| 1. |
- Knudsen, D. J., et al.
(författare)
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Sub-kilometer thermal plasma structure near 1750 km altitude in the polar cusp/cleft
- 1994
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Ingår i: Geophysical Research Letters. - 0094-8276. ; 21:17, s. 1907-1910
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Tidskriftsartikel (refereegranskat)abstract
- We present Freja Cold Plasma Analyzer (CPA) measurements from an encounter with the low altitude (approx.1750 km) polar cusp during which the CPA measured 2-D images of the thermal (0-16 eV) particle distributions at 1.2 s time resolution, and simultaneously made rapid estimates (600/s) of integrated thermal particle flux into the instrument. The high resolution data show bursty ion flux enhancements of the order of tens of percent on time scales of tens of ms, or alternatively, hundreds of m spatial scales. The flux of electrons from 0-16 eV also varied by tens of percent and on temporal/spatial scales comparable to those in the ion cases. There is some evidence that the thermal particle flux variations are associated with intense low-frequency electromagnetic fluctuations with temporal/spatial scales identical to those seen by the CPA (tens of ms. hundreds of m).
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| 2. |
- Fahlke, Claudia, 1964, et al.
(författare)
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Involvement of corticosterone in the modulation of ethanol consumption in the rat.
- 1994
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Ingår i: Alcohol (Fayetteville, N.Y.). - 0741-8329. ; 11:3, s. 195-202
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Tidskriftsartikel (refereegranskat)abstract
- Several studies report that rats exposed to stressful conditions may increase their ethanol consumption. Stress is accompanied by a rise in the secretion of adrenocortical hormones, and the possibility that these hormones exert an influence on ethanol consumption should be considered. The present investigation addressed this issue by studying the effect of adrenalectomy (ADX) and subsequent corticosterone (CORT) or aldosterone (ALDO) treatment on ethanol intake. The results showed that ADX rats decreased their ethanol intake compared to the sham-operated controls and that treatment with CORT restored the intake of ethanol to the preoperative level. In contrast, treatment with ALDO (0.25 or 0.75 mg/kg) had no effect on ethanol intake. Biochemical analyses showed increases in monoamine turnover in the brain stem and limbic forebrain after ADX. The reduction of ethanol consumption caused by ADX may thus be specifically attributed to the loss of one of the adrenal hormones, CORT. The results indicate that CORT may be a factor of importance in the modulation of alcohol consumption.
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| 3. |
- Olsson, U, et al.
(författare)
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Effects of selenium deficiency on xenobiotic-metabolizing and other enzymes in rat liver.
- 1993
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Ingår i: International Journal for Vitamin and Nutrition Research. - 0300-9831 .- 1664-2821. ; 63:1
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Tidskriftsartikel (refereegranskat)abstract
- The present study was undertaken to characterize effects of selenium (Se) deficiency on 16 enzymes recovered in either one or more of the subcellular fractions of rat liver (as a basis for future studies on the mechanisms underlying the observed changes). Male rats were fed a Torula-yeast based diet with 0.23 mg Se/kg or the same diet with 0.009 mg Se/kg, from weaning and for 10 weeks. Statistically significant effects of Se deficiency were the following: Se-dependent glutathione peroxidase decreased to 0.14% of the Se-adequate controls, while cytosolic glutathione transferase increased 3-fold in Se deficiency when CDNB was the substrate, but decreased significantly when trans-stilbene oxide (diagnostic for subunit 4) was used as the substrate. Cytosolic DT-diaphorase increased about 7-fold in Se deficiency. Further, DT-diaphorase in the microsomal fraction was also significantly increased in Se deficiency, as were the microsomal and mitochondrial epoxide hydrolases and microsomal glutathione transferase. Furthermore, increased activity of the peroxisomal marker enzyme catalase (P < 0.05) was noted in Se-deficient rats. It is our working hypothesis that changes in enzyme activities in Se deficiency are mainly due to changed levels of endogenously generated metabolites or altered functions of endocrine tissues.
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| 4. |
- Olsson, U, et al.
(författare)
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The involvement of selenium in peroxisome proliferation caused by dietary administration of clofibrate to rats.
- 1992
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Ingår i: Chemico-Biological Interactions. - 0009-2797 .- 1872-7786. ; 85:1
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Tidskriftsartikel (refereegranskat)abstract
- The effects of dietary treatment with clofibrate (0.5% w/w for 10 days) on the livers of selenium-deficient male rats were examined. The peroxisome proliferation (as determined by electron microscopy) in the livers of selenium-deficient animals was much less pronounced than in the case of selenium-adequate rats and no increase in peroxisomal fatty acid beta-oxidation (assayed both as antimycin-insensitive palmitoyl-CoA oxidation and lauroyl-CoA oxidase activity) was observed in the deficient animals. On the other hand, in selenium-deficient rats clofibrate caused increases in the specific activity of microsomal lauric acid omega- and omega-1-hydroxylation and an apparent change in mitochondrial size, seen as a redistribution of mitochondria from the 600 x g(av) pellet to the 10,000 x g(av) pellet, which were approximately 50% as great as the corresponding effects on control animals. Obviously, then, these three different effects of clofibrate are not strictly coupled and may involve at least partially distinct underlying mechanisms. Initial experiments demonstrated that peroxisome proliferation could be obtained by exposing primary hepatocyte cultures derived from selenium-deficient rats to clofibric acid (an in vivo hydrolysis product of clofibrate which is the proximate peroxisome proliferator), nafenopin or mono(2-ethylhexyl)phthalate. This finding suggests that selenium deficiency does not have a direct influence on the basic process(es) underlying peroxisome proliferation, but rather has indirect effects, influencing, for example, the pharmacokinetics of clofibrate and/or hormonal factors.
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| 5. |
- Albrektsson, Tomas, 1945, et al.
(författare)
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Histologic investigations on 33 retrieved Nobelpharma implants.
- 1993
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Ingår i: Clinical materials. - 0267-6605. ; 12:1, s. 1-9
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Tidskriftsartikel (refereegranskat)abstract
- Thirty Nobelpharma implants were retrieved from 17 patients despite a remaining clinical stability, after between 1 and 16 years of clinical function. The reasons for implant removal were bone resorption in combination with soft tissue disorders, psychological causes, implant fracture and post mortem cases. When measured at the cortical passage, there was an average of 84.9% direct bone-to-implant contact and 81.8% average surface bone area in individual threads as evaluated in a computerized morphometric system at the light microscopic level.
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| 6. |
- Allard, Per, et al.
(författare)
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[3H]GBR-12935 binding to dopamine uptake sites in rat striatum.
- 1990
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Ingår i: Neuropsychobiology. - 0302-282X .- 1423-0224. ; 23:4, s. 177-81
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Tidskriftsartikel (refereegranskat)abstract
- The binding of the selective dopamine uptake inhibitor [3H]GBR-12935 to rat striatum was studied. Competition by mazindol and dopamine against [3H]GBR-12935 binding revealed monophasic binding curves. The addition of 100 microM dopamine to the mazindol competition inhibited only 80% of the binding, indicating more than one [3H]GBR-12935 binding site in rat striatum. When a binding fraction that could be discriminated by 1 microM mazindol or 1 mM dopamine was defined as specific binding, a single site binding model was obtained. The [3H]GBR-12935 binding was of protein nature, since it was abolished after protease treatment. Drug inhibition studies with the addition of low concentrations of mazindol and dopamine resulted in alterations in apparent Kd values only, suggesting competitive inhibition by these compounds against [3H]GBR-12935 binding. It is concluded that the [3H]GBR-12935 binding to rat striatum discriminated by 1 microM mazindol reflects binding to the substrate recognition site for the dopamine uptake.
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| 7. |
- Allard, Per, et al.
(författare)
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Loss of dopamine uptake sites labeled with [3H]GBR-12935 in Alzheimer's disease.
- 1990
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Ingår i: European Neurology. - 0014-3022 .- 1421-9913. ; 30:4, s. 181-5
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Tidskriftsartikel (refereegranskat)abstract
- The binding of the dopamine uptake inhibitor [3H]GBR-12935 to postmortem putamen from a control group and patients with Alzheimer's disease/senile dementia of Alzheimer type (AD/SDAT) or vascular dementia (VD) was studied. The binding density (Bmax) in AD/SDAT was significantly reduced to 50% of control. A reduction of Bmax in VD was also noted, but it did not reach statistical significance. No differences in apparent binding affinity (Kd) between controls and dementia groups were obtained. The concentrations of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), 3-methoxytyramine (3-MT) and homovanillic acid were also determined. The concentrations of DA and DOPAC were reduced by 30-40% in AD/SDAT and VD, but the reductions did not reach statistical significance. The concentration of 3-MT was reduced by 40% in AD/SDAT and by 30% in VD. The [3H]GBR-12935-binding densities correlated significantly with corresponding concentrations of DA in control brains. It is suggested that the loss of [3H]GBR-12935-binding sites in human putamen in AD/SDAT reflects a degeneration of dopamine neurites.
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| 8. |
- Allard, Per, et al.
(författare)
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Unaltered [3H]GBR-12935 binding after chronic treatment with dopamine active drugs.
- 1990
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Ingår i: Psychopharmacology. - 0033-3158 .- 1432-2072. ; 102:3, s. 291-4
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Tidskriftsartikel (refereegranskat)abstract
- Rats were injected intraperitoneally with haloperidol 0.5 mg/kg, raclopride 1 mg/kg, bromocriptine 2.5 mg/kg, d-amphetamine 2.5 mg/kg, or cocaine 10 mg/kg twice daily for 21 days. The animals were sacrificed 72 h after last injection. Control rats were injected with saline, following the same schedule. The radioligand [3H]GBR-12935 was used as a presynaptic marker for dopamine neurites. There were no significant differences in [3H]GBR-12935 binding to striatum between drug-treated rats and controls.
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| 9. |
- Andersson, A, et al.
(författare)
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Platelet [3H]paroxetine binding to 5-HT uptake sites in Alzheimer's disease.
- 1991
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Ingår i: Neurobiology of Aging. - 0197-4580 .- 1558-1497. ; 12:5, s. 531-4
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Tidskriftsartikel (refereegranskat)abstract
- Platelet serotonin (5-hydroxytryptamine, 5-HT) uptake sites were studied in a control group (n = 30) and an Alzheimer group (n = 40) using [3H]paroxetine as radioligand. The maximum number of binding sites (Bmax) for control (1250 +/- 60 fmol/mg protein) was not different from the Alzheimer group (1280 +/- 40 fmol/mg protein). There were no differences in apparent binding affinity (Kd): 0.046 (0.024-0.062) nM for control and 0.040 (0.027-0.061) nM for Alzheimer. Thus even though several previous studies have demonstrated marked atrophy of 5-HT containing neurites and 5-HT uptake sites in Alzheimer's disease, these findings are not found in the periphery on platelets. The platelet 5-HT uptake site cannot be used as a peripheral marker of Alzheimer's disease.
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| 10. |
- Andersson-Gäre, Boel, et al.
(författare)
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Incidence and prevalence of juvenile chronic arthritis : a population survey
- 1987
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Ingår i: Annals of the Rheumatic Diseases. - 0003-4967 .- 1468-2060. ; 46:4, s. 277-81
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Tidskriftsartikel (refereegranskat)abstract
- In a population based epidemiological survey of juvenile chronic arthritis (JCA), performed in Western Sweden in 1983, an incidence of 12/100,000 was found. The estimated prevalence was 56/100,000. Subgroup distribution showed a preponderance of mono- and pauciarticular forms. The peak age of onset was between 0 and 4 years of age. Girls predominated over boys in a ratio of 3:2. Overall, 30% were antinuclear antibody (ANA) positive, 9% rheumatoid factor (RF) positive, and eye involvement occurred in 10% of the children. The results suggest differences in population based studies of JCA compared with previously reported hospital based series.
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