Interthalamic adhesion thickness has been previously described as a parameter for quantifying canine brain atrophy and hypothesized to correlate with brain height or ventricular size. However, studies testing this hypothesis are lacking. This retrospective cross-sectional study aimed to compare interthalamic adhesion thickness, interthalamic adhesion thickness/brain height ratio, and interthalamic adhesion thickness/brain height ratio/lateral ventricle to brain height ratio values in dogs with and without cognitive dysfunction. Medical records for dogs meeting the following inclusion criteria were retrieved from two hospitals: available brain magnetic resonance imaging (MRI) or computed tomography (CT) studies, no cerebral parenchymal lesions, and no prior neurological treatment. For each included dog, values of interthalamic adhesion thickness, interthalamic adhesion thickness/brain height ratio, and interthalamic adhesion thickness/brain height ratio/lateral ventricle to brain height ratio were measured by one observer from transverse CT or MRI images and a consensus was reached. A total of 113 dogs met inclusion criteria. Dogs were divided into three groups based on the following criteria: Young group (no cognitive dysfunction, <9-year-old, n = 43), Aging group (no cognitive dysfunction, ≥9-year-old, n = 61), and Dementia group (n = 9). All three parameters were significantly lower in the dementia group than in the Young and Aging groups. In the Young and Aging groups, there was significant negative correlation of all three parameters with age and positive correlation of interthalamic adhesion thickness and interthalamic adhesion thickness/brain height ratio/lateral ventricle to brain height ratio with body weight, while there was no correlation of interthalamic adhesion thickness/brain height ratio with body weight (P < 0.05). There were no differences in all three parameters according to skull type or gender. Findings from the current study supported the use of interthalamic adhesion thickness, interthalamic adhesion thickness/brain height ratio, and interthalamic adhesion thickness/brain height ratio/lateral ventricle to brain height ratio for quantifying brain atrophy in dogs with cognitive dysfunction.

This study aimed to evaluate the usefulness of four microRNAs (miRNAs) in an acute pancreatic injury dog model. Acute pancreatitis was induced by infusion of cerulein for 2 h (7.5 μg/kg/h). The levels of well-known miRNAs, microRNA-216a (miR-216a) and microRNA-375 (miR-375), and new candidates microRNA-551b (miR-551b), and microRNA-7 (miR-7), were measured at 0, 0.5, 1, 2, 6, 12, and 24 h with serum amylase and lipase, and histopathological examination was performed. Among the four miRNAs, miR-216a and miR-375, and serum enzymes were significantly increased by cerulein treatment. The expression levels of miRNAs and serum enzymes peaked at 2–6 h with a similar pattern; however, the overall increases in miR-216a and miR-375 levels were much higher than those of the serum enzyme biomarkers. Increased levels of miR-216a and miR-375 were most highly correlated to the degree of individual histopathological injuries of the pancreas, and showed much greater dynamic response than serum enzyme biomarkers. Twenty-four-hour time-course analysis in this study revealed time-dependent changes of miRNA expression levels, from initial increase to decrease by predose level in acute pancreatitis. Our findings demonstrate that, in dogs, miR-216a and miR-375 have the potential to sensitively detect pancreatitis and reflect well the degree of pancreatic injury, whereas miR-551b and miR-7 do not.

Natural killer (NK) cells are primary immune cells that target cancer cells and can be used as a therapeutic agent against pancreatic cancer. Despite the usefulness of NK cells, NK-cell therapy is limited by tumor cell inhibition of NK-cell homing to tumor sites, thereby preventing a sustained antitumor immune response. One approach to successful cancer immunotherapy is to increase trafficking of NK cells to tumor tissues. Here, we developed an antibody-based NK-cell-homing protein, named NK-cell-recruiting protein-conjugated antibody (NRP-body). The effect of NRP-body on infiltration of NK cells into primary and metastatic pancreatic cancer was evaluated in vitro and in murine pancreatic ductal adenocarcinoma models. The NRP-body increased NK-cell infiltration of tumors along a CXCL16 gradient (CXCL16 is cleaved from the NRP-body by furin expressed on the surface of pancreatic cancer cells). CXCL16 induced NK-cell infiltration by activating RhoA via the ERK signaling cascade. Administration of the NRP-body to pancreatic cancer model mice increased tumor tissue infiltration of transferred NK cells and reduced the tumor burden compared with that in controls. Overall survival of NRP-body-treated mice (even the metastasis models) was higher than that of mice receiving NK cells alone. In conclusion, increasing NK-cell infiltration into tumor tissues improved response to this cancer immunotherapy. The combination of an NRP-body with NK-cell therapy might be useful for treating pancreatic cancer.

The feasibility of using computed tomography (CT) to identify the common bile duct (CBD) and comparison with ultrasonography (US) results were evaluated in normal beagle dogs and dogs without hepatobiliary and pancreatic diseases. In addition, CBD diameters were obtained from CT at the level of the porta hepatis and the duodenal papilla level in dogs with underlying diseases that may cause cholestasis. US is a useful modality in the estimation of gallbladder volume because ejection fraction and CBD diameter from US were not significantly different from those of CT. The normal biliary tract was visible on CT images in 68% of the normal dog group. CBD diameter was not over 3 mm and 3.5 mm at the porta hepatis and duodenal papilla levels, respectively in normal dogs weighing less than 15 kg. Dogs suspected to have cholestasis associated with hepatobiliary or pancreatic diseases had significantly larger CBD than that in normal dogs.

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The purpose of this study was to evaluate the clinical and imaging characteristics of canine splenic tumors and to establish guidelines for the presurgical assessment of splenic tumors in dogs. Fifty-seven dogs that underwent total splenectomy for the treatment of splenic tumors were evaluated by examining medical records, hematologic results, diagnostic imaging results, and histopathologic results. The maximum lesion size from ultrasonography was significantly different between malignant and benign tumors (p = 0.002). There was a correlation between tumor margination and type of splenic tumors (p = 0.045). Precontrast lesion attenuation on computed tomography was significantly different between splenic malignant and benign tumors (p = 0.001). The mean ± SD precontrast lesion attenuation of malignant tumors was 40.3 ± 5.9 Hounsfield units (HU), and for benign tumors, it was 52.8 ± 6.8 HU. In conclusion, some variables of the imaging examination could be used to distinguish the type of splenic tumor. Based on the study results, using a diagnostic flowchart would be effective in increasing the survival rate of patients with splenic malignant tumors. In addition, fine needle aspiration or magnetic resonance imaging prior to surgical exploration and histopathologic examination may be useful in achieving a more accurate diagnosis.

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