How to Assess the Carbon Footprint of a Large University? The Case Study of University of Bologna’s Multicampus Organization

University campuses represent a heterogeneous ecosystem as to social, economic, energetic, and personal travel planning with a huge impact on hosting cities and territories. Sustainable policies are thus fundamental to reduce this impact and to adopt ecological behaviors. The measures for any University Sustainability Plan should be evaluated in terms of GHG emissions, as well as the overall impact of the university itself. Carbon footprint (CF) calculation is a relevant Decision Support tool that allows university organizations to measure and communicate the environmental effects of their activities. The aim of this paper is to present a carbon footprint methodology specifically designed to calculate the carbon footprint of large universities. The methodology was applied to calculate the CF of the University of Bologna by following international standards—i.e., the GHG protocol, the ISO 14064, and the ISO/TR 14069 guide—to understand the environmental impact caused by greenhouse gas emissions from direct and indirect university activities. The study was conducted upon the data available in 2020 and then was compared to the 2018 data, with the aim to recognize if the effect of the pandemic could have altered the results. In 2020, the University of Bologna emitted 16,467 tCO2e which became 15,753 tCO2e considering the offset and avoided emission provided by the internal production of energy from renewable sources. Comparison between 2020 and 2018 shows how, in 2018, most of the emissions came from transportation, representing 74% of the total emissions, while in 2020 almost 50% of total emissions derived by IT procurements. The case application demonstrates the way with which the methodology may be applied to assess environmental impact for complex university campuses

Proresolving lipid mediators resolvin D1, resolvin D2, and maresin 1 are critical in modulating T cell responses.

Resolution of inflammation is a finely regulated process mediated by specialized proresolving lipid mediators (SPMs), including docosahexaenoic acid (DHA)-derived resolvins and maresins. The immunomodulatory role of SPMs in adaptive immune cells is of interest. We report that D-series resolvins (resolvin D1 and resolvin D2) and maresin 1 modulate adaptive immune responses in human peripheral blood lymphocytes. These lipid mediators reduce cytokine production by activated CD8(+) T cells and CD4(+) T helper 1 (TH1) and TH17 cells but do not modulate T cell inhibitory receptors or abrogate their capacity to proliferate. Moreover, these SPMs prevented naïve CD4(+) T cell differentiation into TH1 and TH17 by down-regulating their signature transcription factors, T-bet and Rorc, in a mechanism mediated by the GPR32 and ALX/FPR2 receptors; they concomitantly enhanced de novo generation and function of Foxp3(+) regulatory T (Treg) cells via the GPR32 receptor. These results were also supported in vivo in a mouse deficient for DHA synthesis (Elovl2(-/-)) that showed an increase in TH1/TH17 cells and a decrease in Treg cells compared to wild-type mice. Additionally, either DHA supplementation in Elovl2(-/-) mice or in vivo administration of resolvin D1 significantly reduced cytokine production upon specific stimulation of T cells. These findings demonstrate actions of specific SPMs on adaptive immunity and provide a new avenue for SPM-based approaches to modulate chronic inflammation.This work was supported by Fondazione Italiana Sclerosi Multipla (FISM) to V.C. (grant 2015/R/8) and in part by National Institutes of Health (P01095467 and GM38765) to C.N.S, by Ministero dell’Istruzione, dell’Università e della Ricerca (PRIN grant 2010–2011) to M.M., and by Ministero della Salute (RF-2011- 02346771) and FISM (grant 2013/R/2) to L.B

Occupational Exposure to Metal Engineered Nanoparticles: A Human Biomonitoring Pilot Study Involving Italian Nanomaterial Workers

Advances in nanotechnology have led to an increased use of engineered nanoparticles (ENPs) and the likelihood for occupational exposures. However, how to assess such exposure remains a challenge. In this study, a methodology for human biomonitoring, based on Single Particle Inductively Coupled Plasma Mass Spectrometry (SP-ICP-MS), was developed as a tool to assess the ENPs exposure of workers involved in nanomaterial activities in two Italian Companies. The method was validated for size and number concentration determination of Ag, Au, In2O3, Ir, Pd, Pt, and TiO2 NPs in urine and blood samples. The results showed the presence of In2O3 NPs in blood of exposed workers (mean, 38 nm and 10,371 particles/mL), but not in blood of controls. Silver, Au, and TiO2 NPs were found in urine (mean, Ag 29 nm and 16,568 particles/mL) or blood (mean, Au 15 nm and 126,635 particles/mL; TiO2 84 nm and 27,705 particles/mL) of workers, though these NPs were found also in controls. The presence of ENPs in both workers and controls suggested that the extra-professional exposure is a source of ENPs that cannot be disregarded. Iridium, Pd, and Pt NPs were not detected neither in blood nor in urine. Overall, the findings provided a rational basis to evaluate the exposure assessment to ENPs in cohorts of workers as part of risk assessment and risk management processes in workplaces

Gestational weight gain in overweight and obese women enrolled in a healthy lifestyle and eating habits program

OBJECTIVES: To determine whether changes in lifestyle in women with BMI > 25 could decrease gestational weight gain and unfavorable pregnancy outcomes. METHODS: Women with BMI > 25 were randomized at 1st trimester to no intervention or a Therapeutic Lifestyle Changes (TLC) Program including diet (overweight: 1700 kcal/day, obese: 1800 kcal/day) and mild physical activity (30 min/day, 3 times/week). At baseline and at the 36th week women filled-in a Food Frequency Questionnaire. OUTCOMES: gestational weight gain, gestational diabetes mellitus, gestational hypertension, preterm delivery. Data stratified by BMI categories. RESULTS: Socio-demographic features were similar between groups (TLC: 33 cases, CONTROLS: 28 cases). At term, gestational weight gain in obese women randomized to TLC group was lower (6.7 ± 4.3 kg) versus controls (10.1 ± 5.6 kg, p = 0.047). Gestational diabetes mellitus, gestational hypertension and preterm delivery were also significantly lower. TLC was an independent factor in preventing gestational weight gain, gestational diabetes mellitus, gestational hypertension. Significant changes in eating habits occurred in the TLC group, which increased the number of snacks, the intake of fruits-vegetables and decreased the consumption of sugar. CONCLUSIONS: A caloric restriction associated to changes in eating behavior and constant physical activity, is able to reduce gestational weight gain and related pregnancy complications in obese women.Objectives: To determine whether changes in lifestyle in women with BMI > 25 could decrease gestational weight gain and unfavorable pregnancy outcomes. Methods: Women with BMI > 25 were randomized at 1st trimester to no intervention or a Therapeutic Lifestyle Changes (TLC) Program including diet (overweight: 1700 kcal/day, obese: 1800 kcal/day) and mild physical activity (30 min/day, 3 times/week). At baseline and at the 36th week women filled-in a Food Frequency Questionnaire. Outcomes: gestational weight gain, gestational diabetes mellitus, gestational hypertension, preterm delivery. Data stratified by BMI categories. Results: Socio-demographic features were similar between groups (TLC: 33 cases, Controls: 28 cases). At term, gestational weight gain in obese women randomized to TLC group was lower (6.7 ± 4.3 kg) versus controls (10.1 ± 5.6 kg, p = 0.047). Gestational diabetes mellitus, gestational hypertension and preterm delivery were also significantly lower. TLC was an independent factor in preventing gestational weight gain, gestational diabetes mellitus, gestational hypertension. Significant changes in eating habits occurred in the TLC group, which increased the number of snacks, the intake of fruits-vegetables and decreased the consumption of sugar. Conclusions: A caloric restriction associated to changes in eating behavior and constant physical activity, is able to reduce gestational weight gain and related pregnancy complications in obese women. © 2014 Informa UK Ltd

Plasma heavy metal levels correlate with deregulated gene expression of detoxifying enzymes in osteoporotic patients

Heavy metal levels appear to be associated with low bone mineral density (BMD) and the consequent osteoporosis risk, but the relationship with the disease has not been clearly defined. The altered expression pattern of numerous genes, including detoxifying genes, seems to play a pivotal role in this context, leading to increased susceptibility to several diseases, including osteoporosis. The purpose of this study is to analyse circulating heavy metals levels and the expression of detoxifying genes in osteoporotic patients (OPs, n = 31), compared with healthy subjects (CTRs, n = 32). Heavy metals concentration in plasma samples was determined by Inductively Coupled Plasma Mass Spectrometry (ICP-MS), and the subsequent expression analysis of NAD(P)H quinone dehydrogenase 1 (NQO1), Catalase (CAT), and Metallothionein 1E (MT1E) genes in Peripheral Blood Mononuclear Cells (PBMCs) was assessed by real-time polymerase chain reaction (qRT-PCR). Copper (Cu), mercury (Hg), molybdenum (Mo) and lead (Pb) were found to be significantly higher in the plasma of OPs compared to CTRs. Analysis of the expression levels of detoxifying genes showed a significant decrease in CAT and MT1E in OP group. In addition, Cu correlated positively with the expression levels of both CAT and MT1E in CTRs group and MT1E in OPs. This study shows an increased circulating concentration of certain metals combined with an altered expression pattern of detoxifying genes in OPs, highlighting a novel aspect to be investigated in order to better characterize the role of metals in the pathogenesis of osteoporosis

Interleukin-9 regulates macrophage activation in the progressive multiple sclerosis brain.

BACKGROUND: Multiple sclerosis (MS) is an immune-mediated, chronic inflammatory, and demyelinating disease of the central nervous system (CNS). Several cytokines are thought to be involved in the regulation of MS pathogenesis. We recently identified interleukin (IL)-9 as a cytokine reducing inflammation and protecting from neurodegeneration in relapsing-remitting MS patients. However, the expression of IL-9 in CNS, and the mechanisms underlying the effect of IL-9 on CNS infiltrating immune cells have never been investigated. METHODS: To address this question, we first analyzed the expression levels of IL-9 in post-mortem cerebrospinal fluid of MS patients and the in situ expression of IL-9 in post-mortem MS brain samples by immunohistochemistry. A complementary investigation focused on identifying which immune cells express IL-9 receptor (IL-9R) by flow cytometry, western blot, and immunohistochemistry. Finally, we explored the effect of IL-9 on IL-9-responsive cells, analyzing the induced signaling pathways and functional properties. RESULTS: We found that macrophages, microglia, and CD4 T lymphocytes were the cells expressing the highest levels of IL-9 in the MS brain. Of the immune cells circulating in the blood, monocytes/macrophages were the most responsive to IL-9. We validated the expression of IL-9R by macrophages/microglia in post-mortem brain sections of MS patients. IL-9 induced activation of signal transducer and activator of transcription (STAT)1, STAT3, and STAT5 and reduced the expression of activation markers, such as CD45, CD14, CD68, and CD11b in inflammatory macrophages stimulated in vitro with lipopolysaccharide and interferon (IFN)-γ. Similarly, in situ the number of activated CD68+ macrophages was significantly reduced in areas with high levels of IL-9. Moreover, in the same conditions, IL-9 increased the secretion of the anti-inflammatory cytokine, transforming growth factor (TGF)-β. CONCLUSIONS: These results reveal a new cytokine expressed in the CNS, with a role in the context of MS. We have demonstrated that IL-9 and its receptor are both expressed in CNS. Moreover, we found that IL-9 decreases the activation state and promotes the anti-inflammatory properties of human macrophages. This mechanism may contribute to the beneficial effects of IL-9 that are observed in MS, and may be therapeutically potentiated by modulating IL-9 expression in MS

Interleukin-9 regulates macrophage activation in the progressive multiple sclerosis brain

Background: Multiple sclerosis (MS) is an immune-mediated, chronic inflammatory, and demyelinating disease of the central nervous system (CNS). Several cytokines are thought to be involved in the regulation of MS pathogenesis. We recently identified interleukin (IL)-9 as a cytokine reducing inflammation and protecting from neurodegeneration in relapsing-remitting MS patients. However, the expression of IL-9 in CNS, and the mechanisms underlying the effect of IL-9 on CNS infiltrating immune cells have never been investigated. Methods: To address this question, we first analyzed the expression levels of IL-9 in post-mortem cerebrospinal fluid of MS patients and the in situ expression of IL-9 in post-mortem MS brain samples by immunohistochemistry. A complementary investigation focused on identifying which immune cells express IL-9 receptor (IL-9R) by flow cytometry, western blot, and immunohistochemistry. Finally, we explored the effect of IL-9 on IL-9-responsive cells, analyzing the induced signaling pathways and functional properties. Results: We found that macrophages, microglia, and CD4 T lymphocytes were the cells expressing the highest levels of IL-9 in the MS brain. Of the immune cells circulating in the blood, monocytes/macrophages were the most responsive to IL-9. We validated the expression of IL-9R by macrophages/microglia in post-mortem brain sections of MS patients. IL-9 induced activation of signal transducer and activator of transcription (STAT)1, STAT3, and STAT5 and reduced the expression of activation markers, such as CD45, CD14, CD68, and CD11b in inflammatory macrophages stimulated in vitro with lipopolysaccharide and interferon (IFN)-γ. Similarly, in situ the number of activated CD68+ macrophages was significantly reduced in areas with high levels of IL-9. Moreover, in the same conditions, IL-9 increased the secretion of the anti-inflammatory cytokine, transforming growth factor (TGF)-β. Conclusions: These results reveal a new cytokine expressed in the CNS, with a role in the context of MS. We have demonstrated that IL-9 and its receptor are both expressed in CNS. Moreover, we found that IL-9 decreases the activation state and promotes the anti-inflammatory properties of human macrophages. This mechanism may contribute to the beneficial effects of IL-9 that are observed in MS, and may be therapeutically potentiated by modulating IL-9 expression in MS

Food at the heart of the Empire. Dietary reconstruction for Imperial Rome inhabitants

This paper aims to provide a broad diet reconstruction for people buried in archaeologically defined contexts in Rome (first to third centuries CE), in order to combine archaeological and biological evidence focusing on dietary preferences in Imperial Rome. A sample of 214 human bones recovered from 6 funerary contexts was selected for carbon and nitrogen stable isotope analysis. The baseline for the terrestrial protein component of the diet was set using 17 coeval faunal remains recovered from excavations at Rome supplemented by previously published data for the same geographic and chronological frames. δ13C ranges from − 19.9 to − 14.8‰, whereas δ15N values are between 7.2 and 10.0‰. The values are consistent with an overall diet mainly based on terrestrial resources. All the human samples rely on a higher trophic level than the primary consumer faunal samples. Certainly, C3 plants played a pivotal role in the dietary habits. However, C4 plants also seem to have been consumed, albeit they were not as widespread and were not always used for human consumption. The environment played a critical role also for Romans of lower social classes. The topographical location determined the preferential consumption of food that people could obtain from their neighborhood

Endothelin-Receptor Antagonists beyond Pulmonary Arterial Hypertension: Cancer and Fibrosis.

The endothelin axis and in particular the two endothelin receptors, ETA and ETB, are targets for therapeutic intervention in human diseases. Endothelin-receptor antagonists are in clinical use to treat pulmonary arterial hypertension and have been under clinical investigation for the treatment of several other diseases, such as systemic hypertension, cancer, vasospasm, and fibrogenic diseases. In this Perspective, we review the molecules that have been evaluated in human clinical trials for the treatment of pulmonary arterial hypertension, as well as other cardiovascular diseases, cancer, and fibrosis. We will also discuss the therapeutic consequences of receptor selectivity with regard to ETA-selective, ETB-selective, or dual ETA/ETB antagonists. We will also consider which chemical characteristics are relevant to clinical use and the properties of molecules necessary for efficacy in treating diseases against which known molecules displayed suboptimal efficacy