Secretory products of the haptoral reservoirs and peduncular glands in two species of Bravohollisia (Monogenea : Ancyrocephalidae)

Light and electron microscopy were used to characterize the structure of secretory cells and their products involved in attachment of two monogenean parasites of fish, in order to understand their role in the attachment process. In Bravohollisia rosetta and Bravohollisia gussevi, peduncular gland cells with two nuclei, granular endoplasmic reticulum, and Golgi bodies produce dual electron-dense (DED) secretory bodies with a homogenous electron-dense rind and a less electron-dense fibrillar core (oval and concave in B. rosetta and oval in B. gussevi). The DED secretory bodies are altered as they migrate from the gland cell to the haptoral reservoir, the superficial anchor grooves, and into the gill tissues. The contents of the DED secretory bodies are exocytosed into the reservoirs, fibrillar cores persisting in the matrix, some of which condense, forming highly electron-dense spherical bodies. Small, oval, electron-dense bodies occur in the grooves, while no inclusions are visible in the homogenous exudate within the gill tissues. The single tubular extension of the reservoir enters a bifurcate channel within the anchor via a concealed, crevice-like opening on one side of the anchor. The channel directs secretions into the left and the right grooves via concealed apertures. The secretions, introduced into the tissues by the anchors, probably assist in attachment. The secretions are manifested externally as net-like structures and observed in some cases to be still attached to the point of exudation, on anchors detached from the gill tissues. This suggests that despite having the anchors detached, the worms can still remain anchored to the gill tissues via these net-like structures. Based on this, it is postulated that the net-like secretions probably function as a safety line to anchor the worm during the onset of locomotion and in doing so reduce the risk of tearing host tissues.

Revealing differences in gene network inference algorithms on the network level by ensemble methods

Motivation: The inference of regulatory networks from large-scale expression data holds great promise because of the potentially causal interpretation of these networks. However, due to the difficulty to establish reliable methods based on observational data there is so far only incomplete knowledge about possibilities and limitations of such inference methods in this context.

Results: In this article, we conduct a statistical analysis investigating differences and similarities of four network inference algorithms, ARACNE, CLR, MRNET and RN, with respect to local network-based measures. We employ ensemble methods allowing to assess the inferability down to the level of individual edges. Our analysis reveals the bias of these inference methods with respect to the inference of various network components and, hence, provides guidance in the interpretation of inferred regulatory networks from expression data. Further, as application we predict the total number of regulatory interactions in human B cells and hypothesize about the role of Myc and its targets regarding molecular information processing.

Hyperacetylation in prostate cancer induces cell cycle aberrations, chromatin reorganization and altered gene expression profiles.

Histone acetylation is a fundamental mechanism in the regulation of local chromatin conformation and gene expression. Research has focused on the impact of altered epigenetic environments on the expression of specific genes and their pathways. However, changes in histone acetylation also have a global impact on the cell. In this study we used digital texture analysis to assess global chromatin patterns following treatment with trichostatin A (TSA) and have observed significant alterations in the condensation and distribution of higher-order chromatin, which were associated with altered gene expression profiles in both immortalised normal PNT1A prostate cell line and androgen-dependent prostate cancer cell line LNCaP. Furthermore, the extent of TSA-induced disruption was both cell cycle and cell line dependent. This was illustrated by the identification of sub-populations of prostate cancer cells expressing high levels of H3K9 acetylation in the G2/M phase of the cell cycle that were absent in normal cell populations. In addition, the analysis of enriched populations of G1 cells showed a global decondensation of chromatin exclusively in normal cells.

Many-body theory of gamma spectra from positron-atom annihilation

A many-body theory approach to the calculation of gamma spectra of positron annihilation on many-electron atoms is developed. We evaluate the first-order correlation correction to the annihilation vertex and perform numerical calculations for the noble gas atoms. Extrapolation with respect to the maximal orbital momentum of the intermediate electron and positron states is used to achieve convergence. The inclusion of correlation corrections improves agreement with experimental gamma spectra.

Selection for cuticular melanism reveals immune function and life-history trade-offs in Spodoptera littoralis

Several insect species show an increase in cuticular melanism in response to high densities. In some species, there is evidence that this melanism is correlated with an up-regulation of certain immune system components, particularly phenoloxidase (PO) activity, and with the down-regulation of lysozyme activity, suggesting a trade-off between the two traits. As melanism has a genetic component, we selected both melanic and nonmelanic lines of the phase-polyphenic lepidopteran, Spodoptera littoralis, in order to test for a causative genetic link between melanism, PO activity and lysozyme activity, and to establish if there are any life-history costs associated with the melanic response. We found that, in fact, melanic lines had lower PO activity and higher lysozyme activity than nonmelanic lines, confirming a genetic trade-off between the two immune responses, but also indicating a genetic trade-off between melanism and PO activity. In addition, we found that lines with high PO activity had slower development rates suggesting that investment in PO, rather than in melanism, is costly.

Tri- and tetra-substituted naphthalene diimides as potent G-quadruplex ligands.

A series of tri- and tetra-substituted naphthalene diimides have been designed and synthesized. Several compounds show exceptional affinity for telomeric G-quadruplex DNA in classical and competition FRET assays and SPR studies. They inhibit telomerase in the TRAP assay, and show potent senescence-based short-term anti-proliferative effects on MCF7 and A549 cancer cell lines, and localize in the nucleus and particularly the nucleolus of MCF7 cells.

Functional effect of the C242T polymorphism in the NAD(P)H oxidase p22phox gene on vascular superoxide production in atherosclerosis.

BACKGROUND:

Increased superoxide anion production increases oxidative stress and reduces nitric oxide bioactivity in vascular disease states. NAD(P)H oxidase is an important source of superoxide in human blood vessels, and some studies suggest a possible association between polymorphisms in the NAD(P)H oxidase CYBA gene and atherosclerosis; however, no functional data address this hypothesis. We examined the relationships between the CYBA C242T polymorphism and direct measurements of superoxide production in human blood vessels.

METHODS AND RESULTS:

Vascular NAD(P)H oxidase activity was determined in human saphenous veins obtained from 110 patients with coronary artery disease and identified risk factors. Immunoblotting, reverse-transcription polymerase chain reaction, and DNA sequencing showed that p22phox protein, mRNA, and 242C/T allelic variants are expressed in human blood vessels. Vascular superoxide production, both basal and NADH-stimulated, was highly variable between patients, but the presence of the CYBA 242T allele was associated with significantly reduced vascular NAD(P)H oxidase activity, independent of other clinical risk factors for atherosclerosis.

CONCLUSIONS:

Association of the CYBA 242T allele with reduced NAD(P)H oxidase activity in human blood vessels suggests that genetic variation in NAD(P)H oxidase components may play a significant role in modulating superoxide production in human atherosclerosis.

Referral to an Extracorporeal Membrane Oxygenation Center and Mortality Among Patients With Severe 2009 Influenza A(H1N1)

Context Extracorporeal membrane oxygenation (ECMO) can support gas exchange in patients with severe acute respiratory distress syndrome (ARDS), but its role has remained controversial. ECMO was used to treat patients with ARDS during the 2009 influenza A(H1N1) pandemic.

Genetic susceptibility to invasive meningococcal disease: MBL2 structural polymorphisms revisited in a large case–control study and a systematic review

Invasive infection caused by Neisseria meningitidis is a worldwide public health problem. Previous reports have indicated that carriage of common ‘defective’ structural polymorphisms of the host mannose-binding lectin gene (MBL2) greatly increases an individual’s risk of developing the disease. We report the largest case–control study so far to investigate the effect of these polymorphisms in meningococcal disease (296 PCR-positive cases and 5196 population controls, all of European ancestry) and demonstrate that no change in risk is associated with the polymorphisms overall or in any age-defined subgroup. This finding contrasts with two smaller studies that reported an increase in risk. A systematic review of all studies of MBL2 polymorphisms in people of European ancestry published since 1999, including 24 693 individuals, revealed a population frequency of the combined ‘defective’MBL2 allele of 0.230 (95% confidence limits: 0.226–0.234). The past reported associations of increased risk of meningococcal disease were because of low ‘defective’ allele frequencies in their study control populations (0.13 and 0.04) that indicate systematic problems with the studies. The data from our study and all other available evidence indicate that MBL2 structural polymorphisms do not predispose children or adults to invasive meningococcal disease.

Genetic susceptibility to invasive meningococcal disease: MBL2 structural polymorphisms revisited in a large case-control study and a systematic review.

AbstractInvasive infection caused by Neisseria meningitidis is a worldwide public health problem. Previous reports have indicated that carriage of common 'defective' structural polymorphisms of the host mannose-binding lectin gene (MBL2) greatly increases an individual's risk of developing the disease. We report the largest case-control study so far to investigate the effect of these polymorphisms in meningococcal disease (296 PCR-positive cases and 5196 population controls, all of European ancestry) and demonstrate that no change in risk is associated with the polymorphisms overall or in any age-defined subgroup. This finding contrasts with two smaller studies that reported an increase in risk. A systematic review of all studies of MBL2 polymorphisms in people of European ancestry published since 1999, including 24 693 individuals, revealed a population frequency of the combined 'defective'MBL2 allele of 0.230 (95% confidence limits: 0.226-0.234). The past reported associations of increased risk of meningococcal disease were because of low 'defective' allele frequencies in their study control populations (0.13 and 0.04) that indicate systematic problems with the studies. The data from our study and all other available evidence indicate that MBL2 structural polymorphisms do not predispose children or adults to invasive meningococcal disease.