Durangustafsson8594

Several literature reviews have suggested that pregnancy may trigger the formation of dural arteriovenous fistulae (DAVF). However, few case reports have described DAVF discovered during pregnancy, and treatment strategies remain largely unknown.

A 28-year-old primigravid woman without any medical history of note presented to our hospital for natural twin conception. She started to feel left-sided pulsatile tinnitus in 23 weeks of gestation. Magnetic resonance imaging of the head raised suspicion of left cavernous sinus DAVF with leptomeningeal venous drainage. Considering the risk of intracerebral hemorrhage due to the increased cardiac output in the third trimester of a twin pregnancy, we performed transarterial embolization for the DAVF, which was successfully achieved without complications in 28 weeks of gestation. Tinnitus resolved immediately after the procedure, and the postoperative course proved uneventful. Both fetuses were safely delivered by cesarean section on 37 1/7 weeks of gestation.

We encountered a case of cavernous sinus DAVF during a twin pregnancy. This case suggests that hemodynamic shift due to pregnancy has potential to cause higher shunt flow in an arteriovenous fistula. The timing of treatment should be determined in consideration of the hemodynamic change in the course of pregnancy. If X-ray exposures and iodine contrast media are appropriately managed, endovascular intervention is one treatment option, even during pregnancy.

We encountered a case of cavernous sinus DAVF during a twin pregnancy. This case suggests that hemodynamic shift due to pregnancy has potential to cause higher shunt flow in an arteriovenous fistula. The timing of treatment should be determined in consideration of the hemodynamic change in the course of pregnancy. If X-ray exposures and iodine contrast media are appropriately managed, endovascular intervention is one treatment option, even during pregnancy.

We assessed the safety and efficacy of flow diverter stents (FDSs) in the treatment of recanalized or residual intracranial aneurysms treated endovascularly.

Patients whose recanalized or residual aneurysms were treated with FDSs in five tertiary hospitals were reviewed retrospectively. The patients' demographic data, aneurysm characteristics, types of previous treatment, and clinical complications, or serious adverse events associated with FDSs, as well as the results of neurological and angiographic follow-up assessments, were recorded.

Eighty-six patients (37 males) with 87 aneurysms were included in this study. Eighty (91.9%) aneurysms were in the anterior and seven (8.1%) in the posterior circulation. The initial treatment methods were the primary coiling or balloon remodeling technique in 69 (79.3%) and stent-assisted coiling in 18 (20.7%) aneurysms. The endovascular procedure was successful in all patients. Complications occurred in four patients, for a total complication rate of 4.6%. A technical complication developed in one patient (1.2%). Syrosingopine An in-stent thrombosis treated with tirofiban was seen in two cases. Late in-stent stenosis exceeding 50% was treated with balloon angioplasty in one patient. The mean length of follow-up was 21.0 months. The first angiographic follow-up (3-6 months) revealed the complete occlusion of 74 aneurysms (85.1%). While 76 aneurysms (87.4%) were occluded at the last angiographic follow-up (mean 26.0 months), 11 aneurysms (12.6%) were still filling. Morbimortality was zero.

The drawback of endovascular treatment is aneurysmal remnants or recurrences, which is safely and durably amenable to flow diversion.

The drawback of endovascular treatment is aneurysmal remnants or recurrences, which is safely and durably amenable to flow diversion.Both microRNAs (miRs) and dexmedetomidine (Dex) have been verified to exert functional roles in myocardial ischemia-reperfusion injury (MI/RI). Given that, we concretely aim to discuss the effects of Dex and miR-138-5p on ventricular remodeling in mice affected by MI/RI via mediating leukotriene B4 receptor 1 (Ltb4r1). MI/RI mouse model was established by ligating left anterior descending coronary artery. The cardiac function, inflammatory factors and collagen fiber contents were detected after Dex/miR-138-5p/Ltb4r1 treatment. MiR-138-5p and Ltb4r1 expression in myocardial tissues were tested by RT-qPCR and western blot assay. The target relationship between miR-138-5p and Ltb4r1 was verified by online software prediction and luciferase activity assay. MiR-138-5p was down-regulated while Ltb4r1 was up-regulated in myocardial tissues of MI/RI mice. Dex improved cardiac function, alleviated myocardial damage, reduced inflammatory factor contents, collagen fibers, and Ltb4r1 expression while increased miR-138-5p expression in myocardial tissues of mice with MI/RI. Restored miR-138-5p and depleted Ltb4r1 improved cardiac function, abated inflammatory factor contents, myocardial damage, and content of collagen fibers in MI/RI mice. MiR-138-5p directly targeted Ltb4r1. The work evidence that Dex could ameliorate ventricular remodeling of MI/RI mice by up-regulating miR-138-3p and down-regulating Ltb4r1. Thus, Dex and miR-138-3p/Ltb4r1 may serve as potential targets for the ventricular remodeling of MI/RI.We report results of a phase-1 study evaluating the safety and anti-cancer activity of the small molecule insulin-like growth factor-1 receptor (IGF-1R) inhibitor, linsitinib combined with bortezomib, and dexamethasone in relapsed/refractory multiple myeloma. Nineteen patients were enrolled across four dose-escalation cohorts (75-150 mg bid). The maximum tolerated dose of linsitinib was 125 mg. The most frequent Grade 3/4 AEs occurring in ≥10% of patients were thrombocytopenia (53%), bone pain (26%), neutropenia (21%), diarrhea (14%), anemia (14%), rash (10%), and lung infection (10%). Study discontinuation due to treatment-related AEs was low (16%). Across all cohorts the ORR was 61% (95% CI 28.9-75.6%). Three partial response or greater and one stable disease were observed in proteasome inhibitor (PI) refractory patients (n = 5). Median PFS was 7.1 months (95% CI 3.6-NA). Linsitinib plus bortezomib and dexamethasone demonstrate a manageable safety profile while the clinical benefit particularly in PI refractory patients warrants further exploration.