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Rough scad Trachurus lathami is a key pelagic fish in the Argentinean continental shelf (ACS, south-west Atlantic Ocean), with recent increases in abundance. It is a main prey of fishes and marine mammals, and shares the environment with commercially relevant pelagic species (Engraulis anchoita and Scomber colias), playing an important role linking lower and upper trophic levels in the ecosystem. This study aims to determine the ontogenetic changes in the diet composition, feeding strategy, trophic niche breadth and trophic level of T. lathami in the North Patagonian Shelf (43°-45°30'S). The stomach contents of adult fish (n = 238) were analysed. The results suggest a clear ontogenetic shift in the diet at a size of ~190 mm. Smaller individuals (160-190 mm) were specialized on misidaceans, and showed the highest trophic level, while larger T. lathami (221-230 mm) consumed decapods (Peisos petrunkevitchi) and teleosts (eggs and larvae). Trophic niche breadth was higher at the medium-sized class (191-220 mm), which mainly preyed on copepods (Calanoides carinatus) and chaetognaths (Sagitta spp.), evidencing a more diverse diet and a rather generalist strategy. Updated information on the trophic ecology of T. lathami evidences its extremely plastic feeding behaviour, being able to adapt its trophic niche to the most readily available food items from the mesopelagic community.

Recent studies revealed that molecular events related with the physiology and pathology of αS might be regulated by specific sequence motifs in the primary sequence of αS. The importance of individual residues in these motifs remains an important open avenue of investigation. In this work, we have addressed the structural details related to the amyloid fibril assembly and lipid-binding features of αS through the design of site-directed mutants at position 39 of the protein and their study by in vitro and in vivo assays. We demonstrated that aromaticity at position 39 of αS primary sequence influences strongly the aggregation properties and the membrane-bound conformations of the protein, molecular features that might have important repercussions for the function and dysfunction of αS. Considering that aggregation and membrane damage is an important driver of cellular toxicity in amyloid diseases, future work is needed to link our findings with studies based on toxicity and neuronal cell death. BRIEF STATEMENT OUTLINING SIGNIFICANCE: Modulation by distinct sequential motifs and specific residues of αS on its physiological and pathological states is an active area of research. Here, we demonstrated that aromaticity at position 39 of αS modulates the membrane-bound conformations of the protein, whereas removal of aromatic functionality at position 39 reduces strongly the amyloid assembly in vitro and in vivo. Our study provides new evidence for the modulation of molecular events related with the physiology and pathology of αS.

Let PG$(\mathbb{F}_q^v)$ be the $(v-1)$-dimensional projective space over $\mathbb{F}_q$ and let $\Gamma$ be a simple graph of order ${q^k-1\over q-1}$ for some $k$. A 2$-(v,\Gamma,\lambda)$ design over $\mathbb{F}_q$ is a collection $\cal B$ of graphs (\textit{blocks}) isomorphic to $\Gamma$ with the following properties: the vertex set of every block is a subspace of PG$(\mathbb{F}_q^v)$; every two distinct points of PG$(\mathbb{F}_q^v)$ are adjacent in exactly $\lambda$ blocks. This new definition covers, in particular, the well known concept of a 2$-(v,k,\lambda)$ design over $\mathbb{F}_q$ corresponding to the case that $\Gamma$ is complete. In this work of a foundational nature we illustrate how difference methods allow us to get concrete non-trivial examples of $\Gamma$-decompositions over $\mathbb{F}_2$ or $\mathbb{F}_3$ for which $\Gamma$ is a cycle, a path, a prism, a generalized Petersen graph, or a Moebius ladder. In particular, we will discuss in detail the special and very hard case that $\Gamma$ is complete and $\lambda=1$, i.e., the Steiner 2-designs over a finite field. Also, we briefly touch the new topic of near resolvable 2-$(v,2,1)$ designs over $\mathbb{F}_q$. This study has led us to some (probably new) collateral problems concerning difference sets. Supported by multiple examples, we conjecture the existence of infinite families of $\Gamma$-decompositions over a finite field that can be obtained by suitably labeling the vertices of $\Gamma$ with the elements of a Singer difference set.

BACKGROUND Reliable preprocedural risk scores for the prediction of Contrast-Induced Acute Kidney Injury (CI-AKI) following Percutaneous Coronary Intervention (pPCI) in patients with ST-elevation myocardial infarction (STEMI) are lacking. Aim of this study was to derive and validate a preprocedural Risk Score in this setting. METHODS Two prospectively enrolled patient cohorts were used for derivation and validation (n = 3,736). CI-AKI was defined as creatinine increase ≥0.5 mg/dl 75 years, anterior MI (3 points), Killip class IV (4 points), estimated GFR

Following the discovery of the involvement of the ribonucleoprotein TDP-43 in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD), a major research focus has been to develop treatments that can prevent or alleviate these disease conditions. One pharmacological approach has been to use TDP-43-based disease models to test small molecules and drugs already known to have some therapeutic effect in a variety of neurodegenerative conditions. In parallel, various disease models have been used to perform high-throughput screens of drugs and small compound libraries. The aim of this review will be to provide a general overview of the compounds that have been described to alter pathological characteristics of TDP-43. These include expression levels, cytoplasmic mis-localization, post-translational modifications, cleavage, stress granule recruitment and aggregation. In parallel, this review will also address the use of compounds that modify the autophagic/proteasome systems that are known to target TDP-43 misfolding and aggregation. LINKED ARTICLES: This article is part of a themed issue on Neurochemistry in Japan. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.6/issuetoc.

Small pelagic fishes are used for human consumption, fishmeal and fish oil. They constitute 25% of global fish catch and have been of considerable conservation concern because of their intermediate position in aquatic food webs, often being a dominant dietary component of marine predators. This paper provides an overview of trends in abundance and fishing pressure on small pelagic fish stocks from single-species scientific assessments that constitute 60% of global small pelagic catch. While most individual stocks have exhibited wide variability in abundance (typical of small pelagics compared with other fish taxa), across stocks there has been remarkable stability in average fishing pressure and biomass since 1970. On average, since 1970, the biomass of assessed small pelagic stocks is estimated to have been slightly above the biomass that would produce maximum sustainable yield, but estimation of this quantity for highly fluctuating stocks is quite uncertain. There were significant differences among assessed regions, with the Mediterranean and Black Sea of greatest concern for high and growing fishing pressure. The 40% of global small pelagic fish catch not covered by single-species quantitative stock assessments since 1970 comes largely from Asia, where catches have continued to increase. At regional levels, the average abundance of assessed small pelagic fish is largely unrelated to average fishing pressure, which we argue results both from the portfolio effect, where numerous stocks fluctuate with little correlation in abundance, and from the short life span of small pelagics coupled with recruitment largely independent of spawning abundance. publishedVersion

The guanine exchange factor subunit eEF1Bα encoded by the EEF1B2 gene belongs to the eukaryotic elongation translational machinery. Pathogen variants in genes of the translational machinery have been associated with several neurodevelopmental disorders. However, only one family of three siblings with intellectual disability (ID) has been reported so far with a homozygous variant in EEF1B2. Here, we report a second family with a novel homozygous loss of function (LoF) variant p.(Ser128*), carried by two siblings with moderate ID and seizures. Our findings confirm the role of EEF1B2 variants in the pathogenesis of autosomal-recessive ID, expand the variant spectrum and precisely describe the clinical consequences of the LoF of EEF1B2.

OBJECTIVE Research on retirement suggests that personality can influence the adjustment process, but the mechanisms involved remain still largely unknown. In the present study, we investigate direct and indirect associations between the Big Five personality traits and life satisfaction over the retirement transition. Indirect effects were evaluated through the role of personality for levels and changes in self-esteem, autonomy, social support, self-rated physical health, self-rated cognitive ability, and financial satisfaction. METHOD Our sample consisted of 796 older adults (age 60-66) and four annual measurement waves from the longitudinal population-based HEalth, Ageing, and Retirement Transitions in Sweden (HEARTS) study, including individuals retiring during the study period. RESULTS Results from multivariate latent growth curve analysis revealed multiple indirect associations between personality and life satisfaction. Extraversion, Agreeableness, and Conscientiousness were positively related to life satisfaction through higher levels of self-esteem, autonomy, and social support. Neuroticism was negatively associated with life satisfaction through lower levels of self-esteem and lower levels and negative changes in autonomy and social support. CONCLUSIONS Our findings suggest that retirees with higher levels of Neuroticism are more vulnerable in the transition process and they are also more likely to experience adjustment problems resulting from negative changes in key resources.

The 2012 Emilia earthquake (in Northern Italy) caused extensive damage to existing prefabricated reinforced concrete structures. These buildings were found being extremely vulnerable because, being designed for vertical loads only, they featured friction-based connections between structural elements, most commonly between beams and columns. Given the large diffusion of these structures, their seismic retrofit is critical. Various techniques have been proposed in the literature, in most of which friction-based connections are removed by inserting mechanical connectors that will make beam-column connections hinged. These approaches lead to a significant increase of the base shear and therefore require strengthening of columns. The paper presents dissipative devices based on carbon-wrapped steel tubes to be used as an alternative low-damage solution for the retrofit of beam-column connections. The first part of the paper presents results of experimental tests on the devices and discusses their dissipative behaviour. The succeeding parts of the paper present numerical analyses on simple structures reinforced with the proposed device. The results of the numerical study show how the introduction of the dissipative devices produces a significant reduction of forces transmitted to the structure, by comparing the seismic response of simple frame structures equipped with dissipative devices with the response of equivalent elastic systems.

Knowledge of skeletal muscle adaptations is important to understand the functional deficits in cerebral palsy (CP). This study aimed to investigate the morphofunctional characteristics of skeletal muscle in a CP animal model. Initially, pregnant Wistar rats were injected intraperitoneally with saline or lipopolysaccharide over the last five days of pregnancy. The control group (n = 8) consisted of male pups born to females injected with saline. The CP group (n = 8) consisted of male pups born to females injected with lipopolysaccharide, which were submitted to perinatal anoxia [day of birth, postnatal day 0 (P0)] and sensorimotor restriction (P1‐P30). The open‐field test was undertaken on P29 and P45. On P48, the animals were weighed, and the plantaris muscle was collected and its weight and length were measured. Transverse sections were stained with haematoxylin‐eosin, NADH‐TR, Masson's trichrome and non‐specific esterase reaction for analysis. and transmission electron microscopy was performed. In the CP group, reductions were observed in mobility time, number of crossings and rearing frequency, body weight, muscle weight and length, and nucleus‐to‐fibre and capillary‐to‐fibre ratios. There was a statistically significant increase in the percentage area of the muscle section occupied by collagen; reduction in the area and increase in the number of type I muscle fibres; increase in myofibrillar disorganization and Z‐line disorganization and dissolution; and reduction in the area and largest and smallest diameters of neuromuscular junctions. Thus this animal model of CP produced morphofunctional alterations in skeletal muscle, that were associated with evidence of motor deficits as demonstrated by the open‐field test.

Frontotemporal lobar degeneration (FTLD) is a group of disorders that principally affect the frontal and temporal lobes of the brain. In many parts of the world, FTLD is rapidly becoming a serious health burden on society and, as a result, the molecular mechanisms that underlie its onset and development have been the target of intense research efforts in recent years. Nonetheless, despite crucial pathological and genetic discoveries in this area much is still uncertain about how the many genes associated with this disease cause the observed neurodegeneration. Moreover, it has not been easy to define the molecular mechanisms that account for the clinical and pathological heterogeneity of the various FTLD subtypes, characterized by aggregates of Tau, TAR-DNA-Binding Protein-43 (TDP-43), and less often Fused in Sarcoma (FUS) protein. In this review, we will examine some of the emerging discoveries in this field: from the recent importance of autoimmunity to the presence of substantial variations in the composition and localization of TDP-43 and FUS brain aggregates in patients, and how they might affect the course of the disease. All together, these new results demonstrate how the observed clinical heterogeneity underlies considerable complexity at both the molecular and the disease pathway level. A better characterization of all this complexity will be essential for a more accurate stratification of patient cohorts for further studies and, eventually, for trials of therapy.

The consumption of whole-grain food—including pasta—has been increasing steadily. In the case of whole-grain pasta, given the many different producers, it seems important to have some objective parameters to define its overall quality. In this study, commercial whole-grain pasta samples representative of the Italian market have been characterized from both molecular and electronic-senses (electronic nose and electronic tongue) standpoint in order to provide a survey of the properties of different commercial samples. Only 1 pasta product showed very low levels of heat damage markers (furosine and pyrraline), suggesting that this sample underwent to low temperature dry treatment. In all samples, the furosine content was directly correlated to protein structural indices, since protein structure compactness increased with increasing levels of heat damage markers. Electronic senses were able to discriminate among pasta samples according to the intensity of heat treatment during the drying step. Pasta sample with low furosine content was discriminated by umami taste and by sensors responding to aliphatic and inorganic compounds. Data obtained with this multidisciplinary approach are meant to provide hints for identifying useful indices for pasta quality. Practical Application As observed for semolina pasta, objective parameters based on heat-damage were best suited to define the overall quality of wholegrain pasta, almost independently of compositional differences among commercial samples. Drying treatments of different intensity also had an impact on instrumental sensory traits that may provide a reliable alternative to analytical determination of chemical markers of heat damage in all cases where there is a need for avoiding time-consuming procedures.

Objective Vein of Galen aneurysmal malformation (VGAM) is a rare fetal anomaly, the neurological outcome of which can be good with appropriate perinatal management. However, most fetal series are too small to allow reliable statistical assessment of potential prognostic indicators. Our aim was to assess, in a two-center series of 49 cases, the prognostic value of several prenatal variables, in order to identify possible prenatal indicators of poor outcome, in terms of mortality and cerebral disability. Methods This was a retrospective study involving 49 cases of VGAM diagnosed prenatally and managed at two centers over a 17-year period (1999–2015). All cases had undergone detailed prenatal cerebral and cardiac assessment by grayscale ultrasound, color and pulsed-wave Doppler and magnetic resonance imaging (MRI). Ultrasound and MRI examination reports and images were reviewed and outcome information was obtained from medical reports. Volume of the VGAM (on ultrasound and MRI) was calculated and development of straight-sinus dilatation, ventriculomegaly and other major brain abnormalities was noted. Cardiothoracic ratio, tricuspid regurgitation and reversed blood flow across the aortic isthmus were evaluated on fetal echocardiography. Major brain lesions were considered by definition to be associated with poor outcome in all cases. Pregnancy and fetoneonatal outcome were known in all cases. Fetoneonatal outcome and brain damage were considered as dependent variables in the statistical evaluation. Poor outcome was defined as death, late termination of pregnancy due to association with related severe brain anomalies or severe neurological impairment. Results At a mean follow-up time of 20 (range, 0–72) months, 36.7% of the whole series and 52.9% of the cases which did not undergo late termination were alive and free of adverse sequelae. Five (10.2%) cases showed progression of the lesion between diagnosis and delivery. On univariate analysis, dilatation of the straight sinus, VGAM volume ≥ 20 000 mm3 and tricuspid regurgitation were all significantly related to poor outcome. However, on logistic regression analysis, the only variables associated significantly with poor outcome were tricuspid regurgitation and, to a lesser extent, VGAM volume ≥ 20 000 mm3. The former was also the only variable associated with brain damage. Conclusions Major brain lesions, tricuspid regurgitation and, to a lesser extent, VGAM volume ≥ 20 000 mm3 are the only prenatal variables associated with poor outcome in fetal VGAM. Prenatal multidisciplinary counseling should be based on these variables. Copyright © 2016 ISUOG. Published by John Wiley & Sons Ltd.

Handling a life-supporting yet redox-active metal like iron represents a significant challenge to cells and organisms that must not only tightly balance intra- and extracellular iron concentrations but also chaperone it during its journey from its point of entry to final destinations, to prevent inappropriate generation of damaging reactive oxygen species. Accordingly, regulatory mechanisms have been developed to maintain appropriate cellular and body iron levels. In intracellular compartments, about 95% of iron is protein-bound and the expression of the major proteins of iron metabolism is controlled by an integrated and dynamic system involving multilayered levels of regulation. However, dysregulation of iron homeostasis, which could result from both iron-related and unrelated effectors, may occur and have important pathological consequences in a number of human disorders. In this review, we describe the current understanding of the mechanisms that keep cellular iron balance and outline recent advances that increased our knowledge of the molecular physiology of iron metabolism. © 2017 IUBMB Life, 69(6):389-398, 2017.