CT findings and complete clinical data of 185 cases with closed chest injuries were retrospectively analyzed.The diagnosis of 185 cases were pulmonary contusion ( n = 185 ),pulmonary laceration ( n = 35 ),Macklin effect ( n = 5 ) and lung herniation ( n = 1 ).CT findings of lung contusion appeared as thick and vagur lung marking (n =9),small points shadows (n = 12 ),blotchy shadows (n =48),small pieces shadows (n=10),ground-glass shadows (n=16),large pieces shadows (n =5),diffuse patchy clouding shadows (n = 17) or mixed lesions (n = 68).CT appearance of lung laceration included pulmonary hematomas (n = 12),cavitary lesions with air ( n = 19),cavitary lesions with air-fluid levels ( n = 53 ).Macklin effect appeared as bronchus-,pulmonary vessel-adjacent air collection and mediastinal air collection (n=5).Traumatic pulmonary hernia appeared as lung herniation through an intercostal space.Initial CT scan missed one case of pulmonary contusion and 2 cases of pulmonary laceration.

Osteoarthritis is a chronic disabling disease that tends to occur in middle-aged and elderly population, the main pathological characteristics are the dynamic imbalance between the synthesis and degradation of articular chondrocytes, extracellular matrix and subchondral bone. The occurrence and development is related to many factors. This article reviews the structure, the function and the interaction between α2-macroglobulins and a disintegrin and metallo-proteinase with throm-bospondin motifs in the development of osteoarthritis.

Osteoarthritis (OA) is a kind of chronic and frequently-occurring disease in the elderly.It is also called degenerative disease.Pain,stiffness,swelling,deformity and dysfunction of joints are the main clinical manifestations,which seriously affect the quality of life.Kaschin-Beck Disease (KBD) is a kind of endemic diseases;its main feature is cartilage degeneration and necrosis.Although KBD becomes a typical OA in late stage,it is different from OA.Osteoprotegerin (OPG) and insulin-like growth factor (IGF)-1 participate in the bone growth,repair,and alteration.In this paper,we summarized clinical manifestations and pathological changes of OA,and reviewed the current situation and development of OPG and IGF-1 in OA bone remodeling.

Objective To investigate the risk factors for sensorineural hearing loss (SNHL) in patients with nasopharyngeal carcinoma (NPC) after intensity-modulated radiotherapy (IMRT).Methods From January 2012 to January 2013,29 patients with histopathologically confirmed NPC who received radiotherapy alone or concurrent chemoradiotherapy were included in this study.All patients underwent hearing tests,including pure tone audiometry and acoustic immittance measurement,before and after the IMRT.The cochlear doses for each ear were also collected for analysis.A prospective analysis was performed to investigate the relationship between cochlear dose and SNHL in patients with NPC,and the effects of other factors,including time after radiotherapy,chemotherapy,T stage,and age,were also analyzed.Results Of the 58 ears studied,6(10％) had low-frequency SNHL,and 17 (29％) had highfrequency SNHL.There were significant differences in mean cochlear doses between the patients who developed SNHL after radiotherapy and those who did not (left ears:46.1 Gy vs.35.5 Gy,P =0.006;right ears:45.0 Gy vs.35.8 Gy,P =0.009).When the mean cochlear dose was less than 44 Gy,only 15％ (6/38) of ears had high-frequency SNHL.The invasion of skull base bone was also a significant risk factor for SNHL(P =0.047),but age,chemotherapy,and time after IMRT were not significant risk factors.Conclusions The mean cochlear dose and invasion of skull base bone are significant risk factors for SNHL in patients with NPC after radiotherapy.It is recommended that the mean cochlear dose should be limited to 44 Gy to minimize the incidence of SNHL after IMRT.

Objective To study the pathogenesis of upper gastrointestinal rehaemorrhagia after the transjugular intrahepatic portasystemic shunt (TIPS) and its influencing factor.Methods Fifty postoperative patients with TIPS were selected.The patients were followed-up,and the effect of the various factors in the role of upper gastrointestinal rehaemorrhagia after TIPS was analyzed.Results The portal vein pressure of 50 patients with TIPS decreased from preoperative (39.8 ±9.2) cmH2O (1 cmH2O =0.098 kPa) to postoperative (25.2 ± 5.8) cmH2O,and there was statistical difference (P ＜ 0.05).Fourteen patients appeared upper gastrointestinal rehaemorrhagia after TIPS,which accounted for total of 28％ (14/50) and included 3 cases of postoperative vomiting blood within 3 days.Acute stomach mucosa lesions bleeding was considered,and bleeding was controlled within a short-term medical treatment (1 patient after more than a year in recurrent upper gastrointestinal rehaemorrhagia).Twelve cases of patients appeared upper gastrointestinal rehaemorrhagia within 2 years after TIPS,and the causes of rehaemorrhagia in 6 cases were esophageal variceal rehaemorrhagia,gastric and duodenal ulcer in 3 cases,erosive gastritis in 2 cases,coagulation abnormalities in 1 case.Esophageal variceal rehaemorrhagia rate was 12％ (6/50).Conclusions The main reasons of upper gastrointestinal rehaemorrhagia after TIPS are variceal rehaemorrhagia and non variceal rehaemorrhagia,both of which are important causes of rehaemorrhagia after TIPS.Variceal rehaemorrhagia after TIPS occurs more than 3 months,and non variceal rehaemorrhagia occurs within 3months,so it is very important to protect gastric mucosa with proton pump inhibitor in postoperative patients.

OBJECTIVE To strengthen and explore the effect of target monitoring in ICU.METHODS To put out prospectively the target monitoring of the nosocomial infection in ICU from Jan 2006 to Dec 2007.RESULTS A total of 3917 patients were monitored and 217 of them suffered from infection.The day infection rate was 11.7‰,and the infection rater per thousand day were 13.4‰,10.0‰ in 2006 and 2007,respectively.The infection rate related to urinary catheter,central venous catheter and ventilator were 1.2‰,0.9‰,4.1‰,2.8‰,14.2‰,6.0‰ in the past two years,respectively.It decrease 0.3‰,1.3‰,8.2‰,respectively.Ventilator-associated infection was the main infection part of hospital infection,and the patients after liver transplantation ICU had the highest infectionrate.CONCLUSIONS Prospective target monitoring is a scientific monitoring method that plays an important role in controlling and preventing hospital-acquired infection.It deserves recommendation.

OBJECTIVE: To study the influence of PD173074 on proliferation and apoptosis of nasopharyngeal carcinoma. METHOD: With immunoblotting and RT-PCR, FGFR1 expression was detected in CNE, PONE1 and C666-1 cell lines. With MTT assay,the time-effect and dose-effect correlation between PD173074 and inhibition of CNE proliferation was evaluated. After PD173074 stimulation, the phosphorylation level of FGFR1 and AKT was detected with immunoblotting assay. Furthermore, influence of PD173074 on the activation of Caspase3 and Caspase9 was detected to study the underlying mechanism of why PD173074 could inhibit CNE proliferation. RESULT: FGFR1 has the highest expression in CNE cell line. Under incubation of 10 nmol/L PD173074 stimulation for 36 hours to 72 hours, the phosphorylation of FGFR1 and AKT was impaired significantly, which further reduced the proliferation of CNE. Moreover, PD173074 can activate the intrinsic apoptotic pathway by stimulating Caspase9,which activated Caspase3 and induced the apoptosis. CONCLUSION PD173074 could inhibit proliferation of nasopharyngeal carcinoma cell through reducing the phosphorylation of FGFR1 and AKT. Additionally, PD173074 can induce CNE apoptosis by activating intrinsic apoptotic pathway via cleaving Caspase9 and Caspase3.
Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Carcinoma ; Caspase 3 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; Humans ; Nasopharyngeal Carcinoma ; Nasopharyngeal Neoplasms ; drug therapy ; pathology ; Pyrimidines ; pharmacology

[Objective]This study was conducted to examine the effects of dexmedetomidine on the proliferation and angiogenesis of MHCC97H and SMCC7721 human hepatocellular carcinoma(HCC)cell lines cultured in hypoxia condition in vitro,and investigated the possible mechanism involved.[Methods]MHCC97H and SMCC7721 human HCC cell lines under hypoxia culture condition were treated with presence or absence of dexmedetomidine(100 μmol/L). Cell viability,colony formation,vasculogenic mimicry(VM) formation were assessed. The effects of dexmedetomidine on α-2A adrenergic receptor(α2A),hypoxia induced factor-1a(HIF-1a),and vascular endothelial growth factor(VEGF)protein expression were evaluated with Western blot analysis.[Results]Cell proliferation assay and colony formation assay indicated that hypoxia obviously promoted the proliferation of MHCC 97H and SMCC7721 cells(CoCl2 group vs corresponding control group,the proliferation rate of MHCC97H and SMCC7721:Day 3,142.2%and 133.8%;Day 4,134.7%and 131.0%;Day 5,133.5%and 136.2%;all P<0.05),and VM formation assay suggested that hypoxia increased angiogenesis of MHCC97H and SMCC7721 cells. Whereas dexmedetomidine significantly inhibited the proliferation(Dex+CoCl2 group vs CoCl2 group,the proliferation rate of MHCC97H and SMCC7721:Day 3,55.7%vs 60.7%;Day 4,46.9%vs 58.1%;Day 5,46.4%vs 57.0%,all P<0.05)and angiogenesis of MHCC97H,SMCC7721 cells induced by hypoxia. Dexmedetomidine may exert these functions by activating α-2A adrenergic receptor,causing an decrease in HIF-1a and VEGF protein,while hypoxia activated HIF-1a and VEGF protein to promote the growth and angiogenesis of cells.[Conclusion]The findings provide evidence that hypoxia could promote the proliferation and angiogenesis of MHCC97H and SMCC7721 cells,while dexmedetomidine might inhibit these effects by down-regulating HIF-1a and VEGF protein expression through activatingα-2A adrenergic receptor.

Objective To determine the random spot albuminuria to creatinine ratio (ACR) of normal pregnant women , to track the pregnancy outcome , and to discuss the predictive value of ACR in women with hy-pertensive disorders complicating pregnancy (HDCP). Methods Except for 87 pregnant women suffering from HDCP, 2 038 pregnant women were enrolled in this study. ACR, routine examinations of blood and urine, blood biochemical, 24-hr urinary protein were determined. Results ACR, but not 24-hr urinary protein level,was sig-nificantly higher in women with HDCP. There was positive correlation between the ACR and 24-hr urinary protein quantitation. Age, gestational weeks, ACR, red blood cells, fasting plasma glucose, serum creatinine, total pro-tein were the independent risk factors for HDCP. The sensitivity , specificity and optimal cut off value of ACR for predicting HDCP were 0.78, 0.63, 1.46 mg/mmol. Conclusions There was positive correlation between ACR and 24-hr urinary protein quantitation , and ACR provided a more sensitive pathway for early predictionof HDCP.

AIM:ToobservetheeffectofcepharanthineonhumanlungadenocarcinomaLTEP-a-2cellgrowth, and to explore the changes of related microRNA ( miRNA) expression in the cells .METHODS:LTEP-a-2 cells were trea-ted with cepharanthine at concentrations of 0μmol/L, 10μmol/L, 20μmol/L and 40μmol/L.The growth inhibition rate was detected by MTT assay , and the cell morphological changes were observed under light microscope .The cell apoptosis was analyzed by flow cytometry .The expression of let-7c, miR-34a and miR-34b was measured by real-time PCR.RE-SULTS:Cepharanthine inhibited the cell activity of LTEP-a-2 cells in a dose-dependent manner .With the increase in cepharanthine concentration , the pyknosis of the cells was visible under the inverted microscope .Flow cytometry analysis found that different concentrations of cepharanthine induced the increase in the apoptotic rates of LTEP -a-2 cells.The re-sults of real-time PCR showed that the cepharanthine also increased the expression of let -7c, miR-34a and miR-34b.CON-CLUSION:Cepharanthine inhibits the growth of LTEP-a-2 cells, and induces apoptosis .Cepharanthine increases the ex-pression of let-7c, miR-34a and miR-34b, indicating that these miRNAs in LTEP-a-2 cells has the function as tumor sup-pressor genes .