Although less common than oesophageal varices in portal hypertension, gastric fundal varices carry a higher mortality rate when they rupture. They are less amenable to sclerotherapy. We have developed a minimally invasive balloon-occluded retrograde transverse obliteration (B-RTO) procedure to treat gastric fundal varices. B-RTO involves inserting a balloon catheter into an outflow shunt (gastric-renal or gastric-vena caval inferior) via the femoral or internal jugular vein. Blood flow is then blocked by inflating the balloon, and 5% ethanolamine oleate iopamidol is injected in a retrograde manner. The embolized gastric varix subsequently disappears. B-RTO was performed in 32 patients with gastric varices. Follow-up endoscopies were performed at intervals of 2-4 months for an average observation period of 14 months. Eradication of the varices has been confirmed in 31 of 32 patients. No recurrence occurred in any patients in the follow-up period. There were no significant changes in liver function after the procedure. We conclude that B-RTO is a safe and effective procedure for the treatment of gastric fundal varices.
The present study was conducted to investigate the influence of cell cycle stage of the donor nucleus on chromatin structure and development of mouse embryonic nuclei transplanted into enucleated oocytes. Donor cell-cycle stage was controlled in order to examine, in addition, the developmental potential of nuclei from 2-, 4-, and 8-cell-stage embryos. The cell cycle stage of donor nuclei was classified as early, middle, or late. After nuclear transfer, electrofusion, and activation, early-stage transplants formed a single pronucleus-like structure, but middle-stage transplants formed very irregular types of structures and late-stage transplants extruded a polar body. A high proportion of development to the blastocyst stage (77.8%) and an increased cell number (62.1 cells) were obtained from the early 2-cell-stage transplants as opposed to the middle- (0%) and late-stage (20.8%, 37.0 cells) transplants (p < 0.001). With transplantation of early-stage nuclei, high proportions of development to the blastocyst stage and of offspring were obtained from nuclear transplant embryos with a nucleus from a 2-, 4-, or 8-cell-stage embryo. The results confirm that the donor cell-cycle stage critically affects the chromatin structure and development of nuclear transplant embryos. The results also demonstrate that the nuclei from 2-, 4-, and 8-cell-stage mouse embryos in the early stage of each cell cycle can be reprogrammed when transplanted into enucleated mature oocytes.
Patients with hepatitis C have been reported occasionally to be coinfected with serum marker-negative (silent) hepatitis B virus (HBV). The frequency and significance of such coinfection were investigated. Thirty patients with hepatitis C virus (HCV) infections (10 acute, 10 chronic, 10 cirrhotic) were selected randomly; the acute cases were without serum hepatitis B surface antigen (HBsAg) and anti-hepatitis B core IgM, and the chronic cases were without HBsAg. A nested polymerase chain reaction for the X open reading frame was used to amplify HBV DNA in serum, and immunoperoxidase staining was carried out on liver biopsy specimens. Nucleotide sequencing was carried out to characterize the amplified HBV DNAs. In order to clarify the possibility that the silent HBV mutant promotes HCV replication in the liver, the full-length HCV RNA and the cloned silent HBV DNA dimer were cotransfected into an established cell line, HuH-7, and the amount of secreted HCV RNA was quantified serially. The target HBV DNA was amplified in 26 (86.7%) of the 30 patients. Subsequent direct nucleotide sequencing in 9 selected patients revealed an 8-nucleotide deletion, characteristic of a silent HBV mutant. Immunostaining revealed hepatitis B surface antigen in 15 (50.0%). Cotransfected silent HBV DNA augmented the secretion of HCV RNA by up to 5-fold in comparison with HCV RNA transfection alone. In conclusion, HCV is coinfected frequently with the silent HBV mutant and the latter probably promotes the replication of the former in the liver.
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