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O Eriksson

Publications and source records attributed to O Eriksson.

At least 37 records · Page 2Linked to original sources
PubMed2000

Non-collinear states in magnetic sensors

Certain materials have an electrical conductivity that is extremely sensitive to an applied magnetic field; this phenomenon, termed 'giant magnetoresistance', can be used in sensor applications. Typically, such a device comprises several ferromagnetic layers, separated by non-magnetic spacer layer(s)--a so-called 'super-lattice' geometry. In the absence of a magnetic field, the ferromagnetic layers may be magnetized in opposite directions by interlayer exchange coupling, while an applied external magnetic field causes the magnetization directions to become parallel. Because the resistivity depends on the magnetization direction, an applied field that changes the magnetic configuration may be detected simply by measuring the change in resistance. In order to detect weak fields, the energy difference between different magnetization directions should be small; this is usually achieved by using many non-magnetic atomic spacer layers. Here we show, using first-principles theory, that materials combinations such as Fe/V/Co multilayers can produce a non-collinear magnetic state in which the magnetization direction between Fe and Co layers differs by about 90 degrees. This state is energetically almost degenerate with the collinear magnetic states, even though the number of non-magnetic vanadium spacer layers is quite small.

Journal Article↗
PubMed2000

Characterisation of three novel cationic lipids as liposomal complexes with DNA.

Cationic lipids (CLs) are being increasingly exploited as transfection vectors for the delivery of DNA into eukaryotic cells. To obtain further insight to the complex formation and interactions between cationic liposomes and DNA, we characterised three novel cationic lipids, viz. bis[2-(11-phenoxyundecanoate)ethyl]-dimethylammonium bromide, N-hexadecyl-N-¿10-[O-(4-acetoxy)-phenylundecanoate]ethyl¿- dimethylammonium bromide, and bis[2-(11-butyloxyundecanoate)ethyl]dimethylammonium bromide. These lipids bear the same charged headgroup yet have different hydrophobic parts. Accordingly, we may anticipate their electrostatic interactions with DNA to be similar while differing in both thermal phase behaviour and physicochemical properties of their complexes with DNA. In keeping with the above all three lipids formed complexes with DNA as evidenced by light scattering, fluorescence spectroscopy and Langmuir film balance. Differential scanning calorimetry revealed very different phase behaviours for the binary mixtures of the three CLs with dimyristoylphosphatidylcholine and also provided evidence for DNA-induced lipid phase separation. These data were confirmed by compression isotherms and fluorescence microscopy of monolayers residing on an aqueous buffer, recorded both in the presence and absence of DNA. Importantly, binding to cationic liposomes appears to prevent thermal denaturation of DNA upon heating of the complexes. Likewise, renaturation of heat-treated DNA complexed with the cationic liposomes appears to be abolished as well.

Cations↗
PubMed2000

Implications of the generation of reactive oxygen species by photoactivated calcein for mitochondrial studies.

Calcein is a fluorescent probe that is widely used in studies of cell viability and mitochondrial function by microscopy fluorescence imaging. It was found to have a strong photosensitizing action that prevalently involves the generation of reactive oxygen species (ROS). The photooxidation properties of calcein in solution were studied in the presence of histidine and tryptophan as oxidizable substrates. The photodegradation of histidine was mainly mediated by singlet oxygen (1O2), as shown by the inhibitory effect of sodium azide, a specific 1O2 scavenger. On the other hand, mixed photosensitization mechanisms were present when tryptophan was used as the target of the calcein-stimulated photoprocess. In addition to 1O2, hydroxyl radicals and hydrogen peroxide were involved as reactive species, as shown by using mannitol and catalase as scavengers. The calcein-photosensitized alterations of mitochondria as a potential source of artifacts in confocal microscopy studies of cells were considered. Irradiation of isolated mitochondria with visible light (500-600 nm) in the presence of calcein induced opening of the permeability transition (PT) pore. The extent of the mitochondrial membrane photodamage, however, was modulated by the nature of the calcein environment. Thus, pore opening was triggered at short irradiation times and low dye concentrations when calcein was dissolved in the bulk medium. On the contrary, calcein concentrated in the matrix space was rather inefficient as photosensitizer even at concentrations 10 times higher than those present in the external medium.

Animals↗
PubMed2000

Seed Size and Dispersal Systems of Early Cretaceous Angiosperms from Famalicão, Portugal.

Seeds and fruits of Early Cretaceous (Barremian-Aptian) angiosperms from the Famalicão locality in Portugal were analyzed to establish seed and fruit size (volume) distributions and to infer the proportion of animal-dispersed fruits. On the basis of a sample of 106 angiosperm fruit and seed taxa, the average seed size was 0.78 mm3 (range 0.02-6.86 mm3), whereas the average fruit size was 2.06 mm3 (range 0.12-8.34 mm3). Variation in seed size among taxa is smaller than in modern plant communities, but within-taxon variation is similar to that known for extant plants. No significant difference in the size of "fleshy" versus other fruits was observed. The proportion of fleshy fruits was 24.5%. This high figure was surprising and indicates that the significance of animal dispersal during an early stage in angiosperm evolution has been underestimated. We suggest that reptiles and multituberculates, and perhaps other mammals and birds as well, were the likely seed dispersers and that the early angiosperms from Famalicão probably were herbs or small shrubs that inhabited a semiopen coniferous woodland.

Journal Article↗
PubMed2000

Effects of melagatran, a novel direct thrombin inhibitor, during experimental septic shock.

Sepsis and endotoxaemia initiate the generation of thrombin, which is responsible for the conversion of fibrinogen to fibrin, platelet aggregation and acts as an inflammatory mediator affecting numerous types of cells, including myocardial, smooth muscle and endothelial cells. Human Gram-negative septic shock, frequently seen in intensive care units, is a condition with high mortality. This condition can be replicated in the endotoxaemic pig. As many of the toxic effects of sepsis are due to thrombin generation, it was of interest to study, using this porcine experimental septic shock model, whether inhibition of thrombin could alleviate the effects of endotoxaemia. For this purpose melagatran, a direct synthetic thrombin inhibitor with a molecular weight of 429 Da, was employed. Melagatran does not significantly interact with any other enzymes in the coagulation cascade or fibrinolytic enzymes aside from thrombin. Furthermore, melagatran does not require endogenous co-factors such as antithrombin or heparin co-Factor II for its antithrombin effect, which is important, as these inhibitors are often consumed in septic patients. We have shown that melagatran exerts a beneficial effect on renal function, as evaluated by plasma creatinine and urinary output, during experimental septic shock. These effects were most pronounced during the later phase of the experimental period, after the infusion of melagatran had been discontinued. Prevention of intrarenal coagulation may be attributable to this finding. In addition, melagatran had beneficial effects on systemic haemodynamics (left ventricular stroke work index, pulmonary capillary wedge pressure and systemic vascular resistance index) in endotoxaemic pigs. This result may be explained by the ability of melagatran to inhibit thrombin, thereby counteracting thrombin's cellular effects. Thus, it can be seen, using this experimental model of septic shock, that melagatran may help to alleviate some of the damaging effects of endotoxaemia, although more research is required to test this further.

Animals↗
PubMed2000

Physical symptoms in premenstrual syndrome are related to plasma progesterone and desoxycorticosterone.

Somatic symptoms in the premenstrual syndrome (PMS) may have an etiology separate from that of the mental symptoms. A disturbance in mineralocorticoid action has been discussed, as mineralocorticoids regulate water balance. Desoxycorticosterone (DOC) is interesting, as it has mineralocorticoid effects and is a precursor to the neurosteroid 5 alpha-pregnan-3 alpha,21-diol-20-one (THDOC). THDOC is a steroid with direct benzodiazepine-like effects on the GABA-A receptor in the brain that is metabolized from DOC within the brain and in the periphery. Ten women with PMS having swelling as a major symptom and eight controls were recruited. They marked, on a validated visual-analog scale, three physical symptoms every evening during one menstrual cycle in conjunction with giving blood samples for progesterone and DOC measurements. DOC showed menstrual cycle-linked variation correlating with progesterone. There was no difference in plasma DOC concentrations between patients and controls. The symptoms reached a maximum 1-3 days before the onset of menstruation, with a delay of 3-6 days after the hormone peak. DOC was less strongly correlated with the symptoms than progesterone. These results do not support the hypothesis that DOC is involved in the etiology of physical symptoms in PMS or that physical and mental symptoms have separate etiologies.

Adult↗
PubMed1999

A comparison between in vitro studies of protein lesions generated by brain electrodes and finite element model simulations.

The aim of this study was to develop a finite element model for simulation of the thermal characteristics of brain electrodes and to compare its performances with an in vitro experimental albumin model. Ten lesions were created in albumin using a monopolar electrode connected to a Leksell Neuro Generator and a computer-assisted video system was used to determine the size of the generated lesions. A finite element model was set up of the in vitro experiments using the same thermal properties. With a very simple heat source applied to the finite element model in the proximity of the upper part of the tip, a good agreement (no deviations in width and distance from tip but a deviation in length of -1.6 mm) with the in vitro experiments (width 4.6 +/- 0.1 mm and length 7.4 +/- 0.1 mm) was achieved when comparing the outline of the lesion. In addition, a gelatinous albumin-model was set up and compared to computer simulations resulting in deviations in width of -0.4 mm, length of -2.2 mm and distance from the tip of -0.1 mm. Hence, the utilisation of finite element model simulations may be a useful complement to in-vitro experiments.

Albumins↗
PubMed1999

In vitro evaluation of brain lesioning electrodes (Leksell) using a computer-assisted video system.

Radiofrequency (RF) generated thermal brain lesions are widely used in functional neurosurgery. The size, shape and development of the lesions depends on system parameter settings and the electrode configuration. Difficulties in studying the effect of these factors in vivo stimulated us to develop an in vitro system for standardized comparison between different electrodes and physical parameters. A computer-assisted video system was set-up allowing continuous video recording of RF-generated coagulations in either a standard albumin solution or in the fresh white of a hen's egg as transparent test substrates. Ten lesions were made with each test electrode (two bipolar and three monopolar) in each of the two substrates at 70 degrees, 80 degrees and 90 degrees C (t = 60 sec). Due to the better homogeneity the lesions in the albumin solution were much more regular and reproducible. This made it possible to calculate the size (width 2.2 +/- 0.1 to 5.3 +/- 0.1 mm and length 3.0 +/- 0.1 to 8.7 +/- 0.3 mm) as well as the volume (8.5 +/- 1.4 mm3 to 133.5 +/- 26.8 mm3). It is concluded that this in vitro system offers a reproducible way to study and document the effect of different electrode configurations and RF-generator settings on the formation of a heat lesion. Even if the results are not directly applicable to the living human brain they give an estimate of the form and size of a coagulation lesion and can be of value for standardized comparisons between different electrodes.

Brain↗
PubMed1999

Regulation of total mitochondrial Ca2+ in perfused liver is independent of the permeability transition pore.

Triggering of the permeability transition pore (PTP) in isolated mitochondria causes release of matrix Ca2+, ions, and metabolites, and it has been proposed that the PTP mediates mitochondrial Ca2+ release in intact cells. To study the role of the PTP in mitochondrial energy metabolism, the mitochondrial content of Ca2+, Mg2+, ATP, and ADP was determined in hormonally stimulated rat livers perfused with cyclosporin A (CsA). Stimulation of livers perfused in the absence of CsA with glucagon and phenylephrine induced an extensive uptake of Ca2+, Mg2+, and ATP plus ADP by the mitochondria, followed by a release on omission of hormones. In the presence of CsA, the PTP was fully inhibited, but neither the hormone-induced uptake of Ca2+, ATP, or ADP by mitochondria nor their release after washout of hormones was significantly changed. We conclude that the regulation of sustained changes in mitochondrial Ca2+ content induced by hormonal stimulation is independent of the PTP.

Adenosine Diphosphate↗
PubMed1998

Regulation of the permeability transition pore in skeletal muscle mitochondria. Modulation By electron flow through the respiratory chain complex i.

We have investigated the regulation of the permeability transition pore (PTP), a cyclosporin A-sensitive channel, in rat skeletal muscle mitochondria. As is the case with mitochondria isolated from a variety of sources, skeletal muscle mitochondria can undergo a permeability transition following Ca2+ uptake in the presence of Pi. We find that the PTP opening is dramatically affected by the substrates used for energization, in that much lower Ca2+ loads are required when electrons are provided to complex I rather than to complex II or IV. This increased sensitivity of PTP opening does not depend on differences in membrane potential, matrix pH, Ca2+ uptake, oxidation-reduction status of pyridine nucleotides, or production of H2O2, but is directly related to the rate of electron flow through complex I. Indeed, and with complex I substrates only, pore opening can be observed when depolarization is induced with uncoupler (increased electron flow) but not with cyanide (decreased electron flow). Consistent with pore regulation by electron flow, we find that PTP opening is inhibited by ubiquinone 0 at concentrations that partially inhibit respiration and do not depolarize the inner membrane. These data allow identification of a novel site of regulation of the PTP, suggest that complex I may be part of the pore complex, and open new perspectives for its pharmacological modulation in living cells.

Animals↗
PubMed1998

Chemical modification of arginines by 2,3-butanedione and phenylglyoxal causes closure of the mitochondrial permeability transition pore.

We have investigated the role of arginine residues in the regulation of the mitochondrial permeability transition pore, a cyclosporin A-sensitive inner membrane channel. Isolated rat liver mitochondria were treated with the arginine-specific chemical reagent 2, 3-butanedione or phenylglyoxal, followed by removal of excess free reagent. After this treatment, mitochondria accumulated Ca2+ normally, but did not undergo permeability transition following depolarization, a condition that normally triggers opening of the permeability transition pore. Inhibition by 2,3-butanedione and phenylglyoxal correlated with matrix pH, suggesting that the relevant arginine(s) are exposed to the matrix aqueous phase. Inhibition by 2,3-butanedione was potentiated by borate and was reversed upon its removal, whereas inhibition by phenylglyoxal was irreversible. Treatment with 2,3-butanedione or phenylglyoxal after induction of the permeability transition by Ca2+ overload resulted in pore closure despite the presence of 0.5 mM Ca2+. At concentrations that were fully effective at inhibiting the permeability transition, these arginine reagents (i) had no effect on the isomerase activity of cyclophilin D and (ii) did not affect the rate of ATP translocation and hydrolysis, as measured by the production of a membrane potential upon ATP addition in the presence of rotenone. We conclude that reaction with 2,3-butanedione and phenylglyoxal results in a stable chemical modification of critical arginine residue(s) located on the matrix side of the inner membrane, which, in turn, strongly favors a closed state of the pore.

Animals↗
PubMed1998

Characterization of a high capacity calcium transport system in mitochondria of the yeast Endomyces magnusii.

The Ca2+ transport system of Endomyces magnusii mitochondria has been shown previously to be activated by spermine. Here we report it to be regulated also by low, physiological ADP concentrations, by the intramitochondrial NADH/NAD+ ratio, and by Ca2+ ions. The combination of all these physiological modulators induced high initial rates of Ca2+ uptake and high Ca2+-buffering capacity of yeast mitochondria, enabling them to lower the medium [Ca2+] to approximately 0.2 microM. The mechanisms of stimulation by these agents are discussed.

Adenosine Diphosphate↗
PubMed1998

The mitochondrial permeability transition.

This review summarizes recent work on the regulation of the permeability transition pore, a cyclosporin A-sensitive mitochondrial channel that may play a role in intracellular calcium homeostasis and in a variety of forms of cell death. The basic bioenergetics aspects of pore modulation are discussed, with some emphasis on the links between oxidative stress and pore dysregulation as a potential cause of mitochondrial dysfunction that may be relevant to cell injury.

Animals↗
PubMed1998

Retinyl palmitate injections reduce serum levels and effects of endotoxin on systemic haemodynamics and oxygen transport in the pig.

BACKGROUND: Retinyl palmitate [(RP) 230 IU.kg(-1)] modulates the circulatory and respiratory responses of a subsequent infusion of endotoxin in the pig. The aims of this study were: I. To determine if RP (2300 IU.kg(-1)) affects the serum endotoxin levels in this model. II. To evaluate the effect of this dose of RP on circulatory and respiratory variables in our porcine model. III. To investigate the levels of RP and neutrophil count in porcine endotoxaemia. METHODS: Ten anaesthetized pigs were randomly given 2300 IU.kg(-1) of RP or the solvent i.m. prior to the continuous i.v. infusion of E. coli endotoxin (10 microg.kg(-1).h(-1)). Another 4 sham animals were given either i.m. RP (n=2) or i.m. solvent (n=2) followed by an infusion of saline. Haemodynamics and oxygen extraction were monitored and samples taken for analysis of endotoxin, RP and blood cells. RESULTS: I. Endotoxin levels in serum were lower (P<0.001) in the RP-pretreated pigs. II. These animals had higher cardiac index (P<0.05), mean arterial pressure and left ventricular stroke work index (both P<0.001), and lower oxygen extraction (P<0.01). III. RP-Pre=pretreatment caused a paradoxical decrease in serum retinyl (P<0.001) and a more rapid restitution of neutrophil count (P<0.05). CONCLUSION: Pretreatment with RP (2300 IU.kg(-1)) counteracts the progressive increase in serum endotoxin levels in porcine endotoxaemia.

Animals↗
PubMed1997

The Gothenburg breast screening trial: first results on mortality, incidence, and mode of detection for women ages 39-49 years at randomization.

BACKGROUND: The effect of mammography screening on breast carcinoma mortality in women ages < 50 years remains unclear. METHODS: A randomized trial of invitation to breast carcinoma screening with mammography was performed in the city of Gothenburg, Sweden. The purpose was to estimate the effect of mammographic screening on breast carcinoma mortality in women ages < 50 years. Randomization was initially by day-of-birth cluster (18% of subjects), and subsequently by individual (82% of subjects). Between September 1983 and April 1984, 11,724 women ages 39-49 years were randomized to the study group. This group was invited to mammographic screening every 18 months. Two-view mammography was used at each screen unless the density of the breast at the previous screen indicated that single view was adequate. Fourteen thousand two hundred and seventeen women in the same age range were randomized to a control group that was not invited to undergo screening until the fifth screen of the study group (between 6 and 7 years after randomization). Women with breast carcinoma diagnosed up to the time immediately after the first screen of the control group were followed for death from breast carcinoma until the end of December 1994. RESULTS: A 45% reduction in mortality from breast carcinoma was observed in the study group compared with the control group (relative risk [RR] = 0.55, P = 0.035, 95% confidence interval [CI], 0.31-0.96). A conservative estimate based on removal of the tumors detected at the first screen of the control group gave a mortality reduction of 44% (RR = 0.56, P = 0.046, 95% CI, 0.31-0.99). In both cases, the effect was statistically significant. CONCLUSIONS: Mammographic screening can reduce mortality from breast carcinoma in women ages < 50 years. The mortality reduction can be substantial if high quality mammography is used and an 18-month interscreening interval is strictly adhered to.

Adult↗
PubMed1997

Inhibition of the mitochondrial cyclosporin A-sensitive permeability transition pore by the arginine reagent phenylglyoxal.

The mitochondrial permeability transition pore, a cyclosporin A-sensitive channel, is controlled by the transmembrane electric potential difference across the inner membrane. Here, we show that treatment of rat liver mitochondria with the arginine reagent phenylglyoxal inhibits the permeability transition pore triggered by depolarization with uncoupler after Ca2+ accumulation. Phenylglyoxal does not change the extent of mitochondrial Ca2+ uptake or the extent of membrane depolarization, indicating that covalent modification of arginine (and possibly lysine) residues directly affects the open probability of the pore. We propose that arginine residues play a role in the physiological control of the permeability transition pore by the mitochondrial transmembrane potential.

Animals↗
PubMed1997

Effect of butylhydroxytoluene and related compounds on permeability of the inner mitochondrial membrane.

Mitochondrial inner membrane contains a latent pore (PTP) that when opened uncouples mitochondrial energy transduction and allows rapid equilibration of low-molecular-weight solutes between the matrix and exterior. Based on sensitivity of the PTP to well-known free radical scavenger butylhydroxytoluene (BHT), it has been proposed that increased steady-state level of oxygen radicals, and subsequent radical attack of proteins and lipids, is a central event in activation of this pore (Novgorodov et al., J. Bioenerg. Biomembr. 19, 191-202, 1987; Carbonera and Azzone, Biochim. Biophys. Acta 943, 245-255, 1988). Present studies revealed that DBT, a derivative of BHT devoid of radical scavenging activity, exerts an analogous effect on the permeability of the inner membrane. Inhibition of the Ca2+-induced PTP opening is essentially complete at dose range of 50-60 nmol/mg protein with IC50 values of about 32 and 23 nmol/mg protein for DBT and BHT, respectively. Electron microscopy and osmotic experiments utilizing polyethylene glycols with different Stokes radii showed that the apparent lack of inhibition seen at high concentrations of these compounds results from cyclosporin A- and Ca2+-insensitive pore formation in the inner membrane. Experiments employing antioxidants with similar structure but dissimilar hydrophobicity provided evidence for localization of the antioxidant binding sites within the hydrophobic zone of the inner membrane or in the matrix space. The data obtained do not refute the notion that oxygen radicals modulate the PTP, but rather indicate that BHT operates independently of its free radical scavenging activity. Overall, the sensitivity to BHT and other antioxidants is not always a reliable criterion for the involvement of free radical reactions in the processes under study.

Animals↗