2,670 research outputs found
Università G. d’Annunzio Chieti-Pescara, DdA Dipartimento di Architettura con P. Misino, M. Angrilli, S. Ferrini, R. Ottaviani
No full textPresentazioen del progetto elaborato dal gruppo dell'Università di Chieti-Pescara composto da P. Misino, M. Angrilli, S. Ferrini, R. Ottaviani, C. Varagnol
IL SUBLIME URBANO. Architettura e new media
No full textI “new media” determinano nuove forme di relazione tra spazi urbani e spazi della comunicazione. Attivando meccanismi alternativi alla pubblicità “packaging” e avvalendosi di diverse strategie “low profile”: quelle dei “guerrilla marketing”, di “temporary store” e di campagne “no-name”. Per i cultori della condizione post, si potrebbe oggi parlare di una condizione iniziale di “post marketing”, contrapposta a quella tradizionale; di un nuovo “sublime urbano”. Testi di: L. Altarelli, R. Ottaviani, G. Donini, A. Bordi, M. De Licio, V. Sassanelli, A. Tzompanakis, A. Llerandi Gonzales, D. Mancini,M. Memo, A. Rocca, A. Cornaro, A. Lacerenza, L. De Licio, A. Del Re, V. De Vitiis, S. La Pergola, E. Tagliacollo, A. Greco, E. Vitaletti, P. Cagnazzi, G. Turano, A. Lanzetta
Sudden Intrauterine Unexplained Death (SIUD) «Gray Zone» or borderline
No full textThe author reports the histopathological findings of 9 fetuses (3 females and 6 males, ranging in age from 34 to 41 gestational weeks) that died suddenly and unexpectedly in utero. They presented brainstem and cardiac conduction system lesions together with abnormalities of the fetal adnexa. A complete autopsy was performed, including detained investigation of the brainstem and cardiac conduction system on serial sections, as well as of the fetal adnexa, according to our guidelines. Histological examination of the fetal adnexa disclosed the presence of chorioamnionitis (7 cases), an abnormally short umbilical cord (1 case), and placental infection by parvovirus (1 case). These lesions were associated with brainstem lesions, i.e., hypoplasia of the arcuate nucleus (6 cases), inflammatory infiltrates in the brainstem (2 cases), hypoplasia of the raphe obscurus nucleus (2 cases), hypoplasia of the parabrachial Kölliker-Fuse complex (1 case), hypoplasia of the pre-Bötzinger complex (1 case), agenesis of the facial/parafacial complex (1 case), as well as conduction system lesions, i.e., dispersion or septation of the atrio-ventricular junction (9 cases), islands of the conduction system inside the central fibrous body (5 cases) resorptive degeneration (4 cases), cartilaginous meta-hyperplasia (2 cases), Mahaim fibers (1 case). Each SIUD victim presented at least one of these brainstem and/or cardiac conduction abnormalities, more than one change being present in the same fetus. The SIUD «gray zone», or borderline cases, are hereby described as those cases in which the lesions of the fetal adnexa alone might not have accounted for the sudden deaths, had it not been for the concomitant presence of brainstem and cardiac conduction lesions representing the morphological substrates for SIUD, as well as for SIDS. Our 9 cases are consistent with the triple-risk model, a hypothesis introduced for SIDS postulating an underlying biological vulnerability to exogenous stressors or triggering factors in a critical developmental period. In conclusion, we are convinced that there is a continuum between SIUD and SIDS and the triple-risk model is herein considered for the first time also for SIUD “gray zone” victims
Sudden infant and perinatal unexplained death : Are we moving forward yet?
No full textAutonomic nervous system and cardiac conducting system dysfunctions have been proposed to be implied in the pathogenesis of sudden
infant death syndrome (SIDS). However, most clinicians and even pathologists lack experience with detailed examination of the brainstem and
cardiac conducting system and may not recognize lesions within those systems that potentially could be crucial factors in the sudden unexpected
perinatal and infant death. Recent anatomical, pathological, and bacteriological studies in SIDS confirm that the multidisciplinary approach
provides the best approach to the challenging problems of SIDS and sudden unexplained perinatal death
Sudden death and coronary intimal thickening
No full textAmong 22 fetuses dying suddenly and unexpectedly
after 35 weeks of gestation, in 12 (55%) cases, multifocal
structural alterations of all the coronary arteries were
reported, and these were more severe along the anterior
descending branch of the left coronary artery. In seven
(32%) of these fetuses, foci of altered architecture of the
media with thinning and fiber fragmentation were
observed, even in fields far from the bifurcations. The
smooth muscle cells (SMCs) showed loss of polarity,
forming columns of myocytes located perpendicular to the
axis of the media itself and infiltrating the subendothelial
connective tissue. In five (23%) additional fetuses, besides
this intense reaction of the SMCs of the media, increased
amounts of mucoid ground substance were observed in the
subendothelial connective tissue, with formation of intimal
lesions of proliferative aspect. Such processes
also seem to determine fragmentation and detachment of
the internal elastic membrane
Defining Sudden Infant Death and Sudden Intrauterine Unexpected Death Syndromes with Regard to Anatomo-Pathological Examination
No full textCrib death, or sudden infant death syndrome (SIDS), is the most frequent form of death in the first year of life, striking one baby in every 1,700–2,000. Yet despite advances in maternal-infant care, sudden intrauterine unexplained/unexpected death syndrome (SIUDS), has a six-eightfold greater incidence than that of SIDS. Frequent congenital abnormalities, likely morphological substrates for SIDS-SIUDS, were detected, mainly represented by alterations of the cardiac conduction system, such as accessory pathways and abnormal resorptive degeneration, and hypoplasia/agenesis of the vital brainstem structures. On the basis of these considerations, the new common definition of the SIDS-SIUDS complex is The sudden death of a fetus after the 25th gestational week or infant under one year of age which is unexpected by history and remains unexplained after a thorough case investigation, including examination of the death scene, performance of a general autopsy and examination of the fetal adnexa. Therefore, given that the general autopsy does not disclose any cause of death, a more in-depth histopathological analysis of the cardiac conduction system and autonomic nervous system by specialized pathologists will become necessary
Vincenzo Ottaviani
No full textBotanico: Ottaviani, Vincenzo (1790-1853).
Professore di botanica e chimica nell\u27Università di Camerino.
Titolo manoscritto sul recto, dove compaiono anche le note: n. 1790; m. 1853; Primo prefetto (1826-1841) dell’Orto camerte; Da un ritratto ad olio nella bibliot. d’Urbino; Dono del prof. G. B. De Toni, X. 900.
Timbro ad inchiostro sul verso: Costantino Della Casa Fotografo Urbino.
Montata su cartone 185 x 140 mm.
1 fotografia : aristotipo ; 171 x 124 mm.
Vai alla scheda bibliografica: https://galileodiscovery.unipd.it/discovery/fulldisplay?context=L&vid=39UPD_INST:VU1&search_scope=MyInst_and_CI&tab=Everything&docid=alma99001597770020604
Arrhythmogenic sudden death in the modern setting SIDS. An overview
No full textBesides the quoted pathogenetic backgrounds of cardiac SIDS, and even overcoming the statistical exaggerations of Schwartz' group who arbitrarily put forward the LQTS (1), the present authors stand convinced that the presence of accessory AV pathways can play an important role, in an unprecised but significant number of cardio-arrhythmogenic SIDS. These authors themselves studied an uncommonly numerous case group of SIDS who exhibited (and likely succumbed to) as a unique histopathological evidence, accessory AV communications, however "silent" on the clinical plane, since they lacked EKG-confirmed tachy-arrhythmias (2). To favour their own conviction, the present upholders of this thesis do point out the anatomoclinical knowledge that most of the high-risk tachy-arrythmias in early infancy show a typical EKG of a junctional reentry, together with the inherent implications of a potential or actual degeneration into ventricular fibrillation. The fact that the lethal event, or its threat, would not be recorded electrically, depends on the very same circumstantial "limitations" emphasised by Schwartz and co-workers among the over 34.000 EKGs of the never-ascertained suspicion of an LQTS pathogenesis: indeed, this was only documented by objective proof 2 years after the publication of the original article. In this article no case (i.e. less than 1:34.000) ever presented with confirmed risk neither of arrhythmic death nor of related dysfunctions. To confirm the missing reliability of Schwartz's thesis, even after the sporadic and numerically limited set of inherent controls by genetic investigations (3): yet, accurate as they were, such controls did not take into consideration the newer data concerning the genetic background of high-risk dysarrhythmias, both sudden and lethal, as causes of SIDS beyond cases of cardiac failure and/or hypertrophy. Such gene, namely the KvCHIPz (or Kv channel-interacting protein or Ito) provides the Ca-independent regulation of K+ ionic channels during early repolarization, thereby playing a key-role in regular myocell's electrical activation. For this reason such a genetic mechanism configures a plausible alternative to the exclusivistic Schwartz' hypothesis focused on the equation SIDS/LQTS alone. Recent studies have also borne out further close clinico-patho-genetic analogies with arrhythmogenic lethal late repolarization, attended by fetal developmental impairments of the conduction system, often resulting into accessory AV pathways, whose high frequency in SIDS has been documented in the present authors' cases and is entirely consistent with junctional tachycardia (2). It is important to underline, in this connection, that Hai-Chien Kuo and al.(4) emphasize the possible role of the conduction system among the ontogenic substrates of the Ito's abnormalities; such a genetic clinico-pathological suggestion is further substantiated by the recent work of one of the present authors (5) on the life-threatening potential of WPW syndrome, whose commonplace accessory AV pathway substrate was proven to occasionally rely on genetic familiarity (6).
All in all, under the light of these late findings, which aligne among the developmental backgrounds of an arrhythmogenic SIDS the postnatal persistence of AV junctional accessory pathways, one must better re-consider, critically, the overemphasised and overinsistent LQTS/SIDS equation of the Schwartz' school. Indeed, the basic arguments of this, rely on data that are being overcome, at the probable unawareness of the upholders themselves.
References
1. Schwartz PJ, Stramba-Badiale M, Segantini A, Austoni P, Bosi G, Giorgetti RR, Grancini F, Marini ED, Perticone F, Rositi D, Salice P. Prolongation of the QT interval and the sudden infant death syndrome. N Engl J Med 338: 1709, 1998.
2. Matturri L, Ottaviani G, Ramos SG, Rossi L. Sudden Infant Death Syndrome (SIDS): a study of cardiac conduction system. Cardiovasc Pathol 9:137, 2000.
3. Priori SG, Bloise R, Crotti L The long QT syndrome (Review). Europace. 3(1): 16-27, 2001.
4. Kuo HC, Cheng CF, Clark RB, Lin JJ, Lin JL, Gu Y, Ikeda Y, Chu PH, Ross Jr J , Giles WR Chien KR. A defect in the Kv channel-interacting protein 2 (KchIP2) gene leads to a complete loss of Ito and confers susceptibility to ventricular tachycardia. Cell 107:801, 2001.
5. Basso C, Corrado D, Rossi L, Thiene G. Ventricular pre-exccitation in children and young adults: atrial myocarditis as a possible trigger of sudden death. Circulation, 103:269, 2001.
6. Gollob MH, Green MS, Tang A S-L, Gollob T, Karibe A, Hassa A, Ahmad F, Lozado R, Shah G, Fananapazir L, Bachinski L, Roberts R. Identification of a gene responsible for familial Wolff-Parkinsons-White syndrome. N Engl J Med 344:1823, 2001
Role of post-mortem investigations in determining the cause of sudden unexpected death in infancy
No full textPost-mortem bacteriological examination is of great importance, but it should be stressed that post-mortem investigations in every case of sudden unexpected death in infancy should primarily focus on the possibility of pathological findings in the brainstem and the cardiovascular system. Based on careful evaluation of recent anatomo-pathological studies on sudden unexpected death in infancy, there is now sound evidence to rely on for a new approach to this thorny problem
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