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Sökning: WFRF:(Wickstrom K.)

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1.
  • Johannsson, Gudmundur, 1960, et al. (författare)
  • Growth Hormone Research Society perspective on biomarkers of GH action in children and adults
  • 2018
  • Ingår i: Endocrine Connections. - 2049-3614. ; 7:3, s. R126-R134
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: The Growth Hormone Research Society (GRS) convened a Workshop in 2017 to evaluate clinical endpoints, surrogate endpoints and biomarkers during GH treatment of children and adults and in patients with acromegaly. Participants: GRS invited 34 international experts including clinicians, basic scientists, a regulatory scientist and physicians from the pharmaceutical industry. Evidence: Current literature was reviewed and expert opinion was utilized to establish the state of the art and identify current gaps and unmet needs. Consensus process: Following plenary presentations, breakout groups discussed questions framed by the planning committee. The attendees re-convened after each breakout session to share the group reports. A writing team compiled the breakout session reports into a document that was subsequently discussed and revised by participants. This was edited further and circulated for final review after the meeting. Participants from pharmaceutical companies were not part of the writing process. Conclusions: The clinical endpoint in paediatric GH treatment is adult height with height velocity as a surrogate endpoint. Increased life expectancy is the ideal but unfeasible clinical endpoint of GH treatment in adult GH-deficient patients (GHDA) and in patients with acromegaly. The pragmatic clinical endpoints in GHDA include normalization of body composition and quality of life, whereas symptom relief and reversal of comorbidities are used in acromegaly. Serum IGF-I is widely used as a biomarker, even though it correlates weakly with clinical endpoints in GH treatment, whereas in acromegaly, normalization of IGF-I may be related to improvement in mortality. There is an unmet need for novel biomarkers that capture the pleiotropic actions of GH in relation to GH treatment and in patients with acromegaly.
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  • Zhou, Kai, et al. (författare)
  • Lithium protects hippocampal progenitors, cognitive performance and hypothalamus-pituitary function after irradiation to the juvenile rat brain
  • 2017
  • Ingår i: Oncotarget. - 1949-2553. ; 8:21, s. 34111-34127
  • Tidskriftsartikel (refereegranskat)abstract
    • Cranial radiotherapy in children typically causes delayed and progressive cognitive dysfunction and there is no effective preventive strategy for radiation-induced cognitive impairments. Here we show that lithium treatment reduced irradiation-induced progenitor cell death in the subgranular zone of the hippocampus, and subsequently ameliorated irradiation-reduced neurogenesis and astrogenesis in the juvenile rat brain. Irradiation-induced memory impairment, motor hyperactivity and anxiety-like behaviour were normalized by lithium treatment. Late-onset irradiation-induced hypopituitarism was prevented by lithium treatment. Additionally, lithium appeared relatively toxic to multiple cultured tumour cell lines, and did not improve viability of radiated DAOY cells in vitro. In summary, our findings demonstrate that lithium can be safely administered to prevent both short- and long-term injury to the juvenile brain caused by ionizing radiation.
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4.
  • Dahl, S., et al. (författare)
  • High prevalence of pituitary hormone deficiency in both unilateral and bilateral optic nerve hypoplasia
  • 2019
  • Ingår i: Acta Paediatrica. - : WILEY. - 0803-5253 .- 1651-2227. ; 108:9, s. 1677-1685
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim This study examined the prevalence of neurological impairment and pituitary hormone deficiency (PHD) in patients with unilateral and bilateral optic nerve hypoplasia (ONH). Methods A population-based cross-sectional cohort study of 65 patients (51% female) with ONH was conducted in Stockholm. Of these were 35 bilateral and 30 unilateral. The patients were below 20 years of age, living in Stockholm in December 2009 and found through database searching. The median age at the analysis of the results in January 2018 was 16.1 years (range 8.1-27.5 years). Neurological assessments and blood sampling were conducted, neuroradiology was reviewed and growth curves were analysed. Diagnoses of PHDs were based on clinical and biochemical evidence of hormone deficiency. Results Neurological impairments were identified in 47% of the patients and impairments in gross and fine motor function were more prevalent in bilateral ONH (p < 0.001). In addition, 9% had cerebral palsy and 14% had epilepsy. The prevalence of PHD was 29 and 19% had multiple PHD. Conclusion Children with ONH had a high risk of neurological impairment, especially in bilateral disease. Both unilateral and bilateral ONH signified an increased prevalence of PHD and all these children should be endocrinologically followed up until completed puberty.
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5.
  • Henriksson, Karin, et al. (författare)
  • A pilot study of facial, cranial and brain MRI morphometry in men with schizophrenia: Part 2.
  • 2006
  • Ingår i: Psychiatry Research. - : Elsevier. - 1872-7123 .- 0165-1781. ; 147:2-3, s. 187-195
  • Tidskriftsartikel (refereegranskat)abstract
    • This pilot study applies a new 3D morphometric MR method to test the hypothesis that men with schizophrenia (vs. controls) have deviant facial shapes and landmark relations in cranio/facialibrain (CFB) regions. This constitutes Part 2 of paired articles in this issue of Psychiatry Research: Neuroimaging, in which Part 1 presents the new method in detail. MRI coordinates from CFB landmarks of 23 patients and 15 controls were identified and then aligned with the Procrustes model, leaving shape as the only unitless geometrical information. Men with schizophrenia had significantly longer mid- and lower-facial heights, and greater lower (left) facial depth, with a tendency toward rotation along the facial midline. This supports findings from earlier anthropometric and 3D studies of the "exterior" (face). In contrast, none of the patient-control differences for the new "interior" (cranial-brain) distances reached statistical significance. These results need to be retested on a larger sample of both sexes. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
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6.
  • Wickstrom, K., et al. (författare)
  • Responsiveness of the Endometriosis Health Profile-30 questionnaire in a Swedish sample : an observational study
  • 2017
  • Ingår i: CLINICAL AND EXPERIMENTAL OBSTETRICS & GYNECOLOGY. - : I R O G CANADA, INC. - 0390-6663. ; 44:3, s. 413-418
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: The objective was to evaluate the responsiveness of the Endometriosis Health Profile-30 (EHP-30) questionnaire in a Swedish sample. Materials and Methods: Forty-two patients with endometriosis were included in a prospective observational study. Main outcome measures: The changes on the EHP-30 questionnaire after pertubation treatment were compared with the patients' self-estimated change in pain intensity. The responsiveness to change was evaluated with effect sizes and significance of change (paired t-test). The changes in scores between those who improved / not improved were compared with independent t-test. Results: The changes in the scores were significant for all dimensions on the core questionnaire (p = 0.04-0.0002) for improved patients in contrast to the patients in the stable group where there were no significant changes in any dimension (p = 0.16-0.63). The effect sizes were large (> 0.8) on all core scales except for self-image (0.51) for the improved patients and small on all scales in the non-improved (stable) group (- 0.17-0.35). There were significant differences between the improved and the stable group considering change in most of the core EHP-30 scores. Conclusions: The EHP-30 is responsive to improvement on all core scales and is acceptable, understandable, and applicable in this Swedish sample.
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7.
  • Wickström, Malin, et al. (författare)
  • The novel melphalan prodrug J1 inhibits neuroblastoma growth in vitro and in vivo
  • 2007
  • Ingår i: Molecular Cancer Therapeutics. - 1535-7163 .- 1538-8514. ; 6:9, s. 2409-2417
  • Tidskriftsartikel (refereegranskat)abstract
    • Neuroblastoma is the most common extracranial solid tumor of childhood. The activity of J1 (l-melphalanyl-p-l-fluorophenylalanine ethyl ester), an enzymatically activated melphalan prodrug, was evaluated in neuroblastoma models in vitro and in vivo. Seven neuroblastoma cell lines with various levels of drug resistance were screened for cytotoxicity of J1 alone or in combination with standard cytotoxic drugs, using a fluorometric cytotoxicity assay. J1 displayed high cytotoxic activity in vitro against all neuroblastoma cell lines, with IC50 values in the submicromolar range, significantly more potent than melphalan. The cytotoxicity of J1, but not melphalan, could be significantly inhibited by the aminopeptidase inhibitor bestatin. J1 induced caspase-3 cleavage and apoptotic morphology, had additive effects in combination with doxorubicin, cyclophosphamide, carboplatin, and vincristine, and synergistically killed otherwise drug-resistant cells when combined with etoposide. Athymic rats and mice carrying neuroblastoma xenografts [SH-SY5Y, SK-N-BE(2)] were treated with equimolar doses of melphalan, J1, or no drug, and effects on tumor growth and tissue morphology were analyzed. Tumor growth in vivo was significantly inhibited by J1 compared with untreated controls. Compared with melphalan, J1 more effectively inhibited the growth of mice with SH-SY5Y xenografts, was associated with higher caspase-3 activation, fewer proliferating tumor cells, and significantly decreased mean vascular density. In conclusion, the melphalan prodrug J1 is highly active in models of neuroblastoma in vitro and in vivo, encouraging further clinical development in this patient group.
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8.
  • Boström, Pontus, 1982, et al. (författare)
  • The SNARE protein SNAP23 and the SNARE-interacting protein Munc18c in human skeletal muscle are implicated in insulin resistance/type 2 diabetes.
  • 2010
  • Ingår i: Diabetes. - : American Diabetes Association Inc.. - 1939-327X. ; 59:8, s. 1870-8
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Our previous studies suggest that the SNARE protein synaptosomal-associated protein of 23 kDa (SNAP23) is involved in the link between increased lipid levels and insulin resistance in cardiomyocytes. The objective was to determine whether SNAP23 may also be involved in the known association between lipid accumulation in skeletal muscle and insulin resistance/type 2 diabetes in humans, as well as to identify a potential regulator of SNAP23. RESEARCH DESIGN AND METHODS: We analyzed skeletal muscle biopsies from patients with type 2 diabetes and healthy, insulin-sensitive control subjects for expression (mRNA and protein) and intracellular localization (subcellular fractionation and immunohistochemistry) of SNAP23, and for expression of proteins known to interact with SNARE proteins. Insulin resistance was determined by a euglycemic hyperinsulinemic clamp. Potential mechanisms for regulation of SNAP23 were also investigated in the skeletal muscle cell line L6. RESULTS: We showed increased SNAP23 levels in skeletal muscle from patients with type 2 diabetes compared with that from lean control subjects. Moreover, SNAP23 was redistributed from the plasma membrane to the microsomal/cytosolic compartment in the patients with the type 2 diabetes. Expression of the SNARE-interacting protein Munc18c was higher in skeletal muscle from patients with type 2 diabetes. Studies in L6 cells showed that Munc18c promoted the expression of SNAP23. CONCLUSIONS: We have translated our previous in vitro results into humans by showing that there is a change in the distribution of SNAP23 to the interior of the cell in skeletal muscle from patients with type 2 diabetes. We also showed that Munc18c is a potential regulator of SNAP23.
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9.
  • Dyberg, C., et al. (författare)
  • Rho-associated kinase is a therapeutic target in neuroblastoma
  • 2017
  • Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - 0027-8424 .- 1091-6490. ; 114:32, s. E6603-E6612
  • Tidskriftsartikel (refereegranskat)abstract
    • Neuroblastoma is a peripheral neural system tumor that originates from the neural crest and is the most common and deadly tumor of infancy. Here we show that neuroblastoma harbors frequent mutations of genes controlling the Rac/Rho signaling cascade important for proper migration and differentiation of neural crest cells during neuritogenesis. RhoA is activated in tumors from neuroblastoma patients, and elevated expression of Rho-associated kinase (ROCK) 2 is associated with poor patient survival. Pharmacological or genetic inhibition of ROCK1 and 2, key molecules in Rho signaling, resulted in neuroblastoma cell differentiation and inhibition of neuroblastoma cell growth, migration, and invasion. Molecularly, ROCK inhibition induced glycogen synthase kinase 3 beta-dependent phosphorylation and degradation of MYCN protein. Small-molecule inhibition of ROCK suppressed MYCN-driven neuroblastoma growth in TH-MYCN homozygous transgenic mice and MYCN gene-amplified neuroblastoma xenograft growth in nude mice. Interference with Rho/Rac signaling might offer therapeutic perspectives for high-risk neuroblastoma.
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