Biomedical subjects

S Mørk

Publications and source records attributed to S Mørk.

At least 19 recordsLinked to original sources

PubMed2000

[Orbital tumors].

BACKGROUND: Orbital tumours are relatively uncommon, and few series of patients with such tumours have been reported from Scandinavia. Here we present the experience of a Norwegian referral centre. MATERIAL AND METHODS: We have retrospectively evaluated the records of 278 patients with orbital tumours hospitalized at the Department of Ophthalmology, Haukeland University Hospital from 1961 to 1999. RESULTS: In 177 patients, a benign tumour was present, while 96 patients suffered from malignant disease. In five cases, the malignant potential of the tumour could not be assessed. A total of 71 different histological entities were observed. Surgical treatment performed at our department was in 22 patients exenteration, in 87 lateral orbitotomy, in 47 anterior orbitotomy and in 41 biopsy through an anterior approach. INTERPRETATION: This series illustrates the wide panorama of space-occupying lesions that may be present in the orbit. Since the lesions are rare and management in many cases complex, the treatment should be centralized to an eye department with a defined interest in orbital disease.

Adolescent↗

PubMed2000

[Polyneuropathy is an early finding in primary systemic amyloidosis].

BACKGROUND: Polyneuropathy is associated with several pathological conditions. Amyloidosis is a less common cause of polyneuropathy. Amyloidosis is caused by the accumulation of insoluble protein fibrils (amyloid) in the extracellular matrix. Primary systemic amyloidosis is caused by B-lymphocyte dyscrasia. Polyneuropathy is the first sign of primary systemic amyloidosis in about 20% of the cases, and is characterised by relentless progression, painfulness, and prominent symptoms of autonomic neuropathy. MATERIAL AND METHODS: We describe three cases of primary systemic amyloidosis that started with polyneuropathy. RESULTS: The diagnosis of primary systemic amyloidosis is often delayed more than two years after the onset of polyneuropathy. Biopsy of rectum, fat tissue, bone marrow, or peripheral nerve are diagnostic tools. INTERPRETATION: The survival of non-treated patients is about 18 months after the diagnosis. With chemotherapy the survival is prolonged to approximately 38 months.

Aged↗

PubMed2000

[Diffusion-weighted magnetic resonance tomography--a new instrument in the diagnosis of Creutzfeldt-Jakob disease].

Creutzfeldt-Jakob's disease (CJD) is characterised by rapidly progressive dementia, ataxia, myoclonus, and several other neurological deficits. It generally affects older adults and occurs in sporadic, genetic and iatrogenic forms. Death occurs usually within one year after onset of the disease. The diagnosis is based on clinical criteria, neurophysiological and radiological findings, and confirmed by postmortal histopathology. During the last two years several cases of CJD have been reported with diffusion-weighted magnetic resonance imaging (MR) abnormalities, represented by increased signal intensity indicating reduced diffusion in basal ganglia and/or cortex cerebri. These abnormalities seem to be characteristic of CJD. We report a case of CJD in a 54-year-old woman who developed vertigo, nystagmus, ataxia, myoclonus, and dementia over a period of eight months. Diffusion-weighted magnetic resonance imaging showed increased signal intensity in corpus striatum and gyrus cinguli. The diagnosis was postmortally confirmed with histopathology.

Brain↗

PubMed1998

[Cerebral amyloid angiopathy].

Cerebral amyloid angiopathy affects the cerebral vasculature selectively, and there is no systemic amyloidosis. Amyloid is deposited in small and medium-sized vessels of the cortex and leptomeninges. Cerebral amyloid angiopathy is a common cause of spontaneous lobar haemorrhage in elderly patients. However, cerebral amyloid angiopathy may have atypical clinical and radiological presentations. We report on five patients (three males and two females, aged 43-77 years) with histologically verified cerebral amyloid angiopathy. One patient experienced an acute headache attack and classical lobar haemorrhage. The other patients had various neurological symptoms and signs, such as seizure, disturbed vision, pareses, aphasia, and dementia that were initially diagnosed as cerebral infarction or tumour. Two patients with cerebral amyloid angiopathy and granulomatous angiitis responded to immunosuppressive treatment.

Adult↗

PubMed1998

Stimulation of extracellular matrix components in the normal brain by invading glioma cells.

Malignant gliomas are characterized by an extensive invasion of tumor cells into the normal brain parenchyma. A substantial amount of data indicates that cell movement in general is regulated by specific interactions between extracellular matrix components and specific cell-surface receptors. In the present work, multicellular spheroids from 4 human glioma cell lines (U-373Mg, A-172Mg, U-251Mg and HF-66) were confronted with normal rat brain cell aggregates in vitro, which resulted in a progressive invasion of tumor cells into the brain aggregates. The co-cultures were then sectioned and immuno-stained for specific extracellular matrix components (laminin, fibronectin and collagen type IV) and for specific cell-surface receptors which bind to these components (integrins beta1, beta4, alpha3, alpha6). In addition, flow-cytometric measurements and Northern blot analyses showed expression of several different integrins within the cell lines. The alpha3 subunit was expressed strongly in all cell lines. Whereas the beta1 subunit was expressed weakly in exponentially growing monolayer cultures, it showed a pronounced expression in multicellular spheroids, indicating that the integrin expression may vary depending on the micro-environment within a tumor. Furthermore, normal brain tissue was able to produce laminin when confronted with the glioma cells, which also was observed for fibronectin and collagen type IV. The relevance of our observations to the in vivo situation was investigated further by immuno-staining 5 human glioma biopsy samples for laminin. In some areas of the tumors, specific deposits of laminin were observed. In conclusion, we have shown that normal brain tissue has the ability to produce extracellular matrix components, such as laminin, collagen type IV and fibronectin, when confronted with invading glioma cells. Our results show that the glioma cells express specific integrins which can interact with these extracellular matrix components. Such interactions may facilitate tumor cell migration and invasion.

Animals↗

PubMed1997

[Paraneoplastic cerebellar degeneration. A case report].

Paraneoplastic cerebellar degeneration is a rare remote effect of ovarian and breast carcinoma especially, and is characterised clinically by rapidly evolving pancerebellar symptoms. A woman aged 83 developed progressive vertigo, cerebellar ataxia, nystagmus and dysarthria. The cerebrospinal fluid showed slight mononuclear pleocytosis, elevated total protein and IgG concentrations, and oligoclonal bands. A magnetic resonance investigation performed within the first month of symptoms was normal. A left pelvic mass was found, possibly a carcinoma of the colon or the left ovary. Cancer antigen 125 was elevated in the serum and antibodies against Purkinje cells (anti-Yo antibodies) were demonstrated in the serum and cerebrospinal fluid. These results suggested a carcinoma of the ovary as primary site of cancer. Autopsy revealed a left ovarian adenocarcinoma and marked loss of Purkinje cells in the cerebellum. The case illustrates that anti-Yo antibodies may serve as a marker not only for paraneoplastic cerebellar degeneration, but also for the nature of the neoplasm that caused it.

Adenocarcinoma↗

PubMed1997

Neuroblastoma and venous sinus thrombosis in an adult patient.

A 35-year-old woman developed symptoms consistent with intracranial venous sinus occlusions that were demonstrated by MR angiography. After a few weeks of anticoagulant therapy, she became paraplegic due to haemorrhages in the caudal spinal canal. A decompressive laminectomy did not improve her neurological deficits. Up to this point, we assumed her condition to be caused solely by the intracranial venous thrombosis and complications of the treatment. A tumour diagnosis had so far not been considered. A few months later she became tetraplegic. MRI revealed fresh bleeding in the upper spinal cord and a dissemination of tumour along the entire craniospinal axis. Biopsy specimens obtained from the spinal canal contained tumour cells with the characteristics of neuroblastoma.

Adult↗

PubMed1996

[Prion diseases. Review of the literature on the light of two case reports of Creutzfeldt-Jakob disease].

During the last ten years the diseases scrapie in sheep and bovine spongiform encephalopathy (or mad cow disease) in cattle have received increased attention. Through the 1960s it became apparent that scrapie in sheep and kuru and later Creutzfeldt-Jakob disease in man were infectious diseases. During the last decade the appearance of mad cow disease in Great Britain has increased the fear that humans can develop Creutzfeldt-Jakob disease through their food. A special characteristic of the infectious agent, the prion, is its lack of DNA. It has been shown that the prion most probably has a pure protein structure. The prion may exist in two slightly different structural patterns, one of which induces the various prion diseases in animals and man. In 1994 two men with Creutzfeldt-Jakob disease were diagnosed at Haukeland Hospital. Their symptoms and clinical data are presented, together with a review of the literature on prion diseases in animals and man.

Animals↗

PubMed1996

Distribution of immunoglobulin superfamily members ICAM-1, -2, -3, and the beta 2 integrin LFA-1 in multiple sclerosis lesions.

To identify potential molecular substrates for leukocyte trafficking and activation in multiple sclerosis (MS) brain, we determined the immunocytochemical distribution of the beta, integrin lymphocyte-function-associated antigen-1 (LFA-1) and its major ligands, intercellular adhesion molecule (ICAM)-1, ICAM-2, and ICAM-3 in MS tissue. Colocalization of these adhesion molecules with lineage-specific markers was analyzed by dual-labeling immunocytochemistry and confocal microscopy. ICAM-1 and ICAM-2 were detected on endothelial cells, and ICAM-3 immunoreactivity was restricted to infiltrating leukocytes. In control brain, 10% of glucose transporter-1 positive vessels contained ICAM-1 immunoreactivity on their luminal surface and 21% were ICAM-2-positive. A significant increase in ICAM-1-positive vessels was found in MS brains. This increase was greater in MS lesions (81% of vessels) than in nonlesion areas (37% of vessels). A significant increase in ICAM-1-positive vessels was found in encephalitis (55% of vessels) but not in Parkinson's (17% of vessels) brains. The percentage of vessels expressing ICAM-2 was not increased in MS, encephalitis, or Parkinson's brains. Both ICAM-3 and LFA-1 were detected on the vast majority of infiltrating lymphocytes and monocytes in and near MS lesions, and these cells were often closely apposed to each other. In addition, LFA-1 was detected on activated microglia located close to the edge of demyelinating lesions. ICAM-3-positive leukocytes were often closely apposed to LFA-1-positive microglia. These results suggest a role for ICAM-1, -2, and LFA-1 in the transendothelial migration of leukocytes into MS brain and a role for ICAM 3/LFA-1 interactions in the activation of lymphocytes, monocytes, and microglia in MS lesions.

Adolescent↗

PubMed1994

Reactive microglia in multiple sclerosis lesions have an increased expression of receptors for the Fc part of IgG.

Receptors for the Fc part of IgG, FcRI (CD64), FcRII (CD32), and FcRIII (CD16) were studied by indirect immunoperoxidase staining of cryostat sections from normal and multiple sclerosis (MS) brains. Microglia in the parenchyma of normal white matter had a dendritic morphology, and were weakly stained by monoclonal antibodies (mAbs) to FcRI, FcRII, and FcRIII. In active MS lesions reactive microglia were strongly stained by the mAbs 32.2 (FcRI), IV-3 (FcRII), and 3G8 (FcRIII). Perivascular macrophages were stained by all anti-FcR mAbs in both normal white matter and in MS lesions, whereas endothelial cells were stained by the anti-FcRIII mAb only. The FcR on microglia and perivascular macrophages may be of functional importance in antibody-dependent cell-mediated cytotoxicity (ADCC), phagocytosis, and local immunoregulation. FcR on endothelium may be of importance in binding and transportation of immune complexes into the CNS. FcR mediated functions may consequently be highly relevant to the pathogenesis of MS.

Adult↗

PubMed1994

Phenotypic differences between human monocytes/macrophages and microglial cells studied in situ and in vitro.

This report describes a phenotypic differentiation pattern conceived to distinguish invading monocytes from resident microglia in frozen and formalin-fixed human CNS. Phagocytic cells in normal and diseased CNS (multiple sclerosis and encephalitis) were studied immunohistochemically with a panel of antibodies, and phenotypic characteristics were compared with cultured monocytes/macrophages and microglia. Monocytes/macrophages were positive for the markers non-specific esterase, myeloperoxidase, L1, lysozyme, RFD7, and CD14, whereas microglia were negative for the same markers. Both populations of cells were positive for CD11c and CD68. Our results indicate that invading monocytes/macrophages mainly have a perivascular location in active multiple sclerosis lesions, whereas invading monocytes/macrophages also infiltrate the parenchyma in acute inflammatory CNS diseases such as in encephalitis.

Acute Disease↗

PubMed1994

Organ culture of a glioblastoma from a patient with an unusually long survival.

Multicellular tumor spheroids were directly initiated in vitro from the biopsy specimens of a patient who is alive and who has had no neurological changes in 7 years after the gross removal of a glioblastoma. The spheroids were studied alone and in confrontation with aggregates of fetal rat brain tissue. Both in the biopsy and in the tumor spheroids, a very high proportion of cells were proliferating, as flow cytometric deoxyribonucleic acid measurements showed that 40% of the cells in the biopsy specimens and in the tumor spheroids were in the S and G2M phases of the cell cycle. Despite this high proliferation rate, the volume of the spheroids decreased, indicating an even greater cell loss. Light and scanning electron microscopic studies also indicated cell death in the spheroids. This behavior may be related to the long-time survival.

Animals↗

PubMed1994

In situ characterization of leukocytes in the fallopian tube in women with or without an intrauterine contraceptive device.

Histological evaluation of sections from the human fallopian tube revealed an inflammatory reaction in 21 of 31 women using an intrauterine contraceptive device (IUCD) and in four of 29 controls (non-IUCD users). The inflammatory cells were mainly localized at the epithelium-lamina propria interface and at the center of the mucosal folds. The immunohistochemical study revealed leukocytes (CD45+), T lymphocytes (CD3+), T helper cells (CD4+), T suppressor/cytotoxic cells (CD8+), B lymphocytes (CD22+, CD19+), granulocytes, monocytes and null cells (CD11b+) mainly localized at the lamina propria in both groups. T lymphocytes were the predominant cell type, and the ratio between T helper and T suppressor/cytotoxic cells was fairly close to one both in IUCD-users and controls. B lymphocytes were the least frequent cell type identified. In IUCD users, the numbers of the different leukocytes were increased. In both groups, IgA-, IgG- and IgM-positive cells were demonstrated and were predominantly located at the lamina propria of the mucosal folds. The IgA-positive cells dominated in both groups, whereas IgG- and IgM-positive cells were less frequent. Cell positive for IgA, IgG or IgM were significantly increased in number in the IUCD users. The data confirm the presence of an immune system in the normal human fallopian tube and indicate that the IUCD can induce a prominent recruitment of inflammatory cells, with a tubal inflammation as the result. The IUCD may disturb the immunological function of the fallopian tube and its rôle in fertilization.

Adult↗

PubMed1994

The expression of CD59 in normal human nervous tissue.

The expression of CD59, a complement regulator of the formation and function of the terminal cytolytic membrane attack complex, was studied in human normal nervous tissue by immunohistochemical markers using two monoclonal antibodies 1F5 and MEM43. CD59 was present on Schwann cells, neurons and endothelial cells in the peripheral nervous system (PNS), and on Schwann cells in culture. In the central nervous system (CNS) CD59 was found predominantly on endothelial cells. There was also a diffuse staining of white and grey matter of the spinal cord and brain, presumably of microglia, oligodendrocytes, astrocytes and neurons, as these cells were CD59 positive in culture. Furthermore, CD59 was detected in the cerebrospinal fluid (CSF) of healthy individuals. CD59 in the PNS and CNS was glycosyl-phosphatidylinositol linked and had a molecular weight of 19,000-25,000. The presence of CD59 on various cells of the nervous system and in the CSF suggests that regulation of complement activation by this protein is important in neural host defence mechanisms.

Adult↗

PubMed1994

HLA class II molecules (HLA-DR, -DP, -DQ) on cells in the human CNS studied in situ and in vitro.

Human leucocyte antigen (HLA) class II molecules expressed by antigen-presenting cells (APC) are major restriction elements in the interaction between APC and T cells of the CD4+ subtype. To explore the immune accessory function of cells in the central nervous system (CNS), we studied the expression of HLA-DR, -DP, and -DQ molecules on CNS cells in situ and in vitro. Reactive microglia and perivascular cells in multiple sclerosis lesions expressed all three HLA class II molecules, whereas microglia in the normal CNS expressed HLA-DR only. All three HLA class II molecules were up-regulated on cultured microglia after stimulation with interferon-gamma (IFN-gamma). Microglial stimulation of allogeneic CD4+ T cells in a mixed lymphocyte reaction (MLR) was effectively blocked using anti-HLA-DR monoclonal antibodies (mAb) but not using anti-HLA-DQ mAb. HLA class II-positive astrocytes and endothelial cells were not identified in normal or diseased CNS. Cultured astrocytes stimulated with IFN-gamma could, however, be induced to express HLA class II antigens of all subtypes, although great variability was observed between different donors. Our results indicate that although both microglia and astrocytes are capable of expressing all HLA class II subtypes in vitro, subtype expression differs between normal and pathological states in situ. Such selective expression may be associated with functional properties.

Adult↗

PubMed1993

Migratory pattern of fetal rat brain cells and human glioma cells in the adult rat brain.

The migratory behavior of two human glioma cell lines (D-54MG and GaMG) and fetal rat brain cells grafted into the adult rat brain was studied. To trace the implanted cells, they were stained with the carbocyanine vital dye 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate before injecting them into the white matter above the corpus callosum. The animals were sacrificed 2 h and 7 and 21 days after injection, and the brains were removed and cryosectioned. Fluorescence microscopy showed that both the 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate-stained fetal and tumor cells had the same migratory pattern. Implanted cells were found along myelinated fibers in the corpus callosum and in the perivascular space. After immunostaining for several extracellular matrix (ECM) components (laminin, fibronectin, collagen type IV, and chondroitin sulfate), laminin deposits were observed in the border zone between the host tissue and implanted tumor cells as well as fetal cells. By using two different types of antibodies against fibronectin, it is shown that the fibronectin expression observed in the tumor matrix may be host derived. This was further supported by the fact that tumor spheroids obtained from the two glioma cell lines were negative when immunostained for these ECM components. Several of the ECM components may be host derived. This can be caused by neovascularization and repair synthesis or by a local production of guiding substrates which are important for tumor cell locomotion. The present data suggest that the migratory patterns of fetal and glioma cells are indistinguishable when transplanted into the adult rat brain. Thus, glioma cells may be routed by the same ECM components that play a major role during brain development.

Animals↗

PubMed1991

Mast cells in brains during experimental allergic encephalomyelitis in Lewis rats.

We studied the number of mast cells and their extent of degranulation in brains of Lewis rats with acute experimental allergic encephalomyelitis (EAE), activity induced with guinea pig spinal cord and Freund's complete adjuvant. Non-immunized controls and EAE rats were killed on days 10, 11, 12, and 16 post-immunization (p.i.). The percentage of degranulated mast cells was significantly increased in EAE brains. Signs of degranulation were observed as early as day 10 p.i. Clinical EAE signs appeared from day 10 p.i. A significant change in mast cell number was not observed. The percentage of degranulated cells was largest at day 16 p.i., at a time when the inflammation had reached the thalamus. This indicates that mast cell degranulation may occur as a result of the inflammation. Collectively, the data suggest that mast cells may play a role in the pathogenesis of EAE.

Animals↗

PubMed1990

Interaction between human brain tumour biopsies and fetal rat brain tissue in vitro.

The invasiveness of human intracranial tumours was studied in an organ culture system. Biopsies from six glioblastomas, four astrocytomas, two mixed gliomas, one ependymoma, four meningiomas and two carcinoma metastases were cut into fragments of 0.5 mm diameter, and placed in agar overlay tissue culture. The tumour specimens formed spheroids which were co-cultured with cell aggregates or fragments from fetal rat brain for up to 10 days in vitro. The invasiveness of the glioblastoma spheroids was characterised by a gradual destruction of normal brain tissue by tumour cells, followed by replacement of normal tissue by these cells. Co-cultures from two glioblastomas showed lesions in the normal brain tissue in areas removed from the tumour cells. Tumour spheroids from four glioblastomas totally destroyed the normal brain tissue without any change in the original tumour spheroid configuration. The low-grade gliomas were less invasive than the glioblastomas. The meningiomas and the metastases were non-invasive. This organ culture assay appeared to reflect the in situ invasive behaviour of the brain tumours examined. It is suggested that it may be used for evaluating the aggressiveness of individual brain tumours with the specific aim of correlating clinical data with the biological character of the tumour.

Adolescent↗