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Objective: This article describes how one comprehensive cancer center in the Northeast United States reorganized their nursing research fellowship (NRF) with the goals of engaging nurses in research processes, developing a culture of inquiry, building nursing research capacity, and sustaining infrastructures for facilitating high-quality, nurse-led oncology research studies. Methods: The basis for the curriculum, course work, and research practicum is derived from academic courses taught at the undergraduate, graduate, and doctoral levels. Evidence from the current literature, expertise of nurse-scientists, and feedback from former fellows provided the background for a fellowship model that included: (1) amending curriculum timeframes; (2) incorporating protected time; (3) improving access to resources; (4) enhancing the protection, data sharing, and accessibility of data; and (5) involving nurse-scientists as mentors and facilitators of research processes. These factors were incorporated over 3 years. Metrics included individual class and overall course evaluations and ongoing assessments. Results: In three cohorts from 2016 to 2019, a total of 21 nurses were accepted, and 18 (86%) nurses completed the NRF. In cohort 1 through cohort 3, 17 fellows presented their research findings internally, and a total of nine projects were presented at external forums. There were seven fellows whose manuscript submissions resulted in 21 journal publications. Of the 18 fellows, 15 (83%) conducted institutional review board-approved studies and three (17%) fellows developed studies involving one concept analysis and two systematic reviews. Conclusions: Utilizing technology, the fellowship improved access beyond the classroom setting. Improved application processes, the inclusion of protected time for nurses, and mentoring from nurse-scientists demonstrate a commitment to fostering a culture supporting new knowledge and innovation for improving patient care.

Background Ventricular tachycardia (VT) and ventricular fibrillation (VF) remain a challenging problem in patients with implantable cardioverter-defibrillators (ICDs). Objectives This study aimed to determine whether ranolazine administration decreases the likelihood of VT, VF, or death in patients with an ICD. Methods This was double-blind, placebo-controlled clinical trial in which high-risk ICD patients with ischemic or nonischemic cardiomyopathy were randomized to 1,000 mg ranolazine twice a day or placebo. The primary endpoint was VT or VF requiring appropriate ICD therapy or death, whichever occurred first. Pre-specified secondary endpoints included ICD shock for VT, VF, or death and recurrent VT or VF requiring ICD therapy. Results Among 1,012 ICD patients (510 randomized to ranolazine and 502 to placebo) the mean age was 64 ± 10 years and 18% were women. During 28 ± 16 months of follow-up there were 372 (37%) patients with primary endpoint, 270 (27%) patients with VT or VF, and 148 (15%) deaths. The blinded study drug was discontinued in 199 (39.6%) patients receiving placebo and in 253 (49.6%) patients receiving ranolazine (p = 0.001). The hazard ratio for ranolazine versus placebo was 0.84 (95% confidence interval: 0.67 to 1.05; p = 0.117) for VT, VF, or death. In a pre-specified secondary analysis, patients randomized to ranolazine had a marginally significant lower risk of ICD therapies for recurrent VT or VF (hazard ratio: 0.70; 95% confidence interval: 0.51 to 0.96; p = 0.028). There were no other significant treatment effects in other pre-specified secondary analyses, which included individual components of the primary endpoint, inappropriate shocks, cardiac hospitalizations, and quality of life. Conclusions In high-risk ICD patients, treatment with ranolazine did not significantly reduce the incidence of the first VT or VF, or death. However, the study was underpowered to detect a difference in the primary endpoint. In prespecified secondary endpoint analyses, ranolazine administration was associated with a significant reduction in recurrent VT or VF requiring ICD therapy without evidence for increased mortality. (Ranolazine Implantable Cardioverter-Defibrillator Trial [RAID]; NCT01215253)

Riassunto Obiettivi Descrivere l’atteggiamento clinico nella risoluzione dei piu frequenti difetti di cresta da riabilitare con implantologia, sulla base delle metodiche maggiormente validate dalla letteratura scientifica. Materiali e metodi La rigenerazione guidata dell’osso attraverso membrane barriera ad azione occlusiva e praticabile in differenti difetti ossei alveolari. Tale fenomeno si puo comprendere se si conosce la cascata degli eventi biologici a carico dei tessuti duri e molli che si innesca durante la rigenerazione guidata. E indispensabile classificare i difetti localizzati delle creste edentule per poter adottare protocolli chirurgici appropriati laddove la morfologia non si associ a una rigenerazione spontanea. Risultati Mediante casi clinici esemplificativi il lavoro mostra i risultati ottenibili con l’applicazione dei principi della GBR, inserendo gli impianti in maniera protesicamente guidata e non costringendo il protesista a realizzare una protesi di compromesso. Conclusioni I casi clinici trattati, usando un protocollo ripetibile e validato, sono l’esempio che non e solo l’anatomia del difetto l’elemento discriminante la quota di GBR ottenibile quanto il mantenimento dell’“effetto tenda” che il Gore-Tex ® con rinforzo in titanio puo fornire se opportunamente sagomato.

Objective Bicuspid aortic valve (BAV) is associated with high incidence of ascending aortic aneurysm. In BAV sporadic form, changes in outflow's hemodynamic secondary to the valvular morphotype are said to play a prominent role in the aortic dilatation. We aimed at comparing the different ascending aorta segment diameters according to the morphotype and the function of the BAV. Methods We evaluated 174 patients with sporadic BAV by transthoracic echocardiography. The valvular function was defined as either Aortic Insufficiency (AI) if Grade ≥ 2 and aortic Stenosis (AS) if mean gradient > 20 mmHg. Aortic diameters were measured at the Valsalva sinus, tubular ascending aorta and at the aortic arch. Kruskal-Wallis, Mann–Whitney and Spearman tests were used for comparisons. Results Among the non-operated patients, Sievers’ morphotype was type 1LR for 63%, type 1NR for 18%, and other types counted for 19%. The Valsalva sinus diameter did not differ according to the Sievers’ type (P = 0.78). The type 1LR type compared to the type1NR appeared to have a wider tubular aorta, but not significantly (42.3 ± 8.5 vs. 36.4 ± 7.3 mm; P = 0.06). Aortic valve function was distributed as follows: AI: 39%, AS: 20%, Both: 9%, Normal: 32%. Comparison of the different valve dysfunctions revealed a difference at the Valsalva (P Conclusion Our results showed the tremendous role of AI in the aortic dilation of all segments except the arch. However no influence of BAV morphotype was noticed on aortic diameters. Our results give rise to the relatively limited influence of the valvular morphology in the development of aortic dilation.

Acute erythroleukemia is a relatively rare disorder of a multilineal nature. Patients with this type of leukemia traditionally have been treated with a standard myeloid protocol, with a wide variation in prognosis between M6a, which has a similar prognosis to acute myelogenous leukemias, and M6b, with an extremely poor outcome despite aggressive therapy. Forty-eight archival cases of acute erythroleukemia, subtypes M6a (the traditional FAB-M6), M6b (pure erythroleukemia), and M6c (>30% myeloblasts and >30% pronormoblasts by FAB exclusion criteria), were evaluated for multidrug resistance gene (MDR-1) status. Findings were correlated with clinical course and karyotypes. Immunohistochemical stain for the protein product of MDR-1, P-glycoprotein, was variably positive in 11 of 23 patients with M6a, as well as in all of the patients with M6b (strongly positive) and M6c (weakly positive). P-glycoprotein expression positively correlated with unfavorable cytogenetic aberrations, poor response to chemotherapeutic agents, and short survival. Most significant was that P-glycoprotein expression demonstrated a negative additive effect on response to treatment and prognosis with unfavorable cytogenetic anomalies. P-glycoprotein expression and multiple cytogenetic anomalies most probably contribute to the resistance to chemotherapy and poor survival characteristic of the patients with M6b (mean survival, 3.15 +/- 4.2 mo) and M6c (mean survival, 10.5 +/- 12.7 mo). Because patients with M6b and M6c have increased numbers of pronormoblasts in their bone marrow and past chemotherapeutic attempts have failed, chemotherapy directed at these cells is appropriate. Additional therapy directed toward the MDR-1 gene and its protein product seems indicated from our findings.

Acute erythroleukemia is an aggressive leukemia derived from a multipotential stem cell. Three subtypes have been described: (1) M6a with greater than or equal to 30% blasts of the nonerythrocytic component, (2) M6b with greater than or equal to 30% pronormoblasts of the erythrocytic elements, and (3) M6c with greater than or equal to 30% blasts and greater than or equal to 30% pronormoblasts by the aforementioned exclusion criteria. The poor prognosis associated with this disorder positively correlates with a high pronormoblast:myeloblast ratio; unfavorable cytogenetic aberrations; a high proliferative index; and the presence of P-glycoprotein expression (multidrug resistance phenotype). Chemotherapeutic regimens directed toward these specific parameters should be devised in order to improve the characteristically poor outcome of this patient population.