Objective: To study protective effect of taurine on gut barrier after hemorrhagic shock-reperfusion. Method: Twenty-four white rabbits were divided randomly into 3 groups: taurine group (A),shock group (B), control group (C). Result: Malondialdehyde and Ca~(2+) contents of intestinal mucosa remained unchanged in group A, but increased significantly in group B, Incidence of bacterial translocation in B group was markedly higher than that in C group at 30 min following reperfusion. Under light and electronic microscope,in comparsion with A and C groups,intestinl mucosa damage in B group became more severe. Conclusion: Taurine can protect gut barrier from intestinal ischemia reperfusion injury induced by hemorrhagic shock through reducing oxide free radical and preventing calcium overload.

Objective To discuss the surgical method of resection of petroclival tumors used temporal base transtentorial approach.Methods Analyzed 26 cases of petroclival tumors.All of them were surgically treated under intraoperative neurophysiological monitoring by temporal base transtentorial approach.Firstly the supratentorial part of tumors were resected by pieces,and then the tentorium was cut open,in order to resect residue of the subtentorial part of tumors.This surgical maneuver was applied to reduce the retraction to surrounding vessels,nerves and brain stem,as well to protect important structures and to finally achieve radical removal of the tumors.The efficacy and complications were observed.Results Among 26 cases,19 cases (73.1％,19/26) achieved total removal,5 cases (19.2 ％,5/26) achieved subtotal removal and 2 cases (7.7％,2/26) achieved great partial removal.There was no surgery-related death.Eleven cases suffered from partial neurological deficit.All cases were followed up for 3 months to 4 years,3 cases underwent complete recovery,4 cases underwent partial recovery,and 4 cases underwent permanent deficit.Conclusions Using temporal base transtentorial approach to resect petroclival tumors is convenient,applicable,safe and with minimal injury and with high proportionality of total resection.Under intraoperative neurophysiological monitoring,this approach may be an ideal choice for surgical treatment of these tumors.

Objective To investigate the effect of vascular inner diameter and artery flow velocity on the flow of internal arteriovenous fistula. Methods Sixty-two patients received the operation of internal fistula were enrolled. According to the inner diameter (Group A: d ≤ 1.5 mm, Group B: 1.5 mm < d ≤ 2.0 mm, Group C: 2.0 mm < d ≤ 3.0 mm, Group D: d > 3.0 mm), the patients were divided into four groups in terms of artery flow velocity (Group a: v ≤ 20 cm/s, Group b:20 cm/s < v≤50 cm/s, Group c:50 cm/s < v ≤ 100 cm/s, Group d:v > 100 cm/s), the differences of fistula and dialysis flow for two months were analyzed among various groups. Results Compared with Group B/b, patients in Group A/a had higher risk of operation failure, with lowered inner fistula flow and dialysis flow. In terms of inner venous diameter , there were significant differences between Group B and C. Conclusions It is not recommended to carry out the inner vascular fistula operation. Followed with the thickening and increasing of inner artery diameter and artery flow , the inner fistula flow and the dialysis flow increase. The inner venous diameter has no significant impact on the inner fistula flow.

Children with pediatric tumors have better prognosis and longer survival than adults, suggesting that attention should be paid to the long-term complications induced by radiotherapy. In this article, the data from more than 40 clinical studies of pediatric tumor radiotherapy published in the recent decade were retrospectively analyzed. Long-term complications of nervous system, cardio-cerebrovascular system, respiratory system, endocrine system, urinary system, reproductive system, skeletal development, long-term secondary tumors were considered and the corresponding radiation dose-volume parameters were summarized, aiming to guide radiation oncology physicians and physicists to optimize radiotherapy plans for children with pediatric tumors.

Aim To investigate the role of ATP-sensi-tive potassium channels-Akt pathway in exogenous hy-drogen sulfide( H2 S) inhibiting the high glucose( HG)-induced injury in H9c2 cardiac cells. Methods The expression level of Akt protein was tested by Western blot assay. The cell viability was measured by cell counter kit-8(CCK-8 assay). The number of apoptotic cells was tested by Hoechst 33258 nuclear staining fol-lowed by photofluorography. The intracellular levels of reactive oxygen species ( ROS ) were detected by DCFH-DA staining followed by photofluorography. Mi-tochondrial membrane potential ( MMP ) was examined by JC-1 staining followed by photofluorography. Results H9c2 cells were treated with 35 mmol·L-1 glucose (high glucose, HG) for 0 ~24 h respectively. After treating for 3 h, the expression level of phosphorated ( p )-Akt protein began to be obviously reduced, the maximum reduced expression level was observed after the cells were exposed to HG for 24 h. Pretreatment of the cells with 50 μmol · L-1 pinacidil ( Pin, a KATP channel opener) or 400 μmol·L-1 NaHS( a donor of H2 S) prior to exposure to HG considerably blocked the down regulation of p-Akt expression level induced by HG. However, pretreatment with 1 mmol · L-1 KATP channel blocker glibenclamide( Gli) obviously attenua-ted the inhibitory effect of NaHS on HG-induced down-regulation of p-Akt expression level. On the other hand, the protective effects of NaHS against the HG-induced cardiomyocyte injury were markedly blocked by 30 μmol·L-1 Ly294002(an inhibitor of Akt), as indicated by the decrease in cell viability and MMP dissipation as well as the increases in the number of apoptotic cells and ROS generation. Conclution KATP channels-Akt pathway mediates the protective effect of H2 S against the HG-induced cardiac injury.

Objective To evaluate the effects of exogenous insulin like growth factor 1(IGF-1) on postoperative cognitive function in aged rats. Methods One hundred and twenty pathogen-free healthy male Sprague-Dawley rats, aged 18-20 months, weighing 500-600 g, were divided into 4 groups(n=30)using a random number table: control group(group C), sham operation group(group S), opera-tion group(group O)and exogenous IGF-1 group(group I). Splenectomy was performed, IGF-1 50 μg∕kg was subcutaneously injected at the same time point every day for 7 consecutive day starting from the end of surgery on the day of surgery in group I, and splenectomy was performed, and the equal volume of normal saline was given instead in group O. Morris water maze test was performed on 1, 3 and 7 days after surgery, and the escape latency and swimming distance were recorded. The rats were sacrificed after the end of Morris water maze test, and hippocampi were isolated for determination of the expression of amyloid-β(Aβ), amyloid precusor protein(APP)and β-secretase 1(BACE-1)using immunohistochemistry and Western blot methods. Results Compared with group C, the escape latency and swimming distance were significantly prolonged at 1, 3 and 7 days after surgery, and the expression of Aβ, BACE-1 and APP was up-regulated in O and I groups(P<005), and no significant change was found in the parameters mentioned above in group S(P>005). Compared with group O, the escape latency and swimming dis-tance were significantly shortened at 1, 3 and 7 days after surgery, and the expression of Aβ, BACE-1 and APP was down-regulated in group I(P<005). Conclusion Exogenous IGF-1 can improve postoperative cognitive function in aged rats.

AIM:To study whether hydrogen sulfide (H2S) protects H9c2 cardiomyocytes against high glucose ( HG)-induced injury by inhibiting necroptosis .METHODS:The protein levels of RIP3 ( an indicator of necroptosis ) and cleaved caspase-3 were determined by Western blot .The cell viability was measured by CCK-8 assay.The intracellular le-vels of reactive oxygen species (ROS) were detected by 2’, 7’-dichlorfluorescein diacetate staining followed by photofluo-rography.Mitochondrial membrane potential (MMP) was examined by rhodamine 123 staining followed by photofluorogra-phy.The number of apoptotic cells was observed by Hoechst 33258 nuclear staining followed by photofluorography .RE-SULTS:After the H9c2 cells were treated with HG (35 mmol/L glucose) for 0~24 h, the protein expression of RIP3 in the H9c2 cells was significantly increased at 3 h, 6 h, 9 h, 12 h and 24 h, reaching the maximum level at 24 h.Pretreat-ment of the cells with 400μmol/L NaHS (a donor of H2S) or co-treatment of the cells with necrostatin-1 (Nec-1;a speci-fic inhibitor of necroptosis) considerably blocked the up-regulation of RIP3 protein induced by HG.Moreover, pretreatment with NaHS or co-treatment with Nec-1 obviously inhibited HG-induced injuries , leading to an increase in the cell viability , and decreases in the generation of ROS and MMP loss .On the other hand , pretreatment with NaHS also reduced the num-ber of apoptotic cells and the protein level of cleaved caspase-3 in the HG-treated H9c2 cardiomyocytes .CONCLUSION:H2 S protects H9c2 cardiomyocytes against HG-induced injury by inhibiting necroptosis .

Aim To investigate the role of the interac-tion between necroptosis ( Nec ) and p38 mitogen-acti-vated protein kinase ( MAPK) pathway in the high glu-cose (HG)-induced H9c2 cardiac cells injury.Meth-ods The cell viability was measured by cell counter kit-8 assay .The intracellular level of reactive oxygen species ( ROS ) was tested by DCFH-DA stating fol-lowed by photofluorography .Mitochondrial membrane potential ( MMP) was detected by Rhodamine 123 stai-ning followed by photofluorography . The expression levels of receptor interaction protein 3 ( RIP3, an indi-cator of Nec ) and p38 MAPK protein were tested by Western blot assay .Results The treatment of H9c2 cardiac cells with 35 mmol? L-1 glucose ( high glu-cose, HG) for 24 h induced considerable injuries , in-cluding a decrease in cell viability , increases in ROS generation as well as MMP loss .The co-treatment of the cells with 100 μmol? L-1 necrostatin-1(Nec-1,a specific inhibitor of Nec ) and HG for 24 h or the pre-treatment of the cells with 3 μmol? L-1 SB 2 0 3 5 8 0 ( an inhibitor of p38MAPK) for 60 min before HG exposure attenuated the above injuries induced by HG .Moreo-ver, the treatment of the cells with HG for 1,3,6,9, 12 ,24 ,36 and 48 h significantly increased the expres-sion levels of RIP3, peaking at 24 h.The co-treatment of the cells with 100 μmol? L-1 Nec-1 or the pre-treatment of the cells with 3 μmol? L-1 SB203580 considerably blocked the up-regulation of RIP3 expres-sion induced by HG .On the other hand , the co-treat-ment of the cells with 100 μmol? L-1 Nec-1 alleviated the HG-induced up-regulation of the expression of p-p38MAPK.Conclusion The interaction between Nec and p38 MAPK pathway mediates the HG-induced inju-ry in H9c2 cardiac cells.

AIM:To investigate whether the opening of ATP-sensitive K+(KATP) channels protects H9c2 car-diac cells against high glucose ( HG)-induced injury and inflammation by inhibiting the Toll-like receptor 4 ( TLR4 )/nu-clear factor-κB ( NF-κB) pathway.METHODS:The protein levels of TLR4 and NF-κB p65 were determined by Western blot.The levels of interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α) were detected by ELISA.The cell viabil-ity was measured by CCK-8 assay.Mitochondrial membrane potential (MMP) was examined by rhodamine 123 (Rh 123) staining followed by photofluorography.The intracellular levels of reactive oxygen species ( ROS) were detected by 2′, 7′-
dichlorfluorescein-diacetate (DCFH-DA) staining followed by photofluorography.The number of apoptotic cells was ob-served by Hoechst 33258 nuclear staining followed by photofluorography.RESULTS: After the H9c2 cardiac cells were treated with HG (35 mmol/L glucose) for 24 h, the protein levels of TLR4 and phosphorylated NF-κB p65 ( p-NF-κB p65) were significantly increased.Pretreatment of the cells with 100 μmol/L diazoxide ( DZ, a KATP channel opener) for 30 min before exposure to HG considerably blocked the up-regulation of the TLR4 and p-NF-κB protein levels induced by HG.Moreover, co-treatment of the cells with 30 μmol/L TAK-242 (an inhibitor of TLR4) obviously inhibited the HG-in-duced up-regulation of the p-NF-κB p65 protein level.On the other hand, pretreatment of the cells with 100 μmol/L DZ had a clear myocardial protection effect, which attenuated the HG-induced cytotoxicity, inflammatory response, mitochon-drial damage, oxidative stress and apoptosis, evidenced by an increase in the cell viability, and decreases in the levels of IL-1βand TNF-α, MMP loss, ROS generation and the number of apoptotic cells.Similarly, co-treatment of H9c2 cardiac cells with 30μmol/L TAK-242 or 100μmol/L PDTC ( an inhibitor of NF-κB) and HG for 24 h also obviously reduced the above injuries and inflammation induced by HG.CONCLUSION: The opening of KATP channels protects H9c2 cardiac cells against HG-induced injury and inflammation by inhibiting the TLR4/NF-κB pathway.

Objective To evaluate the changes in the expression of hippocampal long non-coding RNAs ( lncRNAs) and bioinformatics analysis in mice with perioperative neurocognitive disorders ( PND) . Methods Thirty clean-grade male C57BL∕6 mice, aged 12-14 weeks, weighing 25-30 g, were divided into 2 groups (n=15 each) according to the random number table method: control group (group C) and PND group. The model of PND was established by performing open tibial fracture with intramedullary fixa-tion under isoflurane anesthesia in anesthetized mice. The Morris water maze test, open field test and fear conditioning test were performed at 1, 3 and 7 days postoperatively. The animals were sacrificed after the end of behavioral testing on 3 days after operation, the hippocampus was obtained, the high-throughput gene sequencing was performed to identify the differentially expressed lncRNAs, and Gene Ontology func-tional analysis and Kyoto Encyclopedia of Genes and Genomes signaling pathway analysis were used to ana-lyze the results. Results Compared with group C, the escape latency was significantly prolonged, and the percentage of time spend in the target quadrant and percentage of freezing time in the fear conditioning test were decreased at different time points after operation in group PND ( P<0. 05) . A total of 121 differential-ly expressed lncRNAs were identified, of which 69 were up-regulated and 52 were down-regulated. The Gene Ontology functional analysis showed that there were differences in various biological processes, such as synaptic transmission, cholinergic neurotransmitters, or adiponectin secretion and regulation. The KEGG signaling pathway analysis showed that there were also differences in cholinergic synapses, MAPK signaling pathway, glucagon signaling pathway, TNF signaling pathway, NOD-like receptors, Toll-like re-ceptors, chemokine signaling pathway and etc. Conclusion There are 121 differentially expressed lncR-NAs in the hippocampus of PND mice, and lncRNAs- and the target gene-related inflammatory responses, synaptic transmission, energy metabolism and etc. may be related to the pathogenesis of PND.