Diffuse Jejunal Lipomatosis and Associated Complications.

Small intestinal lipomatosis is a rare condition with a poorly understood epidemiology and pathophysiology. Cases of small intestinal lipomatosis have been documented in multiple countries over the last century, yet little has been published regarding the natural history of this disease. Therapeutic options are largely surgical and based on limited evidence. We report a unique case of diffuse jejunal lipomatosis in a 62-year-old man with complications of small bowel obstruction, small bowel volvulus, jejunal diverticulosis, pneumatosis intestinalis, malnutrition, small intestinal bacterial overgrowth, and intestinal dysmotility developing over a 12-year period.

Use of a Clinical Electrocardiographic Database to Enhance Atrial Fibrillation/Atrial Flutter Identification Algorithms Based on Administrative Data.

Background Administrative data have limited sensitivity for case finding of atrial fibrillation/atrial flutter (AF/AFL). Linkage with clinical repositories of interpreted ECGs may enhance diagnostic yield of AF/AFL. Methods and Results We retrieved 369 ECGs from the institutional Marquette Universal System for Electrocardiography (MUSE) repository as validation samples, with rhythm coded as AF (n=49), AFL (n=50), or other competing rhythm diagnoses (n=270). With blinded, duplicate review of ECGs as the reference comparison, we compared multiple MUSE coding definitions for identifying AF/AFL. We tested the agreement between MUSE diagnosis and reference comparison, and calculated the sensitivity and specificity. Using a data set linking clinical registries, administrative data, and the MUSE repository (n=11 662), we assessed the incremental diagnostic yield of AF/AFL by incorporating ECG data to administrative data-based algorithms. The agreement between MUSE diagnosis and reference comparison depended on the coding definitions applied, with the Cohen κ ranging from 0.57 to 0.75. Sensitivity ranged from 60.6% to 79.1%, and specificity ranged from 93.2% to 98.0%. A coding definition with AF/AFL appearing in the first 3 ECG statements had the highest sensitivity (79.1%), with little loss of specificity (94.5%). Compared with the algorithms with only administrative data, incorporating ECG data increased the diagnostic yield of preexisting AF/AFL by 14.5% and incident AF/AFL by 7.5% to 16.1%. Conclusions Routine ECG interpretation using MUSE coding is highly specific and moderately sensitive for AF/AFL detection. Inclusion of MUSE ECG data in AF/AFL case identification algorithms can identify cases missed using administrative data-based algorithms alone.

Examining the Effects of Anabolic-Androgenic Steroids on Repetitive Mild Traumatic Brain Injury (RmTBI) Outcomes in Adolescent Rats.

BACKGROUND: Repetitive mild traumatic brain injury (RmTBI) is increasingly common in adolescents. Anabolic-androgenic steroid (AAS) consumption among younger professional athletes is a significant risk factor for impaired neurodevelopment. Given the increased rates and overlapping symptomology of RmTBI and AAS use, we sought to investigate the behavioural and neuropathological outcomes associated with the AAS Metandienone (Met) and RmTBI on rats. METHODS: Rats received either Met or placebo and were then administered RmTBIs or sham injuries, followed by a behavioural test battery. Post-mortem MRI was conducted to examine markers of brain integrity and qRT-PCR assessed mRNA expression of markers for neurodevelopment, neuroinflammation, stress responses, and repair processes. RESULTS: Although AAS and RmTBI did not produce cumulative deficits, AAS use was associated with detrimental outcomes including changes to depression, aggression, and memory; prefrontal cortex (PFC) atrophy and amygdala (AMYG) enlargement; damaged white matter integrity in the corpus callosum; and altered mRNA expression in the PFC and AMYG. RmTBI affected general activity and contributed to PFC atrophy. CONCLUSIONS: Findings corroborate previous results indicating that RmTBI negatively impacts neurodevelopment but also demonstrates that AAS results in significant neuropathological insult to the developing brain.

Examining the Progressive Behavior and Neuropathological Outcomes Associated with Chronic Repetitive Mild Traumatic Brain Injury in Rats.

While the physical and behavioral symptomologies associated with a single mild traumatic brain injury (mTBI) are typically transient, repetitive mTBIs (RmTBI) have been associated with persisting neurological deficits. Therefore, this study examined the progressive changes in behavior and the neuropathological outcomes associated with chronic RmTBI through adolescence and adulthood in male and female Sprague Dawley rats. Rats experienced 2 mTBIs/week for 15 weeks and were periodically tested for changes in motor behavior, cognitive function, emotional disturbances, and aggression. Brain tissue was examined for neuropathological changes in ventricle size and presentation of Iba1 and GFAP. We did not see progressively worse behavioral impairments with the accumulation of injuries or time, but did find evidence for neurological and functional change (motor disturbance, reduced exploration, reduced aggression, alteration in depressive-like behavior, deficits in short-term working memory). Neuropathological assessment of RmTBI animals identified an increase in ventricle size, prolonged changes in GFAP, and sex differences in Iba1, in the corpus callosum, thalamus, and medial prefrontal cortex. Telomere length reduced exponentially as the injury load increased. Overall, chronic RmTBI did not result in accumulating behavioral impairment, and there is a need to further investigate progressive behavioral changes associated with repeated injuries in adolescence and young adulthood.

The behavioural and pathophysiological effects of the ketogenic diet on mild traumatic brain injury in adolescent rats.

Mild traumatic brain injury (mTBI), caused by an insult to the head, results in a cascade of molecular imbalance that includes altered glucose metabolism, mitochondrial dysfunction, and increases in reactive oxygen species. Although glucose is the primary energy source for the brain, it becomes an inefficient substrate following injury, and the brain is primed to use alternative substrates (such as ketones). The ketogenic diet (KD), a high-fat, low-carbohydrate diet, forces the brain to utilize ketones over glucose for energy. Given that mTBIs are commonly experienced during adolescence, our study sought to examine the effects of the KD on recovery from mTBI in adolescent rats. This was done via two experiments; the first of which animals were fed the KD prior to a mTBI in order to investigate the neuroprotective potential of the diet, and the second the animals were fed the KD following a mTBI to examine the therapeutic potential. Male and female Sprague Dawley rats were assigned to receive a control standard diet or the KD (either pre-injury or post-injury), then further randomized to receive a sham or mTBI. Animals were tested on 6 behavioural measures designed to examine post-concussive symptomology, and mRNA analysis of the brain and small intestine were performed. Pre-injury exposure to the KD offered some neuroprotection, reducing balance and motor impairments while increasing exploratory behaviour and telomere length. Consumption of the KD following the injury also provided some therapeutic benefit, reducing both anxiety- and depressive-like behaviours. The timing of KD administration also differentially modified expression of prefrontal cortex, hippocampus, and intestinal mRNA for our genes of interest (Fgf2, Iba1, Opa1, Sirt1, Claudin3, OCC, and ZO1) This study demonstrates the neuroprotective and therapeutic potential of the KD for mTBI and warrants further investigation.

Neuroendocrine Whiplash: Slamming the Breaks on Anabolic-Androgenic Steroids Following Repetitive Mild Traumatic Brain Injury in Rats May Worsen Outcomes.

Sport-related concussion is an increasingly common injury among adolescents, with repetitive mild traumatic brain injuries (RmTBI) being a significant risk factor for long-term neurobiological and psychological consequences. It is not uncommon for younger professional athletes to consume anabolic-androgenic steroids (AAS) in an attempt to enhance their performance, subjecting their hormonally sensitive brains to potential impairment during neurodevelopment. Furthermore, RmTBI produces acute neuroendocrine dysfunction, specifically in the anterior pituitary, disrupting the hypothalamic-pituitary adrenal axis, lowering cortisol secretion that is needed to appropriately respond to injury. Some AAS users exhibit worse symptoms post-RmTBI if they quit their steroid regime. We sought to examine the pathophysiological outcomes associated with the abrupt cessation of the commonly abused AAS, Metandienone (Met) on RmTBI outcomes in rats. Prior to injury, adolescent male rats received either Met or placebo, and exercise. Rats were then administered RmTBIs or sham injuries, followed by steroid and exercise cessation (SEC) or continued treatment. A behavioral battery was conducted to measure outcomes consistent with clinical representations of post-concussion syndrome and chronic AAS exposure, followed by analysis of serum hormone levels, and qRT-PCR for mRNA expression and telomere length. RmTBI increased loss of consciousness and anxiety-like behavior, while also impairing balance and short-term working memory. SEC induced hyperactivity while Met treatment alone increased depressive-like behavior. There were cumulative effects whereby RmTBI and SEC exacerbated anxiety and short-term memory outcomes. mRNA expression in the prefrontal cortex, amygdala, hippocampus, and pituitary were modified in response to Met and SEC. Analysis of telomere length revealed the negative impact of SEC while Met and SEC produced changes in serum levels of testosterone and corticosterone. We identified robust changes in mRNA to serotonergic circuitry, neuroinflammation, and an enhanced stress response. Interestingly, Met treatment promoted glucocorticoid secretion after injury, suggesting that maintained AAS may be more beneficial than abstaining after mTBI.