Javma-journal of The American Veterinary Medical Association最新文献

Nerve growth factor (NGF) is one of several neurotrophic proteins necessary for normal development and function of the mammalian nervous system. Nerve growth factor is necessary for normal brain cholinergic function, and reduced brain cholinergic activity is a hallmark pathological feature of human Alzheimer's disease (AD). In both aging humans and transgenic rodent models, disruption of the normal NGF metabolic pathway (NGF dysmetabolism) leads to brain neuronal damage, loss of synaptic plasticity, and cognitive decline. Nerve growth factor dysmetabolism in AD patients is a gradual process, beginning years prior to the development of mild cognitive impairment. In addition to changes in the levels of specific molecular regulators of the NGF pathway, there are changes in the proportions of the 2 major receptors for NGF and its precursor (proNGF) in the brain: the tropomyosin kinase A (TrkA) receptor and the p75 neurotrophin (p75NTR) receptor. Nerve growth factor has high affinity for TrkA receptors, the stimulation of which has neuroprotective effects. The precursor of NGF has higher affinity than NGF for p75NTR receptors; stimulation of p75NTR receptors by proNGF has deleterious effects on neurons. With NGF dysmetabolism, the respective ratios of available NGF/proNGF and TrkA/p75NTR receptors are decreased, favoring neuronal damage. In rodent models genetically engineered to produce monoclonal antibodies against NGF, neuronal damage and cognitive decline occur, even when the antibodies are targeted specifically against peripheral (ie, not CNS) NGF. Because canine cognitive dysfunction is a naturally occurring model of human AD, NGF dysmetabolism may be relevant to aging dogs. This article will review details of NGF dysmetabolism and how this aberrant pathway contributes to cognitive decline.

Background: Canine enteric coronavirus (CECoV) causes diarrhea and vomiting, often leading to outbreaks in kennels and shelters. The World Small Animal Veterinary Association does not recommend vaccination due to limited evidence of efficacy. This meta-analysis assesses CECoV vaccine immunogenicity and protective efficacy against diarrhea and viral shedding.

Methods: PubMed, Scopus, and Google Scholar were searched for experimental or observational studies of dogs vaccinated against CECoV, published from inception to September 29, 2025. Included studies confirmed dogs were free of CECoV infection and neutralizing antibodies before study. Exclusions applied to noncompliant studies. The Systematic Review Centre for Laboratory Animal Experimentation and funnel plots assessed bias risk. To assess vaccine immunogenicity, ELISA optical density (OD) values and log2 virus neutralization (VN) titers were regressed; pooled risk ratios evaluated protective efficacy.

Results: From 415 studies, 5 experimental studies with unclear bias risks were included. Most reported dog age but omitted sex or breed. Inactivated vaccines significantly increased both OD values and VN titers, whereas attenuated vaccines significantly increased OD values but not VN titers. Vaccination reduced diarrhea risk by 72% (risk ratio, -1.28; 95% CI, -2.05 to -0.51), but did not decrease viral shedding (risk ratio, -0.25; 95% CI, -0.70 to 0.21).

Clinical relevance: CECoV vaccines are immunogenic and reduce diarrhea, but do not significantly reduce viral shedding, potentially masking infections in clinical settings and thus complicating disease control in communal environments. Limited literature and studies from similar research groups suggest removing CECoV vaccines from guidelines. Standardized reporting is recommended to improve future canine epidemiological research reliability.

Objective: To report complications and outcomes following ureteroneocystostomy performed in cats presenting for benign ureteral obstruction or ectopic ureters.

Methods: This was a retrospective, single-institution study of 37 cats. Medical records were reviewed for pre-, intra-, and postoperative variables including preexisting disease, pre- and postoperative bloodwork, location and source of obstruction, surgical technique, ureteral stent placement, postoperative clinical signs, and survival time. Follow-up was ≥ 14 days or until death. The Kaplan-Meier method was used to calculate median survival, and univariable and multivariable logistic regression was used to examine correlation of variables with postoperative complications and mortality.

Results: Overall median survival was 1,980 days, with 92% of cats surviving to discharge. There was no intraoperative mortality and a relatively low incidence of short- (19%) and long-term (24%) complications. Highest mortality rate was within the first 30 days. Factors associated with increased mortality were increased preoperative BUN, creatinine, and phosphorous. Surgical ureteral stent removal occurred in 86% (6 of 7) of cases when placed, secondary to long-term recurrent urinary tract infections and stent migration.

Conclusions: Ureteroneocystostomy was a viable treatment option for benign obstructions and extramural ectopic ureters in cats, with overall longer median survival and lower long-term complication incidence compared to historical subcutaneous ureteral bypass device and ureteral stent literature. Preoperative azotemia was associated with poorer outcomes. Ureteral stents were associated with long-term complications, prompting removal.

Clinical relevance: Ureteroneocystostomy should be highly considered as a treatment option for cats presenting with benign ureteral obstructions and ectopic ureters.

Objective: To estimate the time until reliable echocardiography in healthy dogs by evaluating differences in measured echocardiographic variables in dogs before sedation, during sedation with dexmedetomidine, and after reversal with atipamezole.

Methods: 13 dogs were prospectively enrolled. Two-dimensional echocardiographic measurements on left atrial and ventricular dimensions and ventricular systolic function were obtained at each time point. Dogs underwent IV sedation with 10 µg/kg of dexmedetomidine and 0.2 mg/kg of butorphanol, and dexmedetomidine was reversed with atipamezole IM. Echocardiography was performed before sedation, during sedation, and 30 to 60 minutes, 2 hours, and 6 hours after reversal. Data were analyzed with a Bayesian multivariate hierarchical model.

Results: There were effects of sedation on the mean values of all echocardiographic variables. These effects varied among dogs, with most dogs expected to remain within normal reference ranges during and after sedation for all variables except ejection fraction and fractional shortening. The effects of sedation on ejection fraction and fractional shortening were widespread and persistent, such that 88% and 79% of dogs, respectively, were expected to measure outside the normal ranges during sedation. After reversal with atipamezole, this proportion declined, with approximately 9% of dogs estimated outside the normal reference ranges after 6 hours.

Conclusions: Effects of dexmedetomidine on echocardiographic measurements were detected 6 hours after reversal with atipamezole. Accurate cardiac assessment in dogs sedated with this drug is not likely to be possible on the same day as sedation.

Clinical relevance: Dogs sedated with this protocol and that have echocardiography performed within 6 hours following reversal should have results interpreted with caution.