OBJECTIVE:To prepare core-shell nanocapsules loading nicardipine hydrochloride and to investigate its pharmaceutical characteristics. METHODS: Core-shell nanocapsules were prepared using layer-by-layer electrostatic self-assembly technique. The indexes including the shape and particle size and the loaded drug amount of the nanocapsules were evaluated, and its accumulative release rates in artificial gastric juice and intestinal juice were computed and compared with those of its crude drug. RESULTS: The results showed that the nanocapsules were spherical with a mean particle size of 200 nm and a maximum loaded drug amount of 2.512%. The drug release rate within 12 h reached 18.64% in artificial gastric juice and 70% in artificial intestinal juice, whereas within 3 h the drug release rate of its crude drug in artificial intestinal juice reached 87%. CONCLUSIONS: The prepared core-shell nanocapsules containing nicardipine hydrochloride had a good pharmaceutical property.

Objective To explore of the color Doppler ultrasound diagnosed choledocholithiasis.Methods 100 cases with choledocholithiasis diagnosed by color ultrasonography and cholangiography were analysed retrospectively.The sensitivity,specificity,accuracy and the inspection time of two methods were compared.Results 90 cases were diagnosed after operation,90％ in 100 patients.The diagnostic accuracy of Doppler ultrasound was 88 cases,2 false negative cases,no false positive.The diagnostic accuracy of cholangiography was 87 cases,3 false negative cases,2 false positive cases.The sensitivity,specificity and accuracy of two groups were not statistically significant (x2 =0.23,1.25,0.57,P ＞ 0.05).The inspection time of color ultrasound was 12 ～ 28 min,the average inspection time was (16.57 ±4.12)min.The inspection time of cholangiography was 12 ～37min,the average inspection time was (21.09 ± 6.24) min.The inspection times of two ways were statistically significant (t =6.53,P ＜ 0.05).Followed up between 5 months and 2 years,there was no residual gallstone patients.Conclusion Color Doppler ultrasound is a noninvasive,safe,time-saving,simple,good repeatability,high successful rate,for common bile duct stones in the main examination methods.

ObjectiveTo explore the effects of hemofiltration on serum enzyme (SE),endotoxin (ET) and malonaldehyde (MDA) of dogs with heat stroke caused shock.MethodsSixteen healthy male hybrid dogs were randomly divided into 2 groups,8 for each:as heat stroke group (HS group ) and hemofiltration group (HF group).Severe heat stroke model was induced with high temperature.The dogs were taken out of the heating cabin when it reached heat stroke level,and then observed under normal temperature without treatment.The dogs in HF group was immediately treated with hemofiltration.The changes of SE,ET,MDA of two groups of dogs were observed and the survival time between two groups was compared,ResultsThe time from heat exposure to shock was ( 107.00 ± 28.52 ) and ( 111.38 ± 22.24 )minutes in HS group and HF group respectively ( t =- 0.354,P =0.729 ).The SE ( CK,LDH,ALT,AST) of the dogs were all higher after heat stroke,and the dogs of two groups showed no siginificant difference (P ＞ 0.05).At three hours after heat stroke,the SE increased apparently in HS group and HF group,but the level was significantly lower in HF group. Before heat stroke,the serum ET showed no siginificant difference between two groups ( P ＞ 0.05 ).After heat stroke,the serm ET was much higher than before ( P ＜0.01 ),but there was still no siginificant difference between two groups ( P ＞0.05 ).At three hours after heat stroke,the ET increased both in HF group and HS group,but the level was lower in HF group.Before heat stroke,the serm MDA had no siginificant difference between two groups ( P ＞ 0.05 ).After heat stroke,the serm MDA was much higher than before ( P ＜ 0.0l ),but there was still no siginificant difference between two groups (P ＞ 0.05 ).After heat stroke in three hours,the MDA of HS group rose apparently while HF group slowly declined.The median survival time of HF group was 180 min while HS group was 75 min,the survival rate showed siginificant difference (P ＜ 0.01 ).Conc4usions HF can improve the prognosis of dogs with heat stroke caused shock,prolong its survival time,reduce mortality.The mechanism is probably that HF clear serum MDA,partially clear serum ET and then eventually reduce cell and tissue injury and reduce SE.

Objective To explore the effect of quality control circle (QCC) in reducing the health examination report errors. Methods QCC was founded, activity themes were selected, activity schedule was planned, the reasons of health examination report errors were analyzed, goal setting, countermeasures were planned and implemented jointly by circle members. Totally 11 738 reports of health checkup were selected and analyzed the errors were analyzed during the activity, 6 892 were male, 4 846 were female, their average age was(38.01 ± 11.31)years, 5 000 reports were made before improvement, 5 120 reports during improvement, 1 618 reports after improvement and compared the report error rates were compared. Evaluation of QCC activity results and tracking effect were evaluated. Results Error rate of health checkup report from 17.80‰ decreased to 7.23‰ during improvement, dropped to 2.48‰ after improvement. The rate of standard was 141.9%, progress rate was 86.1%. Tracking results for 8 months, error rate remained below the target value of 3.40‰although error rate roise to 5.25‰in August 2016, the effect was good. The additional benefit, working efficiency of the doctors was improved; Average time for each written report was reduced to 4 minutes from 5 minutes;Saved about 1 hours per person a day to review the accuracy of the report and learning; Formed“communication model between clinical departments”;Established the error registration system for the report has been distributed;Similar error of ECG department has been avoided. Conclusions Application of QCC not only reduced the error rate of the health checkup report, but also ensured quality, objective, and accurate physical examination report; activities not merely help to improve the work efficiency of physician, team's mutual cooperation, and is beneficial to optimize the system of medical institution and avoid the error.

Objective To detect the expressions and clinical significance of Nanog and CD44 protein in lung cancer. Methods The expressions of Nanog and CD44 were detected by immunohistochemistry in 50 cases of lung cancer, 32 cases of benign lesion lung tissue and 18 cases of paraneoplastic normal lung tissue. Then their relationships with clinicopathological factors were analyzed. Results The expression of Nanog in lung cancer was significantly higher than those in benign lesion lung tissue and paraneoplastic normal lung tissue (P < 0.05). There was no significant difference of the expression of CD44 among the three groups (P > 0.05). The expressions of Nanog and CD44 in squamous cell carcinomas were higher than those in adenocarcinomas and small cell lung carcinomas (P < 0.05). The expressions of Nanog and CD44 were significantly correlated with lymph node metastasis (P < 0.05), but were not correlated with age, gender, tumour size, TNM stage and differentiation of lung cancer (P>0.05). The positive correlation was also noted between the expressions of Nanog and CD44 in lung cancer (r = 0.564, P < 0.05). Conclusion Nanog and CD44 proteins may participate in the genesis and progression of lung cancer. Nanog protein is a potential diagnostic marker and therapeutic target for lung cancer.

Objective To study whether there is correlation among the VEEG, head B ultrasound examination and NBNA score in evaluation of encephalopathy in premature infants. Methods One hundred cases of premature and low birth weight infants in our hospital from January 2012 to August 2013 admitted to NICU, were graded by video electroencephalogram, head B ultrasound examination and NBNA score to analyze the result of them in the assessment results encephalopathy in premature infants. Results In the treatment process, consistent with the EEG, head B ultrasound examination and NBNA score changes the presence of data results,with statistical significance. Conclusion There is a good correlation between VEEG,head B ultrasound examination and NBNA score.

Objective To investigate the clinical significance of the gray head B ultrasound quantitative determination on early detection for preterm low birth weight infants with cerebral white matter damage. Methods From 2013 January to August 2014 in the NICU department of our hospital, 100 cases of preterm and low birth weight infants were ran-domly divided into the treatment group and the control group. After birth 72 hours, the value of cerebral white matter was measured by head B ultrasound combined with medical image analysis software. The cases, whose early values of cerebral white matter were above 130, were treated with early brain nerve nutrition and rehabilitation. The develop-ment of nerve growth was followed up in 3 months and 6 months after birth, respectively. Results The NBNA score of premature and low birth weight infants was significantly higher than that of the control group. By the follow-up investi-gation in 3 months and 6 months after birth, the nerve growth of the treatment group was significantly better than that of the control group. Conclusion The head B ultrasound gray-scale quantitative analysis has important guiding signifi-cance for early diagnosis of premature and low birth weight infants with cerebral white matter injury,and it can help to judge the prognosis and guide early clinical treatment.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.