Objective: To study the clinical effect of nursing after laparoscopic myomectomy after nursing intervention. Methods: Retrospective analysis of our hospital from 2009 May to 2012 October in our department, laparoscopic myomectomy in the treatment of 148 cases of uterine fibroids patients clinical data, were randomly divided into 2 groups, 74 cases in each group, the control group routine nursing care to patients, nursing intervention on the patients with study group, The quality of life of patients with depression and anxiety scores were compared between the two groups before and after the rate and nursing of exhaust and ambulation time, hospitalization time, complications. Results: Research group of exhaust, ambulation, time of hospitalization, the incidence of complications compared with the control group, showed significant difference; the study group before operation and nursing of patients with anxiety and depression and quality of life scores compared with the control group, there was no significant difference, nursing intervention, there were significant differences. Conclusion: Laparoscopic myomectomy nursing intervention, can promote the rehabilitation, and improve the living condition, patients with significant effect, should be popularized.

Objective To explore the pathological characteristics and prognosis of triple-negative breast cancer(TNBC).Methods The pathological data of 465 cases of operable primary breast cancer were analyzed.TNBC was immunohistochemically defined by a lack of expression of ER,PR and Her-2.The differences of pathological characteristics and prognosis between TNBC and non-TNBC were explored.Results TNBC count for about 15%(73/465)of all breast carcinomas.TNBC correlated with younger(＜50y)and premenopausal women (P＜0.05).The follow-up time of the 369 cases was truncated at January 2009,and 39 cases had recurrence or metastasis,the relapse rate of TNBC(18.3%,11/60)was higher than that of non-TNBC(9.1%,28/309,P=0.033).Conclusions The patients with TNBC were younger,and had an increased likelihood of relapse.

Objective To summarize the progress of clinical research on triple-negative breast cancer(TNBC).Methods Domestic and international publications on the study of TNBC in recent years were collected and reviewed.Results The patients with TNBC were younger,and their prognosis was poorer.Besides operation,chemotherapy was the major therapeutic tool for them.Currently the targeted therapy for epidermal growth factor receptor and its signal conducting system was applied to clinical therapy gradually,and it might benefit the patients with TNBC.Conclusion The study on TNBC may bring a new way for therapy.

Objective To evaluate the role of phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) in 17β estradiol-induced inhibition of propofol-caused neuroapoptosis in the hippocampus of newborn rats.Methods Seventy-eight male Sprague-Dawley rats,aged 7 days,weighing ll-18 g,were divided into 6 groups (n =13 each) using a random number table:dimethyl sulfoxide (DMSO) group,fat emulsion group (group F),17β estradiol group (group E),propofol group (group P),propofol plus 17β estradiol group (group PE) and propofol plusl7β estradiol plus mitogen-activated protein kinase kinase 1/2 inhibitor U0126 group (group PEU).17β estradiol 600 μg/kg was injected subcutaneously every 24 h for 7 consecutive days in group E,and the equal volume of DMSO was given instead in group DMSO.Propofol 75 mg/kg was injected intraperitoneally every 24 h for 7 consecutive days in group P,and the equal volume of fat emulsion was injected instead in group F.Propofol 75 mg/kg was injected intraperitoneally,and 17β estradiol 600 μg/kg was injected subcutaneously every 24 h for 7 consecutive days in group PE.Propofol 75 mg/kg was injected intraperitoneally,17β estradiol 600 μg/kg was injected subcutaneously,and U0126 10 mg/kg was injected intraperitoneally every 24 h for 7 consecutive days in group PEU.At 15 min after the last injection,3 rats in each group were randomly selected,and arterial blood samples from the cardiac apex were collected for determination of arterial oxygen partial pressure.The animals were sacrificed at 24 h after the last injection for determination of the expression of activated caspase-3 (by immunohistochemistry) and p-ERK1/2 (by Western blot).Results There was no significant difference in arterial oxygen partial pressure between the six groups (P＞0.05).Compared with group F,the expression of activated caspase-3 was significantly up-regulated,and the expression of p-ERK1/2 was downregulated in group P (P＜0.05).Compared with group P,the expression of activated caspase-3 was significantly down-regulated,and the expression of p-ERK1/2 was up-regulated in group PE (P＜0.05).Compared with group PE,the expression of activated caspase-3 was significantly up-regulated,and the expression of p-ERK1/2 was down-regulated in group PEU (P＜0.05).Conclusion The mechanism by which 17β estradiol inhibits propofol-caused neuroapoptosis in the hippocampus is related to up-regulation of the expression of p-ERK1/2 in newborn rats.

Objective To investigate the protective effect and the mechanisms of 17β-estradiol on ketamine-induced apoptosis on primary cultured rat cortical neurons. Methods Cortical neurons were primarily cultured for seven days,then divided into four groups :control group ( treated with equal valume of DMSO ),estradiol-treated group ( treated with 0.1 μmol·L-1 17β-estradiol),ketamine-treated group(treated with 100 μmol·L-1 ketamine),ketamine plus 17β-estradiol-treated group( treated with 0. 1 μmol·L-1 17β-estradiol+100μmol·L-1 ketamine). The neurons were treated for 24 hours. The neuron viability was determined by MTT. Neuroapoptosis was measured by nuclear morphometry after Hoechest 33258 dying. Western blotting was performed to detect the expression levels of cleaved-caspase-3 and Bcl-2protein. Results The neuron viability in the ketamine group was(54. 02±7. 78)%,significantly decreased from the control group,whereas ketamine plus 17β-estradiol increased the cell viability to(88. 09±6. 54)%,significantly higher than the ketamine group. The neuroapoptosis rate in the ketamine group was(49. 50±4. 34)%,significantly increased from the control group,while that in the drug combination group was(15. 74 ± 3. 40)%,significantly lower compared with the ketamine group. Meanwhile,the cleaved-caspase-3 expression increased,and Bcl-2 expression decreased remarkably after ketamine treatment,while which was reversed in the drug combination group. Conclusion 17β-estradiol can protect against ketamine-induced injury by inhibiting neuron apoptosis.

Objective To investigate the effect of propofol exposure on neuroapoptosis in pri-mary cultured cortical neurons and its mechanisms.Methods Cortical neurons were primarily cultured for seven days,then divided into two groups:control group (treated with equal volume of 20% in-tralipid),propofol-treated group (treated with 500 μmol/L propofol).The neurons were treated for 12 h.The neuron viability was determined by MTT.Neuroapoptosis was identified by Hoechest 33 258 dying.Mitochondrial membrane potential was measured by the fluorescent dye rhodamine 123 (Rh123).Western blot was performed to detect the level of cyt-c and cleaved-caspase-3.Results Neu-rons survival rate (54.4%±6.4%)in the propofol group was significantly lower than that of control group (99.8% ± 4.1%) (P < 0.05 ), the rate of neuronal apoptosis (46.5% ± 5.3%) was significantly higher than that of control group (7.2%±0.9%)(P <0.05),mitochondrial membrane potential (59.6%±4.3%)was significantly lower than that of the control group (99.9% ± 5.7%) (P <0.05 ),cyt-C protein level (0.38 ± 0.03 )was significantly higher than that of control group (0.1 5±0.02)(P < 0.05 ),level of cleaved-caspase-3 protein level (0.46 ± 0.04)was significantly higher than that of control group (0.13±0.02)(P <0.05).Conclusion Propofol induces neuroapo-tosis in primary cultured cortical neurons,which is associated with the decreased level of MPP and the increase levels of cyt-c and cleaved-caspase-3.

C1q /TNF-related proteins (CTRPs)belong to the same category of C1q /TNF-related protein family,mainly secreted by adipose tissue and widely expressed in human and rodent.Their function turned out to be metabolic modulation,cardiovascular system protection and suppression of inflammation.But for metabolic modulation,enhancing the synthesis of glycogen,promoting fatty acid uptake and oxidation,in-creasing insulin sensitivity is the major role of CTRPs playing in governing the metabolism.Each CTRP has its own unique tissue expression profile and nonredundant function in regulating sugar and /or fat metabo-lism.In this review we focus on the recent progress about the metabolic function of CTRPs.

Objective To investigate the mechanisms of the protective effects of dexmedetomidine against the propofol-induced neuroapoptosis in primary cultured cortical neurons.Methods The neurons were cultured 7days and then divided into four groups: vehicle-control group (treated with equal volume of intralipid), propofoltreated group (treated with 500 μmol/L propofol), propofol plus dexmedetomidine treated group (treated with 500 μmol/L propofol and 0.1 μmol/L dexmedetomidine), and LY294002 pretreated group (treated with 500 μmol/L propofol ,0.1 μ mol/L dexmedetomidine and 10 μmol/L LY294002).12 hours after different treatments, neuron viability was measured by MTT assay,neuroapoptosis was detected by Hoechst33258 staining, and the levels of pAkt and Bcl-2 protein were detected by Western blot.Results Compared with the vehicle-reduced group,propofol reduced neuron viability greatly((53.4±4.2)％ vs (99.9±6.3)％;P＜0.01), but increased neuroapoptosis greatly((44.6±4.3)％ vs (5.8±0.4)％;P＜0.01).The levels of pAkt((0.41±0.03) vs (0.86±0.07))and Bcl-2 ((0.15±0.02) vs (0.72±0.03)) were decreased greatly (both P＜0.01).Compared with propofol treatment group, the neuron viability of propofol plus dexmedetomidine group were increased greatly((86.4±5.3) ％ , P＜0.01) ,the neu roapoptosis was decreased greatly ((23.1 ± 3.5) ％, P＜ 0.01), and the levels of pA kt (0.8 ± 0.03) and Bc1-2 (0.52 ±0.05) were increased greatly (both P＜0.01).Compared with propofol plus dexmedetomidine treated group,LY294002 inhibited the protective effects of dexmedetomidine, decreased neuron viability greatly ((64.3±5.1) ％ ,P＜0.01), increased the number of apoptotic neurons((38.8±4.9) ％, P＜0.01), and reduced the levels of pAkt (0.52±0.04) and Bcl-2(0.31±0.02) significantly (P＜0.01).Conclusion Dexmedetomidine exerts the neuroprotective effects against propofol-induced neuroapoptosis by activating the PI3K-Akt-Bcl-2 signalling pathway.

Objective Dexmedetomidine is known to have a neuroprotective effect.The aim of this study was to investigate the effects of dexmedetomidine on ketamine-induced apoptosis of primarily cultured cortical neurons and its action mechanisms. Methods Rat cortical neurons were primarily cultured for 7 days and treated with ketamine (100μmol/L) and different concentrations of dexmedetomi-dine (0.001, 0.01, 0.1, and 1 μmol/L) for 24 hours, followed by measurement of the viability of the neurons by MTT assay.The neurons were divided into four groups:vehicle control, ketamine ( trea-ted with 100 μmol/L ketamine), dexmedetomidine+ketamine (DD+K, treated with 0.1 μmol/L DD and 100 μmol/L ketamine), and LY294002 ( treated with 0.1 μmol/L DD, 100 μmol/L ketamine, and 10 μmol/L LY294002) .After 24 hours of treatment, the apoptosis rate of the neurons was determined by Hoechst33258 staining, and the expressions of pAkt and cleaved-caspase-3 in the neu-rons detected by Western blot. Results The apoptosis rate of neurons was dramatically increased in the LY294002 and ketamine groups in comparison with the vehicle control and DD+K groups ([36.8 ±4.4] and [43.4 ±4.5]%vs [7.5 ±1.1] and [16.4 ± 3.6]%, P<0.01), the pAkt level remarkably decreased (0.26 ±0.02 and 0.15 ±0.01 vs 0.61 ±0.05 and 0.50 ±0.04, P<0.01), and the expression of cleaved caspase-3 significantly upregulated in the former two as compared with the latter two groups (0.40 ±0.02 and 0.65 ±0.03 vs 0.10 ±0.02 and 0.12 ±0.01, P<0.01). Conclusion Dexmedetomidine exerts a neuroprotec-tive effect against ketamine-induced apoptosis of neurons by activating the PI3K-Akt signaling pathway.

BACKGROUND: It has been reported that Angiotensin Ⅱ (Ang Ⅱ) is related to occurrence and development of dermatofibrosis; however, less is explored about the expression and effect of AT1 and AT2 receptors in the fibroblasts of human hypertrophic scar.OBJECTIVE: To observe the expression of Ang Ⅱ type 1 (AT1) and type 2 (AT2) receptors in human hypertrophic scars, and explore their effects on collagen synthesis of fibroblasts.DESIGN, TIME AND SETTING: Randomized control experiment was performed at the Experimental Center, Guangzhou General Hospital of Guangzhou Military Area Command of Chinese PLA between August 2006 and November 2007. PARTICIPANTS: Samples of hypertrophic scare were taken from 18 patients (10 males and 8 females, 19-47 years Old). Seven specimens of normal skin served as control. All of the specimens collected were divided into two parts, one part for immunohistochemical staining after fixated by 4% paraformaldehyde, the other part for culturing fibroblasts.METHODS: The expression of both AT1 and AT2 receptors in fibroblasts of hypertrophic scare was detected with immunohistochemical staining and radioligand receptor binding assay. Collagen synthesis was examined in cultured fibroblasts of hypertrophic scars by measuring [3H]-proline incorporation into collagenous proteins.MAIN OUTCOME MEASURES: The expression of both AT1 and AT2 receptors in human hypertrophic scars; the [3H]-proline incorporation value in cultured fibroblasts.RESULTS: Positive staining signals of both AT1 and AT2 receptors were found in fibroblasts of hypertrophic scars. Similar results were also observed in cultured fibroblasts of hypertrophic scars, expression level of AT1 and AT2 receptors were (10.69±2.15) fmol/106 cells and (4.9±1.05) fmol/106cells, respectively. In cultured fibreblasts, Ang Ⅱ stimulation significantly increased collagen synthesis, which was inhibited by valsartan, an AT1 receptor blocker, but augmented by PD123319, an AT2 receptor antagonist.CONCLUSION: Both AT1 and AT2 receptors were expressee in the fibreblasts of hypertrophic scars, and Ang Ⅱ regulates collagen synthesis in hypertrophic scar fibroblasts through a negative cross-talk between AT1 and AT2 receptors, which might contribute, at least partly to formation and maturation of human hypertrophic scars.