New Data on Therangospodus oncalensis from the Berriasian Fuentesalvo Tracksite (Villar del Río,Soria, Spain): An Example of Gregarious Behaviour in Theropod Dinosaurs

Therangospodus oncalensis is a Berriasian theropod ichnotaxon from the Cameros Basin (Soria Province, Spain). We discovered new trackways assigned to this ichnotaxon during cleaning and conservation works at the type locality (Fuentesalvo), enabling us to describe it more precisely. Therangospodus oncalensis was made by a medium-sized theropod dinosaur and is characterized by a single tapering pad on each toe, a rounded heel impression and a narrow trackway. In addition to having similar morphometric characteristics, most of the trackways at the Fuentesalvo site show comparable size and biometric features. This indicates that, in terms of size and age, a homogeneous population of a single theropod species could have produced these tracks. Moreover, the similar orientation (lying within a range of only 15°) and estimated speed suggested by most of the trackways, lend weight to the hypothesis that the trackmaker of Therangospodus oncalensis was able, at least at times, to move in structured packs displaying gregarious behaviour. Furthermore, this is the first structured pack of theropods to be described.     

Ehrlich cell plasma membrane redox system is modulated through signal transduction pathways involvingcGMP and Ca2+ as second messengers

Ehrlich cell plasma membrane ferricyanide reductase activity increased in the presence of mastoparan, a generic activator of G proteins, using either whole cells or isolated plasma membrane fractions. Agents that increase intracellularcAMP also increased the rate of ferricyanide reduction by Ehrlich cells. For the first time, evidence is shown on a modulation of plasma membrane redox system bycGMP. In fact, permeant analogs ofcGMP, dibutyrylcGMP, and 8-bromo-cGMP increased the rate of ferricyanide reduction by the Ehrlich cell plasma membrane redox system. Furthermore, specific inhibition ofcGMP-phosphodiesterases by dipyridamole was also accompanied by an enhancement in the rate of ferricyanide reduction. On the other hand, treatments expected to increase cytoplasmic Ca²⁺ concentrations were accompanied by a remarkable stimulation of the reductase activity. Taking all these data together, it seems that the Ehrlich cell plasma membrane redox system is under a multiple and complex regulation by different signal transduction pathways involving G proteins, cyclic nucleotides, and Ca²⁺ ions.     

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.     

Thioredoxin and glutaredoxin system proteins—immunolocalization in the rat central nervous system

Background

The oxidoreductases of the thioredoxin (Trx) family of proteins play a major role in the cellular response to oxidative stress. Redox imbalance is a major feature of brain damage. For instance, neuronal damage and glial reaction induced by a hypoxic–ischemic episode is highly related to glutamate excitotoxicity, oxidative stress and mitochondrial dysfunction. Most animal models of hypoxia–ischemia in the central nervous system (CNS) use rats to study the mechanisms involved in neuronal cell death, however, no comprehensive study on the localization of the redox proteins in the rat CNS was available.

Methods

The aim of this work was to study the distribution of the following proteins of the thioredoxin and glutathione/glutaredoxin (Grx) systems in the rat CNS by immunohistochemistry: Trx1, Trx2, TrxR1, TrxR2, Txnip, Grx1, Grx2, Grx3, Grx5, and γ-GCS, peroxiredoxin 1 (Prx1), Prx2, Prx3, Prx4, Prx5, and Prx6. We have focused on areas most sensitive to a hypoxia–ischemic insult: Cerebellum, striatum, hippocampus, spinal cord, substantia nigra, cortex and retina.

Results and conclusions

Previous studies implied that these redox proteins may be distributed in most cell types and regions of the CNS. Here, we have observed several remarkable differences in both abundance and regional distribution that point to a complex interplay and crosstalk between the proteins of this family.

General significance

We think that these data might be helpful to reveal new insights into the role of thiol redox pathways in the pathogenesis of hypoxia–ischemia insults and other disorders of the CNS.This article is part of a Special Issue entitled Human and Murine Redox Protein Atlases.     

Cyclodextrin production by cyclodextrin glycosyltransferase from Bacillus circulans DF 9R

Cyclodextrins (CD) are cyclic oligosaccharides with multiple applications in the food, pharmaceutical, cosmetic, agricultural and chemical industries. In this work, the conditions used to produce CD with cyclodextrin glycosyltransferase from Bacillus circulans DF 9R were optimized using experimental designs. The developed method allowed the partial purification and concentration of the enzyme from the cultural broth and, subsequently, the CD production, using the same cassava starch as enzyme adsorbent and as substrate. Heat-treatment of raw starch at 70 degrees C for 15 min in the presence of adsorbed cyclodextrin glycosyltransferase allowed the starch liquefaction without enzyme inactivation. The optimum conditions for CD production were: 5% (w/v) cassava starch, 15 U of enzyme per gram of substrate, reaction temperature of 56 degrees C and pH 6.4. After 4h, the proportion of starch converted to CD reached 66% (w/w) and the weight ratio of alpha-CD:beta-CD:gamma-CD was 1.00:0.70:0.16.     

Sterculic acid antagonizes 7-ketocholesterol-mediated inflammation and inhibits choroidal neovascularization

Sterculic acid is a cyclopropene fatty acid with numerous biological activities. In this study we demonstrate that sterculic acid is a potent inhibitor of endoplasmic reticulum (ER) stress and related inflammation caused by 7-ketocholesterol (7KCh). 7KCh is a highly toxic oxysterol suspected in the pathogenesis of various age-related diseases such as atherosclerosis, Alzheimer's disease and age-related macular degeneration. Sterculic acid demonstrated to be 5-10 times more effective than other anti-inflammatory fatty acids at inhibiting 7KCh-mediated inflammatory responses in cultured cells. In vivo, sterculic acid was effective at inhibiting the formation of choroidal neovascularization (CNV) in the laser-injury rat model. Our data suggests that sterculic acid may be useful in treating CNV in certain forms of age-related macular degeneration.     

Variability in the settlement of non-indigenous species in benthic communities from an oceanic island

The introduction of non-indigenous species (NIS) in new environments represents a major threat for coastal ecosystems. A good understanding of the mechanisms and magnitude of the impact of NIS colonisation on native ecosystems is becoming increasingly crucial to develop mitigation measures and prevent new invasions. In this present study, we asked if distinct coastal benthic communities from an oceanic island can have different vulnerability to NIS colonisation process. First, PVC settlement plates were deployed for 1 year on the rocky shore of two different locations of Madeira Island (North versus South coast). Then, we implemented a mesocosm experiment where recruited plate communities were maintained under different levels of NIS propagule pressure in order to assess their vulnerability to NIS colonisation process. Results showed that NIS colonisation success was not influenced by the level of propagule pressure, but however, final colonisation patterns varied depending on the origin of the communities. This variability can be attributed to major structural differences between the preponderant species of each community and therefore to the biotic substrate they offer to colonisers. This study highlights how biotic features can alter the NIS colonisation process and importantly, shows that in an urbanisation context, the nature of the resident communities facing invasions risks needs to be closely assessed.     

Mutations in foregut SOX2+ cells induce efficient proliferation via CXCR2 pathway

Identification of the precise molecular pathways involved in oncogene-induced transformation may help us gain a better understanding of tumor initiation and promotion. Here, we demonstrate that SOX2⁺ foregut epithelial cells are prone to oncogenic transformation upon mutagenic insults, such as Kras^G12D and p53 deletion. GFP-based lineage-tracing experiments indicate that SOX2⁺ cells are the cells-of-origin of esophagus and stomach hyperplasia. Our observations indicate distinct roles for oncogenic KRAS mutation and P53 deletion. p53 homozygous deletion is required for the acquisition of an invasive potential, and Kras^G12D expression, but not p53 deletion, suffices for tumor formation. Global gene expression analysis reveals secreting factors upregulated in the hyperplasia induced by oncogenic KRAS and highlights a crucial role for the CXCR2 pathway in driving hyperplasia. Collectively, the array of genetic models presented here demonstrate that stratified epithelial cells are susceptible to oncogenic insults, which may lead to a better understanding of tumor initiation and aid in the design of new cancer therapeutics.     

Characterization of HTT Inclusion Size,Location, and Timing in the zQ175 Mouse Model of Huntington′s Disease: An In Vivo High-Content Imaging Study

Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder caused by a CAG trinucleotide repeat expansion in the huntingtin gene. Major pathological hallmarks of HD include inclusions of mutant huntingtin (mHTT) protein, loss of neurons predominantly in the caudate nucleus, and atrophy of multiple brain regions. However, the early sequence of histological events that manifest in region- and cell-specific manner has not been well characterized. Here we use a high-content histological approach to precisely monitor changes in HTT expression and characterize deposition dynamics of mHTT protein inclusion bodies in the recently characterized zQ175 knock-in mouse line. We carried out an automated multi-parameter quantitative analysis of individual cortical and striatal cells in tissue slices from mice aged 2–12 months and confirmed biochemical reports of an age-associated increase in mHTT inclusions in this model. We also found distinct regional and subregional dynamics for inclusion number, size and distribution with subcellular resolution. We used viral-mediated suppression of total HTT in the striatum of zQ175 mice as an example of a therapeutically-relevant but heterogeneously transducing strategy to demonstrate successful application of this platform to quantitatively assess target engagement and outcome on a cellular basis.