1,721,170 research outputs found
GSI anomaly and spin-rotation coupling
No full textWe propose a model in which a recently reported modulation in the decay of the hydrogenlike ions 140Pr58+, 142Pm60+ and 122I52+ arises from the coupling of rotation to the spin of electron and nucleus. The model shows that the spin–spin coupling of electron and nucleus does not contribute to the modulation and predicts that the anomaly cannot be observed if the motion of the ions is rectilinear, or if the ions are stopped in a target. It also supports the notion that the modulation frequency is proportional to the inverse of the atomic mass and that no modulation is expected for the β+-decay. The model predicts that for He-like ions the modulation is still present
The role of spin-rotation coupling in the non-exponential decay of hydrogen-like heavy ions
No full textRecent experiments carried out at the storage ring of GSI in Darmstadt reveal an unexpected oscillation in the orbital electron capture and subsequent decay of hydrogen-like 140Pr58+, 142Pm60+ and 122I52+. The modulations have periods of 7.069(8) s, 7.10(22) s and 6.1 s respectively in the laboratory frame and are superimposed on the expected exponential decays.
In this paper we propose a semiclassical model in which the observed modulations arise from the coupling of rotation to the spins of electron and nucleus. We show that the modulations are connected to quantum beats and to the effect of the Thomas precession on the spins of bound electron and nucleus, the magnetic moment precessions of electron and nucleus and their cyclotron frequencies. We also show that the spin–spin coupling of electron and nucleus, though dominant relative to the magnetic moment coupling of electron and nucleus with the storage ring magnetic field, does not contribute to the modulation because these terms average out during the time of flight of the ions, or cancel out. The model also predicts that the anomaly cannot be observed if the motion of the ions is rectilinear, or if the ions are stopped in a target (decay of neutral atoms in solid environments). It also supports the notion that no modulation occurs for the β+β+-decay branch
Increase of protein and lipid oxidation during hyperhomocysteinemia induced by methionine oral loading
No full textIntroduction: Hyperhomocysteinemia (HHcy) is a well-defined risk factor for vascular disease by a not still well clear molecular mechanism. It is known a pro-oxidant effect of Hcy “in vitro” in presence of metal ions (Fe e Cu). To assay a similar effect in vivo, we studied plasma markers of lipid and protein oxidation during hyperhomocysteinemia induced by methionine oral load.Materials and methods: 16 subjects (aged 79 14 years; 16f), 14 of which underwent a methionine (100 mg/Kg) oral load were studied; in all patients we assayed total plasma HCY, malonaldehyde (MDA) and conjugates dienes (DIE), oxidized protein (PTOX) (carbonilic groups) in basal conditions and after 4, 6, 8 and 24 hours from the oral load. In the two subjects who did not take the methionine load (controls), were made the same assays with the same timing of the probands. In all subjects we assayed basal and after 8 hours from the methionine load total plasma antioxidant (ANTOX) capacity.Results: table shows values (mean DS) of considered parameters in subjects who underwent the methionine loadParameterBasal4 h6 h8 h24 hHcy (nmol/ml)20.7 11.550.6 19.157.2 25.561.6 28.3 45.3 30.7PTOX (nmol/mg prot.)0.38 0.210.49 0.270.68 0.390.68 0.270.58 0.40DIE(nmol/ml)493 163562 181526 233590 202545 182MDA(nmol/ml)1.66 0.801.91 0.942.19 1.321.96 0.931.95 0.99ANTOX(nmol/ml)1.76 +/- 0.511.38 +/- 0.86 Conclusions: HHCY induces a correspondent increase of plasma oxidation makers. In absence of HHCY, no significant modifications were observed. This data, together with the reduction of ANTOX in correspondence of maximum plasma HCY increase, are suggestive of pro-oxidant effect of HHCY in vivo
Distribution of homocysteine in plasma lipoproteins
No full textAim of study: Plasma Homocysteine (HCY) is free or bound to plasma proteins (PbHCY). A moderate increase of HCY is a risk factor for vascular disease, even though by mechanism not yet known: it may depend on oxidative HCY-induced modification of lipoproteins (LP). The present study aims to evaluate the LP-HCY binding in vivo. Materials and methods: 53 subjects (mean age 7120 yr) were studied. HCY was measured by HPLC method. Plasma lipoprotein fractions were separated by sequential ultracentrifugation. Single fraction purity was tested on agarose gel electrophoresis. HCY bound to single plasma protein fraction was calculated as difference between total and free HCY. Results: Pb-HCY (mean value: 19.4±2 nmol/ml) results on average about 80% of total plasma HCY (mean values 24.2±2.5 nmol/ml). Distribution (absolute and percentage mean values) of Pb-HCY (nmol/ml) among the different fractions and single fraction HCY/protein ratio (nmol of HCY/mg of protein) are shown in the table. FractionsPb-HCY % of Pb-HCYHCY/protein ratio VLDL1 ± 0.65.10.76 ± 0.4LDL1.5 ± 0.57.70.52 ± 0.3HDL1.9 ± 0.59.70.11 ± 0.1LFF*15.1 ± 277.5 1.21 g/ml) Conclusions: A fraction of plasma HCY circulates bound to LP (about 23% of Pb-HCY); if single Pb-HCY fraction values are considered in terms of ratio between Pb-HCY (nmol) and mg of protein, VLDL and LDL fractions show the highest “affinity” for HCY. These results might explain the damaging effect of HCY on the vessel wall
Correlation between plasma malonyldialdeide levels and paroxonase activity in healthy subjects and in patients with atherosclerotic disease
No full textParaoxonase (PON) is a calcium-dependent HDL-associated ester hydrolase catalizying hydrolysis of organophosphates. Its biological role is still unknown: experimental studies suggest a hydroperoxidasic activity on lipoperoxides formed during LDL-oxidation, thus acting as a protective agent against atherogenesis. We evaluated PON activity in healthy subjects (HS) and in patients with cardiovascular (CHD) and cerebrovascular (CVD) disease ; PON activity was correlated with plasma malonyldialdeide (MDA) levels, as markers of lipid peroxidation Materials and Methods: 33 HS (age 7012 yr), 45 CHD (age 818 yr) and 38 CVD (age 8011 yr) patients were studied. Serum PON and plasma MDA levels were measured spectrophotometrically. Statististical analysis was performed by ANOVA univariate for groups comparation and by Pearson r test for values correlation Results: PON activity (mol min-1 ml-1) is higher in HS (0.0750.03) than in CHD (0.0450.03) and CVD (0.0560.03) patients (p<0.05 HS vs. CHD and CVD; ns CHD vs. CVD). MDA (mol/ml) levels are lower in HS (0.0280.023) than in CHD (0.0630.012) and in CVD (0.0560.036) patients (p<0.05 in HS vs. CHD and CVD, ns in CHD vs CVD). Table shows correlation between PON activity and MDA plasma levels in the three studied groups are shown below. rsignificanceHS-.43 p<0.05CHD-.39 p<0.01CVD-.33 p<0.05Conclusions: PON activity is significatively higher in HS than in CHD and CVD patients; whereas there are no significant difference between CHD e CVD patients. In all groups there is statistically significant negative correlation between PON activity and lipid peroxides content (MDA levels) in plasma. Our results suggest a protective role of PON activity against atherogenesis occurring with higher levels of lipoperoxides
Peroxidation indices and total antioxidant capacity in plasma during hyperhomocysteinemia induced by methionine oral loading
No full textHyperhomocysteinemia is a risk factor for vascular disease, although its mechanism of action is not fully clear. Different experimental studies have suggested that homocysteine (Hcy) exerts a pro-oxidant effect in the presence of metal ions (Fe and Cu). To test for a similar effect in vivo, we studied plasma markers of lipid and protein oxidation du ring hyperhomocysteifiemia induced by an oral methionine load. Twenty-nine subjects (aged 61 +/- 25 years; 17 women), 25 of whom underwent oral methionine (100 mg/kg) loading, were studied; in every case, we measured total plasma Hey, malondialdehyde (MDA), conjugated dienes (DIE), and oxidized protein ([PTOX] carbonylic groups) in basal conditions and 4, 6, 8, and 24 hours after methionine loading. Four participants acted as controls. In every case, we also measured total plasma antioxidant capacity (ANTOX) in basal conditions and 8 hours after methionine loading. Eight hours after methionine loading, plasma Hey increased from 17.6 +/- 11.4 to 54.3 +/- 31.6 nmol/ml, PTOX from 0.33 +/- 0.18 to 0.71 +/- 0.33 nmol/mg protein, DIE from 493 +/- 163 to 590 +/- 202 optical density units, and MDA from 1.66 +/- 0.81 to 2.1 +/- 0.93 nmol/ml. There was a significant correlation (Spearman ́s r) between Hey and both PTOX (r = .86, P = .01) and MDA (r = .47, P < .05) 8 hours after methionine loading. No significant modifications of the plasma parameters were found during the observation period in controls. ANTOX at 8 hours was significantly (paired ttest) reduced in probands (from 1.74 +/- 0.59 to 1.14 +/- 0.55 mmol/ml, P = .014); no significant difference was observed for plasma ANTOX in controls. Hyperhomocysteinemia due to oral methionine loading induced an increase in plasma oxidation markers. In the absence of hyperhomocysteinemia. no significant modifications were observed. These findings, together with the decrease in ANTOX and the corresponding increase in total plasma Hey, are consistent with a pro-oxidant effect of acute hyperhomocysteinemia in vivo. Copyrigh
Hyperhomocysteinemia and related factors in 600 hospitalized elderly subjects
No full textHyperhomocysteinemia (HHcy) is a metabolic disorder frequently occurring in the elderly population. Recently several reports have suggested abnormalities in homocysteine (tHcy) metabolism implicating HHcy as a metabolic link in the multifactorial processes characterizing many geriatric illnesses-with special emphasis on atherosclerotic vascular diseases and cognitive impairment. The present study was undertaken in a large sample of elderly hospitalized subjects to determine (1) the prevalence of HHcy, (2) the association of HHcy with vascular and cognitive disorders, and (3) the factors independently predicting Hhcy. Six hundred elderly subjects (264 men and 336 women; mean age, 79 +/-9 years) were randomly chosen from those admitted as inpatients over a period of 3 years. In all patients, body mass index (BMI), mid-upper arm muscle area (MUAMA), plasma cholesterol, triglycerides, total proteins, albumin, lymphocyte count, creatinine, homocysteine (fasting and 4 hours after methionine oral load), serum vitamin B-6, vitamin B-12, and folate concentrations were measured. The presence of disease or use of medications known to affect homocysteine plasma levels were also recorded. The mean fasting tHcy level was 16.8 +/- 12 mu mol/L in the whole sample, 18.18 +/- 13.25 mu mol/L in men, and 15.86 +/- 12.14 mu mol/L in women (P=.005 men v women). The mean Hcy level 4 hours after methionine load was 37.95 +/- 20.9 in the whole sample. Prevalence of hyperhomocysteinemia (fasting Hcy greater than or equal to 15 mu mol/L or 4 hours after methionine load greater than or equal to 35 mu mol/L) was 61% (365/600) (67% in men and 56% in women, P<.05). HHcy was rarely (8%) an isolated disorder; in addition to diabetes (20%), renal failure (48.2%), and malnutrition (20.2%), it was often associated with heart failure (30%), malignancies (20.5%), and the use of diuretics (56%) and anticonvulsant drugs (13%). Plasma homocysteine progressively increases across subjects from those with no diabetes, malnutrition, renal failure, obesity, inflammatory bowel disease, heart failure to those with 1, 2, or more concurrent diseases. Multiple stepwise regression analysis showed that 72% of plasma total fasting tHcy variability was explained by age, serum folate, plasma albumin, use of diuretics, and renal function (measured as plasma creatinine clearance). In conclusion, the present study documents that hyperhomocysteinemia, in elderly hospitalized patients is (1) a common finding, (2) frequently associated with vascular and cognitive disorders, and (3) probably a secondary phenomenon in most cases. The major predictor of high plasma homocysteine levels were age, serum folate, plasma albumin, plasma creatinine clearance, and use of diuretic drugs. These variables explain a large proportion of plasma Hcy variability. Copyrigh
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