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sample sizes are small. 3 Two types of random error can occur ( Appendix ). When a trial finds no difference in outcome between treatment groups, clinicians must be able to assess the likelihood that an important difference was missed because of type II
injury. Type II collagen and aggrecan make up most of the extracellular matrix of articular cartilage. Disruption of the extracellular matrix is the hallmark of osteoarthritis, and as a result, biomarker development has focused on identifying byproducts
Articular cartilage is composed principally of type II collagen and aggrecan. 1,2 Type II collagen is the most abundant protein of articular cartilage across species and is relatively specific for this tissue. 1 A combination of cytokines and
CAV-2 Canine adenovirus type II CDV Canine distemper virus CI Confidence interval CPV Canine parvovirus Log 2 Logarithm base 2 a. Corvac serum separator tubes, Tyco Healthcare Group LP, Mansfield, Mass. b. Nalgene cryoware, Nalge Nunc
Abstract
Objective—To develop an antibody that specifically recognizes collagenase-cleaved type-II collagen in equine articular cartilage.
Sample Population—Cartilage specimens from horses euthanatized for problems unrelated to the musculoskeletal system.
Procedure—A peptide was synthesized representing the carboxy- (C-) terminus (neoepitope) of the equine type-II collagen fragment created by mammalian collagenases. This peptide was used to produce a polyclonal antibody, characterized by western analysis for reactivity to native and collagenase-cleaved equine collagens. The antibody was evaluated as an antineoepitope antibody by ELISA, using peptides ± an amino acid at the C-terminus of the immunizing peptide. Collagen cleavage was assayed from equine articular cartilage cultured with interleukin-1 (IL-1), ± a synthetic MMP inhibitor, BAY 12-9566. Cartilage specimens from osteoarthritic and nonarthritic joints were compared for antibody staining.
Results—An antibody, 234CEQ, recognized only collagenase- generated 3/4-length fragments of equine type-II collagen. This was a true antineoepitope antibody, as altering the C-terminus of the immunizing peptide significantly decreased competition for binding in an inhibition ELISA. The IL-1-induced release of type-II collagen fragments from articular cartilage was prevented with the MMP inhibitor. Cartilage from an osteoarthritic joint of a horse had increased staining with the 234CEQ antibody, compared with normal articular cartilage.
Conclusions and Clinical Relevance—We generated an antineoepitope antibody recognizing collagenase- cleaved type-II collagen of horses. This antibody detects increases in type-II collagen cleavage in diseased equine articular cartilage. The 234CEQ antibody has the potential to aid in the early diagnosis of arthritis and to monitor treatment responses. (Am J Vet Res 2001;62:1031–1039)
Abstract
Objective—To determine the comparative virulence of 5 isolates of bovine viral diarrhea virus (BVDV) type II by inoculating 6- to 9-month-old beef calves with isolates originating from the tissues of cattle affected with naturally occurring, transient, acute, nonfatal infections or naturally occurring, peracute, fatal infections.
Animals—22 calves that were 6 to 9 months old.
Procedure—The study used BVDV isolates 17011, 713, and 5521 that originated from fetuses aborted from cows with transient, nonfatal, acute BVDV infections and isolates 23025 and 17583 that originated from the tissues of cattle with peracute, fatal BVDV infections. Calves were allotted to 6 groups (1, mockinfected control calves [n = 2]; 2, inoculated with BVDV 17011 [4]; 3, inoculated with BVDV 713 [4]; 4, inoculated with BVDV 5521 [4]; 5, inoculated with BVDV 23025 [4]; and 6, inoculated with BVDV 17583 [4]). Rectal temperatures and clinical signs of disease were recorded daily. Total and differential WBC and platelet counts were performed. Histologic examination and immunohistochemical analysis were conducted to detect lesions and distribution of viral antigens, respectively.
Results—Calves inoculated with BVDV 23025 or 17583 developed more severe clinical signs of disease (fever and diarrhea), more severe lymphopenia, and more severe lesions (alimentary epithelial necrosis, lymphoid depletion, and BVDV antigen deposition in lymphatic tissues), compared with calves inoculated with BVDV 713, 5521, or 17011.
Conclusions and Clinical Relevance—Relative severity of experimentally induced infections corresponded to severity of clinical signs of naturally occurring infections with respective BVDV isolates. (Am J Vet Res 2002;63:1379–1384)
Abstract
Objective—To determine the effect of maternally derived antibodies on induction of protective immune responses against bovine viral diarrhea virus (BVDV) type II in young calves vaccinated with a modified-live bovine viral diarrhea virus (BVDV) type I vaccine.
Design—Blinded controlled challenge study.
Animals—24 neonatal Holstein and Holstein-cross calves that were deprived of maternal colostrum and fed pooled colostrum that contained a high concentration of (n = 6) or no (18) antibodies to BVDV.
Procedure—At 10 to 14 days of age, 6 seropositive and 6 seronegative calves were given a combination vaccine containing modified-live BVDV type I. All calves were kept in isolation for 4.5 months. Six calves of the remaining 12 untreated calves were vaccinated with the same combination vaccine at approximately 4 months of age. Three weeks later, all calves were challenged intranasally with a virulent BVDV type II.
Results—Seronegative unvaccinated calves and seropositive calves that were vaccinated at 2 weeks of age developed severe disease, and 4 calves in each of these groups required euthanasia. Seronegative calves that were vaccinated at 2 weeks or 4 months of age developed only mild or no clinical signs of disease.
Conclusions and Clinical Relevance—Results indicate that a single dose of a modified-live BVDV type-I vaccine given at 10 to 14 days of age can protect susceptible young calves from virulent BVDV type II infection for at least 4 months, but high concentrations of BVDV-specific maternally derived antibodies can block the induction of the response. (J Am Vet Med Assoc 2001;219:351–356)
were assigned a classification of acquired type II vWD rather than inherited type 2 vWD. It was not possible by use of medical histories or follow-up monitoring to establish a clinical disease status. It is therefore possible that the observed reduction
by type and include congenital anal stenosis (Type I), imperforate anus and blind rectal pouch in close proximity to the overlying skin (Type II), imperforate anus with a more cranial termination of the blind rectal pouch (Type III), and discontinuity
samples were analyzed in duplicate, and mean values were calculated. Total pellet collagen type II content —Collagen type II protein concentrations in each pellet were determined by use of a commercially available enzyme immunosorbent assay i according
