Dementia has been recognized as a major public health issue that will grow in prominence as life expectancy increases. It has been proposed that estrogen (E2) deficiency in postmenopausal women may ...predispose older women to increased vulnerability of developing neurodegenerative diseases, such as Alzheimer’s disease (AD), and injury associated with cerebrovascular stroke. Indeed, some epidemiological data (1–3) indicate a higher incidence of dementia in women than in men, especially after the age of 85. Even though the gender differences in risk for dementia are generally shown for AD, not for vascular dementia (VaD), the longitudinal Bronx Aging Study reported that a history of myocardial infarction (MI) increased women’s risk to develop dementia fivefold but had no effect on dementia risk in men (3), suggesting the vascular effect on dementia in relationship to E2 status. In contrast, other studies report no gender differences in the age-adjusted incidence of dementia up to high age (4–6). In fact, the longer life expectancy in women than in men seemingly exposes women to higher risk of cognitive impairment in their late life.
The rates of vanadate-stimulated hydrolysis of 2,3-bisphosphoglycerate in metabolically competent erythrocytes and in hemolysates were determined from data on time courses up to 35 min employing 31P ...nuclear magnetic resonance spectroscopy. The enhanced rate of hydrolysis of the bisphosphate was attributed principally to the activation of the phosphatase activity of 2,3-bisphosphoglycerate synthase both in cell suspensions and in hemolysates. Information on the concentrations of vanadate and vanadyl present in the preparations was obtained employing 51V nuclear magnetic resonance spectroscopy and electron paramagnetic resonance spectroscopy. Redox reactions involving vanadium ions appeared to be important in establishing the final equilibrium concentrations of the oxy- and oxo-ions (vanadate and vanadyl, respectively), but the data suggested that the activation of the enzyme resulted from direct action of the vanadium ions on the enzyme and not as a consequence of the alteration in the equilibrium of intracellular oxidants and reductants.
Plasma arginine vasopressin (PAV) concentration was determined by radioimmunoassay during the diurnal cycle in 8 recombent healthy male subjects. Two subjects were studied again 3 weeks later while ...receiving 1 mycles. In 8 out of 10 cycles, a nocturnal increase in PAV was found; there was a progressive rise during the night in 5 subjects and a peak occurred at 2400 or 3400 h. In 1 subject no variation was detected and in another, the pattern was compleetly different. The mean PAV in the 10 cycles was significantly (P less than 0.001) higher during the night than during the day. Dexamethasone did not modify the pattern of variation, but induced a significant (P less than 0.001) decrease in PAV. Hematocrit remained stable throughout the study as did osmolality, except at 2000 h, when a significant (P less than 0.001) increase (5 mOsm) on average occurred in every subject. Blood sugar, sodium or chloride did not account for the observed rise in osmolality and no simultaneous change in PAV occurred. A rise in PAV explains, to some extent, the known nocturnal decrease in urine output. Diurnal variations in PAV must be taken into account in clinical investigations involving vasopressin.
Longitudinal and transverse relaxation times were measured in aqueous solutions containing haemoglobin and 2,3-bisphosphoglycerate and in dilute lysates of human erythrocytes. Analysis of the data in ...terms of calculated excess relaxation rates shows that Na+ interacts with the protein-organic phosphate complex. The comparable magnitude of the effect in the model system and in dilute lysate suggests that intracellular Na+ binds to the haemoglobin-bisphosphate complex. Results obtained with adenosine triphosphate and D-glucose indicate that there is also interaction between Na+ and haemoglobin complexes of these molecules.
The magnetic potential within and outside a nucleated cell placed in a uniform magnetic field is described for a model consisting of two concentric diamagnetic spheres. The analytical description of ...the magnetic potential in and around a system consisting of a finite number of concentric diamagnetic spheres in a uniform magnetic field was derived. The solution was employed to calculate the field gradients outside and inside a model chicken red blood cell. The form and magnitude of the gradients provide a theoretical basis on which to discuss experimental results relating to the attenuation of signals obtained using proton nuclear magnetic resonance spectroscopy with chicken erythrocyte suspensions. The form of the magnetic field, field difference and field gradients in the external medium of a cell suspension was simulated for a distribution of spheres in a uniform magnetic field, such as might occur in an idealised dilute cell suspension.
Metabolic syndrome is a collection of risk factors that include obesity, hypertension, and dyslipidemia,
which leads to increased incidents of coronary artery disease, stroke, and type 2 diabetes. It ...is a rapidly
growing public health issue in almost all developed and many developing countries. e syndrome
aects 20-30% of adults and is increasing in prevalence worldwide (Han et al., 2010, Meng et al., 2010).
Lipopolysaccharide (endotoxin, LPS) exerts potent proinflammatory effects on neutrophils which may involve membrane phospholipid metabolism. The cellular and plasma membrane phospholipid composition ...of resting neutrophils and those stimulated with 50 μg ml‐1 LPS were studied by 31P NMR and chemical analysis. A rapid new method for plasma membrane purification was employed, involving the direct lysis of cytoplasts. Chemical analyses showed that, although total cellular phospholipid content did not change with LPS stimulation, there was twice the amount of phospholipid present in plasma membranes isolated from stimulated cells, resulting in a lowered cholesterol/phospholipid ratio. Since internal membranes have lower cholesterol content this result is consistent with an origin from insertion of these membranes (most probably from the endoplasmic reticulum) into the plasma membrane, thereby increasing its fluidity. The individual phospholipid classes of both cells and membranes were quantified by 31P‐NMR spectroscopy after dissolution in sodium cholate without prior extraction of lipids, allowing partial resolution of the major phospholipid classes and ether‐linked phospholipids. Ether‐linked lipids were distinguished froin diacyl phospholipids by hydrolysis of lipid extracts with HC1 and phospholipase A1, There was a significant increase in phosphatidylserine in both cells and plasma membranes after stimulation, with a decrease in the phosphatidylethanolamine (diacyl and plasmalogen) content in the cells. Plasma membranes from stimulated cells exhibited a significant decrease in a phospholipid tentatively identified as 2‐arachidonoyl‐1‐alkyl‐sn‐glycero‐3‐phosphocholine, a precursor of the lipid inflammatory mediator, platelet‐activating factor. This report is the first to elaborate the changes in phospholipid composition in human neutrophils as a whole, and in plasma membranes separated from them, before and after stimulation by the physiological activator, LPS.
Lipopolysaccharide (endotoxin, LPS) exerts potent proinflammatory effects on neutrophils which may involve membrane phospholipid metabolism. The cellular and plasma membrane phospholipid composition ...of resting neutrophils and those stimulated with 50 μg ml
‐1
LPS were studied by
31
P NMR and chemical analysis. A rapid new method for plasma membrane purification was employed, involving the direct lysis of cytoplasts. Chemical analyses showed that, although total cellular phospholipid content did not change with LPS stimulation, there was twice the amount of phospholipid present in plasma membranes isolated from stimulated cells, resulting in a lowered cholesterol/phospholipid ratio. Since internal membranes have lower cholesterol content this result is consistent with an origin from insertion of these membranes (most probably from the endoplasmic reticulum) into the plasma membrane, thereby increasing its fluidity. The individual phospholipid classes of both cells and membranes were quantified by
31
P‐NMR spectroscopy after dissolution in sodium cholate without prior extraction of lipids, allowing partial resolution of the major phospholipid classes and ether‐linked phospholipids. Ether‐linked lipids were distinguished froin diacyl phospholipids by hydrolysis of lipid extracts with HC1 and phospholipase A
1
, There was a significant increase in phosphatidylserine in both cells and plasma membranes after stimulation, with a decrease in the phosphatidylethanolamine (diacyl and plasmalogen) content in the cells. Plasma membranes from stimulated cells exhibited a significant decrease in a phospholipid tentatively identified as 2‐arachidonoyl‐1‐alkyl‐
sn
‐glycero‐3‐phosphocholine, a precursor of the lipid inflammatory mediator, platelet‐activating factor. This report is the first to elaborate the changes in phospholipid composition in human neutrophils as a whole, and in plasma membranes separated from them, before and after stimulation by the physiological activator, LPS.
The hemodynamic changes observed in patients with the "hyperkinetic" form of borderline (labile) essential hypertension (BEH) could be related to the hyperresponsiveness of cardiac β -adrenergic ...receptors to catecholantines. The isoproterenol-induced increase in plasma cyclic adenosine 3ʼ:5ʼ-monophosphate (cAMP) reflects the response of adenylate cyclase to β-adrenergic stimulation, whereas a non-β-receptor-mediated increase occurs with the administration of glucagon. Both substances were infused into 13 control subjects and 14 patients with the hyperkinetic form of BEH before and after propranolol administration. Baseline plasma cAMP concentrations were comparable in both groups. After 30 minutes of isoproterenol infusion (20 ng/kg per mini a significantly higher increase in plasma cAMP and heart rate and a smaller decrease in diastolic blood pressure were seen in this type of BEH than in control subjects. The increase in plasma cAMP and in heart rate correlated positively when all subjects were considered together. Propranolol abolished hemodynamic and humoral responses to a similar degree in both groups. The plasma cAMP responses to glucagon (200 ng/kg per min) were slightly lower in our patients with BEH than in control subjects and were not suppressed by propranolol.The data are compatible with a hyperreactivity of the β-adrenergic receptors or of the adenylate cyclase or both in hyperkinetic BEH and could correspond to the previously observed exaggerated β-adrenergic drive to the heart in this type of hypertension. The non-β-receptor-mediated rise in plasma cAMP (glucagon), however, remains comparable in control subjects and BEH.
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