Aerobic fitness impacts sympathoadrenal axis responses to concurrent challenges

The combination of mental and physical challenges can elicit exacerbated cardiorespiratory (CR) and catecholamine responses above that of a single challenge alone. Purpose This study examined the effects of a combination of acute mental challenges and physical stress on cardiorespiratory and catecholamine responses. Method Eight below-average fitness (LF VO2max = 36.58 +/- 3.36 ml(-1) kg(-1) min(-1)) and eight above-average fitness (HF VO2max = 51.18 +/- 2.09 ml(-1) kg(-1) min(-1)) participants completed an exercise-alone condition (EAC) session consisting of moderate-intensity cycling at 60% VO2max for 37 min, and a dual-challenge condition (DCC) that included concurrent participation in mental challenges while cycling. Result The DCC resulted in increases in perceived workload, CR, epinephrine, and norepinephrine responses overall. HF participants had greater absolute CR and catecholamine responses compared to LF participants and quicker HR recovery after the dual challenge. Conclusion These findings demonstrate that cardiorespiratory fitness does impact the effect of concurrent stressors on CR and catecholamine responses

Bacterial Cholangitis, Cholecystitis, or both in Dogs

BACKGROUND: Bacterial cholangitis and cholecystitis are rarely reported, poorly characterized diseases in the dog. OBJECTIVES: To characterize the clinical features of these conditions. ANIMALS: Twenty‐seven client‐owned dogs with bacterial cholangitis, cholecystitis, or both. METHODS: Multicenter, retrospective cases series of dogs with bacterial cholangitis, cholecystitis, or both, presenting January 2000 to June 2011 to 4 Veterinary Schools in Ireland/United Kingdom. Interrogation of hospital databases identified all cases with the inclusion criteria; histopathologically confirmed cholangitis or cholecystitis and bile culture/cytology results supporting a bacterial etiology. RESULTS: Twenty‐seven dogs met the inclusion criteria with approximately 460 hepatitis cases documented over the same study period. Typical clinical pathology findings were increases in liver enzyme activities (25/26), hyperbilirubinemia (20/26), and an inflammatory leukogram (21/24). Ultrasound findings, although nonspecific, aided decision‐making in 25/26 cases. The most frequent hepatobiliary bacterial isolates were Escherichia coli (n = 17; 16 cases), Enterococcus spp. (n = 8; 6 cases), and Clostridium spp. (n = 5; 5 cases). Antimicrobial resistance was an important feature of aerobic isolates; 10/16 E. coli isolates resistant to 3 or more antimicrobial classes. Biliary tract rupture complicated nearly one third of cases, associated with significant mortality (4/8). Discharged dogs had a guarded to fair prognosis; 17/18 alive at 2 months, although 5/10 re‐evaluated had persistent liver enzyme elevation 2–12 months later. CONCLUSION AND CLINICAL SIGNIFICANCE: Bacterial cholangitis and cholecystitis occur more frequently than suggested by current literature and should be considered in dogs presenting with jaundice and fever, abdominal pain, or an inflammatory leukogram or with ultrasonographic evidence of gallbladder abnormalities

The Ticks (Arachnida: Acari: Ixodida) of Arkansas

Although ticks are a nuisance to humans and other animals, they are an important part of the biota of North America. In addition, they are vectors of many tick-borne disease agents that can negatively affect higher vertebrates. In Arkansas, there have been no recent comprehensive summaries of the ticks (Acari: Ixodida) in the last 40+ yrs. Here, we provide a summary of the ticks of the state and note the disease agents they can transmit

Maternal immune activation causes age- and region-specific changes in brain cytokines in offspring throughout development

Maternal infection is a risk factor for autism spectrum disorder (ASD) and schizophrenia (SZ). Indeed, modeling this risk factor in mice through maternal immune activation (MIA) causes ASD- and SZ-like neuropathologies and behaviors in the offspring. Although MIA upregulates pro-inflammatory cytokines in the fetal brain, whether MIA leads to long-lasting changes in brain cytokines during postnatal development remains unknown. Here, we tested this possibility by measuring protein levels of 23 cytokines in the blood and three brain regions from offspring of poly(I:C)- and saline-injected mice at five postnatal ages using multiplex arrays. Most cytokines examined are present in sera and brains throughout development. MIA induces changes in the levels of many cytokines in the brains and sera of offspring in a region- and age-specific manner. These MIA-induced changes follow a few, unexpected and distinct patterns. In frontal and cingulate cortices, several, mostly pro-inflammatory, cytokines are elevated at birth, followed by decreases during periods of synaptogenesis and plasticity, and increases again in the adult. Cytokines are also altered in postnatal hippocampus, but in a pattern distinct from the other regions. The MIA-induced changes in brain cytokines do not correlate with changes in serum cytokines from the same animals. Finally, these MIA-induced cytokine changes are not accompanied by breaches in the blood–brain barrier, immune cell infiltration or increases in microglial density. Together, these data indicate that MIA leads to long-lasting, region-specific changes in brain cytokines in offspring—similar to those reported for ASD and SZ—that may alter CNS development and behavior

Introduction to special issue on neuroimmunology in brain development and disease

Although neural-immune cross-talk during disease and/or trauma has been studied for many years, the dogma has been that there is little interaction between the immune and nervous systems in healthy individuals. This belief was historically based on indications that the blood-brain barrier (BBB) blocks immune cell infiltration into the central nervous system (CNS), leading to limited immune responses in the CNS, and by a lack of classical immune proteins in the brain (Murphy and Sturm, 1923; Joly et al., 1991). However, recent observations from both clinical and basic science research have caused a paradigm shift in our understanding of neural-immune interactions, indicating clearly that there is extensive communication between these systems (McAllister and van de Water, 2009). There is now clear evidence that environmental insults that alter the immune response can affect brain development as well as behavior (Patterson, 2009; Meyer et al., 2011). Moreover, mouse models of neurodevelopmental disorders have provided strong support for immune involvement in CNS development and disease (Patterson, 2009; Patterson, 2011). Finally, several different kinds of immune molecules, including cytokines, major histocompatibility complex (MHC) proteins, and complement, are expressed in the developing and adult brain and have critical functions in brain development and plasticity (Garay and McAllister, 2009; Shatz, 2009; Elmer and McAllister, 2012; Stephan et al., 2012). In this Special Issue, we include reviews covering a range of topics from epidemiology indicating a role for immune dysregulation in neurodevelopmental disorders to basic mechanisms underlying the effects of immune molecules in brain development and disease

An experimental study of the rearrangements of valence protons and neutrons amongst single-particle orbits during double {\beta} decay in 100Mo

The rearrangements of protons and neutrons amongst the valence single-particle orbitals during double {\beta} decay of 100Mo have been determined by measuring cross sections in (d,p), (p,d), (3He,{\alpha}) and (3He,d) reactions on 98,100Mo and 100,102Ru targets. The deduced nucleon occupancies reveal significant discrepancies when compared with theoretical calculations; the same calculations have previously been used to determine the nuclear matrix element associated with the decay probability of double {\beta} decay of the 100Mo system.Comment: 18 pages, 13 figures, 37 pages of supplemental informatio