Impact of a cell salvage device on blood transfusions to dogs undergoing surgery at a referral veterinary hospital.

Objective: To determine the number of homologous blood transfusions received by canine surgical patients after introducing a cell salvage device (CSD), trends in surgeries requiring blood transfusion, and the incidence of transfusion reactions.

Study Design: Retrospective study.

Setting: Single referral hospital.

Ex vivo evaluation of a novel cell salvage device to recover canine erythrocytes.

Objective: To determine the ability of a cell salvage device to recover canine erythrocytes by direct aspiration of diluted packed red blood cells (pRBC) and saline rinse from blood-soaked surgical swabs.

Study Design: Experimental study.

Sample Population: Twelve recently expired units of canine pRBC.

Intraoperative cell salvaging: ex vivo evaluation of two swab-washing methods.

Objective: To compare erythrocyte recovery by a cell salvage device between swab-washing by manual agitation or filtration.

Sample: 12 recently expired units of canine packed RBCs.

Procedure: The packed RBC units underwent quality analysis before donation from a pet blood bank.

Prevalence of pulmonary nodules suggestive of metastasis at presentation in dogs with cutaneous or subcutaneous soft tissue sarcoma.

Objective: To investigate the prevalence of pulmonary nodules suggestive of metastasis at the time of initial presentation in dogs with cutaneous or subcutaneous soft tissue sarcomas (STSs) and no previous related thoracic diagnostic imaging.

Animals: 146 client-owned dogs with a cutaneous or subcutaneous STS.

Procedures: Medical records were retrospectively searched to identify dogs with STSs that underwent initial thoracic diagnostic imaging when presented for referral examination between September 2014 and March 2018.

Hyperpolarisation of cultured human chondrocytes following cyclical pressure-induced strain: evidence of a role for alpha 5 beta 1 integrin as a chondrocyte mechanoreceptor.

Mechanical stimuli influence chondrocyte metabolism, inducing changes in intracellular cyclic adenosine monophosphate and proteoglycan production. We have previously demonstrated that primary monolayer cultures of human chondrocytes have an electrophysiological response after intermittent pressure-induced strain characterised by a membrane hyperpolarisation of approximately 40%. The mechanisms responsible for these changes are not fully understood but potentially involve signalling molecules such as integrins that link extracellular matrix with cytoplasmic components.

Analysis of human articular chondrocyte CD44 isoform expression and function in health and disease.

Interactions between articular chondrocytes and components of the extracellular matrix are of potential importance in the normal function of cartilage and in the pathophysiology of arthritis. Little is known of the basis of these interactions, but cell adhesive molecules such as CD44 are likely to be involved. Immunohistology using six well-characterized anti-CD44 monoclonal antibodies demonstrated standard CD44 isoform (CD44H) expression by all chondrocytes in normal and osteoarthrotic (OA) cartilage but absence of the CD44E variant.

Chondrocyte heterogeneity: immunohistologically defined variation of integrin expression at different sites in human fetal knees.

During development and at maturity different forms of cartilage vary in morphology and macromolecular content. This reflects heterogeneity of chondrocyte activity, in part involving differential interactions with the adjacent extracellular matrix via specialized cell surface receptors such as integrins. We undertook an immunohistological study on a series of human fetal knee joints to assess variation in the expression of integrins by chondrocytes and potential matrix ligands in articular, epiphyseal, growth plate, and meniscal cartilage.

Increase in neutrophil Fc gamma receptor I expression following interferon gamma treatment in rheumatoid arthritis.

The therapeutic potential of interferon gamma (IFN gamma) in a number of disease states is still being explored, but progress is hampered by the lack of a suitable measure of in vivo biological activity. To assess the in vivo biological effects of recombinant human IFN gamma (rhIFN gamma), 14 patients were studied in a randomised, prospective, double blind, placebo controlled trial of this cytokine for the treatment of rheumatoid arthritis. The levels of Fc gamma receptors on peripheral blood neutrophils were measured at baseline and after 21 days of once daily, subcutaneous injections of rhIFN gamma or placebo.

Circulating autoantibodies to recombinant lipocortin-1 in asthma.

One of the postulated mechanisms of corticosteroid action is through the de novo synthesis and release of lipocortins. We assayed circulating antibodies to lipocortin-1 in sera obtained from normal (n = 67) and asthmatic (n = 57) subjects using an ELISA technique. Asthmatic subjects with a wide range of severity, with the mildest needing only occasional inhaled beta-agonist therapy to the most severe needing maintenance oral corticosteroid treatment, were recruited from our Asthma Clinic and classified into five categories according to the need of therapy.

An assay for the assessment of lipocortin 1 levels in human lung lavage fluid.

The physiological function of the lipocortins, proteins which are thought to be glucocorticoid-regulated, is unclear. An improved assay for lipocortins might help to elucidate their role. A rapid and specific sandwich enzyme-linked immunosorbent assay (ELISA) for lipocortin 1 with a working range of 1-2000 ng/ml and an interrun coefficient of variation of less than 10% is described and used in this pilot study to quantify human lipocortin 1 for the first time in acellular bronchoalveolar lavage fluid (BALF), and in media conditioned by BAL cells, from control patients and those with pulmonary sarcoidosis.

Anti-inflammatory lipocortin 1 production by peripheral blood leucocytes in response to hydrocortisone.

The presence and amount of the anti-inflammatory protein lipocortin 1 was determined in plasma and peripheral blood leucocytes by a highly specific, enzyme-linked immunosorbent assay. Within 120 min of a single intravenous dose of 100 mg hydrocortisone, the intracellular concentrations of lipocortin 1 in peripheral monocytes in 7 of 8 healthy men increased by a median of 225% (range 129-507%) compared with pretreatment levels, and mononuclear cell-surface lipocortin increased by a median of 224% (range 76-483%). Placebo injections had no effect.

Bronchial asthma is not associated with auto-antibodies to lipocortin-1.

Corticosteroids may mediate some of their anti-inflammatory action by the induction of lipocortin-1, which inhibits phospholipase A2 activity. Raised levels of antibodies to lipocortin have been found in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) and it has been postulated that these may contribute to steroid resistance. A proportion of asthmatic patients fail to respond to treatment with corticosteroids and one possible mechanism is that these patients have raised levels of anti-lipocortin antibodies.