Fewer peripheral intravenous catheter complications in hospitalized dogs when force-activated separation devices are used versus not used in a randomized controlled clinical trial.

OBJECTIVE: To determine whether the use of a force-activated separation device (FASD) lowers the incidence risk of peripheral intravenous catheter (PIVC) complications in hospitalized dogs. ANIMALS: 367 dogs that were hospitalized and received IV fluids between January 11 and March 25, 2021. PROCEDURES: A prospective, randomized controlled clinical trial was performed. Dogs hospitalized and receiving IV fluids for at least 24 hours were randomized to the FASD group or control group. PIVCs were placed following a standardized protocol. Dogs in the FASD group had the FASD device attached to their PIVC according to manufacturer instructions. For both groups, all PIVC complications were documented, and each complication was classified as extravasation, phlebitis, dislodgement, occlusion, or line breakage. RESULTS: Results from 367 dogs (FASD group = 180, control group = 187) underwent analysis. The proportion of PIVC complications was significantly (P = .004) lower for the FASD group (8.9% [16/180]) versus the control group (24.6% [46/187]). Following adjustment for differences in hospitalization time, the odds of a dog in the FASD group having a PIVC complication was approximately one-third the odds of those in the control group (OR, 0.33; 95% CI, 0.17 to 0.63; P = .001). CLINICAL RELEVANCE: Results indicated that the use of a FASD in hospitalized dogs receiving IV fluids is warranted to lower the incidence of PIVC complications and may also limit patient discomfort, owner expense, and staff time devoted to managing PIVC complications. Further research investigating its use in cats and other species should be considered.

A deficit in face-voice integration in developing vervet monkeys exposed to ethanol during gestation.

Children with fetal alcohol spectrum disorders display behavioural and intellectual impairments that strongly implicate dysfunction within the frontal cortex. Deficits in social behaviour and cognition are amongst the most pervasive outcomes of prenatal ethanol exposure. Our naturalistic vervet monkey model of fetal alcohol exposure (FAE) provides an unparalleled opportunity to study the neurobehavioral outcomes of prenatal ethanol exposure in a controlled experimental setting. Recent work has revealed a significant reduction of the neuronal population in the frontal lobes of these monkeys. We used an intersensory matching procedure to investigate audiovisual perception of socially relevant stimuli in young FAE vervet monkeys. Here we show a domain-specific deficit in audiovisual integration of socially relevant stimuli. When FAE monkeys were shown a pair of side-by-side videos of a monkey concurrently presenting two different calls along with a single audio track matching the content of one of the calls, they were not able to match the correct video to the single audio track. This was manifest by their average looking time being equally spent towards both the matching and non-matching videos. However, a group of normally developing monkeys exhibited a significant preference for the non-matching video. This inability to integrate and thereby discriminate audiovisual stimuli was confined to the integration of faces and voices as revealed by the monkeys' ability to match a dynamic face to a complex tone or a black-and-white checkerboard to a pure tone, presumably based on duration and/or onset-offset synchrony. Together, these results suggest that prenatal ethanol exposure negatively affects a specific domain of audiovisual integration. This deficit is confined to the integration of information that is presented by the face and the voice and does not affect more elementary aspects of sensory integration.

Moderate prenatal alcohol exposure and quantification of social behavior in adult rats.

Alterations in social behavior are among the major negative consequences observed in children with Fetal Alcohol Spectrum Disorders (FASDs). Several independent laboratories have demonstrated robust alterations in the social behavior of rodents exposed to alcohol during brain development across a wide range of exposure durations, timing, doses, and ages at the time of behavioral quantification. Prior work from this laboratory has identified reliable alterations in specific forms of social interaction following moderate prenatal alcohol exposure (PAE) in the rat that persist well into adulthood, including increased wrestling and decreased investigation. These behavioral alterations have been useful in identifying neural circuits altered by moderate PAE(1), and may hold importance for progressing toward a more complete understanding of the neural bases of PAE-related alterations in social behavior. This paper describes procedures for performing moderate PAE in which rat dams voluntarily consume ethanol or saccharin (control) throughout gestation, and measurement of social behaviors in adult offspring.

Prenatal alcohol exposure causes attention deficits in male rats.

Children with fetal alcohol spectrum disorder (FASD) are often diagnosed with attention-deficit/ hyperactivity disorder (ADHD). These children show increases in reaction time (RT) variability and false alarms on choice reaction time (CRT) tasks. In this study, adult rats prenatally exposed to ethanol were trained to perform a CRT task. An analysis of the distribution of RTs obtained from the CRT task found that rats with a history of prenatal ethanol exposure had more variable RT distributions, possibly because of lapses of attention. In addition, it was found that, similar to children with FASD, the ethanol-exposed rats had more false alarms. Thus, rats with prenatal ethanol exposure show attention deficits that are similar to those of children with FASD and ADHD.

Alterations in responsiveness to ethanol and neurotrophic substances in fetal septohippocampal neurons following chronic prenatal ethanol exposure.

Pregnant Long-Evans rats were maintained on three diets: a liquid diet in which ethanol accounted for 35-39% of the total calories, a similar diet with the isocaloric substitution of sucrose for ethanol, and a lab chow control diet. At gestation day 18, the fetuses were taken and cultures of septal and hippocampal neurons prepared. Neuronal survival and neurite outgrowth were compared in cultures from the three diet groups, using the following media supplements: ethanol (1.2, 1.8 or 2.4 g/dl), neurotrophic factors (nerve growth factor [NGF] with the septal cultures, basic fibroblast growth factor [bFGF] with the hippocampal cultures), or ethanol plus neurotrophic factors. Both the septal and hippocampal neurons responded to ethanol in a dose-dependent manner. The neurons from both populations from fetuses which had been exposed prenatally to ethanol, however, tolerated considerably higher ethanol concentrations before decreases in survival or outgrowth were seen. These ethanol-exposed neuronal populations were also less responsive to neurotrophic factors: in hippocampal cultures, process outgrowth was significantly enhanced by bFGF in control but not ethanol-derived cultures, and in septal and hippocampal cultures, the neurotrophic factors significantly ameliorated ethanol neurotoxicity in control cultures, but not in those from the ethanol-exposed fetuses. The possible relevance of these observations to the fetal alcohol syndrome is discussed.

Efectos del consumo prolongado de etanol sobre las etapas tempranas del desarrollo dentario en ratones / Effects of prolonged ethanol use on the early stages of dental development in mice

Se hace un estudio de los efectos del consumo prolongado de etanol sobre las etapas tempranas del desarrollo dentario en ratones, se emplean para ello 6 ratonas albinas preñadas, divididas en un grupo control de 2 ratonas y un grupo experimental de 4 animales. Los 2 grupos se ubicaron en jaulas diferentes, disponían de agua y comida a voluntad. En el grupo experimental el auga contenía el 25 % de alcohol. Todos los animales fueron sacrificados a los 14 días de preñez se les extrajeron los fetos y se obtuvieron fragmentos de maxilar y mandíbula, que fueron procesados por la técnica de parafina y teñidos con HE.Los resultados corroboran la presencia de un alto número de reabsorciones embrionarias, así como se detectan anomalías visibles morfológicamente en la capa basaldel brote y los epitelios adamantinos del casquete. Las alteraciones más relevantes se presentan en el epitelio adamantino interno

Efectos del consumo prolongado de etanol sobre las etapas tempranas del desarrollo dentario en ratones / Effects of prolonged ethanol use on the early stages of dental developent in mice

Se hace un estudio de los efectos del consumo prolongado de etanol sobre las etapas tempranas del desarrollo dentario en ratones, se emplean para ello 6 ratonas albinas preñadas, divididas en un grupo control de 2 ratonas y un grupo experimental de 4 animales. Los 2 grupos se ubicaron en jaulas diferentes, disponían de agua y comida a voluntad. En el grupo experimental el auga contenía el 25

de alcohol. Todos los animales fueron sacrificados a los 14 días de preñez se les extrajeron los fetos y se obtuvieron fragmentos de maxilar y mandíbula, que fueron procesados por la técnica de parafina y teñidos con HE.Los resultados corroboran la presencia de un alto número de reabsorciones embrionarias, así como se detectan anomalías visibles morfológicamente en la capa basaldel brote y los epitelios adamantinos del casquete. Las alteraciones más relevantes se presentan en el epitelio adamantino interno

Fetal alcohol syndrome in the ferret (Mustela putorius).

Gastric intubation of 1.5 g ethanol/kg maternal body weight produced a significant teratogenic response in ferrets (Mustela putorius) treated once daily from gestational days 15 through 35. This response was evident by a rise in the frequency of fetuses with one or more malformations (21%), and by a rise in the frequency of litters with one or more malformed fetuses (50%). Palatoschisis and greater relative intermedial canthi distance observed in this study are diagnostic features of the fetal alcohol syndrome (FAS). Although mean (+/- SEM) peak blood alcohol levels of 207 +/- 9 mg/dl did not affect other reproductive parameters, high doses of alcohol (3.0 g/kg) resulted in the inability of treated females to consume adequate food or water, in the complete resorption of litters, and in significant maternal mortality (88%). Fetal deaths occurred prior to gestation day 17 in the high-dose alcohol group. Based on objective evaluation of differences among ethanol-treated, pair-fed sucrose-treated, and untreated ad libitum diet controls, the ferret would seem a valuable alternative animal species for future studies of FAS.

Measures of alcohol damage in utero in the pigtailed macaque (Macaca nemestrina).

A non-human primate model for the fetal alcohol syndrome (FAS) has been developed in a pilot study on four pigtailed macaques (Macaca nemestrina) receiving ethanol once weekly from 40 days of gestation (2.5 g/kg for three moderate-dose monkeys and 4.1 g/kg for one high-dose monkey). Ethanol and acetaldehyde levels and indices of general health were monitored throughout pregnancy. One pregnancy ended in miscarriage. The three infants born at term were compared to control infants. The infant exposed to the higher ethanol dose showed phenotypic similarities to humans with FAS. Its brain was microcephalic and dysplastic; reflex, motor and cognitive development were retarded. One infant receiving the moderate dose had subtle brain abnormalities; it was hyperkinetic and showed developmental retardation on several behavioral measures. The other moderately dosed infant was normal. A larger study now in progress will comprise six groups of seven monkeys, each group being exposed to 0 (control), 0.3, 0.6, 1.2, 2.5 or 4.1 g/kg of ethanol once weekly throughout gestation. So far, 4.1 g/kg ethanol has been shown to be fetotoxic when given between 8 and 13 days of pregnancy.