Objective To evaluate emergency nursing methods to permanent pacemaker patients with severe complication and acute hemodynamic changes during implantation. Methods The emergency nursing methods were analyzed retrospectively in 9 of 2 027 patients over 6 years, who had serious complication occurred during the pacemaker implantation Results There were 4 patients with pneumothorax, 2 with pericardial tamponed, 1 with ventricular fibrillation and 2 with acute left ventricular failure in 9 patients (0.4%). Observed the changes of symptoms and signs carefully,found the severe complications at the first time and performed the specific nursing based on different kinds of conditions and improved the prognosis of these patients. Conclusions The serious complications during the implantation of permanent pacemaker were life-threatening, and the specific nursing scheme to different types of complications could increase the successful rate of emergency service.

OBJECTIVETo investigate the clinical results of external fixation and AO titanium elastic intramedullary nailing for treatment of tibia-fibula comminuted closed fractures.

METHODSFrom June 2010 to June 2012,58 patients with tibia-fibula comminuted closed fractures were treated with external fixation and AO titanium elastic intramedullary nailing, including 31 males and 27 females with an average age of 38.5 years old ranging from 21 to 57 years old. According to the system of AO Classification, the fractures were classified as type B1 in 9 cases,type B2 in 7 cases, type B3 in 10 cases, type Cl in 14 cases, type C2 in 12 cases,and type C3 in 6 cases. According to the system of Winquist-Hanson,the fractures' comminuted were classified as grade 1 in 23 cases, grade 2 in 17 cases, grade 3 in 12 cases, and grade 4 in 6 cases. According to the system of Johner-Wruhs, clinical results were compared between different type and grade groups by the time of last followed-up.

RESULTSAll 58 patients were followed up with an average time of 6.8 months (ranged from 18 to 36 weeks). All fractures had clinical healing with an average time of 28 weeks (ranged from 24 to 32 weeks). The total rate of good to excellent results was 91.4%. The rate of good to excellent in the group of grade 1 was higher than that of other grades. The complication rates and fracture healing time would increase respectively with higher Winquist-Hanson's grade. The complication rates in the group of type C3 was higher than that of other types, but the rate of good to excellent was lower than that of other types. The complication rates in the group of type B1 was lower than that of other types,but the rate of good to excellent was higher than that of other types.

CONCLUSIONMinimal invasiveusing AO titanium elastic intramedullary nailing combined with external fixation for treatment of tibia-fibula fractures especially for the multiple-segment,long spiral mild-to-moderate comminuted with hidden fracture can get satisfactory reduction and reliable fixation,it conformes to the principle of BO completely, protects the fracture end blood supply,reduces the external fixation time, has less skin soft tissue complications, postoperative function recovered satisfactorily.

Adult ; Bone Nails ; Bone Plates ; External Fixators ; Female ; Fibula ; injuries ; surgery ; Follow-Up Studies ; Fracture Fixation, Intramedullary ; instrumentation ; methods ; Fractures, Closed ; surgery ; Fractures, Comminuted ; surgery ; Humans ; Male ; Middle Aged ; Minimally Invasive Surgical Procedures ; methods ; Tibia ; injuries ; surgery ; Young Adult

Objective To investigate the role of β-arrestin-1 in inhibition of endoxin-induced activation of MAPK signaling pathway in pulmonary microvascular endothelial cells (PMVECs) by penehyclidine hydrochloride (PHC).Methods Human PMVECs were seeded in 6-well plates (2 ml/well) or in culture flasks (4 ml/flask) at the density of 1×105 cells/ml,and randomly divided into 5 groups (n=20 each) using a random number table:empty plasmid transfection group (group C),lipopolysaccharide (LPS) + empty plasmid transfection group (LPS group),PHC + LPS + empty plasmid transfection group (P + LPS group),LPS+β-arrestin-1 short hairpin RNA (shRNA) transfection group (LPS+shRNA group),and PHC + LPS+β-arrestin-1 shRNA transfection group (P+LPS+shRNA group).After the cells were transfected with empty plasmid 1.5 μg or with plasmid containing 15 nmol/L β-arrestin-1 shRNA,the cells were incubated for 24 h.At 24 h of incubation,LPS with the final concentration of 0.1 μg/ml was added,and the cells were then incubated for 1 h in LPS and LPS+ shRNA groups.In P+LPS and P+LPS+shRNA groups,PHC with the final concentration of 2 μg/ml was added,and the cells were incubated for 1 h,and then LPS with the final concentration of 0.1 μg/ml was added,and the cells were incubated for 1 h.The expression of filamentous actin (F-actin) was detected by flow cytometry.The expression of myosin light chain kinase (MLCK) and vascular endothelial-cadherin (VE-cadherin) was detected by immunofluorescence.The expression of phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) and phosphorylated cJun N-terminal kinase (p-JNK) was determined by Western blot.The expression of β-arrestin-1 mRNA was determined by real-time polymerase chain reaction.Results Compared with group C,the expression of Factin,VE-cadherin and β-arrestin-1 mRNA was significantly down-regulated,and the expression of MLCK,p-ERK1/2 and p-JNK was up-regulated in group LPS,and the expression of p-ERK1/2 and p-JNK was significantly up-regulated (P＜0.05),and no significant change was found in the other parameters mentioned above in group P+LPS (P＞0.05).Compared with group LPS,the expression of F-actin,VE-cadherin and β-arrestin-1 mRNA was significantly up-regulated,and the expression of MLCK,p-ERK1/2 and p-JNK was down-regulated in group P+LPS,and the expression of F-actin,VE-cadherin and β-arrestin-1 mRNA was significantly down-regulated,and the expression of MLCK and p-JNK was up-regulated in group LPS+shRNA (P＜0.05).Compared with group P+LPS,the expression of F-actin,VE-cadherin and β-arrestin-1 mRNA was significantly down-regulated,and the expression of MLCK,p-ERK1/2 and p-JNK was up-regulated in group P+LPS+shRNA (P＜0.05).Conclusion The mechanism by which PHC inhibits endoxin-induced activation of MAPK signaling pathway in PMVECs is partially related to up-regulation of β-arrestin-1 expression.

Objective To investigate the effects of penehyclidine hydrochloric(PHC)pretreatment on the expression of β-arrestin-2 in the lung tissue in sepsis-induced acute lung injury in mice.Methods Thirty female Ktmming mice,aged 6 weeks,weighing 18-20 g,were randomly divided into 3 groups(n =10 each):sham operation group(group S); sepsis group(group CLP)and penehyclidine hydrochloric pretreatment group(group PHC).Sepsis was induced by cecal ligation and puncture(CLP)in groups CLP and PHC.Penehyclidine hydrochloric 0.45 mg/kg was injected intraperitoneally at 1 h before CLP in group PHC.While the equal volume of normal saline was given instead of penehyclidine hydrochloric in groups S and CLP.At 12 h of CLP,the animals were sacrificed,and the lung tissues were removed for determination of MPO activity(by colorimetry),IL-6 content(by ELISA),β-arrestin-2 mRNA and protein expression(by RT-PCR and Western blot respectively).Blood samples and bronchoalveolar lavage fluid were collected to calculate pulmonary vascular permeability index(PV PI).Results Compared with group S,PVPI,IL-6 content and MPO activity were significantly increased,the expression of β-arrcstin-2 protein was significantly down-regulaled while the expression of β-arrestin-2 mRNA was up-regulated in group CLP,and PVPI,IL-6 content and MPO activity were significantly incrcased,the expression of β-arrestin-2 protein was significantly up-regulated,while the expression of β-arrestin-2 mRNA was down-regulated in group PHC(P ＜ 0.05).Compared with group CLP,PVPI,IL-6 content,and MPO activity were significantly decreased,the expression of β-arrestin-2 protein was significantly up-regulated,while the expression of β-arrestin-2 mRNA was dow n-regulated in group PHC(P ＜ 0.05).Conclusion PHC pretreatment can attenuate the lung injury induced by sepsis in mice through up-regulating the expression of β-arrestin-2 protein.

Objective To study P300 of the first episode depression and mismatch negativity(MMN) changes after antidepressant treatment. Methods Sixty-four patients with first episode depression were evaluated by HAMD 17, and P300 and MMN tests were performed at the baseline and week 12. The cognitive potentials were compared with those of control group(N=36). Results Compared with the control group, depressive patients had longer latency of P300 and MMN,lower amplitude of P300 and MMN before treatment (P

0.05)and significantly delayed reaction time,(305?109)ms vs(212?70)ms(P

Objective To evaluate the role of β-arrestin-1 in penehyclidine hydrochloride (PHC)-induced inhibition of lipopolysaccharide (LPS)-caused increase in pulmonary microvascular permeability in human pulmonary microvascular endothelial cells (PMVECs).Methods Human PMVECs were seeded in 6-well plates (2 ml/well) or in culture flasks (4 ml/flask) at the density of 1 × 105 cells/ml and divided into 5 groups (n=15 each) using a random number table:empty plasmid transfection group (group C),LPS plus empty plasmid transfection group (LPS group),PHC plus LPS plus empty plasmid transfection group (P+LPS group),LPS plus β-arrestin-1 short hairpin RNA (shRNA) transfection group (LPS+shRNA group) and PHC plus LPS plus β-arrestin-1 shRNA transfection group (P+LPS+shRNA group).In LPS and LPS+shRNA groups,the cells were transfected with empty plasmid 1.5 μg or with plasmid containing 15 nmol/L β-arrestin-1 shRNA,LPS with the final concentration of 0.1 μg/ml was added at 24 h of incubation,and the cells were then incubated for 1 h.In P+LPS and P+LPS+shRNA groups,the cells were transfected with empty plasmid 1.5 μg or with plasmid containing 15 nmol/L β-arrestin-1 shRNA,PHC with the final concentration of 2 μg/ml was added at 24 h of incubation,LPS with the final concentration of 0.1 μg/ml was added at 1 h of incubation,and the cells were then incubated for 1 h.The cell permeability was measured using Transwell chambers.The expression of heat shock protein (HSP27) was detected by immunofluorescence.The expression of β-arrestin-1,p38 mitogen-activated protein kinase (p38MAPK) and phosphorylated p38MAPK (p-p38MAPK) was detected by Western blot.The ratio of pp38MAPK/p38MAPK was calculated.Results Compared with group C,the cell permeability was significantly increased,the expression of HSP27 was up-regulated,p-p38MAPK/p38MAPK ratio was increased,and the expression of β-arrestin-1 was down-regulated in LPS,LPS + shRNA and P + LPS + shRNA groups (P＜0.05),and no significant change was found in the parameters mentioned above in group P+LPS (P＞ 0.05).Compared with group LPS,the cell permeability was significantly decreased,the expression of HSP27 was down-regulated,p-p38MAPK/p38MAPK ratio was decreased,and the expression of β-arrestin1 was up-regulated in group P +LPS,and p-p38MAPK/p38MAPK ratio was significantly increased (P＜0.05),and no significant change was found in the other parameters in group P+LPS+shRNA (P＞0.05).Compared with group P+LPS,the cell permeability was significantly increased,the expression of HSP27 was up-regulated,p-p38MAPK/p38MAPK ratio was increased,and the expression of β-arrestin-1 was down-regulated in group P+LPS+shRNA (P＜0.05).Conclusion The mechanism by which PHC inhibits LPS-induced increase in pulmonary microvascular permeability is totally related to β-arrestin-1 in human PMVECs.

A sensitive, rapid method for determining reduced tiopronin concentration in rat plasma has been developed by using a high-performance liquid chromatography (HPLC) technique in conjunction with the derivatizing agent N-(1-pyrenyl) maleimide (NPM). The analytes were separated on a Kromasil C18 column (250 mm x 4.6 mm, 5 microm) using 0.2% glacial acetic acid aqueous solution including 0.015 mol x L(-1) KH2PO4 and acetonitrile (56:44) as a mobile phase at a flow-rate of 0.8 mL x min(-1), and fluorescence detection wavelength were set at lamda(e x) = 340 nm and lamda(e m) = 375 nm, the column temperature was 30 degrees C. The calibration curve was found to be linear over a range of 0.1 - 10.0 microg x mL(-1), the limit of quantitation was 0. 1 mg x L(-1). The coefficients of the variation for the within-run and between-run precisions ranged from 5.3% to 10.8% and 7.0% to 10.8%, respectively. The percentage of absolute recovery ranged from 73.7% to 79.7%. The method was used to determine the concentration of tiopronin in rat plasma after a single intragastric administration of 25 mg x kg(-1) tiopronin to 6 healthy male Wistar rats. The pharmacokinetic process was fitted to a two-compartment model. The method has been successfully applied to the determination of tiopronin in rat plasma.
Animals ; Area Under Curve ; Chromatography, High Pressure Liquid ; methods ; Fluorescent Dyes ; chemistry ; Male ; Maleimides ; chemistry ; Rats ; Rats, Wistar ; Tiopronin ; blood ; pharmacokinetics

Objective To study the effects of ibuprofen on the growth and development of oligodendrocytes. Methods A total of 6 clean and healthy adult female SD (Sprague Dawley) rats were used for extracting and culturing of oligodendrocytes(OLs).Lysophosphatidic acid(LPA)was then added,and the morphological changes of OLs pre-treatment and post-treatment were observed. Then 6 newborn rats (born 24-48 h) were used for mixed glial cell extraction from the cortex, then the OPCs were inoculated into the culture plates and randomly divided into control group, ibuprofen group, lysophosphatidic acid(LPA)group and LPA+ibuprofen group.After the adhering of the cells in each group for three days, cell morphology was observed,and the drugs were added as interventions.The control group was treated with normal saline, and the other 3 groups were added with saline solution of ibuprofen(100 μmol/L),LPA(1.0 μmol/L)and the mixture of them. The cell morphological changes were observed after 7-day intervention.The morphology of OPCs and OLs were observed by immunofluorescence staining through OPCs'specific immune markers (platelet-derived growth factor receptor alpha, PDGFR-α)and OLs'specific immune markers(myelin basic protein,MBP)along with cell count of mature OLs.Western blot assay was used to detect the relative expression level of MBP in each group. Results After the treatment with LPA to the mature OLs,protrusions were shrinking and became very sparse.The morphology of cells developed well in each group after cell adhering for 3 days. After drug intervention for 7 days, more cell protrusions and branches were observed in ibuprofen group and LPA+ibuprofen group than those of the control group and LPA group.The results of cell count showed that the number of MBP positive cells was significantly higher in the ibuprofen group and LPA+ibuprofen group than that in the control group and LPA group(P<0.01).The results of Western blot assay showed that the MBP protein expression was significantly less in LPA group than the other three groups (P<0.01), and the expression was significantly higher in the ibuprofen group than that of LPA+ibuprofen group (P<0.01). Conclusion LPA has a toxic effect on the growth and development of OPCs, and it has an inhibitory effect on the normal growth of mature OLs. A certain concentration of ibuprofen can significantly inhibit the cytotoxicity of LPA on OPCs and OLs,and promote the formation and maintenance of mature OLs.