88,514 research outputs found
Mario Salvadori Engineer
No full textbiografia di Mario Salvadori ingegnere italiano vissuto a New Yor
On a 3D crack tracking algorithm and its variational nature.
No full textThe crack propagation problem for linear elastic fracture mechanics has been studied by several authors exploiting its analogy with standard dissipative systems theory (see e.g. Nguyen (2000), Mielke (2005) and Francfort and Marigo (1998)). In recent publications Salvadori and Carini (2011) and Salvadori and Fantoni (2013) minimum theorems were derived in terms of crack tip “quasi static velocity” for two- and three-dimensional fracture mechanics. They were reminiscent of Ceradini's theorem Ceradini (1965, 1966) in plasticity.
Such an incremental picture naturally leads to explicit methods for integration in time, with well know drawbacks in terms of accuracy and stability. The present work introduces an implicit Newton–Raphson based crack tracking algorithm which is endowed with a variational formulation
Weight function theory and variational formulations for three-dimensional plane elastic cracks advancing
No full textThe weight function theory for three-dimensional elastic crack analysis received great attention after the
work of Rice (1985, 1989). Several applications have been considered since then, particularly in the context
of configurational stability, crack path prediction, stress intensity factor expansions, perturbation
approaches. In all cases, a specific hypothesis has been made on the variation of crack shape, in order
to formulate the problem in terms of Cauchy principal value. In the present note, such hypothesis is further
investigated and consequences discussed. A variational statement given in Salvadori and Fantoni
(2013a) is thus rephrased in terms of weight functions. Its discrete formulation shows the potential to
accurate approximation of crack front propagation
Minimum theorems in 3D incremental linear elastic fracture mechanics
No full textThe crack propagation problem for linear elastic fracture mechanics has been studied by several authors exploiting its analogy with standard dissipative systems theory (see e.g. Nguyen in Appl Mech Rev 47, 1994, Stability and nonlinear solid mechanics. Wiley, New York, 2000; Mielke in Handbook of differential equations, evolutionary equations. Elsevier, Amsterdam, 2005; Bourdin et al. in The variational approach to fracture. Springer, Berlin, 2008). In a recent publication (Salvadori and Carini in Int J Solids Struct 48:1362–1369, 2011) minimum theorems were derived in terms of crack tip “quasi static velocity” for two-dimensional fracture mechanics. They were reminiscent of Ceradini’s theorem (Ceradini in Rendiconti Istituto Lombardo di Scienze e Lettere A99, 1965, Meccanica 1:77–82, 1966) in plasticity. Following the cornerstone work of Rice (1989) on weight function theories, Leblond et al. (Leblond in Int J Solids Struct 36:79–103, 1999; Leblond et al. in Int J Solids Struct 36:105–142, 1999) proposed asymptotic expansions for stress intensity factors in three dimensions—see also Lazarus (J Mech Phys Solids 59:121–144, 2011). As formerly in 2D, expansions can be given a Colonnetti’s decomposition (Colonnetti in Rend Accad Lincei 5, 1918, Quart Appl Math 7:353–362, 1950) interpretation. In view of the expression of the expansions proposed in Leblond (Int J Solids Struct 36:79–103, 1999), Leblond et al. (Int J Solids Struct 36:105–142, 1999) however, symmetry of Ceradini’s theorem operators was not evident and the extension of outcomes proposed in Salvadori and Carini (Int J Solids Struct 48:1362–1369, 2011) not straightforward. Following a different path of reasoning, minimum theorems have been finally derived
Zosterops novae subsp. guineae Salvadori 1878
No full textZosterops novae guineae Salvadori, 1878 Annali del Museo civico di Storia naturale di Genova, 1878 (12): 341. Current name: Zosterops novaeguineae novaeguineae Salvadori, 1878. Syntype NHMO-BI-86649 [I019616]; Study skin; F; Antonie Augustus Bruijn (b), June 1874; Indonesia: Arfak [Arfak Mountains]; 1.083° S 133.967° E; 16a. Remarks: This specimen was received from Genoa in 1888 and is indicated as ‘tipico’ in the accompanying list (see discussion of Melanocharis chloroptera above). The original label is not present, only a replacement label that has been added at NHMO (Figure 6c). Salvadori (1878) did not specify an exact number of specimens in his original publication, but in Salvadori (1881), he listed eight specimens (a–h) as types of the species. Based on the information available on the current label, the NHMO specimen corresponds to specimen b. Salvadori spelled the specific epithet in two words, ‘ novae guineae’, in both of the mentioned publications, but in accordance with article 32.5.2.2 of the Code (International Commission on Zoological Nomenclature 1999) it has later been changed to the current ‘novaeguineae’. Three other syntypes are in MSNG (C.E. 11526–11528; Arbocco et al. 1979), corresponding to specimens e, g and h in Salvadori (1881), and in MRSN specimen a is registered as MZUT Av4174 (Aimassi et al. 2020; Giorgio Aimassi, pers. comm.). A fifth specimen is in RMNH (RMNH 90782, collected by Bruijn in Arfak, 30 January 1876; Dekker & Quaisser 2006). This was not listed by Salvadori (1881), but as Salvadori in his original description wrote that he had examined several specimens collected by Beccari and Bruijn in the Arfak mountains, also this RMNH specimen must be considered part of the type series.Published as part of Johannessen, Lars Erik & Lifjeld, Jan T., 2022, Type specimens of birds in the Natural History Museum, University of Oslo, Norway, pp. 451-486 in Zootaxa 5150 (4) on pages 469-470, DOI: 10.11646/zootaxa.5150.4.1, http://zenodo.org/record/662675
Sertoli cell-secreted factors have promyogenic and antifibrotic properties on human DMD myoblasts with different mutations.
No full textDuchenne muscular dystrophy (DMD) is a recessive X-linked lethal disease affecting one over 5,000 live male births in which mutations in the dystrophin gene (DMD) lead to lack of a functional protein resulting in susceptibility of myofibers to rupture during contraction. Muscles of DMD patients or experimental models of DMD show progressive necrosis of the myofibers, chronic inflammation and reactive regeneration, which lead to exhaustion of muscle precursor cell pool and replacement of myofibers with fibrous and fatty tissues.1 Although multiple therapeutic approaches have been explored in the last decades and are still under investigation, the standard therapy to DMD remains the use of glucocorticoids despite their limited efficacy and undesired side effects.2 We set up a preclinical approach based on the peculiar properties of Sertoli cells (SeC)3,4 a cell type of the seminiferous tubules of the testis in which they favor the maturation of developing germ cells and protect them against the host immune system. Besides creating a physical barrier (the blood-testis barrier), SeC secrete a plethora of trophic and immunomodulatory factors that confer to these cells the ability to survive long time after engraftment, and protect allo- and xenogenic engraftments of tissues and organs.5 SeC isolated from specific pathogens free (SPF) pre-pubertal pigs were encapsulated in highly biocompatible alginate-based microcapsules (MC-SeC) and injected into the peritoneal cavity of mdx mice, an experimental model of DMD, in the absence of pharmacological immunosuppression.3,4A single i.p. injection of MC-SeC resulted in amelioration of muscle morphology and performance as a consequence of the secretion by SeC of anti-inflammatory factors and heregulin β1, an inducer of the dystrophin paralogue, utrophin, opening new routes in the treatment of DMD. However, information is lacking about possible direct effects of SeC on myoblasts/myotubes. Here, we show that SeC secrete factors able to stimulate cell proliferation in the early phase of the myogenic differentiation process in murine C2C12 and human (healthy and DMD) myoblasts. In DMD myoblasts, SeC-derived factors delayed the expression of the muscle-specific terminal differentiation markers, myogenin and myosin heavy chain (MyHC)-II in the early phase (24h) of the differentiation process; nevertheless, SeC stimulated terminal differentiation (6 days) in these cells, suggesting that the promitogenic activity of SeC does not affect the myogenic potential. Moreover, SeC inhibit the expression of the myofibroblast transdifferentiation markers, COL1A1, FN1 and CTGF/CCN2 in DMD myoblasts, suggesting an antifibrotic effect of the SeC-derived factors. Finally, SeC induced utrophin expression in preformed DMD myotubes regardless of the mutation, with the same mechanism reported in dystrophic mice. Altogether, these results further support the use of MC-SeC or SeC-derived factors in the treatment of DMD patients, and suggest that SeC-based approaches might be useful also in improving the early phase of muscle regeneration, during which myoblasts have to proliferate in order to reach the critical amount required to replace the damaged muscle mass.
Keywords: Duchenne muscular dystrophy; Sertoli cell; muscle differentiation; fibrosis.
References
1. Davies KE, Nowak KJ. Molecular mechanisms of muscular dystrophies: old and new players. Nat Rev Mol Cell Biol. 2006;10:762-73. doi: 10.1038/nrm 2024
2. Muntoni F, Fisher I, Morgan, JE, Abraham D. Steroids in Duchenne muscular dystrophy: from clinical trials to genomic research. Neuromuscul. Disord. 2002;1:S162-5. doi: 10.1016/s0960-8966 (02)00101-3
3. Chiappalupi S, Luca G, Mancuso F, Madaro L, Fallarino F, Nicoletti C, Calvitti M, Arato I, Falabella F, Salvadori L, Di Meo A, Bufalari A, Giovagnoli S, Calafiore R, Donato R, Sorci G. Intraperitoneal injection of microencapsulated Sertoli cells restores muscle morphology and performance in dystrophic mice. Biomaterials. 2016;75:313-26. doi:10.1016/j.biomaterials. 2015. 10.029
4. Chiappalupi S, Luca G, Mancuso F, Madaro L, Fallarino F, Nicoletti C, Calvitti M, Arato I, Falabella F, Salvadori L, Di Meo A, Bufalari A, Giovagnoli S, Calafiore R, Donato R, Sorci G. Effects of intraperitoneal injection of microencapsulated Sertoli cells on chronic and presymptomatic dystrophic mice. Data in Brief. 2015;5:1015-21. doi:10.1016/j.dib.2015.11.016
5. Chiappalupi S, Salvadori L, Luca G, Riuzzi F, Calafiore R, Donato R, Sorci G. Do porcine Sertoli cells represent an opportunity for Duchenne muscular dystrophy? Cell Proliferation. 2019;26:e12599; doi: 10.1111/cpr.12599
Indirizzi selvicolturali per il contenimento dei danni da bostrico nelle foreste delle Alpi orientali
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