Animals ; Cardiac Electrophysiology ; Heart Atria ; innervation ; physiopathology ; Humans ; Vagus Nerve ; physiology

Ectopia Cordis ; surgery ; Humans ; Infant, Newborn ; Male

Objective To increase the quality of blood transfusion medical record and strengthen the management of clinical blood transfusion by establishing a management system for clinical blood transfusion.Methods The management system of clinical blood transfusion was developed by using Sybase PowerBuilder 10.5 program and Oracle 8/8i database,through the function module's development of blood application and evaluation by using C/S structure.Results The management system of clinical blood transfusion realized the exchange of the internal data information with the blood information management system and LIS database,and implemented online audit of transfusion application and evaluation,which improved the work efficiency and reduced the human error.Conclusion The management system of clinical blood transfusion can improve the quality of blood transfusion medical record and realize real-time regulation of clinical blood transfusion to ensure the safety of transfusion.

Electrocardiography ; Humans ; Long QT Syndrome

Animals ; Atherosclerosis ; diet therapy ; physiopathology ; Humans ; Plaque, Atherosclerotic ; drug therapy

AIM To investigate whether Aβ deposit in Alzheimer disease(AD) impairs signal transduction pathway responsible for neuronal survival.METHODSThe rats were randomly divided into six groups:control group and Aβ25-35 group,Aβ25-35+ibuprofen groups (7.5 and 15 mg·kg-1,respectively),Aβ25-35+ibuprofen+LY294002 group,and Aβ25-35+LY294002 group.Rats were given ibuprofen (7.5 and 15 mg·kg-1 daily,ig) for 3 weeks prior to and 1 week after icv single dose of Aβ25-35 (10 μL,1 mmol·L-1).LY294002 was injected icv 1 h before the injection of Aβ25-35.Seven days after Aβ25-35 injection,the hippocampal expressions of P53,Bax,Fas ligand (FasL),Bcl-2 proteins,phospho-Akt/PKB,and phosphorylated 70 ku ribosomal protein S6 kinase (p70S6K) and caspase 3 were determined in the brain tissue preparations from CA1 area with Western blot.The activity of caspase 3 was measured using a caspase 3 colorimetric activity assay kit.RT-PCR was used to show the change of p70s6k mRNA level.RESULTS Aβ25-35 icv injection significantly down-regulated phosphorylated Akt/PKB from 1.32±0.14 to 0.69±0.08 and p70S6K from 0.769±0.028 to 0.479±0.032 in hippocampal CA1 region.These changes were accompanied by increased expressions of the proapoptotic proteins P53,Bax,and FasL and decreased expression of the anti-apoptotic protein Bcl-2 in rat hippocampus.In addition,caspase 3 activity was significantly enhanced in hippocampal CA1 region in Aβ25-35-treated rats compared with control rats.Ibuprofen can reverse these Aβ25-35-induced changes.CONCLUSION Down-regulated anti-apoptotic PI3K/Akt/p70S6K signaling pathway induced by Aβ25-35 in rat hippocampus may contribute to the neuronal damage in AD.Ibuprofen prevents Aβ25-35-induced down-regulation of PI3K/Akt/p70S6K signaling pathway.

AIM To observe the neuroprotective effect and protective mechanisms of ibuprofen on amyloid β-protein fragment 1-40 (Aβ1-40)-induced neurotoxicity in rat hippocampus.METHODS Rats were given ibuprofen (15 mg·kg-1 daily,ig) for 3 weeks prior to icv single dose of Aβ1-40 (5 μL,1 mmol·L-1).Six hours after Aβ1-40 injection,Western blotting was used to determine the expressions of phospho-MAP kinase kinase (MKK)3/MKK6,phospho-p38 MAP kinase,phospho-MAP kinase activating protein kinase 2 (MAPKAPK2),heat-shock protein 27(Hsp27),procaspase 9,3,and 7 cleavage,and poly (ADP-ribose) polymerase (PARP) cleavage in hippocampal CA1 region.RESULTS Intracerebroventricular injection of Aβ1-40 induced an increase in phosphorylated MKK3/MKK6 and p38 MAP kinase expressions in hippocampal CA1.These increases,in combination with reduced phospho-MAPKAPK2 and phospho-Hsp27 expressions,mediated Aβ1-40-induced the activation of caspases cascades.Ibuprofen (15 mg·kg-1·d-1,3 weeks) significantly prevented Aβ1-40-induced increases in phosphorylated MKK3/MKK6 and p38 MAP kinase expressions.In addition,Aβ1-40-induced decreases in phosphorylated MAPKAPK2 and Hsp27 expressions were abrogated by ibuprofen.Aβ1-40-induced changes in activation of caspases cascades were inhibited by ibuprofen.CONCLUSIONIbuprofen prevents Aβ1-40-induced neurotoxicity through suppression of phosphorylated MKK3/MKK6 and p38 MAP kinase expressions and the up-regulation of phospho-Hsp27 expression.

After the antidepressant patents were retrieved from Innography, their distribution, R& D level, hot spots and core patents were analyzed , which showed that the largest number of antidepressant patents was produced in USA, the medicinal preparations containing organic active ingredients were the hot spots, the technological and economic strengths of Pfizer, Novo and Sanofi-Aventis were relatively tremendous.The law-suited patents, reex-amined patents and patent strength were mined.

Objective　To study the protocol that induces adult rat bone marrow stromal cells (MSCs) to express neuron-specific enolase (NSE) in vitro. Methods　MSCs were preinduced with β-mercaptoethanol for 24 h, and then induced for 5 h. The positive percentages of NSE protein expression were measured by immunocytochemistry SABC staining. Results　After the induction, MSCs displayed neuronal morphologies, such as pyramidal cell bodies and processes which formed extensive networks. The positive percentage of NSE protein expression was (63.7±4.5)%. Conclusions　β-mercaptoethanol may induce adult rat MSCs to NSE-positive cells in vitro.

The RV lead position, either RVA or RVHS appears to make no difference in the response to CRT but the LV lead placement play a vital role.9,30 The latest activated regions of LV or areas without transmural myocardial scar for an optimal CRT are preferred. Currently, data demonstrate that no significant difference of clinical outcomes in posterior, anterior, and lateral LV lead position was found, while the ideal pacing site of the LV should be avoided in the apex position as suggested in COMPANION trial and MADIT-CRT trial. And dual-site LV CRT, which is a new technique, is also still in progress and we are looking forward to getting more updates from that.
Cardiac Resynchronization Therapy ; Cardiac Resynchronization Therapy Devices ; Heart Failure ; therapy ; Heart Ventricles ; Hemodynamics ; Humans ; Treatment Outcome