Objective To study the clinical effects of breast-preserving surgery in early-stage breast cancer. Methods From March 2002 to March 2007, 27 cases of early-stage breast cancer were treated with breast-preser-ving surgery. The control group had 28 cases, treated with radical mastectomy. Survival rate and recurrence rate were observed. Results The short-term progress of breast-preserving surgery in early-stage breast cancer had no significant difference with that of radical mastectomy. Plastic effects of breast were satisfied. Conclusion Breast- preserving surgery in early-stage breast cancer had favorable effects both in progress and in plastic. Therefore, it is warranted for wide use.

Objective To investigate the relationship between nonalcoholic fatty liver disease (NAFLD) and benign prostatic hyperplasia (BPH) in elderly patients.Methods 50 elderly BPH men with NAFLD were enrolled in this study,while 30 age-matched BPH men without NAFLD were selected as the control group.Prostate volume (PV),body mass index (BMI),triglycerides (TG),fasting blood glucose (FBG),fasting plasma insulin (FINS) and homeostasis model of assessment for insulin resistanceindex (HOMA-IR) were compared between the two groups,and correlations of PV with FINS and HOMA-IR were analyzed in the NAFLD patients.Results The PV level was significantly higher in NAFLD patients than in control group [(48.2±16.3) ml vs.(33.2± 11.5) ml,P＜0.01].The incidence of severe BPH was higher in NAFLD group than in control group (42.2％ vs.13.3％,P＜0.05).BMI,TG,FBG,FINS and HOMA IR were higher in NAFLD group than in the control group (all P＜0.01).The PV was positively correlated with FINS and HOMA-IR levels in elderly NAFLD patients (r=0.814,0.601,respectively,both P＜ 0.01).Conclusions NAFLD is closely associated with BPH in elderly males,and NAFLD may be one of the risk factors for BPH.

This article systematic reviewed the recent ten years clinical research of acupuncture treatment and rehabilitation on hemiplegia after stroke.The curative effect of acupuncture treatment and rehabilitation on hemiplegia after stroke is certain,and also supported by subsequent clinical researches.At the same time,we found that there are some deficiencies.The author elaborated personal views of clinical research in the future.The main purpose is to review the clinical research progress and forecast of acupuncture treatment and rehabilitation on hemiplegia after stroke briefly.

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+.

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.

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+.

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. [

OBJECTIVETo explore the effects of high altitude on cognitive flexibility.

METHODSSimulated hypoxia at an altitude of 3 600 m was performed in a hypobaric chamber. Twenty-three volunteers without hypoxic experience were selected and the mean age was about 25.1 years. The physiological parameters (heart rate, blood pressure and oxygen saturation) were measured. Task switch paradigm was used to explore the cognitive flexibility in each phase, and the changing anxiety state was evaluated simultaneously.

RESULTSReaction time (RT) switch cost in hypoxia phase showed a significant increase compared with the baseline; anxiety level in hypoxia phase was higher than the adaptation phase; a remarkable negative correlation between anxiety level and RT switch cost was found in adaptation phase, whereas a positive correlation was found in landing phase.

CONCLUSIONHigh altitude (3 600 m) affects cognitive flexibility and anxiety state. Anxiety before the hypoxia exposure improves the cognitive flexibility performance, while anxiety after the hypoxia exposure hampers the performance because of the post-hypoxia effect.

Adult ; Altitude ; Anxiety ; Cognition ; physiology ; Humans ; Hypoxia ; psychology ; Male ; Reaction Time