Objective To introduce the method and to evaluate the therapeutic effect of collagenase chemonucleolysis for treatment of cervical disc herniation.Methods 92 patients with cervical herniated discs were selected from January 2002 to December 2004.The procedure was guided by DSA and the puncture was defined from C_(6~7) or C_7-T_1 extradural cavity.Collagenase(1200~2400 u) was injcted in the herniated extradural cavity through the micrcatheter.Results The procedure of 88 cases was successful.80 cases were followed up from 6 to 12 months.The effect showed that 70 cases(87.5%) were excellent or good.No serious complication occurred.Conclusion The method of collagenase chemonucleolysis for treating cervical disc herniation is safe and effective,it can be used in clinic.

Objective To determine the optimal injection dose of ozone for the treatment of lumbar intervertebral disc protrusion.Methods A total of 240 patients with lumbar intervertebral disc protrusion were randomly and equally divided into four groups,with 60 patients in each group.Under CT guidance intervertebral injection of ozone was performed.The injection dose of ozone(50 ug/ml)used for patients in group A,B,C and D was 10 ml,20 ml,30 ml and 40 ml respectively.Immediately after the procedure CT scanning was made to check the result. A follow-up lasting 6-12 months was carried out.Clinical observation,including the ablation degree of the nucleus puiposus,the therapeutic results and the adverse reactions,was conducted.The results were statistically analyzed and compared among the four groups.Results A significant difference in the therapeutic effect existed between group A(10 ml)and other three groups(P＜0.05),while no significant difference in the therapeutic effect existed among group B(20 ml),group C(30 ml)and group D(40 ml),with P＞0.05.The occurrence of complications was increasing with the injection dose used.Conclusion The optimal injection dose of ozone for the treatment of lumbar intervertebral disc protrusion is 20 ml.

To explore the effects of nutritional risks on clinical outcomes [length of stay (LOS),hospitalization expense & mortality] in chronic kidney disease (CKD) patients.A total of 127 CKD patients completed the screening of nutritional risks by Nutritional Risk Screening 2002 (NRS-2002) within 24-48 hours of admission.The data of nutritional supports within 2 weeks of admission,LOS,hospitalization expense and mortality were collected.① Among them,the prevalence of nutritional risks was 18.1％.And the values were 8.2％,9.4％ and 44.1％ in early,middle and advanced CKD groups respectively; ② LOS and hospitalization expense in nutritional risk group were significantly more than the non-nutritional risk group (12.5 d vs.5.2 d,P =0.00 ; 11 806 vs.5311 yuan,P =0.00).There was a positive correlation between NRS score and LOS or hospitalization expense; ③ The nutritional support rate of nutritional risk group was only 17.4％.The progression of CKD increased the nutritional risks leading to greater LOS and hospitalization expense.We should pay more attention to the nutritional risk screening and nutritional intervention in moderate-advanced CKD patients.

Objective To observe the level of serum hepatocyte growth factor(HGF)in patients with hypertension(HT).Methods HGF,fasting plasma glucose(FBG),postprandial plasma glucose(2hPG),glycosylated hemoglobin A1c(HbA1c),total cholesterol(TC),triglyceride(TG),systolic blood pressure(SBP),diastolic blood pressure(DBP),body mass index(BMI)and waistline(w)were detected in 30 patients with hypertension,30 patients with hypertension complicated by type 2 diabetes mellitus(T2DM),and 30 normal controls such indexes as.Results The level of serum HGF in HT group[(413.87±90.87)ng/L],and HT+T2DM group[(413.72±98.72)ng/L]were higher than that in control group[(120.45±25.11)ng/L](P＜0.05),but there was no significance between HT group and HT+T2DM group(P＞0.05).There existed a positive correlation between HGF and FBG,SBP(r=2.273,r=5.353,P＜0.05).Conclusion Higher levels of HGF is found in patients with hypertension and hypertensin complicated with T2DM,which indicates the severity of dysfunction of vascular endothelium.

Hepatitis B virus core protein (HBc) has become a hot spot in drug carrier protein research due to its natural particle self-assembly ability and ease of modification. The truncation of the C-terminal polyarginine domain (CTD, aa 151-183) of HBc does not affect the self-assembly of the particles. However, it does affect the internal and external charges of the particles, which may subsequently affect drug encapsulation. Thus, the truncated C-terminal polyarginine domain (CTD) of HBc and the inserted RGD peptide were selected to construct and express three HBc variants (RH) encapsulated with ICG (RH/ICG) with different C-terminal lengths to compare the stability and drug activity of their nanoformulations. RH160/ICG was found to have a great advantages in encapsulation efficiency and biological imaging. Compared with other HBc variants, RH160/ICG significantly improved encapsulation efficiency, up to 32.77%±1.23%. Cytotoxicity and hemolysis assays further demonstrated the good biocompatibility of RH160/ICG. Cell uptake and in vivo imaging experiments in mice showed that RH160/ICG could efficiently deliver ICG in tumor cells and tumor sites with good imaging effect. This research provides a new direction for further expanding the diagnosis and treatment application of ICG and development of HBc-based nanoparticle drug carrier platform.
Animals ; Hepatitis B/drug therapy* ; Hepatitis B Core Antigens ; Indocyanine Green/chemistry* ; Mice ; Nanoparticles/chemistry* ; Viral Core Proteins

Huntington's disease (HD) is a deadly neurodegenerative disease with abnormal expansion of CAG repeats in the huntingtin gene. Mutant Huntingtin protein (mHTT) forms abnormal aggregates and intranuclear inclusions in specific neurons, resulting in cell death. Here, we tested the ability of a natural heat-shock protein 90 inhibitor, Gedunin, to degrade transfected mHTT in Neuro-2a cells and endogenous mHTT aggregates and intranuclear inclusions in both fibroblasts from HD patients and neurons derived from induced pluripotent stem cells from patients. Our data showed that Gedunin treatment degraded transfected mHTT in Neuro-2a cells, endogenous mHTT aggregates and intranuclear inclusions in fibroblasts from HD patients, and in neurons derived from induced pluripotent stem cells from patients in a dose- and time-dependent manner, and its activity depended on the proteasomal pathway rather than the autophagy route. These findings also showed that although Gedunin degraded abnormal mHTT aggregates and intranuclear inclusions in cells from HD patient, it did not affect normal cells, thus providing a new perspective for using Gedunin to treat HD.