Blitzkrieg in a Marine Invasion: Caulerpa racemosa var. cylindracea (Bryopsidales, Chlorophyta) Reaches the Canary Islands (North-East Atlantic)

On the basis of morphological and genetic studies (rDNA ITS1, 5.8S, ITS2, and a 18S rDNA intron), we confirm here that Caulerpa racemosa var. cylindracea (Sonder) Verlaque, Huisman et Boudouresque, a southwestern Australian taxon recently introduced into the Mediterranean Sea also occurs in the Canary Islands. This is the first report of C. racemosa var. cylindracea in the Atlantic. It was observed for the first time in the Canary Archipelago in 1997–1998. The speed and regional scale of expansion (north Atlantic Ocean and the Mediterranean Sea) of this invasive species appear to be among the most dramatic ever recorded. The possible outcome of this introduction in the Atlantic is discussed.     

Adenovirus's last trick: you say lysis, we say autophagy

The last stage of the adenovirus replication cycle, lysis, is considered not very efficient and remains poorly understood. Pathogen infection induces autophagy in eukaryotic cells. In the case of viruses, autophagy is a double-edged sword that can either facilitate or impede replication. On one hand, autophagy reduces the replication capability of the herpesviruses. On the other hand, the RNA virus poliovirus uses autophagosomes to form replication complexes. Recently we characterized the autophagy induced by the oncolytic adenovirus Delta-24-RGD in brain tumor stem cells. Late in the adenoviral infectious cycle, we observed remarkable upregulation of the Atg12-Atg5 complex and prominent autophagy. In addition, adenovirus-induced autophagy results in disruption of the cytoplasmic structure and the continuity of the cellular membrane. We speculate that adenoviruses induce autophagy to facilitate the release of viral progeny at the end of the infectious cycle. The substitution of 'autophagy' for 'lysis' is not just semantic. Because autophagy is a genetically programmed process and not a passive phenomenon, it immediately suggests interactions between adenovirus proteins and autophagy regulators. Understanding the mechanism underlying adenovirus-mediated autophagy should propel the development of novel vectors with enhanced capability to release viral progeny and, as a result, morepotent oncolytic effect.     

Selective predation by crevalle jack <Emphasis Type="Italic">Caranx caninus</Emphasis> on engraulid fishes in the SE Gulf of California,Mexico

Feeding habits determine many aspects of living organisms, where it lives, the time of day that it is active, energy flow, biomass consumed and intra- and interspecific interactions, it which provides information to make predictions about the effects of fisheries on predator-prey relationships. Accurate predictions require a thorough understanding of predator diets and prey selection. In this study, specimens of the crevalle jack Caranx caninus were obtained between October 2012 and October 2014 in the SE Gulf of California, Mexico, in order to determine its feeding habits and prey selection. A total of 238 specimens were obtained, of which 94 (39.5%) had stomachs containing food and 144 (60.5%) had empty stomachs. A total of 10 prey items were identified, corresponding to seven families that included fishes, crustaceans and cephalopods. According to the Index of Relative Importance (IRI) the most important prey were Anchoa spp. (IRI = 91.2%), Engraulis mordax (IRI = 1.8%), and fish from the Clupeidae family (IRI = 1.0%). The crevalle jack’s diet did not change with the season (warm or cold). The crevalle jack was considered a tertiary predator (trophic level = 4.3) that tends to feed on a reduced number of prey, characterizing it as a specialist and selective predator of engraulid fishes (Levin’s index, Bi = 0.08; E = 0.6).     

DNA-mounted self-assembly: new approaches for genomic analysis and SNP detection

This article presents an overview of new emerging approaches for nucleic acid detection via hybridization techniques that can potentially be applied to genomic analysis and SNP identification in clinical diagnostics. Despite the availability of a diverse variety of SNP genotyping technologies on the diagnostic market, none has truly succeeded in dominating its competitors thus far. Having been designed for specific diagnostic purposes or clinical applications, each of the existing bio-assay systems (briefly outlined here) is usually limited to a relatively narrow aspect or format of nucleic acid detection, and thus cannot entirely satisfy all the varieties of commercial requirements and clinical demands. This drives the diagnostic sector to pursue novel, cost-effective approaches to ensure rapid and reliable identification of pathogenic or hereditary human diseases. Hence, the purpose of this review is to highlight some new strategic directions in DNA detection technologies in order to inspire development of novel molecular diagnostic tools and bio-assay systems with superior reliability, reproducibility, robustness, accuracy and sensitivity at lower assay cost. One approach to improving the sensitivity of an assay to confidently discriminate between single point mutations is based on the use of target assembled, split-probe systems, which constitutes the main focus of this review.     

Human adenovirus type 5 induces cell lysis through autophagy and autophagy-triggered caspase activity

Oncolytic adenoviruses, such as Delta-24-RGD, are promising therapies for patients with brain tumor. Clinical trials have shown that the potency of these cancer-selective adenoviruses should be increased to optimize therapeutic efficacy. One potential strategy is to increase the efficiency of adenovirus-induced cell lysis, a mechanism that has not been clearly described. In this study, for the first time, we report that autophagy plays a role in adenovirus-induced cell lysis. At the late stage after adenovirus infection, numerous autophagic vacuoles accompany the disruption of cellular structure, leading to cell lysis. The virus induces a complete autophagic process from autophagosome initiation to its turnover through fusion with the lysosome although the formation of the autophagosome is sufficient for virally induced cell lysis. Importantly, downmodulation of autophagy genes (ATG5 or ATG10) rescues the infected cells from being lysed by the virus. Moreover, autophagy triggers caspase activity via the extrinsic FADD/caspase 8 pathway, which also contributes to adenovirus-mediated cell lysis. Therefore, our study implicates autophagy and caspase activation as part of the mechanism for cell lysis induced by adenovirus and suggests that manipulation of the process is a potential strategy to optimize clinical efficacy of oncolytic adenoviruses.     

Two Variants of the C-Reactive Protein Gene Are Associated with Risk of Pre-Eclampsia in an American Indian Population

Background

The etiology of pre-eclampsia (PE) is unknown; but it is accepted that normal pregnancy represents a distinctive challenge to the maternal immune system. C-reactive protein is a prominent component of the innate immune system; and we previously reported an association between PE and the CRP polymorphism, rs1205. Our aim was to explore the effects of additional CRP variants. The IBC (Cardiochip) genotyping microarray focuses on candidate genes and pathways related to the pathophysiology of cardiovascular disease.

Methods

This study recruited 140 cases of PE and 270 matched controls, of which 95 cases met criteria as severe PE, from an American Indian community. IBC array genotypes from 10 suitable CRP SNPs were analyzed. A replication sample of 178 cases and 427 controls of European ancestry was also genotyped.

Results

A nominally significant difference (p value <0.05) was seen in the distribution of discordant matched pairs for rs3093068; and Bonferroni corrected differences (P<0.005) were seen for rs876538, rs2794521, and rs3091244. Univariate conditional logistic regression odds ratios (OR) were nominally significant for rs3093068 and rs876538 models only. Multivariate logistic models with adjustment for mother''s age, nulliparity and BMI attenuated the effect (OR 1.58, P = 0.066, 95% CI 0.97–2.58) for rs876538 and (OR 2.59, P = 0.050, 95% CI 1.00–6.68) for rs3093068. An additive risk score of the above two risk genotypes shows a multivariate adjusted OR of 2.04 (P = 0.013, 95% CI 1.16–3.56). The replication sample also demonstrated significant association between PE and the rs876538 allele (OR = 1.55, P = 0.01, 95% CI 2.16–1.10). We also show putative functionality for the rs876538 and rs3093068 CRP variants.

Conclusion

The CRP variants, rs876538 and rs3093068, previously associated with other cardiovascular disease phenotypes, show suggestive association with PE in this American Indian population, further supporting a possible role for CRP in PE.     

Genome-wide study identifies two loci associated with lung function decline in mild to moderate COPD

Accelerated lung function decline is a key COPD phenotype; however, its genetic control remains largely unknown. We performed a genome-wide association study using the Illumina Human660W-Quad v.1_A BeadChip. Generalized estimation equations were used to assess genetic contributions to lung function decline over a 5-year period in 4,048 European American Lung Health Study participants with largely mild COPD. Genotype imputation was performed using reference HapMap II data. To validate regions meeting genome-wide significance, replication of top SNPs was attempted in independent cohorts. Three genes (TMEM26, ANK3 and FOXA1) within the regions of interest were selected for tissue expression studies using immunohistochemistry. Two intergenic SNPs (rs10761570, rs7911302) on chromosome 10 and one SNP on chromosome 14 (rs177852) met genome-wide significance after Bonferroni. Further support for the chromosome 10 region was obtained by imputation, the most significantly associated imputed SNPs (rs10761571, rs7896712) being flanked by observed markers rs10761570 and rs7911302. Results were not replicated in four general population cohorts or a smaller cohort of subjects with moderate to severe COPD; however, we show novel expression of genes near regions of significantly associated SNPS, including TMEM26 and FOXA1 in airway epithelium and lung parenchyma, and ANK3 in alveolar macrophages. Levels of expression were associated with lung function and COPD status. We identified two novel regions associated with lung function decline in mild COPD. Genes within these regions were expressed in relevant lung cells and their expression related to airflow limitation suggesting they may represent novel candidate genes for COPD susceptibility.