著者

Masaya TSUBOI Kazuyuki UCHIDA Tetsuya IDE Mizue OGAWA Takehiko INAGAKI Shinji TAMURA Miyoko SAITO James K. CHAMBERS Hiroyuki NAKAYAMA

出版者

公益社団法人 日本獣医学会

雑誌

Journal of Veterinary Medical Science (ISSN:09167250)

巻号頁・発行日

pp.12-0224, (Released:2012-11-01)

被引用文献数

5

---

Canine polyneuropathy is a neurological disorder characterized by a dysfunction of multiple peripheral nerves. The etiology of the disease is diverse; it may occur in cases of infectious, immune-mediated, or hereditary conditions or in association with endocrinopathy, neoplasm, or chemical intoxication. It is often difficult to determine the etiology through clinical symptoms. The aim of this study is to investigate pathological differences among three canine polyneuropathy cases with each presumably having a different etiology. Cases included a 13-month-old female border collie (Dog No.1), a 21-month-old male chihuahua (Dog No.2), and an 11-year-old male beagle (Dog No.3). Clinical examinations revealed hindlimb ataxia and sensory loss in Dog No.1, forelimb paralysis and vertebral pain in Dog No.2, and paddling-gait and hypothyroidism in Dog No.3. Histopathologically, axonal swelling and pale myelin were observed in Dog No.1. Giant axons mimicking giant axonal neuropathy were obvious in Dog No.2. Dog No.3 showed atrophic axons and severe interstitial edema. Distributions of peripheral nerve lesions coincided with respective clinical symptoms. According to their clinical and pathological features, Dogs No.1 and No.2 were suspected of hereditary polyneuropathy, while Dog No.3 seemed to have hypothyroidism-associated polyneuropathy. As each case demonstrated unique pathological features, different pathogeneses of peripheral nerve dysfunction were suggested.

著者

Kanae OYAKE Yui KOBATAKE Sanae SHIBATA Hiroki SAKAI Miyoko SAITO Osamu YAMATO Kazuya KUSHIDA Sadatoshi MAEDA Hiroaki KAMISHINA

出版者

公益社団法人 日本獣医学会

雑誌

Journal of Veterinary Medical Science (ISSN:09167250)

巻号頁・発行日

pp.15-0521, (Released:2016-04-24)

被引用文献数

1 14

---

Canine degenerative myelopathy (DM) is characterized by progressive degeneration of the spinal cord. Although atrophic changes in the intercostal muscles were previously reported in the late stage of DM in Pembroke Welsh Corgis (PWCs), changes in respiratory function have not yet been examined. In the present study, we performed an arterial blood gas analysis and measured respiratory movements over progressive disease stages to document changes in respiratory function in DM-affected PWCs. We found that respiratory dysfunction progressed during the later stages of DM and correlated with a change in respiratory movement to the abdominal breathing pattern. These results suggested that hypoventilation occurred due to dysfunctional changes in the intercostal muscles and resulted in hypoxemia in the later stages of DM.

著者

Yasuhiro KURIHARA Takehito SUZUKI Motoharu SAKAUE Ohoshi MURAYAMA Yoko MIYAZAKI Atsushi ONUKI Takuma AOKI Miyoko SAITO Yoko FUJII Masaharu HISASUE Kazuaki TANAKA Tatsuya TAKIZAWA

出版者

公益社団法人 日本獣医学会

雑誌

Journal of Veterinary Medical Science (ISSN:09167250)

巻号頁・発行日

pp.13-0219, (Released:2013-08-27)

被引用文献数

2 15

---

Adipose tissue-derived stem cells (ADSCs) isolated from adult tissue have pluripotent differentiation and self-renewal capability. The tissue source of ADSCs can be obtained in large quantities and with low risks, thus highlighting the advantages of ADSCs in clinical applications. Valproic acid (VPA) is a widely used antiepileptic drug, which has recently been reported to affect ADSC differentiation in mice and rats; however, few studies have been performed on dogs. We aimed to examine the in vitro effect of VPA on canine ADSCs. Three days of pretreatment with VPA decreased the proliferation of ADSCs in a dose-dependent manner; VPA concentrations of 2 mM and above inhibited the proliferation of ADSCs. In parallel, VPA increased p16 and p21 mRNA expression, suggesting that VPA attenuated the proliferative activity of ADSCs by activating p16 and p21. Furthermore, the effects of VPA on adipogenic, osteogenic or neurogenic differentiation were investigated morphologically. VPA pretreatment markedly promoted neurogenic differentiation, but suppressed the accumulation of lipid droplets and calcium depositions. These modifications of ADSCs by VPA were associated with a particular gene expression profile, viz., an increase in neuronal markers, that is, NSE, TUBB3 and MAP2, a decrease in the adipogenic marker, LPL, but no changes in osteogenic markers, as estimated by reverse transcription-PCR analysis. These results suggested that VPA is a specific inducer of neurogenic differentiation of canine ADSCs and is a useful tool for studying the interaction between chromatin structure and cell fate determination.