Neurons descending from the griseum centrale mesencephali, nucleus Darkschewitsch and nucleus interstitialis of Cajal to the nucleus raphe magnus and adjacent reticular formation (nucleus reticularis gigantocellularis and nucleus reticularis pontis caudalis) were identified in 9 adult cats with the retrograde HRP method. In the griseum centrale mesencephali, the labeled neurons were found bilaterally but slightly more ipsilaterally. In the nucleus Darkschewitscb and nucleus interstitialis of Cajal, the labeled neurons were consistently found in its rostral part ipsilateral to the injected side at the level of the posterior commissure. In addition, in 5 of the 9 cases, a few labeled neurons were observed in the nucleus raphe dorsalis.

Objective To investigate the effect of tadpole extract(T871 3) on tumor cells and its mechanism. Methods We studied the effects of T871 3 on proliferation, differentiation and apoptosis of HL 60 cells by cytomorphological observation, cytochemistry and TUNEL method. We also examined gene expression during the induction of apoptosis and differentiation in tadpole extract treated HL 60 cells by in situ hybridization and intact cell mRNA dot blot techniques. Results 1 T871 3 was able to inhibite HL 60 cells proliferation. 2 T871 3 was able to induce HL 60 cells to differentiate along monocyte macrophage lineage at low concentration, and apoptosis at higher concentration. 3 The differentiation of HL 60 cells was accompanied by downregulations of c myc,c myb gene expression, The apoptosis of HL 60 cells was accompanied by downregulations of c\|myc bcl 2 gene expression, suggesting that these genes may be involved in the apoptosis and differentiation process. Conclusion Tadpole extract may have effects on HL 60 cells through changing the oncogene expression. [

BACKGROUND:Bone marrow mesenchymal stem cel s are likely to repair renal injury by differentiating into renal parenchymal cel s. OBJECTIVE:To explore the effect and mechanism of bone marrow mesenchymal stem cel s in the renal repair after mesangial proliferative glomerulonephritis. METHODS:Thirty Sprague-Dawley rats were randomized into normal group, model group and treatment group (n=10 per group). Model group and treatment group were treated with tail vein injection of mouse anti-rat monoclonal antibody Thy1.1 to prepare mesangial proliferative glomerulonephritis models. One week after modeling, rats in the treatment group were given 2×106 bone marrow mesenchymal stem cel s via the tail vein, and rats in the other two groups were given the same volume of normal saline. Two weeks after transplantation, urinary protein, urea nitrogen, creatinine levels were detected;hematoxylin-eosin staining was used for observing pathological changes of the renal tissue under microscope;and the expression of transforming growth factor beta 1 was detected by immunohistochemistry method. RESULTS AND CONCLUSION:The levels of urinary protein, urea nitrogen and creatinine as wel as the expression of transforming growth factor beta 1 in the renal tissue arranged in descending order were listed as fol ows:model group>treatment group>control group, and there were significant differences among three groups (P<0.05). In the model group, diffuse glomerular hyperplasia was observed with the presence of increased extracel ular matrix, partial glomerular sclerosis, and interstitial infiltration of inflammatory cel s;in the treatment group, glomerular hyperplasia, mesangial proliferation and inflammatory cel infiltration were al mitigated compared with the model group. Therefore, bone marrow mesenchymal stem cel transplantation may contribute to renal repair after mesangial proliferative glomerulonephritis, by inhibiting overexpression of transforming growth factor beta 1 in the kidney.