Enzymatic hydrolysis of corn gluten proteins

http://www.worldcat.org/oclc/1808358

Prevalence of ultrasonographic gastrointestinal wall changes in dogs with acute pancreatitis: A retrospective study (2012-2020)

BACKGROUND: Ultrasonographic gastrointestinal wall changes in dogs with acute pancreatitis (AP) are not well characterized in the literature. No detailed studies have described their prevalence, characteristics, distribution, or clinical relevance. HYPOTHESIS/OBJECTIVES: Describe the prevalence of ultrasonographic gastrointestinal wall changes in a population of dogs with AP and evaluate for associations between the presence of gastrointestinal wall changes and clinical or clinicopathological variables. ANIMALS: Referral population of 66 client‐owned dogs with AP. METHODS: Retrospective search of clinical records to identify dogs with AP. Clinical variables, clinicopathological variables and ultrasonographic findings were reported using descriptive statistics. A binary logistic regression model was used to evaluate for associations between the presence of gastrointestinal wall changes and clinical or clinicopathological variables. RESULTS: Sixty‐six dogs were included. Forty‐seven percent of dogs (95% confidence interval [CI], 35.0%‐59.0%; n = 31) with AP had ultrasonographic gastrointestinal wall changes. Gastrointestinal wall changes were most common in the duodenum and identified in 71% (n = 22) of affected dogs. Of dogs with gastrointestinal wall changes, 74.2% (n = 23) had wall thickening, 61.3% (n = 19) had abnormal wall layering, and 35.5% (n = 11) had wall corrugation. In the multivariable model, only heart rate remained an independent predictor of ultrasonographic gastrointestinal wall changes (P = .02). CONCLUSIONS AND CLINICAL IMPORTANCE: Ultrasonographic gastrointestinal wall changes in this population of dogs with AP were common. Increased heart rate was the only independent predictor of gastrointestinal wall changes, which might imply more severe disease. Additional studies are required to elucidate whether ultrasonographic gastrointestinal wall changes reflect disease severity in AP

BCL-xL Regulates ATP Synthase and Synaptic Efficiency

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Bcl-xl Regulates ATP Synthase Activity at the Inner Mitochondrial Membrane

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BAK Alters Neuronal Excitability and Can Switch from Anti- to Pro-Death Function during Postnatal Development

AbstractBAK is a pro-apoptotic BCL-2 family protein that localizes to mitochondria. Here we evaluate the function of BAK in several mouse models of neuronal injury including neuronotropic Sindbis virus infection, Parkinson's disease, ischemia/stroke, and seizure. BAK promotes or inhibits neuronal death depending on the specific death stimulus, neuron subtype, and stage of postnatal development. BAK protects neurons from excitotoxicity and virus infection in the hippocampus. As mice mature, BAK is converted from anti- to pro-death function in virus-infected spinal cord neurons. In addition to regulating cell death, BAK also protects mice from kainate-induced seizures, suggesting a possible role in regulating synaptic activity. BAK can alter neurotransmitter release in a direction consistent with its protective effects on neurons and mice. These findings suggest that BAK inhibits cell death by modifying neuronal excitability

Maternal autoimmunity and inflammation are associated with childhood tics and obsessive-compulsive disorder: Transcriptomic data show common enriched innate immune pathways.

Although genetic variation is a major risk factor of neurodevelopmental disorders, environmental factors during pregnancy and early life are also important in disease expression. Animal models demonstrate that maternal inflammation causes fetal neuroinflammation and neurodevelopmental deficits, and brain transcriptomics of neurodevelopmental disorders in humans show upregulated differentially expressed genes are enriched in immune pathways. We prospectively recruited 200 sequentially referred children with tic disorders/obsessive-compulsive disorder (OCD), 100 autoimmune neurological controls, and 100 age-matched healthy controls. A structured interview captured the maternal and family history of autoimmune disease and other pro-inflammatory states. Maternal blood and published Tourette brain transcriptomes were analysed for overlapping enriched pathways. Mothers of children with tics/OCD had a higher rate of autoimmune disease compared with mothers of children with autoimmune neurological conditions (p = 0.054), and mothers of healthy controls (p = 0.0004). Autoimmunity was similarly elevated in first- and second-degree maternal relatives of children with tics/OCD (p 0.0001 and p = 0.014 respectively). Other pro-inflammatory states were also more common in mothers of children with tics/OCD than controls (p 0.0001). Upregulated differentially expressed genes in maternal autoimmune disease and Tourette brain transcriptomes were commonly enriched in innate immune processes. Pro-inflammatory states, including autoimmune disease, are more common in the mothers and families of children with tics/OCD. Exploratory transcriptome analysis indicates innate immune signalling may link maternal inflammation and childhood tics/OCD. Targeting inflammation may represent preventative strategies in pregnancy and treatment opportunities for children with neurodevelopmental disorders

Bcl-xL regulates mitochondrial energetics by stabilizing the inner membrane potential

To promote cell survival, the antiapoptotic factor Bcl-xL both inhibits Bax-induced mitochondrial outer membrane permeabilization and stabilizes mitochondrial inner membrane ion flux and thus overall mitochondrial energetic capacity

2018 Scholars at Work Conference Program

Program for the 2018 Scholars at Work Conference at Minnesota State University, Mankato on March 30, 2018