Objective To investigate the effects of long-and mid-term indwelling AO clavicular hook plate (CHP) on the shoulder function following surgery for acromioclavicular dislocation(from grade Ⅲ to grade Ⅴ by Rockwood's classification).Methods A retrospective study was done of 95 patients with acromioclavicular dislocation who had been fixed with AO CHP from December 2002 to May 2011.They were 80 men and 15 women,aged from 20 to 63 years (average,45.0 years).By the Rockwood's classification,there were 40 cases of type Ⅲ,35 ones of type Ⅳ and 20 ones of type Ⅴ.Time from injury to surgery ranged from 2 to 7 days (average,4.6 days).The CHP was indwelling in 70 patients but removed in 25 patients from 12 to 23 mouths post-surgery (average,16.5 months).The University of California (UCLA) shoulder scoring system was used to compare the shoulder functions between those with an indwelling CHP and those without,as well as between the healthy and affected shoulders among those with an indwelling plate.Results The follow-up time for all the 95 cases ranged from 7.5 months to 9 years,with an average of 38 months.Of those with an indwelling CHP,subacromial bone erosion occurred in 45,internal implant failure in 3,impingement in 13,screw loosening in 2 and frozen shoulder in 5,giving a complication rate of 97.1％ (68/70).Of those without an indwelling CHP,subacromial bone erosion occurred in 3 and no redislocation was found in this group,giving a complication rate of 12.0％ (3/25).The UCLA score for the affected shoulder among those with an indwelling CHP(27.0 ± 11.0 points) was lower than that for the healthy one (34.0 ± 1.0 points) and lower than that for the affected shoulder among those without an indwelling CHP(32.0 ± 6.5 points).Conclusion Long-and mid-term indwelling AO CHP can have a significant adverse impact on shoulder function,leading to a very high rate of postoperative complications.

Objective To investigate effects of ulinastatin preconditioning on cerebral ischemia-reperfusion injury in patients undergoing operation on aorta with deep hypothermic circulatory arrest.Methods 30 patients aged 30-50 with national institutes of health stroke scale(NIHSS) ＜ 10 undergoing operation on aorta with deep hypothermic circulatory arrest,were randomly divided into 2 groups(n =15):normal saline control group(group C),ulinastatin preconditioning group(group U).In group U,ulinastatin 20 000U/kg was infused via central vein at 500-1000 U · kg-1 · min-1 from after tracheal intubation,until 10 min before ascending aortic cross-clamping.In group C,same volume normal saline was infused instead of ulinastatin.Blood samples were taken from internal carotid vein at 5 min before the beginning of deep hypothermic circulatory arrest(T1),15 min after the beginning of deep hypothermic circulatory arres(T2)and 15 min after the end of deep hypothermic circulatory arrest(T3)for determination of plasma concentrations of S-100β,CK-BB,Glutamate(Glu) 、TNF-α、IL-1 、IL-10、MDA,SOD and TGF-β1.Cerebral funcition was evaluated and scored using NIHSS at 2 day after operation.Results Plasma concentrations of S-100β,CK-BB,Glu,TNF-o、IL-1 and MDA were lower,the levels of SOD,IL-10 and TGF-β1 were higher,and the NIHSS score was lower in group U (P ＜ 0.05).Conclusion Ulinastatin preconditioning can lighten cerebral ischemia-reperfusion injury in patients undergoing operation on aorta with deep hypothermic circulatory arrest.The mechanism is involved in inhibit the formn of reactive oxygen free radical.

Objective To evaluate the role of Fas/FasL signaling pathway in ulinastatin postconditioning-induced attenuation of apoptosis in the myocardial cells of patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Forty patients of both sexes,aged 21-59 yr,of ASA physical status Ⅱ or Ⅲ (NYHA class Ⅱ or Ⅲ),scheduled for elective cardiac valve replacement with CPB,were randomly divided into 2 groups (n =20 each):control group (group C),and ulinastatin postconditioning group (group U).In group U,ulinastatin 10 000 U/kg was perfused via the aortic root at 4 000-5 000 U·kg-1 ·min-1 starting from 5 min before aortic unclamping.In group C,the equal volume of normal saline was infused instead of ulinastatin.Myocardial specimens were taken from the right auricle at 45 min after aortic unclamping for determination of Fas,Fas ligand (FasL),caspase-8,Bcl-2 and Bax expression and cell apoptosis.The ratio of Bcl-2 expression to/Bax expression (Bcl-2/Bax) and apoptotic index were calculated.Results Fas,FasL,caspase-8 and Bax expression and apoptotic index were significantly lower,and Bcl-2 expression and Bcl-2/Bax were higher in group U than in group C.Conclusion Ulinastatin postconditioning attenuates apoptosis in the myocardial cells through inhibiting Fas/FasL signaling pathway in the patients undergoing cardiac valve replacement with CPB.

Objective To evaluate the effects of ulinastatin postconditioning and combination of ulinastatin preconditioning and postconditioning on myocardial apoptosis in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Eighty New York Heart Association (NYHA) class Ⅱ or Ⅲ patients of both sexes,aged 21-59 years,scheduled for cardiac valve replacement with CPB,were randomly divided into four groups (n =20 each):normal saline control group (group C),ulinastatin preconditioning group (group U1),ulinastatin postconditioning group (group U2) and ulinastatin preconditioning plus postconditioning group (group U3).In group U1,uinastatin 20000 U/kg was infused via the central vein at 500-1000 U·kg-1 · min-1 after endotracheal intubation until 10 minutes before blocking the ascending aorta.In group U2,ulinastatin 10000 U/kg was infused via the aortic root at 4000-5000 U· kg-1 · min-1 at 5-7 minutes before opening the aorta.In group U3,ulinastatin preconditioning and postconditioning were performed as described in groups U1 and U2.In group C,the same volume of normal saline was infused instead of ulinastatin.Blood samples were taken from the radial artery at 10 minutes before blocking the ascending aorta,40 minutes after blocking the ascending aorta,45 minutes after opening the aorta and at the end of operation for determination of plasma concentrations of tumor necrosis factor-alpha (TNF-α) and soluble tumor necrosis factor receptor 1 (sTNF-R1).Myocardial tissues were obtained from the right atrial appendage at 45 minutes after opening the aorta for determination of the expression of TNF-α,bcl-2,bax,caspase-3,and apoptosis.The bcl-2/bax ratio and apoptotic index were calculated.Results Plasma concentrations of TNF-α and sTNF-R1 and the expression of TNF-α,bax,caspase-3 and apoptotic index were lower and the expression of bcl-2 and bcl-2/bax ratio were higher in groups U1,U2 and U3 than in group C and they were lower in group U3 than in groups U1 and U2 (P ＜ 0.05).Conclusion Ulinastatin postconditioning can inhibit myocardial apoptosis in patients undergoing cardiac valve replacement with CPB,and the efficacy of combination of ulinastatin preconditioning and postconditioning is stronger than that of ulinastatin postconditioning.The mechanism is involved in balancing the expression of bax and bcl-2 and down-regulating the expression of TNF-α and its receptor.

Objective To investigate the role of phosphatidylinositol 3-kinase (PI3K)/protein-serine-threonine kinases (Akt) signal pathway in ulinastatin postconditioning-induced attenuation of apoptosis in myocardial cells in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Forty NYHA class and ASA physical status Ⅱ or Ⅲ patients of both sexes,aged 21-59 yr,scheduled for cardiac valve replacement with CPB,were randomly divided into 2 groups (n =20 each):normal saline control group (group C) and ulinastatin postconditioning group (group U).In group U,ulinastatin 10 000 U/kg was perfused via the aortic root at 4000-5000 U· kg-1 · min-1 starting from 5 min before aortic unclamping.In group C,the equal volume of normal saline was given instead of ulinastatin.Myocardial specimens were taken from the right auricle at 45 min after aortic unclamping for determination of the expression of Akt,phosphorylated Akt (p-Akt),cytochrome c,caspase-9,Bcl-2 and Bax,and cell apoptosis.Bcl-2/Bax ratio and apoptotic index were calculated.Results The expression of p-Akt and Bcl-2 and Bcl-2/Bax ratio were significantly higher,and the expression of cytochrome c,caspase-9 and Bax and apoptotic index were lower in group U than in group C (P ＜ 0.05).Conclusion Ulinastatin postconditioning attenuates apoptosis in myocardial cells in patients undergoing cardiac valve replacement with CPB through activating PI3K/Akt signal pathway.

Objective To evaluate the effects of ulinastatin on renal ischemia-reperfusion injury in patients undergoing operation on aorta with deep hypothermic circulatory arrest (DHCA ) .Methods Thirty patients ,aged 30-50 yr ,of ASA physical status Ⅲ or Ⅳ (NYHA Ⅱ or Ⅲ) ,scheduled for elective operation on aorta with DHCA ,were randomly divided into 2 groups ( n=15 each) using a random number table :control group (group C ) and ulinastatin group (group U ) .In group U ,ulinastatin 20 000 U/kg was infused via the central vein at 500-1 000 U·kg-1 ·min-1 from the time immediately after tracheal intubation until 10 min before ascending aortic cross-clamping .In group C ,the equal volume of normal saline was infused instead of ulinastatin .At 5 min before the beginning of DHCA (T1 ) and 15 min after the end of DHCA (T2 ) ,blood samples were taken from the extracorporeal circulation for determination of polymorphonuclear leukocyte counts , and plasma levels of intercellular adhesion molecule-1 , tumor necrosis factor-α, iterleukin-6 (IL-6 ) IL-8 , IL-10 , malondialdehyde , myeloperoxidase ,atrial natriuretic peptide ,cystatin C ,and creatinine .Results The polymorphonuclear leukocyte counts and plasma levels of intercellular adhesion molecule-1 , tumor necrosis factor-α, IL-6 , IL-8 , malondialdehyde , myeloperoxidase , cystatin C , and creatinine were significantly lower , and the plasma concentrations of IL-10 and atrial natriuretic peptide were higher in group U than in group C ( P< 0.05 ) . Conclusion Ulinastatin can attenuate renal ischemia-reperfusion injury in patients undergoing operation on aorta with DHCA and inhibition of inflammatory responses is involved in the mechanism .

Objective To evaluate the effects of ulinastatin postconditioning and combination of ulinastatin preconditioning and postconditioning on myocardial apoptosis in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Eighty NYHA class Ⅱ or Ⅲ patients of both sexes,aged 21-59,scheduled for cardiac valve replacement with CPB,were randomly divided into 4 groups ( n =20 each):normal saline control group ( group C ),ulinastatin preconditioning group ( group U1 ),ulinastatin postconditioning group (group U2 ) and ulinastatin preconditioning plus postconditioning group(group U3 ).In group U1,uinastatin 20 000U/kg was infused via central vein at 500-1000 U·kg-1 ·min-1 from after tracheal intubation until 10 min before ascending aortic cross-clamping.In group U2,ulinastatin 10 000 U/kg was perfused via aortic root at 4000-5000 U· kg-1 · min-1 at 5-7 min before aortic unclamping.In group U3,ulinastatin preconditioning and postconditioning were performed as described in groups U1 and U2.In group C same volume normal saline was infused instead of ulinastatin.Blood samples were taken from radial artery at 10 min before ascending aortic cross-clamping,40 min after ascending aortic cross-clamping,45 min after aortic unclamping and the end of operation for determination of plasma concentrations of TNF-α and soluble tumor necrosis factor receptor 1 (sTNF-R1).Myocardial tissues were obtained from right atrial appendage at 45 min after aortic unclamping for determination the expression of TNF-d,Bcl-2,Bax and caspase-3 and apoptosis.The Bcl-2/Bax ratio and apoptotic index were calculated.Results Plasma concentrations of TNF-α and sTNF-R1 and the expression of TNF-α,Bax,caspase-3 and apoptotic index were lower,the expression of Bcl-2 and Bcl-2/Bax ratio were higher in groups U1,U2 and U3 thah group C and in group U3 than groups U1,U2 ( P ＜ 0.05 ).Conclusion Ulinastatin postconditioning can inhibit myocardial apoptosis in patients undergoing cardiac valve replacement with CPB,and efficacy of combination of ulinastatin preconditioning and postconditioning is stronger than that of ulinastatin postconditioning.The mechanism is involved in balancing the expression of Bax and Bcl-2 and down-regulating the expression of TNF-α and its receptor.

ObjectiveTo investigate the effects of ulinastatin postconditioning and combining ulinastatin postconditioning with pretreatment on myocardial inflammatory response in patients undergoing cardiac valve replacement under CPB.MethodsEighty NYHA class Ⅱ or Ⅲ patients of both sexes aged 21-59 yr undergoing cardiac valve replacement under CPB were randomly divided into 4 groups ( n =20 each): group control (group C) ; group ulinastatin pretreatment ( group U1 ) ; group ulinastatin postconditioning (group U2 ) and group ulinastatin pretreatment and postconditioning combined (group U3 ).Ulinastatin 20 000 U/kg was infused via central vein at 500-1000 U·kg-1 ·min-1 after tracheal intubation until 10 min before cross-clamping of ascending aorta in groups U1 and U3.Ulinastatin 10 000 U/kg was infused into root of aorta at 4000-5000 U· kg- 1 · min- 1 at 5-7 min before declamping of aorta in groups U2 and U3.Blood samples were obtained from radial artery before cross clamping of ascending aorta,at 40 min after aortic cross-clamping,at 45 min after declamping of aorta (T3) and at the end of operation for polymorphonuclear leukocyte (PMN) count,routine analysis of blood and determination of plasma concentrations of IL-10,TNF-α,IL-1 and IL-6 (by ELISA).Myocardial specimens were obtained at 45 min after declamping of aorta for determination of IL-1β and IL-6 expression by immune-histochemistry.Results Ulinastatin pretreatment and/or postconditioning significantly increased plasma IL-10 concentration and decreased plasma IL-1,IL-6,TNF-α concentrations and PMN count and myocardial IL-1β and IL-6 expression in groups U1,U2 and U3 as compared with group C.Plasma IL-10 concentration was significantly higher and plasma IL-1,IL-6 and TNF-α concentrations,PMN count and myocardial IL-1β and IL-6 expression were lower in group U3 than in groups U1 and U2.ConclusionUlinastatin postconditioning can inhibit myocardial imflammatory response in patients undergoing valve replacement under CPB.The protective effect can be augmented by combining ulinastatin postconditioning with pretreatment.

Objective To evaluate the effects of ulinastatin on cardiac function in heart valve replacement patients with cardio-pulmonary bypass (CPB).Methods 120 patients received valve replacements were divided into 4 groups at random.Group U 1,preconditioning group:ulinastatin parenteral solution (20 000 U/kg) was injected into the central veins for 10 min before the ascending aorta was clamped.Group U2,postconditioning group:ulinastatin ( 10 000 U/kg) was injected into the aortic root for 5 min before the aortic clamp was opened.Group U3,combined the treatments of group U1 and group U2.Group C was served as control without using ulinastatin.The ST-T of ECG at different 8 time points was recorded from preanesthesia to the end of operation.The dosage of vasoactive agents in the 4 groups was recorded after the aortic clamp was opened.Blood samples were taken from the radial artery at 4 time points during 1O min before the ascending aorta was clamed to the end of operation for determining the serum concentration of H-FABP,IMA,CK-MB,MDA and SOD.The changes in myocardium were examined by microscope.Results The automatic reheating rate of heart in group U1,group U2,and group U3 were 70％,73％ and 90％ respectively,which were all higher than group C (33％) after the aortic clamp was opened in 3 -5 min.The scores of reperfusion arrhythmia,change of ST segments in ECG ( elevation or depression),the dosage of vasoactive drugs ( dopamine and adrenaline) and their using time,the concentration of MDA,H-FABP,IMA and CK-MB in group U1 and group U2 were ＜ than those of group C ( P ＜0.05 ),but was ＞ than those of group U3 ( P ＜0.05 ).The activity of SOD in group U1 and group U2 were ＞ than those of group C ( P ＜ 0.05 ),but was ＜ than those of group U3 ( P ＜ 0.05 ).There were no significant differences between group U1 and group U2( P ＞0.05 ).The myocardium in group C had focal coagulative necrosis.The damage of myocardium in group U3 was minor,the cytoplasm and nucleus was homogeneous,and the boundaries were distinct.Conclusion Ulinastatin parenteral solution preconditioning and postconditioning could improve heart function after valves replacement on CPB.The protective effects were not significantly different regarding ulinastati was administered into the central veins before the ascending aorta was clamped vs.it was injected into the aortic root before the aortic clamp opening.Combined these 2 administration methods and dosages could produce collaborative protection.

OBJECTIVETo observe the clinical effect of modified skin soft tissue expansion in repair of devastating wound on the head due to electrical burn in the early stage.

METHODSTwenty-one patients with partial scalp soft tissue defect accompanying skull exposure and necrosis in different degree due to high-voltage electrical burn were hospitalized from April 2009 to October 2014, with wound area ranging from 7 cm × 5 cm to 15 cm × 13 cm. The wounds were debrided as early as possible, and necrotic skulls were kept in situ and covered with porcine ADM and silver-containing dressing. Bacterial culture of exudate from the residual soft tissue was carried out 3 days after hospitalization. Pertinent antibiotics were applied topically to control infection, and autologous split-thickness skin grafts were transplanted. Two to three weeks after injury when the skin grafts survived, modified skin soft tissue expansion was carried out. The crossbow-form incision was made on the normal scalp 2 cm away from the edge of transplanted skin; a capsule cavity was formed by ladder-like dissection. An expander was inserted with the injection port laying outside. The expander was stretched by inflation and deflation. The incisions were sutured layer by layer. The time of continuing negative pressure drainage in the interval of expansion was extended. Volume of water reaching 2 to 3 times of the capacity of expander was injected for excessive expanding. The expanded skin flap was rotated to repair the wound after expansion was ended.

RESULTSWithin 1 week after debridement, 4 kinds of bacteria were detected in the bacterial culture of wound exudate, including 4 cases of Staphylococcus aureus, 5 cases of Staphylococcus epidermidis, 5 cases of Pseudomonas aeruginosa, and 3 cases of Acinetobacter baumannii. A total of 26 expanders were imbedded. No infection or incision dehiscence in the expanding area or cracking and leakage of expander was observed during expanding period. Two to three months after injury, expanded skin flap transplantation was completed, and the wound was repaired. Raw wounds were seen in 4 expanded skin flaps after transfer, and they healed after dressing change. Punctiform ulceration at the seams of 2 flaps was observed one month after the operation, which healed after removing few pieces of sequestra by themselves. The other expanded skin flaps survived well. During the postoperative follow-up for 3 to 12 months, satisfactory appearance and hair growth was observed in the operation area.

CONCLUSIONSRepair of the devastating wound on the head due to electrical burn with modified skin soft tissue expansion could achieve the result of early wound covering and cosmetic repair without alopecia in one time.

Animals ; Bandages ; Burns, Electric ; surgery ; Craniocerebral Trauma ; surgery ; Debridement ; Female ; Head ; Humans ; Male ; Middle Aged ; Necrosis ; Postoperative Complications ; Reconstructive Surgical Procedures ; methods ; Skin Transplantation ; Skull ; Soft Tissue Injuries ; surgery ; Staphylococcus aureus ; Surgical Flaps ; Swine ; Tissue Expansion ; Treatment Outcome ; Wound Healing