Objective To study the clinical changes of von Willebrand factor( vWF) and interleukin-8 (IL-8) in patients with severe pulmonary contusion. Methods Sixty-three patients with severe pulmonary contusion were divided into three different classifications for the sake of comparison in different respects, namely (1) severe pulmonary contusion with ARDS group and severe pulmonary contusion without ARDS group, (2) survival group and non-survival group, and (3) ISS score <20 group and ISS scored 20 group. In addition, the normal control group was set up. The levels of plasma vWF and serum IL-8 were respectively detected by double-antibody sandwich enzyme-linked immunosorbent assay (ELISA) within 24 hours of injury and 1,3,5 and 7days after injury. The regularity of their changes was observed and the correlation factors were analyzed from the data. Results Compared with normal controls, the concentrations of plasma vWF and serum IL-8 were significantly increased in patients with severe pulmonary contusion in all intervals of detection. The concentrations of plasma vWF escalated gradually in severe pulmonary contusion with ARDS, and reached significantly higher levels in 5 days and 7 days after injury compared with those without ARDS group (P <0. 05). The increase in concentrations of serum IL-8 peaked in 5day after injury, and then declined. The levels of serum IL-8 were higher in patients with severe pulmonary contusion with ARDS group than those in this kind of patients without ARDS group. The levels of plasma vWF and serum IL-8 were higher in non - survival group than those in survival group (P < 0.05). The increase in levels of plasma vWF and serum IL-8 peaked and then declined in 5 days in ISS score 3:20 group, whereas it peaked and declined in 3 days after injury in ISS score < 20 group. The level of plasma vWF was positively correlated with platelets and negatively correlated with oxygenation index. The levels of serum IL-8 was positively correlated with white blood cell count and ISS score, and negatively correlated with oxygenation index. Conclusions The levels of plasma vWF and serum IL-8 were increased in patients with severe pulmonary contusion, reflecting the severity of pulmonary injury. The levels of plasma vWF and serum IL-8 were the sensitive markers for evaluating the severity of pulmonary injury and the prognosis of ARDS caused by severe pulmonary contusion.

Objective To evaluate the effect of interventional vas embolism operation at ICU bedside in severe pelvis fracture patients complicated with hemorrhagic shock. Method Forty-eight severe pelvis fracture patients with hemorrhagic shock were treated by interventional vas embolism operation at bedside as well as intensive monitoring. The clinical results were compared with those of the traditional conservative therapy group. Results In the interventional therapy group, 46 patients with hemorrhage had been controlled within an hour after the operation and the success ratio reached 95.8%. The blood transfusion volume, the complication incidence and mortality rate were all significantly lower than those of the conservative therapy group. Conclusion Interventional vas embolism operation at ICU bedside is a safe, practical and effective treatment on pelvis fracture with iliac vas trauma.

OBJECTIVE: To determine the effect of tetramethylpyrazine (TMP) on the expression of migration inhibitory factor (MIF) in acute spinal cord injury (ASCI) in rats. METHODS: Allen's weight-drop method was used to establish a rat model of ASCI at T10. A total of 110 adult SD rats were divided into a sham operation group (group S, n=10), a control group (group C, n=50), and a TMP group (group T, n=50). Spinal cord functionality was measured by a modified Rivilin loxotic plate degree, BBB score, and combined behavioral score (CBS) at 1, 3, 5, 7, 14 and 21 d postoperatively. The injured spinal cord tissue samples were harvested at 1, 3, 6, 12 h and 1, 3, 5, 7, 14, 21 d postoperatively (n=5 at each time point) and used to prepare continuous histological sections, in which the expression of MIF was analyzed by immunohistochemistry. RESULTS: The degree in group T measured by modified Rivlin loxotic plate test after the ASCI was significantly higher than that in group C at 7, 14, and 21 d (P<0.05). BBB score in group T was significantly higher than that in group C at 5, 7, 14, and 21 d after the ASCI (P<0.05). CBS score in group C was significantly higher than that in group T at 5, 7, 14, and 21 d after the ASCI (P<0.05). The significantly low number of MIF positive cells was shown in group T when compared with that in group C at 12 h and 1, 3, 5, 7 d after the ASCI (P<0.05). As time passed, there was negative correlation between modified Rivlin loxotic plate degree and MIF expression and also between BBB score and MIF, and there was positive correlation between CBB score and MIF expression. CONCLUSION TMP has protective effect after the ASCI, and may promote the repair of injured spinal cord tissues. TMP may decrease the MIF expression in cells after the ASCI.
Animals ; Immunohistochemistry ; Intramolecular Oxidoreductases ; metabolism ; Macrophage Migration-Inhibitory Factors ; metabolism ; Pyrazines ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Injuries ; metabolism

Objective To analyse the risk factors for postoperative infection in traumatic tibial plateau fractures and to construct a Nomogram prediction model.Methods One hundred and forty-eight patients with traumatic tibial plateau fractures who underwent surgery in our hospital from October 2019 to August 2021 were selected for the study,and were divided into an infected group(n=20)and an uninfected group(n=128)according to whether they developed infection after surgery.The general data of the two groups were compared;the predictive value of statistically significant continuous variables was analysed using the ROC experiment;the risk factors affecting postoperative infection in traumatic tibial plateau fractures were analysed using the logistic regression experiment;and the clinical efficacy of the Nomogram model was verified using internal data.Results In the comparison of general data such as age and gender between the two groups,the differences were not statistically significant(P＞0.05).Compared with the uninfected group,patients in the infected group had a higher percentage of diabetes mellitus,open fracture type,and osteofascial compartment syndrome,and longer operative time and hospital stay(P＜0.05);diabetes(yes),fracture type(open),osteofascial compartment syndrome(yes),and operative time(＞3 h)were risk factors affecting postoperative infection in traumatic tibial plateau fractures.The AUCs for operative time and hospital stay were not 0.792 and 0.651;the optimal stage values were not 3 h and 13 d(P＜0.05);the Nomogram model predicted a C-index of 0.744(0.651-0.807)for the risk of postoperative infection in traumatic tibial plateau fractures.The model predicted the risk of infection after traumatic tibial plateau fracture at a threshold of＞0.09.Conclusion Diabetes mellitus(yes),fracture type(open),osteofascial compartment syndrome(yes),and operative time(＞3 h)were risk factors affecting postoperative infection in traumatic tibial plateau fractures,and the Nomogram model constructed based on the above variables had good predictive value.

Objective To explore the underlying mechanism of β2 adrenergic receptor(ADRB2)in fibrogenesis during wound healing.Methods Non-specific ADRB2 gene knockdown adeno-associated virus(AAV-ADRB2 group,6 mice)and control virus(AAV-NC group,6 mice)was injected randomly into the back skin of 12 mice for 21 days,a full-thickness skin defected wound healing murine model was established.Wound healing rates were recorded at the 1st,3rd,5th,and 7th day after operation.Histological examinations by H-E staining,Masson staining,and immunohistochemistry were conducted to observe wounded skin tissue structure,fibrosis,and α-SMA protein expression;quantitative PCR was employed to analyze ADRB2 and matrix metalloproteinase(MMP)mRNA levels;Western blotting was utilized to assess the protein expression levels of COL1A1,COL3A1,TGF-β1,and Smad3.Results On postoperative day 5 and 7,the wound healing rate of the AAV-ADRB2 group significantly decreased(P＜0.05),accompanied by a series pathological changes,including thickened epidermis,exaggerated inflammation,reduced fibroblast count,and inhibited collagen deposition;the α-SMA expression showed a significant decrease(P＜0.05),and the ratio of COL1A1 to COL3A1 decreased(P＜0.05);ADRB2 mRNA levels significantly decreased(P＜0.01),while MMP-1 and MMP-8 mRNA levels increased(P＜0.01);the protein levels of TGF-β1 and Smad3 exhibited a significant decrease(P＜0.05).Conclusions ADRB2 knockdown reduced fibrosis during wound healing and degenerated connective tissue content around the wound bed by inhibiting the TGF-β1/Smad3 signaling pathway,which leads to an increase in MMP mRNA levels and a decrease in the ratio of type Ⅰ to type Ⅲ collagen.

OBJECTIVETransesophageal echocardiography was performed during closed-chest cardiopulmonary resuscitation (CPR) in in-hospital cardiac arrest to further explore the hemodynamic mechanism of CPR.

METHODSCPR attempts were performed according to advanced cardiovascular life support guidelines in 6 cases of in-hospital cardiac arrest. Multi-plane transesophageal echocardiography was carried out within 15 min of initiation of CPR. Throughout CPR, the motion of the mitral, tricuspid and aortic valves, the changes in the left ventricular cavity size and the thoracic aortic diameter were observed. Trans-mitral and trans-aortic Doppler files of blood flow were also documented.

RESULTSA closure of the mitral and tricuspid valves with simultaneous opening of the aortic valve occurred exclusively during chest compression, resulting in forward blood flow in the pulmonary and systemic circulation. Peak forward aortic flow at a velocity of 58.8 +/- 11.6 cm/s was recorded during the compression phase. Whereas, a closure of the aortic valve and rapid opening of the atrioventricular valves associated with ventricular filling during relaxation of chest compression was noted in all 6 patients. Peak forward mitral flow at a velocity of 60.6 +/- 20.0 cm/s was recorded during the release phase. Mitral regurgitation during the chest compression period was detected in 5 patients, reflecting a positive ventricular-to-atrial pressure gradient. A reduction in the left ventricular chamber and an increase in the thoracic aortic diameter during the compression phase was found in all patients, indicating that direct cardiac compression contributed to forward blood flow.

CONCLUSIONThese observations favor the cardiac pump theory as the predominant hemodynamic mechanism of forward blood flow during CPR in human beings.

Aged ; Aged, 80 and over ; Cardiopulmonary Resuscitation ; Echocardiography, Transesophageal ; Female ; Heart Arrest ; diagnostic imaging ; physiopathology ; therapy ; Hemodynamics ; Humans ; Male ; Middle Aged

Objective: To investigate the expression of microRNA-133b (miR-133b) in esophageal squamous cell carcinoma (ESCC), and explore its effect and the underlying molecular mechanisms on cell proliferation and invasion. Methods: Real-time quantitative PCR (qPCR) was used to examine miR-133b expression in 63 ESCC tissues and paired adjacent non-cancerous tissues, several ESCC cells (Eca109, EC9706, EC1, TE1, KYSE70) and normal esophageal epithelial cell Het-1A. MiR-133b mimic, inhibitor and negative control (NC) were transfected into TE1 cells. The effect of miR-133b on cell proliferation and invasion were determined by CCK-8 and Transwell assays, respectively. Subsequently, the target gene of miR-133b was predicted by online tools TargetScan and miRDB, which was verified by dual luciferase reporter assays. Finally, Western blot was utilized to detect the effects of miR-133b overexpression on expression of target gene TAGLN2 as well as EMT-related proteins E-cadherin, N-cadherin, Snail, Slug and Vimentin. Results: Relative levels of miR-133b in ESCC tissues (0.295±0.040) were significantly lower than those in adjacent non-cancerous tissues (1.002±0.011, P<0.001). The expression of miR-133b was tightly associated with clinical staging, lymph node metastasis and prognosis. Moreover, relative levels of miR-133b in ESCC cells Eca109, EC9706, EC1, TE1 and KYSE70 (0.679±0.031, 0.391±0.008, 0.236±0.016, 0.031±0.005 and 0.099±0.020) were evidently lower than that in normal esophageal epithelial cell Het-1A (1.005±0.016, all P<0.001). In TE1 cells, miR-133b mimic significantly increased the level of miR-133b to 6.199±0.627, and suppressed cell proliferation and invasion, whereas miR-133b inhibitor obviously decreased its expression to 0.182±0.023, and promoted cell proliferation and invasion. Most notably, the relative luciferase activities of miR-133b-mimic group (0.320±0.018) in TE1 cells transfected with TAGLN-3′UTR-WT were markedly lower than that in NC group (1.010±0.036, P<0.001), whereas those in TAGLN-3′UTR-MUT transfection cells were 1.019±0.056 and 1.008±0.021, respectively, showing no significantly statistical difference (P>0.05). Furthermore, miR-133b overexpression markedly downregulated TAGLN2, N-cadherin, Snail, Slug and Vimentin levels, and increased E-cadherin expression. Conclusion MiR-133b plays an important role in the proliferation and invasion of ESCC cells by regulating TAGLN2 expression, and it may be a potential therapeutic target for ESCC patients.