Objective To investigate the pathogenistic, clinical and pathologic characteristics and treatment in elder patients with thyroid carcinoma(TC). Methods The clinical and pathologic manifestation, the treatment and prognosis of forty elder patients with thyroid carcinoma were analysed. Results The incidence of TC in elder patients was 14.2% in all of the thyroid carcinomas in the same period. The clinical course was longer and the neoplasm was bigger. A majority of the pathology was follicular adenocarcinoma(35%), followed by adenocarcinoma, undifferentiated carcinoma and pipallary adenocarcinoma. Surgerical management was the primary therapy. 17 cases underwent redical thyroidectomy with neck dissection, 13 total thyroidectomy or subtotal thyroidectomy, 4 palliative resection. Isotopic or radiotherapy as an adjuvant therapy was done if necessary. Five year survival rat was 52.0%, mortality was 45.0% in follow up period. Conclusions The main causes of the poorer prognosis of elder patients with thyroid carcinoma are follows: ① the malignant degree of the tumor is higher; ② the reaction for the tumor in elder patients is duller. So it is important to pay attention to elder patients with thyroid nodule, and an operation should be done as quick as possible.

BACKGROUND:Perioperative treatment of emergency liver transplantation for acute hepatic failure is extremely different from common liver transplantation, due to complex conditions, high risk, several complications, and high mortality. OBJECTIVE:To summarize the experience of emergency liver transplantation for acute hepatic failure during the perioperative period, and to increase the success rate in treatment of acute hepatic failure. METHODS:A retrospective analysis was undertaken on the clinical data of 38 cases undergone emergency liver transplantation for acute hepatic failure. There were 21 male and 17 female, who aged 15-69 years. Among them, 23 cases had hepatitis B virus (including 2 cases with hepatitis B and C virus), 7 cases had Wilsons disease, 3 cases had mushroom poisoning, 2 cases had unknown liver damage, 1 case had Tripterygium wilfordi poisoning, 1 case had decompensation after partial liver resection due to trauma, and 1 case had liver transplantation from corpse. RESULTS AND CONCLUSION:The survival time of the involve patients was 13-1 740 days, and the median survival time was 634 days. Perioperative survival rate was 76%, 1-year survival rate was 63%, and 2-year survival rate was 58%. During the perioperation nine cases died of brain edema and intracranial hypertension, renal failure, severe pulmonary infection, multiple organ failure, coagulation disorders (intracranial hemorrhage, upper digestive tract hemorrhage), acute respiratory distress syndrome and primary graft non-function. At present, emergency liver transplantation is stil the most effective way for acute liver failure. Hemorrhage, infection and rejection are the leading causes of the death. Each perioperative treatment is of great significance for the success of liver transplantation and long-term survival.

Neurofeedback, as an alternative treatment method of behavioral medicine, is a technique which translates the electroencephalogram (EEG) signals to styles as sounds or animation to help people understand their own physical status and learn to enhance or suppress certain EEG signals to regulate their own brain functions after several repeated trainings. This paper develops a neurofeedback system on the foundation of brain-computer interface technique. The EEG features are extracted through real-time signal process and then translated to feedback information. Two feedback screens are designed for relaxation training and attention training individually. The veracity and feasibility of the neurofeedback system are validated through system simulation and preliminary experiment.
Brain-Computer Interfaces ; Electroencephalography ; Female ; Humans ; Neurofeedback

Objective To investigate the role of T-type calcium channel in lidocaine-induced neuronal cytotoxicity . Methods SH-SYSY cell line was a gift from cell biology laboratory of our medical university. The cells were cultured in DMEM liquid culture medium at 37℃ in incubator filled with 5% CO2 , and randomly divided into 4 groups ( n = 66 each) : control group (group C)and M, L and ML groups were exposed to 5 μmol/L mibefradil (a T-type calcium channel blocker), 10 mmol/L lidocaine and 5 μmoL/L mibefradil + 10 mmol/L lidocaine for 24 h. Cell morphology was examined by electronic microscopy at 24 h of drug exposure. Cell viability (by MTT) and neuronal apoptosis (by flow cytometry) were detected immediately before and at 1, 6, 12 and 24 h of exposure to mibefradil or/and lidocaine.Results In C and M groups, the cells demonstrated dendritic protrusions, enlarged nerve processes and dense lattice. After being exposed to lidocaine for 24 h, the dendritic protrusions disappeared,the cells decreased in size, shrinked and became round; the cell viability was significantly decreased while the neuronal apoptosis increased. The lidocaine-induced changes were significantly attenuated by co-incubation with mibefradil. ConclusionT-type calcium channel is involved in lidocaine-induced neuronal cytotoxicity.

Objective To analyze the correlation of preoperative serum vascular endothelial growth factor(VEGF)level with serum CA125 level in patients with epithelial ovarian cancer(EOC),and to evaluate the prognostic value of preoperative serum VEGF in these patients.Methods Forty-one patients with EOC were included as study group,while 20 healthy women were selected as control group.Enzymelinked immunosorbent assay(ELISA)and chemiluminescence assay were used to measure serum VEGF and CA125 level respectively.The correlations of serum VEGF with CA125 level,postoperative recurrence rate and survival time were analyzed retrospectively.Resuits Serum VEGF levels in patients with EOC were higher than those in healthy women,with the median of 415 and 165 ng/L,range 110-2120 and 100-735 ng/L respectively(P＜0.01).No correlation was found between preoperative serum VEGF and CA125 level (Spearman test,P=0.989).High preoperative serum VEGF was positively correlated with postoperative recurrence.Serum VEGF level in patients with postoperative recurrence was higher than that in patients without recurrence,with the median of 490 and 315 ng/L respectively(P=0.035).Univariate analysis showed that higher serum level was reversely correlated with shorter survival.Median overall survival time in patients with higher serum VEGF level and lower serum VEGF level was 18 months and＞35 months respectively(P=0.010).Multivariate Cox model analysis showed that high VEGF level was an independentfactor for the prognosis of EOC(P=0.042).Conclusion Preoperative serum VEGF level is not correlated with CA125 concentration in patients with EOC,and it is an independent risk factor for prognosis.

Objective To investigate the relationship between the neuroprotective effect of epigallocatechin gallate ( EGCG ) for PC12 cells induced by 1-methyl-4-phenyl-pyridinium ( MPP+ ) and activating nuclear factor-related factor 2 ( NRF2 ).Methods Well differentiated PC12 cells treated with MPP+ were used as the in vitro cell models,and PC12 cells were pretreated with different concentrations of EGCG.MTT assay was used to investigate the cell viability.Western blot was used to observe the expression of NRF2 in cells and distribution in the nucleus and the cytoplasm.Real-time PCR was used to observe the antioxidant enzymes,HO-1 and NQO1 mRNA expression.Results Pretreatment of PC12 cells with different concentrations of EG CG for an hour could restore cell viability.Western blot showed that expression of NRF2 in cells treated with MPP+ for 24 hours was increased 148％ +5％ compared with the control group (t =6.102,P ＜0.01 ).The level of NRF2 in EGCG pretreated group was 188％ + 6％ compared with the control group(t =11.172,P ＜0.01 ).Moreover the NRF2 protein level in the nuclear was also increased.Western blot showed that the NRF2 protein level in the nuclear was 258％ +2％ compared with the control group (t =21.995,P ＜ 0.01 ).Further research found U 120,an inhibitor of ERK,could inhibit the effect of EGCG.The levels of NRF2 in both samples were 148％ ± 15％ and 158％ ± 1％ compared with their respective control groups(t =6.118,8.058,both P ＜0.01 ).In accordance with the NRF2 data,real-time PCR indicated that the levels of HO-1 and NQO1 mRNA expression increased obviously in the group pretreated with EGCG.Likewise,U120 could also inhibit HO-1 and NQO1 mRNA expression induced by EGCG.Conclusions EGCG can repair oxidative damage to PC12 cells induced by MPP+.The protective effect may be related through the ways to activate ERK-NRF2 and induce downstream of antioxidant enzyme expression,such as HO-1 and NQO1.

Objective To evaluate the role of calcium/calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ) in the neuronal damage induced by lidocaine.Methods SH-SY5Y cells were seeded in 96-well plates (100 μl/hole) with a density of 5 × 105/ml and randomly divided into 4 groups (n =63 each):normal culture group (C group),CaMK Ⅱ inhibitor KN93 (K group),lidocaine group (L group) and KN93 + lidocaine group (KL group).KN93 (final concentration 1 μmol/L) was added to the culture medium and the cells were then cultured for 24 h in group K.Lidocaine (final concentration 10 mmol/L) was added to the culture medium and the cells were then cultured for 24 h in group L.KN93 (final concentration 1 μmol/L) and lidocaine (final concentration 10 mmol/L) were added to the culture medium and the cells were then cultured for 24 h in group KL.The cell morphology was examined with microscope after 24 h of incubation.The viability of cells was measured by MTT assay before incubation and at 1,6,12 and 24 h of incubation.The apoptosis in the cells was assessed by flow cytometry.The apoptotic rate was calculated.Results Compared with C and K groups,the cell viability was significantly decreased and the apoptotic rate was increased in L and KL groups (P ＜ 0.05).The cell viability was significantly higher and the apoptotic rate was lower in group KL than in group L (P ＜ 0.05).There was no significant difference in the cell viability and apoptotic rate between C group and K group (P ＞ 0.05).The pathological changes were obviousin group L and significantly reduced in group KL.Conclusion CaMK Ⅱ is involved in the neuronal damage induced by lidocaine.

Objective To investigate the effects of dexmedetomidine on perioperative cellular immune function and micro-metastasis in blood circulation in patients undergoing radical operation for colon cancer.Methods Sixty ASA Ⅰ or Ⅱ patients,aged 38-69 yr,weighing 45-67 kg,undergoing radical operation for colon cancer,were randomly divided into 2 groups (n =30 each) ∶ dexmedetomidine group (D group) and control group (C group).Anesthesia was induced with midazolam,cisatracurium and sufentanil,and maintained with propofol,remifentanil and sevoflurane.After tracheal intubation,a loading dose of dexmedetomidine 1 μg/kg was injected intravenously,followed by infusion at 0.5μg· kg-1 · h-1 until the end of operation in D group.The equal volume of normal saline was administered in C group.Venous blood samples were obtained at 5 min before induction of anesthesia (T0),1 h after beginning of operation (T1),the end of operation (T2) and 24 h after the end of operation (T3) for determination of the levels of T lymphocyte subsets (CD3+,CD4+,CD8+) and NK cells by flow cytometry.CD4+/CD8+ ratio was calculated.Cytokeratin 20 (CK20) expression in circulation was detected by RT-PCR at T0 and T3 and the positive rate was calculated.Results Compared with the baseline value at T0,the levels of CD3+ and CD4+,CD4+/CD8+ ratio and level of NK cells were significantly decreased at T2 and T3 in group C,and the levels of CD3+ and CD4+ were significantly decreased at T2 and T3 in group D (P ＜ 0.05).The levels of CD3+,CD4+ and NK cells at T2 and T3 were significantly higher and positive rate at T3 was significantly lower in group D than in group C (P ＜ 0.05).Conclusion Dexmedetomidine can improve the cellular immune function and decrease the probability of micro-metastasis in blood circulation in patients undergoing radical operation for colon cancer.

Objective To observe the expression of calcium/calmodulin dependent protein kinase Ⅱ (CaMK Ⅱ) in the spinal cord of the rats followed lidocaine hydrochloride intrathecal injection.Methods 48 male SD rats weight(230 ± 20) g,after intrathecal indwelling catheter,were randomly divided into four groups (n =12,8 rats for behavioral detection and 4 rats for western blotting):normal group (C group),sham group (S group),DMSO group (D group),10％ lidocaine group (L group).Mechanical withdrawal threshold(MWT) and thermal withdrawal latency(TWL) were detected before and after 2 h,4 h,8 h,12 h,1 d,2 d,3 d,4 d and 5 d with drug treatment.Intumescentia lumbalis of the spinal cord were collected to measure the expression of CaMK Ⅱ with western blotting after drug treatment for 12 h.Results The based MWT of the rats in C,S and D group were (11.2 ± 3.1) g,(11.8 ± 2.2) g and (11.4 ± 2.4) g respectively.There were no differences among the every time points (n=8,P＞0.05).The MWT of the rats in L group significantly increased at 2 h,4 h,8 h,12 h,1 d,2 d,3 d and 4 d after treatment with lidocaine hydrochloride,and the data were (22.0 ± 6.6) g,(22.2 ± 5.3) g,(20.5 ±5.8)g,(18.5 ±4.3)g,(16.7 ±3.2)g,(15.2 ±3.1)g,(15.5 ±3.5)g,(13.7 ±2.4)g respectively (n=8,P＜0.01).TWL had no difference among the rats in C,S,and D group(n=8,P＞0.05).The TWL of the rats in L group significantly increased at 2 h,4 h,8 h,12 h,1 d,2 d and 3 d after treatment with lidocaine hydrochloride(n =8,P＜ 0.01).The expression of CaMK Ⅱ of the rats in C group,S group,D group and L group were 0.17 ± 0.03,0.16 ± 0.03,0.19 ± 0.05,0.42 ± 0.11,and significantly upregulated in L goup (n =4,P ＜ 0.01).Conclusion Lidocaine hydrochloride intrathecal injection can increase the expression of the CaMK Ⅱ in the spinal cord of the rats.Those indicate that CaMK Ⅱ may be involved with the nerve damage induced by lidocaine hydrochloride.

Objective To evaluate the effects of sevoflurane on invasion and migration of mouse lung cancer cells induced by hypoxia.Methods Mouse Lewis lung cancer cells were inoculated in the culture plate.After being cultured for 24 h,the cells were randomly divided into 3 groups (n=18 each) using a random number table:control group (group C),hypoxia group (group H) and hypoxia+ 2％ sevoflurane group (group HS).Cells were exposed to 95％ air-5％CO2 (2 L/min) for 4 h in group C.Cells were exposed to 94％ N2-5％CO2-1％ O2 for 4 h in group H.In group HS,cells were exposed to 2％ sevoflurane and 94％ N2 (2 L/min) for 4 h.The invasion of cells was determined by Transwell assay,and the invaded cells were counted.The migration of cells was evaluated by wound healing assay,and cell migration rates were calculated.The expression of Beclin 1 and LC3 Ⅱ protein in cells was detected by Western blot.Results Compared with group C,the number of invaded cells and cell migration rates were significantly increased,and the expression of Beclin Ⅰ and LC3 Ⅱ was up-regulated in H and HS groups.Compared with group H,the number of invaded cells and cell migration rates were significantly decreased,and the expression of Beclin 1 and LC3 Ⅱ was down-regulated in group HS.Conclusion Sevoflurane can inhibit the invasion and migration of mouse lung cancer cells induced by hypoxia,and inhibition of autophagy is involved in the mechanism.