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- Abrahamsson, Kenneth, et al.
(författare)
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The value of work experience in higher education : a study of work experience as a substitute for formal academic entrance requirements
- 1980
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Rapport (övrigt vetenskapligt/konstnärligt)abstract
- The Swedish policy that work experience can be used as a substitute for formal academic entrance requirements for higher education is assessed. The social and economic background of introducing work experience in higher education policy is described, and the significance of work experience to enrollment patterns and for the form and content of higher education is addressed. The general characteristics of the Swedish admissions system and the effects on recruitment and admissions are outlined. Additionally, the effects of work experience on the educational process are considered from a theoretical viewpoint. Distinctions are made between three different functions of work experience as a ground for admission: work experience as a substitute for upper secondary school education (alternative route) for adults; additional credit in selection for all students; and formal requirement for admission to some study programs. Work experience also is classified as a basis for academic studies according to its content (relevant professional experience, work experience, in general, and life experience). The admissions schemes in Sweden and Denmark are compared, and those found in a few other countries are briefly noted. Some Swedish findings regarding different ways of valuing work experience as an admission criterion are summarized. It is suggested that institutions that are mainly oriented toward traditional groups do not have the same possibilities of using experience as do institutions with an educational design oriented toward nontraditional students. A bibliography is appended
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| 3. |
- Kim, Lillemor
(författare)
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Val och urval till högre utbildning : En studie baserad på erfarenheterna av 1977 års tillträdesreform : [a study based on the experiences of the 1977 admissions reform in Sweden]
- 1998
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The central theme of this study is the process of choice and selectionin recruitment to higher education. The study is based on the experiences of the 1977 admissions reform in Sweden and subsequent developments. The traditional problem of individual choice is complemented by a further perspective-the decision-making process underlying the creation and successive modification of the admissions system-thereby enhancing our understanding of the mechanisms that determine recruitment to higher education.Several studies constitute the empirical basis for the thesis. Three investigations elucidate the effects of the admissions rules on individual choices at the end of secondary school, at the time of application and in the longer run. Two studies analyze the admissions reform from the system side. They all focus on the interplay between the individual and the admissions system. Both quantitative and qualitative methods are used ("multi-method study").The empirical studies revealed that the uniform admissions rules had strong impact on inividuals expectations and produced different effects for different groups of applicants. These effects were less related to social background than to current situation and reactions of applicants. Changes in admission rules during the 1980s appeared to be the result of a complicated interplay between the political and the administrative power structures.The results of the study imply that it is necessary to view admission to higher education as a process over a long time period and as an interplay between the choices of individuals and selection by the system. The process takes on strongly cumulative effects over time, especially in a higher-education system with unchanged admissions capacity, as was the case in Sweden until the early 1990s. The analysis indicates several deficiencies in the underlying policy theory.The results are used to elaborate the conceptual framework, termed Blau's Model, as a basis for continued research. Fundamental features of Sweden's present-day admissions policy, still based on largely the same principles as in 1977, are also questioned on these grounds.
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| 5. |
- Kleer, Jessica S., et al.
(författare)
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Complement C1s deficiency in a male Caucasian patient with systemic lupus erythematosus : a case report
- 2023
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Ingår i: Frontiers in Immunology. - 1664-3224. ; 14
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Tidskriftsartikel (refereegranskat)abstract
- Deficiencies of the early complement components of the classical pathway (CP) are well-documented in association with systemic lupus erythematosus (SLE) or SLE-like syndromes and severe pyogenic infections. Among these, complete C1s deficiency has been reported in nine cases so far. Here, we describe a 34-year-old male patient who presented with severe, recurrent infections since childhood, including meningitides with pneumococci and meningococci, erysipelas, subcutaneous abscess, and recurrent infections of the upper airways. The patient also exhibited adult-onset SLE, meeting 7/11 of the ACR criteria and 34 of the 2019 EULAR/ACR classification criteria, along with class IV-G (A) proliferative lupus nephritis (LN). A screening of the complement cascade showed immeasurably low CH50, while the alternative pathway (AP) function was normal. Subsequent determination of complement components revealed undetectable C1s with low levels of C1r and C1q, normal C3, and slightly elevated C4 and C2 concentrations. The patient had no anti-C1q antibodies. Renal biopsy showed class IV-G (A) LN with complement C1q positivity along the glomerular basement membranes (GBMs) and weak deposition of IgG, IgM, and complement C3 and C4 in the mesangium and GBM. In an ELISA-based functional assay determining C4d deposition, the patient’s absent complement activity was fully restored by adding C1s. The genome of the patient was analyzed by whole genome sequencing showing two truncating variants in the C1S gene. One mutation was located at nucleotide 514 in exon 5, caused by a nucleotide substitution from G to T, resulting in a nonsense mutation from Gly172 (p.Gly172*). The other mutation was located at nucleotide 750 in exon 7, where C was replaced by a G, resulting in a nonsense mutation from Tyr250 (p.Tyr250*). Both mutations create a premature stop codon and have not previously been reported in the literature. These genetic findings, combined with the absence of C1s in the circulation, strongly suggest a compound heterozygote C1s deficiency in our patient, without additional defect within the complement cascade. As in a previous C1s deficiency case, the patient responded well to rituximab. The present case highlights unanswered questions regarding the CP’s role in SLE etiopathogenesis.
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| 7. |
- Perman, Jeanna, 1981, et al.
(författare)
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The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction.
- 2011
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Ingår i: The Journal of clinical investigation. - : American Society for Clinical Investigation. - 1558-8238 .- 0021-9738. ; 121:7, s. 2625-40
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Tidskriftsartikel (refereegranskat)abstract
- Impaired cardiac function is associated with myocardial triglyceride accumulation, but it is not clear how the lipids accumulate or whether this accumulation is detrimental. Here we show that hypoxia/ischemia-induced accumulation of lipids in HL-1 cardiomyocytes and mouse hearts is dependent on expression of the VLDL receptor (VLDLR). Hypoxia-induced VLDLR expression in HL-1 cells was dependent on HIF-1α through its interaction with a hypoxia-responsive element in the Vldlr promoter, and VLDLR promoted the endocytosis of lipoproteins. Furthermore, VLDLR expression was higher in ischemic compared with nonischemic left ventricles from human hearts and was correlated with the total lipid droplet area in the cardiomyocytes. Importantly, Vldlr-/- mice showed improved survival and decreased infarct area following an induced myocardial infarction. ER stress, which leads to apoptosis, is known to be involved in ischemic heart disease. We found that ischemia-induced ER stress and apoptosis in mouse hearts were reduced in Vldlr-/- mice and in mice treated with antibodies specific for VLDLR. These findings suggest that VLDLR-induced lipid accumulation in the ischemic heart worsens survival by increasing ER stress and apoptosis.
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