The Density-Dependent Correlations among Observables in Nuclear Matter and Hyperon-Rich Neutron Stars

The conserving σ-ω-ρ mean-field approximation with nonlinear interactions of hadrons has been applied to examine properties of nuclear matter and hyperonic neutron stars. The nonlinear interactions that will produce density-dependent effective masses and coupling constants of hadrons are included in order to examine density correlations among properties of nuclear matter and neutron stars such as binding energy, incompressibility, K, symmetry energy, a4, hyperon-onset density, and maximum masses of neutron stars. The conditions of conserving approximations in order to maintain thermodynamic consistency to an approximation are essential for the analysis of density-dependent correlations

New Maximum Likelihood Estimators for Eukaryotic Intron Evolution

The evolution of spliceosomal introns remains poorly understood. Although many approaches have been used to infer intron evolution from the patterns of intron position conservation, the results to date have been contradictory. In this paper, we address the problem using a novel maximum likelihood method, which allows estimation of the frequency of intron insertion target sites, together with the rates of intron gain and loss. We analyzed the pattern of 10,044 introns (7,221 intron positions) in the conserved regions of 684 sets of orthologs from seven eukaryotes. We determined that there is an average of one target site per 11.86 base pairs (bp) (95% confidence interval, 9.27 to 14.39 bp). In addition, our results showed that: (i) overall intron gains are ~25% greater than intron losses, although specific patterns vary with time and lineage; (ii) parallel gains account for ~18.5% of shared intron positions; and (iii) reacquisition following loss accounts for ~0.5% of all intron positions. Our results should assist in resolving the long-standing problem of inferring the evolution of spliceosomal introns

Characterization of a Novel Proteinous Toxin from Sea Anemone Actineria villosa.

The sea anemone Actineria villosa expresses a lethal protein toxin. We isolated a novel 120-kDa protein, Avt120, from partially purified toxin and found it to possess extremely strong lethal activity. The 3,453-bp Avt120 gene translates to a 995-amino acid protein. The 50% lethal dose (LD(50)) of purified Avt120 in mice was 85.17 ng. Among several tested cell lines, Colo205 cells were most sensitive to Avt120: 50% of them were damaged by 38.4 ng/mL Avt120. Avt120 exerted ATP degradation activity (10 μmol ATP h(-1) mg(-1)), which was strongly inhibited by ganglioside GM1 to decrease the cytotoxicity of Avt120

Loss of Ribosomal Protein L11 Affects Zebrafish Embryonic Development through a p53-Dependent Apoptotic Response

Ribosome is responsible for protein synthesis in all organisms and ribosomal proteins (RPs) play important roles in the formation of a functional ribosome. L11 was recently shown to regulate p53 activity through a direct binding with MDM2 and abrogating the MDM2-induced p53 degradation in response to ribosomal stress. However, the studies were performed in cell lines and the significance of this tumor suppressor function of L11 has yet to be explored in animal models. To investigate the effects of the deletion of L11 and its physiological relevance to p53 activity, we knocked down the rpl11 gene in zebrafish and analyzed the p53 response. Contrary to the cell line-based results, our data indicate that an L11 deficiency in a model organism activates the p53 pathway. The L11-deficient embryos (morphants) displayed developmental abnormalities primarily in the brain, leading to embryonic lethality within 6–7 days post fertilization. Extensive apoptosis was observed in the head region of the morphants, thus correlating the morphological defects with apparent cell death. A decrease in total abundance of genes involved in neural patterning of the brain was observed in the morphants, suggesting a reduction in neural progenitor cells. Upregulation of the genes involved in the p53 pathway were observed in the morphants. Simultaneous knockdown of the p53 gene rescued the developmental defects and apoptosis in the morphants. These results suggest that ribosomal dysfunction due to the loss of L11 activates a p53-dependent checkpoint response to prevent improper embryonic development

Regulation of the autophagy protein LC3 by phosphorylation

PKA puts the brakes on autophagy by inhibiting LC3 recruitment to autophagosomes

seasonal abundance of the nearctic gall midge obolodiplosis robiniae in italy and the impact of its antagonist platygaster robiniae on pest populations

The Nearctic gall midge Obolodiplosis robiniae (Haldeman, 1847) (Diptera Cecidomyiidae) infesting black locusts, Robinia pseudoacacia L. (Fabaceae), was detected in Asia in 2002 and in Europe (first in Italy) in 2003. Its distribution in Europe has expanded dramatically, probably favored by extensive distribution of its host plant along the main routes. The results of a 3-yr study on the seasonal abundance of O. robiniae in northern Italy are reported here. O. robiniae can develop three to four generations per year by exploiting plants of different ages and vigor. Overwintering takes place as diapausing larvae and adults emerge in spring. Two generations are completed on mature plants where populations decline in summer. Two additional generations can develop on root suckers from midsummer onward. Pest population densities reach their highest levels in late spring. Gall midge larvae were attacked by various predators, but parasitism by the platygastrid Platygaster robiniae Buhl & Duso was particularly significant. The impact of parasitism by P. robiniae is indicated as a key factor in reducing O. robiniae population densities

Detecting early kidney damage in horses with colic by measuring matrix metalloproteinase -9 and -2, other enzymes, urinary glucose and total proteins

BACKGROUND: The aim of the study was to investigate urine matrix metalloproteinase (MMP-2 and -9) activity, alkaline phosphatase/creatinine (U-AP/Cr) and gamma-glutamyl-transpeptidase/creatinine (U-GGT/Cr) ratios, glucose concentration, and urine protein/creatinine (U-Prot/Cr) ratio and to compare data with plasma MMP-2 and -9 activity, cystatin-C and creatinine concentrations in colic horses and healthy controls. Horses with surgical colic (n = 5) were compared to healthy stallions (n = 7) that came for castration. Blood and urine samples were collected. MMP gelatinolytic activity was measured by zymography. RESULTS: We found out that horses with colic had significantly higher urinary MMP-9 complex and proMMP-9 activities than horses in the control group. Colic horses also had higher plasma MMP-2 activity than the control horses. Serum creatinine, although within reference range, was significantly higher in the colic horses than in the control group. There was no significant increase in urinary alkaline phosphatase, gamma-glutamyltranspeptidase or total proteins in the colic horses compared to the control group. A human cystatin-C test (Dako Cytomation latex immunoassay(® )based on turbidimetry) did not cross react with equine cystatin-C. CONCLUSION: The results indicate that plasma MMP-2 may play a role in the pathogenesis of equine colic and urinary MMP-9 in equine kidney damage

Epigenetic Activation of a Subset of mRNAs by eIF4E Explains Its Effects on Cell Proliferation

BACKGROUND: Translation deregulation is an important mechanism that causes aberrant cell growth, proliferation and survival. eIF4E, the mRNA 5′ cap-binding protein, plays a major role in translational control. To understand how eIF4E affects cell proliferation and survival, we studied mRNA targets that are translationally responsive to eIF4E. METHODOLOGY/PRINCIPAL FINDINGS: Microarray analysis of polysomal mRNA from an eIF4E-inducible NIH 3T3 cell line was performed. Inducible expression of eIF4E resulted in increased translation of defined sets of mRNAs. Many of the mRNAs are novel targets, including those that encode large- and small-subunit ribosomal proteins and cell growth-related factors. In addition, there was augmented translation of mRNAs encoding anti-apoptotic proteins, which conferred resistance to endoplasmic reticulum-mediated apoptosis. CONCLUSIONS/SIGNIFICANCE: Our results shed new light on the mechanisms by which eIF4E prevents apoptosis and transforms cells. Downregulation of eIF4E and its downstream targets is a potential therapeutic option for the development of novel anti-cancer drugs