Impact of Volume and Type of Overnight Pages on Resident Sleep During Home Call.

BACKGROUND: Little research exists regarding factors that contribute to resident fatigue during home call. OBJECTIVE: We objectively tracked the number and type of pages received, as well as residents' sleep time, during home call. We then examined the relationship between paging volume, resident sleep, and resident fatigue. METHODS: A total of 4 of 4 urology residents (100%) at a single institution wore a FitBit Charge HR device from July 2015 to July 2016 to track sleep. Between January and July 2016, pages received by the on-call resident were counted as either floor (urology inpatient unit), clinic (after-hours answering service), or other. Postcall residents were defined as fatigued and excused at noon if they reported they were too tired to safely perform clinical duties. RESULTS: Residents slept an average of 408 minutes per night while not on call, versus 368 minutes while on call but not fatigued, and 181 minutes while on call and fatigued (P < .05). The most senior resident received fewer pages per night on average than the most junior resident. Each page was associated with 4.71 fewer minutes asleep on average for all residents. Pages in the other category were associated with 7.74 fewer minutes asleep per page for all residents, but only the most junior resident had significantly less sleep, 9.02 minutes, per floor page. CONCLUSIONS: Objective sleep data correlate with subjective assessment of resident fatigue and with volume and type of pages received. Senior residents spent less time awake per page and received fewer pages.

Urologic Emergencies.

The diagnosis and management of urologic emergencies are incorporated into the basic training of all urology residents. In institutions without access to urologic services, it is usually left to the General Surgeon or Emergency Medicine physician to provide timely care. This article discusses diagnoses that are important to recognize and treatment that is practically meaningful for the non-Urologist to identify and treat. The non-Urology provider, after reading this article, will have a better understanding and a higher comfort level with treating patients with urologic emergencies.

Tau accumulation causes mitochondrial distribution deficits in neurons in a mouse model of tauopathy and in human Alzheimer's disease brain.

Neurofibrillary tangles (NFT), intracellular inclusions of abnormal fibrillar forms of microtubule associated protein tau, accumulate in Alzheimer's disease (AD) and other tauopathies and are believed to cause neuronal dysfunction, but the mechanism of tau-mediated toxicity are uncertain. Tau overexpression in cell culture impairs localization and trafficking of organelles. Here we tested the hypothesis that, in the intact brain, changes in mitochondrial distribution occur secondary to pathological changes in tau. Array tomography, a high-resolution imaging technique, was used to examine mitochondria in the reversible transgenic (rTg)4510, a regulatable transgenic, mouse model and AD brain tissue. Mitochondrial distribution is progressively disrupted with age in rTg4510 brain, particularly in somata and neurites containing Alz50-positive tau aggregates. Suppression of soluble tau expression with doxycycline resulted in complete recovery of mitochondrial distribution, despite the continued presence of aggregated tau. The effect on mitochondrial distribution occurs without concomitant alterations in neuropil mitochondrial size, as assessed by both array tomography and electron microscopy. Similar mitochondrial localization alterations were also observed in human AD tissue in Alz50+ neurons, confirming the relevance of tau to mitochondrial trafficking observed in this animal model. Because abnormalities reverted to normal if soluble tau was suppressed in rTg4510 mice, even in the continued presence of fibrillar tau inclusions, we suggest that soluble tau plays an important role in mitochondrial abnormalities, which likely contribute to neuronal dysfunction in AD.

Structural abnormalities in the cortex of the rTg4510 mouse model of tauopathy: a light and electron microscopy study.

rTg4510 transgenic (TG) mice overexpress mutant (P301L) human tau protein. We have compared the dorsal premotor cortex of TG mice versus non-transgenic (NT) mice at 4, 9, and 13 months of age, using light (LM) and electron microscopy (EM). LM assessment shows that cortical thickness in TG mice is reduced by almost 50% from 4 to 13 months of age, while at the same time layer I thickness is reduced by 80%, with most of the cortical thinning occurring between 4 and 9 months. In TG mice, spherical, empty vacuoles, up to 60 µm in diameter, become increasingly abundant with age and by 9 months, pyramidal and non-pyramidal neurons with large intracellular tangles of tau protein are common throughout the cortex. These tangles occur in the perikarya; we have not observed them entering into cellular processes, nor have we observed ghost tangles in the intercellular matrix. In TG mice, nerve fiber pathology is widespread by 13 months, and split myelin sheaths, ballooned sheaths, and swollen axons containing mitochondrial aggregations are all common. Astrocytes become increasingly filled with glial filaments as TG mice age, and microglial cells almost always contain phagocytic inclusions. However, no glial cells are seen to contain tau in their cytoplasm. These observations add to the base of knowledge available on this commonly employed model of tauopathy.