Objective To investigate the evolution of diffusion indices in the pyramidal tract with Wallerian degeneration(WD)due to cerebral infarction using diffusion tensor imaging(DTI),and to study the relationship between early changes of diffusion indices and motor deficit.Methods Fifteen patients (13 males and 2 females)with acute cerebral infarction(within 7 days)were recruited from the Neurology Department from Mar 2006 to Jan 2007.A11 patients were assessed with DTI.National Institutes of Health Stroke Scale(NIHSS),Bathel Index(BI),modified Rankin Scale(mRS)and Motricity Index(MI)within 7 days from onset,and at the second week.DTI was performed with SIEMENS Trio 3.0 T MR scanner.The placement of region of interest(ROI),measurement of diffusion indices were performed by DTI Studio software.The mean diffusivity(MD),the fractional anisotropy(FA),the first eigenvalue (λ1),the second eigenvalue(λ2),and the third eigenvalue(λ3)were computed.Results At the second week.NIHSS was 6.93±3.39.BI 45.33±26.01,mRS 4.33±0.90.and MI 69.47± 60.71.At the second week from onset.MD of the pyramidal tract at the levels of the middle slice of pons and the superior slice of medulla oblongata showed no significant differences between both the two sides at second week from onset. Other ROI showed significant differences between both sides.MD.FA and λ1 of affected side were lower than the unaffected side.λ2 and λ3 of the affected side were higher than the unaffected side.Positive correlations were found between FA and BI(r=0.530,P=0.042),FA and MI(r=0.543,P=0.036)at the second week.Negative correlations were found between FA and NIHSS(r=-0.613,P=0.015)at the second week.Conclusions DTI can detect the changes in the pyramidal tract due to WD within 7-14 days after ischemic stroke.including a decrease of the fractional anisotropy.the first eigenvalue and increased the second and the third eigenvalues.The fractional anisotropy of the second week from onset is related to the outcome of the motor function.

BACKGROUND: Orotracheal intubation with conventional Macintosh laryngoscope often makes strong alterations in hemodynamic responses. Compare with the Macintosh laryngoscope, the Airtraq~((R)) laryngoscope has weak effect on throat irritation. However, the contrast effect on hemodynamics remains still unknown. OBJECTIVE: To compare the hemodynamical responses to orotracheal intubation between Airtraq~((R)) laryngoscope and Macintosh laryngoscope. DESIGN, TIME AND SETTING: A randomized comparative observation was performed at Department of Anesthesiology, Dalian Second People's Hospital between October 2008 and April 2009. PARTICIPANTS: A total of 40 patents scheduled for surgery under general anesthesia requiring orotracheal intubation were randomly divided into Airtraq~((R)) laryngoscope group and Macintosh laryngoscope group, with 20 cases in each group. METHODS: After standard intravenous anesthetic induction, orotracheal intubation was performed with Airtraq~((R)) laryngoscope or Macintosh laryngoscope. Common Airtraq~((R)) laryngoscope was used in the Airtraq~((R)) laryngoscope group, and an endotracheal tube with internal diameter of 8.0 was inserted. No. 3 lens were used in the Macintosh laryngoscope group, and an endotracheal tube with internal diameter of 8.0 was inserted. MAIN OUTCOME MEASURES: Glottic exposure time, tracheal intubation time, noninvasive heart rate (HR), systolic blood pressure (SBP) and diastolic blood pressure (DBP) before (T0) and after (T1) anesthetic induction as well as at 0 minute (T2), 1 minute (T3), 2 minutes (T4), and 3 minutes (T5) after intubation, as well as rate-pressure product (RPP). RESULTS: The glottic exposure time in Airtraq~((R)) laryngoscope group was significantly longer than that in Macintosh laryngoscope group (P < 0.01), while the tracheal intubation time in Airtraq~((R)) laryngoscope group was significantly shorter than that in Macintosh laryngoscope group (P < 0.01). Compared with pre-induction (T0), the SBP, DBP, and RPP of the two groups decreased significantly after anesthetic induction (T1) (P < 0.05), but the HR did not change remarkably (P > 0.05). Compared with T1, all hemodynamical values at T2, T3, T4 and T5 in Airtraq~((R)) laryngoscope group did not increased sign ificantly (P > 0.05). In Macintosh laryngoscope group, HR and RPP at T4, SBP, DBP, HR and RPP at T2 and T3 increased significantly compared with T1 (P < 0.05). In Macintosh laryngoscope group, HR and RPP at T2, T3 and T4 were significant higher than that in Airtraq~((R)) laryngoscope group (P< 0.05). CONCLUSION: In comparison to the Macintosh laryngoscope, tracheal intubation with the Airtraq~((R)) laryngoscope resulted in less alterations in hemodynamical responses.

0.05). In Macintosh laryngoscope group, HR and RPP at T4, SBP, DBP, HR and RPP at T2 and T3 increased significantly compared with T1 (P

Objective To explore the clinical correlation of the variation of plasma homocysteine (HCY), melatonin (MLT) and ulceative colitis (UC). Methods The clinical data of 112 UC patients was collected, and 110 normal healthy persons as control. The level of plasma HCY and MLT was detected by high pressure liquid chromatography-fluorescence detection (HPLC-FD) method. The level of plasma folate ( FA) and vitamin B12 was detected by enzyme-linked immunosorbent assay (ELISA) method. The correlation of these four indexes and UC was analyzed. Results The serum level of HCY in UC patients was significantly higher than that in normal healthy persons [(11. 27± 7.26) μmol/L vs (8. 19±4. 81) μmol/L, P = 0. 000]. The serum level of MLT in UC patients was significantly lower than that in normal healthy persons [(49. 06 + 31. 40) pg/ml vs (64. 28±41. 16) pg/ml,P=0. 008]. The serum level of FA in UC patients was significantly lower than that in normal healthy persons [(7. 64 + 1.95) nmol/L vs (9. 14 + 1.23) nmol/L, P = 0. 005]. The serum level of vitamin B12 in UC patients was significantly lower than that in normal healthy persons [(108. 64 ±32. 22) pmol/L vs (112. 64±33. 33) pmol/L, P = 0. 004]. There was no correlation between plasma HCY, MLT and UC disease activity degree, range, disease duration, erythrocyte sedimentation rate (ESR), or C reactive protein (CRP) in UC patients. There was no significant correlation between MLT and HCY in UC patients. Conclusions The serum level of HCY is higher in UC patients than that in normal control, and MLT is lower than that in normal control. However there is no significant correlation between them.

Objective To investigate the effect and mechanism of anti-tumor necrosis factor (TNF)-α on the intestinal mucosal permeability in dextran sulfate sodium (DSS) induced colitis mice.Methods Eighteen C57BL/6J mice were evenly divided into healthy control group,model group and anti-TNF-α treated group.The mice of model group and anti-TNF-α treated group were fed with 5％DSS solution for 7 days.The mice of anti-TNF-α treated group were injected anti-TNF-α (5 mg/kg)intraperitoneally on the first and fourth day; control group and model group were substituted with equal volume saline injection.The mice were sacrificed at 7 days after modeling.The disease activity index (DAI) score was evaluated everyday.The intestinal permeability was examined by Evan′s blue (EB) method and FITC-dextran (FITC-D) method.The colon tissue was collected for observation under microscope and histological index (HI).The small intestinal tissues were examined under electron microscope.The 10％ homogenate of colon and intestinal mucosa was prepared,the activity of myeloperoxidase (MPO),the content of TNF-α and epithelial myosin light chain kinase (MLCK) concentration were determined with kits respectively.The expression of MLCK in intestinal mucosa was tested by Western blot assay.Single factor of variance between groups were analyzed.Results Compared with control group,the DAI of model group increased daily.Compared with model group,the DAI of anti-TNF-α treated group improved.In model group,mice intestinal epithelial cells junctional complex shortened and widened and the cell gap expanded.In anti-TNF-α treated group,the connection structure of mice intestinal epithelial cells was tighter.The activity of HI and MPO and the content of TNF-α of model group were higher than those of control group (P ＝ 0.008,0.006 and 0.001,respectively),all of those of anti-TNF-α treated group were lower than those of model group (P=0.004,0.008 and 0.005,respectively).The F value of three groups was 131.98,218.28 and 58.93,respectively.The contents of EB in mice intestinal wall and serum FITC-D of model group were higher than those of control group (P=0.003 and 0.010),and those of anti-TNF-α treated group were lower model group (P＝0.001 and 0.009).The F value of three groups was 69.36 and 17.96.The MLCK concentration in mice intestinal mucosa of model group [(71.10± 7.52) ng/g] was higher than that of control group [(18.56±9.92) ng/g,P＜0.01],that of anti-TNF-α treated group [(37.56±15.84) ng/g] was lower than model group (P=0.008),and the difference among these three groups was statistically significant (F＝ 17.23).The Western blot results indicated the expression of MLCK in intestinal mucosa of model group was higher than that of control group,and that of anti-TNF-α treated group was lower than model group.Conclusions Anti-TNF-α play an important role in improving colitis,and the intestinal mucosal permeability.The mechanism may be related with the regulation of MLCK expression.

Objective To investigate the effects of limb ischemic post-conditioning (LIpostC) alone or its combination with therapeutic hypothermia (TH) on systemic inflammatory response and lung injury after cardiac arrest (CA) and resuscitation. Methods Twenty-one healthy male pigs weighing (37±2) kg were randomly divided into 3 groups (n = 7 each): control group, LIpostC group, and LIpostC+TH group. The animal model was established by 10 minutes of untreated CA and then 5 minutes of cardiopulmonary resuscitation (CPR).Coincident with the start of CPR, LIpostC was induced by four cycles of 5 minutes of limb ischemia followed by 5 minutes of reperfusion in the LIpostC and LIpostC+TH groups. After successful resuscitation, TH was implemented by surface cooling to reach a temperature of 32-34℃ until 4 hours post-resuscitation, followed by a re-warming rate of 1 ℃/h for 4 hours in the LIpostC+TH group. Normal temperature was maintained in the control and LIpostC groups. The resuscitation outcomes in each group were recorded during CPR. At 15 minutes prior to CA (baseline) and during 4 hours post-resuscitation, the level of arterial lactate was measured and PaO2/FiO2 was calculated, and extra-vascular lung water index (EVLWI) and pulmonary vascular permeability index (PVPI) were measured meanwhile by a PiCCO monitor. At 15 minutes prior to CA (baseline) and during 24 hours post-resuscitation, the levels of serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured by enzyme linked immunosorbent assay (ELISA). Results Six animals in each group were successfully resuscitated. Coronary perfusion pressure (CPP), duration of resuscitation, number of shocks and epinephrine dosage during CPR were not statistically significant among the three groups. The baseline of arterial lactate, PaO2/FiO2, EVLWI, PVPI and cytokines prior to CA were also not statistically significant among the three groups. The levels of serum TNF-α and IL-6 after resuscitation were gradually increased in all the three groups; however, the values of TNF-αand IL-6 were significantly lower in the LIpostC and LIpostC+TH groups than that in the control group, and they were further decreased in the LIpostC+TH group when compared to the LIpostC group [TNF-α (ng/L): 305±22 vs. 343±26 at 4 hours, 350±29 vs. 389±18 at 24 hours; IL-6 (ng/L): 239±14 vs. 263±19 at 24 hours, all P < 0.05]. The levels of lactate reached the peak at 2 hours post-resuscitation and then gradually decreased in all the three groups; it finally returned to the baseline in the LIpostC and LIpostC+TH groups, which was markedly lower than that in the control group (mmol/L: 1.4±0.7, 1.2±0.3 vs. 3.1±1.7, both P < 0.05). During 4 hours post-resuscitation, PaO2/FiO2 was significantly higher and EVLWI and PVPI were markedly lower in the LIpostC and LIpostC+TH groups than that in the control group; additionally, PaO2/FiO2 and EVLWI were further improved in the LIpostC+TH group than the LIpostC group [4-hour PaO2/FiO2 (mmHg, 1 mmHg = 0.133 kPa): 391±26 vs. 361±20; 4-hour EVLWI (mL/kg): 10.1±1.5 vs. 12.1±1.2, both P < 0.05]. Conclusion LIpostC can be used to alleviate systemic inflammatory response and lung injury after porcine CA and CPR, and its combination with TH further enhanced its protective effects.

Objective To evaluate the effects of hypothermia on Ca2+∕calmodulin-dependent pro-tein kinase Ⅱ ( CaMKⅡ) and cell autophagy in brain tissues after cardiac arrest and cardiopulmonary re-suscitation ( CA-CPR) in swine. Methods Twenty-one healthy male white swine, weighing 33-40 kg, were divided into 3 groups using a random number table method: sham operation group ( group S, n=5) , CA-CPR group ( n=8) and hypothermia group ( group H, n=8) . The experimental model of CA-CPR was established in CA-CPR and H groups. The Swan-Ganz catheters were placed in the right femoral artery and vein to monitor the pressure of thoracic aorta and right atrium and body temperature and to collect blood sam-ples. A pacing catheter was advanced from the right external jugular vein into the right ventricle. Ventricu-lar fibrillation was induced by using a 1 mA alternating current through the pacing catheter. Once ventricular fibrillation was successfully induced, mechanical ventilation was discontinued for 8 min, and then CPR was initiated. Epinephrine 20 μg∕kg was intravenously injected at 2. 5 min of CPR, followed by repetition once every 3 min. Defibrillation was delivered at 5 min of CPR, and then spontaneous circulation was evaluated. If the spontaneous circulation was not restored, CPR was immediately resumed for 2 min, and then defibril-lation was delivered again. Mechanical ventilation was continued for 30 h after successful CPR. At 5 min af-ter successful resuscitation, body temperature was decreased to 33 ℃ by using a cooling blanket, then maintained at 33 ℃ until 24 h after resuscitation, and finally increased at a rate of 1℃∕h for 5 h in group H. The temperature was maintained at a normal level of 37. 5-38. 5 ℃ with the aid of a cooling blanket in S and CA-CPR groups. At 1, 6, 12, 24 and 30 h after resuscitation (T1-5), blood samples were collected from the femoral vein for measurement of the concentration of neuron specific enolase ( NSE) and S100βprotein in serum by enzyme-linked immunosorbent assay. Five animals in each group were then sacrificed, and brains were removed to determine the expression of CaMKⅡ, microtubule-associated protein 1 light chain 3 Ⅱ( LC3Ⅱ) and p62 in cerebral cortex by Western blot. Neurological deficit score was evaluated in the remaining three swine at 48, 72 and 96 h after resuscitation (T6-8) in CA-CPR and H groups. Results Compared with group S, the concentrations of NSE and S100β protein in serum were significantly in-creased at T1-5 , the expression of CaMKⅡand LC3Ⅱin cerebral cortex was up-regulated, and the expres-sion of p62 in cerebral cortex was down-regulated in CA-CPR and H groups (P<0. 05). Compared with group CA-CPR, the concentrations of NSE and S100βprotein in serum were significantly decreased at T3-5, the neurological deficit score was decreased at T6-8 , the expression of CaMKⅡand LC3Ⅱin cerebral cortex was down-regulated, and the expression of p62 in cerebral cortex was up-regulated in group H ( P<0. 05) . Conclusion The mechanism by which hypothermia alleviates brain injury after CA-CPR may be related to inhibiting CaMKⅡ activation and reducing cell autophagy in brain tissues of swine.

Objective To investigate the effects of therapeutic hypothermia (TH) on myocardial Ca2+/calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ) and cell autophagy after cardiopulmonary resuscitation (CPR) in swine.Methods Twenty healthy male domestic swine weighing 33-40 kg were randomly (random number) divided into 3 groups:sham group (n=4),CPR group (n=8) and TH group (n=8).Sham animals only underwent general preparation without experiencing cardiac arrest and resuscitation.The animal model was established by 8 min of electrically induced ventricular fibrillation and then 5 min CPR in the CPR and TH groups.Successful resuscitation was regarded as an organized rhythm with a mean arterial pressure of greater than 50 mmHg for 5 min or more.After successful resuscitation,body temperature was decreased to 33 ℃ by a cooling blanket and then maintained until 24 h post-resuscitation,and followed by a rewarming at a rate of 1 ℃/h for 5 h in the TH group.A normal temperature was maintained by the blanket throughout the experiment in the sham and CPR groups.At 6,12,24 and 30 h after resuscitation,the values of stroke volume (SV) and global ejection fraction (GEF) were measured by PiCCO,and meanwhile the serum concentrations of cardiac troponin Ⅰ (cTnI) were measured by ELISA assay and the serum activities of creatine kinase-MB (CK-MB) were evaluated by an automatic biochemical analyzer.At 30 h after resuscitation,the animals were sacrificed and left ventricular myocardium was obtained for the determination ofCaMK Ⅱ,microtubule-associated protein light chain 3 Ⅱ (LC3 Ⅱ) and p62 expressions by Western blot.The variables were compared with One way analysis of variance and then the Bonferroni test among the three groups.Results Compared with the sham group,myocardial dysfunction and injury after resuscitation were observed in the CPR and TH groups,which were indicated by decreased SV and GEF and also increased cTnI concentration and CK-MB activity in serum (all P＜0.05).Compared with the CPR group,the values of SV and GEF were significantly increased at 6 h after resuscitation,and serum cTnI concentration and CK-MB activity were significantly decreased starting 12 h after resuscitation in the TH group [SV (mL):25.0±6.9 vs 31.9±3.3 at 6 h,26.7±5.1 vs 34.6±3.7 at 12 h,28.8±3.3 vs 35.7±3.2 at 24 h,29.2±5.2 vs 36.7±3.3 at 30 h;GEF (％):17.1±2.7 vs 19.9±1.8 at 6 h,18.7±1.9 vs 21.6±1.8 at 12 h,19.3±2.3 vs 23.0±2.4 at 24 h,21.0±1.7 vs 23.7±1.7 at 30 h;cTnI (pg/mL):564±51 vs 466±56 at 12 h,534±38 vs 427±60 at 24 h,476±55 vs 375±46 at 30 h;CK-MB (U/L):803±164 vs 652±76 at 12 h,693±96 vs 557±54 at 24 h,633±91 vs 480±77 at 30 h,all P＜0.05].Tissue detection indicated that the expression of CaMK Ⅱ and LC3 Ⅱ were increased while the expression of p62 was decreased in post-resuscitation myocardium in the CPR and TH groups compared with the sham group (all P＜0.05).However,the expression of CaMK Ⅱ and LC3 Ⅱ were decreased and the expression of p62 was increased in postresuscitation myocardium in the TH group compared to the CPR group (CaMK Ⅱ:0.73±0.06 vs 0.58±0.05;LC3 Ⅱ:0.69±0.09 vs 0.50±0.07;p62:0.40±0.07 vs 0.68±0.14,all P＜0.05).Conclusion The mechanism of TH alleviating post-resuscitation myocardial dysfunction and injury may be related to the inhibition of CaMK Ⅱ expression and cell autophagy.

Objective:To investigate the risk factors and their warning value for the occurrence of sepsis in patients with severe multiple trauma.Methods:A retrospective cohort study was conducted to analyze the clinical data of 92 patients with severe multiple trauma admitted to Yuyao People′s Hospital from July 2019 to October 2021. There were 71 males and 21 females, with the age range of 36-55 years [(45.5±13.6)years]. The injury severity score (ISS) was 20-29 points [(25.3±6.4)points]. The patients were divided into sepsis group ( n=32) and non-sepsis group ( n=60) according to whether sepsis occurred during hospitalization. Data were recorded for the two groups, including gender, age, basic diseases, cause of injury, number of injury sites, ISS, post-injury complications, and levels of aryl hydrocarbon receptor (AHR), C-reactive protein (CRP) and procalcitonin (PCT) at 1, 3 and 5 days after injury. The above data were analyzed to identify their correlation with the occurrence of sepsis in patients with severe multiple trauma by univariate analysis. The independent risk factors for sepsis in patients with severe multiple trauma were determined by multivariate Logistic regression analysis. The warning value of the single or combined risk factors for the occurrence of sepsis in patients with severe multiple trauma was evaluated by the receiver operating characteristic (ROC) curve and area under the curve (AUC). Results:By univariate analysis, it was demonstrated that the occurrence of sepsis was correlated with ISS, level of AHR at day 1 after injury, level of CRP at day 3 after injury and level of PCT at day 3 after injury ( P<0.05 or 0.01), but not with age, sex, basic diseases, level of AHR at 3, 5 days after injury, level of PCT at 1, 5 days after injury and level of CRP at 1, 5 days after injury (all P>0.05). By multivariate Logistic regression analysis, higher ISS ( OR=1.12, 95% CI 1.01, 1.24, P<0.05), level of AHR at day 1 after injury ( OR=1.30, 95% CI 1.10, 1.52, P<0.01) and level of PCT at day 3 after injury ( OR=1.81, 95% CI 1.08, 3.03, P<0.05) were found to be strongly correlated with the occurrence of sepsis. ROC curve analysis showed that higher ISS (AUC=0.69, 95% CI 0.57, 0.76) and level of AHR at day 1 after injury (AUC=0.79, 95% CI 0.68, 0.90) had warning value for the occurrence of sepsis, and the warning efficiency of combined panel was much better (AUC=0.86, 95% CI 0.77, 0.95). Conclusions:Higher ISS, level of AHR at day 1 after injury and level of PCT at day 3 after injury are independent risk factors for the occurrence of sepsis in patients with severe multiple trauma. ISS, AHR and combination of both exhibit good warning value for the occurrence of sepsis in patients with severe multiple trauma.

Objective To evaluate the effect of mild hypothermia on inositol-requiring enzyme 1 (IRE1) signaling pathway during myocardial injury after cardiac arrest and resuscitation in swine.Methods Twenty-one healthy male white swine,weighing 33-41 kg,were divided into 3 groups using a random number table method:sham operation group (group S,n =5),cardiac arrest-cardiopulmonary resuscitation group (group CA-CPR,n=8),and mild hypothermia group (group MH,n=8).The model of cardiac arrest and resuscitation was established based on the previously reported method.The catheters placed in the left femoral artery and right internal jugular vein were connected to the PiCCO Monitor system,and another pacing catheter was advanced from the right external jugular vein into the right ventricle.Ventricular fibrillation was induced by using a 1 mA alternating current through the pacing catheter.Once ventricular fibrillation was successfully induced,mechanical ventilation was discontinued for 8 min,and then cardiopulmonary resuscitation was initiated.Epinephrine 20 μg/kg was administered at 2.5 min of resuscitation followed by repetition every 3 min.Defibrillation was delivered at 5 min of resuscitation,and then spontaneous circulation was evaluated.If return of spontaneous circulation was not achieved,cardiopulmonary resuscitation was immediately resumed for 2 min and then defibrillation was delivered again.Mechanical ventilation was continued for 30 h after successful resuscitation.Animals in group S only underwent surgical preparation without experiencing cardiac arrest and resuscitation.At 5 min after successful resuscitation,body temperature was cooled down to 33 ℃ by using a cooling blanket,and then maintained at this level until 24 h after resuscitation,followed by 5 h of re-warming at a rate of 1 ℃/h in group MH.The temperature was maintained at 37.5-38.5 ℃ with the aid of surface cooling blanket in the other two groups.At 1,6,12,24 and 30 h after resuscitation (T1-5),the values of stroke volume (SV) and global ejection fraction (GEF) were recorded,and meanwhile 2 ml of blood samples was obtained via the femoral vein to measure the concentration of serum cardiac troponin Ⅰ (cTnI) (by enzyme-linked immunosorbent assay) and activity of serum creatine kinase-MB (CK-MB) (by immunosuppression).The swine were sacrificed at 30 h after resuscitation,and then myocardial specimens from the left ventricle were obtained for determination of the expression of caspase-3 (by immunohistochemistry),cell apoptosis (by TUNEL),and expression of IRE1 and casepase-12 (by Western blot).Apoptosis index was calculated.Results Compared with group S,SV and GEF were significantly decreased and the serum CK-MB activity was increased at T1-5,the concentration of serum cTnI was increased at T2-5,the expression of IRE1,caspase-12 and caspase-3 in myocardium was up-regulated,and apoptosis index was increased in CA-CPR and MH groups (P＜0.05).Compared with group CA-CPR,the SV and GEF were significantly increased and the concentration of serum cTnI was decreased at T2-5,the activity of serum CK-MB was decreased at T3-5,the expression of IRE1,caspase-12 and caspase-3 in myocardium was down-regulated,and apoptosis index was decreased in group MH (P＜0.05).Conclusion The mechanism by which mild hypothermia mitigates myocardial injury after cardiac arrest and resuscitation may be related to inhibiting IRE1 signaling pathway in swine.