumors and the influencing factors so as to provide health departments with basis for improvement. Methods(Using) methods of interviews and questionnaires,investigations were made on the quality of life for 639 patients with malignant tumors diagnosed between January 2001 and July 2002 in the various cities and regions of Sichuan and the influencing factors by means of filling out quality of life assessment scales.(Results) The quality of life for patients with malignant tumors was in general pretty low,scoring 54.40?10.95.Careers in management were positively related to psychological status(P

Pleomorphic adenoma ranks first among parotid gland tumors. Surgical procedure, which includes enucleation, ex-tra-capsular resection, partial superficial parotidectomy (PSP), superficial parotidectomy (SP), and total parotidectomy (TP), remains to be the treatment of choice for pleomorphic adenoma. In the last century, physicians lacked understanding on the pathological character-istics of pleomorphic adenoma and facial neurotomia. Thus, simple enucleation of tumors has always been the major therapy for pa-tients to reduce the rate of facial nerve injury. However, postoperative recurrence was frequently observed in patients that have under-gone simple enucleation. In this study, the surgeons attempted to control the relapse rate by enlarging the scope of excision when remov-ing a pleomorphic adenoma, and by performing an extra-capsular resection procedure that was developed in the clinic. Although the tu-mor peplos was excised, the surgeons failed to control the relapse rate. SP and TP apparently decreased the relapse rate of the pleomor-phic adenomas. However, these therapies seem to be overcorrected by the aggravation of facial nerve injuries. PSP is a relatively ad-vanced technique that is currently used in parotid surgery. PSP reduces the rate of relapse and facial nerve injury, as verified by basic pa-thology research. Nevertheless, the controversy between advanced PSP and classic SP still exists. Plastic surgery, pathology research, and gene testing were used to evaluate the advantages of advanced PSP and classic SP. However, the research failed to derive a con-firmed result that can determine which treatment method is fit and unfit to treat pleomorphic adenoma. Our study reviews the trend of parotid surgery from a historic point of view.

Head and Neck Neoplasms ; surgery ; Humans ; Imaging, Three-Dimensional ; Reconstructive Surgical Procedures

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+.

Adenocarcinoma ; Carcinoma, Papillary ; Estrogens ; metabolism ; Humans ; Receptors, Estrogen ; metabolism ; Thyroid Neoplasms ; metabolism

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+.

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

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.