OBJECTIVE:To observe clinical efficacy of urinary kallidinogenase in the treatment of acute cerebral watershed in-farct (WSI). METHODS:128 patients with WSI were randomly divided into control group and treatment group,each of the 64 cases. Control group was given Shuxuening 15 ml added into 0.9% Sodium chloride 250 ml,ivgtt,qd;treatment group received urinary kallidinogenase 0.15 PNA added into 0.9% Sodium chloride 100 ml,ivgtt,qd. Both groups were treated for consecutive 14 days. Neurologic impairment score(NIHSS)and clinical efficacy were observed in 2 groups before treatment and 3,7 and 14 days after treatment. The blood specimens were collected after 7 and 14 days treatment,to determine serum levels of TCC. RESULTS:After treatment,NIHSS and total effective rate of treatment group were significantly higher than those of control group,with statis-tical significance(P<0.01). There was no statistical significance in TCC between 2 groups before treatment(P>0.05);7 days af-ter treatment,TCC level of 2 groups increased significantly,to 14 days,and a declive;the treatment group was higher than the control group,with statistical significance (P<0.05). CONCLUSIONS:Urinary kallidinogenase can improve clinical efficacy of WSI significantly,and promote neurologic impairment symptom and TCC levels.

Objective: To investigate the effects of the repair and restitution of ear-shaped cartilage by adipose tissue-derived stem cells(ADSC) and cartilage acellular extracellular matrix. Methods: ADSC were extracted by digesting with collagenase type II from the adipose tissue from 32 patients with adiposity whose fats were drawn, and were cultured and subcultured in vitro. The natural biological scaffolds were prepared by acellular method using porcine ear cartilage, and then the second generation ADSC(5.0×10⁷/ml) were inoculated on the preformed natural bio-scaffold scaffold by culturing in vitro for 3 days to form a cell scaffold complex. 32 New Zealand white rabbits were randomly divided into the experimental groups, the control group A, the control group B and the control group C. All New Zealand white rabbits were modeled by ear cartilage defects. The cell scaffolds composite was implanted into the experimental group of the ear cartilage defects of rabbits, the ADSC were implanted into the control group A, the cartilage acellular extracellular matrix scaffold was implanted into the control group B and the control group C was modeled only by ear cartilage defects. After 16 weeks, the animals were sacrificed and the repair effect was observed by gross appearance and histological examinations including HE, Toluidine blue staining, Safranin O and typeⅡ collagen staining. Its were quantitatively analyzed by positive staining results of type Ⅱ collagen. Ear cartilage tissue elasticity was detected. SPSS 17.0 software was used to analyze the data. Results: The cartilage defects in the experimental group were repaired well by general shape observation and those in the control group was filled in with granulation tissue. There were significant differences between the experimental group and the control group in the wet weight(P<0.05). HE staining showed that cartilage cavities formed in articular cartilage defects, and only the fibrous tissue was filled with the ear cartilage defect in the control groups. In the repair area, Toluidine blue staining, Safranin O and type Ⅱ collagen staining were positive in the experimental group, and negative in the control groups. There was no significant difference between the experimental group and the normal ear cartilage in the ear cartilage elastic constant detection(P>0.05). Conclusions The mechanics and histology of rabbit ear neonatal cartilage constructed by ADSC combined with cartilage acellular matrix are close to normal ear cartilage. Cartilage acellular matrix material combined with adipose-derived stem cells has good repair and reconstruction ability for ear cartilage defects, which possesses potential clinical application value.