| 1. |
- Araujo, Carlos Moyses, et al.
(författare)
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Pressure-induced structural phase transition in NaBH4
- 2005
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Ingår i: Physical Review B. Condensed Matter and Materials Physics. - 1098-0121 .- 1550-235X. ; 72:5, s. 054125-
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Tidskriftsartikel (refereegranskat)abstract
- We present a combined experimental and theoretical study of the technologically important NaBH4 compound under high pressure. Using Raman spectroscopy at room temperature, we have found that NaBH4 undergoes a structural phase transformation starting at 10.0 GPa with the pure high-pressure phase being established above 15.0 GPa. In order to compare the Raman data recorded under high pressure with the low-temperature tetragonal phase of NaBH4, we have also performed a cooling experiment. The known order-disorder transition from the fcc to the tetragonal structure was then observed. However, the new high pressure phase does not correspond to this low-temperature structure. Using first-principle calculations based on the density functional theory, we show that the high-pressure phase corresponds to the alpha-LiAlH4–type structure. We have found a good agreement between the measured and calculated transition pressures. Additionally, we present the electronic structure of both the fcc and the high-pressure phases.
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| 2. |
- Warme, Jonatan, et al.
(författare)
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Helicobacter pylori and Pro-Inflammatory Protein Biomarkers in Myocardial Infarction with and without Obstructive Coronary Artery Disease
- 2023
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Ingår i: International Journal of Molecular Sciences. - : MDPI AG. - 1661-6596 .- 1422-0067. ; 44
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Tidskriftsartikel (refereegranskat)abstract
- Myocardial infarction (MI) with obstructive coronary artery disease (MI-CAD) and MI in the absence of obstructive coronary artery disease (MINOCA) affect different populations and may have separate pathophysiological mechanisms, with greater inflammatory activity in MINOCA compared to MI-CAD. Helicobacter pylori (Hp) can cause systemic inflammation and has been associated with cardiovascular disease (CVD). We aimed to investigate whether Hp infection is associated with concentrations of protein biomarkers of inflammation and CVD. In a case-control study, patients with MINOCA (n = 99) in Sweden were included, complemented by matched subjects with MI-CAD (n = 99) and controls (n = 100). Protein biomarkers were measured with a proximity extension assay in plasma samples collected 3 months after MI. The seroprevalence of Hp and cytotoxin-associated gene A (CagA) was determined using ELISA. The associations between protein levels and Hp status were studied with linear regression. The prevalence of Hp was 20.2%, 19.2%, and 16.0% for MINOCA, MI-CAD, and controls, respectively (p = 0.73). Seven proteins were associated with Hp in an adjusted model: tissue plasminogen activator (tPA), interleukin-6 (IL-6), myeloperoxidase (MPO), TNF-related activation-induced cytokine (TRANCE), pappalysin-1 (PAPPA), soluble urokinase plasminogen activator receptor (suPAR), and P-selectin glycoprotein ligand 1 (PSGL-1). Hp infection was present in one in five patients with MI, irrespective of the presence of obstructive CAD. Inflammatory proteins were elevated in Hp-positive subjects, thus not ruling out that Hp may promote an inflammatory response and potentially contribute to the development of CVD.
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