No abstract

Thyroid hormones are involved in the regulation of many physiological processes and regulate gene transcription by binding to their nuclear receptors TR␣ and TR␤. In the absence of triiodothyronine (T3), the unliganded receptors (aporeceptors) do bind DNA and repress the transcription of target genes. The role of thyroid hormone aporeceptors as repressors was observed in hypothyroid adult mice, but its physiological relevance in nonpathological hypothyroid conditions remained to be determined. Here we show that, in the normal mouse fetus, TR␣ aporeceptors repress heart rate as well as the expression of TR␤ and several genes encoding ion channels involved in cardiac contractile activity. Right after birth, when T3 concentration sharply increases, liganded TR␣ (holoreceptors) turn on the expression of some of these same genes concomitantly with heart rate increase. These data describe a physiological situation under which conversion of TR␣ from apo-receptors into holo-receptors, upon changes in T3 availability, plays a determinant role in a developmental process.

Cerebrovascular accidents, or strokes, and gliomas are common intraaxial brain lesions in dogs. An accurate differentiation of these two lesions is necessary for prognosis and treatment decisions. The magnetic resonance (MR) imaging characteristics of 21 dogs with a presumed cerebrovascular accident and 17 with a glioma were compared. MR imaging findings were reviewed retrospectively by three observers unaware of the final diagnosis. Statistically significant differences between the appearance of gliomas and cerebrovascular accidents were identified based on lesion location, size, mass effect, perilesional edema, and appearance of the apparent diffusion coefficient map. Gliomas were predominantly located in the cerebrum (76%) compared with presumed cerebrovascular accidents that were located mainly in the cerebellum, thalamus, caudate nucleus, midbrain, and brainstem (76%). Gliomas were significantly larger compared with presumed cerebrovascular accidents and more commonly associated with mass effect and perilesional edema. Wedge-shaped lesions were seen only in 19% of presumed cerebrovascular accidents. Between the three observers, 10-47% of the presumed cerebrovascular accidents were misdiagnosed as gliomas, and 0-12% of the gliomas were misdiagnosed as cerebrovascular accidents. Diffusion weighted imaging increased the accuracy of the diagnosis for both lesions. Agreement between observers was moderate (j ¼ 0.48, Po0.01). r

This article describes the findings in three dogs with histopathologically confirmed pancreatic insulinoma using dual-phase computed tomographic angiography (CTA). In all three dogs, dual-phase CTA findings identified lesions not seen on ultrasonography, including the actual identification of the primary pancreatic neoplasm in two dogs. CTA findings were in agreement with the surgical and histopathological findings. In two dogs, the insulinomas were found to have a strong enhancement during the arterial phase of the study but not at the other phases, which stresses the importance of dual-phase computed tomography for the diagnosis of this type of pancreatic neoplasia, in agreement with current knowledge in humans.

Abdominal lymph node enlargement is frequently noted sonographically. Certain sonographic features can be used to suggest whether lymphadenopathy is more likely benign or malignant. Specific changes in size, shape, echogenicity, and Doppler flow patterns have an association with malignancy. In this retrospective case-control study, the association between abdominal lymph node heterogeneity and malignancy was evaluated. Twenty-three canine and 18 feline patients with ultrasonographically heterogeneous abdominal nodes were evaluated for presence of benign or malignant lymphadenopathy. Controls were animals with lymph node enlargement of uniform echogeneity. Twenty-one (91%) of heterogeneous canine lymph nodes were malignant, and there was a significant association between heterogeneity and malignancy in canine abdominal lymph nodes (P= 0.024). Seven (63%) heterogeneous feline lymph nodes were malignant, with no significant association between heterogeneity and malignancy (P = 0.537).

Sensitivity and positive predictive value of CT for bulla detection were low. Results suggested that CT is potentially an ineffective preoperative diagnostic technique in dogs with spontaneous pneumothorax caused by bulla rupture because lesions can be missed or incorrectly diagnosed. Bulla size may affect visibility on CT.

BACKGROUND AND PURPOSE: Sparganosis is a rare parasitic infection in humans by a larval cestode of the genus Spirometra. Preoperative diagnosis of cerebral sparganosis in the past has been very difficult. Our objective was to evaluate the CT and MR features of cerebral sparganosis in order to make a definite diagnosis.

Protein arginylation mediated by arginyltransferase (ATE1) is essential for heart formation during embryogenesis, however its cell-autonomous role in cardiomyocytes and the differentiated heart muscle has never been investigated. To address this question, we generated cardiac muscle-specific Ate1 knockout mice, in which Ate1 deletion was driven by α-myosin heavy chain promoter (αMHC-Ate1 mouse). These mice were initially viable, but developed severe cardiac contractility defects, dilated cardiomyopathy, and thrombosis over time, resulting in high rates of lethality after 6 months of age. These symptoms were accompanied by severe ultrastructural defects in cardiac myofibrils, seen in the newborns and far preceding the onset of cardiomyopathy, suggesting that these defects were primary and likely underlay the development of the future heart defects. Several major sarcomeric proteins were arginylated in vivo. Moreover, Ate1 deletion in the hearts resulted in a significant reduction of active and passive myofibril forces, suggesting that arginylation is critical for both myofibril structural integrity and contractility. Thus, arginylation is essential for maintaining the heart function by regulation of the major myofibril proteins and myofibril forces, and its absence in the heart muscle leads to progressive heart failure through cardiomyocyte-specific defects.