Companion animals and human health: benefits, challenges, and the road ahead for human-animal interaction.

There is ample evidence that human-animal interaction (HAI) is associated with health. Studies encompass three general categories: those that compare companion animal owners with individuals who do not own companion animals, those examining brief, 'one-off' contacts with animals, and those that review animal-assisted interventions. The health benefits demonstrated typically include reductions in depression and loneliness, while enhancing social interaction or social skills, and decreasing anxiety and arousal. Other health benefits associated with companion animals include the promotion of exercise or physical activity. The types of human-animal contact that have been evaluated include visual contact, physical contact, and looking at images of animals. The species used in interventions include dogs, cats, horses, rabbits, goats, hamsters and crickets. Despite these benefits, HAIs are also associated with problems, including allergies, asthma, zoonoses, animal bites and scratches, and human falls. Other problems include grief and negative emotions when a companion animal is injured or dies. Companion animal ownership is also expensive. Inconsistent policies concerning keeping animals in housing and enabling service animals to access public places make it difficult to live with companion animals or keep service animals in some circumstances. Additional research is needed to provide an evidence base to evaluate the efficacy of particular types of HAI using a given type of animal. This will document specific outcomes for an individual with certain characteristics and assist in promoting the future use of HAI to enhance human and animal health and well-being.

L'existence d'un lien entre la santé, d'une part, et l'interaction humains­animaux d'autre part, est amplement démontrée. Les études en la matière se répartissent en trois catégories principales : comparaisons entre la situation de propriétaires d'animaux de compagnie et celle d'individus ne possédant pas d'animal de compagnie ; études sur des contacts brefs et ponctuels avec des animaux ; études analysant les interventions thérapeutiques recourant à des animaux. Parmi les bénéfices pour la santé mis en évidence dans ces études figurent l'atténuation des états dépressifs et du sentiment de solitude, une meilleure interaction sociale, un renforcement des compétences sociales et une diminution des états d'anxiété et d'agitation. Les animaux de compagnie encouragent à avoir une activité physique, ce qui est un facteur bénéfique pour la santé. Les contacts humains­animaux étudiés sont le contact visuel, le contact physique et la contemplation d'images d'animaux. Les espèces suivantes sont utilisées à des fins thérapeutiques : chiens, chats, chevaux, lapins, chèvres, hamsters et grillons. En dépit de ces avantages, les interactions humains­animaux peuvent aussi provoquer certains problèmes tels qu'allergies, asthme, maladies zoonotiques, blessures dues à des morsures et griffures et chutes. Il y a aussi le chagrin et les émotions négatives qui peuvent s'emparer d'une personne en cas de blessures ou de mort de son animal de compagnie. La possession d'un animal de compagnie entraîne des coûts. L'incohérence des réglementations sur la présence d'animaux dans les logements et sur l'accès des animaux aidants dans les espaces publics rend parfois difficile la vie avec des animaux de compagnie ou le recours aux animaux aidants. Il convient de poursuivre les recherches afin de pouvoir évaluer l'efficacité de certaines catégories d'interactions humains­animaux suivant le type d'animal utilisé. Cela permettra de connaître les résultats spécifiques que l'on peut attendre chez un individu présentant des caractéristiques particulières et contribuera à promouvoir l'utilisation future d'interactions humains­animaux pour améliorer la santé et le bien-être humain et animal.

Existen abundantes pruebas de que la interacción de humanos y animales reporta salud. Los estudios realizados corresponden a tres grandes categorías: aquellos que comparan a las personas que tienen una mascota con las que no tienen; aquellos que estudian contactos breves y excepcionales con animales; y aquellos que se centran en las intervenciones auxiliadas por animales. Los beneficios para la salud más comúnmente observados y probados son un menor grado de depresión y sentimiento de soledad, acompañado de una mejora de las relaciones y aptitudes sociales, así como menores niveles de ansiedad y agitación. Entre otros beneficios para la salud asociados a la presencia de animales de compañía destaca el incremento del ejercicio físico. Los tipos de contacto entre humanos y animales que se han evaluado son el contacto visual, el contacto físico y la visión de imágenes de animales. Las especies utilizadas en las intervenciones son principalmente el perro, el gato, el caballo, el conejo, la cabra, el hámster y el grillo. Pese a todos los beneficios que deparan, las relaciones entre humanos y animales también pueden provocar problemas como alergias, asma, zoonosis, mordeduras y arañazos de animal o caídas de las personas. Asimismo, a veces surgen dificultades como el duelo o las emociones negativas que acompañan las lesiones o la muerte de una mascota. Además, la propiedad de un animal de compañía resulta cara. En algunas circunstancias, la aplicación de políticas incoherentes sobre el hecho de tener animales en las viviendas o de permitir el acceso de animales de servicio a lugares públicos dificulta la vida con mascotas o la posesión de animales de servicio. Para evaluar la eficacia de ciertas clases particulares de relación entre humanos y animales con el uso de un determinado tipo de animal se requieren más investigaciones que aporten una sólida base probatoria. Con ello será posible demostrar la obtención de resultados específicos con una persona de determinadas características y promover en el futuro la utilización de la relación entre humanos y animales para procurar a ambas partes mayores cotas de salud y bienestar.

Effect of liquid flavor supplementation of the diet on dairy cows in the transition period.

A 9-wk trial was conducted to study the performance of 24 Holstein cows during the transition period (3 wk prepartum to 6 wk postpartum). Cows were assigned to either a control or liquid-flavored (0.52 mL/kg of feed) total mixed ration in a randomized complete block design. The diets contained corn silage, alfalfa haylage, cottonseed, and a grain mix based on ground corn and soybean meal. Cows were fed to ensure 10% orts, and the diet provided (on a dry matter basis) 13% crude protein, 32% acid detergent fiber, 44% neutral detergent fiber, and 1.54 Mcal/kg of NEL prepartum and 17.5% crude protein, 30% acid detergent fiber, 40% neutral detergent fiber, and 1.57 Mcal/kg of NEL postpartum. An additional 2.3 kg of alfalfa hay was fed during the first 5 d postpartum. Weekly means of dry matter intake (DMI), milk yield, milk protein, milk fat, SNF, somatic cell counts, and body weight (BW) were analyzed using a repeated measures procedure. There was no effect of treatment on these variables, and least squares means were 16.9 and 15.7 kg/d for DMI, 38 and 35.3 kg/d for milk yield, 3.10 and 3.11% for milk protein, 3.69 and 3.74% for milk fat, 8.37 and 8.16% for SNF, 1.99 x 10(5) and 4.33 x 10(5) for somatic cell count, and 631 and 651 kg for BW for cows fed control and flavored diets, respectively. Individual cow daily DMI data were fitted to an exponential model describing pre- and postpartum feed consumption [DMI = a - b x e(-c x t), where DMI was measured in kg, a = asymptotic DMI, b = potential fractional increase in DMI, c = fractional rate of increase in DMI, and t = days prior to calving or days in milk]. Fractional rates of increase in DMI were similar: 0.139 and 0.123/d for control and flavored diets, respectively. Data for both groups were separately analyzed using multiple regression with 3.5% fat-corrected milk as the dependent variable and BW and DMI as independent variables. More BW was mobilized per unit increase in 3.5% fat-corrected milk in cows fed the control than in cows fed the flavored diet. Cows fed the control diet tended to be in more negative energy balance during early lactation than cows fed the flavored diet. It was concluded that feeding flavor improved energy balance of cows in early lactation and may reduce the risk of health or reproductive problems.

Stimulated D(1) dopamine receptors couple to multiple Galpha proteins in different brain regions.

Previous studies have revealed that activation of rat striatal D(1) dopamine receptors stimulates both adenylyl cyclase and phospholipase C via G(s) and G(q), respectively. The differential distribution of these systems in brain supports the existence of distinct receptor systems. The present communication extends the study by examining other brain regions: hippocampus, amygdala, and frontal cortex. In membrane preparations of these brain regions, selective stimulation of D(1) dopamine receptors increases the hydrolysis of phosphatidylinositol/phosphatidylinositol 4,5-biphosphate. In these brain regions, D(1) dopamine receptors couple differentially to multiple Galpha protein subunits. Antisera against Galpha(q) blocks dopamine-stimulated PIP(2) hydrolysis in hippocampal and in striatal membranes. The binding of [(35)S]GTPgammaS or [alpha-(32)P]GTP to Galpha(i) was enhanced in all brain regions. Dopamine also increased the binding of [(35)S]GTPgammaS or [alpha-(32)P]GTP to Galpha(q) in these brain regions: hippocampus = amygdala > frontal cortex. However, dopamine-stimulated binding of [(35)S]GTPgammaS to Galphas only in the frontal cortex and striatum. This differential coupling profile in the brain regions was not related to a differential regional distribution of the Galpha proteins. Dopamine induced increases in GTPgammaS binding to Galpha(s) and Galpha(q) was blocked by the D(1) antagonist SCH23390 but not by D(2) receptor antagonist l-sulpiride, suggesting that D(1) dopamine receptors couple to both Galpha(s) and Galpha(q) proteins. Co-immunoprecipitation of Galpha proteins with receptor-binding sites indicate that in the frontal cortex, D(1) dopamine-binding sites are associated with both Galpha(s) and Galpha(q) and, in hippocampus or amygdala, D(1) dopamine receptors couple solely to Galpha(q). The results indicate that in addition to the D(1)/G(s)/adenylyl cyclase system, brain D(1)-like dopamine receptor sites activate phospholipase C through Galpha(q) protein.

Increased association of brain protein kinase C with the receptor for activated C kinase-1 (RACK1) in bipolar affective disorder.

BACKGROUND: Membrane protein kinase C (PKC) activity is increased in frontal cortex of subjects with bipolar affective disorder, and lithium was demonstrated to inhibit PKC translocation to membranes. Protein kinase C is anchored to the membrane via the receptor for activated C kinase-1 (RACK1), suggesting that interactions between these proteins may be altered in bipolar disease. METHODS: The levels of RACK1 coimmunoprecipitating with PKC isozymes were compared in homogenates of frontal cortex slices from postmortem bipolar subjects and matched control subjects. RESULTS: Receptor for activated C kinase-1 was located exclusively in membranes and, in control brains, the levels of RACK1 that coimmunoprecipitated with most PKC isozymes were increased by stimulation with the PKC activator, phorbol 12-myristate, 13-acetate (PMA). The association of RACK1 with membrane gammaPKC and zetaPKC was increased under basal conditions in bipolar relative to control brains. Stimulation with PMA increased the amount of RACK1 that coimmunoprecipitated with the alpha, beta, gamma, delta, and varepsilonPKC isozymes, but not zetaPKC, in bipolar tissues over that elicited in control tissues. CONCLUSIONS: These data suggest that the increased association of RACK1 with PKC isozymes may be responsible for the increases in membrane PKC and in its activation that were previously observed in frontal cortex of bipolar affective disorder brains.

Mechanism of decreased adenosine protection in reperfusion injury of aging rats.

The purpose of this study was to determine whether the protective effects of adenosine on myocardial ischemia-reperfusion injury are altered with age, and if so, to clarify the mechanisms that underlie this change related to nitric oxide (NO) derived from the vascular endothelium. Isolated perfused rat hearts were exposed to 30 min of ischemia and 60 min of reperfusion. In the adult hearts, administration of adenosine (5 micromol/l) stimulated NO release (1. 06 +/- 0.19 nmol. min(-1). g(-1), P < 0.01 vs. vehicle), increased coronary flow, improved cardiac functional recovery (left ventricular developed pressure 79 +/- 3.8 vs. 57 +/- 3.1 mmHg in vehicle, P < 0.001; maximal rate of left ventricular pressure development 2,385 +/- 103 vs. 1,780 +/- 96 in vehicle, P < 0.001), and reduced myocardial creatine kinase loss (95 +/- 3.9 vs. 159 +/- 4.6 U/100 mg protein, P < 0.01). In aged hearts, adenosine-stimulated NO release was markedly reduced (+0.42 +/- 0.12 nmol. min(-1). g(-1) vs. vehicle), and the cardioprotective effects of adenosine were also attenuated. Inhibition of NO production in the adult hearts significantly decreased the cardioprotective effects of adenosine, whereas supplementation of NO in the aged hearts significantly enhanced the cardioprotective effects of adenosine. The results show that the protective effects of adenosine on myocardial ischemia-reperfusion injury are markedly diminished in aged animals, and that the loss in NO release in response to adenosine may be at least partially responsible for this age-related alteration.

Cocaine administration in pregnant rabbits alters cortical structure and function in their progeny in the absence of maternal seizures.

Previous studies have reported that cocaine exposure in utero results in structural and functional alterations in the development of the anterior cingulate cortex (ACC). In the present study, the effects of maternal cocaine dosage and of cocaine-elicited maternal seizures on the progeny were studied. The incidence of maternal generalized tonic clonic seizures (GTCSs) elicited by cocaine was recorded. No GTCSs were elicited in pregnant rabbits by doses of 2 or 3 mg/kg of cocaine, but GTCSs were sometimes elicited by the highest dose (4 mg/kg per injection). We analyzed the offspring of cocaine-exposed and control animals using three assays of ACC development: (i) the structure of apical dendrites of pyramidal neurons, (ii) the distribution of a calcium binding protein (parvalbumin) in the dendrites of GABAergic neurons, and (iii) coupling of D1-like receptors and their G proteins. In all progeny of rabbits exposed to 3 or 4 mg/kg of cocaine during pregnancy, there was a significant change in the structure of apical dendrites, a significant increase in the number of dendrites of GABAergic neurons which were parvalbumin immunoreactive, and a significant reduction in D1/G protein coupling. In assays of apical dendrites, the effects on offspring of rabbits given 2 mg/kg cocaine were as pronounced as in offspring of rabbits given 3 or 4 mg/kg, but the effects on parvalbumin immunoreactivity and D1/G protein coupling were reduced at this low dose. Thus, previous findings of ACC developmental abnormalities in offspring of rabbits given a dose of 4 mg/kg were replicated, the effects were shown to be dose-related and to be independent of maternal seizures. A mechanism by which dysfunction of the D1 receptor system could mediate cocaine-associated changes in all three parameters of ACC structure and function is discussed.

Fulfilling the sisters' promise. The heritage of healthcare's early days.

Members of religious orders--the sisters--built not just Catholic healthcare, but healthcare in America. A good 50 years before Henry and Edgar Kaiser got the idea, prepaid capitated health insurance was being offered by sisters who looked at what was needed and realized this was simply the best way to get it done. The sisters also created the integrated healthcare system at a time when the emerging medical elite wanted nothing to do with any patient who was not socially acceptable and potentially curable. They arranged a continuum of care for the aging sisters within their own communities. And they understood the concept of social medicine, of population-based healthcare, of healthy communities, long before these ideas became commonplace. But the sisters are gone, most of them. The question today is, How do we preserve the sisters' heritage and transfer it to a new millennium, a new healthcare system, and a new set of rules? First, it is important to understand that much of what we remember the sisters for--courage, compassion, vision-was not unique. They created many of the structures that today are the new models; but they were not alone. However, three aspects of how they expressed their vision and their faith were unique to the sisters and must be understood by those who wish to treat the path the sisters blazed. The purity of their commitment and its underlying philosophy--that the helpless and the sick must always be the point of the exercise--should pervade Catholic healthcare to its soul. These women, living in poverty, represented, and still represent, a singular group: a group of women who, having told the world that their only wish is to serve others, humble became CEOs of vast systems and trustees of huge enterprises, without ever abandoning that simple, original pledge. Although they bowed to the rule of obedience, and they were humble, the were fighters. They spoke out against poverty, bigotry, the shunning of those with certain diseases, lack of access to healthcare, stupidity, ignorance, and hate.

Receptor-mediated activation of G proteins is increased in postmortem brains of bipolar affective disorder subjects.

Guanine nucleotide binding proteins (G proteins) have been implicated in the pathophysiology of bipolar affective disorder. In the present investigation receptor-mediated G protein activation and changes in G protein trimeric state were examined in frontal cortical membranes obtained from postmortem brains of bipolar affective disorder subjects and from age-, sex-, and postmortem interval-matched controls. Stimulation of cortical membranes with serotonin, isoproterenol, or carbachol increased guanosine 5'-O-(3-[35S]thiophosphate) ([35S]GTP gamma S) binding to specific G alpha proteins in a receptor-selective manner. The abilities of these receptor agonists to stimulate the binding of [35S]GTP gamma S to the G alpha proteins was enhanced in membranes from bipolar brains. Immunoblot analyses showed increases in the levels of membrane 45- and 52-kDa G alpha S proteins but no changes in the amounts of G alpha i, G alpha o, G alpha Z, G alpha q/11, or G beta proteins in membrane or cytosol fractions of bipolar brain homogenates. Pertussis toxin (PTX)-activated ADP-ribosylations of G alpha i and G alpha o were enhanced by approximately 80% in membranes from bipolar compared with control brains, suggesting an increase in the levels of the trimeric state of these G proteins in bipolar disorder. Serotonin-induced, magnesium-dependent reduction in PTX-mediated ADP-ribosylation of G alpha i/G alpha o in cortical membranes from bipolar brains was greater than that observed in controls, providing further evidence for enhanced receptor-G protein coupling in bipolar brain membranes. In addition, the amounts of G beta proteins that coimmunoprecipitated with the G alpha proteins were also elevated in bipolar brains. The data show that in bipolar brain membrane there is enhanced receptor-G protein coupling and an increase in the trimeric state of the G proteins. These changes may contribute to produce exaggerated transmembrane signaling and to the alterations in affect that characterize bipolar affective disorder.

The efficacy of erythropoietin in human immunodeficiency virus-infected end-stage renal disease patients treated by maintenance hemodialysis.

The superimposition of human immunodeficiency virus (HIV) infection, associated opportunistic infections, and anti-retroviral therapy further worsens the severity of anemia in patients also suffering from end-stage renal disease. A major cause of anemia in renal failure is a deficiency of erythropoietin. The causes of anemia in HIV disease include direct and indirect stem cell inhibition by the virus, increased peripheral destruction of red blood cells, and bone marrow suppression by various opportunistic infections and therapeutic drugs, particularly zidovudine. We compared the efficacy of recombinant human erythropoietin (rHuEPO) therapy in improving the anemia in HIV-infected end-stage renal disease patients (group I) with that in nondiabetic (group II) and diabetic (group III) hemodialysis patients without HIV infection. All three groups of patients were comparable in dialysis prescription and serum iron studies. Iron supplementation was prescribed to all patients, and none received blood transfusions. After 8 weeks of rHuEPO therapy (administered intravenously in a dose of 100 U/kg body weight thrice weekly), the mean increase in hematocrit was similar in all responders (5.8% increase in hematocrit in 23 of 30 HIV patients and 6.7% increase in 24 of 30 non-HIV patients). Response in hematocrit was noted in HIV patients despite the presence of opportunistic infections in 15 and zidovudine administration in 11. Seven HIV-positive patients and six non-HIV patients failed to respond to rHuEPO. Irrespective of the HIV status, the baseline serum EPO levels in patients responding to rHuEPO were significantly lower than those in nonresponders.(ABSTRACT TRUNCATED AT 250 WORDS)

Diet restriction prevents aging-induced deficits in brain phosphoinositide metabolism.

Receptor-activated hydrolysis of [3H]inositol-labeled phosphoinositides was evaluated in brain slices of 6-month-old (6M) and 24-month-old (24M) F344 rats that had been fed ad libitum (AL) or restricted (60% of normal) diet (RD). The muscarinic cholinergic agonist, carbachol, and the dopamine receptor agonist, SKF3893, stimulated significantly lower accumulation of [3H]inositol phosphates in striatal and cortical slices of the 24M AL rats compared to the 6M AL group. This observation suggests a decreased capacity of the aged brain to respond to receptor-activated phosphoinositide hydrolysis. Furthermore, the 24M RD tissues gave significantly higher responses to carbachol (p < .01) or SKF38393 (p < .01) compared to the 24M AL group. The 24M RD responses were not significantly different from corresponding responses in the 6M AL rats, implying complete prevention of the aging effect in the diet-restricted animals up to at least 24 months of age. Concomitant observations of decreased phosphoinositide labeling in the 24M AL tissues and prevention of this decrease in diet restriction may contribute to the observed effects of aging on inositol phosphate formation.

Time-dependent effects of peer separation on lymphocyte proliferation responses in juvenile squirrel monkeys.

This study evaluated the immunological, hormonal, and behavioral responses of juvenile squirrel monkeys to repeated social separations of varying length. Following a 3-hr separation, lymphocyte responses to stimulation with the mitogen concanavalin A (Con A) declined significantly, and these alterations were sustained after a 24-hr separation period. The responses to Con A and to a second mitogen, phytohemagglutinin (PHA), were suppressed after 2 days. At the end of a 7-day separation period, immune responses were not significantly different from basal values. Plasma cortisol levels were elevated above basal levels in all animals after the 3-hr, 24-hr, and 2-day separations, but were not elevated after the 7-day separation. While we observed no statistically significant changes in locomotor activity or calling behavior during any of the separations, the monkeys tended to be most active and to call most immediately following separation. Our findings concur with earlier reports indicating that social stressors can influence lymphocyte proliferation in nonhuman primates and that certain cell types might be differentially sensitive to stress, but also indicate that these influences are transient.