Splenic artery embolisation for portal hypertention in children

Background: Bleeding from esophageal varices is one of the most common causes of serious gastrointestinal haemorrhage in children. We analysed our experience with the use of splenic artery embolisation and variceal sclerotherapy for bleeding oesophageal varices.Patients and Methods: Records of all patients treated for bleeding oesophageal varices caused by portal hypertension from 1998 to 2004 were retrospectively analysed. Patients were followed up for five years.Results: Out of 25 patients treated, ten belonged to sclerotherapy (group A), eight to combined sclerotherapy and embolisation (group B), and seven to only embolisation (group C). The patients were selected randomly, only two patients who had active bleed recently were directly sclerosed. The splenic artery was embolised at the hilum using steel coils in 15 patients with portal hypertension and hypersplenism. Follow-up findings showed decrease in splenic mass,varices, and hyperdynamic flow.Conclusion: In spite of few patients and a short period of follow-up, our results pointed out that a serious consideration should be given to this procedure, as it slowed the sequel of portal hypertension and thecomplications associated with it. Patients who were embolised and followed up for five years had lesser rebleeds and complications than sclerotherapy patients

Robotic Treatment of Utricular Cysts

none5noMüllerian duct remnants (MDR) derive from incomplete regression of female structures, presumably as a consequence of delayed or insufficient production or effect of anti-Müllerian hormone (AMH) [1–3]. Dilatation of the Müllerian duct remnants can lead to an enlarged prostatic utricle or a Müllerian duct cyst which is known to be present in 4% of newborns and 1% of adults [4]. The prevalence of symptomatic remnants is still unknown. In 11–14% of cases an enlarged prostatic utricle is associated to distal hypospadias or disorders of sexual differentiation (DSD) and to a perineal hypospadias in 50% of cases [5, 6].noneLima, Mario; Gargano, Tommaso; Maffi, Michela; Ruggeri, Giovanni; Libri, MicheleLima, Mario; Gargano, Tommaso; Maffi, Michela; Ruggeri, Giovanni; Libri, Michel

Molecular analysis of the subtype-selective inhibition of cloned K(ATP) channels by PNU-37883A

1. In this study, we have used Kir6.1/Kir6.2 chimeric proteins and current recordings to investigate the molecular basis of PNU-37883A inhibition of cloned K(ATP) channels. 2. Rat Kir6.1, Kir6.2 and Kir6.1/Kir6.2 chimeras were co-expressed with either SUR2B or SUR1, following RNA injection into Xenopus oocytes, and fractional inhibition of K(ATP) currents by 10 μM PNU-37883A reported. 3. Channels containing Kir6.1/SUR2B were more sensitive to inhibition by PNU-37883A than those containing Kir6.2/SUR2B (mean fractional inhibition: 0.70, cf. 0.07). 4. On expression with SUR2B, a chimeric channel with the Kir6.1 pore and the Kir6.2 amino- and carboxy-terminal domains was PNU-37883A insensitive (0.06). A chimera with the Kir6.1 carboxy-terminus and Kir6.2 amino-terminus and pore was inhibited (0.48). These results, and those obtained with other chimeras, suggest that the C-terminus is an important determinant of PNU-37883A inhibition of Kir6.1. Similar results were seen when constructs were co-expressed with SUR1. Further chimeric constructs localised PNU-37883A sensitivity to an 81 amino-acid residue section in the Kir6.1 carboxy-terminus. 5. Our data show that structural differences between Kir6.1 and Kir6.2 are important in determining sensitivity to PNU-37883A. This compound may prove useful in probing the structural and functional differences between the two channel subtypes