OBJECTIVE To compare complications and outcome following unilateral, staged bilateral, and single-stage bilateral ventral bulla osteotomy (VBO) in cats. ANIMALS 282 client-owned cats treated by VBO at 25 veterinary referral and academic hospitals from 2005 through 2016. PROCEDURES Medical records of cats were reviewed to collect information on signalment, clinical signs, diagnostic test results, surgical and postoperative management details, complications (anesthetic, surgical, and postoperative), and outcome. Associations were evaluated among selected variables. RESULTS Unilateral, staged bilateral, and single-stage bilateral VBO was performed in 211, 7, and 64 cats, respectively, representing 289 separate procedures. Eighteen (9%), 2 (29%), and 30 (47%) of these cats, respectively, had postoperative respiratory complications. Cats treated with single-stage bilateral VBO were significantly more likely to have severe respiratory complications and surgery-related death than cats treated with other VBO procedures. Overall, 68.2% (n = 197) of the 289 procedures were associated with Horner syndrome (19.4% permanently), 30.1% (87) with head tilt (22.1% permanently), 13.5% (39) with facial nerve paralysis (8.0% permanently), and 6.2% (18) with local disease recurrence. Cats with (vs without) Horner syndrome, head tilt, and facial nerve paralysis before VBO had 2.6, 3.3, and 5.6 times the odds, respectively, of having these conditions permanently. CONCLUSIONS AND CLINICAL RELEVANCE Findings suggested that staged bilateral VBO should be recommended over single-stage bilateral VBO for cats with bilateral middle ear disease. Cats with Horner syndrome, head tilt, and facial nerve paralysis before surgery were more likely to have these conditions permanently following surgery than were cats without these conditions.

Objective To determine which of 2 suture materials would be superior in terms of closure time and leakage pressure in open single‐layer cystotomy closure. Study design Experimental study. Animals Twenty‐four freshly harvested porcine urinary bladders. Methods A cystotomy was performed and the incision closed with a single layer simple continuous suture pattern with barbed (n = 12) or smooth (n = 12) suture. Time required for closure was measured. Each bladder was connected to a system for monitoring intraluminal pressure while inflated with saline until leakage occurred. Intraluminal pressure at time of initial leakage and leakage site were recorded. Two‐sample t tests were used to compare maximum leakage pressure and closure time between the 2 groups. P < .05 was considered significant. Results All bladders were sutured successfully with no difference in mean closure time (barbed suture 296 ± 46 seconds; smooth suture 293 ± 26 seconds) (P = .821). There was no difference in mean leakage pressure of porcine urinary bladder incisions closed in a single layer with barbed suture (28.8 ± 10.4 mm Hg) compared with smooth suture (30.6 ± 8.8 mm Hg) (P = .642). Conclusions Barbed suture provides comparable cystotomy repair to smooth suture, and no benefit to its use was identified in an open procedure. Barbed suture closure should be evaluated for adequate tensile strength in the presence of urine, satisfactory in vivo healing of cystotomies, and lack of long‐term urolith formation in dogs and cats.

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21The adhesion protein L-selectin (CD62L) is expressed at high levels by circulating 22 neutrophils and has a critical role in initiating their recruitment at sites of inflammation. 23 L-selectin expression is rapidly downregulated upon neutrophil activation by various 24 stimuli through a proteolytic process referred to as ectodomain shedding, which regulates 25 L-selectin's binding avidity and neutrophil recruitment. In humans and mice, L-selectin 26 shedding is primarily mediated by ADAM17 (a disintegrin and metalloproteinase 17). L-27 selectin expression is also rapidly downregulated by canine neutrophils upon their 28 activation; however, the role of ADAM17 in this process has not been previously 29 investigated. We show that a highly selective inhibitor of ADAM17, but not an inhibitor 30 of its most closely related family member ADAM10, effectively blocked L-selectin 31 downregulation from the surface of canine neutrophils following their activation. The 32 ADAM17 inhibitors did not block the rapid upregulation of the CD18 integrin Mac-1 33 (CD11b/CD18), showing that they did not broadly impair neutrophil activation. To 34 directly examine the expression of ADAM17, we used several anti-human ADAM17 35 mAbs. Many did not stain canine neutrophils; however, the ADAM17 function-blocking 36 mAbs MEDI3622 and D1(A12) did stain and also blocked L-selectin downregulation.37 Taken together, our findings provide the first direct evidence that ADAM17 is a primary 38 sheddase of canine L-selectin, which may serve as an important therapeutic target to 39 prevent neutrophil dysfunction during conditions of excessive inflammation, such as 40 sepsis. 3 41 Introduction 42 L-selectin (CD62L), where "L" signifies leukocyte, is a member of the Selectin 43 family of adhesion proteins [1, 2]. L-selectin facilitates the accumulation of neutrophils 44 along the vascular endothelium, the initial step of a "multi-step" process of their 45 migration from the blood vessel lumen, through the vascular wall, and into the underlying 46 tissue at sites of inflammation [3]. L-selectin is expressed at high levels by resting 47 neutrophils and is primarily distributed on the ends of cellular microvilli [4]. This 48 distribution pattern facilitates their capture and rolling along the vascular wall under 49 hydrodynamic shear stress [3]. In addition to its role in the direct attachment of free-50 flowing neutrophils to the vascular endothelium, L-selectin also mediates neutrophil 51 attachment to previously tethered neutrophils, and this process of indirect capture can 52 greatly amplify neutrophil accumulation [5-7]. 53 Unlike most adhesion molecules expressed by neutrophils, L-selectin undergoes a 54 process referred to as ectodomain shedding. This proteolytic event occurs upon cell 55 activation and results in a rapid downregulation of L-selectin expression from the cell 56 surface [1, 2, 8]. L-selectin shedding, in part, regulates the avidity of its interactions with 57 vascular ligands and neutrophil tethering efficiency [9]. However, exce...