Objective To study the value of color Doppler ultrasound in diagnosis of deep vein thrombosis (DVT) of lower extremity and pulmonary embolism (PE) in spinal cord injury (SCI). Methods 60 PE patients (PE group) and 35 SCI patients without PE (control group) received color Doppler ultrasound examination for DVT of lower extremity. Results PE group included 36 SCI patients (PE-SCI group) and 24 no-SCI patients (PE-no-SCI group). There were 15 cases with lower extremity thrombosis in PE-SCI group, and 9 cases in PE-no-SCI group (P>0.05), while there were 5 cases in the control group. There was significantly different in lower extremity thrombosis between PE group and the control group (P<0.01). In PE group, the detection rate was not significantly different between acute PE (detected 11 cases out of 37 cases) and chronic PE (detected 10 cases out of 23 cases) (P>0.05). 31 cases were rechecked as lower extremity venous valve regurgitation and calf muscle vein dilation (51.7%) in PE group while 8 cases in the control group (22.9%) (P<0.01). Conclusion There is not significantly different in the detection rate of DVT of lower extremity in PE patients with and without spinal cord injury, which are higher than in the patients without PE. Color Doppler ultrasound is necessary to check DVT in acute and chronic PE patients.

Objective To investigate expressional pattern of the Connexin 43 in atrial myocytes of ventricular septal defect children. Methods The expressional role of the Connexin 43 in atrial myocytes of ventricular septal defect children were observed and determinated by immunohistochemistry and digital image analysis technology. Results 1.The Connexin 43 granules of 1-3 year-old-group normal children were mainly distributed on cell side surface,which took on beening spot-,belt-or chain-shaped,but seldom at intercalated disks. The Connexin 43 of 7-16 year-old-group normal children were abundantly distributed on cell side surface and intercalated disks. 2.The Connexin 43 of 1-3 year-old-group ventricular septal defect children were not noly distributed on cell side surface but could be detected at intercalated disks and cytoplasm,a few granules were irregular in arrangement.The Connexin 43 of 7-16 year-old-group ventricular septal defect children were distributed on cell side surface and in cytoplasm but seldom existed at intercalated disks,and arranged in irregular order. 3.The experimental results showed insignificant difference in the expressional amount of the Connexin 43 in atrial myocytes between the ventricular septal defect children and normal children. Conclusion The Cx 43 distributional pattern in atrial myocytes of ventricular septal defect children was changed,but its expressional amount was indistinct,which suggested that ventricular septal defect affected only the Cx43 expressional pattern.

Objective To systematically evaluate the clinical efficacy of Lanqin Oral Liquid(LOL)and ribavirin on infantile hand-foot-mouth disease(HFMD).Methods The randomized controlled trials(RCT)of LOL and ribavirincombined for treating HFMD were retrieved from EMbase, PubMed, CNKI, CBM and VIP(from establish to Oct 2014), the methodological quality of included literature was evaluated, and data analyses were performed with RevMan 5.2 software.Results Fifteen studies involving 2 016 patients were ultimately identified.The meta-analysis results showed that the effective rate of LOL group was superior to that of the control,OR(95%CI)was 5.80 (3.94, 8.52), and there were significant differences in the antifebrile time, erythra regression time, herpes regression time and oral ulcer regression time between the groups,MD (95%CI): -1.29 (-1.45,-1.13), -1.88 (-2.44,-1.33), -1.57 (-2.36,-0.78), -1.57 (-2.07,-1.08), respectively. Conclusion Based on the present clinical evidence, the meta-analysis results indicate that LOL and ribavirin treating HFMD is effective and safe. However, due to the uneven quality of these included studies, this conclusion need more large sample size and high-quality clinical RCTs to be confirmed.

Objective: To observe the protective roll of atorvastatin on post-operative cardiac remodeling induced by transverse aortic constriction (TAC) in experimental mice with its possible mechanism.
Methods: A total of 48 C57BL/6 mice were randomly divided into 4 groups: Sham group, TAC group, TAC + valsartan group and TAC + atorvastatin group,n=12 in each group. Myocardial hypertrophy model was successfully established at 4 weeks after the operation, and then the animals were further treated by normal saline, valsartan 5mg/kg and atorvastatin 10mg/kg respectively for 8 weeks. Left ventricular anterior wall thickness at diastole (LVAWd), left ventricular posterior wall thickness at diastole (LVPWd), LVEF and left ventricular fractional shortening (FS) were examined by echocardiography, cardiac hypertrophy indexes were calculated. Protein expression of NF-κB was detected by Western blot analysis, cardiac tissue hydroxyproline (Hyp) level was measured by alkaline hydrolysis, serum levels of TNF-α, IL-1β were determined by ELISA, cardiac collagen deposition was identiifed by HE and Masson staining.
Results: Compared with Sham group, TAC group had increased LVAWd, LVPWd, cardiac hypertrophy indexes and increased area of cardiac fibrosis, allP<0.01; elevated protein expressions of NF-κB, Hyp, TNF-α, IL-1β, all P<0.01. Compared with TAC group, TAC + valsartan group and TAC + atorvastatin group presented improved cardiac hypertrophy indexes, decreased LVAWd, LVPWd and decreased area of cardiac ifbrosis, allP<0.01; reduced protein expressions of NF-κB, Hyp, TNF-α, IL-1β, allP<0.01.
Conclusion: Atorvastatin had protective roll on myocardial hypertrophy induced by pressure overload in experimental mice, which might be related to its anti-inlfammatory effect.

Objective To study the inhibitory effects of TPP,a desmosdumotin-C B ring para-fluoro modified derivative,on human breast cancer MCF-7 cell proliferation,and investigate the possible mechanisms.Methods MTT assay was used to measure the proliferation suppression of MCF-7 cells after treated with 1.0,2.5,5.0,10.0,and 20.0 μg/mL TPP for 48 h,and then the cell apoptosis rate and expression rate of NF-κB P65 positive cells were tested by flow cytometry after 20.0 μg/mL TPP treatment for 0,24,and 48 h.Results MTT assay showed that,after treatment for 48 h,1.0,2.5,5.0,10.0,and 20.0 μg/mL TPP all exhibited the inhibitory effects and showed a dose-dependent relationship.Flow cytometry results showed that 20.0 μg/mL TPP induced cell apoptosis after treatment for 24 and 48 h.TPP (20.0 μg/mL) significantly reduced the rate ofNF-κB P65-positive cells in MCF-7 cells after treatment for 48 h.Conclusion TPP could inhibit the proliferation of MCF-7 cells,which may be induced by cell apoptosis.Down-regulation of NF-κB is possible to be related with apoptosis.

Objective To construct the risk model for healthcare-associated infection (HAI)with multidrug-re-sistant organisms(MDROs)in intensive care unit (ICU).Methods 836 patients who were admitted to ICU for more than 48 hours between October 2012 and September 2015 were analyzed retrospectively,logistic regression model of HAI was constructed,the model was conducted goodness of fit tests and the area under ROC curve analysis. Results Among 836 patients,incidence of HAI with MDROs was 14.23%(n=119).15 variables that were statis-tically significant in univariate analysis were included in logistic multivariate analysis,the results showed that the following variables entered into logistic regression equation:length of ICU stay (OR,2.493 [95%CI ,1 .816 -3.494]),underlying diseases (OR,1 .536 [95%CI ,1 .243 - 1 .898 ]),hypoproteinemia (OR,87.211 [95%CI , 36.165-210.304]),ventilator days (OR,1 .723 [95%CI ,1 .399-2.121 ]),fever(OR,20.639 [95%CI ,3.462 -123.043]),and primary pulmonary infection (OR,0.295 [95%CI ,0.133 -0.664]).Evaluation of model effect:sensitivity 95%,specificity 87.9%,the area under ROC curve 0.973.Conclusion Logistic regression model has a high goodness of fit in predicting HAI among ICU patients.

Objective To investigate the characteristics of sleep structures in patients with multiple dreams through the retrospective analysis of polysomnography in patients with multiple dreams,and to provide a theoretical basis for the treatment of multiple dreams.Methods Twenty-two cases with multiple dreams in Department of Neurology,the People's Hospital of Zhengzhou University from July 2015 to Ferbuary 2018 were included in multi-dream group and 12 healthy people in control group.The sleep parameters related to polysomnography during the visit were collected and recorded,and the differences between the two groups were compared.Resluts There was no statistically significant difference in apneahypopnea index,sleep latency,rapid eye movement (REM) sleep latency,slow-wave sleep ratio,and REM-arousal index between the two groups.Compared with the control group,sleep efficiency (73.46％ ± 12.41％ vs 90.43％ ± 4.42％,t=-4.555,P=0.000),REM period ratio (16.28％ ± 5.59％ vs 21.59％ ± 2.70％,t =-3.727,P =0.001) decreased in the multi-dream group;whereas ratio of light sleep (66.49％ ±9.97％ vs 59.85％ ±3.01％,t =2.966,P =0.006),awakening numbers (13.4 ±6.98 vs 6.08 ± 3.34,t =3.411,P =0.002),arousal index (20.11 ± 10.69 vs 11.82 ± 8.09,t =2.338,P =0.026),non-REM arousal index (20.22 ± 10.53 vs 12.08 ± 8.69,t =2.283,P =0.029) increased.Conclusion The sleep efficiency of patients with multiple dreams is reduced,and their perceived dreams may originate from light sleep periods.

Objective:To explore the laboratory characteristics and diagnostic methods for therapy-related acute megakaryocytic leukemia (t-AMKL).Methods:The data of one child with acute lymphoblastic leukemia (ALL) in the Blood Disease Hospital of Chinese Academy of Medical Sciences & Peking Union Medical College in September 2014 was retrospectively analyzed. After inducing remission for more than 43 months, the child was diagnosed as t-AMKL.Results:After the diagnosis of ALL, the child was given chemotherapy with standard childhood ALL regimen. After 43 months, t-AMKL was diagnosed by comprehensive morphology, cytogenetics, and molecular biology. Bone marrow morphology showed that the proportion of primitive cells was 0.44; flow cytometry showed the phenotype was abnormal myeloid primitive cells; the pathology result showed that the abnormal cells weakly expressed CD42b and CD61; the electron microscopy showed platelet peroxidase (PPO)-positive and myeloperoxidase (MPO)-negative; the bone marrow immunohistochemistry showed the positive rate of CD41 was 34%; the child had a complex karyotype. After reviewing his medical history, he was diagnosed as t-AMKL.Conclusion:The t-AMKL is relatively rare, and it is helpful to improve the prognosis of patients by completing the relevant examinations for early diagnosis.

OBJECTIVETo investigate the changes of the two- pore K channel TASK-1 in diabetic rats with myocardial injury.

METHODSThirty-six SD rats were divided into normal group (N), diabetes at 4 weeks (DM 4W) group, and diabetes at 8 weeks (DM 8W) group. The cardiac functions of the rats were determined using cardiac ultrasonography, and the body weight and heart weight of the rats at different time points were measured to calculate the heart/body weight ratio (HW/BW). Myocardial fibrosis in the rats was assessed using Masson's staining. The protein expression of TASK-1 in the myocardium was detected using Western blotting. Whole- cell patch clamp technique was used to record the action potential duration (APD) and twopore domain potassium channel TASK- 1 current in acutely isolated rat ventricular myocytes. meanwhile, The inhibition of TASK-1 current was observed by the TASK-1 specific inhibitor ML-365.

RESULTSCompared with the normal group, the diabetic rats showed significantly increased HW/BW ( < 0.05), end- diastole left ventricular diameter (LVIDd), end- systolic left ventricular diameter (LVIDs), and TASK-1 protein expression, with obviously decreased left ventricular diameter shortening rate (FS) and ejection fraction (EF) ( < 0.01). Masson staining showed that in diabetic rats, the collagen fibers were thickened, interwoven into a network with uneven arrangement and increased deposition. Compared with DM 4W group, the rats in DM 8W group exhibited progressive increases in LVIDd, LVIDs, HW/BW, and TASK-1 expression ( < 0.01 or 0.05); FS and EF were further decreased ( < 0.01). Masson staining showed worsened morphological changes of the myocardium with increased deposition. Compared with that in the normal group, the current of TASK- 1 in diabetic rats at 8 weeks was significantly reduced ( < 0.01) and the duration of action potential was extended ( < 0.05). The TASK-1 current was successfully inhibited by ML-365.

CONCLUSIONSDiabetes can induce myocardial fibrosis and aggravate myocardial injury possibly in relation to changes in the protein expression and current of the two-port potassium channel TASK-1.

OBJECTIVE: To investigate whether autophagy mediates the effects of aldehyde dehydrogenase 2 (ALDH2) on the proliferation of neonatal rat cardiac fibroblasts cultured in high glucose. METHODS: Cardiac fibroblasts were isolated from neonatal (within 3 days) SD rats and subcultured. The fibroblasts of the third passage, after identification with immunofluorescence staining for vimentin, were treated with 5.5 mmol/L glucose (control group), 30 mmol/L glucose (high glucose group), or 30 mmol/L glucose in the presence of Alda-1 (an ALDH2 agonist), daidzin (an ALDH2 2 inhibitor), or both. Western blotting was employed to detect ALDH2, microtubule-associated protein 1 light chain 3B subunit (LC3B) and Beclin-1 in the cells, and a hydroxyproline detection kit was used for determining hydroxyproline content in cell culture medium; CCK- 8 kit was used for assessing the proliferation ability of the cardiac fibroblasts after the treatments. RESULTS: Compared with the control cells, the cells exposed to high glucose exhibited obviously decreased expressions of ALDH2, Beclin-1 and LC3B and increased cell number and hydroxyproline content in the culture medium. Treatment of the high glucose-exposed cells with Alda-1 significantly increased Beclin-1, LC3B, and ALDH2 protein expressions and lowered the cell number and intracellular hydroxyproline content, whereas the application of daidzin resulted in reverse changes in the expressions of ALDH2, Beclin-1 and LC3B, viable cell number and intracellular hydroxyproline content in high glucose-exposed cells. CONCLUSIONS Mitochondrial ALDH2 inhibits the proliferation of neonatal rat cardiac fibroblasts induced by high glucose, and the effect is possibly mediated by the up-regulation of autophagy-related proteins Beclin-1 and LC3B.
Aldehyde Dehydrogenase ; Aldehyde Dehydrogenase, Mitochondrial ; metabolism ; Animals ; Animals, Newborn ; Autophagy ; Beclin-1 ; physiology ; Fibroblasts ; Glucose ; Microtubule-Associated Proteins ; Mitochondrial Proteins ; Rats ; Rats, Sprague-Dawley