Background: Dental diseases are common in dogs and cats, and accurate measurements of dentoalveolar structure are important for planning of treatment. The information that the comparison computed tomography (CT) with dental radiography (DTR) is not yet reported in veterinary medicine. Objectives: The purpose of this study was to compare the DTR with CT of dentoalveolar structures in healthy dogs and cats, and to evaluate the CT images of 2 different slice thicknesses (0.5 and 1.0 mm). Methods: We included 6 dogs (2 Maltese and 1 Spitz, Beagle, Pomeranian, mixed, 1 to 8 years, 4 castrated males, and 2 spayed female) and 6 cats (6 domestic short hair, 8 months to 3 years, 4 castrated male, and 2 spayed female) in this study. We measured the pulp cavity to tooth width ratio (P/T ratio) and periodontal space of maxillary and mandibular canine teeth, maxillary fourth premolar, mandibular first molar, maxillary third premolar and mandibular fourth premolar. Results: P/T ratio and periodontal space in the overall dentition of both dogs and cats were smaller in DTR compared to CT. In addition, CT images at 1.0 mm slice thickness was generally measured to be greater than the images at 0.5 mm slice thickness. Conclusions The results indicate that CT with thin slice thickness provides more accurate information on the dentoalveolar structures. Additional DTR, therefore, may not be required for evaluating dental structure in small-sized dogs and cats.

Movement defects in obesity are associated with peripheral muscle defects, arthritis, and dysfunction of motor control by the brain. Although movement functionality is negatively correlated with obesity, the brain regions and downstream signaling pathways associated with movement defects in obesity are unclear. A dopaminergic neuronal pathway from the substantia nigra (SN) to the striatum is responsible for regulating grip strength and motor initiation through tyrosine hydroxylase (TH) activity-dependent dopamine release. We found that mice fed a high-fat diet exhibited decreased movement in open-field tests and an increase in missteps in a vertical grid test compared with normally fed mice. This motor abnormality was associated with a significant reduction of TH in the SN and striatum. We further found that phosphorylation of c-Jun N-terminal kinase (JNK), which modulates TH expression in the SN and striatum, was decreased under excess-energy conditions. Our findings suggest that high calorie intake impairs motor function through JNK-dependent dysregulation of TH in the SN and striatum.
Animals ; Arthritis ; Brain ; Diet, High-Fat* ; Dopamine ; Dopaminergic Neurons* ; Hand Strength ; JNK Mitogen-Activated Protein Kinases ; Mesencephalon* ; Mice ; Obesity ; Phosphorylation ; Substantia Nigra ; Tyrosine 3-Monooxygenase

Background and Objectives: Large clinical studies of sodium/glucose cotransporter 2 (SGLT2) inhibitors have shown a significant beneficial effect on heart failure-associated hospitalization and cardiovascular events. As SGLT2 is known to be absent in heart cells, improved cardiovascular outcomes are thought to be accounted for by the indirect effects of the drug. We sought to confirm whether such benefits were mediated through SGLT2 expressed in the heart using myocardial infarction (MI) model. Methods: Mice pre-treated with empagliflozin (EMPA), an SGLT2 inhibitor, showed a significantly reduced infarct size compared with the vehicle group three days post-MI.Interestingly, we confirmed SGLT2 localized in the infarct zone. The sequential changes of SGLT2 expression after MI were also evaluated. Results: One day after MI, SGLT2 transiently appeared in the ischemic areas in the vehicle group and increased until 72 hours. The appearance of SGLT2 was delayed and less in amount compared with the vehicle group. Additionally, there was a significant difference in metabolites, including glucose and amino acids in the 1 H nuclear magnetic resonance analysis between groups. Conclusions Our work demonstrates that SGLT2 is transiently expressed in heart tissue early after MI and EMPA may directly operate on SGLT2 to facilitate metabolic substrates shifts.

Background and Objectives: Large clinical studies of sodium/glucose cotransporter 2 (SGLT2) inhibitors have shown a significant beneficial effect on heart failure-associated hospitalization and cardiovascular events. As SGLT2 is known to be absent in heart cells, improved cardiovascular outcomes are thought to be accounted for by the indirect effects of the drug. We sought to confirm whether such benefits were mediated through SGLT2 expressed in the heart using myocardial infarction (MI) model. Methods: Mice pre-treated with empagliflozin (EMPA), an SGLT2 inhibitor, showed a significantly reduced infarct size compared with the vehicle group three days post-MI.Interestingly, we confirmed SGLT2 localized in the infarct zone. The sequential changes of SGLT2 expression after MI were also evaluated. Results: One day after MI, SGLT2 transiently appeared in the ischemic areas in the vehicle group and increased until 72 hours. The appearance of SGLT2 was delayed and less in amount compared with the vehicle group. Additionally, there was a significant difference in metabolites, including glucose and amino acids in the 1 H nuclear magnetic resonance analysis between groups. Conclusions Our work demonstrates that SGLT2 is transiently expressed in heart tissue early after MI and EMPA may directly operate on SGLT2 to facilitate metabolic substrates shifts.