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Biomedical subjects

C Brunner

Publications and source records attributed to C Brunner.

At least 55 records · Page 3Linked to original sources

Differential ultrastructural localization of myelin basic protein, myelin/oligodendroglial glycoprotein, and 2',3'-cyclic nucleotide 3'-phosphodiesterase in the CNS of adult rats.

In a light and electron microscopic immunocytochemical study we have examined the distribution of myelin basic protein (MBP), 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP), and myelin/oligodendroglial glycoprotein (MOG) within CNS myelin sheaths and oligodendrocytes of adult Sprague-Dawley rats. Ultrastructural immunocytochemistry allowed quantitative analysis of antigen density in different myelin and oligodendrocyte zones: MBP was detectable in high density over the whole myelin sheath, but not in regions of loops, somata, or the oligodendrocyte plasma membrane. CNP reactivity was highest at the myelin/axon interface, and found in lower concentration over the outer lamellae of myelin sheaths, at the cytoplasmic face of oligodendrocyte membranes, and throughout the compact myelin. MOG was preferentially detected at the extracellular surface of myelin sheaths and oligodendrocytes and in only low amounts in the lamellae of compacted myelin and the myelin/axon border zone. Our studies, thus, indicate further the presence of different molecular domains in compact myelin, which may be functionally relevant for the integrity and maintenance of the myelin sheath.

Animals↗

Tau and ubiquitin immunoreactivity at different stages of formation of Alzheimer neurofibrillary tangles.

In his original 1911 publication Alois Alzheimer classified neurofibrillary tangles (ANT) into three morphologically defined subgroups according to their stage of maturation. The present study shows that changes in the morphological appearance of ANT during their maturation process are accompanied by changes in their antigenic profile. As shown by several immunocytochemical studies these abnormal phosphorylated microtubule-associated protein tau and of ubiquitin. In this study, immunoreactivity for the altered tau is not only seen in a subset of tangles but also in the cytoplasm of some nerve cells lacking ANT, which we believe to be at a stage of neuronal alteration preceding the formation of compact tangles (Stage 0 tangles). Similar numbers of Stage 0 tangles are present in the brains of age-matched non-demented individuals as in Alzheimer cases, but are absent in young controls lacking ANT. In extracellular "ghost tangles", the ultimate stage of neurofibrillary degeneration, immunoreactivity for tau is accessible to antibodies only when tissue sections are pretreated with formic acid to uncover the binding sites. In contrast to tau, presence/accessibility of an epitope residing on residues 50-65 of ubiquitin recognized by a monoclonal antibody raised to paired helical filaments (3-39) increases during the maturation of ANT and is most pronounced in "ghost tangles". Appearance/uncovering of the 3-39 epitope and masking of tau reactivity during tangle maturation may reflect degradation or conformational changes in the pathological filaments due to their aging and the final loss of their parent nerve cells.

Aged↗

[Drug addiction and pregnancy. Principal obstetrical and pediatric complications].

The principal obstetrical and paediatric sequelae were studied in 22 heroin addicts who were followed up at Lariboisière Hospital in Paris between 1980 and 1984. The main effects were on the fetus with 45% showing growth retardation below the 10th percentile, 65% fetal distress, 9% prematurity; 33% had infections and 66% had the withdrawal syndrome. Because of this pathology a high number had to be transferred. Considering the period of study, HIV infection could not be evaluated. The most dramatic result seems to be the long-term effect on these children because only a third apparently live with their families and several suffer from abnormalities in psychomotor development.

Adult↗

Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions.

The effect of a circulating monoclonal antibody recognizing an antigen located on the surface of myelin sheaths (myelin/oligodendroglia glycoprotein, MOG) on clinical and histopathological expression of experimental allergic encephalomyelitis (EAE) was tested in a model of EAE passively transferred by monospecific T lymphocytes. Intravenous injection of anti-MOG antibody at the onset of the disease massively augmented clinical impairment as well as primary demyelination. The structure of the CNS lesions depended on the balance between encephalitogenic T cells and anti-MOG antibody: when EAE was induced with high numbers of T cells, circulating anti-MOG antibody resulted in ubiquitous perivenous demyelination in the spinal cord and medulla oblongata. On the contrary, focal confluent demyelinated lesions were observed in animals injected with low numbers of T cells (even as few as 10(4] and anti-MOG antibody. Our studies, thus, indicate that the formation of inflammatory demyelinating lesions may be due to a synergistic action of cellular and humoral immune mechanisms.

Animals↗

[Traumatic hip dislocation in the child].

We report on 20 own cases of the past 20 years. Traumatic hip dislocation in children, which is a rare event, should be primarily reduced under anaesthesia as quickly as possible. An open reduction is only necessary with the luxatio obturatoria if a sole conservative reduction attempt is unsuccessful. A possible ipsilateral femur shaft fracture must be treated operatively at the same time.

Anesthesia, General↗

Augmentation of demyelination in rat acute allergic encephalomyelitis by circulating mouse monoclonal antibodies directed against a myelin/oligodendrocyte glycoprotein.

In this study the authors have developed a model with which can be studied directly the influence of circulating anti-myelin antibody on the clinical and pathologic course of inflammatory T-cell-mediated experimental allergic encephalomyelitis (EAE) in the rat. EAE was induced by passive transfer of either myelin basic protein (MBP)-activated spleen cells derived from sensitized donors or long-term-cultured MBP-specific T-cell lines. At the onset of the disease, monoclonal antibodies against a myelin/oligodendrocyte glycoprotein (MOG) were injected intravenously. This antigen is exposed on the surface of central nervous system myelin and oligodendrocytes. Intravenous injection of the antibody in the course of T-cell-mediated transfer EAE augmented the severity and duration of clinical signs and resulted in the formation of large, confluent demyelinated plaques.

Animals↗

[BCG osteitis in Switzerland. A report of 6 cases].

BCG osteitis is a rare complication after vaccination in the newborn. On the basis of various, not yet fully known mechanisms, an increase in the number of cases is nevertheless possible. In the period 1980-1985 the authors recorded 6 instances of BCG osteitis. The clinical findings and diagnostic criteria are described. The incidence, pathogenesis and therapy of the disease are discussed.

Antitubercular Agents↗

Therapy of rat autoimmune disease by a monoclonal antibody specific for T lymphoblasts.

The central role of T lymphocytes in the initiation, regulation and propagation of autoimmune diseases defines them as most suitable targets for selective immunotherapy. The recent advance in culturing human and animal T cell lines allows us to select monoclonal antibodies specific for differentiation antigens expressed by activated T lymphocytes. We selected a monoclonal antibody cytotoxic for a subpopulation of activated rat T cells. In vivo, this antibody effectively blocks immune responses to foreign antigens or autoantigen and prevents development of autoimmune diseases like experimental allergic encephalomyelitis and adjuvant arthritis. Even already established disease can be blocked by a single injection of antibody. Furthermore, this monoclonal antibody can be used to monitor the course of autoimmune disease progression from peripheral blood samples.

Animals↗

Peripheral nervous system lesions in experimental allergic encephalomyelitis. Ultrastructural distribution of T cells and Ia-antigen.

The distribution of T cells and Ia-antigen in peripheral nervous system (PNS) lesions of experimental allergic encephalomyelitis was studied by light- and electron-microscopic immunocytochemical techniques. Sprague Dawley rats, sensitized with guinea pig spinal cord tissue, developed a biphasic disease with acute inflammatory and chronic inflammatory demyelinating lesions in the PNS. In both the acute non-demyelinating and the chronic demyelinating disease inflammatory infiltrates were composed of T cells and Ia-positive monocytes/macrophages. Dependent upon the stage of the disease a variable percentage of T-lymphocytes carried the Ox 8 antigen (suppressor/cytotoxic cells). In demyelinating lesions no evidence for an interaction of T cells with myelin or Schwann cells was observed, thus arguing against a direct T-cell cytotoxicity in demyelination. The whole sequence of myelin destruction and digestion was performed by W3/13-, Ia+ mononuclear cells with ultrastructural features of monocytes/macrophages. In contrast to the acute inflammatory stage of the disease, high titers of anti-myelin antibodies were present in sera of affected animals sampled during the chronic inflammatory demyelinating stage. The sera from the latter animals also showed pronounced in vivo demyelinating activity when transferred into the cerebrospinal fluid (CSF) of normal recipient rats. It is thus suggested that demyelination in this model is induced by a co-operation of cell-mediated and humoral immune mechanisms. We did not find evidence for Ia-antigen expression on local elements of the PNS (Schwann cells, axons, or endothelial cells).

Animals↗

BCG osteomyelitis. Case report and review.

A 6-month-old boy is described presenting with BCG osteomyelitis of the distal metaphysis of the left femur extending into the epiphysis. Epidemiological, diagnostic and therapeutical problems of BCG osteomyelitis after BCG vaccination in the newborn period are discussed reviewing 89 published records of this late onset complication of BCG vaccination.

BCG Vaccine↗

[Congenital non-union of the clavicle (author's transl)].

The isolated congenital non-union of the clavicle is an extremely rare condition. We report on of one case of bilateral congenital non-union of the clavicle in which the left side became painful. Treatment with compression plate osteosynthesis and homologous cancellous bone grafting was successful. Surgical treatment of this rare condition is only indicated when the non-union becomes painful.

Adolescent↗