Objective To summarize the experience in endovascular repair of De Bakey type Ⅲ aortic dissection in recent years and summarize the prevention and management of the related perioperative complications.Methods From January 2009 to January 2011,49 cases of endovascular repair for De Bakey type Ⅲ aortic dissection were performed under general anesthesia in our department.There were 45 male and 4 female.The follow-up was performed in the outpatient department or by telephone.Results There was no inhospital death and no paraplegia events.Severe complication included:coma,2 cases ( 4.1％ ) ; endoleak,2 cases (4.1％ ) ; upper limb ischemia,2 cases (4.1％ ).Recurrent proximal aortic dissection,1 case.Fever was occurred in most of those cases.Conclusion Endovascular repair of aortic dissection improves the outcome of aortic dissection patients.But more attention should be pay to prevent the severe complications,It will help to improve the prognosis and life quality by reducing the risk of retrograde dissection,acute brain ischemia and endoleak.

Objective To explore the etiology,clinical manifestations of infantal viral pneumonia in Luzhou area.Methods Five viral specific serum IgM antibodies were detected by enzyme-linked immunosorbent assay(ELISA) in acute period of viral pneumonia.Five kinds of virus were separated,as respiratory syncytial virue(RSV),influenza virus(IFV),adenovirus(ADV),cytonegalo virus(CMV),and parainfluenza virus(PIV).Serum specific IgM was positive,C-reactive protein(CRP) was less than 8 mg/L,and there was no(clini-)cal and laboratory proof of other pathogenic infection detected in 221 infants with pneumonia.Results 1.One hundred and four cases of viral infection were detected from 221 infants with pneumonia.The viral positive detected rate was 47.1%,and there were 75 cases of single viral infection(72.1%) and 29 cases of mixed viral infection(27.9%) among them.2.In the single viral infection,RSV was the first,IFV,ADV,PIV and CMV being the second,the third,the fourth,and the fifth respectively.3.The types of likely infection virus were different in different age-stage and seasons in infants.Conclusions The etiology of infantal pneumonia is complicated.The types of viral infection are various besides germ infection and the epidemic season peak;clinical manifestations are different.Earlier detection of(etiology) in infection will make clear the etiology and then take appropriate treatment measures to improve curative effect.

Objective To explore the protective effects of diazoxide on injury of human renal tubular cell(HK-2)induced by serum obtained from neonates with asphyxia.Methods HK-2 cells was used as the target cel1.The attacking concentration of serum obtained from neonates with asphyxia was 200 mL/L.The experiment was designed as 3 groups.HK-2 cells were divided into control group,asphyxia group,and diazoxide group.Control group:joined nutrient fluid including 100 mL/L embryo cow blood serum.Asphyxia group:joined nutrient fluid including the isometric 200 mL/L serum obtained from neonates with asphyxia.Diazoxide group:the diazoxide was joined nutrient including the isometric 200 mL/L serum obtained from neonates with asphyxia fluid.The diazoxide density finally was 100 ?mol/L.Then the change of morphology was observed and photographed under inverted microscope,and the cell viability was measured by methyl thiazolyl tetrazolium method,and the leakage rate oflactate dehydrogenase(LDH)was determined by biochemical methods.Results Under inverted microscopy,HK-2 cells in control group pastes the wall to be good,assumes the paving stone type,into flat polygon,fission many,the cell arrangement was close,connection large expanse,quantity were many.Compared with control group,the HK-2 cell to suffer injury obviously,the shape changed,become the anomalous circular or the ellipse by the model flat polygonal cell,the intercellular space crevice enlarged,the connection was loose,intercellular space obviously many cell fragmented.Living cell quantity reduced obviously,the cell vigor dropped,and the leakage rate of LDH increased significantly in asphyxia group(P

OBJECTIVETo investigate the expression of serine protease Omi/HtrA2 in kidneys of postasphyxial neonatal rats, and to study the effects of Ucf-101 on apoptosis and the expression of Omi/HtrA2 in these rats.

METHODSSeventy-two neonatal Wistar rats of 7-10 days old were randomly divided into 3 groups: control, postasphyxial model, Ucf-101-treated postasphyxialThe postasphyxial model was established by normobaric asphyxiaExpression of Omi/HtrA2 was determined with streptavidin-peroxidase immunohistochemistry 2, 24 and 48 hrs after asphyxia. Terminal deoxynuleotidyl-mediated nick end labeling (TUNEL) was used to ascertain the apoptosis of renal cells.

RESULTSCompared with the control group, OmiHtrA2 expression in renal cells began to increase 2 hrs after asphyxia and peaked at 24 hrs. The expression of Omi/HtrA2 in the Ucf-101-treated postasphyxial group was significantly lower than that in the postasphyxial model group (P<0.01). TUNEL-positive cells began to increase 2 hrs after asphyxia and peaked at 24 hrs in the postasphyxial model group when compared with the control group. The number of TUNEL-positive cells in the Ucf-101-treated postasphyxial group was significantly lower than that in the postasphyxial model group at all time points (P<0.01).

CONCLUSIONSThe expression of Omi/HtrA2 in kidneys is increased in postasphyxial neonatal rats. The increased Omi/HtrA2 expression may play an important role in the development of postasphyxial renal injury. Treatment with Ucf-101 can reduce the expression of Omi/HtrA2 in kidneys of postasphyxial neonatal rats and thus reduce renal tububar epithelial cell apoptosis.

Animals ; Animals, Newborn ; Apoptosis ; drug effects ; Asphyxia Neonatorum ; drug therapy ; metabolism ; pathology ; Female ; High-Temperature Requirement A Serine Peptidase 2 ; Humans ; Immunohistochemistry ; In Situ Nick-End Labeling ; Infant, Newborn ; Kidney ; chemistry ; Male ; Mitochondrial Proteins ; analysis ; antagonists & inhibitors ; Pyrimidinones ; pharmacology ; therapeutic use ; Rats ; Rats, Wistar ; Serine Endopeptidases ; analysis ; Thiones ; pharmacology ; therapeutic use

OBJECTIVETo explore the protective effects of mitochondrial ATP-sensitive potassium channel opener diazoxide on hyperoxia-induced apoptosis of type II alveolar epithelial cells (A549 cells) and possible mechanisms.

METHODSA549 cells were cultured in vitro and divided randomly into control, hyperoxia and diazoxide group. The hyperoxia group was exposed to a mixture of O2 (900 mL/L) and CO2 (50 mL/L) for 10 minutes, then cultured in a closed environment. The diazoxide group was pretreated with diazoxide of 100 μmol/L for 24 hrs before hyperxia induction. The cells were collected 12, 24 and 48 hrs after culture. The morphologic changes of A549 cells were observed under an inverted microscope. A549 cell apoptosis was detected by flow cytometry. The expression of Omi/HtrA2 in the endochylema of A549 cells was determined by immunohistochemistry.

RESULTSA549 cells were damaged and the changes in morphology of the cells were serious in the hyperoxia group. The apoptosis rate of A549 cells and the expression of Omi/HtrA2 in the endochylema increased in the hyperoxia group compared with the control group (P<0.05). The growth and the morphology of A549 cells were greatly improved and the cell injuries were obviously alleviated in the diazoxide group. The expression of Omi/HtrA2 in the endochylema and the apoptosis rate of A549 cells were significantly reduced in the diazoxide group compared with the hyperoxia group (P<0.05).

CONCLUSIONSDiazoxide as an opener of mitoKATP channel can reduce the expression of Omi/HtrA2 and the apoptosis rate of A549 cells, thus relieves the injury of A549 cells induced by hyperoxia.

Apoptosis ; Cells, Cultured ; Cytoprotection ; Diazoxide ; pharmacology ; High-Temperature Requirement A Serine Peptidase 2 ; Humans ; Hyperoxia ; complications ; Lung ; pathology ; Mitochondrial Proteins ; analysis ; Potassium Channels ; physiology ; Serine Endopeptidases ; analysis

OBJECTIVETo explore the effect of silence of Pin1 expression on hyperoxia-induced apoptosis in alveolar epithelial cells A549.

METHODSA549 cells were divided into four groups: control, hyperoxia, negative lentivirus and Pin1-shRNA hyperoxia. The hyperoxia group was exposed to a mixture of 95%O2 and 5%CO2 for 10 minutes. Then cells were cultured in a closed environment. After 24 hours, the changes of morphology were observed under an inverted microscope. Cell apoptosis was detected by flow cytometry (FCM). The expression of X-linked inhibitor of apoptosis protein (XIAP) and Caspase-9 were detected by immunohistochemistry. The production of reactive oxygen species (ROS) and cellular mitochondria membrane potential (△Ψm) were determined by fluorescence microscopy.

RESULTSUnder the inverted microscope, the A549 cells grew slowly and the changes in morphology of the cells were most obvious in the hyperoxia and negative lentivirus groups. The changes in morphology of A549 cells were obviously improved in the Pin1-shRNA hyperoxia group. The FCM results showed that the apoptosis rate of A549 cells increased, Caspase-9 expression increased, XIAP expression decreased, mitochondrial ROS production increased and mitochondrial membrane potential decreased in the hyperoxia and negative lentivirus groups compared with the control group (P<0.05). Compared with the hyperoxia and negative lentivirus groups, the apoptosis rate of A549 cells decreased, Caspase-9 expression decreased, XIAP expression increased, mitochondrial ROS production decreased and mitochondrial membrane potential increased in the Pin1-shRNA hyperoxia group (P<0.05), although the levels of the indexes did not reach to those of the control group.

CONCLUSIONSSilencing of Pin1 could suppress hyperoxia-induced apoptosis of A549 cells.

Apoptosis ; Caspase 9 ; genetics ; Humans ; Hyperoxia ; pathology ; Membrane Potential, Mitochondrial ; NIMA-Interacting Peptidylprolyl Isomerase ; Peptidylprolyl Isomerase ; physiology ; Reactive Oxygen Species ; metabolism ; X-Linked Inhibitor of Apoptosis Protein ; genetics

OBJECTIVETo explore the roles of PKCβ/P66Shc oxidative stress signal pathway in mediating hyperoxia-induced reactive oxgen species (ROS) production in alveolar epithelial cells (A549) and the protective effects of PKCβ inhibitor on hyperoxia-induced injuries of alveolar epithelial cells.

METHODSA549 cells were cultured in vitro and randomly divided into three groups: control, hyperoxia and PKCβ inhibitor LY333531 treatment. The hyperoxia group was exposed to a mixture of O2 (950 mL/L) and CO2 (50 mL/L) for 10 minutes and then cultured in a closed environment. The LY333531 group was treated with PKCβ inhibitor LY333531 of 10 µmol/L for 24 hours before hyperoxia induction. Cells were collected 24 hours after culture and the levels of PKCβ, Pin1, P66Shc and P66Shc-Ser36 were detected by Western blot. The intracellular translocation of P66Shc, the production of ROS and cellular mitochondria membrane potential were measured using the confocal microscopy.

RESULTSCompared with the control group, the levels of PKCβ, Pin1, P66Shc and P-P66Shc-Ser36 in A549 cells 24 hours after culture increased significantly in the hyperoxia group. These changes in the hyperoxia group were accompanied with an increased translocation rate of P66Shc from cytoplasm into mitochondria, an increased production of mitochondrial ROS, and a reduced mitochondrial membrane potential. Compared with the hyperoxia group, the levels of Pin1, P66Shc and P66Shc-Ser36 in A549 cells, the translocation rate of P66Shc from cytoplasm into mitochondria and the production of mitochondrial ROS decreased significantly, while the mitochondrial membrane potential increased significantly in the LY333531 treatment group. However, there were significant differences in the above mentioned measurements between the LY333531 treatment and control groups.

CONCLUSIONSHyperoxia can increase the expression of PKCβ in alveolar epithelial cells and production of mitochondrial ROS and decrease mitochondrial membrane potential. PKCβ inhibitor LY333531 can partially disrupt these changes and thus alleviate the hyperoxia-induced alveolar epithelial cell injury.

Cell Hypoxia ; Cells, Cultured ; Epithelial Cells ; metabolism ; Humans ; Indoles ; pharmacology ; Maleimides ; pharmacology ; Oxidative Stress ; Protein Kinase C beta ; physiology ; Pulmonary Alveoli ; cytology ; metabolism ; Reactive Oxygen Species ; metabolism ; Shc Signaling Adaptor Proteins ; physiology ; Signal Transduction ; physiology ; Src Homology 2 Domain-Containing, Transforming Protein 1

OBJECTIVETo evaluate the efficacy and feasibility of bortezomib plus dexamethasone (BD) in patients with primary systemic (AL) amyloidosis.

METHODSEleven AL amyloidosis patients, including four relapsed or progressed after previous therapies and 7 newly diagnosed were treated with BD. Ten patients had two or more organs involved. Precursor protein analysis showed that 1 was κ light chain, 9 λ light chain; 5 patients with positive immunofixation including 1 IgG κ, 3 IgG λ and 1 IgA λ. BD was administered according to standard two-week schedule.

RESULTSEight patients were evaluable, the median number of treatment cycles was 3 (range 1 - 6). Median follow-up duration was 6 months. At least one affected organ response was observed in six patients and median time to organ response was 2 months. Three patients progressed and two of them died. Toxicities were mainly diarrhea, thrombocytopenia, peripheral neuropathy, fatigue and herpes zoster, and 7 evaluable patients who had toxicities were adjusted dosage and 2 of them interrupted therapy. Epilepsia, paralytic ileus, acute cardiac dysfunction, and postural hypotention were occurred in 3 inevaluble patients.

CONCLUSIONBortezomib plus dexamethasone is effective in AL amyloidosis. Adverse events are common, and in some patients are severe.

Amyloidosis ; drug therapy ; Boronic Acids ; therapeutic use ; Bortezomib ; Dexamethasone ; administration & dosage ; Humans ; Multiple Myeloma ; drug therapy

Adolescent ; Adult ; Aged ; Antibodies, Viral ; blood ; Child ; Child, Preschool ; China ; epidemiology ; Female ; Humans ; Infant ; Influenza A virus ; immunology ; Influenza B virus ; immunology ; Influenza, Human ; epidemiology ; virology ; Male ; Middle Aged ; Seroepidemiologic Studies

OBJECTIVETo explore the effect of resveratrol on the levels of sirtuin 1 (SIRT1) and reactive oxygen species (ROS) in peripheral blood mononuclear cells (PBMCs) of premature infants exposed to hyperoxia.

METHODSPeripheral blood and isolated PBMCs from premature infants (gestational age<32 weeks) without oxygen supplement were collected and were randomly assigned into four groups: control, air+resveratrol, hyperoxia, and hyperoxia+resveratrol. The PBMCs were cultured in vitro for 48 hours, then the ROS content in PBMCs was measured by laser scanning confocal microscopy. Malondialdehyde (MDA) content in the medium was measured by the whole spectrum spectrophotometer. SIRT1 positioning was assessed by immunofluorescence. SIRT1 expression levels in PBMCs were measured by Western bolt.

RESULTSCompared with the control group, the level of SIRT1 in the air+resveratrol group increased significantly (P<0.05). The levels of ROS and MDA and the SIRT1 transposition rate in the hyperoxia group increased significantly, while the expression level of SIRT1 decreased significantly compared with the control group (P<0.05). The levels of ROS and MDA and the SIRT1 transposition rate decreased significantly (P<0.05), and the expression level of SIRT1 increased significantly in the hyperoxia+resveratrol group (P<0.05).

CONCLUSIONSResveratrol can increase SIRT1 expression in PBMCs and inhibit SIRT1 shuttle from nucleus to cytoplasm in order to increase the ability of antioxidative stress in premature infants exposed to hyperoxia, thereby reducing the oxidative stress injury in premature infants.

Female ; Humans ; Hyperoxia ; metabolism ; Infant, Newborn ; Infant, Premature ; Leukocytes, Mononuclear ; metabolism ; Lipid Peroxidation ; Male ; Oxidative Stress ; Sirtuin 1 ; blood ; Stilbenes ; pharmacology