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Now showing items 33 - 48 of 48

  • Transected myofibres may remain permanently divided in two parts

    Vaittinen, S   Hurme, T   Rantanen, J   Kalimo, H  

    During regeneration of transected myofibres a scar is formed between their stumps. Myofibres restore their tendon-muscle-tendon continuity and contractile function by attaching to the scar with new myotendinous junctions. The scar contracts with time, and thereby the stumps are pulled close to each other. During early regeneration, myoblasts and myotubes can fuse with the surviving parts of the transected myofibres. However, it is not known whether it is possible that the opposite stumps could eventually fuse to reunite the divided parts of the transected fibres. In this study, we show in rat that even after 12 months the stumps remain attached to the separating scar by myotendinous junctions without showing definite fusion of the stumps. We conclude that transected myofibres probably remain permanently divided in two consecutive tendon-muscle-tendon units. (C) 2002 Elsevier Science B.V. All rights reserved.
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  • X-linked myopathy with excessive autophagy: a new hereditary muscle disease.

    Kalimo, H   Savontaus, M L   Lang, H   Paljarvi, L   Sonninen, V   Dean, P B   Katevuo, K   Salminen, A  

    We report on 3 brothers with a myopathy that also affected their maternal grandfather and great-uncle. Characteristic features are onset in early childhood, very slow progression, normal life expectancy, weakness of proximal limb muscles, especially in the legs, elevation of serum creatine kinase, and no cardiac or intellectual involvement. In biopsy material muscle fibers are almost never necrotic but show excessive autophagic activity and exocytosis of the phagocytosed material. We suggest that this family has an undescribed type of congenital myopathy, for which we propose the name X-linked myopathy with excessive autophagy.
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  • Evaluation of brain tumor metabolism with [C-11] choline PET and H-1-MRS

    Utriainen, M   Komu, M   Vuorinen, V   Lehikoinen, P   Sonninen, P   Kurki, T   Utriainen, T   Roivainen, A   Kalimo, H   Minn, H  

    Background: The signal of choline containing compounds (Cho) in proton magnetic resonance spectroscopy (H-1-MRS) is elevated in brain tumors. [C-11] choline uptake as assessed using positron emission tomography (PET) has also been suggested to be higher in brain tumors than in the normal brain. We examined whether quantitative analysis of choline accumulation and content using these two novel techniques would be helpful in non-invasive, preoperative evaluation of suspected brain tumors and tumor malignancy grade. Methods: 12 patients with suspected brain tumor were studied using [C-11] choline PET, gadolinium enhanced 3-D magnetic resonance imaging and H-1-MRS prior to diagnostic biopsy or resection. Eleven normal subjects served as control subjects for H-1-MRS. Results: The concentrations of Cho and myoinositol (mI) were higher and the concentration of N-acetyl signal/group (NA) lower in brain tumors than in the corresponding regions of the normal brain. There were no significant differences in metabolite concentrations between low- and high-grade gliomas. In non-tumorous lesions Cho concentrations were lower and NA concentrations higher than in any of the gliomas. Enormously increased lipid peak differentiated lymphomas from all other lesions. The uptake of [C-11] choline at PET did not differ between low- and high-grade gliomas. The association between Cho concentration determined in H-1-MRS and [C-11] choline uptake measured with PET was not significant. Conclusion: Both H-1-MRS and [C-11] choline PET can be used to estimate proliferative activity of human brain tumors. These methods seem to be helpful in differential diagnosis between lymphomas, non-tumorous lesions and gliomas but are not superior to histopathological methods in estimation of tumor malignancy grade.
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  • METABOLIC, CIRCULATORY, AND STRUCTURAL ALTERATIONS IN THE RAT-BRAIN INDUCED BY SUSTAINED PENTYLENETETRAZOLE SEIZURES

    INGVAR, M   SODERFELDT, B   FOLBERGROVA, J   KALIMO, H   OLSSON, Y   SIESJO, BK  

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  • PIGMENTED PRIMITIVE NEUROECTODERMAL TUMOR WITH MULTIPOTENTIAL DIFFERENTIATION IN CEREBELLUM (PIGMENTED MEDULLOMYOBLASTOMA) - A CASE WITH LIGHT-MICROSCOPIC AND ELECTRON-MICROSCOPIC, AND IMMUNOHISTOCHEMICAL ANALYSIS

    KALIMO, H   PALJARVI, L   EKFORS, T   PELLINIEMI, LJ  

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  • Mast cells and IgE-containing cells in gastric mucosa of Hellicobacter pylori infected and non-infected patients with chronic urticaria

    Liutu, M   Kalimo, K   Kalimo, H   Uksila, J   Leino, R  

    Background Several studies have indicated that antibiotic therapy aimed at eradication of Helicobacter pylori has effects on symptoms of chronic urticaria (CU) patients. However, the possible connections and pathomechanism by which H. pylori might be linked to CU have remained largely unknown. The IgE-mediated pathway might be a possible link between H. pylori infection and CU. We therefore clarified the role of H. pylori as an inducer of IgE response. Materials and methods Gastroscopy was performed and mucosal biopsy specimens were taken to evaluate the histology, as well as the presence of H. pylori bacteria, mast cells and IgE-containing cells in the antral mucosa, in 21 CU patients. Controls (n = 48) included 19 patients with lichen planus, nine patients with atopic dermatitis and 20 patients with no skin or allergic disease. Results The mean densities of IgE-containing cells were significantly higher in H. pylori-infected patients and in patients with skin disease compared to non-H. pylori-infected patients with no skin or allergic disease. No significant difference was found in the number of IgE-containing cells between H. pylori-infected and non-infected patients with CU. There was no significant difference in the mean densities of mast cells in the different patient groups. Conclusions Our findings suggest that H. pylori gastritis leads to increased lgE production. However, we could not show a significant difference in IgE staining between H. pylori-infected and non-infected patients with CU.
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  • Neuropsychological functions in variant Alzheimer's disease with spastic paraparesis

    Verkkoniemi, A   Ylikoski, R   Rinne, JO   Somer, M   Hietaharju, A   Erkinjuntti, T   Viitanen, M   Kalimo, H   Haltia, M  

    Few data exist on the effects of specific Alzheimer's disease (AD)-related mutations on cognitive function. We present neuropsychological test results in eight members of a large kindred with variant Alzheimer's disease (VarAD) due to a deletion of the presenilin 1 (PS-1) gene, encompassing exon 9. The disease was neuropathologically characterized by the presence of large, unusual, "cotton wool" plaques (CWP). Four surviving patients were prospectively tested, and retrospective neuropsychological data were collected from additional four deceased patients. The neuropsychological evaluation was based on tests of verbal and visual memory, abstract thinking, and visuoconstructive and spatial functions. In addition, psychiatric symptoms were evaluated. In four patients, brain glucose metabolism was examined by positron emission tomography (PET). PET showed temporoparietal hypometabolism typical of AD. In addition, variable patterns of hypometabolism (hemispherical asymmetry and occipital accentuation) were related to individual deficits of cognitive performance. However, all these early-onset patients (age range 43-63 years) with a deletion mutation of PS-1 gene showed prominent memory impairment and deficits in visuoconstructive and intellectual functions. (C) 2003 Elsevier B.V. All rights reserved.
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  • Skeletal muscle HSP expression in response to immobilization and remobilization.

    Venojarvi, M   Kvist, M   Jozsa, L   Kalimo, H   Hanninen, O   Atalay, M  

    Heat shock proteins play an important regulatory role in the cellular defence. Oxidative stress is one of the factors inducing heat shock protein expression. This study tested the effects of 4 weeks of immobilization and subsequent remobilization on heat shock protein expression and oxidative stress in the lateral gastrocnemius and plantaris muscles of the rat. Active mobilization or free mobilization protocols were used for remobilization. In active mobilization, strenuous uphill treadmill running, twice a day, was started immediately after the immobilization and lasted for six days. Rats in the free mobilization group moved freely in their cages immediately after the immobilization. Expression of heat shock proteins was upregulated during the recovery from immobilization, especially in the lateral gastrocnemius muscle in the active mobilization group. However, markers of oxidative stress, such as protein carbonyls and 4-hydroxynonenal protein adducts, or activities of the antioxidant enzymes glutathione peroxidase and glutathione reductase, did not change after the immobilization and subsequent recovery. In summary, following immobilization, both intensive and spontaneous exercise upregulated the heat shock protein expressions in the lateral gastrocnemius muscle and partly in the plantaris muscle, which may contribute to the recovery from immobilization atrophy.
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  • Specific and innervation-regulated expression of the intermediate filament protein nestin at neuromuscular and myotendinous junctions in skeletal muscle.

    Vaittinen, S   Lukka, R   Sahlgren, C   Rantanen, J   Hurme, T   Lendahl, U   Eriksson, J E   Kalimo, H  

    The intermediate filament proteins nestin, vimentin, and desmin show a specific temporal expression pattern during the development of myofibers from myogenic precursor cells. Nestin and vimentin are actively expressed during early developmental stages to be later down-regulated, vimentin completely and nestin to minimal levels, whereas desmin expression begins later and is maintained in mature myofibers, in which desmin participates in maintaining structural integrity. In this study we have analyzed the expression levels and distribution pattern of nestin in intact and denervated muscle in rat and in human. Nestin immunoreactivity was specifically and focally localized in the sarcoplasm underneath neuromuscular junctions (NMJs) and in the vicinity of the myotendinous junctions (MTJs), ie, in regions associated with acetylcholine receptors (AChRs). This association prompted us to analyze nestin in neurogenically and myogenically denervated muscle. Immunoblot analysis disclosed a marked overall increase of accumulated nestin protein. Similar to the extrajunctional redistribution of AChRs in denervated myofibers, nestin immunoreactivity extended widely beyond the NMJ region. Re-innervation caused complete reversion of these changes. Our study demonstrates that the expression levels and distribution pattern of nestin are regulated by innervation, ie, signal transduction into myofibers.
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  • Electromyography and morphology during regeneration of muscle injury in rats.

    Hurme, T   Lehto, M   Falck, B   Tainio, H   Kalimo, H  

    Healing of the partially ruptured rat gastrocnemius muscle was studied correlating electromyographical findings with morphological changes. Fibrillation potentials and positive sharp waves were seen both proximal and distal to the injury 7 days after the injury and disappeared in the proximal part by day 14 and in the distal part by day 21. Late components of motor action potential were observed from day 14 onwards. Denervation was mainly myogenic, i.e. caused either by rupture of myofibres, whence the abjunctional stump lost its contact with the neuromuscular junction on the adjunctional stump, or by necrosis of the segment of the ruptured myofibre lying underneath the neuromuscular junction. Lesser extent of denervation was neurogenic, i.e. caused by damage to intramuscular nerve fibres. The reinnervation occurs either by regeneration of the necrotized myofibres, by regeneration of the severed nerves, or by collateral innervation of new neuromuscular junctions in the abjunctional stumps. The present study indicates that electromyography may be useful in the diagnosis and follow-up of skeletal muscle injuries.
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  • Variant Alzheimer's disease with spastic paraparesis and cotton wool plaques is caused by PS-1 mutations that lead to exceptionally high amyloid-beta concentrations

    Houlden, H   Baker, M   McGowan, E   Lewis, P   Hutton, M   Crook, R   Wood, NW   Kumar-Singh, S   Geddes, J   Swash, M   Scaravilli, F   Holton, JL   Lashley, T   Tomita, T   Hashimoto, T   Verkkoniemi, A   Kalimo, H   Somer, M   Paetau, A   Martin, JJ   Van Broeckhoven, C   Golde, T   Hardy, J   Haltia, M   Revesz, T  

    We describe 3 new families affected by Alzheimer's disease with spastic paraparesis. In affected individuals, including the earliest known patient with this clinical syndrome, neuropathological examination revealed large "cotton wool" plaques similar to those we have previously described in a Finnish family. In the families in which DNA was available, presenilin-1 mutations were observed. Transfection of cells with these mutant genes caused exceptionally large increases in secreted A beta 42 levels. Furthermore, brain tissue from individuals with this syndrome had very high amyloid-beta concentrations. These findings define the molecular pathogenesis of an important subgroup of Alzheimer's disease and have implications for the pathogenesis of the disease in general.
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  • Benzodiazepine sensitivity in Leber's hereditary optic neuroretinopathy.

    Nikoskelainen, E   Asola, M   Kalimo, H   Savontaus, M L   Majander, A  

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  • Cell cycle regulators (p21, p53, pRb) in oligodendrocytic tumors: A study by novel tumor microarray technique

    Miettinen, HE   Paunu, N   Rantala, I   Kalimo, H   Paljarvi, L   Helin, H   Haapasalo, H  

    Using the novel tissue microarray technique, we studied immunohistochemical expression of cell cycle regulators p53, p21, pRb in 42 grade II oligodendrogliomas, 16 grade III anaplastic oligodendrogliomas, 10 primary and 4 recidive grade II oligoastrocytomas, 10 grade III oligoastrocytomas and 2 other grade II mixed gliomas. The p53 immunopositivity associated with malignant histology of the tumor (p = 0.01, Mann-Whitney test) and high pRb expression (p = 0.015). The p21 score associated strongly with histological grade (p < 0.001). The immunopositive tumors had a significantly higher rate of proliferation (p = 0.021). The p21 immunopositivity correlated positively with p53 immunopositivity: among the 33 p21 immunopositive tumors 30 (91%) were p53 immunopositive and only 3 were p53 immunonegative (p = 0.017). Patients with p21 immunonegative primary tumors had significantly better prognosis: among them 42 of the 46 (91%) survived, whereas only 18 of the 30 patients (60%) with p21 immunopositive primary tumors survived until the follow-up date (p = 0.0017). Statistical significance was reached in multivariate analysis as well (p = 0.01, exp(B) = 5.5). The pRb immunopositive tumors had higher proliferation rate than immunonegative tumors (p = 0.002). In multivariate variance analysis, comparing the effects of different regulatory proteins on cell proliferation, only the amount of pRb expression reached statistical significance (p = 0.004). In conclusion, the expression of p21 in oligodendrocytic tumors seems to be upregulated by p53 expression which rises with cell proliferation and malignancy as in attempt to halt cell cycle but seems to be overrun by other factors. The amount of p21 expression has independent prognostic significance and could be used in diagnosis to help the difficult evaluation of the malignancy potential of oligodendrogliomas and oligoastrocytomas.
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  • MYELOCYSTOCELE WITH CEREBELLAR HETEROTOPIA - CASE-REPORT

    SUNESON, A   KALIMO, H  

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  • Enrichment of the R77C alpha-sarcoglycan gene mutation in Finnish LGMD2D patients

    Hackman, P   Juvonen, V   Sarparanta, J   Penttinen, M   Aarimaa, T   Uusitalo, M   Auranen, M   Pihko, H   Alen, R   Junes, M   Lonnqvist, T   Kalimo, H   Udd, B  

    Limb-girdle muscular dystrophy 2D (LGMD2D) is caused by mutations in the alpha-sarcoglycan gene (SGCA). The most frequently reported mutation, 229CGC>TGC (R77C) in exon 3 of SGCA, results in the substitution of arginine by cysteine. We present here the clinical, immunohistochemical, and genetic data of 11 Finnish patients with LGMD2D caused by mutations in SGCA. Mutational analysis showed 10 patients homozygous and 1 compound heterozygous for R77C. A wide spectrum of SGCA mutations has been reported previously. Our results show an enrichment of R77C in Finland, further underlined by the observed carrier frequency of 1 per 150. According to the annual birth rate of similar to60.000 in Finland, one LGMD2D patient with a homozygous mutation is expected to be born every 1 or 2 years on average. The presence of an ancient founder mutation is indicated by the fact that all patients shared a short common haplotype extending greater than or equal to790 kilibases. Our results emphasize the need to include the SGCA gene R77C mutation test in routine DNA analyses of severe dystrophinopathy-like muscular dystrophies in Finland, and suggest that the applicability of this test in other populations should be studied as well.
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  • CD44-HYALURONATE INTERACTION MEDIATES IN-VITRO LYMPHOCYTE BINDING TO THE WHITE-MATTER OF THE CENTRAL-NERVOUS-SYSTEM

    AHO, R   JALKANEN, S   KALIMO, H  

    The cell adhesion molecule CD44 is expressed in the central nervous system, especially on glial cells in the white matter, the extracellular matrix of which also contains one of its ligands, hyaluronate. We investigated the role of CD44 and hyaluronate in the adhesion of human peripheral blood lymphocytes to myelinated areas of cerebellum by an in vitro binding assay. Hermes-1 epitope, which recognizes the hyaluronate binding site of CD44, and Hermes-3 epitope, involved in lymphocyte binding to mucosal high endothelial venules, were both immunohistochemically expressed in the white matter. No immunoreactivity was observed with mAb Var3.1, which sees variant forms of CD44 containing the exon v6 encoding region. The molecular weight analysis showed that CD44 of the white matter was identical to the major 90 kD form of CD44 present on lymphocytes. The binding of both T and B lymphocytes was significantly inhibited by pretreatment of both cells and sections with mAb Hermes-1 but not with Hermes-3. Digestion of the sections and/or lymphocytes with hyaluronidase also reduced lymphocyte binding. These findings implicate that CD44-hyaluronate mediates lymphocyte adhesion to the white matter and this interaction may be involved in the pathogenesis of inflammations and lymphomas of the central nervous system.
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