Objective To discuss the value of multi-slice spiral CT angiography (MSCTA)and digital subtraction angiography (DSA)in lower extremity arteriosclerosis obliterans.Methods MSCTA and DSA of lower extremity arteries were performed in 41 patients with lower extremity arteriosclerosis obliterans sequentially.The interval of these two examinations was no more than 2 weeks.DSA served as the reference standard and compared with MSCTA in terms of grading of stenoocclusive lesions,visualization of collaterals in lower extremity arteries.Results No significant differences of grading of stenoocclusive lesions,visualization of col-laterals were observed between MCTA and DSA in lower extremity arteries.Compared with the results of DSA,the sensitivity,spe-cificity,accuracy,positive and negative predictive value of MSCTA in the detection of arterial stenosis (≥ 50%)were 97.2%, 98.2%,93.8%,94.6%,98.2%,respectively.Conclusion MSCTA shows relatively high sensitivity and specificity in the diagnosis of lower extremity arteriosclerosis obliterans,can provide effective guidance of planning treatment in lower extremity arteriosclerosis obliterans.

Purpose To establish myocardial infarction model in rabbits and to evaluate cardiac function and pathological changes.Materials and Methods In 35 New Zealand white rabbits, the left anterior descending branch (LAD) of the coronary artery was ligated. The cardiac function was evaluated using echocardiography, and the blood serum brain natriuretic peptide (BNP) level was examined preoperatively, on postoperative day 1, and in 1 week, 2 weeks, 4 weeks and 8 weeks for comparison. Pathological sections and HE staining were performed to observe pathological changes. Results The death rate was 28.6% (10/35). There was progressive increase in left ventricular end systolic diameter (LVESD) and left ventricular end diastolic diameter (LVEDD) at 1 week, 2 weeks and 4 weeks (P<0.05). There was progressive decrease in left ventricular ejection fraction (LVEF) and left ventricular fractional shortening fraction (LVFS) at 1 day, 1 week, 2 weeks and 4 weeks (P<0.05). The BNP level started increasing in 1 day, peaked in 1 week, then gradually decreased but remained higher than preoperative level in 8 weeks (P<0.01). Pathological section showed typical myocardial cell degeneration, necrosis, ifbrosis, calciifcation and scar formation. Conclusion This myocardial infarction model is satisfactory with signiifcant decrease of cardiac function and increase of BNP level.

Objective To study the protective mechanism of adenosine on intestinal barrier function in acute hemorragic necrotizing pancreatitis (AHNP) pigs; Methods Twelve small pigs were equally devided into two groups randomly after the AHNP model sitted up: (1) AHNP controll group (group A) and adenosine treated group (group B). The intestinal blood flow, intestinal permeability, bacterial culture and endotoxin in portal blood were compared between the two groups in pre and post AHNP. Results (1)The intestinal blood flow was dramatically decreased in group A, and much higher in group B than that in group A at the 8 h, 24 hour and day 7 after ANHP model was setted up (P0.001,P

This paper reports some histochemical,scanning and transmission electron mic-roscopical features of thymic nurse cell(TNC)of human fetuses.The results showedthat TNCs were all negative for ANAE,AcP,AlP,ATPase,5'-Nase and PAS.TNCcontained various numbers of lymphocytes.Some intracytoplasmic lymphocytes werepositive for ANAE,AcP,AlP and ATPase.Their ANAE positive percentage deter-mined were 26.8%.However,ANAE positive percentage of extracytoplasmic lym-phocytes of TNC were 51.3%.Our data demonstrated that there was significant dif-ference between these two ANAE positive percentages,P

The chemokine CXCL10 and its receptor CXCR3 play a role in breast cancer metastasis to bone and osteoclast activation. However, the mechanism of CXCL10/CXCR3-induced intracellular signaling has not been fully investigated. To evaluate CXCL10-induced cellular events in the mouse breast cancer cell line 4T1, we developed a new synthetic CXCR3 antagonist JN-2. In this study, we observed that secretion of CXCL10 in the supernatant of 4T1 cells was gradually increased during cell growth. JN-2 inhibited basal and CXCL10-induced CXCL10 expression and cell motility in 4T1 cells. Treatment of 4T1 cells with CXCL10 increased the expression of P65, a subunit of the NF-κB pathway, via activation of the NF-κB transcriptional activity. Ectopic overexpression of P65 increased CXCL10 secretion and blunted JN-2-induced suppression of CXCL10 secretion, whereas overexpression of IκBα suppressed CXCL10 secretion. These results indicate that the CXCL10/CXCR3 axis creates a positive feedback loop through the canonical NF-κB signaling pathway in 4T1 cells. In addition, treatment of osteoblasts with conditioned medium from JN-2-treated 4T1 cells inhibited the expression of RANKL, a crucial cytokine for osteoclast differentiation, which resulted in an inhibitory effect on osteoclast differentiation in the co-culture system of bone marrow-derived macrophages and osteoblasts. Direct intrafemoral injection of 4T1 cells induced severe bone destruction; however, this effect was suppressed by the CXCR3 antagonist via downregulation of P65 expression in an animal model. Collectively, these results suggest that the CXCL10/CXCR3-mediated NF-κB signaling pathway plays a role in the control of autonomous regulation of CXCL10 and malignant tumor properties in breast cancer 4T1 cells.
Animals ; Breast Neoplasms* ; Breast* ; Cell Line ; Cell Movement ; Chemokine CXCL10 ; Coculture Techniques ; Culture Media, Conditioned ; Down-Regulation ; Macrophages ; Mice ; Models, Animal ; Neoplasm Metastasis ; Osteoblasts ; Osteoclasts

Background and Objectives: Stem cell therapy is a promising strategy for treating neurological diseases but its effectiveness is influenced by the route of administration and the characteristics of the stem cells. We determined whether neural induction of mesenchymal stem cells (MSCs) was beneficial when the cells were delivered intra-arterially through the carotid artery. Methods: and Results: MSCs were neurally induced using a retroviral vector expressing the neurogenic transcription factor neurogenin-1 (Ngn1). The LacZ gene encoding bacterial β-galactosidase was used as a control. Ischemic stroke was induced by transluminal occlusion of the middle cerebral artery and 3 days later the MSCs were delivered intra- arterially through the internal carotid artery. Magnetic resonance imaging analysis indicated that compared to MSCs expressing LacZ (MSCs/LacZ), MSCs expressing Ngn1 (MSCs/Ngn1) exhibited increased recruitment to the ischemic region and populated this area for a longer duration. Immunohistochemical analysis indicated that compared to MSCs/LacZ, MSCs/Ngn1 more effectively alleviated neurological dysfunction by blocking secondary damage associated with neuronal cell death and brain inflammation. Microarray and real-time PCR analysis indicated that MSCs/Ngn1 exhibited increased expression of chemotactic cytokine receptors, adherence to endothelial cells, and migration ability. Conclusions Neural induction with Ngn1 increases the homing ability of MSCs, enhancing their engraftment efficiency in the ischemic rat brain. Intra-arterial delivery of neurally induced MSCs/Ngn1 3 days after ischemic injury blocks neuronal cell death and inflammation, and improves functional recovery. Thus, intra-arterial administration of stem cells with neural properties may be a novel therapy for the treatment of ischemic stroke.