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Efficacy of prophylactic clipping for postpolypectomy bleeding: A multicenter randomized controlled trial

ABSTRACT: Interventions: Colonoscopic polypectomy Prophylactic clipping after colonoscopic polypectomy Primary outcome(s): Postpolypectomy bleeding rate Study Design: Parallel Randomized

DISEASE(S): Colorectal Neoplasms

PROVIDER: 2627524 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Evaluation of Nexpowder Application to Prevent Delayed Bleeding After Colorectal Endoscopic Mucosal Resection

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Novel single nucleotide polymorphism markers for low dose aspirin-associated small bowel bleeding

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Project description:Uterine NK cells (uNK) play a role in the regulation of placentation but their functions in non-pregnant endometrium are not understood. We have previously reported suppression of endometrial bleeding and alteration of spiral artery morphology in women exposed to asoprisnil, a progesterone receptor modulator (PRM). We now compare global endometrial gene expression in asoprisnil-treated versus control women and demonstrate a statistically significant reduction of genes in the IL-15 pathway, known to play a key role in uNK development and function. Suppression of IL-15 by asoprisnil was also observed at mRNA level (p<0.05), and immunostaining for NK cell marker CD56 revealed a striking reduction of uNK in asoprisnil-treated endometrium (p<0.001). IL-15 levels in normal endometrium are progesterone-responsive. Progesterone receptor (PR) positive stromal cells transcribe both IL-15 and IL-15RA. Thus, the response of stromal cells to progesterone will be to increase IL-15 trans-presentation to uNK, supporting their expansion and differentiation. In asoprisnil-treated endometrium, there is a marked down-regulation of stromal PR expression and virtual absence of uNK. These novel findings indicate that the IL-15 pathway provides a missing link in the complex interplay between endometrial stromal cells, uNK and spiral arteries affecting physiological and pathological endometrial bleeding. 39 Samples

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INCREASED HEAT SHOCK PROTEIN 70 EXPRESSION BY CM-695 ASSOCIATES WITH STRONG ANTITROMBOTIC EFFECT WITHOUT INCREASING BLEEDING

Project description:BACKGROUND Antithrombotic medications target coagulation factors. Their use is associated with an increased bleeding risk. Safer drugs are needed. We described that the heat shock protein 70 (Hsp70) exhibits antithrombotic properties that do not influence bleeding. OBJECTIVES By using murine models, we want to test the hypothesis that overexpressing Hsp70 with CM-695, a dual inhibitor of HDAC6 and phosphodiesterase 9, protects against thrombosis while leaves bleeding tendency unaltered. METHODS CM-695 was used to induce Hsp70 overexpression. Hsp70 overexpressing mice were submitted to three thrombosis-triggering procedures. The ferric chloride carotid artery model was used to compare the antithrombotic role of CM-695 and rivaroxaban, a direct oral anticoagulant. The mouse tail transection model was used to compare the bleeding tendency upon CM-695 or rivaroxaban administration. RESULTS Intraperitoneal (i.p.) 20 mg/kg CM-695 increased Hsp70 expression markedly in the murine aortic tissue. This treatment delayed thrombosis in the collagen/epinephrine [P=0.04 (Log-Rank test), n=10], Rose Bengal/laser [median vessel occlusion time (OT): 58.6 vs. 39.0 minutes (min) in the control group (CG), P=0.008, n≥10] and ferric chloride (OT: 14.7 vs. 9.2 min in the CG, P=0.032, n≥10) models. I.p. 80 mg/kg CM-695 (n≥9) and intravenous 3 mg/kg rivaroxaban (n≥8) significantly delayed thrombosis. CM-695 did not induce bleeding [median bleeding time (BT): 8.5 vs. 7.5 min in the CG, n≥10]. However, this was dramatically increased by rivaroxaban (BT: 30.0 vs. 13.7 min in the CG, P=0.001, n=10). CONCLUSIONS CM-695 is a new antithrombotic drug devoid of bleeding risk that may be envisioned as a useful clinical tool.

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