We evaluated the preoperative and intraoperative general condition of 33 pediatric kidney recipients. Eighteen patients were anaesthetized with lumbar epidural anaesthesia. Ten patients were with nitrous oxide-oxygen-halothane, 5 cases were with NLA. Preoperatively many children had cardiovascular and metabolic complications. For example 39% of patients had history of hypertension. Sixty-seven percent of patients were found to have cardiomegaly (cardio-thoracic ratio > 50%) with chest X-ray film. Seven of 9 patients undergoing echocardiogram had abnormality of cardiac wall motion, valvular impairment, pericardial effusion. In forty-eight percent of patients, hyperlipidemia was found. During operation we could not maintain the cardiovascular stability following intratracheal intubation and manipulation of vena cava or abdominal aorta under NLA or nitrous oxide-oxygen-halothane anesthesia. Epidural analgesia inhibited the cardiovascular fluctuation following these surgical stresses. We concluded that epidural analgesia is the best anaesthesia for pediatric renal transplantation and phentolamine or PGE1 are useful to maintain cardiovascular stability and transplanted kidney function.
Cell ablation technology is useful for studying specific cell lineages in a developing organ in vivo . Herein, we established a novel anti-Müllerian hormone ( AMH )-toxin receptor-mediated cell knockout (Treck) mouse line, in which the diphtheria toxin ( DT ) receptor was specifically activated in Sertoli and granulosa cells in postnatal testes and ovaries respectively. In the postnatal testes of Amh -Treck transgenic (Tg) male mice, DT injection induced a specific loss of the Sertoli cells in a dose-dependent manner, as well as the specific degeneration of granulosa cells in the primary and secondary follicles caused by DT injection in Tg females. In the testes with depletion of Sertoli cell, germ cells appeared to survive for only several days after DT treatment and rapidly underwent cell degeneration, which led to the accumulation of a large amount of cell debris within the seminiferous tubules by day 10 after DT treatment. Transplantation of exogenous healthy Sertoli cells following DT treatment rescued the germ cell loss in the transplantation sites of the seminiferous epithelia, leading to a partial recovery of the spermatogenesis. These results provide not only in vivo evidence of the crucial role of Sertoli cells in the maintenance of germ cells, but also show that the Amh -Treck Tg line is a useful in vivo model of the function of the supporting cell lineage in developing mammalian gonads.
Congenital biliary atresia is an incurable disease of newborn infants, of unknown genetic causes, that results in congenital deformation of the gallbladder and biliary duct system. Here, we show that during mouse organogenesis, insufficient SOX17 expression in the gallbladder and bile duct epithelia results in congenital biliary atresia and subsequent acute 'embryonic hepatitis', leading to perinatal death in ~95% of the Sox17 heterozygote neonates in C57BL/6 (B6) background mice. During gallbladder and bile duct development, Sox17 was expressed at the distal edge of the gallbladder primordium. In the Sox17(+/-) B6 embryos, gallbladder epithelia were hypoplastic, and some were detached from the luminal wall, leading to bile duct stenosis or atresia. The shredding of the gallbladder epithelia is probably caused by cell-autonomous defects in proliferation and maintenance of the Sox17(+/-) gallbladder/bile duct epithelia. Our results suggest that Sox17 plays a dosage-dependent function in the morphogenesis and maturation of gallbladder and bile duct epithelia during the late-organogenic stages, highlighting a novel entry point to the understanding of the etiology and pathogenesis of human congenital biliary atresia.
In early embryogenesis, the posteroventral foregut endoderm gives rise to the budding endodermal organs including the liver, ventral pancreas and gallbladder during early somitogenesis. Despite the detailed fate maps of the liver and pancreatic progenitors in the mouse foregut endoderm, the exact location of the gallbladder progenitors remains unclear. In this study, we performed a DiI fate-mapping analysis using whole-embryo cultures of mouse early somite-stage embryos. Here, we show that the majority of gallbladder progenitors in 9–11-somite-stage embryos are located in the lateral-most domain of the foregut endoderm at the first intersomite junction level along the anteroposterior axis. This definition of their location highlights a novel entry point to understanding of the molecular mechanisms of initial specification of the gallbladder.
