Résumé
Objective A surface feedback-stimulation gastric-pacing device was designed to extract gastric surface information,determine the status of gastric and surface stimulation.Methods The characteristic parameters of gastric electrical formed by processing signal and extracting parameter.By that,the state of stomach could be confirmed,and stimulus signal of stomach pace-making in different frequency and intensity could be decided as needed.During the processes of the stimulation,the variations of gastric electrical parameters can be analyzed in real-time and the stimulation parameters could be modified to achieve the self-feedback mode.Results Self-feedback model in different gastric motility analog environment could be realized.Conclusion The preliminary validation of experimental results proved the effectiveness of self-feedback of gastric pacing devices and its application prospects in some areas.
Résumé
Constant direct current stimulation has facilitation for cellular growth of many histiocytes.This paper primarily introduces the systemic and detailed design of the software as well as its achievement.The system can accomplish controlling action of peripheral circuitry through computer interface.In this way,it can run stably,harmoniously and safely.
Résumé
30 sexually mature, virgin female SD rats, weighed 200-270 g were mated and used for the study of the teratogenic effect of N, N-methylene-bis (2-amino-1,3,4-thiadiazole) (Bis-A-TDA) on fetal neural tube formation and to explore the possible morphological mechanism of neural tube defects (NTD). In the morning of day 10 of gestation, the experimental group was administered with 10mg/kg body weight Bis-A-TDA mixed in peanut oil, and the control group with the same amount of peanut oil only. The results Showed that the incidence of NTD was 52.9% and the majority of NTD were excencephaly and encephalocele in the experimental group. In the early stage of NTD formation, some neuroepithelial cells showed vacuolated degeneration and necrosis, and the mitochondria became swollen and with indistinct or even disappeared crista. The intercellular spaces widened, and some cells escaped into the lumen of neural tube. The mitotic index of neuroepitbelial cells were sharply decreased. In the closure region of the telencephalon, similar changes of the neuroepithelium were present also, and decreased migration of mesodermal cells was noted. We consider the failure of cranial neural folds to approximate and closure was caused mainly by the damage of neuroepithelial cells, inhibition of cell proliferation, alteration of intercellular junctions and the changes of topographical arrangement of the neuroepithelium. The damage and delayed migration of mesodermal cells might also be involved in this event.