In order to summarize the clinical diagnosis and treatment methods for 42 cases of multiple injuries with pancreatic injury, a retrospective analysis on 42 cases of multiple injuries with pancreatic injury from January 1990 to January 2006 was carried out in our hospital. Most cases were associated with hemopneumothorax and rib fractures (52.3%), shock (50%), multiple fractures (47.6%), and severe brain injury (26.1%). In 42 cases, one case died of severe hemorrhagic shock, and the remaining 41 cases (97.6%) were cured (including 40 cases receiving surgical operation and one case receiving the conservative treatment). Postoperative complications occurred in 16 cases (21 cases/times): pancreatic fistula (5 cases/times) and incisional wound infection (5 cases/times), intra-abdominal infection (3 cases/times), stress ulcer (3 cases/times), pleural effusion (3 cases/times), pulmonary infection (one case) and wound dehiscence (1 case). The principle therapy of multiple injuries with pancreatic injury is to rescue life, followed by active treatment to prevent injuries which giving rise to the abnormal respiratory and circulatory functions, management of cerebral hernia and other injuries which endangers life at last, and the pancreatic injury to increase the survival rate and survival quality.
To enhance the fusion of graft bone in thoracolumbar vertebrae and minimize the postoperative loss of correction, short-segment pedicle screw fixation was reinforced with posterior moselizee bone grafting in vertebrae for spinal fusion in patients with thoracrolumbar vertebrate fractures. Seventy patients with thoracrolumbar vertebrate fractures were treated by short-segment pedicle screw fixation and were randomly divided into two groups. Fractures in group A (n=20) were reinforced with posterior morselized bone grafting in vertebrae for spinal fusion, while patients group B (n=50) did not receive the morselized bone grafting for bone fusion. The two groups were compared in terms of kyphotic deformity, anterior vertebral height, instrument failure and neurological functions after the treatment. Frankel grading system was used for the evaluation of neurological evaluation and Denis scoring scale was employed for pain assessment. The results showed that the kyphosis correction was achieved in both group A and group B (group A: 6.4 degree; group B: 5.4 degree)/ At the end of follow-up, kyphosis correction was maintained in group A but lost in group B (P=0.0001). Postoperatively, greater anterior height was achieved in group A than in group B (P<0.01). During follow-up study, anterior vertebral height was maintained only in Group A (P<0.001). Both group A and group B showed good Denis pain scores (P1 and P2) but group A outdid group B in terms of control of severe and constant pain (P4 and P5). By Frankel criteria, the changes in neurological functions in group A was better than those of group B (P<0.001). It is concluded that reinforcement of short-segment pedicle fixation with morselized bone grafting for the treatment of patients with thoracolumbar vertebrae fracture could achieve and maintain kyphosis correction, and it may also increase and maintain anterior vertebral height. Morselized bone grafting in vertebrae offers immediate spinal stability in patients with thoracolumbar vertebrate fractures, decreases the instrument failure and provides better postoperative pain control than without the morselized bone grafting.
To investigate the effect of proteasome inhibitor MG132 on the apoptosis of bovine lens epithelial cells (BLECs), the cells were treated with MG132 at different concentrations for12, 24 and 36 h. The cell viability was analyzed by MTT assay and the effect of MG132 on the apoptosis of BLECs was assessed by flow cytometry (FCM). The results showed that after treatment for the same period, the inhibitory effect of MG132 on BLECs proliferation was enhanced with the increment of the concentration of MG132 (0, 2, 5, 10, μmol/L) (P<0.05). The 50% inhibiting concentration (IC50) was 2.03 μmol/L when the BLECs were treated with MG132 for 36 h. MG132 also induced the apoptosis of BLECs obviously. FCM showed that the apoptosis index of the cells treated by MG132 at 2 μmol/L for 12 h was (20.24±1.51)%, and that of the control was (0.98±0.20)% respectively (P<0.01, n=3). It was concluded that MG132 could lead to apoptosis of BLECs. The decrease of proteasome activity may play an important role in the formation and development of cataract.
The protein expression of cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated Cl− channel, in ovarian stimulated premature female rat ovary during a cycle of follicle development and corpus luteum formation was investigated. Animals were injected with 10 U pregnant Mare’s serum gonadotropin (PMSG) and subsequently 10 U hCG 48 h later. Time-dependent immunohistochemistry and Western blotting experiments were performed before and 24, 48, 72 h after hCG treatment. The immunohistochemistry revealed that administration of PMSG stimulated the CFTR expression in thecal cell layer and granulosa cell layer of mature follicles 48 h post injection, coincident with the PMSG-induced peak in follicular estradiol. However, the expression of CFTR in the granulose lutein cell layer and thecal lutein cell layer was time-dependently reduced following hCG injection, in accordance with the gradually increased progestogen level during luteum corpus formation. Western blotting analysis demonstrated that rat ovarian tissue expressed the special CFTR band at 170 kD. It is concluded that cAMP-dependent Cl− channels are involved in regulation of follicle development and luteum formation.
This study observed the protective effect of hypercapnic acidosis preconditioning on rabbit heart suffered from ischemia-reperfusion injury. Hypercapnic acidosis was established in animals with mechanical hypoventilation before ischemia-reperfusion. Thirty-two rabbits were randomly divided into 4 groups, with each having 8 aminals in term of the degree of acidification: hypercapnic acidosis group A (group A), hypercapnic acidosis group B (group B), hypercapnic acidosis group C (group C), ischemia and reperfusion group (group IR). Animals in group IR were ventilated normally (tidal volume: 15 mL/kg, breathing rate 35 bpm). The PETCO2 was maintained at the level of 40–50 mmHg for 30 min. Animals in groups A, B, C received low-frequency, low-volume ventilation to achieve hypercarbonic acidosis and the target levels of PETCO2 were 75–85,65–75, 55–65 mmHg, respectively, with levels being maintained for 5 min. The animals then were ventilated normally to lower PETCO2 to 40–50 mmHg. The left anterior branch artery of all the animals was ligated for 30 min and reperfused for 180 min. Then the infarct size was calculated. The cardiomyocytes were morphologically observed and ECG and hemodynamics were monitored on continuous basis. Acid-base balance was measured during procedure. Our results showed that the infarct size was (48.5±11.5)% of the risk area in the control group and (42.4±7.9)% in group C (P>0.05). Mean infarct size was significantly smaller in group B (34.5%±9.4%) (P<0.05 vs control group) and group A (31.0%±9.1%) (P<0.01 vs control group). It is concluded that HA-preconditioning can effectively protect the myocardium.