Objective To explore related influencing factors for postoperative delirium in elderly patients, to provide a reference for the prevention and treatment. Methods Fifty-four patients with delirium after surgery were used as observa?tion group, and a total of 150 subjects with no delirium after surgery during the same period were selected as the control group. Data of age, gender, malnutrition, disorders of water and electrolyte metabolism, postoperative mechanical ventilation, postoperative hypoxemia, severe infection and postoperative pain degree, and the combination of basic diseases were com?pared and analysed between two groups. The binary logistic regression analysis was used to analyse the influencing factors of postoperative delirium. The outcome and prognosis were observed and analyzed in observation group. Results The average age was significantly higher in observation group than that of control group (P<0.05). The percentages of postoperative hy?poxemia and severe infection were significantly higher in observation group than those of control group ( P<0.05). Patients with higher age, postoperative hypoxemia and severe infection were risk factors for postoperative delirium. In observation group,1 case died of lung infection, 1 case died of multiple organ failure, the remaining 52 patients were improved and dis?charged from hospital after three months. Conclusion For patients with higher age, postoperative hypoxemia and severe in?fection are the risk factors for occurrence of postoperative delirium. More attention should be paid to clinical preoperative and postoperative periods.

Objective To investigate the feasibility and security of omentum minus cavity xenotransloantation of alginic-polylysine-alginic(APA) microencapsulated neonatal swine islet cells by laparoscopic procedure. Methods 5 patients with IDDM received the xenotransloantation of APA microencapsulated neonatal pig islets in omentum minus cavity by laparoscopic procedure.The patients' general conditions,the change in fast blood glucose level,serum C-peptide and the dose of insulin used were observed before and after the xenotransplantation. Results No complications occurred during operation and after operation.The levels of serum C-peptide increased by 3 to 23 times respectively and the post-operative dose of insulin needed decreased obviously.Insulin independency was achieved in one recipient for up to 31 months. Conclusions Omentum minus cavity xenotransplantation of APA microencapsulated neonatal pig islets for the treatment of IDDM patients by laparoscopic technique is safe and practicable.

Objective To evaluate the effect and result of xenotransplantation with alginic polylysine alginic(APA) microencapsulated neonatal swine islets for the treatment of IDDM patients.[WT5”HZ] Method [WT5”BZ] The neonatal pig islets were microencapsulated with APA technique and cultured in vitro. The secretion of insulin, glucose stimulated insulin release test and histological examination between the microencapsulated and unmicroencapsulated neonatal pig islets were compared. 3 patients with IDDM received a xenotransplantation of microencapsulated neonatal pig islets by laparoscopic procedure. The change in blood glucose level, C peptide and the dose of insulin used were observed before and after the xenotransplantation. [WT5”HZ]Results [WT5”BZ] No significant difference was found between microencapsulated and unmicroencapsulated neonatal pig islets in vitro in terms of biological activity of the islets. The levels of serum C peptide in two of the 3 recipients increased by 11 and 23 times respectively, the postoperative dose of insulin needed decreased by 63% in one, insulin independency was achieved in the other recipient.In these two cases,the microencapsulated islets have functioned effectively for up to 80 ds.[WT5”HZ] Conclusion [WT5”BZ] APA microencapsulated neonatal pig islets have good biological activity and survived while transplanted into IDDM recipients. Omentum minus cavity xenotransplantation of microencapsulated neonatal pig islets by laparoscopic technique is safe, capable of repeated transplantation.

Objective To evaluate the changes in the expression of transient receptor potential vanilloid 1 (TRPV1) in dorsal root ganglions (DRGs) during remifentanil-induced hyperalgesia in the rats with incisional pain.Methods Thirty-two SPF healthy male Sprague-Dawley rats,weighing 240-260 g,aged 2-3 months,in which caudal catheters were successfully implanted,were divided into 4 groups (n=8 each) using a random number table:control group (group C),incisional pain group (group Ⅰ),remifentanil group (group R),and incisional pain + remifentanil group (group I+R).A 1 cm longitudinal incision was made through skin,fascia and muscle of the plantar aspect of the left hindpaw to establish the model of incisional pain.In group R,remifentanil was intravenously infused for 60 min at a rate of 1.2 μg · kg-1 · min-1.In group Ⅰ,the model of incisional pain was established,and the equal volume of normal saline was intravenously infused for 60 min at the same time.In group I+R,the model of incisional pain was established,and remifentanil was intravenously infused for 60 min at a rate of 1.2 μg · kg-1 · min-1 at the same time.In group C,the equal volume of normal saline was intravenously infused for 60 min.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawl latency (TWL) were measured at 24 h before normal saline or remifentanil infusion (To) and 2,6,24 and 48 h after the end of infusion (T1-4).The rats were sacrificed after the last measurement of pain threshold,and the DRGs of the lumbar segment (L4-6) were removed for determination of the expression of TRPV1 protein and mRNA by Western blot and real-time polymerase chain reaction,respectively.Results Compared with group C,the MWT was significantly decreased,and the TWL was shortened at T1-4,and the expression of TRPV1 protein and mRNA was up-regulated in R,I and I+R groups (P＜0.05).Compared with group R or group I,the MWT was significantly decreased,and the TWL was shortened at T1-4,and the expression of TRPV1 protein and mRNA was up-regulated in group I+R (P＜0.05) Conclusion Up-regulated expression of TRPV1 in DRGs may be involved in the mechanism underlying remifentanil-induced hyperalgesia in the rats with incisional pain.

Hepatocellular carcinoma (HCC) is a malignant tumor with a high incidence in China. Bone is a common extra hepatic metastasis site of HCC. Bone metastasis of HCC not only has a serious impact on the quality of life of patients, but also shortens their survival time. However, the pathogenesis of bone metastasis of HCC remains unclear. This review summarizes the clinical features, pathogenesis, prognostic factors, diagnosis and treatment progress and other aspects of bone metastasis of HCC, in order to provide new ideas for the clinical diagnosis and treatment.

Objective To investigate the changes in the expression of Ca2+/calmodulin-dependent protein kinase Ⅱ α (CaMK Ⅱ α) in the spinal cord and dorsal root ganglia (DRG) during remifentanil-induced hyperalgesia in a rat model of incisional pain (IP).Methods Thirty-two male Sprague-Dawley rats in which caudal vein catheter was successfully placed,aged 260-280 g,were divided into 4 groups (n=8 each) using a random number table method:control group (group C),IP group,remifentanil group (group R) and remifentanil plus IP group (group RIP).Normal saline was infused via the caudal vein for 60 min at a rate of 0.1 ml · kg-1 · min-1 in group C.Normal saline was infused via the caudal vein for 60 min at a rate of 0.1 ml · kg-1 · min-1,and the model of IP was simultaneously established in group IP.Remifentanil was infused via the caudal vein for 60 min at a rate of 1.0 μg · kg-1 · min-1 in group R.Remifentanil was infused via the caudal vein for 60 min at a rate of 1.0 μg · kg-1 · min-1,and the model of IP was simultaneously established in group RIP.Mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 24 h before infusion and 2,6,24 and 48 h after infusion (T0-4).The rats were sacrificed after the last behavioral test,and L4-6 segment of the spinal cord and DRGs were removed for determination of the expression of total and phosphorylated CaMK Ⅱ α (tCaMK Ⅱ α,pCaMK Ⅱ α) by Western blot.The ratio of pCaMK Ⅱ /tCaMK Ⅱ α was calculated.Results Compared with group C,MWT was significantly decreased,TWL was shortened,the expression of tCaMK Ⅱ α and pCaMK Ⅱ α in the spinal cord and DRGs was up-regulated,and the ratio of pCaMK Ⅱ α/tCaMK Ⅱ α was increased in I,R and RIP groups (P＜0.05 or 0.01).Compared with group IP and group R,MWT was significantly decreased,TWL was shortened,the expression of tCaMK Ⅱ α and pCaMK Ⅱ α in the spinal cord and DRGs was up-regulated,and the ratio of pCaMK Ⅱ α/tCaMK Ⅱ α was increased in group RIP (P＜0.05 or 0.01).Conclusion The mechanism by which remifentanil induces hyperalgesia may be related to upregulated expression of CaMK Ⅱ α in the spinal cord and DRGs in a rat model of IP.

Objective: To evaluate the role of spinal COX-1 and COX-2 in remifentanil-induced hyperalgesia in mice with incisional pain. Methods: Thirty-two male C57BL/6J mice, aged 8-10 weeks, weighing 20-25 g, were divided into 4 groups (n=8 each) using a random number table method: control group (group C), incisional pain plus remifentanil group (group IR), incisional pain plus remifentanil plus selective COX-1 inhibitor group (group IR+ SC560), and incisional pain plus remifentanil plus selective COX-2 inhibitor group (group IR+ SC236). In IR, IR+ SC560 and IR+ SC236 groups, normal saline 10 μl, SC560 25 μg and SC236 25 μg were intrathecally injected, respectively, 15 min later remifentanil 10 μg/kg was injected via the tail vein for 4 times at 15 min intervals.An incisional pain model was established after the first injection of remifentanil.The mechanical paw withdrawal threshold (MWT) was measured at 24 h before normal saline or remifentanil injection and 3, 6, 24 and 48 h after the last injection (T₀-T₄). The mice were sacrificed after the last measurement of pain threshold, and the L_4-6 segments of the spinal cord were removed for determination of the expression of COX-1 and COX-2 (by Western blot) and expression of COX-1 and COX-2 mRNA (by quantitative real-time polymerase chain reaction). Results: Compared with group C, the MWT was significantly decreased, and the expression of COX-2 protein and mRNA was up-regulated in IR, IR+ SC560 and IR+ SC236 groups (P<0.05). Compared with group IR, the MWT was significantly increased in IR+ SC560 and IR+ SC236 groups (P<0.05). There was no significant difference in the MWT at each time point between IR+ SC560 and IR+ SC236 (P>0.05) .There was no significant difference in the expression of COX-2 protein and mRNA among group IR, group IR+ SC560 and group IR+ SC236 (P>0.05). There was no significant difference in the expression of COX-1 protein and mRNA among the four groups (P>0.05). Conclusion Compared with COX-1, spinal COX-2 plays a major role in the pathophysiological mechanism of remifentanil-induced hyperalgesia in mice with incisional pain.

Objective To investigate the relationship remifentanil-induced hyperalgesia and func-tion of nitrated glutamate transportor-1 ( GLT-1) and glutamine synthetase ( GS) in the spinal cord of rats with incisional pain. Methods Thirty-two male Sprague-Dawley rats, weighing 260-280 g, aged 2-3 months, in which caudal catheters were successfully implanted, were divided into 4 groups (n=8 each) u-sing a random number table method: control group ( group C) , incisional pain group ( group I) , remifen-tanil group ( group R) and remifentanil plus incisional pain group ( group RI) . Normal saline was intrave-nously infused for 60 min at 0. 1 ml · kg-1 · min-1 in group C. The model of incisional pain was estab-lished, and normal saline was simultaneously infused for 60 min via the tail vein at 0. 1 ml·kg-1 ·min-1 in group I. Remifentanil was infused for 60 min via the tail vein at 1. 0 μg· kg-1 ·min-1 in group R. The model of incisional pain was established, and remifentanil was infused for 60 min via the tail vein at 1. 0μg· kg-1 ·min-1 in group RI. The mechanical paw withdrawal threshold ( MWT) and thermal paw with-drawal latency ( TWL) were measured at 24 h before infusion of remifentanil or normal saline ( T0 ) and at 2, 6, 24 and 48 h after infusion ( T1-4 ) . The rats were sacrificed after the last measuremnet of pain thresh-old, and the L4-6 segment of the spinal cord was removed for determination of the expression of GLT-1 and GS (by Western blot) and expression of nitrated GLT-1 (nGLT-1) and nitrated GS (nGS) (by Western blot) . Ratios of nGLT-1∕GLT-1 and nGS∕GS were calculated. Results Compared with group C, the MWT was significantly decreased and TWL was shortened at T1-4 , the expression of GLT-1 and GS was down-regu-lated, the expression of nGLT-1 and nGS was up-regulated, and ratios of nGLT-1∕GLT-1 and nGS∕GS were increased in I, R and RI groups ( P<0. 05) . Compared with group I and group R, the MWT was signifi-cantly decreased and TWL was shortened at T1-4 , the expression of GLT-1 and GS was down-regulated, the expression of nGLT-1 and nGS was up-regulated, and ratios of nGLT-1∕GLT-1 and nGS∕GS were increased in group RI ( P<0. 05) . Conclusion The mechanism of remifentanil-induced hyperalgesia may be related to impaired function of GLT-1 and GS in the spinal cord of rats with incisional pain.

Objective To evaluate the relationship between remifentanil-induced hyperalgesia and Antamins family member membrane protein 16C ( TMEM16C) and Slack channel in the spinal dorsal horn of rats with incisional pain. Methods Forty-eight male Sprague-Dawley rats, aged 1 month, were studied. The study was performed in two parts. Experiment Ⅰ Twenty-four rats were divided into 4 groups ( n=6 each) using a random number table method: normal saline group ( S group ) , virus vector group ( V group) , virus vector plus remifentanil plus incisional pain group ( VRI group) , and AAV5-TMEM16C o-ver-expression plus remifentanil plus incisional pain group (ORI group). Normal saline (S group), virus vector (V group and VRI group) or AAV5-TMEM16C (ORI group) 1 μl was injected via the L4,5 spinal dorsal horn. Remifentanil 1 μg ·kg-1 ·min-1 was infused for 60 min via the caudal vein at 30 days, and the incisional pain model was simultaneously established in VRI and ORI groups. The thermal paw withdrawal latency ( TWL) and mechanical paw withdrawal threshold ( MWT) were measured at 24 h before remifen-tanil infusion ( T0 ) and 2, 6, 24, and 48 h after stopping infusion ( T1-4 ) . The L4,5 segments of spinal dorsal horns were obtained at the end of the behavioral testing, and the expression of TMEM16C and Slack in total and membrane proteins was determined by Western blot. ExperimentⅡ Twenty-four rats were di-vided into 4 groups ( n=6 each) using a random number table method: normal saline plus artificial cerebro-spinal fluid (ACSF) group (SA group), virus vector plus ACSF group (VA group), virus vector plus remifentanil group ( VR group ) , and AAV5-TMEM16C over-expression plus remifentanil group ( OR group). Normal saline (SA group), virus vector (VA group and VR group) or AAV5-TMEM16C (OR group) 1μl were injected via the spinal dorsal horn at the level of L4,5 . L4,5 spinal cord slices were obtained at 30 days and incubated for 60 min in ACSF ( SA and VA groups ) or in ACSF containing 4 nmol∕L remifentanil ( VR group and OR group) . The whole-cell patch-clamp was used to measure the frequency and amplitude of the Slack channel current after the end of incubation in each group. Results ExperimentⅠCompared with S group, the TWL was significantly shortened and the MWT was decreased at T1-4 , and the expression of TMEM16C and Slack in total and membrane proteins was down-regulated in VRI group ( P<0. 05) . Compared with VRI group, the TWL was significantly prolonged and the MWT was increased at T1-4 , and the expression of TMEM16C and Slack in total and membrane proteins was up-regulated in ORI group ( P<0. 05) . Experiment Ⅱ Compared with SA group, the amplitude and frequency of Slack chan-nel current in spinal dorsal horns were significantly decreased in VR group ( P<0. 05) . Compared with VR group, the amplitude and frequency of the Slack current were significantly increased in OR group ( P<0. 05) . Conclusion The mechanism of remifentanil-induced hyperalgesia is related to down-regulating the expression of TMEM16C and further down-regulating the expression of the Slack channel in the spinal dorsal horn of rats with incisional pain.

Objective: To evaluate the role of neuroligin 1 (NL-1) in trafficking of GluR1-containing AMPA receptor to cell membrane in spinal cord dorsal horns during remifentanil-induced hyperalgesia in mice with incisional pain. Methods: Forty SPF healthy male C57BL/6J mice, aged 8-10 weeks, weighing 18-22 g, were divided into 5 groups (n=8 each) using a random number table method: control group (group C), NL1-shRNA plasmid group (group NL), incisional pain plus remifentanil group (group I+ R), incisional pain plus remifentanil plus blank vector group (group I+ R+ B), and incisional pain plus remifentanil plus NL-1-shRNA plasmid group (group I+ R+ NL). Negative lentivirus was intrathecally injected in group I+ R+ B.In NL and I+ R+ NL groups, 10 μl NL-1-shRNA lentivirus at 1×10⁸ IFU/ml was intrathecally injected once a day for 3 consecutive days.Normal saline 10 μl was intrathecally injected at the same time point in C and I+ R groups.After transfection was stable, normal saline 0.1 ml was injected via the caudal vein for 4 consecutive times at 15 min intervals in C and NL groups.In I+ R, I+ R+ B and I+ R+ NL groups, 0.1 ml remifentanil 10 μg/kg was injected via the caudal vein for 4 consecutive times at 15 min intervals, and the model of incisional pain was established after the first administration.The mechanical paw withdrawal threshold (MWT) and tail-flick latency (TFL) were measured at 24 h before normal saline or remifentanil administration (T₀) and at 3, 6, 24 and 48 h after the end of administration (T_1-4). The animals were sacrificed after measurement of pain threshold at T₄, and L_4-6 segments of the spinal dorsal horn were then collected for determination of the expression of NL-1 protein and mRNA and AMPA receptors, and the ratio of AMPA receptor expression in the membrane protein to that in the total protein (m/t ratio) was calculated. Results: Compared with group C, the MWT was significantly decreased, and TFL was shortened at T_1-4, the expression of NL-1 protein and mRNA and GluR1-containing AMPA receptors in membrane and total proteins was up-regulated, and m/t ratio was increased in I+ R and I+ R+ B groups (P<0.05). Compared with I+ R and I+ R+ B groups, the MWT was significantly increased and TFL was prolonged at T_1-4, the expression of NL-1 protein and mRNA and GluR1-containing AMPA receptors in membrane and total proteins was down-regulated, and m/t ratio was decreased in group I+ R+ NL (P<0.05). Conclusion NL-1 in spinal cord dorsal horns can promote the trafficking of GluR1-containing AMPA receptors to cell membrane, which is involved in the development and maintenance of remifentanil-induced hyperalgesia in mice with incisional pain.