Publications by authors named "Roberta Turner"

Background: Amyotrophic Lateral Sclerosis (ALS) is a terminal neuromuscular disease with patients dying within 3-5 years of diagnosis. Most patients choose to forego invasive life sustaining measures. Timing of hospice referral can be challenging given the advancement of non-invasive ventilation (NIV) technology.

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Background: Increased relapse rates in multiple sclerosis (MS) as a consequence of peripheral immune system activation, owing to infection for example, have been widely reported, but the mechanism remains unclear. Acute brain injury models can be exacerbated by augmenting the hepatic acute phase response (APR). Here, we explored the contribution of the hepatic APR to relapse in two rodent models of MS.

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Background: Patients with end-stage liver disease have a predictable and progressive decline in their quality of life because of physical symptoms and psychological distress. Early palliative care intervention (EPCI) correlates with better symptom control and mood. We aimed to improve symptomatology and mood in liver transplant candidates by implementing a longitudinal multidisciplinary EPCI.

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Unlabelled: Infection with adenovirus triggers the cellular DNA damage response, elements of which include cell death and cell cycle arrest. Early adenoviral proteins, including the E1B-55K and E4orf3 proteins, inhibit signaling in response to DNA damage. A fraction of cells infected with an adenovirus mutant unable to express the E1B-55K and E4orf3 genes appeared to arrest in a mitotic-like state.

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Adenoviral infection is a major risk factor for otitis media. We hypothesized that adenovirus promotes bacterial ascension into the middle ear through the disruption of normal function in the Eustachian tubes due to inflammation-induced changes. An intranasal infection model of the chinchilla was used to test the ability of type 5 adenovirus to promote middle ear infection by Streptococcus pneumoniae.

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Adenovirus inundates the productively infected cell with linear, double-stranded DNA and an abundance of single-stranded DNA. The cellular response to this stimulus is antagonized by the adenoviral E1B and E4 early genes. A mutant group C adenovirus that fails to express the E1B-55K and E4orf3 genes is unable to suppress the DNA-damage response.

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