Objective To explore the effect of dexmedetomidine on phosphoinositide 3-kinase/protein kinase B (PI3K/Akt ) pathway in hippocampus of propofol anesthetized neonatal rats. Methods Eighty Sprague-Dawley male rats,aged 7 days,weighing 10-1 5 g,were randomly divided into 8 groups (n= 10 each):normal saline group (group N),DMSO group (group D),intralipid group (group I),propofol group (group P),dexmedetomidine 25 μg/kg,50 μg/kg and 75 μg/kg +propofol 100 mg/kg groups (groups PD25 ,PD50 and PD7 5 ),LY294002 25 μg + dexmedetomidine 75μg/kg + propofol 100 mg/kg group (group LYPD).The hippocampus of rats in all groups were taken 2 h after the animals fully awake.The ultrastructure of hippocampal neurons was observed by transmission electron microscope.The pAkt-(ser473 )protein and Akt protein in the hippocampus were evaluated by Western blot analysis.Results There was no significant difference in the expression of Akt protein among the eight groups.Compared with group N,the expression of pAkt (ser473)protein was significantly down-regulated in groups P,PD25 ,PD50 ,PD7 5 and LYPD (P <0.05).Compared with group P,the expression of pAkt (ser473)protein was increased significantly in groups PD7 5 and LYPD (P <0.05).Compared with group PD7 5 ,the expression of pAkt (ser473) protein was significantly down-regulated in group LYPD (P <0.05 ).The structure of hippocampal neurons was normal in groups N,I and D.Nuclear nuclei swelling,chromatin decreasing and mito-chondrion vacuolar degeneration were observed in group P while improved gradually with dexmedeto-midine in a dose-dependent manner in groups PD25 ,PD50 and PD7 5 .Neurons karyopyknosis,partial dissolution of nuclear membrane,chromatin condensation,mitochondria vacuolar degeneration were observed in group LYPD.Conclusion Dexmedetomidine pretreatment provides neuroprotection against propofol-induced hippocampal destruction by preserving PI3K/Akt pathway activity in the de-veloping brains.

Objective To investigate the utility value of monoexponential and biexponential DWI in the differential diagnosis between benign and malignant liver neoplasms.Methods Seventy three patients with pathologically or clinically confirmed liver mass,were analyzed retrospectively and categorized into benign and malignant groups between January 2013 and October 2013.Malignant group included 46 patients with 53 lesions,while 27 patients in benign group had 35 lesions.All patients underwent MR examinations on 3.0T system (GE 750).Conventional MR T1WI,T2WI,DWI(b=0,800 s/mm2) (to obtain ADC with monoexponential modeling),multi-b value DWI(b=0,20 50,100,200,400,600,800 and 1 200 s/mm2) (to obtain Slow-ADC,Fast-ADC,f with biexponential modeling) and dynamic enhancement were performed.The ADC,Slow-ADC,Fast-ADC and f mean values of benign and malignant liver neoplasms were measured and analyzed by using independent samples t test.Diagnostic efficacy of these parameters in malignant group was evaluated by using receiver operating characteristic curve,with histopathologic findings as the gold standard.Results ADC,Slow-ADC,Fast-ADC and f of malignant group were lower than those of benign group [ADC:(1.79±0.35)× 10-3 mm2/s vs (1.16±0.36) × 10-3 mm2/s; Slow-ADC:(1.67±0.25) × 10-3 mm2/s vs(0.94±0.22)×10-3mm2/s; Fast-ADC(72.40±23.70)×10-3mm2/s vs(34.62±17.43)×10-3mm2/s; and f:(33.59± 11.77)％ vs (22.28±8.97)％ in benign and malignant groups,respectively).Significant inter-group difference was observed in ADC,Fast-ADC,Slow-ADC and f (t=0.89,14.77,8.96 and 5.47,respectively and P＜0.05).The areas under the ROC curve (AUC) of ADC,Slow-ADC,Fast-ADC and fwere 0.938,0.974,0.895 and 0.789,respectively.The sensitivity and specificity of ADC,Slow-ADC,Fast-ADC and fwere 90.6％ (48/53),96.2％ (51/53),90.6％ (48/53) and 90.6％ (48/53) and 85.7％ (30/35),91.4％ (32/35),82.9％ (29/35) and 57.1％ (20/35)respectively for differentiating benign from malignant hepatic lesions.Conclusion ADC obtained with mono-exponential modeling and Fast-ADC,Slow-ADC,f obtained with biexponential modeling are useful parameters in distinguishing benign and malignant hepatic lesions,among which slow-ADC demonstrates the highest diagnostic efficacy.

Modern Chinese medicine is rooted in classical literature and the legacies provided by ancient doctors and their patients.It is also grounded in the practices of expert clinicians and increasingly informed by clinical and experimental research.Considering Chinese medicine's stage of international development,a whole-evidence approach is an appropriate method for compiling and synthesizing different types and levels of evidence for specific types of interventions.This approach can be used for the wide range of clinical conditions that Chinese medicine commonly treats.

Objective To evaluate the role of cyclic adenosine monophosphate-protein kinase A-cAMP response element-binding protein (cAMP-PKA-CREB) signaling pathway in hypoxic preconditioninginduced reduction of propofol-induced central neurotoxicity in the developing rats.Methods A total of 70 SPF male Sprague-Dawley rats,aged 7 days,weighing 10-15 g,were divided into 7 groups (n=10 each) using a random number table method:normal saline group (N group),propofol group (P group),hypoxic preconditioning plus propofol group (HP group),hypoxic preconditioning plus propofol plus PKA inhibitor H89 group (HPH group),propofol plus PKA agonist SP-CAMP group (PS group),normal saline injected via the lateral cerebral ventricle group (NI group),and 5％ dimethyl sulfoxide (DMSO) injected via the lateral cerebral ventricle group (DI group).In P group,propofol 50 mg/kg was intraperitoneally injected,and an increment of propofol 50 mg/kg was given after recovery of righting reflex.The equal volume of normal saline was given instead in N group.In HP group,hypoxic preconditioning (rats were subjected to 5 cycles of 10-min hypoxia of 8％ O2 and 1O-min normoxia of 21％ O2) was performed,and propofol was intraperitoneally injected at 2 h after the end of hypoxic preconditioning and the method was similar to those previously described in P group.In HPH group,H89 5 μmol/5 μl was injected via the lateral cerebral ventricle,and 30 min later the other treatment was similar to those previously described in HP group.In PS group,SP-CAMP 20 nmol/5 μl was injected via the lateral cerebral ventricle,and 30 min later propofol was injected using the method previously described in P group.In NI and DI groups,5 μl normal saline and 5％ DMSO were injected via the lateral cerebral ventricle,respectively.Rats were immediately sacrificed after the righting reflex was recovered,brains were removed and hippocampi were isolated and cut into sections which were stained with haematoxylin and eosin for determination of PKAc and p-CREB positive cells (by i mmuno-histochemistry) and expression of cleaved caspase-3,Bcl-2,Bax,PKAc and posphorylated (p-CREB) protein (by Western blot).Results Compared with N group,the expression of cleaved caspase-3 and Bax was significantly up-regulated,the expression of Bcl-2,PKAc and p-CREB was downregulated,and the percentage of PKAc and p-CREB positive cells was decreased (P＜0.05),hippocampal cells had irregular arrangement,and cells was atrophied in P group.Compared with P group,the expression of cleaved caspase-3 was significantly down-regulated,the expression of Bcl-2,PKAc and p-CREB was up-regulated,and the percentage of PKAc and p-CREB positive cells was increased in HP and PS groups,and the expression of Bax was down-regulated (P＜0.05),the hippocampal cells were arranged neatly,the cytoplasm was abundant,and the nuclei were visible in HP group.Compared with HP group,the expression of cleaved caspase-3 was significantly up-regulated,the expression of Bcl-2,PKAc and p-CREB protein was down-regulated and the percentage of PKAc and p-CREB positive cells was decreased (P＜0.05),the cells had irregular arrangement and shrinked,and nuclear condensation was found in cells in HPH group.Conclusion The mechanism by which hypoxic preconditioning reduces propofol-induced central neurotoxicity may be related to activating cAMP-PKA-CREB signaling pathway in the developing rats.

Objective: To investigate clinicopathological features of carcinoma showing thymus-like elements (CASTLE) in the head and neck regions. Methods: Clinicopathological data of 7 patients with CASTLE in the head and neck regions were retrospectively reviewed.Immunohistochemical staining and in situ hybridization for EBER were performed. BRAF^V600E mutation was examined by ARMS method in 6 cases. Results: There were 5 females and 2 males with age between 49 and 78 years (average of 65.6 years). All tumors were solitary nodular lesions with an infiltrative border, including 6 intrathyroid tumors and 1 extrathyroid tumor in the laryngeal pharynx.The tumors were 1.7-4.1 cm in diameter (average of 3.0 cm). Four cases demonstrated lymph node metastasis.All patients were alive without metastasis during follow-up, except one consultation case (with FNA sample) developed recurrence at the primary site. The cases showed different immunoreaction to CD5, diffuse immunoreaction with p63, CK5/6 and CD117, but negative staining for TTF1, TG and calcitonin. One case showed positive immunoreaction with Synin less than 30% tumor cells. The Ki-67 labeling index was between 3% and 90%. No BRAF^V600E mutation and EB virus infection were detected. Conclusions Extrathyroid CASTLE involving laryngeal pharynx shows the similar morphological and immunohistochemical features with intrathyroid CASTLE.Immunohistochemical markers of CD5 and CD117 are helpful in the diagnosis. Ki-67 labeling index can be high in CASTLE, especially in lymphoepithelioma type. CD5-negative CASTLE may have neuroendocrine differentiation. BRAF^V600E mutation and EB virus may not be involved in the carcinogenesis of CASTLE.

Objective: To analyze the impact of dual antiplatelet (DAPT) therapy combining with or without proton pump inhibitors (PPI) on the main outcomes after percutaneous coronary intervention (PCI). Methods: The PubMed, EMBASE and Cochrane Library were searched for relevant literature and the references obtained from these sources were retrieved manually from inception till September 2017. Inclusion and exclusion criteria were established follow the Cochrane review standard. A total of 977 literatures were included, 193 duplicates were excluded, 74 reviews, case reports, letters and systematic reviews were excluded, 667 literatures were excluded after reading the title and abstract, 34 literatures were excluded due to non-randomized control studies and unrelated outcome indicators, and 9 literatures were finally included with a total of 16 589 patients. RevMan 5.3 software was used to compare the incidence of major adverse cardiovascular events (MACE), cardiogenic death, recurrent myocardial infarction, target vessel revascularization, all-cause death, stent thrombosis, stroke, gastrointestinal bleeding and gastrointestinal events in patients with DAPT combining with or without PPI after PCI. Results: MACE was observed in 8 out of the 9 included literatures, and the results showed that MACE occurred in 561 out of 6 282 patients receiving DAPT combining with PPI therapy and in 951 out of 9 632 patients using DAPT alone (OR=1.15, 95%CI 0.88-1.51, P>0.05). Cardiogenic death was observed in 7 out of the 9 included literatures, and the results showed that cardiogenic death occurred in 172 out of 6 453 patients receiving DAPT combining with PPI treatment and in 321 out of the 9 839 patients using DAPT alone (OR=0.97, 95%CI 0.80-1.18, P>0.05). Recurrent myocardial infarction was observed in 7 out of the 9 included literatures, the results showed 416 out of 6 282 cases in DAPT combining with PPI therapy group experienced recurrent myocardial infarction and 691 out of 9 632 cases in DAPT group experienced recurrent myocardial infarction (OR=1.01, 95%CI 0.89-1.16, P>0.05). Four out of 9 literatures observed revascularization. The results showed that revascularization was performed in 64 out of 2 173 patients receiving DAPT combining with PPI therapy and in 105 out of the 2 770 patients using DAPT alone (OR=1.33, 95%CI 0.55-3.24, P>0.05). All-cause death was observed in 7 out of the 9 included literatures, and the results showed that all-cause death occurred in 172 out of the 6 453 patients in DAPT combining with PPI therapy group and in 321 out of the 9 839 patients using DAPT alone (OR=0.97, 95%CI 0.80-1.18, P>0.05). Three out of the 9 included articles observed stent thrombosis, and the results showed that stent thrombosis occurred in 99 out of 2 997 patients receiving DAPT combining with PPI therapy and in 245 out of the 6 198 patients treated with DAPT (OR=1.07, 95%CI 0.83-1.37, P>0.05). Stroke was observed in 2 out of the 9 included literatures. The results showed that stroke occurred in 5 out of 2 019 patients receiving DAPT combining with PPI therapy, and in 4 out of the 2 033 patients treated with DAPT (OR=1.00, 95%CI 0.29-3.49, P>0.05). Gastrointestinal bleeding was observed in 6 out of the 9 included literatures. The results showed that gastrointestinal bleeding occurred in 26 out of 3 517 patients receiving DAPT combined with PPI therapy, and in 93 out of the 3 506 patients treated with DAPT, gastrointestinal bleeding was significantly lower in the DAPT combining with PPI group than DAPT alone group (OR=0.27, 95%CI 0.17-0.41, P<0.01). Gastrointestinal events were reported in 6 out of the 9 included articles. Similarly, gastrointestinal events were observed in 51 out of 3 517 patients receiving DAPT combined with PPI therapy, and in 190 out of the 3 506 patients treated with DAPT alone, the incidence of gastrointestinal events in the DAPT combined with PPI group was significantly lower than DAPT alone group (OR=0.24, 95%CI 0.14-0.42, P<0.01). Conclusions The incidence of MACE, cardiogenic death, recurrent myocardial infarction, target vessel revascularization, all-cause death, stent thrombosis and stroke are not affected by DAPT combined with PPI therapy after PCI, while the incidence of gastrointestinal bleeding and gastrointestinal events could be reduced by adding PPI to DAPT in patients undergoing PCI.