Embryonic development within carotenoid-enriched eggs influences the post-hatch carotenoid status of the chicken

Carotenoids in the diet of the laying hen are incorporated into the egg yolk and subsequently into the liver and other tissues of the chicken embryo. Since these pigments are known to provide a range of health benefits to a variety of animals, it is of interest to know whether the effects of maternally derived carotenoids are strictly limited to the embryonic period or if they persist in the progeny after hatching. The aim of this study is to compare the effectiveness of pre-hatch (from the hen's diet) with that of post-hatch (from the progeny's diet) supplementation with carotenoids on the carotenoid status of the chick during the first 4 weeks of post-hatch life. Hens were fed a control diet or a diet supplemented with a carotenoid-rich extract of alfalfa. Eggs from the supplemented hens contained up to 22 times more carotenoids than the controls. The concentration of carotenoids in the livers of chicks hatching from the enriched eggs was initially 29 times greater than in the control chicks. Hepatic carotenoid concentrations in chicks from enriched eggs maintained post-hatch on the control diet were sustained at higher values compared with chicks from control eggs that were fed post-hatch on the carotenoid-supplemented diet, for at least the first 7 days. However, by 14 days, the latter group had overtaken the former in terms of liver carotenoid levels. Thus, under these conditions, maternal effects predominate for at least the first week after hatching, whereas from 2 weeks onwards, the progeny's diet becomes the main determinant of its carotenoid status. Since the antioxidant and immunostimulatory roles of carotenoids are likely to be especially important during the immediate post-hatch period, maternal dietary intake of carotenoids may have important ramifications for the viability of the offspring.     

Molecularly imprinted ligand-exchange recognition assay of glucose by quartz crystal microbalance

Molecular imprinted polymers (MIP) as a recognition element for sensors are increasingly of interest and MIP-quartz crystal microbalance (QCM) have started to appear in the literature. In this study, we have combined quartz crystal microbalance with MIP to prepare a sensor using the ability of glucose to chelate of copper (II) ion of methacrylamidohistidine (MAH) monomer to create ligand exchange (LE) assembled monolayer which is suitable for glucose determination. The study includes the measurement of binding interaction of molecularly imprinted QCM sensor via ligand interaction, investigation of the pH effect on frequency shift and recognition selectivity studies of glucose-imprinted polymer with respect to methyl-alpha-d-glucopyranoside and sucrose. Bmax (number of binding sites) and K(D) (dissociation constant of the metal-chelate copolymer) were also calculated using Scathard plot and the detection limit was found as 0.07 mM. MIP showed higher glucose-binding affinity than a well-known glucose binding protein, conconavalin A.     

NADPH oxidase links endoplasmic reticulum stress, oxidative stress, and PKR activation to induce apoptosis

Endoplasmic reticulum (ER)-induced apoptosis and oxidative stress contribute to several chronic disease processes, yet molecular and cellular mechanisms linking ER stress and oxidative stress in the setting of apoptosis are poorly understood and infrequently explored in vivo. In this paper, we focus on a previously elucidated ER stress-apoptosis pathway whose molecular components have been identified and documented to cause apoptosis in vivo. We now show that nicotinamide adenine dinucleotide phosphate reduced oxidase (NOX) and NOX-mediated oxidative stress are induced by this pathway and that apoptosis is blocked by both genetic deletion of the NOX subunit NOX2 and by the antioxidant N-acetylcysteine. Unexpectedly, NOX and oxidative stress further amplify CCAAT/enhancer binding protein homologous protein (CHOP) induction through activation of the double-stranded RNA-dependent protein kinase (PKR). In vivo, NOX2 deficiency protects ER-stressed mice from renal cell CHOP induction and apoptosis and prevents renal dysfunction. These data provide new insight into how ER stress, oxidative stress, and PKR activation can be integrated to induce apoptosis in a pathophysiologically relevant manner.     

Effect of denture adhesive on the micro-organisms in vivo

doi: 10.1111/j.1741‐2358.2010.00381.x Effect of denture adhesive on the micro‐organisms in vivo Background: Denture adhesives increase the retention and stability of dentures in edentulous patients, especially in cases where salivary flow is impaired or in the management of traumatised oral mucosa. Objectives: The effect of a denture adhesive on the oral flora at different time intervals. Method: Thirty denture‐wearing patients were involved in this study. While half of the group received a denture adhesive, the other half did not. At baseline, 1 and 2 months after delivering the dentures, smear samples were obtained from the saliva, palate and the dentures. Candida albicans, Candida krusei, Candida glabrata, Candida spp., Staphylococcus aureus, Moraxella catarrhalis, α‐haemolytic streptococci, β‐haemolytic streptococci, Pneumococcus aureus, S. anginosus, S. intermedius, S. constellatus, S. sanguis, S. gordonii, S. mitis, S. mutans, S. salivarius, and yeasts were investigated. The data were statistically analysed using anova and repeated measures. Results: Most types of the micro‐organisms were not seen and could not be analysed statistically except α‐haemolytic streptococci and C. albicans. No statistically significant difference was found for α‐haemolytic streptococci and C. albicans in saliva, palate and the denture at all time intervals. Conclusions: Prolonged use of the denture adhesive tested up to 2 months did not yield to increase in micro‐organisms of the oral flora.     

Increased risk of advanced prostate cancer associated with MnSOD Ala-9-Val gene polymorphism

We aimed to investigate the association between manganese superoxide dismutase (MnSOD) Ala-9-Val gene polymorphism and the initiation and/or progression of prostate cancer (PCa) as well as to evaluate its potential interactions with advanced age and smoking status. MnSOD Ala-9-Val gene polymorphism was carried out in 134 (mean age 64.1 ± 7.48) PCa patients and 159 (mean age 62.5 ± 7.53) healthy controls with serum prostate specific antigen (PSA) levels (<4 ng/ml) and normal digital rectal examination (DRE) findings in this prospectively designed study. PCa patients were classified as low stage disease (T₁ or T₂ and N₀M₀ stages) and high stage disease (T₃ or T₄ and N₀M₀ or N₁ or M₁ stages). Genotypes for MnSOD Ala-9-Val gene polymorphism were identified by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFPL). Despite lack of association between different genotypes of MnSOD Ala-9-Val gene polymorphism and the presence of PCa, patients with Ala/Ala genotype were at an increased risk of high stage disease compared with those with the Val/Val genotype [odds ratio (OR), 3.77; 95% CI, 1.30–10.94; P = 0.012]. However, no significant difference was observed in the distribution of each genotype among PCa patients, with respect to tumor grade. On the other hand, smoking status and aging did not seem to change the association between genotypes and PCa risk. Ala/Ala genotype of MnSOD polymorphism may have an effect on adverse features of PCa such as high stage disease.     

RIG‐I detects infection with live Listeria by sensing secreted bacterial nucleic acids

Immunity against infection with Listeria monocytogenes is not achieved from innate immune stimulation by contact with killed but requires viable Listeria gaining access to the cytosol of infected cells. It has remained ill‐defined how such immune sensing of live Listeria occurs. Here, we report that efficient cytosolic immune sensing requires access of nucleic acids derived from live Listeria to the cytoplasm of infected cells. We found that Listeria released nucleic acids and that such secreted bacterial RNA/DNA was recognized by the cytosolic sensors RIG‐I, MDA5 and STING thereby triggering interferon β production. Secreted Listeria nucleic acids also caused RIG‐I‐dependent IL‐1β‐production and inflammasome activation. The signalling molecule CARD9 contributed to IL‐1β production in response to secreted nucleic acids. In conclusion, cytosolic recognition of secreted bacterial nucleic acids by RIG‐I provides a mechanistic explanation for efficient induction of immunity by live bacteria.