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Now showing items 17 - 32 of 48

  • ULTRASTRUCTURAL STUDIES ON HYPOTHALAMIC NEUROSECRETORY NEURONES OF RAT .1. PARAVENTRICULAR NEURONES OF NON-TREATED RAT

    KALIMO, H  

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  • MAST-CELLS AND IGE IN INTESTINAL-MUCOSA IN ADULT ATOPIC-DERMATITIS PATIENTS

    KALIMO, K   LAMMINTAUSTA, K   KLEMI, P   LEINO, R   PANULA, P   KALIMO, H  

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  • Epidemiology of hereditary neuropathy with liability to pressure palsies (HNPP) in south western Finland

    Meretoja, P   Silander, K   Kalimo, H   Aula, P   Meretoja, A   Savontaus, ML  

    An epidemiological study of hereditary neuropathy with liability to pressure palsies (HNPP) was carried out in south western Finland, with a population of 435 000. The diagnosis was established in 69 patients from 23 unrelated families through family and medical history, clinical neurological and neurophysiological examinations and with documentation of the deletion at gene locus 17p11.2 in at least one member of each family. This gave a prevalence of at least 16/100 000, which is remarkably high. However, due to the insidious nature of HNPP, most probably it is still an underestimation. This is the first population-based prevalence figure reported for HNPP. The prevalence is somewhat lower than that obtained for CMT in the same population, which agrees with the proposal that HNPP and CMT 1A are reciprocal products of the same unequal crossing-over. The clinical pictures of our patients were, in general, similar to those previously described in HNPP. (C) 1997 Elsevier Science B.V.
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  • ENDOGENOUS SERUM-ALBUMIN CONTENT IN BRAIN AFTER SHORT-LASTING EPILEPTIC SEIZURES

    SOKRAB, TEO   KALIMO, H   JOHANSSON, BB  

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  • LYMPHOCYTE MIGRATION INTO THE SKIN - THE ROLE OF LYMPHOCYTE HOMING RECEPTOR (CD44) AND ENDOTHELIAL-CELL ANTIGEN (HECA-452)

    JALKANEN, S   SAARI, S   KALIMO, H   LAMMINTAUSTA, K   VAINIO, E   LEINO, R   DUIJVESTIJN, AM   KALIMO, K  

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  • Intracranial aneurysms in three patients with disseminated Lyme borreliosis: cause or chance association?

    Oksi, J   Kalimo, H   Marttila, RJ   Marjamaki, M   Sonninen, P   Nikoskelainen, J   Viljanen, MK  

    Methods-Three patients with Borrelia burgdorferi infection and intracranial aneurysms are described. Results-All three patients had neurological symptoms. Perivascular and vasculitic lymphocytic inflammation were detected in the brain biopsy specimen of one patient. The aneurysm was located in the internal carotid arteries in two patients and in the basilar artery in one patient. The aneurysm ruptured in two patients. Conclusions-Cerebral lymphocytic vasculitis and intracranial aneurysms may be associated with B burgdorferi infection. It is suggested that inflammatory changes caused by B burgdorferi in vessel walls may be a pathogenetic mechanism for the formation of aneurysms.
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  • EARLY ULTRASOUND DIAGNOSIS OF FETAL INTRACRANIAL TUMORS

    PALO, P   PENTTINEN, M   KALIMO, H  

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  • MITOCHONDRIAL-DNA POLYMORPHISM IN FINNISH FAMILIES WITH LEBERS HEREDITARY OPTIC NEURORETINOPATHY

    VILKKI, J   SAVONTAUS, ML   KALIMO, H   NIKOSKELAINEN, EK  

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  • Etiologic aspects of chronic urticaria

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

    Background Urticaria is a common disease that is always a challenge to the dermatologist due to its evasive etiology. Patients and methods One hundred and seven chronic urticaria patients were studied. Routine laboratory investigations were performed and Helicobacter pylori (H. pylori) immunoglobulin G (IgG) antibody determinations, autoimmune reactivity, infections, allergies, and hyperreactivities were investigated. Results Pathologic findings were seen in 92 patients. Concomitant diseases suggesting autoimmune reactivity were detected in nine patients and, in 16 patients, infections including maxillary sinusitis, streptococcal tonsillitis, and tooth infection were found. Elevated total IgE level was detected in 37 out of 75 patients and positive skin prick test results in 47 out of 91 patients. Fifty-five patients had a history of recent dyspeptic symptoms. A diagnosis of adult celiac disease was made in two patients and, additionally, IgA antigliadin antibodies were seen in four patients. H, pylori IgG antibodies were found in 40 out of 107 patients. Active gastritis was verified by esophagogastroduodenoscopy in 30 out of 32 patients with positive Helicobacter staining in 24 samples. An elevated IgE level was detected in 64% of H. pylori-positive and in 39% of H, pylori-negative patients. Conclusions In this study, several findings suggesting aberrant immunologic activation were detected in chronic urticaria patients, inflammation in the gastrointestinal tract, e.g. caused by H. pylori infection, may have an important role in the etiology of chronic urticaria.
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  • Prognostic value of the expression of tumor suppressor genes p53, p21, p16 and pRb, and Ki-67 labelling in high grade astrocytomas treated with radiotherapy

    Kirla, R   Salminen, E   Huhtala, S   Nuutinen, J   Talve, L   Haapasalo, H   Kalimo, H  

    Cumulative inactivation of tumor suppressor genes and/or amplification of oncogenes lead to progressively more malignant astrocytic tumors. We have analyzed the significance of tumor suppressor genes p53, p21, p16 and retinoblastoma protein (pRb) and proliferative activity for survival in 77 high grade astrocytic tumors. After operation, the patients - 25 anaplastic astrocytomas (AA) and 52 glioblastomas (GBs) - were treated with similar radiotherapy. The expression of the suppressor genes and the proliferative activity were analyzed immunohistochemically. p53 immunopositivity was found in 44% of AAs and 46% of GBs. Tumors with aberrant p53 expression had lower proliferation indices than p53 immunonegative tumors. Neither p53 expression nor p21 immunonegativity (52% of AAs and 48% of GBs) correlated with survival, p16 immunostaining was negative in 16% of AAs and in 44% of GBs, and it correlated inversely with survival in both uni- and multivariate analyses. pRb immunostaining was negative only in 8% of both AAs and GBs and the absence of p16 and pRb were mutually exclusive. Ki-67 labelling index (LI) was significantly higher in GBs (26.8%) than in AAs (20.3%), and in multivariate analysis it was an independent prognostic factor for survival. In 48% of AAs Ki-67 LI exceeded 20% and this subset of AAs had similar prognosis as GB. In high grade astrocytic tumors p16 immunonegativity was an independent indicator of poor prognosis in addition to the previously established patient's age, histopathology and Ki-67 LI. Furthermore, there was a subset of AAs with a high proliferation rate (> 20%) in which the histopathological hallmarks of GB were lacking, but which had similarly dismal prognosis as GB.
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  • Alzheimer changes are common in aged drivers killed in single car crashes and at intersections

    Viitanen, M   Johansson, K   Bogdanovic, N   Berkowicz, A   Druid, H   Eriksson, A   Krantz, P   Laaksonen, H   Sandler, H   Saukko, P   Thiblin, I   Winblad, B   Kalimo, H  

    With increasing age, diseases affecting the cognitive functions are more frequent. These diseases may increase the risk for fatal car crashes. We analyzed the frequency of neuropathological alterations characteristic of Alzheimer's disease (i.e. neuritic and diffuse plaques, and neurofibrillary tangles) in two association areas of the brain, parietal and frontal cerebral cortex, from 98 fatally injured aged drivers. In the age groups of 65-75 and over 75 years of age, 50% and 72% of the drivers, respectively, had neuritic plaques in either parietal and/or frontal cortex. In 14% of all killed drivers the number of neuritic plaques reached the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) age-related histologic score C, which indicates the diagnosis of Alzheimer's disease (AD), and an additional 33% had score B, which suggests the diagnosis of AD. Neuropathological AD changes were most common in the brains of drivers killed in single vehicle crashes, followed by multivehicle crashes at intersections and least common in multivehicle crashes elsewhere, but the differences did not reach statistical significance. In a great majority (80-85%) of cases the killed aged driver was the guilty party of the crash. The results imply, that incipient AD may contribute to fatal crashes of aged drivers, and therefore the forensic autopsy of these victims should include neuropathological examination. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.
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  • The firing rate of motor units in neuromuscular disorders.

    Halonen, J P   Falck, B   Kalimo, H  

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  • Distribution and modulation of histamine H-3 receptors in basal ganglia and frontal cortex of healthy controls and patients with Parkinson's disease

    Anichtchik, OV   Peitsaro, N   Rinne, JO   Kalimo, H   Panula, P  

    Parkinson's disease (PD) is a brain degenerative disorder with unknown etiology, and specific degeneration of mesencephalic dopaminergic cells is a morphological manifestation of the disease. The central histaminergic system appears to be activated in PD, since the histaminergic innervation is increased in the substantia nigra. The aim of the present study was to investigate the expression and function of histamine H-3 receptors in PD, using receptor mRNA in situ hybridization with oligonucleotide probes, receptor binding assay with a specific radioactive agonist, and GTP-gamma-[S-35]-binding assay as a tool to study the activation of the receptor G-protein. H-3 receptor binding sites were detected using N-alpha -methylhistamine autoradiography in the basal ganglia and cortex, being most abundant in the substantia nigra and striatum. In PD substantia nigra we detected an increase of the receptor binding density. In situ hybridization study of the receptor mRNA revealed prominent sites of H-3 receptor synthesis in the putamen, cortex, and globus pallidus, whereas very low mRNA expression was seen in the substantia nigra. In the PD pallidum externum, H-3 receptor mRNA expression was elevated as compared with the normal brains. GTP-gamma-[S-35]-binding assay did not reveal any significant difference between PD and normal brains, although the density values in PD substantia nigra tended to be lower than in the normal brain, and density values in PD striatum were higher. The dopaminergic neurons did not express significant amount of H-3 receptor mRNA, suggesting that the effects of H-3 receptor-mediated modulation of dopamine release are indirect. Our data indicates modulation of the histamine H-3 receptor in PD at the level of the mRNA expression in the striatum and receptor density in the substantia nigra. The receptor activity seems to be unchanged or decreased, as revealed by GTP-gamma-[S-35]-binding assay. Modulation of the histamine H-3 receptor may influence the activity of other neurotransmitter systems, e.g., the GABAergic one, in the substantia nigra. (C) 2001 Academic Press
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  • INCLUSION BODY MYOSITIS AND PARAMYXOVIRUSES

    KALLAJOKI, M   HYYPIA, T   HALONEN, P   ORVELL, C   RIMA, BK   KALIMO, H  

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  • PITFALLS IN PREPARATION OF BUFFERS FOR ELECTRON-MICROSCOPY

    KALIMO, H   PELLINIEMI, LJ  

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  • Low TENS treatment on post-stroke paretic arm: a three-year follow-up

    Sonde, L   Kalimo, H   Fernaeus, SE   Viitanen, M  

    Objective: To determine whether stroke patients with initial increases in arm motor recovery following low-frequency transcutaneous electrical nerve stimulation (low TENS) treatment go on to show long-term benefits. Also whether the same therapy results in long-term improvements in motor function, spasticity or activities of daily living (ADL). Design: A three-year follow-up study. Subjects: Twenty-eight stroke patients, who had participated in a randomized trial of daily treatment with low-frequency (1.7 Hz) transcutaneous electrical nerve stimulation (low TENS) on the paretic arm for three months starting 6-12 months after stroke. Outcomes: Fugl-Meyer Motor Performance Scale for evaluation of changes in arm motor function, A 6-point Ashworth Scale to measure spasticity. Barthel Index to evaluate performance in ADL, Results: Motor function of the paretic arm had deteriorated in both treatment and control groups. Increased spasticity was seen in both groups. ADL score remained at a similar level in the low TENS group, whereas the control group had deteriorated during the same time period. Conclusions: Low TENS stimulation started 6-12 months after stroke may not have a specific effect on arm motor function years after completion of treatment.
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