Transforming cancer survivorship care through quality improvement initiatives.

Oncology nurses must become better prepared to conduct quality improvement projects that will optimize quality of care and patient safety for long-term cancer survivors. The growing interest in survivorship care has led to the availability of multiple versions of cancer survivorship care plans (SCPs). Despite the availability of SCPs, research is lacking evidence-based processes to evaluate whether providers comply with planning and issuing SCPs.

D-dimer levels remain elevated in acute aortic dissection after 24 h.

Background: D-dimer levels are elevated in patients with acute aortic dissection (AAD). Although D-dimer levels have been used to rule out AAD within 24 h of symptom onset, it is unknown whether they may be used reliably after 24 h but within the acute period. Here, we tested the hypothesis that D-dimer levels remain elevated in AAD patients for at least 10 d after dissection onset.

Molecular mechanisms of thoracic aortic dissection.

Thoracic aortic dissection (TAD) is a highly lethal vascular disease. In many patients with TAD, the aorta progressively dilates and ultimately ruptures. Dissection formation, progression, and rupture cannot be reliably prevented pharmacologically because the molecular mechanisms of aortic wall degeneration are poorly understood.

Genome-wide association study identifies a susceptibility locus for thoracic aortic aneurysms and aortic dissections spanning FBN1 at 15q21.1.

Although thoracic aortic aneurysms and dissections (TAAD) can be inherited as a single-gene disorder, the genetic predisposition in the majority of affected people is poorly understood. In a multistage genome-wide association study (GWAS), we compared 765 individuals who had sporadic TAAD (STAAD) with 874 controls and identified common SNPs at a 15q21.1 locus that were associated with STAAD, with odds ratios of 1.

Recurrent chromosome 16p13.1 duplications are a risk factor for aortic dissections.

Chromosomal deletions or reciprocal duplications of the 16p13.1 region have been implicated in a variety of neuropsychiatric disorders such as autism, schizophrenia, epilepsies, and attention-deficit hyperactivity disorder (ADHD). In this study, we investigated the association of recurrent genomic copy number variants (CNVs) with thoracic aortic aneurysms and dissections (TAAD).

Epidemiology of thoracic aortic dissection.

Thoracic aortic dissection (TAD) is estimated to occur at a rate of 3-4 cases per 100,000 persons per year and is associated with a high mortality. Reported rates are probably underestimates of the true incidence of TAD because of difficulties in diagnosis. The incidence of TAD appears to have been increasing over time.

Rare copy number variants disrupt genes regulating vascular smooth muscle cell adhesion and contractility in sporadic thoracic aortic aneurysms and dissections.

Thoracic aortic aneurysms and dissections (TAAD) cause significant morbidity and mortality, but the genetic origins of TAAD remain largely unknown. In a genome-wide analysis of 418 sporadic TAAD cases, we identified 47 copy number variant (CNV) regions that were enriched in or unique to TAAD patients compared to population controls. Gene ontology, expression profiling, and network analysis showed that genes within TAAD CNVs regulate smooth muscle cell adhesion or contractility and interact with the smooth muscle-specific isoforms of α-actin and β-myosin, which are known to cause familial TAAD when altered.