| 11. |
- 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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| 12. |
- Fredriksson, K, et al.
(författare)
-
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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| 13. |
- 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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| 14. |
- Joborn, H, et al.
(författare)
-
Serum electrolytes and parathyroid hormone in patients in a coronary care unit
- 1989
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Ingår i: Journal of Internal Medicine. - 1365-2796. ; 225:1, s. 9-14
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Tidskriftsartikel (refereegranskat)abstract
- A prospective study was carried out in 499 patients admitted to a coronary care unit (CCU) in order to evaluate the incidence of clinically significant electrolyte disturbances. Low serum potassium values (less than 3.6 mmol l) occurred in 7% of the CCU patients and low serum magnesium values (less than 0.70 mmol l-1) in 6%. Few patients had low values of both these ions (1.9%). In 49 patients the contents of these electrolytes in muscle biopsies were similar to the values of control subjects and were unrelated to treatment with diuretics. Serum calcium was determined in 444 of the patients and was above the reference range in 11 (2.5%). If we consider their concomitant parathyroid hormone (PTH) values, primary hyperparathyroidism was likely to occur in at least seven patients (1.5%). Patients with acute myocardial infarction (AMI) had mean PTH and electrolyte values similar to those of individuals without this disease. In conclusion, the present study indicates that clinically important disturbances of magnesium, potassium or calcium homeostasis are rare among unselected patients admitted to a CCU.
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| 15. |
- Johansson, Bengt O. H., 1934-2021
(författare)
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Byggnadsminneslagen : ett prejudikat
- 1986
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Ingår i: Kulturminnesvård. - Stockholm : Riksantikvarieämbetet. - 0346-9077. ; :1, s. 3-8
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Tidskriftsartikel (populärvet., debatt m.m.)abstract
- Det är ont om rättsfall i anslutning till byggnadsminneslagen. Den utgår från att byggnadsminnesförklaring skall göras frivilligt och att skyddsföreskrifter skall utformas med minsta möjliga tvång. Genom beslut i regeringsrätten och efter tre års domstolsförhandling avgjordes dock fallet med länsstyrelsens byggnadsminnesförklaring av Oscarsteatern och Kungsbropalatset i Stockholm. Länsantikvarie Bengt O H Johansson rapporterar.
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| 16. |
- Johansson, Bengt O H, 1934-2021
(författare)
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Docklands : en kritisk skrivövning
- 1988
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Ingår i: Kulturminnesvård. - Stockholm : Riksantikvarieämbetet. - 0346-9077. ; :6, s. 2-3
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Tidskriftsartikel (populärvet., debatt m.m.)
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| 17. |
- Johansson, Bengt O H, 1934-
(författare)
-
English Heritage
- 1988
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Ingår i: Kulturminnesvård. - Stockholm : Riksantikvarieämbetet. - 0346-9077. ; :6, s. 40-45
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Tidskriftsartikel (populärvet., debatt m.m.)abstract
- Riksantikvarieämbetets motsvarighet i England — English Heritage — får här en presentation av Bengt O H Johansson.
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| 18. |
- Johansson, Bengt O H, 1934-
(författare)
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Riksintressen : en resa i historien
- 1988
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Ingår i: Kulturminnesvård. - Stockholm : Riksantikvarieämbetet. - 0346-9077. ; :1, s. 15-19
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Tidskriftsartikel (populärvet., debatt m.m.)abstract
- Nu är det gjort! De kulturhistoriskt mest intressanta områdena i Sverige har valts ut i ett samarbete mellan länsstyrelser, länsmuseer och riksantikvarieämbetet. Bengt O H Johansson, chef för den nya Kulturmiljöavdelningen, berättar om arbetet.
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| 19. |
- 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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| 20. |
- 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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