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L-type amino acid transporter 1 (LAT1) is upregulated in various malignant tumors in humans. LAT1 expression correlates with the grade of cancer and prognosis. LAT1 is responsible for the supply of many essential amino acids to cancer cells. Inhibition of LAT1 reduces the amino acids that enter the cell and inhibits cancer cell growth. Therefore, novel anticancer drugs targeting LAT1 have attracted much attention in recent years. In this study, to explore the applicability of using LAT1 expression in intracranial tumors as a prognostic factor and therapeutic target, we investigated the expression of LAT1 in surgically resected primary and secondary intracranial tumor tissues from dogs and cats. Immunohistochemical analysis of LAT1 was performed on intracranial tumor tissue from 14 dogs and 3 cats. Primary intracranial tumors were seen in 10 dogs and included meningiomas, histiocytic sarcomas, pituitary tumors, and gliomas, and 9 out of 10 cases were positive for LAT1. Primary intracranial tumors were seen in 2 cats and included meningioma and lymphoma; both cases were positive for LAT1. Secondary intracranial tumors were positive for LAT1 in 3 out of 4 cases in dogs and 1 out of 1 in cats. Since the majority of intracranial tumors in dogs and cats were positive for LAT1, immunostaining for LAT1 is expected to be a prognostic indicator and therapeutic target in the future.

Canine brain tumors are best diagnosed using magnetic resonance imaging (MRI). However, opportunities of MRI examination are restricted due to its limited availability in veterinary facilities; thus, numerous canine brain tumors are diagnosed at an advanced stage. Therefore, development of a noninvasive diagnostic biomarker is required for the early detection of brain tumors. In the present study, plasma free amino acid (PFAA) profiles between dogs with and without brain tumors were compared. A total of 12 dogs with brain tumors, diagnosed based on clinical signs, and on the results of intracranial MRI and/or pathological examination were evaluated. In addition, eight dogs diagnosed with idiopathic epilepsy and 16 healthy dogs were also included. A liquid chromatography system with automated pre-column derivatization functionality was used to measure the levels of 20 amino acids. As a result, the levels of three amino acids (alanine, proline and isoleucine) were increased significantly (1.6-, 1.5- and 1.6-fold, respectively) in the plasma of dogs with brain tumors as compared with the levels in control dogs (all P

Background Electroencephalography (EEG) is required for the diagnosis of canine idiopathic epilepsy as a highest confidence level of diagnosis by the International Veterinary Epilepsy Task Force; however, EEG is seldom used and a standardised assessment method has not been reported. Methods Interictal EEG was performed under medetomidine sedation in dogs with idiopathic epilepsy and in control dogs. Epileptiform discharge (ED) frequency was compared between dogs with more severe and less severe seizures during one month before EEG and control dogs. Results All 10 dogs with more severe seizures had ED, as had 7 of 11 with less severe seizures. All epileptic dogs without ED had good long-term outcomes. ED frequency (number of ED per five minutes) was significantly higher in dogs with more severe (median, 4.5) than with less severe seizure (median, 0.46) and in the control dogs (median, 0.15). An ED frequency greater than 0.8 was considered to indicate epilepsy. Conclusion Interictal EEG in a light sleep state under medetomidine sedation had a high detection rate of ED, and ED frequency had a positive correlation with the recent severity of epileptic seizures. This allows interictal EEG recordings to be used as a simplified and objective test that may help to diagnose epilepsy and to assess the recent severity of the disease in dogs.

An 8 yr old male golden retriever was evaluated because of chronic, progressive, multiple neurologic signs. Physical examination showed marked obesity and facial swelling with a “tragic facial expression.” Neurologic evaluation revealed the dog had multiple cranial nerve deficits and lower motor neuron signs in the pelvic limbs. Serum biochemical analysis and thyroid function tests were consistent with hypothyroidism. A biopsy from the common peroneal nerve revealed a loss of myelinated fibers, inappropriately thin myelinated fibers, and resolving subperineurial edema. The diagnosis of polyneuropathy associated with hypothyroidism was made. Levothyroxine therapy was initiated. Response to levothyroxine treatment was slow, with most neurologic abnormalities persisting for >6 wk. However, the dog made a full neurologic recovery within 6 mo. Although the occurrence of polyneuropathy in dogs resulting from hypothyroidism has been controversial, the study authors demonstrated that hypothyroid polyneuropathy can occur in dogs as documented in humans. This is the first report describing long-term follow-up information together with detailed pathological features of hypothyroid polyneuropathy in a dog. In hypothyroid polyneuropathy, the response to thyroid replacement may be slow, but a recovery can be expected if treatment is initiated before peripheral nerve fiber loss becomes severe.