First description of early developmental stages of the native invasive fireworm Hermodice carunculata (Annelida, Amphinomidae): A cue to the warming of the mediterranean sea

Observations on the reproductive behavior and larval development of the bristled fireworm Hermodice carunculata, a common inhabitant of shallow marine rocky bottoms in the Southern Mediterranean Sea, are reported here. In recent years, an increase in abundance and a northward expansion of the populations along the Southern Italian coast were jointly detected, presumably linked to rising water temperature in the Mediterranean Sea. After making in situ observations on two consecutive spawning events, live worms and fresh spawn were brought into the lab, kept at either 27°C or 22°C and followed through development. Complete and normal development was observed only at 27°C. By contrast, embryonic and larval development appeared to be slowed down at 22°C, stopping at the protrochophora stage. Early development of H. carunculata suggests the existence of a long pre-metamorphic, planktotrophic period in the water column that can explain the genetic cohesion of this species and the low genetic divergence found among populations across the Atlantic Ocean. The observed increase in abundance, invasiveness potential, and geographical northern distribution of the bearded fireworms is probably determined by a progressive northward latitudinal shift of the sea surface temperature coincident with the temperature threshold required for the developmental and reproductive success of the worm

Lack of coupling of D-2 receptors to adenylate cyclase in GH-3 cells exposed to epidermal growth factor. Possible role of a differential expression of Gi protein subtypes.

Exposure of GH-3 cells to epidermal growth factor for 4 consecutive days induced the expression of both D-2(415) and D-2(444) dopamine-receptor isoforms. Epidermal growth factor also promoted a remarkable increase in the content of Gi3 protein, which is responsible for receptor-induced activation of potassium channels in GH-3 cells. D-2 receptors in this model apparently activate a specific transducing pathway, leading to opening of potassium channels and inhibition of prolactin release by cAMP-independent mechanisms. This is shown by: 1) the selective D-2 agonist quinpirole, while inactive on vasoactive intestinal peptide-induced prolactin release, strongly inhibited the hormone secretion induced by neurotensin; 2) quinpirole, up to 100 microM, did not inhibit cAMP production evoked by vasoactive intestinal peptide both in intact cells and in broken cell membrane preparations; and 3) quinpirole and other D-2 agonists strongly potentiated Rb+ efflux when measured in a nominally calcium-free reaction solution containing 100 mM potassium (voltage-dependent component), but did not modify Rb+ efflux if measured in a reaction solution containing 1 mM calcium and 5 mM potassium (calcium-activated, cAMP-dependent component)

Energy Absorption Mechanisms in Layer-to-Layer 3D Woven Composites

3D woven composites provide improved out-of-plane performance over their two-dimensional counterparts. This sort of reinforced through thickness behaviour is desirable in crashworthiness applications where energy absorption can be increased by the composite material's resistance to delamination. The behaviour of these 3D materials in not well understood and fundamental data that can be used to validate and improve material models is not yet sufficiently comprehensive. Here we demonstrate that a modified layer-to-layer type 3D woven architecture can be effectively used in energy absorbing elements to produce repeatable and predictable progressive failure under axial crush conditions. Specific energy absorption (SEA) values in glass and carbon coupons of up to 62J/g and 95J/g respectively are achieved in the quasi-static regime; values up 93J/g to were achieved in the dynamic regime when carbon coupons are tested. Carbon specimens displayed uncharacteristic mixed mode failure with elements of ductile and brittle failure. The addition of a toughening agent showed mixed results in this study, providing quasi-static improvements (+8%) in SEA but significant diminishment in dynamic SEA (-22%). The failure modes present in all cases are explored in depth and the suitability of this material for industry crash applications is investigated

High-levelexpression of functional recombinant human coagulation factor VII in insect cells

Abstract: Recombinant coagulation factor VII (FVII) is used as a potential therapeutic intervention in hemophilia patients who produce antibodies against the coagulation factors. Mammalian cell lines provide low levels of expression, however, the Spodoptera frugiperda Sf9 cell line and baculovirus expression system are powerful systems for high-level expression of recombinant proteins, but due to the lack of endogenous vitamin K-dependent carboxylase, expression of functional FVII using this system is impossible. In the present study, we report a simple but versatile method to overcome the defect for high-level expression of the functional recombinant coagulation FVII in Sf9 cells. This method involves simultaneous expression of both human γ-carboxylase (hGC) and human FVII genes in the host. It may be possible to express other vitamin K-dependent coagulation factors using this method in the future. Keywords: Baculovirus; γ-carboxylase; Coagulation FVII; Factor VII; Insect cel

Temperature and wavelength drift tolerant WDM transmission and routing in on-chip silicon photonic interconnects

We demonstrate a temperature and wavelength shift resilient silicon transmission and routing interconnect system suitable for multi-socket interconnects, utilizing a dual-strategy CLIPP feedback circuitry that safeguards the operating point of the constituent photonic building blocks along the entire on-chip transmission-multiplexing-routing chain. The control circuit leverages a novel control power-independent and calibration-free locking strategy that exploits the 2nd derivative of ring resonator modulators (RMs) transfer function to lock them close to the point of minimum transmission penalty. The system performance was evaluated on an integrated Silicon Photonics 2-socket demonstrator, enforcing control over a chain of RM-MUX-AWGR resonant structures and stressed against thermal and wavelength shift perturbations. The thermal and wavelength stress tests ranged from 27 degrees C to 36 degrees C and 1309.90 nm to 1310.85 nm and revealed average eye diagrams Q-factor values of 5.8 and 5.9 respectively, validating the system robustness to unstable environments and fabrication variations. (C) 2022 Optica Publishing Group under the terms of the Optica Open Access Publishing Agreemen

Inhibition of Notch pathway arrests PTEN-deficient advanced prostate cancer by triggering p27-driven cellular senescence.

Activation of NOTCH signalling is associated with advanced prostate cancer and treatment resistance in prostate cancer patients. However, the mechanism that drives NOTCH activation in prostate cancer remains still elusive. Moreover, preclinical evidence of the therapeutic efficacy of NOTCH inhibitors in prostate cancer is lacking. Here, we provide evidence that PTEN loss in prostate tumours upregulates the expression of ADAM17, thereby activating NOTCH signalling. Using prostate conditional inactivation of both Pten and Notch1 along with preclinical trials carried out in Pten-null prostate conditional mouse models, we demonstrate that Pten-deficient prostate tumours are addicted to the NOTCH signalling. Importantly, we find that pharmacological inhibition of γ-secretase promotes growth arrest in both Pten-null and Pten/Trp53-null prostate tumours by triggering cellular senescence. Altogether, our findings describe a novel pro-tumorigenic network that links PTEN loss to ADAM17 and NOTCH signalling, thus providing the rational for the use of γ-secretase inhibitors in advanced prostate cancer patients

Down syndrome-recent progress and future prospects

Down syndrome (DS) is caused by trisomy of chromosome 21 (Hsa21) and is associated with a number of deleterious phenotypes, including learning disability, heart defects, early-onset Alzheimer's disease and childhood leukaemia. Individuals with DS are affected by these phenotypes to a variable extent; understanding the cause of this variation is a key challenge. Here, we review recent research progress in DS, both in patients and relevant animal models. In particular, we highlight exciting advances in therapy to improve cognitive function in people with DS and the significant developments in understanding the gene content of Hsa21. Moreover, we discuss future research directions in light of new technologies. In particular, the use of chromosome engineering to generate new trisomic mouse models and large-scale studies of genotype-phenotype relationships in patients are likely to significantly contribute to the future understanding of DS