Hovgaardmaynard7713

Insomnia commonly co-occurs with depression, chronic pain, and opioid use. Both insomnia and chronic opioid analgesic use (OAU) are independent risk factors for a new depression episode (NDE). This study determined if the association between longer OAU duration and NDE was stronger in those with versus without insomnia.

Retrospective cohort.

Veterans Health Administration electronic medical records (2000-2012).

New opioid users in follow-up (2002-2012), free of depression for two years prior to follow-up, and aged 18-80 (n = 70,997).

NDE was ≥ 2 ICD-9 codes in a 12-month period. Insomnia before OAU initiation was ≥1 ICD-9 code. Cox proportional hazard models stratified on insomnia assessed the relationship between initiating a 1-30, 31-90, or > 90 day period of OAU and NDE while controlling for confounders using inverse probability of treatment-weighted propensity scores (PS).

Compared to 1-30 day OAU, 31-90 day was associated with NDE in those without (HR = 1.20; 95 percent CI 1.12-1.28) but not with insomnia (HR = 1.06; 95 percent CI 0.86-1.32). Results showed a stronger effect of chronic (>90) OAU in those with insomnia (HR = 1.59; 95 percent CI 1.27-1.98) compared to those without (HR = 1.31; 95 percent CI 1.21-1.42). However, all stratum-specific effects were not significantly different (p = 0.136).

Although stratum-specific risks were statistically similar, there was evidence for a trend that chronic OAU is a stronger risk factor for NDE in those with versus without insomnia. Providers are encouraged to monitor sleep impairment among patients on opioid therapy, as sleep may be associated with greater risk for NDE in patients with chronic OAU.

Although stratum-specific risks were statistically similar, there was evidence for a trend that chronic OAU is a stronger risk factor for NDE in those with versus without insomnia. Providers are encouraged to monitor sleep impairment among patients on opioid therapy, as sleep may be associated with greater risk for NDE in patients with chronic OAU.Astrocytes, the most abundant glial cells in the central nervous system (CNS), have numerous integral roles in all CNS functions. Litronesib They are essential for synaptic transmission and support neurons by providing metabolic substrates, secreting growth factors and regulating extracellular concentrations of ions and neurotransmitters. Astrocytes respond to CNS insults through reactive astrogliosis, in which they go through many functional and molecular changes. In neuroinflammatory conditions reactive astrocytes exert both beneficial and detrimental functions, depending on the context and heterogeneity of astrocytic populations. In this review we profile astrocytic diversity in the context of neuroinflammation; with a specific focus on multiple sclerosis (MS) and its best-described animal model experimental autoimmune encephalomyelitis (EAE). We characterize two main subtypes, protoplasmic and fibrous astrocytes and describe the role of intermediate filaments in the physiology and pathology of these cells. Additionally, we outline a variety of markers that are emerging as important in investigating astrocytic biology in both physiological conditions and neuroinflammation.

Clinical experience with continuous flow ventricular assist devices (VADs) in patients with transposition of the great arteries (TGA) including dextro-TGA and congenitally corrected TGA is rare, and indications as well as potential benefits or specific hurdles remain unclear. Therefore, our goal was to report on our experience regarding VAD therapy in adult patients with TGA as a bridge to candidacy.

We performed a single-centre retrospective study of all adult patients with TGA with systemic right ventricular failure who had continuous flow VAD implants between 2010 and 2018. Study end points were all causes of death, major cardiac and cerebrovascular adverse events or pump thrombosis. Follow-up continued until the time of the heart transplant.

A total of 6 patients (4 men) had a continuous flow VAD implanted in the context of a failing systemic right ventricle (dextro-TGA after the Mustard procedure n = 3; congenitally corrected TGA n = 3). Demographics mean age 32 ± 5.7 years; median Interagency Regie to candidacy and a bridge to a heart transplant.Mutations play a key role in the development of disease in an individual and the evolution of traits within species. Recent work in humans and other primates has clarified the origins and patterns of single-nucleotide variants, showing that most arise in the father's germline during spermatogenesis. It remains unknown whether larger mutations, such as deletions and duplications of hundreds or thousands of nucleotides, follow similar patterns. Such mutations lead to copy-number variation (CNV) within and between species, and can have profound effects by deleting or duplicating genes. Here, we analyze patterns of CNV mutations in 32 rhesus macaque individuals from 14 parent-offspring trios. We find the rate of CNV mutations per generation is low (less than one per genome) and we observe no correlation between parental age and the number of CNVs that are passed on to offspring. We also examine segregating CNVs within the rhesus macaque sample and compare them to a similar data set from humans, finding that both species have far more segregating deletions than duplications. We contrast this with long-term patterns of gene copy-number evolution between 17 mammals, where the proportion of deletions that become fixed along the macaque lineage is much smaller than the proportion of segregating deletions. These results suggest purifying selection acting on deletions, such that the majority of them are removed from the population over time. Rhesus macaques are an important biomedical model organism, so these results will aid in our understanding of this species and the disease models it supports.

As thoracic aortic aneurysm disease continues to cause significant morbidity and mortality in the general population, the cardiovascular community continues the search for the golden threshold of elective surgical replacement of the ascending aorta.

Thoracic aortic aneurysm is a common disease, classified within the 20 most common causes of death in patients over 65 years old. Once aortic complications like dissection or rupture occur, they can prove fatal. Prophylactic surgical replacement of the ascending aorta remains the mainstay of treatment to prevent these complications. Current American and European guidelines agree that the threshold for the diameter for elective replacement of the ascending aorta in non-syndromic, asymptomatic aneurysmal disease is 5.5 cm. Overall, aortic dissection is related to poor prognosis, thus making early intervention paramount.

There is a critical size above which the risk of dissection or rupture becomes extremely high. However, a significant post-dissection increase in diameter is reported, thus rendering the predissection aortic diameter well below the current threshold for elective surgical replacement of the ascending aorta.