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202 results on '"Busque S"'

3. 137P Combining protein and mRNA spatial profiles to identify distinct cell population in metaplastic breast cancer

Author

Kuasne, H., primary, Savage, P., additional, Khadang, B., additional, Lai, J., additional, Martinez Ramirez, C., additional, Monast, A., additional, Fortier, A-M., additional, Busque, S., additional, Asselah, J., additional, Bouganim, N., additional, Meterissian, S., additional, Omeroglu, A., additional, Basik, M., additional, Riazalhosseini, Y., additional, and Park, M., additional

Published
2022
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33. Stimulatory pathways of the Calcium-sensing receptor on acid secretion in freshly isolated human gastric glands

Author

Remy, C, Kirchhoff, P, Hafner, P, Busque, S M, Mueller, M K, Geibel, John P, Wagner, Carsten A; https://orcid.org/0000-0002-9874-8898, Remy, C, Kirchhoff, P, Hafner, P, Busque, S M, Mueller, M K, Geibel, John P, and Wagner, Carsten A; https://orcid.org/0000-0002-9874-8898

Abstract

Gastric acid secretion is not only stimulated via the classical known neuronal and hormonal pathways but also by the Ca(2+)-Sensing Receptor (CaSR) located at the basolateral membrane of the acid-secretory gastric parietal cell. Stimulation of CaSR with divalent cations or the potent agonist Gd(3+) leads to activation of the H(+)/K(+)-ATPase and subsequently to gastric acid secretion. Here we investigated the intracellular mechanism(s) mediating the effects of the CaSR on H(+)/K(+)-ATPase activity in freshly isolated human gastric glands. Inhibition of heterotrimeric G-proteins (G(i) and G(o)) with pertussis toxin during stimulation of the CaSR with Gd(3+) only partly reduced the observed stimulatory effect. A similar effect was observed with the PLC inhibitor U73122. The reduction of the H(+)/K(+)-ATPase activity measured after incubation of gastric glands with BAPTA-AM, a chelator of intracellular Ca(2+), showed that intracellular Ca(2+) plays an important role in the signalling cascade. TMB-8, a ER Ca(2+)store release inhibitor, prevented the stimulation of H(+)/K(+)-ATPase activity. Also verapamil, an inhibitor of L-type Ca(2+)-channels reduced stimulation suggesting that both the release of intracellular Ca(2+) from the ER as well as Ca(2+) influx into the cell are involved in CaSR-mediated H(+)/K(+)-ATPase activation. Chelerythrine, a general inhibitor of protein kinase C, and Go 6976 which selectively inhibits Ca(2+)-dependent PKC(alpha) and PKC(betaI)-isozymes completely abolished the stimulatory effect of Gd(3+). In contrast, Ro 31-8220, a selective inhibitor of the Ca(2+)-independent PKCepsilon and PKC-delta isoforms reduced the stimulatory effect of Gd(3+) only about 60 %. On the other hand, activation of PKC with DOG led to an activation of H(+)/K(+)-ATPase activity which was only about 60 % of the effect observed with Gd(3+). Incubation of the parietal cells with PD 098059 to inhibit ERK1/2 MAP-kinases showed a significant reduction of the Gd(3+) effect

Published
2007

36. INDUCING TOLERANCE IN CLINICAL KIDNEY TRANSPLANTATION

Author

Strober, S., primary, Busque, S., additional, Dejbakhsh-Jones, S., additional, Benike, C., additional, Li, L., additional, Shizuru, J., additional, Lowsky, R., additional, Engleman, E., additional, Sarwal, M., additional, and Scandling, J. D., additional

Published
2010
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39. Sizzling Issues in Clinical Renal TransplantationTransplant nephrectomy improves survival following a failed renal allograft.J Am Soc Nephrol21: 324–380, 2010The success of continued steroid avoidance after kidney transplantation in the US.Am J Transplant9: 2768–2776, 2009Factors associated with progression of interstitial fibrosis in renal transplant patients receiving tacrolimus and mycophenolate mofetil.Transplantation88: 897–903, 2009

Author

Rubin, Mario F., primary, Ayus, JC, primary, Schold, JD, primary, Rush, DN, primary, Achinger, SG, additional, Lee, S, additional, Sayegh, MH, additional, Go, AS, additional, Santos, A, additional, Rehman, S, additional, Magliocca, J, additional, Meier-Kriesche, HU, additional, Cockfield, SM, additional, Nickerson, PW, additional, Arlen, DJ, additional, Boucher, A, additional, Busque, S, additional, Girardin, CE, additional, Knoll, GA, additional, Lachance, JG, additional, Landsberg, DN, additional, Shapiro, RJ, additional, Shoker, A, additional, and Yilmaz, S, additional

Published
2010
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50. Randomized Phase 2b Trial of Tofacitinib (CP‐690,550) in De NovoKidney Transplant Patients: Efficacy, Renal Function and Safety at 1 Year

Author

Vincenti, F., Tedesco Silva, H., Busque, S., O’Connell, P., Friedewald, J., Cibrik, D., Budde, K., Yoshida, A., Cohney, S., Weimar, W., Kim, Y. S., Lawendy, N., Lan, S.‐P., Kudlacz, E., Krishnaswami, S., and Chan, G.

Abstract

In this Phase 2b study, 331 low‐to‐moderate risk de novokidney transplant patients (approximately 60% deceased donors) were randomized to a more intensive (MI) or less intensive (LI) regimen of tofacitinib (CP‐690, 550), an oral Janus kinase inhibitor or cyclosporine (CsA). All patients received basiliximab induction, mycophenolic acid and corticosteroids. Primary endpoints were: incidence of biopsy‐proven acute rejection (BPAR) with a serum creatinine increase of ≥0.3 mg/dL and ≥20% (clinical BPAR) at Month 6 and measured GFR at Month 12. Similar 6‐month incidences of clinical BPAR (11%, 7% and 9%) were observed for MI, LI and CsA. Measured GFRs were higher (p < 0.01) at Month 12 for MI and LI versus CsA (65 mL/min, 65 mL/min vs. 54 mL/min). Fewer (p < 0.05) patients in MI or LI developed chronic allograft nephropathy at Month 12 compared with CsA (25%, 24% vs. 48%). Serious infections developed in 45%, 37% and 25% of patients in MI, LI and CsA, respectively. Anemia, neutropenia and posttransplant lymphoproliferative disorder occurred more frequently in MI and LI compared with CsA. Tofacitinib was equivalent to CsA in preventing acute rejection, was associated with improved renal function and less chronic allograft histological injury, but had side‐effects at the doses evaluated.

Published
2012
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