Localization of ghrelin and its receptor in the reproductive tract of Holstein heifers.

The aim of this experiment was to localize the mRNA and protein of ghrelin and its active receptor, growth hormone secretagogue 1A (GHS-R1A), within the reproductive tract of dairy cattle. Ghrelin is an orexigenic hormone that has been identified as a potent regulator of energy homeostasis. Recent evidence suggests that ghrelin may also serve as a metabolic signal to the reproductive tract. Ghrelin and GHS-R1A have been identified in the reproductive tract of several species, including humans, mice, and rats. However, ghrelin and GHS-R1A expression have not been described within bovine reproductive tissues. Therefore, the ampulla, isthmus, uterine body, corpus luteum, and follicles were harvested from 3 Holstein heifers (15.91±0.07 mo of age) immediately following exsanguination. Duodenum and hypothalamus were collected as positive controls for ghrelin and GHS-R1A, respectively. Tissues were fixed in 10% formalin and embedded in paraffin for microscopy. Additional samples were stored at -80°C for detection of mRNA. Ghrelin and GHS-R1A mRNA and protein were observed in all tissue types within the reproductive tract of dairy heifers; however, expression appeared to be cell specific. Furthermore, ghrelin protein appeared to be localized to the cytoplasm, whereas GHS-R1A protein was found on the plasma membrane. Within the reproductive tissues, ghrelin mRNA and protein were most abundantly expressed in the ampulla of the oviduct. Concentrations of GHS-R1A were lower than those of ghrelin but differed between tissues. This is one of the first studies to provide molecular evidence for the presence of ghrelin and GHS-R1A within the entire reproductive tract. However, implications for fertility remain to be determined.

T-lymphocyte predominance in lesions of canine coccidioidomycosis.

Coccidioidomycosis is a systemic fungal infection endemic to the southwestern United States. Although cell-mediated immunity is considered critical in control of the infection, little is known of the cellular population in naturally occurring lesions. To characterize the lymphocytic infiltration, archived formalin-fixed, paraffin-embedded tissues (subcutis, pericardium/heart, lung, bone, and synovium) from 18 dogs with coccidioidomycosis were studied with immunohistochemistry for CD3 and CD79a. In nearly all lesions, T lymphocytes were more numerous than B lymphocytes and were distributed throughout the lesion with concentration in the periphery of granulomas, whereas B lymphocytes were mostly confined to the periphery of granulomas. The predominance of T lymphocytes in lesions of canine coccidioidomycosis was independent of the tissue evaluated, the number of intralesional organisms, and the nature or severity of the inflammatory response.

Corticosteroid-responsive thrombocytopenia in two beef cows.

Corticosteroid-responsive thrombocytopenia was identified in 2 beef cows. Clinical findings in 1 cow included hematoma formation, petechiation of mucous membranes, anemia, and persistent thrombocytopenia. Cow 2 was in its fourth month of gestation and had epistaxis, nasal mucosal petechiation, anemia, and thrombocytopenia. Treatment included parenteral administration of corticosteroids at immunosuppressive dosages. Cow 1 had a history of chronic hematoma formation and responded to long-term treatment with dexamethasone, but it relapsed 2 months after treatment was discontinued. Cow 2 had acute onset of clinical signs, responded to short-term treatment with prednisone, delivered a full-term, healthy calf, and remained clinically normal for at least 1 year after treatment was completed. Reported causes of thrombocytopenia in ruminants were ruled out or seemed unlikely; a definitive cause for thrombocytopenia in the 2 cows could not be established.

Urine glycosaminoglycan concentrations in mucopolysaccharidosis VI-affected cats following bone marrow transplantation or leukocyte infusion.

Urinary glycosaminoglycan (GAG) concentrations were determined in nineteen normal cats (eleven kittens and eight adult cats), eighteen mucopolysaccharidosis VI (MPS VI)-affected untreated cats (ten kittens and eight adult cats), thirteen cats MPS VI-affected cats following bone marrow transplants (BMT), and two MPS VI-affected cats following intravenous infusion of leukocytes from normal cats. Mucopolysaccharidosis VI-affected cats treated with BMT had a precipitous decrease in urinary GAG by day 7 post-BMT, then a transient increase just prior to engraftment, followed by a sustained decrease to within, or near, the range of urinary GAG concentration established for normal cats. The pre-engraftment changes in urinary GAG excretion were reproduced by leukocyte infusion. After infusion of comparable members of normal peripheral blood leukocytes, a significant decrease in urinary GAG concentrations, specifically dermatan sulfate (DS), was seen with a nadir at day 5 post-infusion, followed by a return by day 9 to pre-infusion values. Post-engraftment, a continued low urinary GAG concentration with a specific decrease in DS can be utilized to document successful autologous engraftment in MPS VI-affected cats.

Evaluation of shelf arthroplasty as a treatment for hip dysplasia in dogs.

OBJECTIVE: To evaluate effects of shelf arthroplasty on coxofemoral joint laxity and progression of degenerative joint disease in young dogs with hip dysplasia. DESIGN: Prospective, controlled study. ANIMALS: 10 dogs between 10 and 24 months old and weighing between 20 and 27 kg. All dogs had bilateral coxofemoral joint laxity (i.e., an Ortolani's sign). PROCEDURE: In all dogs, shelf arthroplasty was performed on the right coxofemoral joints, and a sham procedure was performed on the left. Dogs were evaluated before and after surgery by means of lameness assessment, coxofemoral joint palpation and goniometry, thigh circumference measurement, and radiography. RESULTS: There were no significant changes in coxofemoral joint mobility, range of motion, joint laxity, degree of degenerative joint disease, or thigh circumference during the study. A greater amount of periacetabular bone formed on the right side than on the left side; however, dogs did not develop large bony shelves, and the amount of periarticular bone decreased over time. The polymer implants remained in their original position and were encapsulated by fibrous tissue. There was no histologic evidence of osteoconduction by the implants. CLINICAL IMPLICATIONS: The polymer implants used in this procedure do not appear to be osteoconductive. Shelf arthroplasty was associated with minimal morbidity and was not associated with serious adverse sequelae in this study, but the procedure did not alter the progression of hip dysplasia in these dogs. We cannot advocate shelf arthroplasty using this polymer as a treatment for dogs with hip dysplasia.

Clinicopathologic evaluation of the liver.

Clinicopathologic data are important tools in the evaluation of a patient with liver dysfunction. It is imperative, however, that the data not be looked at with a dogmatic approach. Many of the laboratory tests are sensitive indicators of hepatic dysfunction; however, they seldom, if ever, indicate a specific cause of hepatic dysfunction. History, physical, radiographic, and ultrasonographic examination findings, and laboratory data must be used together to fully evaluate a patient with biochemical abnormalities related to hepatic function. The prevalence of secondary hepatic disease and the difficulty of differentiating it from primary hepatic disease based on laboratory data must always be kept in mind.

Efficacy of 4-methylpyrazole for treatment of ethylene glycol intoxication in dogs.

4-Methylpyrazole (4-MP), an alcohol dehydrogenase inhibitor, was administered to dogs to treat ethylene glycol (EG) intoxication. Eleven dogs were given 10.6 g of EG/kg of body weight; 5 dogs were treated with 4-MP 5 hours after EG ingestion and 6 dogs were treated with 4-MP 8 hours after EG ingestion. 4-Methylpyrazole was administered IV as a 50-mg/ml [corrected] solution in 50% polyethylene glycol: initial dose, 20 mg/kg; at 12 hours after initial dose, 15 mg/kg; at 24 hours after initial dose, 10 mg/kg; and at 30 hours after initial dose, 5 mg/kg. Physical, biochemical, hematologic, blood gas, serum and urine EG concentrations, and urinalysis findings were evaluated at 0, 1, 3, 6, 9, 12, 24, 48, 72 hours, and at 1 week and 2 weeks after EG ingestion. Dogs of both groups developed clinicopathologic signs associated with EG intoxication, including CNS depression, hyperosmolality, high anion gap metabolic acidosis, polydipsia, polyuria, calcium oxalate monohydrate and dihydrate crystalluria, and isosthenuria. Fractional excretion of sodium was increased in all dogs between 1 and 9 hours after EG ingestion, but remained increased beyond 24 hours only in the 2 dogs treated at 8 hours after EG ingestion that developed acute renal failure. All dogs treated 5 hours after EG ingestion recovered without morphologic, biochemical, or clinical evidence of renal impairment. Of the 6 dogs treated 8 hours after EG ingestion, 2 developed acute renal failure. One of the dogs treated 8 hours after EG ingestion remained isosthenuric for 2 months, but did not manifest any other signs of renal impairment.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of ethanol and 4-methylpyrazole as treatments for ethylene glycol intoxication in cats.

The efficacy of 4-methylpyrazole (4-MP) and ethanol as treatment for ethylene glycol (EG) intoxication in cats was compared. Twenty-two cats were assigned at random to 6 experimental groups. Cats of 1 experimental group were given only 4-MP; those of another experimental group were given only EG. Cats of 3 experimental groups were intoxicated with EG and given 4-MP at 0 hour or 2 or 3 hours after EG ingestion, and those of 1 experimental group were given EG and treated with ethanol 3 hours after EG ingestion. Physical, biochemical, hematologic, blood gas, serum and urine EG concentrations, and urinalysis findings were evaluated at 0, 1, 3, 6, 9, 12, 24, 48, and 72 hours, 1 weeks, and 2 weeks after EG ingestion or 4-MP treatment in cats of the 4-MP only group. The half-life of EG and percentage of ingested EG excreted unchanged were determined for each group. 4-Methylpyrazole treatment at 0 hour was most effective at preventing metabolism of EG. 4-Methylpyrazole was not effective in preventing development of renal failure when given 2 or 3 hours after EG ingestion. Ethanol given 3 hours after EG ingestion was successful in preventing development of renal dysfunction in 2 of the 6 cats treated 3 hours after EG ingestion. Of the remaining 4 cats treated with ethanol, 2 developed transient renal dysfunction and 2 developed acute oliguric renal failure and were euthanatized. 4-Methylpyrazole given 2 or 3 hours after EG ingestion was less effective in preventing EG metabolism than was ethanol given 3 hours after EG ingestion. Therefore 4-MP, at the dose found to be effective in dogs, cannot be recommended as an alternative to ethanol for treatment of EG intoxication in cats.

4-Methylpyrazole as treatment for naturally acquired ethylene glycol intoxication in dogs.

Eight dogs with ethylene glycol intoxication were treated with 4-methylpyrazole, an alcohol dehydrogenase inhibitor. Dogs had clinical signs referable to ethylene glycol ingestion including ataxia, depression, vomiting, polyuria, and dehydration. Metabolic abnormalities included high anion gap metabolic acidosis, serum hyperosmolality, isosthenuria, and monohydrate and dihydrate calcium oxalate crystalluria. Serum and urine ethylene glycol concentrations were determined to confirm ingestion of ethylene glycol. A 50-mg/ml solution of 4-methylpyrazole in propylene glycol was administered iv as follows: initial treatment, 20 mg/kg of body weight; at 17 hours after admission, 15 mg/kg; at 25 hours after admission, 5 mg/kg. By 24 hours after admission, all dogs had clinical and metabolic improvement. Of the 8 dogs, 7 were released within 3 days of admission. Four of the 8 dogs returned for follow-up evaluation, at which time biochemical or hematologic abnormalities were not observed.

Identification of calcium oxalate monohydrate crystals by X-ray diffraction in urine of ethylene glycol-intoxicated dogs.

Urine sediments of dogs with experimentally induced ethylene glycol poisoning were examined by light microscopy and X-ray diffraction. Massive calcium oxalate crystalluria was observed in all poisoned dogs. By light microscopy, the frequency with which six-sided hippurate-like prisms and envelope forms of calcium oxalate dihydrate occurred was approximately equal. The hippurate-like crystals were shown to be calcium oxalate monohydrate by X-ray diffractometry.