Objective To investigate the change of aquaporin 2 (AQP2) mRNA and protein levels in renal collecting duct of SD rats after hypoxin caused by rising of the altitude to 4600 m. Methods Forty male SD rats were randomly divided into 4 groups (24 h, 48 h, 72 h and 1 week group), and 10 rats in Xining city were used as control group. All the 40 SD rats were transported to Kekexili Natural Reservation areas (4600 m) in Qinghai province. Rats of four experimental groups were sacrificed and renal tissue samples were harvested at different time point respectively, the control group rats were treated in Xining city (2260 m) as well. The concentration of plasma antidiuretic hormone (ADH) was measured by radioimmunity method. The expression of AQP2 mRNA and proteins was evaluated by real-time fluorescent quantitative-PCR, Western blot and immunofluorescence assay. Results The concentration of plasma ADH was decreased at 24 h and was only 28.5% of that of control group, reaching the lowest concentration at 48 h [(86.94±6.49) μg/L vs (302.5±310.48) μg/L], then it increased gradually and was similar to the control group at 7 d [(306.46±11.14) μg/L vs (302.53±10.48)μg/L, P＞ 0.05]. There were significant differences of the control group with 24 h, 48 h and 72 h groups, respectively[(302.53± 10.48) μg/L vs (142.46±10.57)μg/L, (86.94±6.49)μg/L, (169.65±11.15) μg/L respectively, P＜0.01]. The change of AQP2 gene expression level was consistent with the change of ADH. It was decreased at the begining when exposure to altitude and it reached its lowest level at 48 h. It was then returned to high level similarly to that of the control group at 7 d (0.09±0.01 vs 0.09± 0.008, P＞0.05 ). There were significant differences of the control group with 24 h, 48 h and 72 h group, respectively (0.09±0.008 vs 0.04±0.005, 0.03±0.002, 0.04±0.003 respectively, P＜0.01 ). Conclusions AQP2 expression in the renal collecting duct of SD rats is altered over the period exposed to altitude. It is decreased in the early hypoxia period, and is increased in later period. This change may be related to the intensity of hypoxia, which is mediated by a potential adaptation mechanisms against hypoxia caused by high altitude.

Objective To investigate the effect of intrathecal hyperbaric bupivacaine on spinal cord neurons apoptosis in diabetic neuropathic rats.Methods Thirty-two healthy male Sprague-Daw-ley rats weighing 220-300 g,8 normal rats randomly served as control group (group C),the other rats were intraperitoneal injection 1% streptozotocin (STZ)60 mg/kg to induce diabetic neuropathic (DN),and last induced thirty-seven diabetic neuropathic rats.group C and diabetic neuropathic rats administer intrathecal catheter,respectively.Twenty-four rats in which DN was successfully intrathe-cal catheter were randomly divided into 3 groups (n=8):hyperbaric bupivacaine group (group HB), isobaric bupivacaine group (group IB),glucose group (group G).Hyperbaric bupivacaine 10 μl were injected intrathecally in groups C and HB respectively,isobaric lidocaine 10 μl were injected intrathe-cally in group IB,10% glucose 10 μl were injected intrathecally in group G,once daily for 3d.After rats each administration 2 min,motor block duration were recorded;The paw withdrawal threshold to von Frey filament stimulation (PWT)were measured before induced diabetes model (T1 ),before in-jected intrathecally (T2 ),after 30 min administered 1 d (T3 ),2 d (T4 ),3 d (T5 )and end administered 4 d (T6 ).All rats were sacrificed at T6 and their lumbar intumescential spinal cord tissue were re-moved for microscopic examination.And using TUNEL assay to measure spinal neuronal apoptosis. Results PWT was lower at T2-5 in groups HB,IB and G comparing with T1 (P <0.05 ).Comparing with group C,the motor block duration was significantly prolonged(P <0.05)and spinal cord neuro-nal apoptosis cells were increased(P <0.05)in group HB.Comparing with group IB,the motor block duration was significantly prolonged(P <0.05)and spinal cord neuronal apoptosis cells were increased (P <0.05)in group HB,too.PWT was increased at T6 in group HB at T2-T5 (P <0.05).Group G did not appear motor block and spinal cord neuronal apoptosis.Conclusion Intrathecally hyperbaric bupi-vacaine can promote spinal cord neuronal apoptosis in diabetic neuropathic rats.

Objective To evaluate the effect of hyperbaric factor on lidocaine-induced apoptosis in spinal neurons in rats with diabetic neuropathic pain.Methods Healthy male Sprague-Dawley rats,weighing 220-300 g,were used in the study.Diabetic neuropathic pain was induced by high-sugar high-fat diet + intraperitoneal 1％ streptozotocin (STZ) 30 mg/kg and confirmed by blood glucose level ＞ 16.65 mmol/L at 3 days after STZ injection and then intrathecal catheter was placed.Twenty-four rats with diabetic neuropathic pain in which IT catheters were successfully implanted were randomly divided into 3 groups (n =8 each):hyperbaric lidocaine group (group HL),isobaric lidocaine group (group IL),and glucose group (group G).Another 8 rats in which IT catheters were successfully inserted served as control group (group C).2％ hyperbaric lidocaine 10 μl (in C and HL groups),2％ isobaric lidocaine 10 μl (in group IL),or 10％ glucose 10 μl (in group G) was injected intrathecally once a day for 3 consecutive days.The duration of motor block was recorded at 2 min after each administration.The paw withdrawal threshold to von Frey filament stimulation (PWT) was measured before STZ injection (T1),before IT injection (T2),at 30 min after administration on 1st,2nd and 3rd days and on day 5 after the end of administration (T3-6).All the rats were sacrificed at T6 and their L4,5 segments of the spinal cord were removed for microscopic examination.The apoptosis in spinal neurons was detected using TUNEL assay.Results Compared with the baseline value at T1,PWT was significantly decreased at T2-5 in HL,IL and G groups.PWT was significantly higher at T6 than at T2-5 in group HL.Compared with group C,the duration of motor block was significantly prolonged and the apoptotic index was increased in group HL.Compared with group IL,the duration of motor block was significantly prolonged and the apoptotic index was increased in group HL.Conclusion Hyperbaric factor can promote lidocaine-induced apoptosis in spinal neurons in rats with diabetic neuropathic pain.

Objective To evaluate the role of p38 MAPK signal transduction pathway in dexmedetomidine against neurotoxicity induced by bupivacaine.Methods Seventy-two adult male SD rats,successfully implanted with intrathecal catheter without complications,were randomly divided into 6 groups: control group (group C);p38MAPK inhibitor group(group SB);dexmedetomidine group (group D);bupivacaine group (group B);dexmedetomidine and bupivacaine group (group DB);p38MAPK inhibitor and bupivacaine group (group SBB).DMSO 20 μl were injected intrathecally in group C;p38MAPK inhibitor 30 μg and 5% bupivacaine were respectively injected intrathecally in group SB and B;group DB and SBB were respectivel pretreated with dexmedetomidine 75 μg/kg intraperitoneally and p38MAPK inhibitor 30 μg intrathecal injection 20 min before intrathecally injected 5% bupivacaine.Dexmedetomidine 75 μg/kg was injected intraperitoneally in group D.Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were measured before intrathecal catheter was implanted (T0),before intrathecal administration (T1) and at 4,8 and 12 h and on 1,2,3,4,5 and 6 days after intrathecal administration (T2-T10).At 24 h after intrathecal administration,6 rats were randomly chosen from each group and sacrificed.The lumbar segment (L4-5) of the spinal cord was removed for detecting neuronal apoptosis (by TUNEL) and phosporylated p38MAPK(p-p38MAPK) expression (by Western blot).Results Compared with T0,MWT was significantly increased and TWL was prolonged at T2-T9 in group B,MWT at T2-T7 was significantly increased and TWL at T2-T6 was prolonged in group DB,MWT was significantly increased and TWL was prolonged at T2-T5 in group SBB (P<0.05).Compared with group C,no significant difference was found in MWT,TWL,the apoptotic index and expression of p-p38MAPK in groups D and SB.MWT was significantly increased and TWL was prolonged at T2-T9 in group B,the apoptotic index and expression of p-p38MAPK were significantly increased in group B (P<0.05).Compared with group B,MWT and TWL at T2-T9,the apoptotic index and expression of p-p38MAPK were significantly decreased in groups DB and SBB (P<0.05).Conclusion Dexmedetomidine can inhibit spinal neurotoxicity induced by bupivacaine in rats via inhibiting apoptosis in spinal cord,and inhibition of p38 MAPK signal transduction pathway may be involved in the underlying mechanism.

Hydroxycinnamoyl-CoA:shikimate/quinate hydroxycinnamoyltransferase(HCT) is an key enzyme involved in the biosynthesis of chlorogenic acid in Lonicera japonica. In this study, eight putative HCT genes were cloned with RACE (rapid amplification of cDNA ends) technology based on the analysis of transcriptome in L. japonica. Among them, one was suggested as HCT gene (LjHCT) in L. japonica through analysis of sequence similarity, physical and chemical properties, and domain conservation of the proptein. LjHCT gene containing 1 275 bp encodes a protein with the molecular weight of 47 kDa. These results will provide foundation for exploring the function of LjHCT in Lonicera japonica.

Objective To explore the similarities and differences between finger photoplethysmogram (PPG) and CSI in monitoring the depth of anaesthesia in Chinese adults under general anaesthesia. Methods Ninety-three patients, ASA ⅠorⅡ, aged 20-67, under general anaesthesia were enrolled. Anaesthesia was induced with target-controlled infusion (TCI) of propofol. The initial TCI concentration of propofol was set at 0.5 mg·L-1 followed by increments of 0.5 mg·L-1 at 3-min interval until the score of Modified Observer's Assessment of Alertness/Sedation Scale (MOAAS)reached 0. PPG and CSI were continuously monitored and their values were recorded every 2-4 seconds. MOAAS was recorded every 30 seconds to evaluate the sedation level in the study period. ResultsFor the periodfrom pre-induction to pre-intubation, the difference of photoplethysmogram amplitudevalues had statistical significance between level 4 and level 3, level 3 and level 2 of MOAAS (P<0.05). CSIvalues declined along with the decrease of MOAAS levels and were statistically different between every two neighboring levels of MOAAS (P < 0.05). Photoplethysmogram amplitude (PPGA) and pulse beat interval (PBI) values showed significant differences before and after intubation, pre- and post-incision (P < 0.05). Conclusions PPGA and PBI appear to be suitable to monitor the nociceptive component of balanced general anesthesia , while the CSI exhibits a good performance in monitoring the sedation or hypnotic component of balanced general anesthesia , thusthe combination of PPGA and CSI would benefit the monitoring of the adequacy of depth of anaesthesia.

Objective To evaluate the role of C-Jun N-Terminal kinase (JNK) signaling pathway in dexmedetomidine-induced reduction of spinal neurotoxicity induced by lidocaine in rats.Methods Seventy-two adult male Sprague-Dawley rats, weighing 280-320 g, in which intrathecal catheters were successfully implanted without complications, were randomly divided into 6 groups (n =12 each) using a random number table: control group (group C);SP600125 (JNK signaling pathway blocker) group (group SP);dexmedetomidine group (group D);lidocaine group (group L);dexmedetomidine + lidocaine group (group DL);SP600125+lidocaine group (group SPL).Dimethyl sulfoxide (DMSO) 20 μl was injected intrathecally in group C.SP600125 30 μg and 10％ lidocaine 20 μl were injected intrathecally in SP and L groups, respectively.At 20 min after intrathecal injection of 10％ lidocaine, dexmedetomidine 75 μg/kg was injected intraperitoneally in group DL, and SP600125 30 μg was injected intrathecally in group SPL.Dexmedetomidine 75 μg/kg was injected intraperitoneally in group D.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured before intrathecal catheters were implanted (T0), before intrathecal administration (T1), and at 4, 8 and 12 h and 1, 2, 3, 4, 5 and 6 days after intrathecal administration (T2-10).At 24 h after intrathecal administration, 6 rats randomly selected from each group were sacrificed.The lumbar segment (L4-5) of the spinal cord was removed for detection of cell apoptosis (by TUNEL) and phosphorylated JNK (p-JNK) expression (by Western blot).The apoptotic index was calculated.Results Compared with group C, no significant change was found in the MWT, TWL, apoptotic index and expression of p-JNK in SP and D groups (P＞0.05), the MWT at T2-8 in group L, at T2-6 in group DL and at T2-5 in group SPL were significantly increased, the TWL at T2-8 in group L, at T2-5 in group DL and at T2-4 in group SPL were prolonged, and the apoptotic index and expression of p-JNK were increased in DL, SPL and L groups (P＜0.05).Compared with group L, the MWT was significantly decreased, and the TWL was shortened at T2-8, and the apoptotic index and expression of p-JNK were decreased in DL and SPL groups (P＜0.05).Conclusion The mechanism by which dexmedetomidine mitigates spinal neurotoxicity induced by lidocaine is related to inhibited activation of JNK signaling pathway in rats.

Objective To study the effects of Rhodiolae Crenulatae Radix ET Rhizoma extracts on sexual behavior of male mice.Methods 50 healthy male mice were randomly divided into the low dose, middle dose and the high dose Rhodiola group, theNanbao capsules group and the normal control group, 10 mice per group. The low dose, middle dose and high dose group were drenched with 0.05, 0.20 and 0.80 g/kg Rhodiola diluent respectively. TheNanbao capsules group mice were drenched with 2.00 g/kg turbid liquid. The normal control group were drenched with saline in the same volume. Liquid is drenched two times each day for 21 days. After 21 days, 50 female mice were matched with to the ratio of 1:1. The number of free movement and swimming test were observed before execution. After the execution, the organ indexes were calculated, and then the contents of SOD and MDA in the testis and liver were measured.Results Compared with the normal control group, capturing latency period of low dose group and middle dose group (20.88 ± 19.94 s, 35.40 ± 22.02 svs.78.11 ± 43.33 s) significantly decreased (P<0.05 orP<0.01). Testicular coefficient of the middle dose group (0.72% ± 0.10 %vs. 0.64% ± 0.08%) was significantly increased (P<0.05); the content of SOD in testicular of the middle dose group, the high dose groups and theNanbao capsules group (152.71 ± 38.10 U/mg, 122.32 ± 52.76 U/mg, 94.38 ± 22.20 U/mgvs. 25.30 ± 14.21 U/mg) increased (P<0.01); the content of SOD in liver of the middle dose group and theNanbaocapsules group (77.71 ± 26.35 U/mg, 74.10 ± 26.04 U/mgvs. 57.92 ± 17.17 U/mg) significantly increased (P<0.05).Conclusion Rhodiola extract can improve the ability of sexual behavior of male mice, and improve the antioxidant capacity of testis and liver.

Objective To investigate the effects of Saikosaponin A (SSA)on cognitive function and cAMP/CREB signaling pathway and expression of BDNF in mice after traumatic brain injury. Methods Sixty SD male mice were randomized into three groups:shame operation group (group S, n =20),trauma group (group T,n =20)and SSA treatment group (group A,n =20).Mice received an administration of SSA 5 mg/kg (group A)or equal volume saline (group S,group T)immediately and once daily for 5 consecutive days after trauma.The cognitive function was detected by Morris wa-ter maze test on day 1,3,7 and 14 after trauma.The hippocampal tissues were harvested after be-havioral tests and homogenized for measuring the levels of brain derived neurophic factor (BDNF)and cyclic AMP (cAMP)by ELISA as well as the levels of cAMP-response element binding protein (CREB)and phosphorylation-cAMP-response element binding protein (pCREB)by western bolt. Results Compared with group S,the escape latency and swimming distance were significantly pro-longed in group T on day 1,3,7 and 14 and group A on day 1,3 after trauma (P <0.05 );while compared with group T,they were significantly shorter in group A on day 7,14 after trauma (P <0.05).Compared with group S,the levels of BDNF,cAMP,CREB and pCREB were significantly de-creased in group T(P < 0.05 ).Compared with group T,the levels of BDNF,cAMP,CREB and pCREB were significantly increased in group A (P <0.05).Conclusion SSA can significantly improve cognitive dysfunction in mice after traumatic brain injury,and the mechanism may be related to the activation of cAMP/CREB signaling pathway and up-regulation of BDNF.

OBJECTIVE To summarize the clinical experience of endoscopic thyroidectomy via suprasternal approach. METHODS Endoscopic thyroidectomy via suprasternal approach was performed in 35 patients with ultrasonic scalpel. RESULTS Operations were successfully performed in 35 patients. The mean operation times were 130 (105～190) minutes in 24 cases with subtotal lobectomy and 4 case with total lobectomy, 60 (50~70) minutes in 2 cases with isthmectomy, 228 (185～270) minutes in 2 case with bilateral subtotal lobectomy, 163 (140～215) minutes in 3 case with subtotal lobectomy and the contralateral ademona resection. The bleeding during operation was 5 to 40ml and the average hospital stay time was 4 (3～5) days. CONCLUSION Endoscopic thyroidectomy via suprasternal approach is a safe way with good cosmetic value.