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The main purpose of a quantum key distribution network is to provide secret keys to any users or applications requiring a high level of security, ideally such as to offer the best protection against any computational attack, even of a quantum nature. The keys shared through a point-to-point link between a source and a detector using a quantum key distribution protocol can be proven information-theoretically secure based on the quantum information theory. However, evaluating the security of a quantum key distribution network, especially if it is based on relay nodes, goes far beyond the quantum security of its single quantum links, involving aspects of conventional security for devices and their communication channels. In this contribution, we perform a rigorous threat analysis based on the most recent recommendations and practical network deployment security issues. We show that, at least in the current state of our understanding of quantum cryptography, quantum key distribution networks can only offer computational security and that their security in practical implementations in the shorter term requires resorting to post-quantum cryptography. [ABSTRACT FROM AUTHOR]

In this work, we elaborate on the concept of process authenticity, which intuitively corresponds to the validity of all process steps and their proper binding. It represents the most exciting forefront of distributed ledger technology research concerning the primary challenge of reliably connecting distributed ledger networks to the physical context it must operate. More in detail, the paper describes a novel methodological approach to ensure the authenticity of business processes through blockchain and several security mechanisms applied to the digital twins of the actual processes. We illustrate difficulties and opportunities deriving from implementing process authenticity in concrete case studies in which we were involved as software designers belonging to three critical application domains: document dematerialization, e-voting, and healthcare. [ABSTRACT FROM AUTHOR]

Background. Long-term home noninvasive mechanical ventilation (NIV) is beneficial in COPD but its impact on inflammation is unknown. We assessed the hypothesis that NIV modulates systemic and pulmonary inflammatory biomarkers in stable COPD. Methods. Among 610 patients referred for NIV, we shortlisted those undergoing NIV versus oxygen therapy alone, excluding subjects with comorbidities or non-COPD conditions. Sputumand blood samples were collected after 3months of clinical stability and analyzed for levels of human neutrophil peptides (HNP), interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor-alpha (TNF-alpha). Patients underwent a two-year follow-up. Unadjusted, propensity-matched, and pH-stratified analyses were performed. Results. Ninety-three patients were included (48 NIV, 45 oxygen), with analogous baseline features. Sputum analysis showed similar HNP, IL-6, IL-10, and TNF-alpha levels (P > 0.5). Conversely, NIV group exhibited higher HNP and IL-6 systemic levels (P < 0.001) and lower IL-10 concentrations (P < 0.001). Subjects undergoing NIV had a significant reduction of rehospitalizations during follow-up compared to oxygen group (P = 0.005). These findings were confirmed after propensity matching and pH stratification. Conclusions. These findings challenge prior paradigms based on the assumption that pulmonary inflammation is per se detrimental. NIV beneficial impact on lung mechanics may overcome the potential unfavorable effects of an increased inflammatory state. [ABSTRACT FROM AUTHOR]

Objectives and design: To date, no sufficiently sensitive and specific single marker has been found to predict the clinical course of sarcoidosis. We designed a cohort study to investigate whether a panel of biomarkers measured in bronchoalveolar lavage (BAL) and peripheral blood could help predict pulmonary function worsening during the clinical course of sarcoidosis. Methods: We analyzed 30 individuals with histologically proven sarcoidosis. At baseline, participants underwent pulmonary function tests (PFTs), fiberoptic bronchoscopy and radiological investigations. BAL and blood cellular profiles were obtained from all individuals and six pro-inflammatory molecules were quantified in BAL and serum. PFTs were performed at follow-up visits over a 2-year period. Using discriminant function analysis, a canonical variable was generated to optimize the accuracy of selected variables in predicting pulmonary function worsening and was validated on a subset of nine consecutive individuals with sarcoidosis. Results: A combination of 6 markers from BAL was able to predict pulmonary function worsening in 96 % of patients [95 % confidence interval (CI) 84.4-99.81]. We validated the generated formula on a group of nine patients with sarcoidosis, obtaining 77.8 % correct classification (95 % CI 45.3-93.7). Conclusions: Our results show that a combinational approach could contribute to identifying individuals likely to experience pulmonary function worsening, thus helping to decide the correct therapeutic strategies. [ABSTRACT FROM AUTHOR]

The pivotal role of neutrophils and macrophages in smoking-related lung inflammation and COPD development is well-established. We aimed to assess whether sputum concentrations of Human Neutrophil Peptides (HNP), Neutrophil Elastase (NE), Interleukin-8 (IL-8), and Metalloproteinase-9 (MMP-9), major products of neutrophils and macrophages, could be used to trace airway inflammation and progression towards pulmonary functional impairment characteristic of COPD. Forty-two symptomatic smokers and 42 COPD patients underwent pulmonary function tests; sputum samples were collected at enrolment, and 6 months after smoking cessation. HNP, NE, IL-8, MMP-9 levels were increased in individuals with COPD (p < 0.0001). HNP and NE concentrations were higher in patients with severe airways obstruction, as compared to patients with mild-to-moderate COPD (p =0.002). A negative correlation was observed between FEV_{1} and HNP, NE and IL-8 levels (p < 0.01), between FEV_{1}/FVC and HNP, NE and IL-8 levels (p< 0.01), and between NE enrolment levels and FEV_{1} decline after 2 years (p =0.04). ROC analysis, to discriminate symptomatic smokers and COPD patients, showed the following AUCs: for HNP 0.92; for NE 0.81; for IL-8 0.89; for MMP-9 0.81; for HNP, IL-8 and MMP-9 considered together 0.981. The data suggest that the measurement of sputum markers may have an important role in clinical practice for monitoring COPD. [ABSTRACT FROM AUTHOR]

Background: Acute respiratory failure (ARF) occurring during idiopathic pulmonary fibrosis (IPF) is associated with a poor prognosis. In this subset of individuals, mechanical ventilation (MV) may be required. Objectives: We analysed the characteristics of a group of IPF patients undergoing MV for ARF in order to give some indications on the supposed prognosis. Methods: Hospital records of 34 consecutive patients with IPF, who underwent MV for ARF, were retrospectively examined. Demographic data, time from diagnosis, gas exchange, Acute Physiology and Chronic Health Evaluation (APACHE) II score, ARF causes and MV failure were recorded. Results: Fifteen subjects (group A) underwent invasive MV and 19 patients (group B) non-invasive ventilation (NIV). The 2 groups were different for disease severity (APACHE II score 24.2 ± 6 vs. 19.5 ± 5.9; p = 0.01). Both ventilatory strategies temporarily increased PaO2/FiO2 as compared with spontaneous breathing (group A: 148.5 ± 52 vs. 99 ± 39, p = 0.0004; group B: 134 ± 36 vs. 89 ± 26, p = 0.0004). NIV reduced the respiratory rate (26 ± 7 vs. 36 ± 9 with spontaneous breathing; p = 0.002). Duration of MV correlated with the time of evolution of IPF (r = 0.45; p = 0.018). The in-hospital mortality rate was 85% (100% for invasive MV, 74% for NIV). Four of the 5 survivors died within 6 months from hospital discharge (range 2–6 months). Conclusions: MV does not appear to have a significant impact on the survival of patients with end-stage IPF. NIV may be useful for compassionate use, providing relief from dyspnoea and avoiding aggressive approaches. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

There has been growing interest over recent years in the potential preventive role of the Mediterranean diet in the development of cardiovascular disease and cancer. The present study was designed to evaluate the relationship between the components of the Mediterranean diet and lung cancer. A hospital-based, case-control study of lung cancer was conducted on subjects aged 35+ yr living in the Lazio region and admitted to one of the main hospitals in Rome in the period from 1993 to 1996. Cases (n = 342) were patients with newly diagnosed primary lung cancer. Controls (n = 292) were recruited from departments of general surgery, orthopedics, ENT, and general medicine and were frequency matched by sex and age(±5yr) to the cases. Exposure characteristics were obtained by interviewing study subjects. A self-administered food-frequency questionnaire was used. After careful control for several smoking variables, we found a protective effect for high consumption of carrots (odds ratio [OR] = 0.67, 95% confidence interval [CI] = 0.42-1.05), tomatoes (OR = 0.59, 95% CI = 0.34-1.03), white meat (OR = 0.66, 95% CI = 0.42-1.02), exclusive use of olive oil (OR = 0.67, 95% CI = 0.45-0.99),and regular consumption of sage(OR=0.43,95% CI=0.29-0.65). In a multivariate model, considering all food items simultaneously, the protective effect of exclusive olive oil use and sage remained statistically significant. Our results indicate that some food items typical of the Mediterranean diet are associated with decreased lung cancer risk. [ABSTRACT FROM AUTHOR]

The level of activity of O6-alkylguanine-DNA-alkyltransferase (AGT), a DNA repair enzyme, in blood lymphocytes may be a marker of susceptibility to lung cancer. We measured the AGT activity level, expressed as pmoles of repaired bases/mg protein, in leukocytes of 153 lung cancer cases (of whom 80 were never smokers) and 106 controls (76 never smokers) enrolled in eight centres from seven countries. Subjects were interviewed with respect to active smoking and exposure to environmental tobacco smoke (ETS). Among never smokers, the odds ratios (ORs) of lung cancer were 1.3 (95% confidence interval 0.5–3.9), 1.5 (0.6–4.1) and 1.4 (0.5–3.8) in quartiles of decreasing AGT activity level, as compared to the upper quartile (P value of test for linear trend 0.6). Corresponding ORs among smokers were 3.4 (0.9–13), 2.0 (0.5–8.3) and 0.4 (0.1–1.6) (P value of test for linear trend 0.4). No interaction was suggested between AGT activity level and either cumulative smoking or exposure to ETS. Reduced AGT activity was not clearly associated with increased lung cancer risk in either smokers or non-smokers. However, the small size of our study argues for a prudent interpretation of our results. [Copyright &y& Elsevier]

A letter to the editor about a study of human neutrophil peptides is presented.