Better red than dead: carotenoid-based mouth coloration reveals infection in barn swallow nestlings.
(49/1930)
Nestling birds solicit food from their parents by displaying their open brightly coloured gapes. Carotenoids affect gape colour, but also play a central role in immunostimulation. Therefore, we hypothesize that, by differentially allocating resources to nestlings with more brightly coloured gapes, parents favour healthy offspring which are able to allocate carotenoids to gape coloration without compromising their immune defence. We demonstrated that, in the barn swallow Hirundo rustica, (i) parents differentially allocate food to nestlings with an experimentally brighter red gape, (ii) nestlings challenged with a novel antigen (sheep red blood cells, SRBCs) have less bright gape colour than their control siblings, (iii) nestlings challenged with SRBCs but also provided with the principal circulating carotenoid (lutein) have more brightly coloured red gapes than their challenged but unsupplemented siblings and (iv) the gape colour of nestlings challenged with SRBCs and provisioned with lutein exceeds that of siblings that were unchallenged. This suggests that parents may favour nestlings with superior health by preferentially feeding offspring with the brightest gapes. (+info)
Neuroimaging evidence implicating cerebellum in support of sensory/cognitive processes associated with thirst.
(50/1930)
Recent studies implicate the cerebellum, long considered strictly a motor control structure, in cognitive, sensory, and affective phenomenon. The cerebellum, a phylogenetically ancient structure, has reciprocal ancient connections to the hypothalamus, a structure important in vegetative functions. The present study investigated whether the cerebellum was involved in vegetative functions and the primal emotions engendered by them. Using positron emission tomography, we examined the effects on the cerebellum of the rise of plasma sodium concentration and the emergence of thirst in 10 healthy adults. The correlation of regional cerebral blood flow with subjects' ratings of thirst showed major activation in the vermal central lobule. During the development of thirst, the anterior and posterior quadrangular lobule, lingula, and the vermis were activated. At maximum thirst and then during irrigation of the mouth with water to alleviate dryness, the cerebellum was less activated. However, 3 min after drinking to satiation, the anterior quadrangular lobule and posterior cerebellum were highly activated. The increased cerebellar activity was not related to motor behavior as this did not occur. Instead, responses in ancient cerebellar regions (vermis, fastigal nucleus, archicerebellum) may be more directly related to vegetative and affective aspects of thirst experiences, whereas activity in neocerebellar (posterior) regions may be related to sensory and cognitive aspects. Moreover, the cerebellum is apparently not involved in the computation of thirst per se but rather is activated during changes in thirst/satiation state when the brain is "vigilant" and is monitoring its sensory systems. Some neocerebellar activity may also reflect an intentionality for gratification by drinking inherent in the consciousness of thirst. (+info)
Extensive glycosylation changes revealed by lectin histochemistry in morphologically normal prenatal tissues of the mouse mutant undulated (un/un).
(51/1930)
Recently we observed that in human embryos and fetuses with a variety of malformations, not only malformed tissues, but also several non-malformed tissues displayed alterations in the glycosylation pattern. It was the aim of this work to investigate this more or less inexplicable phenomenon under experimental conditions. To this end, we studied a well known mouse model, the mouse mutant undulated, which has an exactly defined genetic defect (substitution in the pax-1 gene) leading to a localized malformation in the vertebral column. The glycosylation pattern was studied using lectin histochemistry. Distribution of binding sites for the lectins RCA I, Con A, SNA, SBA, PNA, LTA and WGA was studied during the organogenesis stages (i.e., days 11-18). It was striking that in mutants, changes in the glycosylation pattern were found not only in the malformed organ (i.e., vertebral anlage), but also in other embryonic tissues, which showed normal morphology. This suggests that the altered glycosylation seems to be a part of genetically determined phenomena throughout the entire organism. Our results show that a defect in a gene with a very restricted expression can cause universal changes in the glycosylation pattern during development. (+info)
Susceptibilities of oral and nasal isolates of Streptococcus mitis and Streptococcus oralis to macrolides and PCR detection of resistance genes.
(52/1930)
The susceptibility of viridans group streptococci to macrolides was determined. Thirteen isolates (17%) were resistant to erythromycin. Five strains carried an erm gene that was highly homologous to that in Tn917. Four strains had mefE genes that coded erythromycin efflux ability. (+info)
Induction of apoptotic cell death in peripheral blood mononuclear and polymorphonuclear cells by an oral bacterium, Fusobacterium nucleatum.
(53/1930)
It is largely unknown why a variety of bacteria present in the oral cavity are capable of establishing themselves in the periodontal pockets of nonimmunocompromised individuals in the presence of competent immune effector cells. In this paper we present evidence for the immunosuppressive role of Fusobacterium nucleatum, a gram-negative oral bacterium which plays an important role in the generation of periodontal disease. Our studies indicate that the immunosuppressive role of F. nucleatum is largely due to the ability of this organism to induce apoptotic cell death in peripheral blood mononuclear cells (PBMCs) and in polymorphonuclear cells (PMNs). F. nucleatum treatment induced apoptosis of PBMCs and PMNs as assessed by an increase in subdiploid DNA content determined by DNA fragmentation and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling assays. The ability of F. nucleatum to induce apoptosis was abolished by either heat treatment or proteinase digestion but was retained after formaldehyde treatment, suggesting that a heat-labile surface protein component is responsible for bacterium-mediated cell apoptosis. The data also indicated that F. nucleatum-induced cell apoptosis requires activation of caspases and is protected by NF-kappaB. Possible mechanisms of F. nucleatum's role in the pathogenesis of periodontal disease are discussed. (+info)
Reflex effects of oral, gastrointestinal and hepatoportal glutamate sensors on vagal nerve activity.
(54/1930)
Glutamate sensors in the oral cavity, gastrointestinal canal and hepatoportal region are thought to function in the reflex regulation of vagal activity to the gastrointestinal tract and pancreas. In support of this notion, the findings summarized in this report demonstrate that the infusion of monosodium glutamate (MSG) into the stomach (150 mmol/L, 3 mL), duodenum (150 mmol/L, 3 mL) and portal vein (10 mmol/L, 0.1 mL) increases afferent activity in the vagal gastric, celiac and hepatic nerves, suggesting the existence of glutamate sensors in the gastric wall, intestinal wall and hepatoportal region. Further, oral, gastric and intestinal infusions of MSG (150 mmol/L, isotonic solution) and the infusion of MSG (10 mmol/L, 0.1 mL) into the portal vein resulted in reflex activation of the efferent gastric and pancreatic branches of the vagus. The intravenous injection of 10 mmol/L MSG (0.1 mL) also induced a reflex activation of the efferent discharges of the gastric branch of the vagus; however, in hepatic and celiac vagotomized rats, the intravenous injection of MSG (1 or 3mol/L, 1 mL) produced no effect on gastric vagal activity. The results of these experiments demonstrate the importance of the afferent nerve signals from visceral glutamate sensors in generating the reflex activation of gastrointestinal and pancreatic functions in response to MSG administration. (+info)
Ecological effects of triclosan and triclosan monophosphate on defined mixed cultures of oral species grown in continuous culture.
(55/1930)
The effects of triclosan and its phosphorylated derivative, triclosan monophosphate were studied using a continuous culture microcosm model. Two conditions were simulated, a caries-like state (pH 5.5 with artificial saliva plus glucose as growth medium) and a periodontal disease-like state (pH 7.5 with BHI plus yeast extract, haemin and cysteine as growth medium). Both cultures were maintained anaerobically at 37 degrees C at a growth rate of 0.1/h. Steady-state chemostats were pulsed with triclosan or triclosan monophosphate (initial concentrations between 20 and 40 mg/L) and changes in the ecological composition noted after 6 h. The caries-like microcosm steady state was dominated by streptococci, Lactobacillus and Veillonella sp. with low but detectable levels of Neisseria, Actinomyces and Fusobacterium sp. No significant ecological shifts occurred following pulses of either antimicrobial agent; all species were affected to approximately the same degree. The periodontal disease-like microcosm steady state was dominated by streptococci, Fusobacterium, Veillonella, Actinomyces, Prevotella and Porphyromonas sp. with low numbers of Neisseria and Lactobacillus sp. Significant ecological shifts were apparent following pulses of triclosan. The streptococci became the dominant group followed by Fusobacterium sp. For triclosan monophosphate, the streptococci again became dominant although Lactobacillus and Actinomyces were now the main sub-dominant species and Gram-negative anaerobes including Fusobacterium sp. were markedly inhibited. It is concluded that in the periodontal disease state, both triclosan and triclosan monophosphate affected the Gram-negative anaerobes to a greater extent than the Gram-positive groups and that this effect was more marked for triclosan monophosphate. (+info)
Oral colonization by Candida albicans.
(56/1930)
Candida albicans is a commensal yeast normally present in small numbers in the oral flora of a large proportion of humans. Colonization of the oral cavity by C. albicans involves the acquisition and maintenance of a stable yeast population. Micro-organisms are continually being removed from the oral cavity by host clearance mechanisms, and so, in order to survive and inhabit this eco-system, C. albicans cells have to adhere and replicate. The oral cavity presents many niches for C. albicans colonization, and the yeast is able to adhere to a plethora of ligands. These include epithelial and bacterial cell-surface molecules, extracellular matrix proteins, and dental acrylic. In addition, saliva molecules, including basic proline-rich proteins, adsorbed to many oral surfaces promote C. albicans adherence. Several adhesins present in the C. albicans cell wall have now been partially characterized. Adherence involves lectin, protein-protein, and hydrophobic interactions. As C. albicans cells evade host defenses and colonize new environments by penetrating tissues, they are exposed to new adherence receptors and respond by expressing alternative adhesins. The relatively small number of commensal Candida cells in the oral flora raises the possibility that strategies can be devised to prevent oral colonization and infection. However, the variety of oral niches and the complex adherence mechanisms of the yeast mean that such a goal will remain elusive until more is known about the contribution of each mechanism to colonization. (+info)