NAFLD (non-alcoholic fatty liver disease), associated with obesity and the cardiometabolic syndrome, is an important medical problem affecting up to 20% of western populations. Evidence indicates that mitochondrial dysfunction plays a critical role in NAFLD initiation and progression to the more serious condition of NASH (non-alcoholic steatohepatitis). Herein we hypothesize that mitochondrial defects induced by exposure to a HFD (high fat diet) contribute to a hypoxic state in liver and this is associated with increased protein modification by RNS (reactive nitrogen species). To test this concept, C57BL/6 mice were pair-fed a control diet and HFD containing 35% and 71% total calories (1 cal≈4.184 J) from fat respectively, for 8 or 16 weeks and liver hypoxia, mitochondrial bioenergetics, NO (nitric oxide)-dependent control of respiration, and 3-NT (3-nitrotyrosine), a marker of protein modification by RNS, were examined. Feeding a HFD for 16 weeks induced NASH-like pathology accompanied by elevated triacylglycerols, increased CYP2E1 (cytochrome P450 2E1) and iNOS (inducible nitric oxide synthase) protein, and significantly enhanced hypoxia in the pericentral region of the liver. Mitochondria from the HFD group showed increased sensitivity to NO-dependent inhibition of respiration compared with controls. In addition, accumulation of 3-NT paralleled the hypoxia gradient in vivo and 3-NT levels were increased in mitochondrial proteins. Liver mitochondria from mice fed the HFD for 16 weeks exhibited depressed state 3 respiration, uncoupled respiration, cytochrome c oxidase activity, and mitochondrial membrane potential. These findings indicate that chronic exposure to a HFD negatively affects the bioenergetics of liver mitochondria and this probably contributes to hypoxic stress and deleterious NO-dependent modification of mitochondrial proteins.
A 4 yr old castrated male Jack Russell terrier was presented with a 2 mo history of vomiting, anorexia, and weight loss. Abdominal radiographs and ultrasound supported the diagnosis of gastric outflow obstruction. Celiotomy and gastrotomy revealed a large, narrowly based mass originating from the mucosa of the dorsal gastric body, occupying the lumen of the stomach and protruding through the pylorus into the duodenum. A partial gastrectomy was performed to excise the mass along with a 1 cm margin of grossly normal tissue. Giant hypertrophic gastritis was diagnosed via histopathology of the excised tissue. Giant hypertrophic gastritis is a rarely diagnosed disease of canines, characterized by giant gastric folds, hypoalbuminemia, and mucosal hypertrophy. Long-term treatment success has not been previously reported. In the case described herein, surgical excision of the affected gastric tissue provided complete resolution of clinical signs. Twelve mo following surgery, no recurrence of either vomiting or weight loss had been noted and the dog was clinically normal.
Cortical thickness and bone density measurements were obtained from multiple regions of the canine humerus using QCT. Use of short monocortical screws may contribute to failure of locking plate fixation of humeral fractures, especially when placed in the condyle. When bicortical screw placement is not possible, maximizing monocortical screw length may optimize fixation stability for distal humeral fractures.
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