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C Lubetzki

Publications and source records attributed to C Lubetzki.

71 records · Page 4Linked to original sources

[Pseudotumoral spinal cord dilatation during multiple sclerosis. 2 cases with magnetic resonance imaging].

We report 2 patients presenting with signs and symptoms of a medullary lesion. Spinal magnetic resonance imaging (MRI) using surface coils showed a volume increase of the spinal cord. Multiple sclerosis (MS) was suspected on the clinical evolution, the cerebrospinal fluid oligoclonal pattern in one case and the return of the cervical cord to an almost normal calibre on successive MRI. This diagnosis was further supported by the results of encephalic MRI. Such a pseudotumoral aspect of the spinal cord in MS has rarely been reported, and probably has been underestimated. MS should be considered in the differential diagnosis of localised enlargement of the spinal cord.

Adult↗

Myelination by oligodendrocytes isolated from 4-6-week-old rat central nervous system and transplanted into newborn shiverer brain.

Oligodendrocytes isolated from 4-6-week-old rat brains were transplanted into newborn shiverer brains. Cells were identified as mature oligodendrocytes both by immunocytological and ultrastructural criteria. Normal myelin was detected using immunolocalisation (with an anti-MBP antiserum) and electron microscopy (presence of the major dense line). Patches of normal myelin (made by transplanted oligodendrocytes), widely spread throughout the host brains, were detected between 20 and 130 days after grafting. No sign of acute rejection was observed, but the graft became progressively delimited by astrocytic processes forming a continuous basal lamina.

Animals↗

Immunological determination of galactosylceramide level in blood as a serum index of active demyelination.

An enzyme-linked immunosorbent assay (ELISA) to determine the level of galactosylceramide (GalC) in biological fluids is described. The assay uses GalC-coated plastic microtiter plates, with binding of an antibody to GalC detected by a peroxidase-labeled second antibody. The GalC level was directly estimated in the biological samples, without prior extraction, by competition with the coated hapten. This method allows the detection of 62 pmol of GalC (1.2 nmol/ml). Results using this procedure revealed positive sera only among patients suffering a myelin-destructive process: either primary, as in multiple sclerosis, or secondary to brain damage, as during ischemic strokes.

Cerebrosides↗

[Benign intracranial hypertension and minocycline].

A 19 year-old woman complained of headache and nausea occurring while she was taking minocycline for acne. Examination showed bilateral papilloedema and a bilateral VIth nerve palsy. Symptoms and signs rapidly resolved after the drug was stopped. Benign intracranial hypertension due to tetracyclines is well known in infants. It is rare in adults. Its pathophysiology remains unknown. The role of vitamin A is inconsistent. Others biological factors or personal susceptibility could be involved.

Acne Vulgaris↗

[Binding of immunoglobulins of the cerebrospinal fluid of multiple sclerosis patients to oligodendrocytes in culture].

There is often, in multiple sclerosis (MS) an intrathecal synthesis of immunoglobulin G (IgG) with an electrophoretic oligoclonal pattern. The target of those IgG, as well as their possible pathogenic role in the demyelinating process remain unknown and have led to many controversies. We have tested the hypothesis of an oligodendroglial target for those Ig, using a double labelling indirect immunofluorescent assay. Cerebrospinal fluid (CSF) Ig were collected from 28 MS patients (with either progressive or remitting-relapsing disease) and 25 patients with other neurological diseases. Ig binding has been tested on rat and human oligodendrocytes, isolated on a Percoll gradient and maintained 24 to 48 hours in culture. In our experimental conditions, we have never been able to detect any specific binding of MS CSF Ig on those oligodendrocytes, identified by double labelling immunofluorescence with an anti-galactocerebroside antibody.

Animals↗

[Intracerebral transplantation of oligodendrocytes in mice].

We describe in this paper experiments in which oligodendrocytes (from newborn mouse, human embryonic brain, or isolated from adult rat brain) have been transplanted into the brain of the newborn mouse. Experimental conditions (Shiverer model) allowed the detection of myelin formed by transplanted oligodendrocytes into the Shiverer brain. The transplanted oligodendrocytes have been shown to survive, migrate over long distances and myelinate host axons. The maturation of transplanted oligodendrocytes depends upon the age of the brain tissue in which they differentiate.

Animals↗

Schwann cell marker defined by a monoclonal antibody (224-58) with species cross-reactivity. I. Cellular localization.

We have demonstrated by indirect immunofluorescence the cellular localization of a monoclonal antibody (mAb 224-58), produced after immunization of a mouse with human central nervous system (CNS) myelin. Serologically, mAb 224-58 was found to be specific for 3'-sulfomonogalactosylglycolipids, namely 3'-sulfogalactosylceramide (SGC) and 3'-sulfogalactosyl 1-O-alkyl ether 2-O-acylglycerol (seminolipid). This mAb did not bind to SGC-containing tissues such as kidney, liver, spleen, or brain, nor to muscle. However mAb 224-58 did stain positively mouse, rat, and human peripheral nerve sections. In these latter sections, mAb 224-58 was bound to Schwann cell bodies and processes. The specificity of mAb 224-58 for Schwann cells was ascertained on teased rat sciatic nerves and rat Schwann cell cultures. Cells positive for mAb 224-58 were also positive for laminin, and negative for Thy 1-1 antigens both in teased fibers and Schwann cell cultures. In addition, in teased nerve preparations, mAb 224-58-positive cells were also galactosylceramide (GalC)- and SGC-positive. Isolated Schwann cells also expressed 224-58 antigen, even after prolonged time in culture. On testis sections, which contain both SGC and seminolipid, the SGC-positive cells, i.e., the spermatogonia, were always 224-58-negative. But the other germinal cells were 224-58-positive. This suggests that although 224-58 does not discriminate between SGC and seminolipid in serological tests, these lipids in their naturally occurring membrane acquire a spatial configuration that renders them distinguishable to their respective antibody.

Animals↗

Multiple sclerosis: rat and human oligodendrocytes are not the target for CSF immunoglobulins.

CSF Ig from 28 patients with MS and 25 patients with other neurologic diseases (OND) were examined for their capacity to bind to rat or human oligodendrocytes in culture. We have used a double-label approach combining CSF Ig with antibodies against galactocerebroside (GalC). As normal human IgG at a concentration higher than 250 micrograms/ml were found to bind nonspecifically to oligodendrocytes in culture, patients' CSFs were used unconcentrated, at a final IgG concentration never exceeding 115 micrograms/ml. In these experimental conditions, we have not been able to detect any fixation of CSF Ig from MS (or OND) patients to rat or human GalC+ oligodendrocytes.

Animals↗

The M2 autoantigen of central nervous system myelin, a glycoprotein present in oligodendrocyte membrane.

Autoantibodies with in-vitro demyelinating capacity induced in Hartley and strain 13 guinea pigs with homologous central nervous system (CNS) tissue were used to characterize the target autoantigen M2. Using the Dot Immunobinding technique, M2 was found to be a component of CNS myelin different from basic protein (BP) and from cerebroside. The expression of M2 on oligodendrocytes, cells known to produce CNS myelin, also confirmed that M2 was a component of CNS myelin. Furthermore, the autoradiography of immunoprecipitates formed with radiolabelled guinea pig myelin and analysed in sodium dodecyl sulphate gels showed that M2 was specific to CNS myelin and absent in peripheral nervous system (PNS) myelin. On electrophoresis M2 appeared as two CNS myelin protein bands at the 27 and 54 KD molecular weight levels, distinct from the major protein bands of proteolipid and BP. M2 bands were of glycoprotein nature, as was demonstrated by affinity chromatography of CNS myelin on wheat germ agglutinin (WGA)-Sepharose. A monoclonal antibody induced by BP-free CNS glycoproteins recognized the same bands as anti-M2 serum in guinea pig CNS myelin. This would imply that both M2 bands share common determinants. M2 bands similar to the above in guinea pig were also shown in rat, rabbit and bovine CNS myelin with guinea pig antibodies. The same type of anti-M2 antibodies were induced in rabbit immunized with homologous CNS tissue. Although only a minor component of myelin, M2 is strongly immunogenic compared to BP. M2 antigen could thus be the target of chronic demyelinating processes such as experimental allergic encephalomyelitis.

Animals↗

[Painful legs and unstable toes].

Five patients presented with the painful legs and moving toes syndrome as defined by Spillane et al. (1971). A peripheral nervous disorder was present in 4 of these cases while the fifth patient showed evidence of a central lesion. Results of clinical and electrophysiologic investigations in the 4 peripheral cases, are compared with data from the literature.

Adult↗

[Right hemiasomatognosia and sensation of amputation caused by left subcortical lesion. Role of callosal disconnection].

A 72-year-old right-handed hypertensive man presented with a right brachial monoplegia, and hypesthesia of the right half of the body to touch and pricking, sparing the face. A CT scan 2 weeks later showed a spontaneous hyperdense area corresponding to a left subcortical parietal hematoma. The patient used his spontaneous language to express body image disturbances: intense prolonged feeling of amputation related to the upper limb and foot on the right side, hemiasomatognosia without anosognosia, autotopagnosia. Also associated were a right-sided visual negligence and a more general inability to handle spatial data leading to a temporospatial disorientation. Mild language disorders were suggestive of subcortical aphasia: normal incitation and repetition; with semantic paraphasias, poor verbal fluency. Furthermore comprehension of orders or propositions concerning spatial data were poor. Finally, there were signs suggestive of callosal disconnection: paradoxical extinction of the left ear during dichotic listening, agraphia and anomia of the left hand, ideomotor apraxia of the left upper limb, difficulty in visual transfer. The lesion interrupted thalamic tracts to parietal regions and callosal fibers linking parieto-occipital association areas. This twofold lesion was analyzed for each of the neuropsychological disturbances observed. Certain aspect of cerebral function in this patient were reminiscent of "split-brain" disorders. The left hemisphere which "speaks" fails to understand the feelings of the right hemisphere: unfamiliarity of places, sensations of illness, resulting in an unadapted speech. The pathophysiology of feeling of amputation is discussed.

Aged↗

[2 cases of post-measles myelitis].

Two cases of a very rare complication of rubella i.e. a strictly spinal cord lesion developing during the course of the viral infection, are reported. In the first case, there was a flaccid paraplegia which incompletely regressed after two months. In the second case there were only sensory disorders and sphincter disturbances and recovery was complete after one month. The post-eruption encephalomyelitis lesions are of uncertain paphogenesis but the most common hypothesis suggested is that of a delayed hypersensitivity mechanism involving a cell-mediated immunologic reaction. The prognosis of these post-injection neurologic manifestations is difficult to assess, but spinal cord lesions could have a good prognosis.

Adolescent↗

Local and distal effects induced by unilateral striatal application of opiates in the absence or in the presence of naloxone on the release of dopamine in both caudate nuclei and substantiae nigrae of the cat.

Halothane-anesthetized cats implanted with push-pull cannulae in both caudate nuclei (CN) and substantiae nigrae (SN) were used to study the effects of naloxone and various opiates when applied into the left CN on the release of newly synthetized tritiated dopamine (DA) from nerve terminals and dendrites of the two nigro-striatal dopaminergic pathways. In all cases, the drugs (naloxone, opiates alone or in the presence of naloxone) were applied for 30 min into the left CN. When applied alone, naloxone (10(-6) M) induced a delayed reduction in tritiated DA release both in the ipsilateral and contralateral CN. These effects were seen after removal of the drug from the superfusion fluid. Complementary experiments made with tritiated naloxone (10(-6) M) revealed that the contralateral effect on DA release was not due to a diffusion of the opiate antagonist from its application site. Locally, D-Ala2, Met-enkephalinamide (D-Ala2, Met-Enk, 10(-6) M) and the potent delta agonist Tyr-D-Ser-Gly-Phe-Leu-Thr (DSThr, 5 X 10(-8) M) induced a biphasic increase in tritiated DA release. The local changes in tritiated DA release evoked by morphine (10(-6) M) and mu agonists such as Tyr-D-Ala-Gly-NH-C6H13 (10(-8) M) and fentanyl (10(-8) M) differed from those of delta agonists and furthermore differed from each other. For instance, morphine induced a delayed increase in tritiated DA release whereas a biphasic increase followed by a delayed inhibition occurred with fentanyl. Among all the opiates tested D-Ala2-Met-Enk was the only one which elicited a distal effect, that is a reduction of tritiated DA release in the ipsilateral SN. Marked differences in these opiates' effects on tritiated DA release occurred both locally and in distal structures when opiates were applied simultaneously with naloxone (10(-6) M). Locally, the changes induced by mu agonists were particularly altered since during morphine's application with naloxone a reduction of tritiated DA release occurred. In addition, the opiate antagonist prevented the second increase and the delayed inhibition of tritiated DA release evoked by fentanyl (10(-8) M). Interestingly, the combined application of naloxone with either D-Ala2, Met-Enk (10(-6) M), DSThr (5 X 10(-8) M) or morphine (10(-6) M) resulted in the appearance of changes in tritiated DA release in contralateral structures. The most striking effect was seen with D-Ala2, Met-Enk which enhanced tritiated DA release in the contralateral CN and SN. These results are discussed in the light of the involvement of several types of opiate receptors and of the polysynaptic pathways responsible for the distal changes in dopaminergic transmission.

Animals↗

Modulation of dopamine release in rat striatal slices by delta opiate agonists.

The effects of various opiates on the spontaneous release of [3H]dopamine ([3H]DA) continuously formed from [3H]tyrosine has been studied in rat striatal slices. Morphine (5 x 10(-6) M), fentanyl (5 x 10(-8) M) and the tripeptide Tyr-D-Ala-Gly-NH-CH(CH3)CH2-CH(CH3)2 (10(-6) M) were without effect, whereas D-Ala2-Met-enkephalinamide (3 x 10(-7) to 10(-5) M), D-Ala2-D-Leu2-enkephalin (5 x 10(-9) M) and the hexapeptide Tyr-D-Ser-Gly-Phe-Leu-Thr (10(-7) M) enhanced [3H]DA release in vitro. The D-Ala2-Met-enkephalinamide stimulation of [3H]DA release was not accompanied by any increase in [3H]DA synthesis and persisted in the presence of tetrodotoxin (5 x 10(-7) M). Naloxone (5 x 10(-7) M) completely blocked the effect of Tyr-D-Ser-Gly-Phe-Leu-Thre (10(-7) M) on [3H]DA release. However, the opiate antagonist did not affect the action of the hexapeptide or of D-Ala2-Met-enkephalinamide when used at a concentration equal to or lower than the agonist. This suggests that both peptides act on opiate receptors having a low sensitivity to naloxone. According to these various results and to the pharmacological characteristics of the opiates tested as described in peripheral organs or in the brain, it is concluded that opiates acting on delta opiate receptors may presynaptically regulate the release of DA in the striatum.

Animals↗