Many hereditary disorders in dogs have equivalents in humans and thus attract attention as natural animal models. Breed predisposition to certain diseases often provides promising clues to explore novel hereditary disorders in dogs. Recently, cases of gastrointestinal (GI) polyps in Jack Russell Terriers (JRTs) have increased in Japan. In 21 affected JRTs, polyps were found in either or both the stomach and colorectum, with a predilection for the gastric antrum and rectum. Multiple polyps were found in 13 of 21 examined dogs, including 5 dogs with both gastric and colorectal polyps. Some dogs were found to have GI polyps at an early age, with the youngest case being 2.3 years old. Histopathologically, 43 of 46 GI polyps (93.5%) were diagnosed as adenomas or adenocarcinomas. Immunohistochemical analysis revealed cytoplasmic and nuclear accumulation of β-catenin in the tumor cells. As in the case of human patients with familial adenomatous polyposis, all examined JRTs with GI polyps (n = 21) harbored the identical heterozygous germline APC mutations, represented by a 2-bp substitution (c.[462A>T; 463A>T]). The latter substitution was a non-sense mutation (p.K155X) resulting in a truncated APC protein, thus suggesting a strong association with this cancer-prone disorder. Somatic mutation and loss of the wild-type APC allele were detected in the GI tumors of JRTs, suggesting that biallelic APC inactivation was involved in tumor development. This study demonstrated that despite differences in the disease conditions between human and dog diseases, germline APC mutation confers a predisposition to GI neoplastic polyps in both dogs and humans.

Resistin, one of the adipokines that has a cycteine-rich C-terminus, is considered to relate to the development of insulin resistance in rats. However, in cats, there is little knowledge regarding resistin. In this study, we cloned the feline resistin cDNA from adipose tissue by RT-PCR. The feline resistin clone contained an entire open reading frame encoding 107 amino acids that had 72.8%, 75.4%, 50.9% and 51.8% homology with bovine, human, mouse and rat homologues, respectively. In both subcutaneous and visceral adipose tissues, the transcription levels of feline resistin mRNA were significantly higher in obese cats than normal cats, and those of feline adiponectin mRNA were significantly lower in obese cats than normal cats. However, there was no difference in the expression of feline leptin between normal and obese cats. On the other hand, in both normal and obese cats, there were no significant differences in resistin, leptin and adiponectin mRNA levels between subcutaneous and visceral adipose tissues. In cats, the altered expression of resistin and adiponectin mRNA with obesity may contribute to the pathogenesis of insulin resistance and subsequent diabetes mellitus. In addition to feline adiponectin, the feline resistin cDNA clone obtained in this study will be useful for further investigation of the pathogenesis of obesity in cats.

ABSTRACT. A sero-epidemiological survey of human and equine H3 influenza A virus infections in dogs and cats using the hemagglutination inhibition (HI) and neuraminidase inhibition (NI) tests was conducted. Serum samples were collected from 582 dogs and 237 cats in Japan during the periods 2002-2008 and 1997-2008, respectively. Although no HI antibodies against equine H3 virus were detected, 9 (3.8%) from cats and 12 (2.1%) from dogs were HI-positive against human H3 virus. Only one serum each from dogs and cats was NI-positive against N2 virus. These findings suggest that although equine H3 influenza virus infections have not been prevalent in companion animals, human H3N2 influenza A virus infections have occurred in dogs and cats in recent years in Japan.

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ABSTRACT. Serum concentrations of growth hormone (GH) and insulin-like growth factor-1 (IGF-1) were determined in 5 calves in the same lineage with growth retardation. They had normal appetites, activities, body proportion, and laboratory test results. Calves with growth retardation had higher serum GH concentrations and lower serum IGF-1 concentrations. These findings suggested defects in the GH-IGF-1 axis, such as in the GH-receptor.KEY WORDS: growth hormone, growth-retarded cattle, insulin-like growth factor-1.J. Vet. Med. Sci. 63(2): 167-170, 2001 The growth of animals is regulated by many hormones and growth factors acting both in an endocrine (systemic) and autocrine/paracrine (local) manner, and requires the coordinated action of several hormones; growth hormone (GH, somatotropin), insulin-like growth factor-1 (IGF-1, somatomedin), thyroid hormone, insulin, leptin, glucocorticoid and sex steroids. Of these, the somatotropic (GH to IGF-1) axis is the most important hormonal system for growth, primarily consisting of GH, IGF-1, their carrier proteins and receptors [3,16].Considerable numbers of cattle with growth retardation have been produced in populations of Japanese cattle [6]. Most of them are considered to result from infectious diseases such as pneumonia, diarrhea or parasitic diseases [9]. The cattle with hereditary diseases [17,18] showed signs of prostration, anorexia and/or typical abnormal body shape in addition to growth retardation. We observed some Japanese Black cattle with marked growth retardation despite normal activity, appetite and proportional body shapes. In order to clarify the cause of growth retardation in these cattle, we determined the serum GH and IGF-1 concentrations in them.Five Japanese Black calves with growth retardation were used. Their ages ranged from 3 to 13 months. Two calves were males and 3 were females. These calves were of the congenital strain (Fig. 1). Their father was in consensus, YIH, and the paternal grandfather was YF. The maternal grandfather was also YF in 4 calves (Nos. 4371, 4374, 4441 and 4451) and TM in 1 calf (No. 4315). DIZ was the maternal grandfather of YIH, and the father of TM. Nos. 4374 and 4451 were full sibs. Their dam delivered 2 affected calves at the 4th and 5th deliveries, consecutively, mating with YIH. Four dams of the calves with growth retardation had procreated 10 normal calves mating with other sires before mating with YIH. The sire YIH produced 100 calves during 2 years (1997 to 1998) by artificial inseminations in the G region, and 9 calves (9.0%) were dwarfs. Gestations of all 5 calves were normal (288-295 days). They were delivered normally, and neonatal body weights (BW) were normal or slightly below (20 to 26 kg) [2]. These calves showed normal growth with no abnormal clinical signs until 3 or 4 months of age. At the first examinations, 3 calves (Nos. 4315 (160 kg in BW, 13 months of age), 4374 (144 kg in BW, 10 months of age) and 4441 (76 kg in BW, 5 months of age)) showed normal signs of appetite and activity, with no abno...

The aim of the current study was to identify independent risk factors for thyroid axis alterations in dogs with non-thyroidal diseases. In this retrospective cross-sectional study, data and plasma samples from 207 dogs with non-thyroidal diseases was used. The involvement of various factors (disease severity, sex, age, breed, category and duration of disease, and medication) in the alteration of plasma thyroxine (T4) or thyroid-stimulation hormone (TSH) concentrations was analyzed using multivariate logistic regression. Among the 207 dogs analyzed, 99 (47.8%) had low plasma T4 concentrations, while 45 (21.7%) had high TSH concentrations. Intact male sex [odds ratio (OR), 3.25; 1.67–6.35; P <0.001], Labrador Retrievers (OR, 18.70; 2.32–151.00; P =0.006), moderate (OR, 2.39; 1.21–4.74; P =0.012) and severe diseases (OR, 6.84; 2.27–20.70; P <0.001) were associated with increased risk for low plasma T4 concentrations. Meanwhile, intact male (OR, 3.93; 1.51–10.30; P =0.005), spayed female (OR, 4.22; 1.59–11.20; P =0.004), older age (OR, 2.73; 1.28–5.84; P =0.009), and Miniature Dachshunds (OR, 5.39; 2.38–12.20; P <0.001) had increased risk for high plasma TSH concentrations. Disease severity had been determined as an independent risk factor for canine NTIS. In addition, sex, age and breed were also associated with thyroid axis alterations in dogs with non-thyroidal diseases.

ABSTRACT. To investigate the relationship between the decreased immunity associated with infirmity and low body weight at birth as a consequence of intrauterine growth retardation in Japanese Black calves with stillbirth/perinatal weak calf syndrome, the thymuses and spleens of 13 calves with this syndrome, weighing less than 20 kg at birth, were examined histopathologically. Cytokeratin staining of the thymus was also carried out to examine its composition. The thymus and spleen were classified as grades 0-4 and I-III according to their hypoplasia, respectively. All calves showed a decreased number of thymocytes. One calf was classified as grade 1, which was characterized by a starry sky appearance. Five calves were classified as grade 2, demonstrating a reversion of the cortex-to-medulla ratio, and the rest were classified as grades 3 and 4 showing an indistinguishable boundary between the cortex and medulla. The thymuses of grade 3 and 4 were occupied by stroma cells, and their Hassall bodies and other structures were rarely observed. Six of 13 calves showed a decreased number of splenocytes, grade II or III, and their red and white pulp regions were unclear. The intrauterine growth retardation caused by lack of growth factors during the fetal period might have induced thymic hypoplasia associated with decreased immunity in the calves with stillbirth/perinatal weak calf syndrome. Therefore, intrauterine growth retardation might be associated with one of the causes of decreased immunity involved in infirmity in this syndrome. KEY WORDS: intrauterine growth retardation, Japanese Black cattle, low body weight, stillbirth/perinatal weak calf syndrome, thymic hypoplasia.

ABSTRACT. Two intact female dogs were admitted for growing mammary tumors. They had symptoms of acromegaly including weight gain, enlargement of the head, excessive skin folds, and inspiratory stridor. Serum concentrations of growth hormone (GH), insulinlike growth factor-I (IGF-I), and insulin were elevated in the two cases. From these findings, both dogs were diagnosed with acromegaly. In case 1, the GH, IGF-I, and insulin levels subsided after removal of the focal benign mammary tumors and ovariohysterectomy. In case 2, those levels subsided after removal of only focal mammary carcinoma. In both cases, immunohistochemical investigations for GH were positive in the mammary tumor cells but not in the normal mammary glands. We concluded that GH-producing mammary tumors caused the present acromegaly.