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Biomedical subjects

T Olsson

Publications and source records attributed to T Olsson.

At least 343 records · Page 19Linked to original sources
PubMed1989

Hypercortisolism revealed by the dexamethasone suppression test in patients [corrected] with acute ischemic stroke.

Using the dexamethasone suppression test, we studied the activity of the hypothalamic-pituitary-adrenal axis within the first week after onset in 62 patients with acute ischemic stroke. Compared with two control groups (one comprising 25 elderly patients with various acute medical disorders and the other comprising 33 80-year-old volunteers), stroke patients had higher postdexamethasone cortisol levels (p = 0.08 and p = 0.001, respectively). By multiple regression analysis, high postdexamethasone cortisol levels in the stroke patients were significantly associated with proximity of the lesion to the frontal pole of the brain (p = 0.008) and with disorientation (p = 0.03), whereas no association with major depression was seen. Many stroke patients are exposed to hypercortisolism, which may have negative consequences upon organ functions. The extent to which dexamethasone administration suppresses cortisol levels seems to be determined mainly by the site of brain lesion and cannot be used as an indicator of major depression early after stroke.

Acute Disease↗
PubMed1989

Gamma-interferon-like immunoreactivity in axotomized rat motor neurons.

Major histocompatibility complex (MHC) encoded antigens, absent or present at only low levels in normal brain tissue, are induced locally around axotomized motor neurons. We here report that immunoreactivity for the potent MHC-inducing factor, gamma-interferon (IFN-gamma), appears in the cytoplasm of such neurons. Rat facial nerves were interrupted (crushed or cut), and later, at various intervals, cryosections from the facial nuclei were subjected to immunohistochemistry with monoclonal antibodies reacting with IFN-gamma and MHC antigens. IFN-gamma-like immunoreactivity appeared briskly in the cytoplasm of the axotomized motor neurons. The immunoreactivity subsided after a nerve crush as the target muscles were reinnervated, but persisted when nerve regeneration was prevented after a nerve cut. These results point to a role for nerve cell-derived IFN-gamma-like molecules in eliciting the neural cell responses to axotomy.

Animals↗
PubMed1989

Cells producing antibody to measles and herpes simplex virus in cerebrospinal fluid and blood of patients with multiple sclerosis and controls.

The B cell response against measles and herpes simplex virus (HSV) was evaluated in cerebrospinal fluid (CSF) and peripheral blood from patients with multiple sclerosis (MS) and controls by enumeration of cells secreting anti-measles and anti-HSV antibodies of IgG, IgA and IgM isotypes. We used a nitrocellulose immunospot assay which enables parallel enumeration of numbers of cells secreting total IgG, IgA and IgM. Anti-measles IgG antibody-secreting cells were present in CSF from 21 of 24 MS patients (mean 24 cells/10(4) mononuclear cells), and against HSV in CSF from seven of eight patients (mean 23/10(4) cells). No antibody-secreting cells were detectable in the patients' blood. Ten MS patients examined were negative for cells in CSF and blood producing anti-measles antibodies of IgA and IgM isotypes. Anti-measles IgG antibody secreting cells were also found in CSF from four of 18 controls, and anti-HSV IgG antibody-secreting cells in six of 13, especially in patients with subacute or chronic inflammatory nervous system diseases. Our results confirm that viral antibodies in MS are produced within CSF and that this B cell response is preferentially sequestered to this compartment. Whether this viral B cell response in MS reflects specific activation due to persistence of viral antigens or an epiphenomenon remains to be clarified.

Adult↗
PubMed1988

Axotomy induces MHC class I antigen expression on rat nerve cells.

Immunomorphological staining demonstrates that class I major histocompatibility complex (MHC)-coded antigen expression can be selectively induced on otherwise class I-negative rat nerve cells by peripheral axotomy. Induction of class I as well as class II antigen expression was simultaneously seen on non-neural cells in the immediate vicinity of the injured nerve cells. As nerve regeneration after axotomy includes growth of new nerve cell processes and formation of new nerve cell contacts, the present findings raise the question of a role for MHC-coded molecules in cell-cell interactions during nerve cell growth.

Animals↗
PubMed1988

HLA-DR-expressing cells and T-lymphocytes in sural nerve biopsies.

Thirty-five sural nerve biopsies were stained immunohistochemically for HLA-DR antigen. HLA-DR was expressed on nonmyelinating Schwann cells, macrophages, vascular endothelium, and perineurium. By means of double immunofluorescence staining the identity of the HLA-DR presenting structures was confirmed. HLA-DR expression was found in all biopsies and thus was not restricted to any particular type of neuropathy. The HLA-DR expression appeared to correlate with severity and activity of the neuropathy. HLA-DR-expressing macrophages wrapping myelinated fibers were prominent in primary demyelinating neuropathies. T-cells were found in 6 out of 15 nerves examined. Their presence correlated with moderate to strong HLA-DR expression of nonmyelinating Schwann cells, and they occurred during active disease.

Adult↗
PubMed1988

Modulation of experimental allergic neuritis in rats by in vivo treatment with monoclonal anti T cell antibodies.

Monoclonal antibodies (MCA) to different T lymphocyte cell surface antigens have been used to treat rats during different phases of the development of experimental allergic neuritis (EAN). The effects of this treatment were followed by clinical evaluation and in some instances by immunohistochemical analysis of lymphoid organs and affected nerves of the antibody-treated rats. Several MCA, W3/13 (pan T cell reactive), W3/25 (anti-rat CD4), Ox 8 (anti-rat CD8) as well as Ox 6 (anti-Ia) partly prevented clinical signs of EAN when given shortly before expected onset of disease, whereas W3/13 and Ox 8 given at the height of disease did not further affect disease development. However, Ox 19 (anti-rat CD5) given at the same time as immunization partly prevented clinical signs of EAN, while Ox 19 given shortly before expected onset of disease or during height of disease drastically exaggerated disease symptoms. Immunohistochemical studies after Ox 8 or Ox 19 treatment showed a complete absence of staining for the respective antibodies, while staining was preserved with the other MCA. It is concluded that: (1) Ox 8 positive "suppressor/cytotoxic" T lymphocytes do not exert any suppressive effects on EAN during the now investigated phases of disease, and that (2) anti T lymphocyte antibodies (here Ox 19) may exert opposite effects on autoimmune disease when given at different phases of disease development. This may have implications for potential therapeutic trials of MCA therapy for putative autoimmune demyelinating diseases in man.

Animals↗
PubMed1988

Effects of parity and stage of lactation on adenosine triphosphate, somatic cell count and antitrypsin content in cows' milk.

Significant effects of parity and stage of lactation were found on ATP content, somatic cell count and antitrypsin content when using morning milk samples from 39 cows over a period of 18 months. A close similarity was evident between variation in ATP and somatic cell count, except during the first 10 d after parturition when the variation in ATP was more pronounced. The same result was obtained in the whole material as well as in a healthy subset. This study shows clearly that parity and stage of lactation must be taken into account when establishing normal values for ATP as an indicator of mastitis.

Adenosine Triphosphate↗
PubMed1988

Elimination of CD8+ T cells in vivo does not break induced immunospecific tolerance to experimental allergic neuritis in rats.

The role of CD8+ T 'cytotoxic/suppressor' T cells in induced immunospecific tolerance and during recovery after actively induced disease was examined by means of elimination of CD8+ cells from Lewis rats using in vivo treatment by Ox8 monoclonal antibodies, in experimental allergic neuritis (EAN). Animals depleted of CD8+ T cells after recovery from EAN did not show any clinical signs of relapse. Other animals were pretreated with the peripheral nerve basic protein P2 and thereby rendered resistant to disease induction with a potentially neuritogenic emulsion. The elimination of CD8+ T cells did not result in EAN here either. Thus, the CD8+ T-cell population does not seem to participate in the suppression of this autoimmune disease under these experimental conditions.

Animals↗
PubMed1988

Occurrence and isotype of antibodies against peripheral nerve myelin in serum from patients with peripheral neuropathy and healthy controls.

Antibodies against peripheral nerve myelin have previously been demonstrated in serum from patients with peripheral neuropathy and IgM paraproteinaemia, and a causal relationship has been suggested. Using enzyme-linked immunosorbent assay (ELISA), anti-myelin antibodies were found in sera from eight of 16 patients with polyneuropathy and paraproteinaemia, but also in 17% of 109 patients with peripheral neuropathy lacking monoclonal immunoglobulin, including five of 10 patients with Charcot-Marie-Tooth disease, and in 16% of 142 blood donors. The antibodies were mostly of IgM class in the two neuropathy groups, while blood donors had mostly IgA antibodies, and a few subjects of each group had antimyelin antibodies of two different isotypes. Western blot confirmed the ELISA results in a majority of antibody positive sera and revealed a 25-30 kD myelin target antigen for sera from the three groups, and for some of the non-paraproteinaemic sera also a 100 kD myelin target antigen. Our results demonstrate that the presence of serum autoantibodies against peripheral nerve myelin does not necessarily indicate a pathological event.

Adult↗