Effect of continuous positive airway pressure helmet on respiratory function following surgical procedures in brachycephalic dogs: A randomized controlled trial.

OBJECTIVE: To evaluate the effect of continuous positive airway pressure (CPAP) on respiratory function in the early postoperative period of brachycephalic dogs. STUDY DESIGN: Prospective, randomized clinical trial. ANIMALS: A total of 32 dogs. METHODS: Dogs were assigned to recover with or without CPAP (control) and assessed at specific time points over 1 h. Treatment was discontinued for dogs with a CPAP tolerance score of 3 or more (from a range of 0-4). The primary outcome was pulse oximetry (SpO2). Secondary outcomes were arterial O2 pressure (PaO2)/FiO2 ratio (PaO2/FiO2), arterial CO2 pressure (PaCO2), and rectal temperature. For dogs that reached a CPAP tolerance score of 3 or more, only the data collected up to the time point before discontinuation were included in the analysis. The treatment effect (ß) was analyzed using random effects models and the results were reported with 95% confidence intervals. RESULTS: Dogs were assigned randomly to each protocol. Baseline characteristics in both groups were comparable. Arterial blood gases were obtained in seven control group dogs and nine CPAP group dogs. Treatment did not affect SpO2 (ß = -0.1, -2.1 to 2.0) but affected the PaO2/FiO2 ratio (ß = 58.1, 2.6 to 113.6), with no effects on PaCO2 (ß = -4.3, -10.5 to 1.9) or temperature (ß = 0.4, -0.8 to 1.6). CONCLUSION: In postoperative brachycephalic dogs, CPAP had no effect on SpO2 but improved the PaO2/FiO2 ratio in brachycephalic dogs postoperatively. CLINICAL SIGNIFICANCE: Continuous positive airway pressure offers a valuable solution to improve gas exchange efficiency, a prevalent concern in postoperative brachycephalic dogs, with the potential to enhance overall outcomes.

CpG-creating mutations are costly in many human viruses.

Mutations can occur throughout the virus genome and may be beneficial, neutral or deleterious. We are interested in mutations that yield a C next to a G, producing CpG sites. CpG sites are rare in eukaryotic and viral genomes. For the eukaryotes, it is thought that CpG sites are rare because they are prone to mutation when methylated. In viruses, we know less about why CpG sites are rare. A previous study in HIV suggested that CpG-creating transition mutations are more costly than similar non-CpG-creating mutations. To determine if this is the case in other viruses, we analyzed the allele frequencies of CpG-creating and non-CpG-creating mutations across various strains, subtypes, and genes of viruses using existing data obtained from Genbank, HIV Databases, and Virus Pathogen Resource. Our results suggest that CpG sites are indeed costly for most viruses. By understanding the cost of CpG sites, we can obtain further insights into the evolution and adaptation of viruses.