The corner failure in a masonry building damaged by the 2016-2017 Central Italy earthquake sequence

Although still poorly investigated, the failure of corners is a frequent event in masonry buildings and clearly recognizable in the aftermath of a seismic event. It is characterized by the formation of a masonry wedge, mainly due to the thrust of roof elements in addition to inertial forces, and it generally involves rocking-sliding motion along the cracks on the interlocked orthogonal walls. In this paper, the case study of the corner failure in a masonry building located in Visso (Italy) is analyzed. The building was seriously damaged by the seismic events of August 24th, 2016 and October 26th and 30th, 2016. In particular, one of the free corners at the first storey completely collapsed. The seismic capacity with respect to the onset of this failure mode is analyzed by means of a refined macro-block model and by adopting the linear kinematic approach of limit analysis, accounting for frictional resistances and the thrust of roof elements. The key aspect of the proposed approach is the introduction of a criterion to evaluate the contribution of the actual frictional resistances depending on the inclination angles of the crack lines. Moreover, the loads transmitted from the roof to the walls are defined by assuming simplified static conditions according to the typology of the hipped roof. Lastly, the achieved results are compared to the seismic demand obtained by adopting the Italian Technical Standards for Constructions, both the earlier version (2008) and the current one (2018), together with that obtained using in situ recorded floor accelerations

Homozygous mutation in the prokineticin-receptor2 gene (Val274Asp) presenting as reversible Kallmann syndrome and persistent oligozoospermia: case report.

Prokineticin 2 (Prok2) or prokineticin-receptor2 (Prok-R2) gene mutations are associated with Kallmann syndrome (KS). We describe a new homozygous mutation of Prok-R2 gene in a man displaying KS with an apparent reversal of hypogonadism. The proband, offspring of consanguineous parents, presented at age 19 years with absent puberty, no sense of smell, low testosterone and gonadotrophin levels. Magnetic resonance imaging showed olfactory bulb absence. The patient achieved virilization and spermatogenesis with gonadotrophin administration. Two years after discontinuing hormonal therapy, he maintained moderate oligozoospermia and normal testosterone levels. Prok2 and Prok- R2 gene sequence analyses were performed. The proband had a homozygous mutation in Prok-R2 exon 2 that harbours the c.T820>A base substitution, causing the introduction of an aspartic acid in place of valine at position 274 (Val274Asp). His mother had the same mutation in heterozygous state. This report describes a novel homozygous mutation of Prok-R2 gene in a man with variant KS, underlying the role of Prok-R2 gene in the olfactory and reproductive system development in humans. Present findings indicate that markedly delayed activation of gonadotrophin secretion may occur in some KS cases with definite gene defects, and that oligozoospermia might result from a variant form of reversible hypogonadotrophic hypogonadism

Autologous Fat Grafting Reduces Pain in Irradiated Breast: A Review of Our Experience

Introduction. Pain syndromes affect women after conservative and radical breast oncological procedures. Radiation therapy influences their development. We report autologous fat grafting therapeutical role in treating chronic pain in irradiated patients. Materials and Methods. From February 2006 to November 2014, we collect a total of 209 patients who meet the definition of "Postmastectomy Pain Syndrome" (PMPS) and had undergone mastectomy with axillary dissection (113 patients) or quadrantectomy (96 patients). Both procedures were followed by radiotherapy. We performed fat grafting following Coleman's procedure. Mean amount of adipose tissue injected was 52\u2009cc (\ub18.9\u2009cc) per breast. Seventy-eight in 209 patients were not treated surgically and were considered as control group. Data were gathered through preoperative and postoperative VAS questionnaires; analgesic drug intake was recorded. Results. The follow-up was at 12 months (range 11.7-13.5 months). In 120 treated patients we detected pain decrease (mean \ub1 SD point reduction, 3.19 \ub1 2.86). Forty-eight in 59 patients stopped their analgesic drug therapy. Controls reported a mean \ub1 SD decrease of pain of 1.14 \ub1 2.72. Results showed that pain decreased significantly in patients treated (p < 0.005, Wilcoxon rank-sum test). Conclusion. Our 8-year experience confirms fat grafting effectiveness in decreasing neuropathic pain

Antinociceptive effects of tetrazole inhibitors of endocannabinoid inactivation: Cannabinoid and non-cannabinoid receptor-mediated mechanisms

Background and purpose: Tetrazoles were recently developed as inhibitors of the cellular uptake of the endocannabinoid anandamide or of its hydrolysis by fatty acid amide hydrolase (FAAH), but were proposed to act also on non-endocannabinoid-related serine hydrolases. Experimental approach: We tested, in a model of inflammatory pain induced in mice by formalin, five chemically similar inhibitors: (i) OMDM119 and OMDM122, two potent carbamoyl tetrazole FAAH inhibitors with no effect on anandamide uptake; (ii) LY2183240, a carbamoyl tetrazole with activity as both FAAH and uptake inhibitor; (iii) OMDM132, a non-carbamoyl tetrazole with activity only as uptake inhibitor and iv) OMDM133, a non-carbamoyl tetrazole with no activity at either FAAH or uptake. Results: All compounds (2.5-10 mg kg -1, i.p.) inhibited the second phase of the nocifensive response induced by intraplantar injection of formalin. The effects of OMDM119, OMDM122 and OMDM133 were not antagonized by pretreatment with cannabinoid CB 1 receptor antagonists, such as rimonabant or AM251 (1-3 mg kg -1, i.p.). The effects of LY2183240 and OMDM132 were fully or partially antagonized by rimonabant, respectively, and the latter compound was also partly antagonized by the CB 2 receptor antagonist, AM630. Conclusions and implications: (i) non-FAAH hydrolases might be entirely responsible for the antinociceptive activity of some, but not all, tetrazole FAAH inhibitors, (ii) the presence of a carbamoylating group is neither necessary nor sufficient for such compounds to act through targets other than FAAH and (iii) inhibition of anandamide uptake is responsible for part of this antinociceptive activity, independently of effects on FAAH. © 2008 Macmillan Publishers Limited All rights reserved

MIRA: a Multiphysics Approach to Designing a Fusion Power Plant

Fusion systems codes (SCs) are deployed to produce the baseline of the European fusion power reactor (DEMO) within its conceptual design. A DEMO baseline is mostly defined by a radial/vertical reactor sketch and major reactor parameters, such as fusion and net electric power, magnetic fields, and plasma burn time. A baseline shall also meet a set of prescribed reactor requirements, constraints, and architectural features. According to the conceptual design workflow implemented within the EU-DEMO programme, the output from the SC is transferred to the detailed physics and engineering design codes. Presently-available fusion SCs rely on rather basic physics and engineering models (mostly at zero or one-dimensional level). The design codes, instead, are very detailed but run on much longer computing times. To fill the gap between systems and design codes, the multi-fidelity systems/design tool modular integrated reactor analysis (MIRA)—has been recently developed. MIRA incorporates the physics and the engineering insights of the utmost domains of tokamak reactors and relies on a higher spatial resolution, spanning from 1D up to 3D modelling frames. The MIRA approach has been applied to the DEMO 2017 baseline, generated by the EU reference SC PROCESS and used as input to MIRA. In the paper, the architectural and mathematical insights of the MIRA package are described, along with an EU-DEMO 2017 baseline analysis

SIRT3 Modulates Endothelial Mitochondrial Redox State during Insulin Resistance

Emerging evidence indicates that defects in sirtuin signaling contribute to impaired glucose and lipid metabolism, resulting in insulin resistance (IR) and endothelial dysfunction. Here, we examined the effects of palmitic acid (PA) treatment on mitochondrial sirtuins (SIRT2, SIRT3, SIRT4, and SIRT5) and oxidative homeostasis in human endothelial cells (TeloHAEC). Results showed that treatment for 48 h with PA (0.5 mM) impaired cell viability, induced loss of insulin signaling, imbalanced the oxidative status (p &lt; 0.001), and caused negative modulation of sirtuin protein and mRNA expression, with a predominant effect on SIRT3 (p &lt; 0.001). Restoration of SIRT3 levels by mimic transfection (SIRT3+) suppressed the PA-induced autophagy (mimic NC+PA) (p &lt; 0.01), inflammation, and pyroptosis (p &lt; 0.01) mediated by the NLRP3/caspase-1 axis. Moreover, the unbalanced endothelial redox state induced by PA was counteracted by the antioxidant δ-valerobetaine (δVB), which was able to upregulate protein and mRNA expression of sirtuins, reduce reactive oxygen species (ROS) accumulation, and decrease cell death. Overall, results support the central role of SIRT3 in maintaining the endothelial redox homeostasis under IR and unveil the potential of the antioxidant δVB in enhancing the defense against IR-related injuries