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This paper is devoted to a brief presentation of the main results obtained within the FREEDAM research project. The project has been completed and, recently, also the dissemination of the results has reached the finish line. The project was devoted to the development of low-damage beam-to-column connections based on the use of friction dampers conceived to substitute the traditional dissipative zones of moment-resisting frames, i.e. the beam ends. The conception of these innovative connections is presented and the experimental tests carried out at the University of Salerno during the FREEDAM project are summarized dealing with the friction dampers, the beam-to-column joints sub-assemblages and the seismic simulation of a real scale one-bay two-storey building with the pseudo-dynamic testing method. Finally, the design procedures for seismic-resistant steel frames equipped with such connections are presented in the framework of Eurocode 8 and according to TPMC., Freedam Plus RFCS Project

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

The growing incidence of degenerative musculoskeletal disorders as well as lifestyle changes has led to an increase in the surgical procedures involving implanted medical devices in orthopedics. When studying implant/tissue interface in hard materials (i.e., metals or dense plastics) and/or in large bone segments, the hard plastic embedding of the intact undecalcified tissue envelope with the implant in situ is needed. The aim of this work is to describe the advances and the possibilities of high-temperature methyl methacrylate (MMA) embedding for the histological, histomorphometrical, and biomechanical assessment of bone-implanted medical devices. Unlike routine techniques, undecalcified bone processing histology, using high-temperature MMA, requires a complex and precise sample processing methodology and the availability of sophisticated equipment and software for both sample preparation and analyses. MMA embedding permits the evaluation of biological responses to the presence of implanted medical devices without implant removal, allowing simultaneous qualitative and quantitative histological evaluation, both static and dynamic histomorphometry, and biomechanical analyses not possible with tissue decalcification. MMA embedding, despite being a demanding procedure, is still preferred to other kinds of resin-based embedding because of its peculiar characteristics, which allow the study of samples of big dimensions also implanted with hard materials without reducing the sample or removing the material. Dynamic measurements are allowed together with biomechanical investigations at the bone-biomaterial interface, obtaining a comprehensive and precise evaluation of the safety and effectiveness of medical devices for orthopedic regenerative, reconstructive, and reparative surgery.

Background & Aims The guidelines of the European Society of Pediatric Gastroenterology, Hepatology, and Nutrition allow for diagnosis of celiac disease without biopsies in children with symptoms and levels of immunoglobulin A against tissue-transglutaminase (TGA-IgA) 10-fold or more the upper limit of normal (ULN), confirmed by detection of endomysium antibodies (EMA) and positivity for HLA-DQ2/DQ8. We performed a large, international prospective study to validate this approach. Methods We collected data from consecutive pediatric patients (18 years or younger) on a gluten-containing diet who tested positive for TGA-IgA from November 2011 through May 2014, seen at 33 pediatric gastroenterology units in 21 countries. Local centers recorded symptoms; measurements of total IgA, TGA, and EMA; and histopathology findings from duodenal biopsies. Children were considered to have malabsorption if they had chronic diarrhea, weight loss (or insufficient gain), growth failure, or anemia. We directly compared central findings from 16 antibody tests (8 for TGA-IgA, 1 for TGA-IgG, 6 for IgG against deamidated gliadin peptides, and 1 for EMA, from 5 different manufacturers), 2 HLA-DQ2/DQ8 tests from 2 manufacturers, and histopathology findings from the reference pathologist. Final diagnoses were based on local and central results. If all local and central results were concordant for celiac disease, cases were classified as proven celiac disease. Patients with only a low level of TGA-IgA (threefold or less the ULN) but no other results indicating celiac disease were classified as no celiac disease. Central histo-morphometry analyses were performed on all other biopsies and cases were carefully reviewed in a blinded manner. Inconclusive cases were regarded as not having celiac disease for calculation of diagnostic accuracy. The primary aim was to determine whether the nonbiopsy approach identifies children with celiac disease with a positive predictive value (PPV) above 99% in clinical practice. Secondary aims included comparing performance of different serological tests and to determine whether the suggested criteria can be simplified. Results Of 803 children recruited for the study, 96 were excluded due to incomplete data, low level of IgA, or poor-quality biopsies. In the remaining 707 children (65.1% girls; median age, 6.2 years), 645 were diagnosed with celiac disease, 46 were found not to have celiac disease, and 16 had inconclusive results. Findings from local laboratories of TGA-IgA 10-fold or more the ULN, a positive result from the test for EMA, and any symptom identified children with celiac disease (n = 399) with a PPV of 99.75 (95% confidence interval [CI], 98.61–99.99); the PPV was 100.00 (95% CI, 98.68–100.00) when only malabsorption symptoms were used instead of any symptom (n = 278). Inclusion of HLA analyses did not increase accuracy. Findings from central laboratories differed greatly for patients with lower levels of antibodies, but when levels of TGA-IgA were 10-fold or more the ULN, PPVs ranged from 99.63 (95% CI, 98.67–99.96) to 100.00 (95% CI, 99.23–100.00). Conclusions Children can be accurately diagnosed with celiac disease without biopsy analysis. Diagnosis based on level of TGA-IgA 10-fold or more the ULN, a positive result from the EMA tests in a second blood sample, and the presence of at least 1 symptom could avoid risks and costs of endoscopy for more than half the children with celiac disease worldwide. HLA analysis is not required for accurate diagnosis. Clinical Trial Registration no: DRKS00003555. © 2017 AGA Institute

AIM: Laparoscopic adrenalectomy is considered the standard technique for the surgical removal of the adrenal gland. This report is about a 4-year single experience in our Endocrine and General Surgery Unit with laparoscopic adrenalectomy. METHODS: A total of 24 lateral transperitoneal laparoscopic adrenalectomies were performed. The indications for laparoscopic surgery were: aldosteronoma in 3 patients, pheochromocytoma in 6 patients, nonfunctioning adenoma in 6 patients, adenoma causing Cushing’s syndrome in 3 patients, 1 lymphangioma-like adenomatoid tumor, 1 myelolipoma, 1 complicated adrenal cyst, 2 adrenocortical carcinomas, 1 lung metastasis. RESULTS: All except two had successful laparoscopic adrenalectomy. Complication occurred in one patient. 3 patients underwent other associated laparoscopic procedures. Operative time ranged from 100 to 240 minutes for laparoscopic adrenalectomy, from 180 to 210 minutes in the cases with two associated laparoscopic procedures, 5 hours for bilateral adrenalectomy; the postoperative hospital stay for laparoscopic adrenalectomy ranged from 4 to 8 days (6,79 days) and from 7 to 13 days (9,12 days) for patients undergoing the open or converted procedure. CONCLUSIONS: Laparoscopic adrenalectomy is technically feasible and reproducible. We evaluate the effectiveness of laparoscopic adrenalectomy for a variety of endocrine disorders except in the case of invasive carcinoma or large masses. “Antonio Cardarelli” Endocrine and General Surgery Unit in Naples is known as a specialized center for thyroid and parathyroid surgery; in future, we could also become a high-volume laparoscopic referral center for adrenal gland pathologies.

Background: Gliadins, a family of wheat proteins, are central to the pathogenesis of celiac disease (CD). In addition to 'immunogenic' effects, gliadin directly affects cultured cells and intestine preparations, and produces damage in vivo, via a separate 'toxic' peptide, such as A-gliadin p31-43 (P31-43). Aims: Understanding the molecular mechanisms underlying direct non T-cell mediated effects of gliadin peptides, and assessing their potential role in promoting CD. Method: Gliadin effects were tested on a number of cell lines and on cultured mucosa samples by evaluating cytoskeleton rearrangements, endocytosis, proliferation and apoptosis. Standard biochemical methods were used to assess prolonged epidermal growth factor receptor (EGFR) activation. Results: Crude gliadin peptic-tryptic peptides [PTG], or P31-43 alone, fully reproduce the effects of epidermal growth factor [EGF] on actin cytosketon, cell cycle and cell proliferation of various cell lines. Inhibitor studies demonstrate the role of EGFR in the early response to gliadin exposure, pointing to activation of the EGFR pathway. Peptide P31-43 is not similar to any EGFR ligand, but can delay inactivation of the EGFR interfering with its endocytosis. Gliadin-induced delay of EGFR endocytosis in cultured intestinal biopsies, together with S-phase entry of epithelial intestinal cells, confirm a role for EGFR activation in CD. Conclusion: The ability of gliadin peptides to delay EGFR inactivation through interference with the endocytic pathway suggests a model where gliadin fragments amplify the effects of trace amounts of EGF, and possibly of other growth factors, by prolonging receptor activation. The results, using cultures of coeliac intestinal biopsies, highlight the role of the EGF pathway in establishing and maintaining the typical atrophic and proliferative alterations of the small intestine in CD.

The intravenous administration of 12 μg Buserelin acetate (GnRH) causes a ready pituitary response, increasing LH and FSH levels. However, only 57.1% of treated buffaloes show a significative increase of progesterone blood levels (Neglia et al., 2005). The aim of this study was to verify the follicular diameter and the incidence of ovulations after the treatment with GnRH or hCG, performed on day 26 of pregnancy. The trial was carried out between January and March on 109 pluriparous buffaloes (DIM =163 ± 75 days). The animals were synchronized by using the Ovsynch-TAI Program. Buffaloes diagnosed pregnant by ultrasound on day 25 after AI, were randomly assigned in two treatment groups GnRH (12 μg of Buserelin Acetate i.m) and HCG (1000 I.U. i.m.) after measurements of follicular diameter. Two days after treatment the ovulation was evaluated by ultrasound of the ovaries and on day 45 of pregnancy it was verified the presence of an accessory corpus luteum. Differences between the follicular diameters of responsive and not responsive buffaloes were tested by ANOVA. The incidences of animals which responded to the two treatments were analysed by chi square test. No significant differences between the two treatments were found in terms of ovulatory response, which was present in 57.3% of animals. The mean follicular diameter which results sensible to the hormonal treatment was 8.9mm (Table 1) in both treatments, with varying between 4.2 and 1.3 mm. It is interesting to observe that the dimensions of the follicles recorded in buffaloes responsive to the treatments were similar to those of buffaloes in which ovulation did not occurr. These data are in accordance with those reported in bibliography in buffalo and in cattle regarding the incidence of subjects responsive to the treatment with GnRH and the dimensions of responsive follicles. In conclusion, the treatment with GnRH or HCG may be utilised in order to induce the formation of an accessory corpus luteum and, hence, to increase P4 levels, which are critical for maintaining the gestation.

BACKGROUND AND OBJECTIVES: Damage to intestinal mucosa in celiac disease (CD) is mediated both by inflammation due to adaptive and innate immune responses, with IL-15 as a major mediator of the innate immune response, and by proliferation of crypt enterocytes as an early alteration of CD mucosa causing crypts hyperplasia. We have previously shown that gliadin peptide P31-43 induces proliferation of cell lines and celiac enterocytes by delaying degradation of the active epidermal growth factor receptor (EGFR) due to delayed maturation of endocytic vesicles. IL-15 is increased in the intestine of patients affected by CD and has pleiotropic activity that ultimately results in immunoregulatory cross-talk between cells belonging to the innate and adaptive branches of the immune response. Aims of this study were to investigate the role of P31-43 in the induction of cellular proliferation and innate immune activation. METHODS/PRINCIPAL FINDINGS: Cell proliferation was evaluated by bromodeoxyuridine (BrdU) incorporation both in CaCo-2 cells and in biopsies from active CD cases and controls. We used real-time PCR to evaluate IL-15 mRNA levels and FACS as well as ELISA and Western Blot (WB) analysis to measure protein levels and distribution in CaCo-2 cells. Gliadin and P31-43 induce a proliferation of both CaCo-2 cells and CD crypt enterocytes that is dependent on both EGFR and IL-15 activity. In CaCo-2 cells, P31-43 increased IL-15 levels on the cell surface by altering intracellular trafficking. The increased IL-15 protein was bound to IL15 receptor (IL-15R) alpha, did not require new protein synthesis and functioned as a growth factor. CONCLUSION: In this study, we have shown that P31-43 induces both increase of the trans-presented IL-15/IL5R alpha complex on cell surfaces by altering the trafficking of the vesicular compartments as well as proliferation of crypt enterocytes with consequent remodelling of CD mucosa due to a cooperation of IL-15 and EGFR