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- Hedström, Brita, et al.
(author)
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Visby Innerstad : En användningsplan
- 1973
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Reports (pop. science, debate, etc.)abstract
- Sedan lång tid föreligger i stort sett enighet om att bevara innerstadens bebyggelse och att anpassa eventuella nytillskott till det redan bestående. Med den inställningen har förändringsprocessen både dämpats och mildrats men ändå inte bragts att avstanna. Förändringar sker ständigt om det också huvudsakligen i smått: de många synbart så anspråkslösa byggnadsåtgärderna adderar efterhand ihop sig till något större och mer genomgripande. Långsamt, nästan omärkligt, ändrar innerstaden sitt ansikte.Ändå är det inte själva husen som förändrats mest utan användningen av dem. Ur funktionell synpunkt har 1950 - och 60-talen har varit något av en omstörtning i innerstadens historia: den har förlorat nästan hälften av de boende, en stor del av detaljhandeln och praktiskt taget helt sin gamla roll som skolcentrum. I gengäld har ytterstaden vuxit ut till ett sammanhängande kilometerbrett bälte. Till stor del av denna funktionella förändring en följd av beslutet att bevara innerstadens bebyggelse. Vad som inte fått plats inom den gamla ramen har etablerats utandör den.Föreliggande arbete vill ge en översiktlig bild av förändringsförloppen, sedda i ett långt tidsperspektiv men med tonvikt på dagsläget. Bebyggelsen tas upp till utförlig granskning men också användningen av den. Det är just samspelet mellan husen och de funtkioner, de fyller, som kan sägas utgöra bokens huvudtema. I de flesta fall är detta sammanhang hus-användning alldeles konfliktfritt och föranleder därför inte heller någon diskussion. Vad som behandlas är de relativt få problematiska fallen, hus som borde rustas upp för att fylla sin uppgift, hus som är olämpligt nyttjade eller inte använda alls. En serie sådana fall tas upp till systematisk genomgång; samtidigt berörs också de trafik - och miljömässiga konsekvenserna. Bokens syfte är alltså klart: den ger ett underlag av fakta för arbetet med att jämka samman byggnader och användningsformer. I den meningen kan skriften kallas en anvädningsplan för Visby innanför murarna.Arkitekturskolanas arbete har bedrivitis parallellt med den kommunala Innerstadskommitténs verksamhet. Något organiserat samarbete har inte förekommit med de informella kontakterna har varit både täta och goda. Att likheterna mellan Innerstadskommittén och Arkitekturskolans slutsatser blivit så pass stora, kan tillskrivas en gemensam helhetssyn.En av Arkitekturskolans elever, arkitekt Lars-Ingvar Larsson, har tidigare självständigt genomfört en undersökning av förändringar i innerstaden 1945-70- Denna studie publicerats separat och bör uppfattas som ett komplement till den hör föreliggande.Förutom de i innehållsförteckningen nämnda har ytterligare några aktivt medverkat i arbetet. Studiet av trafikfrågorna i innerstaden, i hamnen och öster om ringmuren leddes av Åke Claesson, I fältstudier och diskussioner medverkande Göran Månsson.Arkitekturskolan har fått god hjälp av ett antal initierade personer i Visby. Särskild tacksamhet är vi skyldiga byggnadsnämnden ordförande Henning Jacobson, kommunalrådet C B Stenström, stadsarkitekten Måns Hagbergm f. länsbostadsdorektören Åke Malmberg och landsantikvarien Gunnar Svahnström. I boken publiceringskostnaderna har ekonomiskt bidrag lämnats av Gotlands kommun och Riksantikvarieämbetet.Boken har redigerats av Sture Balgård och Ann Mari Westerlind med hjälp av Henrik O Andersson, Bo Ek, Göran Lindahl, Fredrik von Platen, John Sjöström Gunnar Westerlind och Hans Wetterfors.Skeppsholmen, Stockholm, sommaren 1973.Arkitekturskolans lärare och elever.
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2. |
- Danielson, Mattias, et al.
(author)
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Effects of methylprednisolone on blood-brain barrier and cerebral inflammation in cardiac surgery-a randomized trial
- 2018
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In: Journal of Neuroinflammation. - : Springer Science and Business Media LLC. - 1742-2094. ; 15
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Journal article (peer-reviewed)abstract
- Background: Cognitive dysfunction is a frequent complication to open-heart surgery. Cerebral inflammation caused by blood-brain barrier (BBB) dysfunction due to a systemic inflammatory response is considered a possible etiology. The effects of the glucocorticoid, methylprednisolone, on cerebrospinal fluid (CSF) markers of BBB function, neuroinflammation, and brain injury in patients undergoing cardiac surgery with cardiopulmonary bypass were studied. Methods: In this prospective, randomized, blinded study, 30 patients scheduled for elective surgical aortic valve replacement were randomized to methylprednisolone 15 mg/kg (n = 15) or placebo (n = 15) as a bolus dose administered after induction of anesthesia. CSF and blood samples were obtained the day before and 24 h after surgery for assessment of systemic and brain inflammation (interleukin-6, interleukin-8, tumor necrosis factor-alpha), axonal injury (total-tau, neurofilament light chain protein), neuronal injury (neuron-specific enolase), astroglial injury (S-100B, glial fibrillary acidic protein), and the BBB integrity (CSF/serum albumin ratio). Results: In the control group, there was a 54-fold and 17-fold increase in serum interleukin-6 and interleukin-8, respectively. This systemic activation of the inflammatory cytokines was clearly attenuated by methylprednisolone (p < 0. 001). The increase of the CSF levels of the astroglial markers was not affected. A postoperative BBB dysfunction was seen in both groups as the CSF/serum albumin ratio increased from 6.4 +/- 8.0 to 8.0 in the placebo group (p < 0.01) and from 5. 6 +/- 2.3 to 7.2 in the methylprednisolone group (p < 0.01) with no difference between groups (p = 0.98). In the CSF, methylprednisolone attenuated the interleukin-6 release (p < 0.001), which could be explained by the fall in systemic interleukin-6, and the serum to CSF gradient of IL-6 seen both at baseline and after surgery. In the CSF, methylprednisolone enhanced the interleukin-8 release (p < 0.001) but did not affect postoperative changes in CSF levels of tumor necrosis factor alpha. Serum levels of S-100B and neuron-specific enolase increased in both groups with no difference between groups. CSF levels of total tau, neurofilament light chain protein, and neuron-specific enolase were not affected in any of the groups. Conclusions: Preventive treatment with high-dose methylprednisolone attenuated the systemic inflammatory response to open-heart surgery with cardiopulmonary bypass, but did not prevent or attenuate the increase in BBB permeability or the neuroinflammatory response.
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3. |
- Dellgren, Göran, 1961, et al.
(author)
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Continuous improvement in outcome after heart transplantation - Long-term follow-up after three decades of experience.
- 2017
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In: International journal of cardiology. - : Elsevier BV. - 1874-1754 .- 0167-5273. ; 231, s. 188-194
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Research review (peer-reviewed)abstract
- Heart transplantation (HTx) has become the standard treatment for patients with end-stage heart disease. We report on the long-term outcome after HTx at our centre and investigate trends in outcome over time.During the period, between 1984 and 2014, a total of 610 HTx procedures were performed in 595 patients (median 48years; IQR 31-57years; range 24days-71years; mean 43years; 75% male) in our institution. Long-term outcome was investigated in the whole cohort, among children (n=76), bridged with mechanical circulatory support (MCS, n=131), re-transplanted (n=17), and concomitant kidney transplantation (n=12).Long-term survival was at 1, 5, 10, 15 and 20years: 86% (95CI 0.83-0.89); 77% (95CI 0.73-0.80); 63% (95CI 0.59-0.68); 48% (95CI 0.43-0.54) and 30% (95CI 0.25-0.36), respectively. The median survival for the whole cohort was 14.1years. Patients transplanted during the most recent time period (2010-2014) had a better survival compared to previous eras, with a 1- and 3-year survival of 94% (95CI 0.89-0.97) and 93% (95CI 0.88-0.96), respectively (p<0.001). However, when survival was analysed for long-term MCS (n=80) versus short term MCS (n=35), there was a significantly poorer survival for the short-term MCS group (p=0.001). Independent predictors of long-term mortality included recipient age (p=0.041); previous smoking (p=0.034); ischemic heart disease (p=0.002); and preoperative ventilator therapy (p=0.004).We have shown that continuous improvement in outcome after HTx still occurs. In the last time era, direct transplantation from short-term MCS was abandoned, which may have inflicted outcome during the last time era.
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4. |
- Gruselius, B., et al.
(author)
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Mediaprojektet
- 1979
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Reports (other academic/artistic)
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9. |
- Reinsfelt, Björn, et al.
(author)
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Open-heart surgery increases cerebrospinal fluid levels of Alzheimer-associated amyloid β
- 2013
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In: Acta anaesthesiologica Scandinavica. - : Wiley. - 1399-6576 .- 0001-5172. ; 57:1, s. 82-88
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Journal article (peer-reviewed)abstract
- BACKGROUND: Neurocognitive dysfunction occurs frequently after open-heart surgery. It has been suggested that cognitive decline after cardiac surgery with cardiopulmonary bypass (CPB) could be a functional consequence of Alzheimer's disease (AD)-like neuropathological changes. The aim of the present study was to evaluate the cerebrospinal fluid (CSF) levels of amyloid β peptide (Aβ(1-42) ) and soluble fragments of amyloid precursor protein (sAPP) as well as the cerebral inflammatory response to open-heart surgery. METHODS: Ten patients undergoing aortic valve replacement with CPB were included. CSF was obtained the day before and 24h after surgery for assessment of CSF levels of Aβ(1-42) α-cleaved sAPP and β-cleaved sAPP (sAPP-β). Furthermore, CSF and serum levels of the inflammatory cytokines: tumour necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and interleukin-8 (IL-8) were also assessed. RESULTS: Cardiac surgery with CPB increased CSF levels of Aβ(1-42) from 447±92 to 641±83ng/l (P=0.011), while CSF levels of sAPP-β decreased from 276±35 to 192±21ng/ml (P=0.031). CSF levels of TNF-α increased from ≤0.60 to 0.79±0.26ng/l (P=0.043), IL-6 from 1.89±0.53 to 22.8±6.9ng/l (P=0.003) and IL-8 from 39.8±7.8 to 139±18.3ng/l (P<0.001). CONCLUSIONS: Cardiac surgery with CPB causes a profound cerebral inflammatory response, which was accompanied by increased post-operative CSF levels of the AD biomarker Aβ(1-42) . We hypothesize that these changes may be relevant to Alzheimer-associated amyloid build-up in the brain and cognitive dysfunction after cardiac surgery with CPB.
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10. |
- Reinsfelt, Björn, et al.
(author)
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Transcranial Doppler microembolic signals and serum marker evidence of brain injury during transcatheter aortic valve implantation.
- 2012
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In: Acta anaesthesiologica Scandinavica. - : Wiley. - 1399-6576 .- 0001-5172. ; 56:2, s. 240-24
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Journal article (peer-reviewed)abstract
- BACKGROUND: Recent studies have shown that transcatheter aortic valve implantation (TAVI) is associated with new foci of restricted diffusion on cerebral magnetic resonance imaging suggestive of cerebral microembolism. The aim of the present investigation was to quantify the cerebral embolic load and to evaluate during which phase of the TAVI procedure microembolism occurs. We also evaluated the association between the cerebral embolic load and post-procedural release of S100B, a serological marker of cerebral injury. METHODS: In 21 patients, we described the extent and intra-procedural distribution of microemboli during the TAVI procedure using the transcranial Doppler technique. S100B, a marker of astroglial injury, was measured for 24h after the procedure, and the area under the curve (AUC(24h) ) relating S100B to time was calculated. RESULTS: During the TAVI procedure, a mean of 282±169 emboli was detected, 37% occurred during manipulation of the aortic arch/root/valve by guide wires and catheters, 22% occurred immediately after balloon dilatation of the native valve and 41% occurred during frame expansion of the valve prosthesis. S100B increased in all patients with a peak at 1h after the procedure and returned to baseline after 4h. There was a positive correlation between the total amount of cerebral microemboli and the AUC(24h) for S100B (r=0.68, P<0.001). None of the patients developed neurological impairment. CONCLUSION: TAVI is associated with a substantial amount of cerebral microemboli. The microembolic load correlates to the degree of post-procedural release of a marker of cerebral injury.
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11. |
- Westerlind, Helga, et al.
(author)
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Dense genotyping of immune-related loci identifies HLA variants associated with increased risk of collagenous colitis.
- 2017
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In: Gut. - : BMJ Publishing Group Ltd. - 0017-5749 .- 1468-3288. ; 66:3, s. 421-428
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Journal article (peer-reviewed)abstract
- OBJECTIVE: Collagenous colitis (CC) is a major cause of chronic non-bloody diarrhoea, particularly in the elderly female population. The aetiology of CC is unknown, and still poor is the understanding of its pathogenesis. This possibly involves dysregulated inflammation and immune-mediated reactions in genetically predisposed individuals, but the contribution of genetic factors to CC is underinvestigated. We systematically tested immune-related genes known to impact the risk of several autoimmune diseases for their potential CC-predisposing role.DESIGN: Three independent cohorts of histologically confirmed CC cases (N=314) and controls (N=4299) from Sweden and Germany were included in a 2-step association analysis. Immunochip and targeted single nucleotide polymorphism (SNP) genotype data were produced, respectively, for discovery and replication purposes. Classical human leucocyte antigen (HLA) variants at 2-digit and 4-digit resolution were obtained via imputation from single marker genotypes. SNPs and HLA variants passing quality control filters were tested for association with CC with logistic regression adjusting for age, sex and country of origin.RESULTS: Forty-two markers gave rise to genome-wide significant association signals, all contained within the HLA region on chromosome 6 (best p=4.2×10(-10) for SNP rs4143332). Among the HLA variants, most pronounced risk effects were observed for 8.1 haplotype alleles including DQ2.5, which was targeted and confirmed in the replication data set (p=2.3×10(-11); OR=2.06; 95% CI (1.67 to 2.55) in the combined analysis).CONCLUSIONS: HLA genotype associates with CC, thus implicating HLA-related immune mechanisms in its pathogenesis.
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