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- Brandström, Per, 1959, et al.
(författare)
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Renal damage in children randomized to prophylaxis, endoscopic injection, or surveillance
- 2010
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Ingår i: European Society for Paediatric Urology Annual Meeting, 28 april-1 maj 2010, Antalya, Turkiet.
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- PURPOSE To compare the development of new renal damage in small children with dilating vesicoureteral reflux randomly allocated to antibiotic prophylaxis, endoscopic treatment or surveillance (control group). MATERIAL AND METHODS Included were 203 children, 128 girls and 75 boys, aged 1 to less than 2 years with reflux grade III to IV. Voiding cystourethrography and 99mTcdimercaptosuccinic acid scintigraphy were performed before randomization and after 2 years. Febrile urinary tract infections were recorded during the follow-up. Data analysis was performed according to the intention-to-treat principle. RESULTS New renal damage in a previously unscarred area was seen in 15 children, 13 girls and 2 boys. Eight of these 13 girls were in the surveillance, 5 in the endoscopic, and none in the prophylaxis group (p=0.0155). New damage was seen more often in children with (11/49, 22%) than without (4/152, 3%) febrile recurrence (p<0.0001). CONCLUSIONS In boys the rate of new renal damage was low. It was significantly higher in girls, being most frequent in the surveillance (control) group. There was also a strong association between febrile UTI recurrence and development of new renal damage in girls.
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| 2. |
- Halbritter, Aud H., et al.
(författare)
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Plant trait and vegetation data along a 1314 m elevation gradient with fire history in Puna grasslands, Perú
- 2024
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Ingår i: SCIENTIFIC DATA. - 2052-4463. ; 11:1
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Tidskriftsartikel (refereegranskat)abstract
- Alpine grassland vegetation supports globally important biodiversity and ecosystems that are increasingly threatened by climate warming and other environmental changes. Trait-based approaches can support understanding of vegetation responses to global change drivers and consequences for ecosystem functioning. In six sites along a 1314 m elevational gradient in Puna grasslands in the Peruvian Andes, we collected datasets on vascular plant composition, plant functional traits, biomass, ecosystem fluxes, and climate data over three years. The data were collected in the wet and dry season and from plots with different fire histories. We selected traits associated with plant resource use, growth, and life history strategies (leaf area, leaf dry/wet mass, leaf thickness, specific leaf area, leaf dry matter content, leaf C, N, P content, C and N isotopes). The trait dataset contains 3,665 plant records from 145 taxa, 54,036 trait measurements (increasing the trait data coverage of the regional flora by 420%) covering 14 traits and 121 plant taxa (ca. 40% of which have no previous publicly available trait data) across 33 families.
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| 4. |
- Licht, S. de Fine, et al.
(författare)
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Hepatoblastoma in the Nordic countries
- 2012
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 131:4, s. E555-E561
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Tidskriftsartikel (refereegranskat)abstract
- Little is known about the etiology of hepatoblastoma. Because of the young age at diagnosis, several studies have looked at various birth characteristics. The purpose of our study was to investigate the incidence of hepatoblastoma in the Nordic countries and the association between selected birth characteristics and hepatoblastoma. Data from national cancer registries and birth registries in Denmark, Sweden, Norway and Finland 19852006 was used. Overall, 155 children with hepatoblastoma aged 0-14 years were included and individually matched to five controls drawn randomly from national population registries. The incidence rate of hepatoblastoma was 1.7 per million person-years with a predominance of boys (1.5:1). Incidence rate was highest before the age of 1 year (8.3 per million person-years). A higher risk of hepatoblastoma was found in children with birth weight <1,500 g [odds ratio (OR) = 9.5; 95% confidence interval (CI): 2.338.2], born preterm in week 22-32 (OR = 4.5; CI: 1.811.5) and Apgar scores <7 after 1 min (OR = 3.1; CI: 1.37.1) and 5 min (OR = 7.5; CI: 1.832.4). A doubling in risk was found in children who were large for gestational age (OR = 2.3; CI: 1.05.3). No associations were found with birth order, maternal age or maternal smoking. Our study indicates that intrauterine and/or neonatal factors are associated with increased risk of hepatoblastoma. These may include low birth weight and asphyxia leading to neonatal intensive care. Alternatively, the factors may be a consequence of hepatoblastoma developing in utero.
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| 5. |
- Meeths, M, et al.
(författare)
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Familial hemophagocytic lymphohistiocytosis type 3 (FHL3) caused by deep intronic mutation and inversion in UNC13D
- 2011
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Ingår i: Blood. - Washington : American Society of Hematology. - 0006-4971 .- 1528-0020. ; 118:22, s. 5783-5793
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Tidskriftsartikel (refereegranskat)abstract
- Familial hemophagocytic lymphohistiocytosis (FHL) is an autosomal recessive, often-fatal hyperinflammatory disorder. Mutations in PRF1, UNC13D, STX11, and STXBP2 are causative of FHL2, 3, 4, and 5, respectively. In a majority of suspected FHL patients from Northern Europe, sequencing of exons and splice sites of such genes required for lymphocyte cytotoxicity revealed no or only monoallelic UNC13D mutations. Here, in 21 patients, we describe 2 pathogenic, noncoding aberrations of UNC13D. The first is a point mutation localized in an evolutionarily conserved region of intron 1. This mutation selectively impairs UNC13D transcription in lymphocytes, abolishing Munc13-4 expression. The second is a 253-kb inversion straddling UNC13D, affecting the 3'-end of the transcript and likewise abolishing Munc13-4 expression. Carriership of the intron 1 mutation was found in patients across Europe, whereas carriership of the inversion was limited to Northern Europe. Notably, the latter aberration represents the first description of an autosomal recessive human disease caused by an inversion. These findings implicate an intronic sequence in cell-type specific expression of Munc13-4 and signify variations outside exons and splice sites as a common cause of FHL3. Based on these data, we propose a strategy for targeted sequencing of evolutionary conserved noncoding regions for the diagnosis of primary immunodeficiencies.
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