The capacity of crab megalopae to autotomize body appendages and the consequences upon their feeding ability–the price to pay to live another day

During the mass settlement events of brachyuran crabs, there is a significant chance of density-dependent injury in the megalopae (last larval stage) because cannibalism can occur by larger conspecifics. Laboratory observations revealed that the appendages that are more prone to injury are eyestalks, as well as first (P1) and fifth (P5) pereiopods. The ability of Carcinus maenas megalopae to autotomize these structures and the effect of such injuries in their feeding ability and metamorphosis were investigated. All tested specimens were able to autotomize one or both of their P1 and P5, but not their eyestalks. Megalopae missing a single P1, as well as one or both P5, were able to capture and ingest prey, as well as intact specimens. Megalopae with either P1 and P5 appendages or at least one damaged eyestalk failed to ingest sufficient food to reach the nutritional threshold required to successfully metamorphose.     

Chromothripsis: Breakage-fusion-bridge over and over again

The acquisition of massive but localized chromosome translocations, a phenomenon termed chromothripsis, has received widespread attention since its discovery over a year ago. Until recently, chromothripsis was believed to originate from a single catastrophic event, but the molecular mechanisms leading to this event are yet to be uncovered. Because a thorough interpretation of the data are missing, the phenomenon itself has wrongly acquired the status of a mechanism used to justify many kinds of complex rearrangements. Although the assumption that all translocations in chromothripsis originate from a single event has met with criticism, satisfactory explanations for the intense but localized nature of this phenomenon are still missing. Here, we show why the data used to describe massive catastrophic rearrangements are incompatible with a model comprising a single event only and propose a molecular mechanism in which a combination of known cellular pathways accounts for chromothripsis. Instead of a single traumatic event, the protection of undamaged chromosomes by telomeres can limit repetitive breakage-fusion-bridge events to a single chromosome arm. Ultimately, common properties of chromosomal instability, such as aneuploidy and centromere fission, might establish the complex genetic pattern observed in this genomic state.     

Evaluation of the impact of recreational dive activity on the community structure of some coral reefs at Los Roques Archipelago National Park, Venezula

In order to evaluate if snorkeling had significant effects on coral community structure, three different coral reefs (Madrizquí, Pelona de Rabusquí and Crasquí) located at Archipelago Los Roques National Park, Venezuela, were surveyed. For each site, the coral community structure of two different areas, one subjected to intense snorkeling use (FB) and other not frequently used (PFB), were compared. Community structure was determined with 1 m2-quadrants and 20 m-long transects. These communities were described in terms of species richness, diversity (Shannon-Wiener) and evenness indexes, live and dead coral cover and cover of other organisms (sponges, octocorals and algae). Comparisons within sites were performed with a Kruskall-Wallis test. A total of 24 species of scleractinian corals were found. Live coral cover ranged from 29.9% +/- 26.43 (Crasquí) to 34.55% +/- 6.43 (Madrizquí), while dead coral cover ranged from 32.51% +/- 2.86 (Madrizquí) to 60.78% +/- 21.3 (Pelona de Rabusquí). The PFB areas showed higher live coral cover compared to FB areas; however, significant differences were only found in Crasquí and Pelona de Rabusquí (p < 0.05). Species richness, diversity and evenness were variable and no trends were observed between FB and PFB areas. The frequency of both damaged and diseased colonies were low (< 1%), most damages observed were natural (parrotfish predation). Damages caused by divers such as fin impacts, were not found at the reefs studied. These results suggest that, currently, diving pressure is not as high to cause massive loses of live coral cover in these reefs. However, the lack of strict controls for these activities might produce long-term changes in the structure of these coral communities.     

Status of activation of circulating vaccine-elicited CD8+ T cells

Selective blunting of the status of activation of circulating tumor-specific T cells was invoked to explain their paradoxical coexistence with unhampered tumor growth. By analogy, lack of tumor regression in the face of observable melanoma vaccine-induced T cell responses might be attributed to their status of activation. We enumerated with HLA-A*0201/peptide tetramers (tHLA) vaccine-elicited T cell precursor frequency directly in PBMC of patients with melanoma undergoing vaccination with the HLA-A*0201-associated gp100:209-217(210 M) epitope (g209-2 M). Furthermore, we tested by intracellular (IC)-FACS analysis and quantitative real-time PCR (qRT-PCR) the ability of postvaccination PBMC to produce cytokine in response to challenge with vaccine-related epitopes or vaccine-matched (HLA-A*0201) melanoma cells. Vaccine-induced enhancement of T cell precursor frequency could be detected with tHLA in PBMC from six of eight patients studied at frequencies ranging between 0.3 and 2.3% of the total CD8+ population. Stimulation with vaccine-related epitopes induced IFN-gamma expression detectable by IC-FACS or qRT-PCR, respectively, in five and six of these patients. Furthermore, down-regulation of tHLA staining was noted upon cognate stimulation that could be utilized as an additional marker of T cell responsiveness. Finally, we observed in six patients an enhancement of reactivity against vaccine-matched tumor targets that was partly independent of documented vaccine-specific immune responses. A strong correlation was noted between tHLA staining of postvaccination PBMC and IFN-gamma expression by the same samples upon vaccine-relevant stimulation and assessed either by IC-FACS or qRT-PCR. Thus, blunting of the status of T cell activation on itself cannot easily explain the lack of clinical responses observed with vaccination.     

Atheromatous plaque from human carotid artery: Potential involvement of the endothelin-1 and their receptors

Endothelin-1 (ET-1) is a potent vasoconstrictor peptide that can modulate the behaviour of vascular smooth muscle cells and thus impact on the development of human atherosclerosis. Circulating plasma levels of ET-1 were measured from 82 patients with ischemic cardiomyopathy (ICM) and 42 healthy controls. A significant increase was found in plasma levels of ET-1 in the patients compared to the controls. These circulating levels of ET-1 were greater in patients with diabetes or involvement of several territories. Gene expression of pre-proET-1 and its receptors ET_A and ET_B was analyzed in the atheromatous plaques from carotid arteries (n = 8) and the internal mammary artery (IMA) (n = 8). Our group observed an increase in pre-proET-1 and ET_A in IMA compared with the atheromatous plaques. Immunohistochemical studies in the atherosclerotic plaque showed that the expression of ET-1 was greater in the areas where the macrophages and lipid nucleus were located.Our findings in this group of patients with symptomatic vascular disease suggest that the endothelin system may play an important role in atherothrombosis.     

Regulation of brain anandamide by acute administration of ethanol

FgFtr1 and FgFtr2 are putative iron permeases, and FgFet1 and FgFet2 are putative ferroxidases of Fusarium graminearum. They have high homologies with iron permease ScFtr1 and ferroxidase ScFet3 of Saccharomyces cerevisiae at the amino acid level. The genes encoding iron permease and ferroxidase were localized to the same chromosome in the manner of FgFtr1/FgFet1 and FgFtr2/FgFet2. The GFP (green fluorescent protein)-fused versions of FgFtr1 and FgFtr2 showed normal functions when compared with FgFtr1 and FgFtr2 in an S. cerevisiae system, and the cellular localizations of FgFtr1 and FgFtr2 in S. cerevisiae depended on the expression of their putative ferroxidase partners FgFet1 and FgFet2 respectively. Although FgFtr1 was found on the plasma membrane when FgFet1 and FgFtr1 were co-transformed in S. cerevisiae, most of the FgFtr1 was found in the endoplasmic reticulum compartment when co-expressed with FgFet2. Furthermore, FgFtr2 was found on the vacuolar membrane when FgFet2 was co-expressed. From the two-hybrid analysis, we confirmed the interaction of FgFtr1 and FgFet1, and the same result was found between FgFtr2 and FgFet2. Iron-uptake activity also depended on the existence of the respective partner. Finally, the FgFtr1 and FgFtr2 were found on the plasma and vacuolar membrane respectively, in F. graminearum. Taken together, these results strongly suggest that FgFtr1 and FgFtr2 from F. graminearum encode the iron permeases of the plasma membrane and vacuolar membrane respectively, and require their specific ferroxidases to carry out normal function. Furthermore, the present study suggests that the reductive iron-uptake system is conserved from yeast to filamentous fungi.     

The CD44 standard/ezrin complex regulates Fas-mediated apoptosis in Jurkat cells

The transmembrane receptor CD44 conveys important signals from the extracellular microenvironment to the cytoplasm, a phenomena known as “outside-in” signaling. CD44 exists as several isoforms that result from alternative splicing, which differ only in the extracellular domain but yet exhibit different activities. CD44 is a binding partner for the membrane-cytoskeleton cross-linker protein ezrin. In this study, we demonstrate that only CD44 standard (CD44s) colocalizes and interacts with the actin cross-linkers ezrin and moesin using well-characterized cell lines engineered to express different CD44 isoforms. Importantly, we also show that the association CD44s-ezrin-actin is an important modulator of Fas-mediated apoptosis. The results highlight a mechanism by which signals from the extracellular milieu regulate intracellular signaling activities involved in programmed cell death. Electronic supplementary material The online version of this article (doi: ) contains supplementary material, which is available to authorized users.