| 1. |
- Biasin, Pietro, et al.
(författare)
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From borophene polymorphs towards a single honeycomb borophane phase : reduction of hexagonal boron layers on Al(111)
- 2023
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Ingår i: Nanoscale. - 2040-3364. ; 15:45, s. 18407-18414
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Tidskriftsartikel (refereegranskat)abstract
- The recent interest in characterizing 2D boron polymorphs has led to claims of the first stabilization of a honeycomb phase with conical Dirac-like electron dispersion. However, the synthesis of chemically stable, single, and homogeneous 2D boron phases still represents a significant experimental challenge. This is ascribed to the intrinsic boron electronic configuration that, at variance with carbon, leads to the formation of multi-center covalent bonds. External charge compensation by substrate-induced doping can steer the geometry of the layer, both in the buckling and in the density of B vacancies, like in the case of the recently achieved stabilization of honeycomb boron layers on Al(111). The price to pay is however a strong boron-support interaction, resulting in general in a limiting kinetic hindrance with respect to the synthesis of homogenous single phases. In the specific case of Al(111) an AlB2 layer is known to form at the surface, quite far from a desirable quasi-freestanding borophene monolayer and at variance with graphene, which can be easily synthesized in an almost freestanding configuration e.g. on Ir(111). We provide here evidence for the (reversible) formation of well-ordered honeycomb borophane upon hydrogenation of the honeycomb boron phase on Al(111).
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| 2. |
- Biasin, Pietro, et al.
(författare)
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Growth and Redox Properties of Boron on Al(111) : Competing Affinities in the Case of Honeycomb AlB2
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Ingår i: ACS Nano. - 1936-0851.
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Tidskriftsartikel (refereegranskat)abstract
- The complexity of the geometric and electronic structure of boron allotropes is associated with the multicentric bonding character and the consequent B polymorphism. When growth is limited to two-dimensions (2D), the structural and electronic confinement yields the borophenes family, where the interaction with the templating substrate actually determines the stability of inequivalent boron phases. We report here a detailed study of the growth of the honeycomb AlB2 phase on Al(111), followed by an investigation of its oxidation and reduction properties. By means of a combined experimental and theoretical approach, we show that the structure of the B/Al interface is affected by the complex interplay between B, Al, and common reactive agents like oxygen and hydrogen. While kinetic effects associated with diffusion and strain release influence the AlB2 growth in vacuo, Al, B, O, and H chemical affinities determine its redox behavior. Reduction with atomic hydrogen involves the B layer and yields an ordered honeycomb borophane H/AlB2 phase. Instead, oxidation takes place at the Al interface, giving origin to buried and 1D surface aluminum oxide phases.
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| 3. |
- Fabris, Stefano, et al.
(författare)
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Oxygen Dissociation by Concerted Action of Di-Iron Centers in Metal
- 2011
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Ingår i: Nano Letters. - 1530-6992 .- 1530-6984. ; 11, s. 5414-
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Tidskriftsartikel (refereegranskat)abstract
- The high chemical reactivity of unsaturated metalsites is a key factor for the development of novel devices withapplications in sensor engineering and catalysis. It is also centralin the research for sustainable energy concepts, e.g., the efficientproduction and conversion of chemical fuels. Here, we study theprocess of oxygen dissociation by a surface-supported metal organic network that displays close structural and functionalanalogies with the cofactors of non-heme enzymes. We synthesizea two-dimensional array of chemically active di-iron sites ona Cu(001) surface wheremolecular oxygen readily dissociates atroom temperature. We provide an atomic-level structural and electronic characterization before and after reaction by combiningscanning tunneling microscopy, X-ray absorption spectroscopy, and density functional theory. The latter identifies a novelmechanism for O2 dissociation controlled by the cooperative catalytic action of two Fe2+ ions. The high structural flexibility of theorganic ligands, the mobility of the metal centers, and the hydrogen bonding formation are shown to be essential for the functionalityof these active centers allowing to mimick biologically relevant reactions in a confined environment.
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| 4. |
- Bailetti, D., et al.
(författare)
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ANGPTL4 gene E40K variation protects against obesity-associated dyslipidemia in participants with obesity
- 2019
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Ingår i: Obesity Science & Practice. - : Wiley. - 2055-2238. ; 5:1, s. 83-90
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Tidskriftsartikel (refereegranskat)abstract
- Objective ANGPTL4 inhibits lipoprotein lipase in adipose tissue, regulating plasma triglycerides levels. In persons with obesity plasma ANGPTL4 levels have been positively correlated with body fat mass, TG levels and low HDL. A loss-of-function E40K mutation in ANGPTL4 prevents LPL inhibition, resulting in lower TGs and higher HDLc in the general population. Since obesity determines metabolic alterations and consequently is a major risk factor for cardiovascular disease, the aim was to explore if obesity-related metabolic abnormalities are modified by the ANGPTL4-E40K mutation. Methods ANGPTL4-E40K was screened in 1206 Italian participants, of which 863 (71.5%) with obesity. All subjects without diabetes underwent OGTT with calculation of indices of insulin-sensitivity. Results Participants with obesity carrying the E40K variant had significantly lower TG (p = 0.001) and higher HDLc levels (p = 0.024). Also in the whole population low TGs and high HDLc were confirmed in E40K carriers. In the obese subpopulation it was observed that almost all E40K carriers were within the lowest quartile of TGs (p = 1.1 x 10(-9)). E40K had no substantial effect of on glucose metabolism. Finally, none of the obese E40K carriers had T2D, and together with the favourable lipid profile, they resemble a metabolically healthy obese (MHO) phenotype, compared to 38% of E40E wild-type obese that had diabetes and/or dyslipidaemia (p = 0.0106). Conclusions In participants with obesity the ANGPTL4-E40K variant protects against dyslipidemia. The phenotype of obese E40K carriers is that of a patient with obesity without metabolic alterations, similar to the phenotype described as metabolic healthy obesity.
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| 5. |
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| 6. |
- Burza, Maria Antonella, 1980, et al.
(författare)
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PNPLA3 I148M (rs738409) genetic variant is associated with hepatocellular carcinoma in obese individuals
- 2012
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Ingår i: Digestive and Liver Disease. - : Elsevier BV. - 1590-8658. ; 44:12, s. 1037-1041
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Tidskriftsartikel (refereegranskat)abstract
- Background: Obesity is a risk factor for cancer, including hepatocellular carcinoma. Patatin-like phospholipase domain-containing 3 (PNPLA3) I148M (rs738409) genetic variant has been associated with hepatocellular carcinoma (HCC) in individuals with chronic alcohol abuse or hepatic viral infection. In the present study we examined the association between the PNPLA3I148M genetic variant and hepatocellular carcinoma in obese individuals from the Swedish Obese Subjects cohort (n=4047). Methods: We performed a matched, prospective, controlled, interventional trial, investigating the effect of bariatric surgery (surgery group) compared to conventional treatment (control group) for obesity. Results: A total of 9 events were observed in the 15-year median follow up (5 in the control group and 4 in the surgery group). A significantly higher incidence of hepatocellular carcinoma in PNPLA3 148M allele carriers was found in obese individuals in the control group (log-rank P-value=0.001), but not in the surgery group (log-rank P-value=0.783). Consistently, an increased risk (for each PNPLA3 148M allele, hazard ratio: 5.9; 95% confidence interval 1.5-23.8; P-value=0.013) of developing hepatocellular carcinoma was observed only in the control group. Conclusion: The current study is the first prospective report showing the association of the PNPLA3I148M genetic variant and hepatocellular carcinoma in severely obese individuals.
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| 7. |
- Cavallo, M. G., et al.
(författare)
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Altered Glucose Homeostasis Is Associated with Increased Serum Apelin Levels in Type 2 Diabetes Mellitus
- 2012
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Ingår i: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 7:12
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Tidskriftsartikel (refereegranskat)abstract
- Background: Apelin is an adipokine that plays a role in the regulation of glucose homeostasis and in obesity. The relationship between apelin serum concentration and dysmetabolic conditions such as type 2 diabetes (T2D) is still controversial. Aims of our study are: 1) determine the circulating levels of apelin in a large cohort of Italian subjects with T2D, T1D and in non-diabetic controls; 2) identify putative metabolic determinants of modified apelin concentrations, in order to search possible mechanism of apelin control; 3) investigate changes in apelin levels in response to sharp modifications of glucose/insulin metabolism in T2D obese subjects before and 3 days after bariatric surgery. Methods: We recruited 369 subjects, 119 with T2D, 113 with T1D and 137 non-diabetic controls. All subjects underwent a complete clinical examination, including anthropometric and laboratory measurements. Serum apelin levels were determined by EIA (immunoenzyme assay). Results: Patients with T2D had significantly higher serum apelin levels compared to controls (1.23 +/- 1.1 ng/mL vs 0.91 +/- 0.7 ng/mL, P<0.001) and to T1D subjects (0.73 +/- 0.39 ng/mL, P<0.001). Controls and T1D subjects did not differ significantly in apelin levels. Apelin concentrations were directly associated with fasting blood glucose (FBG), body mass index (BMI), basal Disposition Index (DI-0), age, and diagnosis of T2D at bivariate correlation analysis. Multiple regression analysis confirmed that diagnosis of T2D, basal DI-0 and FBG were all determinants of serum apelin levels independently from age and BMI. Bariatric surgery performed in a subgroup of obese diabetic subjects (n = 12) resulted in a significant reduction of apelin concentrations compared to baseline levels (P = 0.01). Conclusions: Our study demonstrates that T2D, but not T1D, is associated with increased serum apelin levels compared to non-diabetic subjects. This association is dependent on impaired glucose homeostasis, and disappears after bariatric surgery, providing further evidence regarding the relationship between apelin and the regulation of glucose metabolism.
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| 8. |
- Maglio, Cristina, 1983, et al.
(författare)
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The IRS1 rs2943641 Variant and Risk of Future Cancer Among Morbidly Obese Individuals.
- 2013
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Ingår i: The Journal of clinical endocrinology and metabolism. - : The Endocrine Society. - 1945-7197 .- 0021-972X. ; 98:4
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Tidskriftsartikel (refereegranskat)abstract
- Context:Obesity and insulin resistance are risk factors for cancer development. The IRS1 rs2943641 genetic variant has been widely associated with insulin resistance.Objective:The aim of the study was to examine whether the IRS1 rs2943641 associates with cancer incidence in obese individuals.Design, Setting and Patients:The IRS1 rs2943641 was genotyped in participants from the Swedish Obese Subjects (SOS) study, an intervention trial on the effect of bariatric surgery on mortality and morbidity compared with usual care and in the population-based Malmö Diet and Cancer (MDC) cohort. In both studies, the median follow-up for cancer incidence was about 15 years.Intervention and Main Outcome Measure:Cancer incidence was assessed in both the SOS and the MDC cohorts through national and local registers.Results:The IRS1 T allele was associated with lower insulin resistance in both the SOS and the MDC studies. A lower cancer incidence was found in T allele carriers from the SOS control group (hazard ratio [HR] 0.77, 95% confidence interval [CI] 0.62-0.96; P = .021) and was restricted to morbidly obese individuals (HR 0.67, 95% CI 0.50-0.91; P = .011). No evidence of such association was detected in the surgery group (interaction P = .005). In the MDC cohort, a nonsignificant tendency for lower cancer incidence in T allele carriers was observed only in morbidly obese individuals. A meta-analysis of morbidly obese individuals (body mass index > 40 kg/m(2)) from the two cohorts strengthened the evidence for the association (HR 0.66, 95% CI 0.50-0.87; P = .004).Conclusions:Our results suggest that the T allele of rs2943641 near IRS1 may associate with lower cancer incidence in morbidly obese individuals.
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| 9. |
- Mancina, Rosellina Margherita, et al.
(författare)
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COBLL1 rs7607980 genetic variant and insulin resistance in overweight and obese children.
- 2013
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Ingår i: Diabetes/metabolism research and reviews. - : Wiley. - 1520-7560 .- 1520-7552. ; 29:5, s. 413-6
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Childhood obesity is a growing epidemic worldwide and it is associated with metabolic complications, such as insulin resistance. Recently, a genetic variation (rs7607980) in the cordon-bleu protein-like 1 (COBLL1) gene has been associated with lower insulin resistance in adults. The aim of the study was to investigate if the association between COBLL1 rs7607980 genetic variant and lower insulin resistance was present early in life. METHODS: This sequence variant was genotyped in 878 overweight and obese children (mean age: 10years) from Sardinia, Italy, from the outpatient clinic of the Pediatric Endocrine Unit, at the Regional Hospital for Microcitaemia in Cagliari. Insulin resistance was assessed by measurement of fasting circulating insulin levels before and after an oral glucose tolerance test (OGTT) and by homeostatic model assessment of insulin resistance (HOMA-IR). RESULTS: The COBLL1 rs7607980 C allele was associated with lower fasting insulin and HOMA-IR levels (P=0.002 and P=0.035, respectively) in overweight and obese children. Importantly, lower insulin levels were also observed two hours after OGTT in C allele carriers (P=0.009). CONCLUSIONS: The present study shows for the first time the association between COBLL1 rs7607980 C allele, lower serum insulin levels and lower insulin resistance in overweight and obese children. Copyright © 2013 John Wiley & Sons, Ltd.
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