CO2 conversion into hydrocarbons via modified Fischer-Tropsch synthesis by using bulk iron catalysts combined with zeolites

To effectively address the challenges posed by global warming, a prompt and coordinated effort is necessary to conduct an extensive study aimed at reducing CO2 emissions and overcoming the obstacles presented by expensive and scarce fossil fuel resources. This study primarily focuses on comparing two different methodologies for preparing Na-promoted Fe3O4-based catalysts for the CO2 hydrogenation into hydrocarbon mixtures. Three catalysts were synthesized and tested: two samples were impregnated with a different amount of Na (1 wt% and 5 wt%), while a third one was obtained via coprecipitation with NaOH. As the latter catalyst exhibited the best performance, it was combined with zeolites in two ways: physical mixtures and core-shell structures. MFI-type zeolites were used in both configurations and a conventional structure was compared to a hierarchical one. As a result, mesopores increased successfully both the CO2 conversion from 37% to 40% and the liquid hydrocarbon (C6+) selectivity from 29% to 57%, doubling the C6+ yield. On the other hand, NH3-TPD and XPS measurements demonstrated that the intimate contact between the two materials in the core-shell structures led to the migration of Na from the oxide to the zeolite reducing the concentration of strong acid sites and, consequently, the liquid hydrocarbon yield

Baseline and postoperative C-reactive protein levels predict mortality in operable lung cancer.

Background Higher blood levels of C-reactive protein (CRP) have been associated with shorter survival in patients with cardiovascular, chronic obstructive pulmonary disease and cancer. We investigated the impact of baseline and postoperative CRP levels on survival of patients with operable lung cancer (LC). Patients and methods CRP values at baseline (CRP0) and 3 days after surgery (CRP3) were measured in a consecutive series of 1750 LC patients who underwent complete resection between 2003 and 2015. Patients were classified as having 0 (N = 593), 1 (N = 658) or 2 (N = 553) risk factors: CRP0 and/or CRP3 values above the respective median value. The effect of higher CRP was evaluated by Kaplan–Meier mortality curves and adjusted hazard ratio (HR) with 95% confidence interval (CI), by fitting Cox proportional hazards models. Results Cumulative proportions of 5-year survival were 67% for 0 risk factors, 58% for 1 risk factor and 41% for 2 risk factors (P < 0.0001). The overall 5-year mortality risk was significantly higher in patients with 1 risk factor (adjusted hazard ratio [aHR] 1.43 [95% CI 1.14–1.79]), or 2 risk factors (aHR 2.49 [95% CI 1.99–3.11]). A significant impact on survival was observed in each tumour-node-metastasis stage group, and in the subset of non-smokers. Postoperative 30-day mortality was significantly higher in patients with 2 risk factors only (aHR 2.2% versus 0.6%, p < 0.0475). Conclusions Baseline and postoperative CRP levels predict immediate and long-term mortality in all stages of operable lung cancer. Patients with higher CRP levels could be candidate to randomised adjuvant trials with anti-inflammatory agents

The role of heat shock proteins in the inflammatory state of vernal keratoconjunctivitis

The aim of the study was to analyse the role of heat shock proteins (HSPs) in vernal keratoconjunctivitis (VKC), a recurrent allergic ocular inflammatory disease. We evaluated the expression of some HSPs (Hsp10, Hsp27, Hsp40, Hsp60, Hsp70, Hsp90) in the mucosal biopsies of VKC patients by immunohistochemistry, and in conjunctival cells cultures treated with inflammatory stimuli (IL-1β, histamine, IL-4, TNFβ, UVB irradiation) by western blotting. Immunohistochemical analysis revealed that Hsp10, Hsp27, Hsp40, Hsp70 and Hsp90 expression was significantly increased in VKC whereas the Hsp60 level was unaltered. In vitro induction by inflammatory stimuli in Chang epithelial conjunctival cells revealed that Hsp70 protein expression was significantly increased in epithelial cells line after 4-10 h from histamine and IL-4 stimulation. The same molecule was also overexpressed in conjunctival fibroblast cultures after TNFβ treatment. Hsp90 protein level was increased in the same cell cultures by IL-1β at 4-10-24 h. The Hsp40 protein expression was increased both in epithelial and fibroblast cultures induced by all inflammatory stimuli. Moreover, UVB irradiation significantly increased Hsp90 expression in primary fibroblast culture and Hsp27 in conjunctival epithelial cells after 10 hours. These results indicate that HSPs levels increase in VKC. In particular, Hsp40 expression is up-regulated by all the typical inflammatory stimuli involved in VKC pathogenesis. The specific role of each one of these chaperonins to further induce or counteract inflammation need to be further investigated

Stopping Smoking Reduces Mortality in Low-Dose Computed Tomography Screening Participants

Abstract Introduction The National Lung Screening Trial has achieved a 7% reduction in total mortality with low-dose computed tomography (LDCT) screening as compared with in the chest radiography arm. Other randomized trials are under way, comparing LDCT screening with no intervention. None of these studies was designed to investigate the impact of smoking habits on screening outcome. In the present study, we tested the effect of stopping smoking on the overall mortality of participants undergoing repeated LDCT screening for many years. Methods Between 2000 and 2010, 3381 smokers aged 50 years or older were enrolled in two LDCT screening programs. On the basis of the last follow-up information, subjects were divided into two groups: current smokers throughout the screening period and former smokers. Results With a median follow-up time of 9.7 years and a total of 32,857 person-years (PYs) of follow-up, a total of 151 deaths were observed in the group of 1797 current smokers (17,846 PYs) versus 109 among 1584 former smokers (15,011 PYs), corresponding to mortality rates of 8.46 and 7.26 for every 1000 PYs, respectively. Compared with current smokers, former smokers had an adjusted mortality hazard ratio of 0.61 (95% confidence interval: 0.44–0.83), with a 39% reduction in mortality. A similar reduction in mortality was observed in the subset of 712 late quitters, with a hazard ratio of 0.65 (95% confidence interval: 0.44–0.96). Conclusions Stopping smoking significantly reduces the overall mortality of smokers enrolled in LDCT screening programs. The beneficial effect of stopping smoking on total mortality appears to be threefold to fivefold greater than the one achieved by earlier detection in the National Lung Screening Trial

Heat shock proteins levels and expression in chronic obstructive pulmonary disease and vernal keratoconjunctivitis

Inflammatory response in different organs share many similarities, but site-specific signs. Symptoms can be related to mucosal structure changes. The aim of the study was to compare heat shock proteins (HSPs) levels and expression in chronic obstructive pulmonary disease (COPD) to other inflammatory status of mucosa, such as vernal keratoconjunctivitis (VKC), a recurrent ocular inflammatory disease in which autoimune aggression may have a pathogenetic role. We examined bronchial mucosal biopsies from COPD patients (moderate to severe stage) and conjunctival biopsies from VKC patients; age-matched controls were selected for each group. We evaluated levels (by immunohistochemistry) and expression (by RT-PCR) of a panel of HSPs, among which Hsp10, Hsp27, Hsp40, Hsp60, Hsp70, Hsp90, and of the main heat shock transcription factor (both HSF-1 and pHSF-1). Hsp10 levels and expression increased in all pathological conditions, Hsp27 in VKC, Hsp40 in COPD and VKC, Hsp60 in COPD, Hsp70 and Hsp90 in VKC, as compared to their appropriate controls. Transcription factor pHSF-1 positive cells were significantly increased in COPD compared to controls, while was unaltered in VKC. Moreover, all pathological tissues showed increased levels of macrophages (CD68 positive) in lamina propria, COPD showed increased levels of neutrophils (elastase positive) and VKC increased levels of eosinophils (EG2 positive). Finally, Hsp60 colocalize with elastase positive cells in COPD. These results indicate that HSPs levels and expression change during development of different types of inflammation. Further studies will prove their active involvement and functions in triggering and/or maintaining the inflammatory status

Improved Prognostic Prediction in Never-Smoker Lung Cancer Patients by Integration of a Systemic Inflammation Marker with Tumor Immune Contexture Analysis

Almost 25% of lung cancers (LCs) occur in never-smokers. LC inflammatory profile, based on plasma C-reactive protein levels (CRP), predicts mortality, independently by smoking-status. We hypothesized that: CRP could be associated with tumor immune contexture (TIC) in never-smokers and both these two parameters may improve their prognosis. Sixty-eight never-smokers LC patients with high or low CRP were selected. The programmed cell death protein 1 (PD-1) and its ligand (PD-L1), the human leukocyte antigens (HLA-DR and HLA-I), CD8, CD4, CD3, CD33, CD163, and CD68 were evaluated by immunohistochemistry on surgical samples given TIC evaluation. The classification model based on TIC scores was generated by Classification and Regression Tree analysis. Tumor mutational burden was evaluated by targeted next-generation sequencing. Exclusively high CRP (H-CRP) subset showed PD-L1 expression in 35% of LC as well as lower HLA-I and HLA-DR in their stromal cells. CD3, CD4, CD8, HLA-I, HLA-DR tumor cells staining were associated with a "low inflammatory profile" subset. CRP and LC immune profiles drive clinical outcome: 5-year survival 88% against 8% was associated with low and high-risk profiles (p&lt; 0.0001). Clinical outcome prediction in never-smoker LC patients may be improved by both CRP and tumor immune contexture evaluation

Tubulin tyrosination regulates synaptic function and is disrupted in Alzheimer's disease

: Microtubules play fundamental roles in the maintenance of neuronal processes and in synaptic function and plasticity. While dynamic microtubules are mainly composed of tyrosinated tubulin, long-lived microtubules contain detyrosinated tubulin, suggesting that the tubulin tyrosination/detyrosination cycle is a key player in the maintenance of microtubule dynamics and neuronal homeostasis, conditions which go awry in neurodegenerative diseases. In the tyrosination/detyrosination cycle, the C-terminal tyrosine of α-tubulin is removed by tubulin carboxypeptidases and re-added by tubulin tyrosine ligase. Here we show that tubulin tyrosine ligase hemizygous mice exhibit decreased tyrosinated microtubules, reduced dendritic spine density, and both synaptic plasticity and memory deficits. We further report decreased tubulin tyrosine ligase expression in sporadic and familial Alzheimer's disease, and reduced microtubule dynamics in human neurons harboring the familial APP-V717I mutation. Finally, we show that synapses visited by dynamic microtubules are more resistant to oligomeric amyloid β peptide toxicity and that expression of tubulin tyrosine ligase, by restoring microtubule entry into spines, suppresses the loss of synapses induced by amyloid β peptide. Together, our results demonstrate that a balanced tyrosination/detyrosination tubulin cycle is necessary for the maintenance of synaptic plasticity, is protective against amyloid β peptide-induced synaptic damage, and that this balance is lost in Alzheimer's disease, providing evidence that defective tubulin retyrosination may contribute to circuit dysfunction during neurodegeneration in Alzheimer's disease

Nuclear localization and new isoforms detection give new insights on Hsp10 functions in normal and cigarette smoke-stressed lung cells

Heat-shock protein (Hsp)10 is the co-chaperone for Hsp60 inside mitochondria, but it also resides outside the organelle. Variations in its levels and intracellular dis- tribution have been documented in pathological conditions, e.g. cancer and chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) is a potent stressor for the respiratory system, but its effects on the expression, function, and cellular locali- zation of mitochondrial chaperonins are still largely unknown. We studied in vivo (airways biopsies) the localization of Hsp10 and Hsp60 in patients (smokers and non-smokers) affected by mild-moderate COPD, and charac- terized the effects of non-lethal doses of CS extract (CSE) on the expression of these molecules in two human cell lines: lung fibroblasts (HFL-1) and bronchial epithelial cells (16HBE). We applied various in vitro methods: IHC, subcellular fractionation analyses (SFA), western blotting (WB), ICC, transmission electron microscopy (TEM) immunogold, chromati protein extracts (CPE), as well as 2D-gel based proteomics analyses. Bioinformatics was used to gather structural in silico data. IHC showed that Hsp10 occurred in nuclei of epithelial and lamina propria cells of bronchial mucosa from non-smokers and smokers. ICC, SFA, and WB showed that 16HBE and HFL-1 cells featured nuclear Hsp10, before and after CSE exposure; TEM immunogold further confirmed this observation. Proteomics data showed that CSE stimulation did not increase the levels of Hsp10 but did elicit qualitative changes as indicated by molecular weight and isoelectric point shifts. Bioinformatics analyses indicated that Hsp10 can localize in extramitochondrial sites, such as the nucleus, even if Hsp10 lacks known DNA-binding motifs or nuclear import signals. Hsp10 nuclear levels increased after CSE stimulation in HFL-1, indicating cytosol to nucleus migration, and although Hsp10 did not bind DNA, it bound a DNA-associated protein as suggested by CPE/gel retardation experiments. Data reported here indicate that in human cells of the respiratory mucosa there are at least three different intracellular locales for Hsp10: mitochondrial, nuclear, and cyto- solic. Further experiments are en route for the definition of the mechanisms underlying the transfer of Hsp10 to the nucleus and other cellular/extracellular compartments. This work was supported by grants from University of Palermo (FFR 2012) to GLR

Public awareness of the link between alcohol and cancer in England in 2015: A population-based survey

Background: Public knowledge of the association between alcohol and cancer is reported to be low. We aimed to provide up-to-date evidence for England regarding awareness of the link between alcohol and different cancers and to determine whether awareness differs by demographic characteristics, alcohol use, and geographic region. Methods: A representative sample of 2100 adults completed an online survey in July 2015. Respondents were asked to identify which health outcomes, including specific cancers, may be caused by alcohol consumption. Logistic regressions explored whether demographic, alcohol use, and geographic characteristics predicted correctly identifying alcohol-related cancer risk. Results: Unprompted, 12.9% of respondents identified cancer as a potential health outcome of alcohol consumption. This rose to 47% when prompted (compared to 95% for liver disease and 73% for heart disease). Knowledge of the link between alcohol and specific cancers varied between 18% (breast) and 80% (liver). Respondents identified the following cancers as alcohol-related where no such evidence exists: bladder (54%), brain (32%), ovarian (17%). Significant predictors of awareness of the link between alcohol and cancer were being female, more highly educated, and living in North-East England. Conclusion: There is generally low awareness of the relationship between alcohol consumption and cancer, particularly breast cancer. Greater awareness of the relationship between alcohol and breast cancer in NorthEast England, where a mass media campaign highlighted this relationship, suggests that population awareness can be influenced by social marketing