This study was aimed to investigate the changes of hemodynamic parameters, pathology and c kit mRNA expression in myocardium after acute myocardial infarctionin (AMI) in rats, and to elucidate the relationship between these three kinds of changes. Sixty six adult male SD rats were randomly divided into normal group, Sham groups and ligation groups. The rat model of AMI was set up by ligating the left anterior descending artery. Hemodynamic parameters, pathological changes and c kit mRNA expression in myocardiam were examined. The results revealed that there were no statistically significant differences in hemodynamic parameters between normal group and Sham groups. Compared with the normal group, all ligation groups exhibited significantly decreased left ventricular systolic pressure (LVSP) and +/-dp/dtmax (P<0.01), and increased left ventricular end diastolic pressure (LVEDP, P<0.01). In the other ligation groups, compared with 6th hour group after ligation, there appeared striking increase of LVSP, LVEDP and +/-dp/dtmax (P<0.05). HE staining in myocardiam showed that there are necrosis and derangement at 24th hour group after ligation ,and a great number of inflammatory cells infiltration around the infarct zone at 3rd day group after ligation, and granulation tissue infiltrated into the infarct zone at 14th day group after ligation. In all five time points groups after ligation, the levels of c-kit mRNA expression were 0.99 fold, 1.06 fold, 1.46 fold, 1.91 fold and 2.67 fold, respectively, compared with Sham groups. The results suggest that cardiac stem cells in myocardium might contribute to the role of regenerating myocardium via self proliferation after acute myocardial infarction, but further investigation is still needed.
Animals ; Hemodynamics ; physiology ; Male ; Myocardial Infarction ; metabolism ; pathology ; physiopathology ; Myocardium ; metabolism ; pathology ; Myocytes, Cardiac ; cytology ; Proto-Oncogene Proteins c-kit ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Stem Cells ; cytology

This study was aimed at observing the effects of ovariectomy and estradiol on the microarchitecture of cancellous bone and exploring the influence of microarchitectural change on the biomechanical properties. Thirty 6-month-old unmated female SD rats were randomly divided into 3 groups (10 rat each): sham-operated control group (Sham), ovariectomized group (OVX)and Estradiol Benzoate treated group (EBT). All rats were housed in standard environmental conditions. Five months after operation, the rats were sacrificed. The biomechanical properties of the third lumbar vertebras (L3) were measured with compression testing in vitro. Micro-CT scanning was performed on the fourth lumbar vertebras (L4) in vitro. In comparison with the corresponding variables of Sham, the bone volume fraction (BV/TV) and the trabecular number (Tb. N) of OVX were reduced remarkably, and the trabecular separation (Tb. Sp) and the structural model index (SMI) of OVX were enhanced obviously. These facts implicated that the bone trabecular plate-like structure of OVX were decreased. BV/TV, Tb. N and the trabecular thickness (Tb. Th) of EBT were greater than those of OVX. Tb. Sp and SMI of EBT were much smaller than those of OVX. The results of mechanical test showed that the maximum forioe (Fmax), the maximum stress (sigmamax) and the elastic modeulus (E) of the lumbar vertebral cancellous bone of OVX were declined sharply, while the aforesaid biomechanical index of EBT was improved distinctly. The performance of three-dimensional micro-CT and the mechanical testing to assess microarchitecture of cancellous bone are useful for evaluating the state of osteoporosis and the antiosteoporotic effect of agents.
Animals ; Biomechanical Phenomena ; Estradiol ; pharmacology ; Female ; Imaging, Three-Dimensional ; Lumbar Vertebrae ; diagnostic imaging ; pathology ; Osteoporosis ; pathology ; Ovariectomy ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Tomography, X-Ray Computed

Objective To compare the effectiveness and safety of endoscopic submucosal dissection ( ESD) with endoscopic piecemeal mucosal resection ( EPMR) for early esophageal cancer and precancerous lesions with length more than 5 cm. Methods A retrospective analysis was performed on data of 85 patients diagnosed as early esophageal cancer and precancerous lesions with length more than 5 cm in Fujian Medical Association of Early Esophageal Carcinoma from January 2012 to July 2017. The patients were divided into ESD group (52 cases) and EPMR group (33 cases), and the effectiveness and safety between the two groups were compared. Results There was no significant difference on the complete resection rate between the two groups[86. 5％ (45/52) VS 87. 9％ (29/33), P>0. 05]. The operative time (58. 53±30. 50 min VS 32. 06±9. 12 min), postoperative fasting time (4. 18±1. 30 d VS 3. 67±0. 96 d), postoperative hospital-stay time (7. 45±2. 44 d VS 6. 54±1. 73 d), and postoperative antibiotics using time (3. 48±2. 33 d VS 1. 96±2. 20 d) in ESD group were higher than those in EPMR group (all P<0. 05). There were no significant difference in the rate of intraoperative complication and short-term postoperative complication, such as fever, chest pain, and postoperative bleeding, between the two groups ( all P>0. 05 ) . But the postoperative stricture rate of ESD group was higher than that of EPMR group[23. 1％ (12/52) VS 6. 1％(2/33), P<0. 05]. During the follow-up of 3-63 months, 5 cases recurred in ESD group and 1 case in EPMR group, with no significant difference ( P>0. 05). Conclusion ESD and EPMR have equivalent efficacy and safety on the treatment of early esophageal cancer and precancerous lesion. EPMR has a shorter operative time, lower rate of post-operative stricture, and is easier to master.

Macrophages play critical roles in renal fibrosis. However, macrophages exhibit ontogenic and functional heterogeneities, and which population of macrophages contributes to renal fibrosis and the underlying mechanisms remain unclear. In this study, we genetically targeted Notch signaling by disrupting the transcription factor recombination signal binding protein-Jκ (RBP-J), to reveal its role in regulation of macrophages during the unilateral ureteral obstruction (UUO)-induced murine renal fibrosis. Myeloid-specific disruption of RBP-J attenuated renal fibrosis with reduced extracellular matrix deposition and myofibroblast activation, as well as attenuated epithelial-mesenchymal transition, likely owing to the reduced expression of TGF-β. Meanwhile, RBP-J deletion significantly hampered macrophage infiltration and activation in fibrotic kidney, although their proliferation appeared unaltered. By using macrophage clearance experiment, we found that kidney resident macrophages made negligible contribution, but bone marrow (BM)-derived macrophages played a major role in renal fibrogenesis. Further mechanistic analyses showed that Notch blockade reduced monocyte emigration from BM by down-regulating CCR2 expression. Finally, we found that myeloid-specific Notch activation aggravated renal fibrosis, which was mediated by CCR2 macrophages infiltration. In summary, our data have unveiled that myeloid-specific targeting of Notch could ameliorate renal fibrosis by regulating BM-derived macrophages recruitment and activation, providing a novel strategy for intervention of this disease.