| 1. |
- Levin, J.C., et al.
(författare)
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Production of very cold, highly charged ions by synchrotron radiation: Comparisons of the “scalpel” and “hammer” methods
- 1987
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Ingår i: Nuclear Instruments & Methods in Physics Research. Section A: Accelerators, Spectrometers, Detectors, and Associated Equipment. - : Elsevier BV. - 0168-9002. ; 262:1, s. 106-109
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Tidskriftsartikel (refereegranskat)abstract
- Measurements of kinetic energies of highy charged argon ions produced by inner-shell photoionization and by ion-beam impact have been made using time-of-flight techniques. High-charge-state recoil ions produced by beams of ∼ 0.5-1 MeV/u Cl5+ are found to have energies one to two orders of magnitude higher than ions of the same charge produced by vacancy cascades following inner-shell photoionization by synchrotron radiation. The results may have application to the development of a very cold ion source useful for angle-resolved atomic collision studies.
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| 2. |
- Malmqvist, K. G., et al.
(författare)
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PIXE and proton microprobe advances at the Lund Institute of Technology
- 1989
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Ingår i: Nuclear Inst. and Methods in Physics Research, B. - 0168-583X. ; 40-41:PART 1, s. 685-689
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Tidskriftsartikel (refereegranskat)abstract
- A review of recent advances in high-energy ion beam analysis at the Lund Institute of Technology is presented. A nonvacuum specimen chamber allows chemical speciation using a combination of ion beam analysis and controlled heating. The development of a new versatile scanning proton microbeam based on a new dedicated accelerator, an achromatic triplet lens and an advanced specimen chamber is outlined together with the performance of a microVAX-II/VMEbus-based data acquisition system.
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| 3. |
- Short, R. T., et al.
(författare)
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Production of very-low-energy highly charged ions by synchrotron radiation
- 1986
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Ingår i: Physical Review Letters. - 1079-7114. ; 56:24, s. 2614-2617
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Tidskriftsartikel (refereegranskat)abstract
- Very-low-energy highly charged ions have been produced by use of white and monochromatic x rays from a wiggler line at the Stanford Synchrotron Radiation Laboratory to generate vacancy cascades following inner-shell photoionization. Recoil-ion energies have been determined and are shown to correspond essentially to room temperatures, even for high charge states. Promising applications to study of the interaction of stellar radiation with cold matter, to high-brightness ionsource development, to precision spectroscopy, and to angle-resolved chemical-physics reactive-scattering studies are discussed.
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| 4. |
- Blomström-Lundqvist, C, et al.
(författare)
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Cardioangiographic findings in patients with arrhythmogenic right ventricular dysplasia
- 1988
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Ingår i: British Heart Journal. - 0007-0769. ; 59:5, s. 556-563
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Tidskriftsartikel (refereegranskat)abstract
- The dimension, contractility, and regional wall motion of the right and left ventricles were scored on the angiograms of 13 patients with arrhythmogenic right ventricular dysplasia. In 10 patients the right ventricle was enlarged, in eight the contractility of the right ventricle was reduced, and in all but one patient there were regional wall motion abnormalities of the right ventricle. The most common abnormality of regional wall motion was mild hypokinesia. There were bulging or dyskinetic areas in seven patients. Regional wall motion abnormalities of the left ventricle were found in five patients, two of whom also had bulging or dyskinetic areas. The reproducibility of right ventricular dimension, contractility, and regional wall motion scores was generally fair but varied unexpectedly both within and between two observers (Kendall's Tau 0.38-0.92). The score values of regional wall motion for some of the segments differed considerably within and between observers. One of the observers consistently gave higher scores than the other. These data suggest that a more objective approach is needed for evaluating angiographic changes in arrhythmogenic right ventricular dysplasia.
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| 5. |
- Fredriksson, K, et al.
(författare)
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Cerebral microangiopathy in stroke-prone spontaneously hypertensive rats. An immunohistochemical and ultrastructural study
- 1988
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Ingår i: Acta Neuropathologica. - 1432-0533. ; 75:3, s. 241-252
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Tidskriftsartikel (refereegranskat)abstract
- The morphology of cerebral microvessels was studied immunohistochemically and ultrastructurally in 6- to 9-month-old normotensive Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP) with a systolic blood pressure of 138 +/- 15 mm Hg, 189 +/- 9 mm Hg, and 258 +/- 30 mm Hg respectively. Regions with major opening of the blood-brain barrier (BBB) were revealed by an i.v. injection of Evans Blue. Multifocal BBB opening with massive leakage of plasma constituents rich in fibrinogen-fibrin-related antigen occurred in SHRSP with a blood pressure above 210-220 mm Hg. BBB-leakage sites were found in the cerebral cortex and the basal ganglia, most frequently in the arterial border zones. The perivascular tissue spaces were dilated within the BBB-leakage sites, in particular around arterioles. Damaged endothelial and smooth muscle cells were replaced by fibrin-like material, multiple layers of basement membranes and bundles of collagen fibrils surrounded by proliferated fibroblasts. The degenerative-infiltrative-proliferative disease process transformed short segments of single arterioles into severely thickened, tortuous and stenotic vessels. Fibrinoid degeneration, formation of microaneurysms and fibrin-rich vascular occlusions were observed. In contrast, only minor or no vascular alterations were seen in regions with preserved BBB in SHRSP and SHR. A severely increased intraluminal pressure load appears to be of major pathogenetic importance for breakdown of the BBB and initiation of the vascular disease process in SHRSP. However, since only short segments of a limited number of widely separated vessels are severely affected, and the number of affected vessels increase towards arterial end and border zones, additional predisposing and aggravating factors may play significant roles in the development of fibrinoid vascular lesions in arterial hypertension.
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| 6. |
- Fredriksson, K, et al.
(författare)
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Cerebrovascular lesions in stroke-prone spontaneously hypertensive rats
- 1985
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Ingår i: Acta Neuropathologica. - 1432-0533. ; 68:4, s. 284-294
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Tidskriftsartikel (refereegranskat)abstract
- The cerebrovascular lesions of severe chronic hypertension were studied by light microscopy in perfusion-fixed, subserially sectioned brains from stroke-prone spontaneously hypertensive rats (SHRSP). The leakage and spread of plasma proteins were visualized by immunohistochemical detection of extravasated fibrinogen and by using an exogenous marker (Evans blue injected i.v.) for blood-brain barrier (BBB) dysfunction. In most SHRSP the hypertension did not lead to major BBB lesions in spite of a mean arterial pressure around 200 mm Hg at 6-9 months of age. Multifocal BBB damage occurred in a minor group of SHRSP, particularly within the cortex and the deep gray matter. A close spatial correlation was found between the leakage-spread of plasma constituents and the neuropathologic alterations. Fibrinoid degeneration of penetrating arterioles was found within the leakage sites. The surrounding gray matter showed petechial hemorrhages and abundant proteinaceous exudates rich in antifibrinogen-positive material. The current leakage of Evans blue and wide spread of fibrinoid substances suggested long-lasting damage to the BBB. Most neurons within the edematous gray matter had well preserved nuclei surrounded by a rim of cytoplasm with ill-defined outline as if vacuolation or lysis of the peripheral cytoplasm had occurred. The sponginess of the tissue progressed in severe cases to formation of necrotic cysts. Condensed acidophilic neurons were seen in the border zone between the edematous and more compact gray matter. The appearance and distribution of the gray matter lesions deviated in many respects from those commonly seen in regional ischemic infarcts. The fibrin thrombi found close to the cysts might be regarded as secondary events. The extensive spread of antifibrinogen-positive material within the white matter seemed to originate mainly from the chronic leakage sites in the gray matter. Increased number of large astrocytes were seen within the leakage sites and along the spreading pathways for the edema constituents. The white matter showed a rarefied texture with widely dispersed nerve fiber tracts, volume expansion, and occasional cyst formation. The results indicate a crucial pathophysiologic role for the egress, spread, and accumulation of vasogenic edema in the development of the cerebrovascular lesions in SHRSP.
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| 7. |
- Fredriksson, K, et al.
(författare)
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Cyst formation and glial response in the brain lesions of stroke-prone spontaneously hypertensive rats
- 1988
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Ingår i: Acta Neuropathologica. - 1432-0533. ; 76:5, s. 441-450
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Tidskriftsartikel (refereegranskat)abstract
- The brain lesions in spontaneously hypertensive stroke-prone rats (SHRSP) are characterised by multifocal microvascular damage, breakdown of the blood-brain barrier, massive extravasation of plasma constituents and severe brain oedema, with consequent spongy and cystic tissue destruction in the cerebral cortex and basal ganglia as well as loosening of the white matter. In this paper we analyse in greater detail the pathogenetic mechanisms by which the spongy and cystic lesions are formed and the response of astrocytic cells. For this purpose, tracer (Evans blue)-stained brain lesions were examined in 8-month-old SHRSP immunohistochemically and electron microscopically. Sponginess of the neuropil in small lesions and at the periphery of larger lesions was due to swollen neuronal and astrocytic cell processes, i.e. at this stage the oedema was mainly intracellular. Cystic lesions were formed in the grey matter both by expansion of the extracellular space (ECS) containing protein-rich oedema fluid, and by rupture and subsequent loss of massively swollen cellular elements. In the white matter small slit-formed cysts along the fibre tracts were also formed by the expansion of ECS. In apparently recent lesions astrocytes displayed cyto-plasmic oedema but otherwise were still fairly normal. In more chronic lesions increased numbers of enlarged astrocytes with prominent staining for glial fibrillary acidic protein were present. Their distribution corresponded well to the spread of oedema, i.e. they were prominent around the leaky vessels in the grey matter, in the subpial zone and in the white matter. In the reparative phase the grey matter cysts became lined by astrocytic processes, a new glia limitans. Profuse sheets of glial processes in the neuropil around the cysts reestablished the compactness of the brain parenchyma.
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| 8. |
- Fredriksson, K, et al.
(författare)
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Nerve cell injury in the brain of stroke-prone spontaneously hypertensive rats
- 1988
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Ingår i: Acta Neuropathologica. - 1432-0533. ; 76:3, s. 227-237
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Tidskriftsartikel (refereegranskat)abstract
- The brain lesions in stroke-prone spontaneously hypertensive rats (SHRSP) are characterized by multifocal microvascular and spongy-cystic parenchymal alterations particularly in the gray matter. An essential feature of the lesions is the presence of edema with massive extravasation of plasma constituents as evidenced by specific gravity measurements, Evans blue technique and immunohistochemistry. The nerve cell injury occurring in the brain lesions in SHRSP is further characterized by light and electron microscopy in the present study. Two types of neuronal changes were seen within the blood-brain barrier (BBB) leakage sites. A small number of neurons with dark condensed nucleus and cytoplasm were found most often at the periphery of recent lesions. The majority of injured neurons were pale and showed intracellular edema confined to the dendrites and perikarya sparing axons and synapses. Their nuclei were well preserved with finely dispersed chromatin. The swollen and watery cell processes of neurons and astrocytes gave a spongy appearance to the neuropil. The intracellular edema seemed to result in cytolysis. The results suggest that primary anoxia-ischemia is not the major pathogenetic mechanism behind the nerve cell injury in severely hypertensive SHRSP, rather it is the massive BBB leakage and consequent brain edema that causes cytolytic destruction of neurons. Secondary focal ischemia as a consequence of occlusion in microvessels may, however, contribute to the nerve cell destruction.
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| 9. |
- Kutti, Jack, et al.
(författare)
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The relation between platelet reactivity and coronary angiographic findings in young female survivors of acute myocardial infarction.
- 1986
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Ingår i: Thrombosis and haemostasis. - 0340-6245. ; 56:2, s. 207-10
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Tidskriftsartikel (refereegranskat)abstract
- In 31 women who had survived their first acute myocardial infarction (MI) studies of platelet reactivity were related to coronary angiographic findings. The results were compared to those obtained from 38 age-matched control women. According to the cardioangiographic findings the group of MI was subdivided into: 9 patients with 1-vessel disease (VD), 10 patients with 2-VD, and 5 patients with 3-VD; 7 subjects did not reveal significant coronary stenosis. When each of these 4 subgroups of MI-patients were compared with the control material significant difference with respect to PF4 was found only for subjects with 1-VD (20.0 +/- 4.8 vs. 10.3 +/- 0.6 ng/ml). As regards BTG the difference was significant for 1-VD and 2-VD patients (69 +/- 12 and 59 +/- 3, respectively vs. 40 +/- 2 ng/ml). The cumulative frequency for secondary aggregation differed only as regards 1-VD patients (78 vs 40%).
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| 10. |
- Nardella, F A, et al.
(författare)
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Fc epitopes for human rheumatoid factors and the relationships of rheumatoid factors to the Fc binding proteins of microorganisms
- 1988
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Ingår i: Scandinavian Journal of Rheumatology. Supplement. - : Informa UK Limited. - 1502-7740 .- 0300-9742 .- 1502-7732. ; 17:Suppl. 75, s. 190-198
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Tidskriftsartikel (refereegranskat)abstract
- Work from our laboratories has shown that the major antigenic determinants for rheumatoid factors (RFs) are in the C gamma 2-C gamma 3 interface region of IgG in the same area that binds staphylococcal protein A (SPA). Furthermore, the Fc binding proteins of groups A, C and G streptococci as well as the Fc binding proteins induced on cell surfaces by herpes simplex virus type I also bind to the same area of IgG. These binding site similarities between RFs and the microbial Fc binding proteins suggested conformational similarities between the RF antigen combining regions and the Fc binding regions of the microbial proteins. This hypothesis was supported by the observation that antibodies to SPA bind to the antigen combining regions of most RFs as well as to the Fc binding region of the T15 group A streptococcal Fc binding protein. These findings indicate that RFs bear the conformational internal image of these microbial proteins and suggest that RFs could arise as antibodies to the idiotypic determinants on antibodies to microbial Fc binding proteins. Alternatively, microbial Fc binding proteins could present IgG to the immune system in a way that renders specific areas of the C gamma 2-C gamma 3 interface region immunogenic. These relationships between RFs and microbial Fc binding proteins may prove to be important for our understanding of the generation of RFs in rheumatoid arthritis.
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