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ABSTRACT: Intimal hyperplasia is the leading cause of late vein graft failure. Smooth muscle cell proliferation and migration is the underlying mechanism. Pharmacological approaches to prolong vein graft patency have produced limited results. AP-1 proteins play a role in the expression of many genes involved in cellular proliferation and cell cycle progression. Previously we reported inhibition of vascular smooth muscle cell migration, proliferation, and intimal hyperplasia in the balloon-injured rat carotid artery using an AP-1 decoy with HVJ-liposomes. In this report, we evaluated the effect of the AP-1 decoy on intimal hyperplasia in a large animal model. The jugular vein was transfected with hemagglutinating virus of Japan-liposomes containing the AP-1 decoy or scrambled oligonucleotides. An interposition graft was performed with the pretreated jugular vein between the transected femoral arteries. The graft was harvested at 16 weeks after the procedure. The intimal area was compared: the intimal area of the AP-1 decoy-treated versus control group was 47.3 +/- 15.2 versus 102.3 +/- 15.9 (P < .05), respectively. In conclusion, AP-1 decoy using HVJ-liposomes effectively prevented intimal hyperplasia of an autogenous vein graft in mongrel dogs.
Transplantation Proceedings 10/2006; 38(7):2161-3. · 1.00 Impact Factor
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ABSTRACT: Gitelman's syndrome is a primary renal tubular disorder with hypokalemic metabolic alkalosis, hypocalciuria, and magnesium deficiency. Short stature is one of clinical manifestations in children. The pathogenesis of short stature in Gitelman's syndrome is not known. To evaluate whether growth hormone (GH) is deficient and whether recombinant human GH (rhGH) improves growth rate, rhGH therapy was tried in a child with Gitelman's syndrome. Both height and body weight were less than the third percentile. Laboratory and radiologic findings suggested GH deficiency. During the first 6 months, rhGH therapy with potassium supplement markedly elevated growth rate from 3.8 cm/yr to 12.0 cm/yr. After cessation of rhGH, height increment markedly decreased to the pretreatment level of 3.6 cm/yr during the second 6 months. Additionally, hypomagnesemia was corrected after rhGH therapy. Accordingly, GH deficiency may contribute to short stature in children with Gitelman's syndrome, and rhGH therapy would be an excellent adjunctive treatment for short children with Gitelman's syndrome whose condition is resistant to conventional therapies in terms of growth.
American Journal of Kidney Diseases 05/1999; 33(4):778-81. · 5.43 Impact Factor
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Laboratory Investigation 03/1974; 30(2):115-8. · 3.64 Impact Factor
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ABSTRACT: The clinical histories of two infants who had severe hypertension and stenoses of the renal arteries are reported. In both children blood pressure fell significantly after surgical correction of renal ischemia. However, both infants had persistent mild hypertension for several months after surgical treatment. Similar results were found in other infants with renovascular hypertension, reported previously (11 cases). The mortality rate in this total group of 13 infants reviewed was high if renal ischemia was not corrected surgically (4/4). The reason why some infants have persistent hypertension after apparently adequate surgical relief of renal ischemia is not known.
Journal of Pediatrics 02/1974; 84(1):39-44. · 4.11 Impact Factor
