118,946 research outputs found
Introduzione a: «Amate palesemente e generosamente le lettere e la vostra nazione». Ugo Foscolo nell’Ateneo pavese
No full textL' Introduzione ricostruisce il soggiorno di Foscolo a Pavia durante il breve periodo del suo insegnamento universitario, dal dicembre 1808 al giugno 1809. Il Catalogo comprende 99 schede, interamente compilate da G. Lavezzi
Oltre l' "Opera in versi": ricostruzione di un mosaico poetico
No full textRiflessioni ed annotazioni critiche in margine alle poesie lasciate inedite da Montale e pubblicate in “La casa di Olgiate e altre poesie” (a cura di R. Cremante e G. Lavezzi, Milano, Mondadori, 2006)
U. Foscolo, "Viaggio sentimentale", "Dell'origine e dell'ufficio della letteratura", "Essays on Petrarch"
No full textIl volume è il secondo dell'edizione delle "Opere" di Foscolo diretta da F. Gavazzeni. G. Lavezzi ha curato testo, scheda introduttiva e commento scientifico di tre opere: la traduzione del "Sentimental Journey" di L. Sterne, "Dell'origine e dell'ufficio della letteratura" e "Essays on Petrarch"
Proliferating cell nuclear antigen (PCNA) and apoptosis in hyperacute and acute myocardial infarction
No full textThe aim of this study was to determine whether cell proliferation and/or apoptotic cell death occur in hyperacute and acute infarction. Proliferating cell nuclear antigen (PCNA) and apoptosis were investigated in ten autoptic hearts within a few hours of infarction and in three normal hearts as controls. The PCNA Labeling Index (PCNA-LI) ranged from 0 to 3.1 in hyperacute infarction (mean 1.38), from 0.3 to 4 in acute infarction (mean 2.04) and from 0 to 1.2 in controls (mean 0.7). Although the results were not statistically significant, PCNA-LI was higher in acute than in hyperacute myocardial infarctions; and it was higher in hyperacute infarctions than in controls. Regarding apoptosis, the Apoptotic Index (AI) in hyperacute infarctions ranged from 0.7 to 3 (mean 1.78), in acute infarctions from 0.9 to 5 (mean 3.24) and in controls from 0 to 0.4 (mean 0.1). The AI was significantly higher in hyperacute and acute infarctions than in controls (p<0.05)
Pathology of the central autonomic nervous system in stillbirth
No full textThe aim of this study was to identify in stillbirth a possible involvement of morphological and/or physiological alterations of structures of the central autonomic nervous system in the mechanism of death. The study, including the in-depth histological examination of brainstem and cerebellum, was performed on 42 stillbirths, aged from 22 to 40 gestational weeks, 12 of which were explained and 30 were unexplained deaths. In the sudden unexplained stillbirths a variety of morphological and/or biological abnormalities of different structures and nuclei was found, above all the hypoplasia of the parafacial complex, frequently associated with hypoplasia of the arucate and pre-Bötzinger nuclei, and with thyrosine-hydroxilase immunonegativity in the locus coeruleus. A significant correlation was also observed between the neuropathologic findings and mother’s smoking habit
Fetal arterial changes in response to maternal cigarette smoking: revisiting the natural history of the earliest stage of atherosclerosis
No full textThe current knowledge of the development and progression of atherosclerotic lesions is largely owed to exptl. studies carried out in animals fed a high cholesterol diet. Only a few studies have addressed the atherogenic effects of other important exogenous risk factor, namely cigarette smoking. The results of our research into the effects of cigarette smoking on the fetal arterial wall have demonstrated that the first reactive event is a severe alteration of the architecture of the tunica media, forming perpendicularly oriented columns of smooth muscle cells (SMCs), infiltrating the intima. These histopathol. alterations go hand in hand with a marked change in the biol. homeostasis of the SMCs. Our mol. biol. research has shown that the first reaction of these cells to the nicotine is an intense activation of the c-fos proto-oncogene, followed by the transformation of the SMCs to \"myofibroblasts\", characterized by the presence of b-actin and acquisition of both synthetic and ameboid activity. If the harmful effects of passive smoke persist, the myofibroblasts start to proliferate, as demonstrated by positivity of the PCNA, together with the onset of chromosomal alterations. These peculiar changes of the tunica media are the prerequisites for lipid accumulation that thereafter overwhelm the myofibroblast reaction. [on SciFinder (R)
Functional neuroanatomy of the human pre-Bötzinger complex with particular reference to sudden unexplained perinatal and infant death
No full textThe authors are the first to identify in man the pre-Bötzinger complex, a structure of the brainstem critical for respiratory rhythmogenesis, previously investigated only in rats. The evaluation of the neurokinin 1 receptors and somatostatin immunoreactivity in a total of 63 brains from 25 fetuses, nine newborns and 29 infants, allowed to delineate the anatomic structure and the boundaries of this human neural center in a restricted area of the ventrolateral medulla at the obex level, ventral to the semicompact ambiguus nucleus. The neurons of the pre-Bötzinger complex were roundish in fetuses before 30 gestational weeks and lengthened after birth, embedded in a dendritic system belonging to the reticular formation. Besides, structural and/or functional alterations of the pre-Bötzinger complex were present in a high percentage of sudden deaths (47%), prevalent in late fetal deaths. In particular, different developmental defects (hypoplasia with a decreased neuronal number and/or dendritic hypodevelopment of the reticular formation, abnormal neuronal morphology, immunonegativity of neurotransmitters, and agenesis) were found. The authors suggest that the pre-Bötzinger complex contains a variety of neurons not only involved in respiratory rhythm generation, but more extensively, essential to the control of all vital functions. Sudden death and in particular sudden unexpected fetal death could therefore be ascribed to a selective process when developmental alterations of the pre-Bötzinger complex arise
Proposal of the Acronym “SIUDS” for Unexplained Stillbirths, Like “SIDS”
No full textThe authors, propose that also a sudden death during pregnancy that remains unexplained after an in-depth autopsy, should be considered as a syndrome and referred with the acronym “SIUDS”, e.g., “Sudden Intrauterine Unexplained Death Syndrome”, like “SIDS” for “Sudden Infant Death Syndrome”. This suggested definition is based on the presence in these pathologies of common developmental abnormalities of both the autonomic nervous system and the cardiac conduction system, associated to the same preventable risk factors
MORTE FETALE versus SIDS (Legge n.31)-PATOLOGIE (CONGENITE) DEL SISTEMA NEUROVEGETATIVO E DI CONDUZIONE CARDIACO LEGATE ALL’EMBRIOGENESI E ALLO SVILUPPO NELLA MORTE INSPIEGABILE PERINATALE E NELLA SIDS
No full textL’applicazione della Legge 31/2006 “Disciplina del riscontro diagnostico sulle vittime della sindrome della morte improvvisa
del lattante (SIDS) e di morte inaspettata del feto” ha consentito di sviluppare approfondite indagini anatomo-cliniche.
Attraverso lo studio neuropatologico è stata individuata l’eziopatogenesi sia della morte fetale inaspettata e inspiegabile
che della SIDS. Trattasi di anomalie congenite comuni a queste patologie. L’acquisizione dell’origine comune di tali
patologie consente di unificare l’inquadramento nosografico, anche ai fini di valutazioni epidemiologiche. Nel complesso
le anomalie congenite sono più diffuse nelle morti fetali inspiegabili ante-partum. In tale ambito caratteristico è il difetto
di sviluppo del complesso facciale/parafacciale, modulatore delle attività vitali. Nelle morti fetali intra-partum frequente
è il riscontro di ipoplasia/agenesi del complesso parabrachiale/nucleo di Kölliker-Fuse che presiede all’inizio dell’attività
respiratoria. Nelle morti inaspettate neonatali precoci e nella SIDS le anomalie sono più limitate e comprendono l’ipoplasia
del nucleo arcuato e della formazione reticolare respiratoria. Frequente è il riscontro di vie accessorie atrio-ventricolari,
substrato di aritmie anche mortali da rientro; esse sono spesso associate alle anomalie del sistema nervoso autonom
Recurrent chromosome alterations in non-small cell lung cancer.
No full textCytogenetic analysis of 28 cases of non-small cell lung cancer (NSCLC) was carried out in an attempt to determine karyotype changes involved in the early state of disease. Our findings indicate that, even though karyotypes are very complex, recurrent cytogenetic changes can be identified. The most common structural rearrangements were deletions of chromosomes 3, 17 and 9. The most frequent numerical alterations were gain of chromosomes 7 and 20 and loss of chromosomes 1 and Y. In particular, the high frequency of deletions suggests a critical role of suppressor oncogenes in these chromosome regions in tumor development
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