Development and preliminary validation of the cognitive behavioral dieting scale.

OBJECTIVE: The purpose of this research was to empirically develop the Cognitive Behavioral Dieting Scale (CBDS), a measure of current dieting. METHOD: The first study involved item generation and a procedure to boost internal consistency while reducing scale length. Study 2 involved a factor analysis and measures of scale reliability. The third study evaluated the ability of the CBDS to predict calorie intake and negative calorie balance from a 24-hr diet recall. Study 4 evaluated construct validity by comparing the CBDS to dietary restraint, body image, and health behavior self-efficacy. RESULTS: The CBDS is a 14-item scale which measures current dieting behavior and related thoughts within the past 2 weeks. Internal consistency was alpha = .95 and 2-day test-retest reliability was r = .95. This scale provides a method for operationalizing dieting, provides a construct that is different from restraint, and assess dieting behavior on a continuum. Additionally, this scale was able to predict calorie intake and negative calorie balance above and beyond the predictive ability of physical variables (i.e., body mass index BMI] and exercise calories). An additional study of construct validity showed the CBDS was related to poor body image esteem and dietary restraint, but minimally related to healthy eating self-efficacy. DISCUSSION: In conclusion, the CBDS shows promise as a valid and reliable measure of dieting behavior. This scale should have utility in future research on how current dieting relates to eating disorders, dietary restraint, and obesity.

Bacterial isolates from blood cultures of dogs undergoing dentistry.

Bacteria in blood cultures in 30 dogs undergoing high-speed dental scaling and tooth extraction were examined. One or more positive blood cultures were identified in 9 of 30 (30%) dogs. Pasteurella spp. were most frequently (5 dogs) isolated and were sensitive to ampicillin, penicillin, cephalothin, chloramphenicol, tetracycline, amoxicillin with clavulanic acid, and sulfamethoxazole with trimethoprim. Two groups of 15 dogs each, anesthetized or sedated but not undergoing dental procedures, served as non-dentistry controls. There were no significant (p < .05) differences between the number of positive cultures in dentistry and non-dentistry groups. In healthy dogs undergoing high-speed dental scaling and tooth extraction, the occurrence of bacteria in blood cultures was much lower than previously reported. The clinical significance of positive blood cultures was uncertain.

Evaluation of intra-articularly administered sodium monoiodoacetate-induced chemical injury to articular cartilage of horses.

Three doses of sodium monoiodoacetate (MIA) were used to induce degenerative changes in articular cartilage in middle carpal joints of horses. Twelve young (2- to 5-year-old) horses, free of lameness, were randomly allotted to 3 groups. One middle carpal joint of each horse was injected with 0.9% NaCl solution (control joint). The contralateral middle carpal joint was injected with 0.09 mg of MIA/kg of body weight (group 1); 0.12 mg/kg (group 2); or 0.16 mg/kg (group 3). After MIA administration, horses were allowed ad libitum exercise in a 2-acre paddock for 12 weeks. At the end of the study, gross and microscopic tissue changes were evaluated and biochemical analyses of articular cartilage were done. Grossly, diffuse partial-thickness articular cartilage lesions were observed in group-2 (n = 2) and group-3 (n = 4) horses, but not in group-1 horses. Articular cartilage uronic acid content was significantly (P less than 0.03) decreased in all MIA-injected joints, compared with controls. Articular cartilage matrix staining with safranin-O was decreased in 3 of 4 MIA-injected joints of group-1 horses and in all MIA-injected joints of group-2 and group-3 horses, compared with controls (P less than 0.06). Microscopic degenerative changes in articular cartilage were not significantly different between MIA-injected and control joints in group-1 horses, but were increased (P less than 0.06) in all MIA-injected joints of group-2 and group-3 horses, compared with controls. Qualitatively, decreased matrix staining and degenerative changes were more severe in group-3 horses. On the basis of articular cartilage gross and microscopic changes, as well as biochemical changes, 0.12 mg of MIA/kg injected intra-articularly was determined to induce moderate degrees of articular cartilage degeneration. This model of chemically induced articular cartilage injury could be useful for evaluating treatment effects of anti-arthritic drugs in horses.

Conservative management of uroperitoneum in a gelding.

Uroperitoneum as a sequela to urethral calculus in an adult gelding was successfully managed by use of subischial urethrotomy and abdominal drainage. Necrosis of bladder mucosa was seen endoscopically, but a tear or rupture was never identified. Peritonitis developed but was controlled with antibacterial treatment. Although uroperitoneum is usually a sequela to bladder rupture and the ideal treatment is surgical repair, conservative management may be warranted in selected cases.

Comparison of the effect of polysulfated glycosaminoglycan, corticosteroids, and sodium hyaluronate in the potentiation of a subinfective dose of Staphylococcus aureus in the midcarpal joint of horses.

Four groups of 8 horses each had 1 midcarpal joint injected with 33 colony-forming units (CFU) of viable Staphylococcus aureus plus: 1 ml of saline solution (group 1, control), 250 mg of polysulfated glycosaminoglycan (PSGAG, group 2), 100 mg of methylprednisolone acetate (group 3), or 20 mg of sodium hyaulronate (group 4). Horses were euthanatized, and samples were obtained on the basis of clinical signs of septic arthritis that were nonresponsive to phenylbutazone administration. One group-1 horse, all 8 group-2 horses, 3 group-3 horses, and 4 group-4 horses were culture-positive for S aureus and had clinical signs, results of synovial fluid analysis, and histopathologic findings that were consistent with sepsis. The addition of 250 mg of PSGAG increased the development of sepsis significantly (P = 0.001), compared with results in control horses. Differences in the development of sepsis between horses injected with methylprednisolone acetate or sodium hyaluronate and control horses were not significant.

Further investigations into the potentiation of infection by intra-articular injection of polysulfated glycosaminoglycan and the effect of filtration and intra-articular injection of amikacin.

Polysulfated glycosaminoglycan (PSGAG) recently have been reported to potentiate the infectivity of Staphylococcus aureus in horses with experimentally induced septic arthritis. Four groups of 8 horses each had 1 midcarpal joint injected with approximately 33 viable colony-forming units (CFU) of S aureus plus either 1 ml of saline solution (group 1), 250 mg of PSGAG (group 2), 250 mg of PSGAG passed through a 0.6-microns filter (group 3), or 250 mg of PSGAG plus 125 mg of amikacin (group 4). Horses that developed clinical signs consistent with sepsis were euthanatized, and samples were collected at necropsy. Horses that survived had samples obtained by use of arthroscopy at days 13 and 14 after injection. Staphylococcus aureus was isolated from 1 group-1 horse, 8 group-2 horses, and 7 of 7 group-3 horses that met protocol, but was not isolated from any group-4 horses. All 16 aforementioned horses had clinical signs, results of synovial fluid analysis, and gross pathologic and synovial membrane histopathologic findings that were consistent with septic arthritis. Polysulfated glycosaminoglycan (250 mg) increased the infectivity of 33 CFU of S aureus (P = 0.001); filtering the PSGAG had no effect. Intra-articular injection of 125 mg of amikacin immediately after inoculating the joint with 33 CFU of S aureus significantly (P = 0.001) decreased potentiation of infection by the PSGAG.