Objective To investigate the protective effects of isoflurane preconditioning plus mild hypothermia on isolated rat hearts against ischemia-reperfusion (I/R) injury. Methods Fifty male SD rats weighing 250-300 g were randomly divided into 5 groups ( n = 10 each): group Ⅰ control (group C); group Ⅱ I/R; group Ⅲ isoflurane preconditioning (group P); group Ⅳ mild hypothermia (group M) and group Ⅴ isoflurane preconditioning + mild hypothermia (group PM). The animals were anesthetized with intraperitoneal pentobarbital 40 mg/kg. The hearts were immediately removed and perfused with Krebs-Hensleit (K-H) solution aerated with 95% O2 and 5% CO2 at 10 kPa via aorta at 37℃ in a Langendorff apparatus. The hearts were made globally ischemic for 30 min followed by 60 min reperfusion in group Ⅱ-Ⅴ. In group P and PM the hearts were perfused with K-H solution saturated with 1.0% isoflurane for 15 min followed by 15 min washout before ischemia.In group M and PM the hearts were made ischemic at 31 ℃ and perfused at 37℃. LVEDP, LVSP, dp/dtmax,dp/dtmm and HR were measured after equilibration (baseline), immediately before ischemia, and at 30 and 60 min reperfusion. The infarct size and cytochrome C level in cytoplasm and mitochondria of myocytes were measured.Motochondrial ultrastructure was examined using electron microscope. Results Cardiac function was significantly better, the infarct size significantly smaller, the cytochrome C level in cytoplasm significantly lower, while the cytochrome C level in mitochondria of myocytes significantly higher in group Ⅲ-Ⅴ than in group Ⅱ and in group Ⅴ than in group Ⅲ. The cytochrome C level in cytoplasm was significantly lower, while the cytochrome C level in mitochondria of myocytes significantly higher in group Ⅴ than in group Ⅳ. Less damage to mitochondria was observed in group PM than in group I/R, P and M. Conclusion Isoflurane preconditioning combined with mild hypothermia provides better protection against myocardial I/R injury by attenuating the release of cytochrome C from mitochrondria.

Objective To investigate the protective effects of cardioplegic solution containing different concentrations of Shenfu injectio on isolated rabbit heart against ischemia-reperfusion(I/R)injury.Methods Forty adult long-ear white rabbits weighing 3.8-4.2 kg were anesthetized with intraperitoneal thiopental 40 mg?kg~(-1).Heparin 4 mg?kg~(-1) was injected Ⅳ.Hearts were immediately removed and mounted on a Langendorff apparatus and perfused via aorta with Krebs-Henseleit solution aerated at 37℃ with 95 % O_2 and 5 % CO_2.Forty isolated hearts were randomly divided into 5 groups(n=8 each):control group in which cardiac arrest was induced with St Thomas hyperkkaelemic cardioplegic solution and 4 Shenfu groups(SF)in which cardiac arrest was induced with St Thomas cardioplegic solution containing different concentrations of Shenfu injectio:1%(SF1), 5%(SF5),10%(SF10)and 15%(SF15).All hearts in the 5 groups were subjected to global ischemia for 45 min followed by 40 min reperfusion.Coronary effluent was collected after reperfusion for determination of CK-MB activity.Mitochondria were isolated arid Ca~(2+) and MDA content was measured.Myocardial ultrastructure was observed using electron microscope.Mitochondrial injury was assessed by using Flameng score and stereology(NA and ?).Results The CK-MB activity in coronary effluent,mitochondrial MDA and Ca~(2+) content and Flameng score were decreased and NA was increased in group SF1,SF5 and SF10 as compared with control group(P＜ 0.05 or 0.01).The ? of mitochondria was increased in group SF5 and SF10 as compared with control group(P＜ 0.01).The CK-MB activity and Ca~(2+) content were increased and MDA content was decreased in group SF15 as compared with control group(P＜0.05).The pathological damage to myocardium was significantly less in group SF5 and SF10 than in control group.Conclusion Shenfu injectio added to St Thomas cardioplegic solution at concentration of 5%～10% can protect myocardial mitochondria against I/R injury.

In order to clinically differentiate the pulmonary hypertention stage and the heart failure stage in infants with pneumonia, RPEP/RVET and RPEP/T were used as an objective standard for observing the clinical manifestations of these two stages. Many different clinical features were found which would help the physician to select a suitable time to use vasodilator drugs.

Objective To investigate if ketamine protects cultured rat cerebellar granule neurons (CGNs) from apoptosis induced by glutamate and its possible mechanism of signal transduction. Methods Primarily cultured CGNs prepared by enzymatical digestion of cerebellum isolated bom 7-8 day old SD rats were randomly divided into 8 groups: (1) control group (C); (2) glutamate group (G) in which CGNs were incubated with 300 ?mol?L-1 glutamate; (3) (4) (5) ketamine groups (K1 , K2, K3) in which CGNs were incubated with ketamine 10 (K1 ) 100 (K2) or 1 000 (K3) ?mol ? L-1 for 1h before glutamate was added; (6) Ly 294002 - K3 group (LK3) in which CGNs were incubated with 20 ?mol?L-1 Ly 294002 (a specific phosphatidyl-inositol 3-kinase inhibitor) for 30 min before ketamine 1 000 ? mol ? L-1 and glutamate were added as in group K3; (7) Ly 294002 group (L) in which CGNs were incubated with Ly 294002 20?mol ? L-1 and (8) Ly 294002-glutamate group (LG) in which CGNs were incubated with Ly 294002 20 ?mol ? L-1 for 30 min before glutamate was added. After 20 h incubation the apoptosis in CGNs was detected by Hoechst 33258 nucleus staining, phase-contrast microscopy and DNA fragmentation agarose gel electrophoresis. The neuronal survival was determined by fluorescein diacetate (FDA) staining.Results Glutamate 300 ?mol ? L-1 induced apoptosis in CGNs as characterized by cytoplasmic blebbing, heterochromatic clumping, condensation of nuclear chromatin and a typical apoptotic DNA ladder revealed by agarose gel electrophoresis. Ketamine improved the survival of CGNs incubated with glutamate (300 ?mol ? L-1) and blocked the glutamate-induced apoptosis in a concentration-dependent manner. Ly 294002 (20 ?mol ? L-1) antagonized the anti-apoptotic effects of ketamine. Conclusion Ketamine can protect CGNs from apoptosis induced by glutamate. Phosphatidyl-inositol 3-kinase/Akt pathway may be involved in the antiapoptotic action of ketamine.

Humans ; Non-alcoholic Fatty Liver Disease ; diagnosis ; therapy

Adenocarcinoma ; diagnosis ; genetics ; metabolism ; therapy ; Animals ; Barrett Esophagus ; metabolism ; Biomarkers, Tumor ; metabolism ; Carcinoma, Squamous Cell ; diagnosis ; genetics ; metabolism ; therapy ; Esophageal Neoplasms ; diagnosis ; genetics ; metabolism ; therapy ; Gene Expression Profiling ; Genetic Therapy ; Humans ; MicroRNAs ; genetics ; metabolism ; Precancerous Conditions ; metabolism ; Prognosis

In order to arouse the working enthusiasm of the entire staff and give expression to the value of labor and skills, our hospital has implemented reform in the distribution system. Bonus given to clinical departments is linked both to the amount and quality of work and to economic profits; bonus to medico technical departments is given by means of deducting a percentage from the income and expenditure surplus in a way of progressive decrease; bonus given to functional departments is equivalent to 90% of the average bonus given to medical service departments; and bonus to logistical service departments is given, if possible, by the piece and mark. As a result of the reform, the distribution system has become more rational, the working enthusiasm and efficiency of the staff have been enhanced, operational income and income structure have improved, and social benefits bave been raised, with the satisfaction rate reaching over 90%. Of course, there still exist some difficulties in the reform.

Objective To explore the necessity of EGFR?targeted therapy combined with synchronized whole brain radiotherapy ( WBRT ) for non?small?cell lung cancer ( NSCLC ) with mutated EGFR and brain metastasis by comparing the effects on prognosis between WBRT combined with tyrosine kinase inhibitor ( TKI) and TKI alone. Methods A retrospective analysis was performed in 43 patients with EGFR mutation?positive NSCLC and brain metastasis. In those patients, 24 patients received WBRT plus TKI and 19 patients TKI alone. Results The overall response rate ( RR) and 6?month intracranial disease control rate ( CR) were significantly higher in the WBRT+TKI group than in the TKI group ( 79% vs. 37%, P=0. 002;79% vs. 63%, P=0. 008). The median intracranial progression?free survival (IPFS) time was significantly longer in the WBRT+TKI group than in the TKI group ( 23. 7 vs. 8. 3 months, P=0. 025) . The multivariate analysis indicated that the control of lung cancer, WBRT+TKI, and single brain metastasis were favorable factors for substantially longer IPFS time ( P=0. 033,0. 019,0. 019) . In 23 patients with exon 19 deletion, 12 patients received WBRT+TKI and 11 patients TKI alone;compared with the TKI group, the WBRT+TKI group had significantly higher RR and 6?month CR as well as significantly longer IPFS ( 100%vs. 35%, P=0. 000;100% vs. 55%, P=0. 008;23. 7 vs. 8. 4 months, P=0. 003). In 20 patients without exon 19 deletion, however, there were no significant differences in RR or 6?month CR between the WBRT+TKI group (n=12) and the TKI group (n=8)(64% vs. 50%, P=1. 000;58% vs. 75%, P=0. 642).The median IPFS was 14. 4 and 8. 4 months ( P=0. 864) . Conclusions WBRT combined with TKI is superior to TKI alone in the treatment of NSCLC with brain metastasis. Patients with exon 19 deletion have substantially better treatment outcomes.

Objective To investigate the changes in the expression of phosphor-p38 mitogen-activated protein kinase (p-p38MAPK) in the distal cerebrospinal fluid contacting neurons (CSF-CNs) in rats with neuropathic pain.Methods Forty-eight male adult SD rats aged 2-3 months weighing 230-270 g were randomly divided into 2 groups (n =24 each): sham operation group (group S) and chronic constrictive injury group (group CCI).Neuropathic pain was induced by CCI.Sciatic nerve was exposed and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 silk thread.Thermal withdrawal latency (TWL) was measured with radiation heat stimulus before (baseline) and 1,3,5,7,14 d after CCI in 4 animals at eachtime point in each group.The animals were then sacrificed.30％ cholera toxin subunit B with horse radish peroxidase 3 μl was injected into the lateral ventricle at 48 h before the animals were sacrificed at each time point.The brain tissue in the region of the midbrain aqueduct was taken.The number of distal CSF-CN expressing p-p38MAPK was calculated.p-p38MAPK was detected by histochemical staining.Results The TWL was significantly shortened at 1-14 d after CCI in group CCI as compared with group S.The number of distal CSF-CNs expressing p-p38MAPK was significantly increased at 5-14 d after CCI in group CCI as compared with group S.Conclusion The distal CSF-CNs may be involved in the neuropathic pain induced by CCI through p38MAPK signaling pathway.p38MAPK may contribute only to the maintenance but not development of neuropathic pain.

AIM: To investigate the effects of pioglitazone , a peroxisome proliferator-activated receptor γ( PPARγ) agonist, on the cognitive impairments and inflammatory cytokine production induced by isoflurane in aged mice . METHODS:Male C57BL/6J mice ( 11-month-old, n =136 ) were assigned randomly into 5 groups: control group ( Con) , isoflurane group ( Iso) , 10 mg/kg pioglitazone +isoflurane group ( Pi10+Iso) , 20 mg/kg pioglitazone +isoflu-rane group (Pi20+Iso) and 20 mg/kg pioglitazone alone group (Pi20).The mice in all isoflurane-treated groups were ex-posed to oxygen mixed with 1.4%isoflurane for 2 h.The mice in Con group and in Pi20 group were exposed to oxygen only for 2 h.Pioglitazone was suspended in 1% carboxymethyl cellulose (CMC).Pioglitazone (10 mg/kg or 20 mg/kg) was gavaged 2 h prior to the exposure of isoflurane or oxygen alone .The same volume of 1% CMC was gavaged in Con group and in Iso group.Fear conditioning tests were performed to determine the learning and memory abilities 48 h after isoflurane exposure.Fresh cerebral cortice and hippocampi were dissected to measure the protein expression of PPAR γby Western blotting, and the contents of IL-1βand TNF-αwere analyzed by ELISA 6 h after isoflurane exposure .RESULTS: Com-pared with Con group, the response of freezing behavior decreased (P<0.05) and IL-1βcontent in the hippocampus in-creased ( P<0.05) in Iso group.Compared with Iso group , the response of freezing behavior and PPARγprotein expres-sion level had no significant change ( P>0.05) in Pi10+Iso group, but the response of freezing behavior and PPARγpro-tein expression level increased significantly (P<0.05) and IL-1βcontent in the hippocampus decreased (P<0.05) in Pi20+Iso group.IL-1βcontent in the cerebral cortex and TNF-αlevels both in the cerebral cortex and the hippocampus showed no significant difference among all groups (P>0.05).CONCLUSION:Pioglitazone attenuates cognitive impair-ments and the elevates the level of IL-1βin the hippocampus induced by isoflurane in aged mice .