Objective—To develop a quality of life (QOL) survey for use in a canine cancer chemotherapy setting, validate the instrument's utility, identify key questions that facilitate client and clinician communication regarding decisions in patient care, and use human and veterinary QOL literature to develop a comprehensive yet simple proxy survey instrument.
Animals—29 canine chemotherapy patients.
Procedures—Patients were evaluated by both owners and veterinarians at the time of initial visit to the clinic and at 3 and 6 weeks after the initiation of chemotherapy. This survey consisted of a longitudinal evaluation of QOL with 6 components addressing the animal's QOL retrospectively, before onset of cancer; changes in the animal's QOL since manifestation of disease; changes in the animal's QOL with regard to treatment response; owner's QOL and its impact on priorities in decision making; clinician's impression of the owner's priorities and QOL; and clinician's impression of the dog's QOL.
Results—Multiple regression analysis indicated 3 significant predictors of canine cancer patient QOL to be play behaviors, signs of illness, and canine happiness as perceived by owners.
Conclusions and Clinical Relevance—The QOL instrument was easy to use and enhanced client perception of patient care and clinician concern. Owners enjoyed the opportunity to complete the survey. Since questions regarding play behaviors, clinical signs of disease, and canine happiness were significant indicators of changes in QOL, these should be included in future studies. Quality of life assessment may facilitate treatment decisions and assessment of canine patients undergoing chemotherapy.
OBJECTIVE To measure blood lead concentrations (BLCs) in dogs living in Flint, Mich, following a declared water crisis and to assess potential associations of BLCs with demographic data, water sources, and clinical signs in these dogs.
DESIGN Cross-sectional study.
ANIMALS 284 dogs residing in Flint, Mich (test population), and 47 dogs residing in East Lansing, Mich (control population), and immediately adjacent areas.
PROCEDURES Blood samples were collected at free screening clinics in Flint (test population) and at the Michigan State University College of Veterinary Medicine Veterinary Medical Center (control population). Owners of test population dogs completed questionnaires providing demographic and clinical information. Hematologic evaluations were performed; BLCs were measured by inductively coupled plasma–mass spectrometry.
RESULTS 4 of 284 test population dogs had BLCs > 50 ppb; an additional 20 had BLCs > 20 ppb. Overall, BLCs of test population dogs were higher than those of control dogs. Within the test population, young dogs (≤ 2 years of age) had higher BLCs than old dogs (≥ 6 years of age). Only 7.2% of test population dogs were drinking unfiltered tap water at the time of screening; however, dogs that had been receiving filtered or bottled water for ≤ 3 months before screening had higher BLCs than did those that received such water for > 3 months.
CONCLUSIONS AND CLINICAL RELEVANCE Taken together, findings suggested that the impact of the Flint water crisis extended to companion animals. Results highlighted the importance of maintaining awareness of lead exposure and considering both human and animal well-being in cases of environmental toxicant exposures.
Objective—To determine the effects of prostaglandin
E2 (PGE2) on recombinant equine interleukin (IL)-1β-stimulated expression of matrix metalloproteinases
(MMP 1, MMP 3, MMP 13) and tissue inhibitor of
matrix metalloproteinase 1 (TIMP 1) in vitro.
Sample Population—Cultured equine chondrocytes.
Procedure—Stationary monolayers of first-passage
chondrocytes were exposed to graduated concentrations
of PGE2 with or without a subsaturating dose
(50 pg/ml) of recombinant equine IL-1β (reIL-1β) to
induce expression of MMP 1, MMP 3, MMP 13, and
TIMP 1, followed by RNA isolation and northern blotting.
In subsequent experiments, gene expression
was similarly quantified from mRNA isolated from cultures
pretreated with phenylbutazone to quench
endogenous PGE2 synthesis, followed by exposure to
reIL-1β and exogenous PGE2 (5 mg/ml) with appropriate
Results—Exogenous PGE2 (10 mg/ml) significantly
reduced reIL-1β-induced expression of MMP 1,
MMP 3, MMP 13, and TIMP 1. Abrogation of
cytokine induction with this dose of PGE2 was comparable
to that for dexamethasone (10–5M) control.
Similarly, pretreatment with phenylbutazone, followed
by exposure to reIL-1β and PGE2 (5 mg/ml),
was associated with a reduced expression of the
genes of interest, an effect that was significant for
MMP 1, MMP 13, and TIMP 1.
Conclusions and Clinical Relevance—The MMP
and TIMP 1 are important mediators in the pathophysiologic
events in osteoarthritis. The potential for
physiologically relevant regulation of expression of
these genes by PGE2 is a consideration in the use of
drugs that inhibit prostanoid synthesis in the treatment
of equine arthropathies. (Am J Vet Res
Objective—To determine the effects of recombinant
equine interleukin -1β (reIL-1β) and 4 anti-inflammatory
compounds on the expression and activity of
cyclooxygenase (COX)-2 in cultured equine chondrocytes.
Sample Population—Articular cartilage from 9
young adult horses.
Procedure—Reverse transcriptase-polymerase chain
reaction methods were used to amplify a portion of
equine COX-2 to prepare a cDNA probe. Northern blot
analysis was used to quantify the expression of
COX-2 in first-passage cultures of equine articular
chondrocytes propagated in media containing dexamethasone
(DEX), phenylbutazone (PBZ), polysulfated
glycosaminoglycan, and hyaluronan, each at concentrations
of 10 and 100 µg/ml and each with or without
reIL-1β. A commercial immunoassay was used to
determine prostaglandin E2 (PGE2) concentrations in
conditioned medium of similarly treated cells to quantify
Results—Addition of reIL-1β increased the expression
of COX-2 in a dose-dependent manner, which was
paralleled by an increased concentration of PGE2 in
culture medium. Concentration of PGE2 in spent
medium from reIL-1β-treated chondrocytes was significantly
reduced by DEX and PBZ; however, only
DEX significantly reduced gene expression of COX-2.
Conclusions and Clinical Relevance—Prostaglandin
E2 is considered to be an important mediator in the
pathophysiologic processes of arthritis, and cultured
chondrocytes respond to interleukin-1 with enhanced
expression and activity of COX-2. Palliative relief in
affected horses is probably attributable, in part, to
inhibition of PGE2 synthesis; however, analysis of
these data suggests that of the 4 compounds tested,
only DEX affects pretranslational regulation of the
COX-2 gene in cultured equine chondrocytes.
(Am J Vet Res 2002;63:1134–1139)
To determine the frequency of previously reported coding variants in the ATP7A, ATP7B, and RETN genes in a US population of Labrador Retrievers and to explore potential associations of these genotypes with pathologic hepatic copper accumulation.
Archived hepatic specimens from 90 Labrador Retrievers collected between 2013 and 2021.
The Michigan State University Veterinary Diagnostic Laboratory database was searched to identify archived tissues from Labrador Retrievers that had undergone hepatic histopathologic assessment. Cases were classified into control, copper-associated hepatopathy (CAH), and intermediate populations on the basis of histopathologic features and hepatic copper accumulation. The DNA was extracted from archived tissues and genotyped for reported variants in the 3 genes. Allele frequencies were determined, and associations of genotypes with CAH status were evaluated.
29 control dogs, 45 CAH dogs, and 16 intermediate dogs were included in the study. The overall ATP7A and RETN variant allele frequencies were 30% and 13%, respectively, and were not significantly different among control, CAH, and intermediate populations. The ATP7B variant allele frequency was significantly higher in the CAH population (30%) as compared to the control population (13%). However, 21 of 45 (47%) CAH dogs did not have an ATP7B variant allele whereas 7 of 28 (25%) control dogs did have an ATP7B variant allele.
Study results supported a contributory role for the ATP7B variant in CAH pathogenesis in Labrador Retrievers. However, the application of genetic testing in a clinical setting is complicated by genotypic variability within healthy and diseased dogs.