[Acute renal failure following rectosigmoidoscopy]. / Insuffisance rénale aiguë après rectosigmoïdoscopie.

We report the case of a 24-year old man with a past history of vesical extrophy and ureterosigmoidostomy in childhood, admitted with acute left flank pain and acute renal failure. The complaints started the day following the endoscopic resection of a sigmoid polyp. The stricture of the ureterosigmoid junction was diagnosed by intravenous urography. Conservative treatment with endo-ureteral dilatation was successfully performed. At 2 years of follow-up, the patient is still asymptomatic, without any residual hydronephrosis.

Human immunodeficiency virus type 1 quasi species that rebound after discontinuation of highly active antiretroviral therapy are similar to the viral quasi species present before initiation of therapy.

In an effort to identify the sources of the viruses that emerge after discontinuation of therapy, analyses of human immunodeficiency virus (HIV) quasi species were done for 3 patients with sustained levels of HIV RNA of <50 copies/mL for 1-3 years. The sequences found in the rebounding plasma virus were closely related to those of the actively replicating form of viruses present before the initiation of combination therapy. All quasi species found in the rebounding plasma virus were also present in proviral DNA, cell-associated RNA in peripheral blood mononuclear cells (PBMC), and virion RNA derived from PBMC coculture during periods when plasma HIV RNA levels were <50 copies/mL. These findings suggest that the rapid resurgence of plasma viremia observed after discontinuation of therapy and the viruses cocultured from PBMC are derived from a relatively stable pool of the replicating form of virus rather than from activation of a previously latent pool.

Impact of HIV-1 infection and highly active antiretroviral therapy on the kinetics of CD4+ and CD8+ T cell turnover in HIV-infected patients.

To evaluate the effects of HIV infection on T cell turnover, we examined levels of DNA synthesis in lymph node and peripheral blood mononuclear cell subsets by using ex vivo labeling with BrdUrd. Compared with healthy controls (n = 67), HIV-infected patients (n = 57) had significant increases in the number and fraction of dividing CD4(+) and CD8(+) T cells. Higher percentages of dividing CD4(+) and CD8(+) T cells were noted in patients with the higher viral burdens. No direct correlation was noted between rates of T cell turnover and CD4(+) T cell counts. Marked reductions in CD4(+) and CD8(+) T cell proliferation were seen in 11/11 patients 1-12 weeks after initiation of highly active antiretroviral therapy (HAART). These reductions persisted for the length of the study (16-72 weeks). Decreases in naive T cell proliferation correlated with increases in the levels of T cell receptor rearrangement excision circles. Division of CD4(+) and CD8(+) T cells increased dramatically in association with rapid increases in HIV-1 viral loads in 9/9 patients 5 weeks after termination of HAART and declined to pre-HAART-termination levels 8 weeks after reinitiation of therapy. These data are consistent with the hypothesis that HIV-1 infection induces a viral burden-related, global activation of the immune system, leading to increases in lymphocyte proliferation.

Effects of a phorbol ester and isoquinoline sulfonamides on rabbit parietal cell function.

The role of protein kinase C (PKC) on gastric H+ secretion, as measured by aminopyrine (AP) uptake and other intracellular signal transduction products, was investigated in isolated rabbit parietal cells using the PKC activator 12-0-tetradecanoyl phorbol 13-acetate (TPA) and several PKC inhibitors, including isoquinoline sulfonamides (H-7, H-8, H-89 and HA-1004) and calphostin-C. TPA dose-dependently inhibited histamine (10(-4) M)- and carbachol (10(-4) M)-stimulated AP uptake without affecting the response to dibutyryl cyclic AMP (10(-3) M). H-7 and calphostin-C dose-dependently augmented secretagogue-stimulated AP uptake, whereas H-8 and H-89 inhibited the response to secretagogues, and HA-1004 had no effect. H-7 and calphostin-C-induced augmentation of AP uptake was blocked by a calcium (Ca++) antagonist, lanthanum chloride, which suggests that the enhanced AP response was regulated by extracellular Ca++. Moreover, H-7 treatment partially reversed the TPA (10(-7) M)-induced inhibition of secretagogue-stimulated AP uptake. TPA reduced histamine- and carbachol-stimulated cAMP and inositol 1,4,5-triphosphate production by 50% and 96%, respectively, with a concomitant reduction of adenylate cyclase and intracellular free Ca++ by 44% and 78%. TPA increased the distribution of membrane-associated PKC by 20% and decreased histamine-stimulated PKA by 30%. In contrast, H-7 inhibited both PKC and protein tyrosine kinase activity in vitro but had no effect on these parameters in vivo. The results indicate that TPA-induced inhibition of secretagogue-stimulated AP uptake in PC is presumably mediated by activation of PKC.

Effects of cyclic adenosine monophosphate-dependent protein kinase and calcium-dependent protein kinase modulators on stimulated gastric acid secretion in the perfused rat stomach.

The effects of cyclic adenosine monophosphate-dependent protein kinase (PKA) and calcium-dependent protein kinase (PKC) modulators on secretagogue-stimulated gastric acid secretion were studied in the continuously perfused stomach of the anesthetized rat. Intravenous histamine (0.25 mg/kg/h) and pentagastrin (2 micrograms/kg/h) increased secretion above baseline by three- and fourfold, respectively. Parenteral administration of a PKC activator, 12-o-tetradecanoylphorbol-13-acetate (TPA; 0.1 nmol/h), decreased histamine- and pentagastrin-stimulated secretion by 64 and 40%, respectively. Administration of PKC inhibitors, calphostin C and 1-(5-isoquinolinyl sulfonyl)-2 methylpiperazine (H-7; 10 nmol/h, each), increased histamine- and pentagastrin-stimulated secretion by 115 and 74% and 42 and 79%, respectively, while equimolar concentrations (10 nmol/h) of three other isoquinoline sulfonamides (HA-1004, H-8, and H-89) had no effect, except for H-89 (100 nmol/h) which inhibited the histamine- and penta-gastrin-stimulated acid secretion by 44%. Basal secretion was not significantly altered by the aforementioned drugs. The TPA-induced inhibition of pentagastrin-stimulated secretion was partially reversed by treatment with H-7. These findings support a role of PKA and PKC in the modulation of stimulated gastric acid secretion in vivo.