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Träfflista för sökning "WFRF:(Karlsson Göran 1954) srt2:(2001-2004)"

Sökning: WFRF:(Karlsson Göran 1954) > (2001-2004)

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1.
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2.
  • Karlsson, Karl-Göran, 1948-, et al. (författare)
  • Läsande och naturvetenskap - några resultat från den svenska PISA-undersökningen
  • 2004
  • Ingår i: Naturfagenes didaktikk - en disiplin i forandring?. - Kristiansand : Høyskoleforlaget i samarbeid med Høgskolen i Agder. - 8276345689 ; , s. 51-63
  • Konferensbidrag (refereegranskat)abstract
    • I denna studie har vi, för ett urval av PISA-uppgifter, detaljstuderat hög- respektive lågpresterande elever för att försöka förstå vilka faktorer som är avgörande för resultaten inom den naturvetenskapliga delen av PISA-undersökningen. Läsförståelse tycks vara av avgörande betydelse för elevernas resultat inom naturvetenskap. I synnerhet gäller detta för de uppgifter där eleverna ska formulera egna svar.
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3.
  • Karlsson, Karin, et al. (författare)
  • Oral cladribine for B-cell chronic lymphocytic leukaemia : Report of a phase II trial with a 3-d, 3-weekly schedule in untreated and pretreated patients, and a long-term follow-up of 126 previously untreated patients
  • 2002
  • Ingår i: British Journal of Haematology. - : Wiley. - 0007-1048 .- 1365-2141. ; 116:3, s. 538-548
  • Tidskriftsartikel (refereegranskat)abstract
    • A phase II study was undertaken to evaluate the efficacy and toxicity of a new schedule of cladribine administration (10 mg/m2 orally daily for 3 d every 3 weeks) in 107 patients with B-cell chronic lymphocytic leukaemia (CLL). To minimize toxicity, treatment withdrawal criteria were defined. The results of the 63 previously untreated patients were retrospectively compared with 63 from an earlier study using a 5-d monthly schedule. The compiled data were analysed for prognostic factors for survival. No significant difference regarding response were seen in the two cohorts of the 126 previously untreated patients. The complete response (CR), nodular partial response (nPR) and partial response (PR) rates were 15%, 21% and 41%. Quality of response had no impact on survival. The 3- and 5-year overall survival for previously untreated patients was 73% and 58%, respectively, with a median follow-up of 54 months. Pretreatment haemoglobin < 11.0 g/dl and elevated beta-2-microglobulin had a negative influence on survival. Major infections occurred in 21% of patients in the 3-d study compared with 35% in the 5-d study. The overall response (OR) and CR rates in the 40 previously treated patients were 34% and 5% respectively. Median overall survival was 24 months and median progression-free survival for responding patients was 14 months. Cladribine used as a single agent is an effective treatment with an acceptable safety profile for pretreated and untreated B-CLL. The achievement of complete remission was not a prerequisite for long-term survival.
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4.
  • Kormi-Nouri, Reza, 1954-, et al. (författare)
  • Is there memory deficit in Parkinson’s disease? Explicit and implicit memory for verbal and action events
  • 2001
  • Ingår i: Advances in Cognitive Sciences. - Tehran : Institute for Cognitive Science Studies, Qalam Gostaran Pajouhesh. - 1561-4174. ; 3:1-2, s. 28-39
  • Tidskriftsartikel (refereegranskat)abstract
    • Three experiments examined both encoding and test variable whether there is any memory deficit in patients with Parkinson's disease in comparison with normal controls. In Experiment 1, the effect of encoding enactment was tested in free recall and cued recall. In Experiment 2, the combinations of enactment/non enactment and well/poorly integration variables were used at encoding. Again, the subjects were tested by free and cued recall. In Experiment 3, recognition memory and sentence-fragment completion tests were used with the same encoding manipulations as in Experiment 2. In general, the results of all three experiments showed no difference between PD patients and normal controls indicating that there is no memory deficit for PD patients. However, it was observed that there was some recognition deficit (especially for well integrated and verbal items) in Parkins on patients. It was suggested that the similarity between encoding and retrieval and the stage of disease should be considered as important factors for any possible memory deficit in Parkinsonian patients. It was also concluded that Parkinson patients are less well able to utilize cognitive support.
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5.
  • Tobin, Gerard, et al. (författare)
  • Subsets with restricted immunoglobulin gene rearrangement features indicate a role for antigen selection in the development of chronic lymphocytic leukemia.
  • 2004
  • Ingår i: Blood. - : American Society of Hematology. - 0006-4971 .- 1528-0020. ; 104:9, s. 2879-85
  • Tidskriftsartikel (refereegranskat)abstract
    • Pseudohypoaldosteronism type I (PHA1) is a condition associated with salt wasting leading to dehydration, hypotension, hyperkalemia, and metabolic acidosis. Sporadic cases and two familial forms, one autosomal dominant and one autosomal recessive form, have been described. The autosomal dominant or sporadic form manifests milder salt wasting that remits with age. Mutations in the gene encoding the mineralocorticoid receptor (MR) have been identified in patients with the autosomal dominant inheritance. However, recent studies suggest that the autosomal dominant and sporadic forms are genetically heterogeneous and that additional genes might be involved. We report on the study of 15 members of a Swedish five-generation family with the autosomal dominant form of PHA1. Interestingly, neuropathy was found in two of five affected individuals. A novel heterozygous nonsense mutation C436X in exon 2 was identified in the index patient by linkage analysis, PCR, and direct sequencing of the MR gene. Analysis of the family demonstrated that the mutation segregated with PHA1 in the family. It is unclear whether the neuropathy is associated with the mutation found. Our results together with previously published data suggest that loss-of-function mutations of the MR gene located at 4q31.1, commonly are associated with the autosomal dominant form of PHA1.
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