Serum Albumin Is Inversely Associated With Portal Vein Thrombosis in Cirrhosis

We analyzed whether serum albumin is independently associated with portal vein thrombosis (PVT) in liver cirrhosis (LC) and if a biologic plausibility exists. This study was divided into three parts. In part 1 (retrospective analysis), 753 consecutive patients with LC with ultrasound-detected PVT were retrospectively analyzed. In part 2, 112 patients with LC and 56 matched controls were entered in the cross-sectional study. In part 3, 5 patients with cirrhosis were entered in the in vivo study and 4 healthy subjects (HSs) were entered in the in vitro study to explore if albumin may affect platelet activation by modulating oxidative stress. In the 753 patients with LC, the prevalence of PVT was 16.7%; logistic analysis showed that only age (odds ratio [OR], 1.024; P = 0.012) and serum albumin (OR, -0.422; P = 0.0001) significantly predicted patients with PVT. Analyzing the 112 patients with LC and controls, soluble clusters of differentiation (CD)40-ligand (P = 0.0238), soluble Nox2-derived peptide (sNox2-dp; P < 0.0001), and urinary excretion of isoprostanes (P = 0.0078) were higher in patients with LC. In LC, albumin was correlated with sCD4OL (Spearman's rank correlation coefficient [r(s)], -0.33; P < 0.001), sNox2-dp (r(s), -0.57; P < 0.0001), and urinary excretion of isoprostanes (r(s), -0.48; P < 0.0001) levels. The in vivo study showed a progressive decrease in platelet aggregation, sNox2-dp, and urinary 8-iso prostaglandin F2 alpha-III formation 2 hours and 3 days after albumin infusion. Finally, platelet aggregation, sNox2-dp, and isoprostane formation significantly decreased in platelets from HSs incubated with scalar concentrations of albumin. Conclusion: Low serum albumin in LC is associated with PVT, suggesting that albumin could be a modulator of the hemostatic system through interference with mechanisms regulating platelet activation

Tendon structure and extracellular matrix components are affected by spasticity in cerebral palsy patients

We studied the effect of spasticity-induced overload on tendons from the gracilis and semitendinosus muscles from cerebral palsy (CP) and healthy subjects (CT) stained with haematoxylineosin, Sirius red and Alcian blue. Vascularity was also characterized using an anti-CD34 antibody. Light microscopy analysis of haematoxylin-eosin stained sections revealed that the overall structure of tendons was maintained, characterized by parallel and slightly wavy collagen fibers in both CT and CP tendons. However, hypercellularity, cell rounding, increased vascularity and lipoid degeneration were observed in CP samples. Sirius red stained collagen fibers were more evident in CP tendons, suggesting an increased collagen content induced by spasticity. Alcian blue staining revealed an overall increase of glycosaminoglycans in CP tendons as observed in tendinopathy. Our results suggest that CP-induced spasticity may be considered as a chronic, persisting and repetitive loading of tendons, inducing ECM remodeling as adaptive response to increased functional demand. At the same time, the evidence of some tendinopathic-like markers in CP tendons suggests that the chronic nature of the CP condition could represent a pathologic condition, possibly leading to a transient weakness of the tissue making it more susceptible to damage from cumulative loading until an overt tendinopathy develop

Selective Effects of the Host Matrix in Hydrogenated InGaAsN Alloys: Toward an Integrated Matrix/Defect Engineering Paradigm

open13In dilute nitride InyGa1−yAs1−xNx alloys, a spatially controlled tuning of the energy gap can be realized by combining the introduction of N atoms—inducing a significant reduction of this parameter—with that of hydrogen atoms, which neutralize the effect of N. In these alloys, hydrogen forms N–H complexes in both Ga-rich and In-rich N environments. Here, photoluminescence measurements and thermal annealing treatments show that, surprisingly, N neutralization by H is significantly inhibited when the number of In-N bonds increases. Density functional theory calculations account for this result and reveal an original, physical phenomenon: only in the In-rich N environment, the InyGa1−yAs host matrix exerts a selective action on the N–H complexes by hindering the formation of the complexes more effective in the N passivation. This thoroughly overturns the usual perspective of defect-engineering by proposing a novel paradigm where a major role pertains to the defect-surrounding matrix.openFilippone, Francesco; Younis, Saeed; Mattioli, Giuseppe; Felici, Marco; Blundo, Elena; Polimeni, Antonio; Pettinari, Giorgio; Giubertoni, Damiano; Sterzer, Eduard; Volz, Kerstin; Fekete, Dan; Kapon, Eli; Amore Bonapasta, AldoFilippone, Francesco; Younis, Saeed; Mattioli, Giuseppe; Felici, Marco; Blundo, Elena; Polimeni, Antonio; Pettinari, Giorgio; Giubertoni, Damiano; Sterzer, Eduard; Volz, Kerstin; Fekete, Dan; Kapon, Eli; Amore Bonapasta, Ald

Tuning of the optical properties of In-rich In[sub x]Ga[sub 1 12x]N (x=0.82 120.49) alloys by light-ion irradiation at low energy

The effects of low-energy irradiation by light ions (H and He) on the properties of In-rich InxGa1−xN alloys are investigated by optical and structural techniques. H-irradiation gives rise to a remarkable blue-shift of light emission and absorption edge energies. X-ray absorption measurements and first-principle calculations address the microscopic origin of these effects

New insights on cytotoxic activity of group 3 and lanthanide compounds: complexes with [N,N,N]-scorpionate ligands

In this work was to evaluate the cytotoxic activity of a series of monomeric group 3 and lanthanide (N,​N,​N)​-​heteroscorpionate-​triflate complexes (M (OTf) 2 (cybpamd) (THF)​) (Ln = Sc (2)​, Y (3)​, La (4)​, Nd (5)​, Sm (6)​, Dy (7)​, Yb (8)​; OTf = SO3CF3; cybpamd = N, N'-​dicyclohexyl-​2,​2-​bis-​(3,​5-​dimethyl-​pyrazol-​1-​yl)​-​acetamidinate) having octahedral geometry around the metal atoms on the human epithelial lung adenocarcinoma (A549)​, human melanoma (A375)​, human cervical epithelial adenocarcinoma, human embryonic kidney (HEK-​293) and murine macrophages (J774.A1) cell lines. Methods All the tested compds. were incubated with cells for 72 h and their growth inhibition assessed by using MTT assay. Key findings On the cell line HEK-​293 complexes 5 and 7 show a reasonable activities, while the murine macrophage cell line (J774.A1)​, only the scandium 2 complex is not very active. All complexes tested are poorly active on human health adenocarcinoma lung epithelial (A549) and human melanoma (A375)​. Conclusions The group 3 and lanthanide (N,​N,​N)​-​heteroscorpionate triflate-​complexes (M(OTf)​2(cybpamd)​(THF)​) on murine macrophage (J774.A1) cell line, except that of scandium, show a reasonable activity. On human epithelial cervix adenocarcinoma (HeLa) complexes 3, 5 and 6 are significantly more active than cis-​platinum, as well as complex 5 is more active on human embryonic kidney (HEK-​293) cell line. All the tested complexes are poorly active on human epithelial lung adenocarcinoma (A549) and human melanoma (A375)​. The different behavior of the complexes examd. (2-​8) let us hypothesize that the cytotoxic activity is related to the mol. as a whole and not only to the ligand or the metal ion sep

Factors Affecting Asbestosis Mortality Among Asbestos-Cement Workers in Italy

Objectives This study was performed with the aim of investigating the temporal patterns and determinants associated with mortality from asbestosis among 21 cohorts of Asbestos-Cement (AC) workers who were heavily exposed to asbestos fibres. Methods Mortality for asbestosis was analysed for a cohort of 13 076 Italian AC workers (18.1% women). Individual cumulative asbestos exposure index was calculated by factory and period of work weighting by the different composition of asbestos used (crocidolite, amosite, and chrysotile). Two different approaches to analysis, based on Standardized Mortality Ratios (SMRs) and Age-Period-Cohort (APC) models were applied. Results Among the considered AC facilities, asbestos exposure was extremely high until the end of the 1970s and, due to the long latency, a peak of asbestosis mortality was observed after the 1990s. Mortality for asbestosis reached extremely high SMR values [SMR: males 508, 95% confidence interval (CI): 446–563; females 1027, 95% CI: 771–1336]. SMR increased steeply with the increasing values of cumulative asbestos exposure and with Time Since the First Exposure. APC analysis reported a clear age effect with a mortality peak at 75–80 years; the mortality for asbestosis increased in the last three quintiles of the cumulative exposure; calendar period did not have a significant temporal component while the cohort effect disappeared if we included in the model the cumulative exposure to asbestos. Conclusions Among heaviest exposed workers, mortality risk for asbestosis began to increase before 50 years of age. Mortality for asbestosis was mainly determined by cumulative exposure to asbestos

[Time trend in mesothelioma and lung cancer risk in asbestos workers in Italy]

This study aims at investigating, in asbestos exposed workers, the time trend of their risk of mesothelioma and of other neoplasm after very long latency and after the cessation of asbestos exposure. We pooled a large number of Italian cohorts of asbestos workers and updated mortality follow-up. The pool of data for statistical analyses includes 51,988 workers, of which 6,058 women: 54.2% was alive at follow-up, 42.6% was dead, and 2.8%was lost. Cause of death is known for 94.3%: 2,548 deaths from lung cancer, 748 frompleural cancer, 173 fromperitoneal cancer, and 434 from asbestosis. An exposure index is being developed to compare the different cohorts. Data analysis is in progress. This study will have the size for analysing not only time trends in mesothelioma, but also the occurrence of rarer diseases and cancer specific mortality in women

Rate advancement measurement for lung cancer and pleural mesothelioma in asbestos-exposed workers

IntroductionExposure to asbestos increases the risk of lung cancer and mesothelioma. Few studies quantified the premature occurrence of these diseases in asbestos-exposed workers. Focus on premature disease onset (rate advancement or acceleration) can be useful in risk communication and for the evaluation of exposure impact. We estimated rate advancement for total mortality, lung cancer and pleural mesothelioma deaths, by classes of cumulative asbestos exposure in a pooled cohort of asbestos cement (AC) workers in Italy. MethodThe cohort study included 12 578 workers from 21 cohorts, with 6626 deaths in total, 858 deaths from lung cancer and 394 from pleural malignant neoplasm (MN). Rate advancement was estimated by fitting a competitive mortality Weibull model to the hazard of death over time since first exposure (TSFE). ResultAcceleration time (AT) was estimated at different TSFE values. The highest level of cumulative exposure compared with the lowest, for pleural MN AT was 16.9 (95% CI 14.9 to 19.2) and 33.8 (95% CI 29.8 to 38.4) years at TSFE of 20 and 40 years, respectively. For lung cancer, it was 13.3 (95% CI 12.0 to 14.7) and 26.6 (95% CI 23.9 to 29.4) years, respectively. As for total mortality, AT was 3.35 (95% CI 2.98 to 3.71) years at 20 years TSFE, and 6.70 (95% CI 5.95 to 7.41) at 40 years TSFE. ConclusionThe current study observed marked rate advancement after asbestos exposure for lung cancer and pleural mesothelioma, as well as for total mortality

Italian pool of asbestos workers cohorts: mortality trends of asbestos-related neoplasms after long time since first exposure

Asbestos is a known human carcinogen, with evidence for malignant mesothelioma (MM), cancers of lung, ovary, larynx and possibly other organs. MM rates are predicted to increase with a power of time since first exposure (TSFE), but the possible long-term attenuation of the trend is debated. The asbestos ban enforced in Italy in 1992 gives an opportunity to measure long-term cancer risk in formerly exposed workers