| 1. |
- Andersson-Gäre, Boel, et al.
(författare)
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The Swedish version of the Childhood Health Assessment Questionnaire (CHAQ) and the Child Health Questionnaire (CHQ)
- 2001
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Ingår i: Clinical and Experimental Rheumatology. - 0392-856X .- 1593-098X. ; 19:4, Suppl 23, s. S146-50
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Tidskriftsartikel (refereegranskat)abstract
- We report herein the results of the cross-cultural adaptation and validation into the Swedish language of the parent's version of two health related quality of life instruments. The Childhood Health Assessment Questionnaire (CHAQ) is a disease specific health instrument that measures functional ability in daily living activities in children with juvenile idiopathic arthritis (JIA). The Child Health Questionnaire (CHQ) is a generic health instrument designed to capture the physical and psychosocial well-being of children independently from the underlying disease. The Swedish CHAQ CHQ were already published and therefore were revalidated in this study. A total of 129 subjects were enrolled: 69 patients with JIA (13% systemic onset, 39% polyarticular onset, 25% extended oligoarticular subtype, and 23% persistent oligoarticular subtype) and 60 healthy children. The CHAQ clinically discriminated between healthy subjects and JIA patients, with the systemic, polyarticular and extended oligoarticular subtypes having a higher degree of disability, pain, and a lower overall well-being when compared to their healthy peers. Also the CHQ clinically discriminated between healthy subjects and JIA patients, with the systemic onset, polyarticular onset and extended oligoarticular subtypes having a lower physical and psychosocial well-being when compared to their healthy peers. In conclusion the Swedish version of the CHAQ-CHQ are reliable, and valid tools for the functional, physical and psychosocial assessment of children with JIA.
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| 2. |
- Björk, Mikael, et al.
(författare)
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One-dimensional heterostructures in semiconductor nanowhiskers
- 2002
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Ingår i: Applied Physics Letters. - : AIP Publishing. - 0003-6951 .- 1077-3118. ; 80:6, s. 1058-1060
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Tidskriftsartikel (refereegranskat)abstract
- We report on the growth of designed heterostructures placed within semiconductor nanowhiskers, exemplified by the InAs/InP material system. Based on transmission electron microscopy, we deduce the interfaces between InAs and InP to be atomically sharp. Electrical measurements of thermionic emission across an 80-nm-wide InP heterobarrier, positioned inside InAs whiskers 40 nm in diameter, yield a barrier height of 0.6 eV. On the basis of these results, we propose new branches of physics phenomena as well as new families of device structures that will now be possible to realize and explore.
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| 3. |
- Björk, Mikael, et al.
(författare)
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One-dimensional steeplechase for electrons realized
- 2002
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Ingår i: Nano Letters. - : American Chemical Society (ACS). - 1530-6992 .- 1530-6984. ; 2:2, s. 87-89
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Tidskriftsartikel (refereegranskat)abstract
- We report growth of one-dimensional semiconductor nanocrystals, nanowhiskers, in which segments of the whisker with different composition are formed, illustrated by InAs whiskers containing segments of InP. Our conditions for growth allow the formation of abrupt interfaces and heterostructure barriers of thickness from a few monolayers to 100s of nanometers, thus creating a one-dimensional landscape along which the electrons move. The crystalline perfection, the quality of the interfaces, and the variation in the lattice constant are demonstrated by high-resolution transmission electron microscopy, and the conduction band off-set of 0.6 eV is deduced from the current due to thermal excitation of electrons over an InP barrier.
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| 4. |
- Björnsson, Jon Mar, et al.
(författare)
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Reduced proliferative capacity of hematopoietic stem cells deficient in hoxb3 and hoxb4
- 2003
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Ingår i: Blood. - 0006-4971 .- 1528-0020. ; 23:11, s. 3872-3883
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Tidskriftsartikel (refereegranskat)abstract
- Several homeobox transcription factors, such as HOXB3 and HOXB4, have been implicated in regulation of hematopoiesis. In support of this, studies show that overexpression of HOXB4 strongly enhances hematopoietic stem cell regeneration. Here we find that mice deficient in both Hoxb3 and Hoxb4 have defects in endogenous hematopoiesis with reduced cellularity in hematopoietic organs and diminished number of hematopoietic progenitors without perturbing lineage commitment. Analysis of embryonic day 14.5 fetal livers revealed a significant reduction in the hematopoietic stem cell pool, suggesting that the reduction in cellularity observed postnatally is due to insufficient expansion during fetal development. Primitive Lin(-) Scal(+) c-kit(+) hematopoietic progenitors lacking Hoxb3 and Hoxb4 displayed impaired proliferative capacity in vitro. Similarly, in vivo repopulating studies of Hoxb3/Hoxb4-deficient hematopoietic cells resulted in lower repopulating capability compared to normal littermates. Since no defects in homing were observed, these results suggest a slower regeneration of mutant HSC. Furthermore, treatment with cytostatic drugs demonstrated slower cell cycle kinetics of hematopoietic stem cells deficient in Hoxb3 and Hoxb4, resulting in increased tolerance to antimitotic drugs. Collectively, these data suggest a direct physiological role of Hoxb4 and Hoxb3 in regulating stem cell regeneration and that these genes are required for maximal proliferative response.
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| 5. |
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| 6. |
- Brun, Ann, et al.
(författare)
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Hoxb4-deficient mice undergo normal hematopoietic development but exhibit a mild proliferation defect in hematopoietic stem cells
- 2004
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Ingår i: Blood. - : American Society of Hematology. - 1528-0020 .- 0006-4971. ; 103:11, s. 4126-4133
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Tidskriftsartikel (refereegranskat)abstract
- Enforced expression of Hoxb4 dramatically increases the regeneration of murine hematopoietic stem cells (HSCs) after transplantation and enhances the repopulation ability of human severe combined immunodeficiency (SCID) repopulating cells. Therefore, we asked what physiologic role Hoxb4 has in hematopoiesis. A novel mouse model lacking the entire Hoxb4 gene exhibits significantly reduced cellularity in spleen and bone marrow (BM) and a subtle reduction in red blood cell counts and hemoglobin values. A mild reduction was observed in the numbers of primitive progenitors and stem cells in adult BM and fetal liver, whereas lineage distribution was normal. Although the cell cycle kinetics of primitive progenitors was normal during endogenous hematopoiesis, defects in proliferative responses of BM Lin(-) Sca1(+) c-kit(+) stem and progenitor cells were observed in culture and in vivo after the transplantation of BM and fetal liver HSCs. Quantitative analysis of mRNA from fetal liver revealed that a deficiency of Hoxb4 alone changed the expression levels of several other Hox genes and of genes involved in cell cycle regulation. In summary, the deficiency of Hoxb4 leads to hypocellularity in hematopoietic organs and impaired proliferative capacity. However, Hoxb4 is not required for the generation of HSCs or the maintenance of steady state hematopoiesis.
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| 7. |
- Fan, Xiaolong, et al.
(författare)
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Transient disruption of autocrine TGF-beta signaling leads to enhanced survival and proliferation potential in single primitive human hemopoietic progenitor cells.
- 2002
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Ingår i: Journal of Immunology. - 1550-6606. ; 168:2, s. 755-762
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Tidskriftsartikel (refereegranskat)abstract
- Hemopoietic stem cells (HSCs) are maintained at relative quiescence by the balance between the positive and negative regulatory factors that stimulate or inhibit their proliferation. Blocking the action of negative regulatory factors may provide a new approach for inducing HSCs into proliferation. A variety of studies have suggested that TGF-beta negatively regulates cell cycle progression of HSCs. In this study, a dominant negatively acting mutant of TGF-beta type II receptor (TbetaRIIDN) was transiently expressed in HSCs by using adenoviral vector-mediated gene delivery, such that the effects of disrupting the autocrine TGF-beta signaling in HSCs can be directly examined at a single cell level. Adenoviral vectors allowing the expression of TbetaRIIDN and green fluorescence protein in the same CD34(+)CD38(-)Lin(-) cells were constructed. Overexpression of TbetaRIIDN specifically disrupted TGF-beta-mediated signaling. Autocrine TGF-beta signaling in CD34(+)CD38(-)Lin(-) cells was studied in single cell assays under serum-free conditions. Transient blockage of autocrine TGF-beta signaling in CD34(+)CD38(-)Lin(-) cells enhanced their survival. Furthermore, the overall proliferation potential and proliferation kinetics in these cells were significantly enhanced compared with the CD34(+)CD38(-)Lin(-) cells expressing green fluorescence protein alone. Therefore, we have successfully blocked the autocrine TGF-beta-negative regulatory loop of primitive hemopoietic progenitor cells.
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| 8. |
- Holst-Ekström, Måns, et al.
(författare)
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Illusion
- 2003
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Ingår i: Floden och tornet : En vägvisare till Tungelsta trädgårdspark - En vägvisare till Tungelsta trädgårdspark. - 9197336106 ; , s. 39-45
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Bokkapitel (populärvet., debatt m.m.)abstract
- Essän handlar om trädgårdsstaden Tungelsta, idén om eremitens hydda, trädgården och platsen.
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| 9. |
- Jönsson, Lars-Eric, et al.
(författare)
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Form och norm : Om arkitekturen i den psykiatriska vården
- 2001
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Ingår i: Konst på SÖS : Essäer om konst på sjukhus och annan institutionsmiljö - Essäer om konst på sjukhus och annan institutionsmiljö. - 9163118874 ; , s. 95-100
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Bokkapitel (refereegranskat)
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| 10. |
- Lomoth, R., et al.
(författare)
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Mixed-valence properties of an acetate-bridged dinuclear ruthenium (II,III) complex
- 2003
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Ingår i: Journal of Physical Chemistry A. - : American Chemical Society (ACS). - 1089-5639 .- 1520-5215. ; 107:22, s. 4373-4380
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Tidskriftsartikel (refereegranskat)abstract
- The mixed-valence dinuclear ruthenium complex [Ru-2(bpmp)(mu-OAc)(2)](2+) (where blimp is the phenolate anion of 2,6-bis[bis(2-pyridylmethyl) aminomethyl]-4-methylphenol, H-bpmp) has been studied by UV-Vis-NIR, IR, and EPR spectroscopic and electrochemical techniques. The Ru-2(II,III) complex undergoes reversible one-electron reduction (E-1/2 = -0.61 V vs Fc(+/0)) and oxidation (E-1/2 = 0.09 V vs Fc(+/0)), resulting in the Ru-2(II,III) and Ru-2(III,III) complexes, respectively. A comproportionation constant of K-c = 1.10 x 10(12) (DeltaG(c)degrees = -68 kJ mol(-1)) indicates considerable stability of the mixed-valence state. The paramagnetic complex displays a rhombic EPR spectrum (g(1) = 2.492; g(2) = 2.242; g(3) = 1.855) arising from a ground state in a S = 1/2 low spin system in a low symmetry environment. Three intense, distinguishable intervalence bands are observed in the NIR to mid-IR spectrum of [Ru-2(bpmp)(mu-OAc)(2)](2+) at 3765 cm(-1) (epsilon = 1840 M(-1)cm(-1)), 5615 cm(-1) (epsilon = 10590 M-1cm-1), and 7735 cm-1 (E = 3410 M-1cm-1). All intervalence bands are symmetric but more narrow than predicted for the classical limit and independent of solvent polarity. The results of the spectroscopic and electrochemical characterization indicate that [RU2(bpmp)(mu-OAc)(2)](2+) is either electronically delocalized (class III, H-ab = 1880 cm(-1)) or at the borderline between localization and delocalization (class II-III, H-ab greater than or equal to 590 cm(-1)) with rapid electron transfer (k(ET) > 4 x 10(12) s(-1)) decoupled from solvent reorientation but with a residual activation barrier (E-a less than or equal to 440 cm(-1)) from inner reorganization.
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