•Impact craters on Ceres show characteristic trends in their spectral properties with respect to their relative geological age.•Spectral slopes mostly reflect different physical properties of the ...surface material.•Regional concentrations of ammonium-bearing phyllosilicates indicate stratigraphic differences within Ceres’ crust and strengthen the theory that ammonia is a primordial constituent.•Local concentrations of H2O ice and carbonates are associated with the youngest, either recently emplaced or excavated, surface deposits.
Impact craters of different geological ages, sizes and morphologies are not only the most obvious surface features on Ceres’ surface. The investigation of their spectral properties in combination with Ceres’ geology and topography reveals not only lateral compositional variations in Ceres’ surface material but also possible stratigraphic differences within Ceres’ crust. Spectral properties of impact craters with different ages do show distinct trends implying variations with increasing exposure duration of the impact material onto Ceres’ surface. Local concentrations of H2O ice and carbonates are associated with the youngest, either recently emplaced or excavated, surface deposits. On the contrary, regionally higher amounts of ammoniated phyllosilicates originate from deeper regions of Ceres’ crust and strengthen the theory of ammonia being a primordial constituent of Ceres. The blue spectral slope, clearly associated with relatively weak absorptions of OH-bearing and/or ammoniated phyllosilicates, is limited to fresh impact material. Either, the blue spectral slope diminishes slowly with increasing geologic age due to space weathering processes, or shortly as a result of gravitation-induced slumping, forming a fine and loosely consolidated regolith.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Previous studies have clearly demonstrated the beneficial effect of β-blockers in patients with stable congestive heart failure (CHF). β-blockers improve left ventricular ejection fraction (LVEF) and ...reduce cardiac mortality. However, there is an interindividual variability in the response to these agents. Two studies have suggested a possible impact of some functional βAR gene polymorphisms on the effects of β-blockade. The objective of the study is to analyse the association between genetic variations in the β1 or the β2 adrenoreceptor (AR) gene and the effects of β-blockade in patients with stable CHF. We studied 199 consecutive patients with stable CHF not treated with β-blockers. Before introduction of β-blockers and 3 months after the maximal tolerated dose was reached, patients underwent an echocardiography and a radionuclide angiography. The β1ARGlyArg, β1ARSerGly, β2ARGlyArg, β2ARGlnGlu and β2ARThrIle polymorphisms were determinedβ-blockade resulted in a significant decrease in heart rate, a significant increase in LVEF (from 30±10% to 40±13%, P<0.0001). There was no association between the five polymorphisms and heart rate or LVEF, either before or after β-blockade. Heart rate and LVEF responses to β-blockade were not associated with the β1AR or the β2AR polymorphisms. βAR polymorphisms did not explain the interindividual variability in the response to β-blockers.
Impaired hepatic glucose and lipid metabolism are hallmarks of type 2 diabetes. Increased sulfide production or sulfide donor compounds may beneficially regulate hepatic metabolism. Disposal of ...sulfide through the sulfide oxidation pathway (SOP) is critical for maintaining sulfide within a safe physiological range. We show that mice lacking the liver- enriched mitochondrial SOP enzyme thiosulfate sulfurtransferase (Tst−/− mice) exhibit high circulating sulfide, increased gluconeogenesis, hypertriglyceridemia, and fatty liver. Unexpectedly, hepatic sulfide levels are normal in Tst−/− mice because of exaggerated induction of sulfide disposal, with associated suppression of global protein persulfidation and nuclear respiratory factor 2 target protein levels. Hepatic proteomic and persulfidomic profiles converge on gluconeogenesis and lipid metabolism, revealing a selective deficit in medium-chain fatty acid oxidation in Tst−/− mice. We reveal a critical role of TST in hepatic metabolism that has implications for sulfide donor strategies in the context of metabolic disease.
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•TST deficiency elevates sulfide, invoking exaggerated hepatic sulfide disposal•Exaggerated sulfide disposal triggers global hepatic protein underpersulfidation•Skewed persulfidation is associated with higher gluconeogenesis and impaired fat oxidation•Diabetogenic hepatic metabolism dominates over apparent peripheral insulin sensitization
Carter et al. show that mice lacking the mitochondrial sulfide oxidation pathway enzyme TST have high systemic sulfide levels that invoke an alternative hepatic sulfide disposal strategy. Consequently, hepatic metabolism is dominantly skewed toward a diabetogenic profile despite peripheral insulin sensitization. This has implications for sulfide donor therapeutic agents.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Experimental studies and retrospective analyses of mortality trials with angiotensin-converting enzyme inhibitors (ACE-Is) have suggested that aspirin may reduce the beneficial effect of these drugs. ...The aim of this study was to assess a possible detrimental effect of aspirin on survival in stable patients with left ventricular systolic dysfunction who had congestive heart failure and had been treated with ACE-Is.
We performed a retrospective analysis in 755 consecutive stable patients with left ventricular systolic dysfunction. A Cox regression model was used to select independent predictors of survival and to test for a possible interaction between aspirin and ACE-Is with an adjustment to differences in clinical characteristics in subgroups of patients. Of the 755 patients, 328 (43.4%) had proven ischemic cardiomyopathy, 693 patients (91.8%) were receiving ACE-Is, and 317 patients were receiving aspirin (mean ± SD dose, 183 ± 65 mg/d; 74% of the patients receiving ≤ 200 mg/d). During a median follow-up period of 1,996 days, there were 273 cardiac-related deaths, 14 urgent transplantations, 71 nonurgent transplantations, and 46 noncardiac-related deaths, and 3 patients were lost to follow-up. The cardiovascular mortality rates were 11.5% and 19.0%, respectively, at 1 and 2 years. There were no interactions among aspirin, ACE-Is, and survival in the overall population (p = 0.21), or in subgroups of patients with ischemic cardiomyopathy (p = 0.41) or with nonischemic cardiomyopathy (p = 0.74).
In this population of stable patients with left ventricular systolic dysfunction, our retrospective analysis did not demonstrate any interaction between the use of aspirin and survival in patients receiving ACE-Is.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Objective:
Discordant results have been published regarding a possible association between beta‐adrenoreceptor (βAR) gene polymorphisms and survival in patients with congestive heart failure (CHF). ...The aim of the study was to analyze the impact of five functional βAR gene polymorphisms in patients with stable CHF.
Methods:
We prospectively studied 444 consecutive patients with CHF related to left ventricular systolic dysfunction. The β1ARSer49Gly, β1ARGly389Arg, β2AR Arg16Gly, β2AR Gln27Glu and β2AR Thr164Ile polymorphisms were determined. Patients underwent echocardiography, radionuclide angiography and a cardiopulmonary exercise test.
Results:
Mean age was 56.6±11.9 years old, left ventricular ejection fraction (LVEF) was 32±12%, and peak VO2 was 15.5±4.9 ml/min/kg or 63±18% of maximal predicted VO2. Most of the patients (95%) were receiving angiotensin converting enzyme inhibitors and 91% β‐blockers. There was no statistically significant differences between baseline characteristics among β1AR and β2AR genotypes. During a median follow‐up period of 1232 days, there were 110 cardiac‐related deaths and five urgent transplantations. Independent predictors of survival were percent (%) of maximal predicted VO2 (p<0.0001), age (p<0.0001), LVEF (p=0.004), creatinine (p=0.02) and atrial fibrillation (p=0.04). No βAR polymorphisms were associated with survival. However, patients with the combined β2ARGly16Gly/β2ARGln27Gln genotype, who express receptors highly sensitive to down‐regulation, had a significantly lower survival rate than patients with other genotypes but only in univariate analysis.
Conclusions:
In this prospective study, we found no association between five functional βAR polymorphisms and survival in patients with stable CHF. However, we demonstrated, only in univariate analysis, a possible association between the combined β2ARGly16Gly/β2ARGln27Gln genotype and survival.
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BFBNIB, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, UL, UM, UPUK
We previously demonstrated that A-type natriuretic peptide (ANP) at peak exercise was an independent predictor of cardiac survival. No data are available concerning the predictive value of B-type ...natriuretic peptide (BNP) at peak exercise.
One hundred and fifty consecutive stable patients with moderate congestive heart failure (CHF) underwent echocardiography and a cardiopulmonary exercise test. Blood samples were drawn at rest and at peak exercise for the determination of plasma levels of ANP, BNP, and norepinephrine.
Exercise significantly increased plasma values of ANP, BNP, and norepinephrine. After a median follow-up period of 1171 days, there were 35 cardiac related deaths. Mortality rates at 1 and 2 years were 4% and 8%, respectively. Independent predictors of cardiac survival were percent of maximal predicted oxygen consumption (RR = 4.8 2.1–11,
P = .002), BNP at rest (RR = 2.5 1.2–5.6,
P = .01), and left atrial diameter (RR = 2.8 1.2–6.5,
P = .02).
In patients with stable, moderate CHF, plasma levels of ANP, BNP, and norepinephrine measured at peak exercise did not improve risk stratification. However, in addition to percent of maximal predicted oxygen consumption and left atrial diameter, plasma level of BNP at rest was an independent predictor of survival in CHF patients with low risk of cardiac events.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Adsorption on sliding surfaces and the chemical changes occurring within a few nanometers of the surface are key to the performance of lubricants and lubricant additives in the boundary lubrication ...regime. By means of the methods of modern surface science, these phenomena are beginning to be elucidated on a molecular level. This knowledge will be essential, both for the development of higher-performance lubricants, capable of high-temperature operation, as well as for the design of environmentally benign alternatives to the lubricant systems in current use.
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IJS, IMTLJ, KILJ, KISLJ, NUK, SBCE, UL, UM, UPCLJ, UPUK
OBJECTIVE: To analyse the potential association of the angiotensin converting enzyme (ACE) and angiotensin II type 1 receptor (AT1R) gene polymorphisms on left ventricular function and mass in ...patients with normal coronary arteries. DESIGN: Consecutive sample. SETTING: University hospital. SUBJECTS: 141 consecutive white patients referred for coronary angiography and with angiographically normal coronary arteries. Patients with valvar diseases, cardiomyopathies, or a history of myocardial infarction were excluded. MAIN OUTCOME MEASURES: Left ventricular variables were measured for all patients. The ACE and AT1R genotypes were determined with a polymerase chain reaction based protocol using DNA prepared from white blood cells. A general linear model was used to compare data according to the ACE and to the AT1R genotypes. RESULTS: A strong association was observed between left ventricular mass and systemic hypertension (mean (SD) hypertension: 114 (31) g/m2; no hypertension 98 (23) g/m2; P < 0.003). However, no influence of ACE and AT1R polymorphisms on left ventricular mass was found, regardless of systemic hypertension. The subjects homozygous for the AT1R CC mutation had a significantly lower ejection fraction than those with allele A (AC+AA) (mean (SD) 62(12)% and 68(10)%, respectively, P < 0.05). No synergistic interaction of ACE and AT1R gene polymorphisms on left ventricular function and mass was found. CONCLUSIONS: These data do not support an association of the ACE and AT1R genotypes on left ventricular hypertrophy in white patients with normal coronary arteries.
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