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  • Welin, Karl-Olof, et al. (författare)
  • Epilepsy in tuberous sclerosis patients in Sweden – Healthcare utilization, treatment, morbidity, and mortality using national register data
  • 2017
  • Ingår i: Seizure. - Elsevier. - 1059-1311. ; 53, s. 4-9
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose This study is designed to estimate the prevalence of epilepsy associated with TSC in Sweden and to describe treatment, morbidity, and mortality of TSC patients with epilepsy. Methods Register data for 2004–2014 was obtained from the National Board of Health and Welfare in Sweden. Patients with TSC were identified using ICD-10 codes. Epilepsy was identified using ICD-10 codes, interventions aimed to treat epilepsy, or prescriptions for antiepileptic drugs. Results The prevalence of TSC was 5.38 per 100 000 individuals. We identified 551 unique patients with TSC, of which 386 (70.1%) had epilepsy. The mean study period was 8.82 years. Antiepileptic drugs were dispensed to 97.9% of patients with epilepsy. The most prescribed antiepileptic drug was sodium valproate. Ketogenic diet was used in 6 (1.6%) patients, vagus nerve stimulation in 23 (6.0%) patients, and epilepsy surgery was performed in 25 (6.5%) patients. The mean number of outpatient visits per year was 4.70 (SD 4.17) and the mean number of inpatient days per year was 3.25 (SD 5.61). The mean number of outpatient visits per year with an ICD-10 code for epilepsy was 1.65 (SD 1.95) and the corresponding number of inpatient days was 2.06 (SD 4.50). A total of 30 patients with TSC and epilepsy died during the study period. Conclusions The prevalence of epilepsy in this study was in the lower range of previously reported numbers, suggesting that epilepsy may be overestimated in non-population based studies. A substantial part of the healthcare utilization was directly related to epilepsy.
  • Aidoukovitch, Alexandra, et al. (författare)
  • Antimicrobial peptide LL-37 and its pro-form, hCAP18, in desquamated epithelial cells of human whole saliva
  • ????
  • Ingår i: European Journal of Oral Sciences. - Wiley-Blackwell. - 0909-8836.
  • Tidskriftsartikel (refereegranskat)abstract
    • The antimicrobial peptide LL-37 is active against oral bacteria and has been demonstrated to be present in human saliva, but its distribution in different fractions of saliva is not known. LL-37 is formed from its intracellular pro-form, hCAP18, in an extracellular enzymatic reaction catalyzed by proteinase 3 and kallikrein 5. Here, we prepared cell-containing and cell-free fractions of unstimulated human whole saliva by centrifugation after depolymerization of mucins with dithiothreitol, and measured the levels of hCAP18/LL-37 in these fractions using ELISA. Cellular expression of hCAP18/LL-37 was determined by western blotting and immunocytochemistry. The ELISA analyses demonstrated that both cells and cell-free saliva contained hCAP18/LL-37. Western blot analysis of cell-pellet homogenates showed a strong band corresponding to hCAP18 at the correct molecular weight and a weak band corresponding to LL-37. Phase-contrast and light microscopy revealed that the cells consisted of desquamated epithelial cells. These cells expressed cytoplasmic immunoreactivity for hCAP18/LL-37. The peripheral part of the cytoplasm, corresponding to the plasma membrane, was particularly rich in hCAP18/LL-37 immunoreactivity. No immunoreactivity was observed after omission of the primary antibody. We conclude that desquamated epithelial cells of human whole saliva contain antimicrobial hCAP18/LL-37, suggesting that these cells may take part in the innate immune system by harboring and releasing these peptides.
  • Aidoukovitch, Alexandra, et al. (författare)
  • Strontium chloride promotes cell proliferation in a human osteoblast cell line
  • 2014
  • Rapport (övrigt vetenskapligt)abstract
    • <p>Strontium ranelate (SrRan) is the active component of drugs currently used for reducing the risk of fractures in patients suffering from osteoporosis. Despite extensive use, the underlying mechanisms of action of Sr2+ are not fully understood. In the present study, we assess the impact of SrCl2 on human osteoblast activity and proliferation. Cultures of the human osteoblast-like cell line MG63 were treated for 72 h in presence of 0.1 mM, 1 mM, 5 mM and 10 mM SrCl2 or vehicle, used in control groups. Cells were counted manually using a Bürker chamber. Total protein content was determined by colorimetric analysis performed by a microplate reader using Bio-Rad protein assay. Alkaline phosphatase (ALP) activity was determined enzymatically and normalized to total protein content in each sample. Cell viability was assessed using the MTT assay. Treatment with 5 mM SrCl2 for 72 h enhanced total MG63 cell protein content by 37% compared to controls (p<0.01). A lower concentration (0.1 mM) of SrCl2 had no effect on total protein. Incubation with 5 mM SrCl2 for 72 h increased MG63 cell number by 38% compared to controls (p<0.001). The SrCl2-induced increase in cell number was associated with enhanced (+14% compared to controls, p<0.05) cell viability. Treatment with a higher concentration (10 mM) of SrCl2 enhanced cell number similar to 5 mM SrCl2 (+54% compared to controls, p<0.05). Treatment with 0.1 or 5 mM SrCl2 for 72 h had no effect (p>0.05) on MG63 cell ALP activity, while 1 mM SrCl2 reduced ALP activity as well as total protein content by about 25% compared to controls (p<0.05). The current results demonstrate that treatment with SrCl2 for 72 h, at concentrations higher than 1 mM promotes cell proliferation in human osteoblast-like cells, suggesting that Sr2+ may enhance bone formation through this mechanism.</p>
  • Aidoukovitch, Alexandra, et al. (författare)
  • The host defense peptide LL-37 is internalized by human periodontal ligament cells and prevents LPS-induced MCP-1 production
  • 2019
  • Ingår i: Journal of Periodontal Research. - Wiley-Blackwell. - 0022-3484. ; 54:6, s. 662-670
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: The human host defense peptide LL-37 both shows antimicrobial effects and modulates host cell properties. Here, we assess the effects of synthesized LL-37 on lipopolysaccharide (LPS)-induced inflammation in human periodontal ligament (PDL) cells and investigates underlying mechanisms. Background: LL-37 has been detected in the periodontal tissues, but its functional importance for PDL cell innate immune responses is not known. Methods: Human PDL cells were obtained from premolars extracted on orthodontic indications. Cellular pro-inflammatory monocyte chemoattractant protein-1 (MCP-1) mRNA expression was determined using quantitative real-time RT-PCR. MCP-1 protein production was assessed by western blot and ELISA. Internalization of LL-37 by PDL cells was visualized by immunocytochemistry. Nuclear factor kappa-light-chain-enhancer of activated B-cell (NF-κB) activity was assessed by western blot of phosphorylated p65, phosphorylated p105, and IκBα proteins. Binding of LL-37 to PDL cell DNA was determined by isolation and purification of DNA and dot blot for LL-37 immunoreactivity. Results: Treatment with LL-37 (1 µmol/L) for 24 hours prevented LPS-induced stimulation of MCP-1 expression analyzed both on transcript and on protein levels. Stimulation with LL-37 (1 µmol/L) for 24 hours had no effect on toll-like receptor (TLR)2 and TLR4 transcript expression, suggesting that LL-37 acts downstream of the TLRs. Preincubation with LL-37 for 60 minutes followed by stimulation with LPS for 24 hours in the absence of LL-37 completely prevented LPS-evoked MCP-1 transcript expression, implying that LL-37 acts intracellularly and not via binding and neutralization of LPS. In PDL cells stimulated with LL-37 for 60 minutes, the peptide was internalized as demonstrated by immunocytochemistry, suggesting an intracellular mechanism of action. LL-37 immunoreactivity was observed both in the cytosol and in the nucleus. Downregulation of LPS-induced MCP-1 by LL-37 was not mediated by reduction in NF-κB activity as shown by unaltered expression of phosphorylated p65, phosphorylated p105, and IκBα NF-κB proteins in the presence of LL-37. Immunoreactivity for LL-37 was observed in PDL cell DNA treated with but not without 0.1 and 1 µmol/L LL-37 for 60 minutes in vitro. Conclusion: LL-37 abolishes LPS-induced MCP-1 production in human PDL cells through an intracellular, NF-κB-independent mechanism which probably involves direct interaction between LL-37 and DNA.
  • Albin, Björn, et al. (författare)
  • Situation for carers of the elderly in Sweden
  • 2008
  • Ingår i: Studies of Community Welfare: Chiiki Fukushi Kenkyu. - Nihon Seimei Saiseikai Osaka. ; :38, s. 72-83
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>In most societies informal care of the elderly (often given by a relative) plays an important role, this article describes the situation and support for carers that exist in Sweden. The description is partly based on the results from the evaluation of a project (“Anhörig 300”) aimed to develop support for carers in the County of Kronoberg as well as from information and documents. Four different typical situations for carers are identified and is an indication of how different situations for carers can be. In the future the support for carers must be paid attention to and further developed. The National Development Plan for the Nursing and Care for elderly in Sweden suggest increased support for carers as a supplement to the public sector elderly care. It is important to involve voluntary organizations to break isolation and loneliness among carers.</p>
  • Allwood, Jens, 1947-, et al. (författare)
  • Språk och tanke
  • 1977
  • Ingår i: Språk och socialisation symposiet, Graninge.
  • Tidskriftsartikel (refereegranskat)
  • Anders, Emma, et al. (författare)
  • Globular C1q receptor (p33) binds and stabilizes pro-inflammatory MCP-1 : a novel mechanism for regulation of MCP-1 production and function
  • 2018
  • Ingår i: Biochemical Journal. - Portland Press Limited. - 0264-6021. ; 475:4, s. 775-786
  • Tidskriftsartikel (refereegranskat)abstract
    • The protein gC1qR (globular C1q receptor), also named p33, was originally identified as a binding partner of the globular heads of C1q in the complement system. gC1qR/p33 is abundantly expressed in many cell types, but the functional importance of this protein is not completely understood. Here, we investigate the impact of gC1qR/p33 on the production and function of the pathophysiologically important chemokine monocyte chemoattractant protein-1 (MCP-1) and the underlying molecular mechanisms. Knockdown of gC1qR/p33 negatively regulated the production of MCP-1, but had no effect on the expression of transcript for MCP-1 in human periodontal ligament cells, suggesting a translational/post-translational mechanism of action. Laser scanning confocal microscopy showed considerable cytosolic co-localization of gC1qR/p33 and MCP-1, and co-immunoprecipitation disclosed direct physical interaction between gC1qR/p33 and MCP-1. Surface plasmon resonance analysis revealed a high-affinity binding (KD = 10.9 nM) between gC1qR/p33 and MCP-1. Using a transwell migration assay, we found that recombinant gC1qR/p33 enhances MCP-1-induced migration of human THP-1 monocytes, pointing to a functional importance of the interaction between gC1qR/p33 and MCP-1. An in vitro assay revealed a rapid turnover of the MCP-1 protein and that gC1qR/ p33 stabilizes MCP-1, hence preventing its degradation. We propose that endogenous gC1qR/p33 physically interacts with MCP-1 causing stabilization of the MCP-1 protein and stimulation of its activity in human periodontal ligament cells, suggesting a novel gC1qR/p33-mediated pro-inflammatory mechanism of action.
  • Anders, Emma, et al. (författare)
  • LL-37-induced human osteoblast cytotoxicity and permeability occurs independently of cellular LL-37 uptake through clathrin-mediated endocytosis
  • 2018
  • Ingår i: Biochemical and Biophysical Research Communications. - Elsevier. - 0006-291X. ; 501:1, s. 280-285
  • Tidskriftsartikel (refereegranskat)abstract
    • The host defense peptide LL-37 is cytotoxic for bacteria but it has also been reported to reduce host cell viability through an intracellular mechanism. LL-37-evoked cytotoxicity may be involved in the loss of bone tissue in periodontitis which is an inflammatory disease characterized by high concentrations of LL-37 observed locally in the periodontal tissue at the inflammation process. Here, we showed that LL-37 reduced human osteoblast-like MG63 cell viability assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and increased plasma membrane permeability determined by measuring intracellular Ca2+ levels and lactate dehydrogenase (LDH) release. Treatment with chlorpromazine, a well-recognized inhibitor of clathrin-mediated endocytosis, reduced cellular uptake of synthesized LL-37 b y about 30% assessed by Western blotting and ELISA, while filipin, an inhibitor of caveolin-mediated endocytosis, had no effect. The chlorpromazine-induced attenuation of LL-37 uptake was not associated with modulation of LL-37-induced cytotoxicity and LL-37-evoked plasma membrane permeability. Clathrin heavy chain 2 is a major protein of the polyhedral coat of coated pits and vesicles encoded by clathrin heavy chain like 1 gene. Down-regulation of clathrin heavy chain like 1 gene activity by siRNA reduced uptake of LL-37 but did not affect LL-37-induced cytotoxicity and permeability. Thus, we show, using both a pharmacological approach and knockdown of clathrin heavy chain like 1 expression, that LL-37-induced MG63 cell cytotoxicity and permeability occurs independently of LL-37 uptake via clathrin-mediated endocytosis.
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