Caratteristiche principali dell'emissione delle regioni H II

Molte delle più spettacolari immagini della nostra Galassia hanno per protagoniste le regioni H II: storicamente, questi plasmi astrofisici sono stati tra i primi ad essere studiati in dettaglio, grazie ai loro luminosi spettri di emissione in banda ottica. Le regioni H II sono regioni di WIM composte perlopiù da idrogeno ionizzato create all'interno del CNM dal flusso di fotoni ultravioletti prodotto da stelle giovani di grande massa, di classe spettrale OB. Si trovano situate principalmente in corrispondenza delle regioni di formazione stellare delle galassie a spirale. Questa discussione tratterà principalmente le caratteristiche osservative delle regioni H II e si occuperà dunque di descriverne i processi di emissione che ne determinano gli spettri osservati. Si partirà dalla descrizione delle regioni H II come zone di equilibrio di fotoionizzazione e se ne definirà il raggio di Stromgren; successivamente verranno discusse le caratteristiche spettrali. La radiazione continua, in particolare la sua componente dovuta all'emissione di Bremsstrahlung e quella dovuta alle polveri, verrà descritta nel capitolo 2. Le linee di emissione molto brillanti dovute a processi di ricombinazione (RLs) e di eccitazione collisionale (CELs), tipiche di queste regioni, sono discusse nel capitolo successivo. Infine, verranno trattate anche le emissioni provenienti dalle particolari zone che delimitano le regioni H II vere e proprie, che prendono il nome di regioni di fotodissociazione: se ne discuterà l'emissione dovuta a particolari molecole come PAHs, H2 e CO, e la loro importanza nella mappatura delle regioni H II nella Galassia. L'argomento trattato nel corso di questa tesi è molto vasto e dotato di un'estesa letteratura: non è possibile in poche pagine descrivere in dettaglio ogni processo fisico all'interno delle regioni H II, ma viene piuttosto fornito un quadro generale dei processi più importanti nel contesto delle emissioni provenienti da queste nebulose

The Coexistence of asthma and Chronic Ostructive Pulmonary Disease (COPD): prevalence and risk factors in young, middle-aged and elderly people from the general population

Background: The joint distribution of asthma and chronic obstructive pulmonary disease (COPD) has not been well described. This study aims at determining the prevalence of self-reported physician diagnoses of asthma, COPD and of the asthma-COPD overlap syndrome and to assess whether these conditions share a common set of risk factors. Methods: A screening questionnaire on respiratory symptoms, diagnoses and risk factors was administered by mail or phone to random samples of the general Italian population aged 20–44 (n = 5163) 45–64 (n = 2167) and 65–84 (n = 1030) in the frame of the multicentre Gene Environment Interactions in Respiratory Diseases (GEIRD) study. Results: A physician diagnosis of asthma or COPD (emphysema/chronic bronchitis/COPD) was reported by 13% and 21% of subjects aged &lt;65 and 65–84 years respectively. Aging was associated with a marked decrease in the prevalence of diagnosed asthma (from 8.2% to 1.6%) and with a marked increase in the prevalence of diagnosed COPD (from 3.3% to 13.3%). The prevalence of the overlap of asthma and COPD was 1.6% (1.3%–2.0%), 2.1% (1.5%–2.8%) and 4.5% (3.2%–5.9%) in the 20–44, 45–64 and 65–84 age groups. Subjects with both asthma and COPD diagnoses were more likely to have respiratory symptoms, physical impairment, and to report hospital admissions compared to asthma or COPD alone (p&lt;0.01). Age, sex, education and smoking showed different and sometimes opposite associations with the three conditions. Conclusion: Asthma and COPD are common in the general population, and they coexist in a substantial proportion of subjects. The asthma-COPD overlap syndrome represents an important clinical phenotype that deserves more medical attention and further research.</br

Increased prevalence of abnormal vertebral patterning in fetuses and neonates with trisomy 21

Purpose: To assess the prevalence of an abnormal number of ribs in a cohort of fetuses and neonates with trisomy 21 and compare this with a subgroup of fetuses without anomalies. Materials and methods: Radiographs of 67 deceased fetuses, neonates, and infants that were diagnosed with trisomy 21 were reviewed. Terminations of pregnancy were included. The control group was composed of 107 deceased fetuses, neonates, and infants without known chromosomal abnormalities, structural malformations, infections or placental pathology. Cases in which the number of thoracic ribs or presence of cervical ribs could not be reliably assessed were excluded. The literature concerning vertebral patterning in trisomy 21 cases and healthy subjects was reviewed. Results: Absent or rudimentary 12th thoracic ribs were found in 26/54 (48.1%) cases with trisomy 21 and cervical ribs were present in 27/47 (57.4%) cases. This prevalence was significantly higher compared to controls (28/100, 28.0%, Χ2(1) = 6.252, p = .012 and 28/97, 28.9%, Χ2(1) = 10.955, p < .001, respectively). Conclusions: Rudimentary or absent 12th thoracic ribs and cervical ribs are significantly more prevalent in deceased fetuses and infants with trisomy 21

The Stimulation of Inducible Nitric-oxide Synthase by the Prion Protein Fragment 106–126 in Human Microglia Is Tumor Necrosis Factor-α-dependent and Involves p38 Mitogen-activated Protein Kinase

A synthetic peptide consisting of amino acid residues 106-126 of the human prion protein (PrP-(106--126)) has been previously demonstrated to be neurotoxic and to induce microglial activation. The present study investigated the expression of the inducible form of the nitric-oxide synthase (NOS-II) in human microglial cells treated with PrP-(106--126). Using reverse transcriptase-polymerase chain reaction, we found that PrP-(106--126) induces NOS-II gene expression after 24 h of treatment and that this effect is accompanied by a peak of nuclear factor kappa B (NF-kappa B) binding at 30 min as evaluated by electrophoretic mobility shift assay. Since our previous data demonstrated tumor necrosis factor-alpha (TNF-alpha) to be a potent inducer of NOS-II in these cells, we analyzed the expression of this cytokine in PrP-(106--126)-treated microglia. PrP-(106--126) caused the release of TNF-alpha as detected by enzyme-linked immunosorbent assay, and a blocking antibody, anti-TNF-alpha, abolished NOS-II induction elicited by this peptide. Moreover, PrP-(106-126) activates p38 mitogen-activated protein kinase, and the inhibition of this pathway determines the ablation of NF-kappa B binding induced by this fragment peptide