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1.
J Urol ; 179(2): 582-6, 2008 Feb.
Article in English | MEDLINE | ID: mdl-18078958

ABSTRACT

PURPOSE: We evaluated the impact of stenting the ureteroileal anastomosis on its competence, upper urinary tract dilatation, gastrointestinal recovery, metabolic parameters and patency rate after cystectomy with ileal bladder substitution or ileal conduit. MATERIALS AND METHODS: A total of 54 patients (37 with an ileal bladder substitute and 17 with an ileal conduit) were prospectively randomized into 2 groups, with (29) or without (25) perioperative stenting of the ureteroileal anastomosis. In all cases an end-to-side ureteroileal refluxing anastomosis was performed. The stents were removed after 5 to 10 days. The parameters assessed postoperative days 1, 3 and 7 were creatinine concentration from the wound drains, upper urinary tract dilatation, time to bowel function recovery, serum creatinine, as well as urea and incidence of metabolic acidosis. RESULTS: Median patient age was 68 years (range 45 to 85). Urine leak on postoperative day 1 was more frequent in those anastomoses without stents, and on postoperative days 3 and 7 the values were comparable. Stenting of the ureteroileal anastomosis resulted in significantly decreased early postoperative upper urinary tract dilatation, improved recovery of bowel function and decreased metabolic acidosis. In either group no patient had clinical evidence of ureteroileal anastomotic stricture during the early postoperative period. Three patients with perioperative stenting required surgical or endoscopic treatment for a stricture of the ureteroileal anastomosis during the 12-month followup. CONCLUSIONS: Stenting of the ureteroileal anastomosis allows for significantly less frequent incidence of early postoperative dilatation of the pelvicaliceal system, bowel activity resumes significantly earlier and metabolic acidosis is significantly less frequent.


Subject(s)
Anastomosis, Surgical/instrumentation , Ileum/surgery , Stents , Ureter/surgery , Urinary Bladder Diseases/surgery , Urinary Diversion , Aged , Aged, 80 and over , Cystectomy , Follow-Up Studies , Humans , Middle Aged , Prospective Studies , Treatment Outcome
2.
J Biol Chem ; 280(26): 25258-66, 2005 Jul 01.
Article in English | MEDLINE | ID: mdl-15870074

ABSTRACT

Pituitary adenylyl cyclase-activating polypeptide 38 (PACAP38) plays an important role in the proliferation and differentiation of neural cells. In the present study, we have investigated how PACAP38 inhibits the proliferation of cultured neocortical astroglial cells. When applied to synchronized cells during the G(1) phase of the cell cycle, PACAP38 diminished the subsequent nuclear uptake of bromodeoxyuridine. When applied for 2 days, it reduced the cell number. PACAP38 did not exert its antiproliferative effect by activating protein kinase A. It also did not reduce the activity of mitogen-activated protein kinases essential for G(1) phase progression. Instead, PACAP38 acted on a member of the Rho family of small GTPases. It reduced the activity of RhoA as was shown with a Rhotekin pull-down assay. The decrease in endogenous RhoA activity induced by treatment of the cells with C3 exotoxin or by expression of dominant negative RhoA also reduced the nuclear uptake of bromodeoxyuridine. In contrast, expression of constitutively active RhoA prevented the effect of PACAP38. Our data show a novel signal transduction pathway by which the neuropeptide influences cell proliferation.


Subject(s)
Astrocytes/cytology , Nerve Growth Factors/physiology , Neuropeptides/physiology , Neurotransmitter Agents/physiology , rhoA GTP-Binding Protein/metabolism , Actins/chemistry , Adenoviridae/genetics , Animals , Animals, Newborn , Astrocytes/metabolism , Bromodeoxyuridine/pharmacology , Cell Cycle , Cell Line , Cell Nucleus/metabolism , Cell Proliferation , Cyclic AMP-Dependent Protein Kinases/metabolism , Enzyme Inhibitors/pharmacology , G1 Phase , GTP Phosphohydrolases/chemistry , GTP-Binding Proteins , Genes, Dominant , Glutathione Transferase/metabolism , Green Fluorescent Proteins/metabolism , Intracellular Signaling Peptides and Proteins/chemistry , MAP Kinase Signaling System , Microscopy, Fluorescence , Nerve Growth Factors/metabolism , Neuropeptides/metabolism , Neurotransmitter Agents/metabolism , Peptides/chemistry , Pituitary Adenylate Cyclase-Activating Polypeptide , RNA, Messenger/metabolism , Rats , Rats, Wistar , Signal Transduction , Tetracycline/metabolism , Time Factors , Transfection
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