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E J Bartholomé

Publications and source records attributed to E J Bartholomé.

9 recordsLinked to original sources
PubMed2004

Could visual neglect induce amblyopia?

Oculomotor nerve disease is a common cause of diplopia. When strabismus is present, absence of diplopia has to induce the research of either uncovering of visual fields or monocular suppression, amblyopia or blindness. We describe the case of a 41-year-old woman presenting with right oculomotor paresis and left object-centred visual neglect due to a right fronto-parietal haemorrhage expanding to the right peri-mesencephalic cisterna caused by the rupture of a right middle cerebral artery aneurysm. She never complained of diplopia despite binocular vision and progressive recovery of strabismus, excluding uncovering of visual fields. Since all other causes were excluded in this case, we hypothesise that the absence of diplopia was due to the object-centred visual neglect. Partial internal right oculomotor paresis causes an ocular deviation in abduction; the image being perceived deviated contralaterally to the left. Thus, in our case, the neglect of the left image is equivalent to a right monocular functional blindness. However, bell cancellation test clearly worsened when assessed in left monocular vision confirming that eye patching can worsen attentional visual neglect. In conclusion, our case argues for the possibility of a functional monocular blindness induced by visual neglect. We think that in presence of strabismus, absence of diplopia should induce the search for hemispatial visual neglect when supratentorial lesions are suspected.

Adult↗
PubMed2003

Antiphospholipid antibodies and ischemic neuropathy following cardiac surgery.

Sciatic nerve palsy is an uncommon complication of cardiac surgery and is thought to be induced by a combination of reduced femoral artery blood flow, small vessel vascular disease or prolonged hypoxia. We here describe a new case which is the first described with transient elevation of antiphospholipid antibodies. Although transient elevation of lupus coagulation inhibitor is known to occur frequently in patients treated in an intensive care unit, there are very few data about the possible role of antiphospholipid antibodies in the generation of ischemic neuropathies. We can not prove that the ischemic neuropathy in our case has been favored by the presence of lupus coagulation inhibitor and antiphospholipid antibodies as the occurrence of the symptoms seemed to precede the transient elevation of lupus coagulation inhibitor. This case suggests that antiphospholipid antibodies and lupus coagulation inhibitor should be included in the work up of patients who present nerve damage after cardiac surgery but further studies are needed to ascertain this association.

Adult↗
PubMed2002

The cerebellum may be directly involved in cognitive functions.

Neuropsychological deficits may occur in infratentorial strokes. Only minor cognitive disturbances are reported in unilateral anterior cerebellar lesions. Here, the authors describe a patient with bilateral anterior ponto-cerebellar ischemic lesions associated with major neuropsychological deficits. Cerebral PET and SPECT demonstrated no metabolic defect in supratentorial areas.

Brain Ischemia↗
PubMed2001

Human monocyte-derived dendritic cells produce bioactive gelatinase B: inhibition by IFN-beta.

We studied the secretion of gelatinase B by dendritic cells (DC) generated by culturing human peripheral blood monocytes in granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4). First, we found the intracellular expression of gelatinase B on sections of fixed DC pellets. Zymography analysis of the supernatants of DC cultured for 72 h demonstrated the presence of gelatinase B. To determine if DC produce net enzymatic activity, bioactive gelatinase, a novel sensitive fluorescent-activated substrate conversion (FASC) assay was used to complement the zymography data. Culture media of unstimulated DC demonstrated reproducible net gelatinolytic activity. Tumor necrosis factor-alpha (TNF-alpha) IL-1beta but not lipopolysaccharide (LPS) stimulation caused a significant increase in gelatinase B production in zymography analysis. Both types of stimulation failed to increase net gelatinase activity in FASC assay. Interestingly, interferon-beta (IFN-beta) significantly diminished both the total zymolytic production and the net bioactive gelatinase produced by DC in a dose-dependent manner. We conclude that human monocyte-derived DC secrete bioactive gelatinase B and that IFN-beta inhibits this production.

Cells, Cultured↗
PubMed1999

IFN-beta interferes with the differentiation of dendritic cells from peripheral blood mononuclear cells: selective inhibition of CD40-dependent interleukin-12 secretion.

We studied the effects of interferon-beta (IFN-beta) on the differentiation of dendritic cells (DC) obtained by culturing plastic-adherent peripheral blood mononuclear cells (PBMC) from a total of 30 healthy volunteers in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4). First, we found that the addition of IFN-beta at the initiation of the culture did not modify DC morphology but caused a reproducible and statistically significant upregulation of HLA-DR, CD86, and CD80 surface expression. CD1a expression was significantly reduced, and CD40 expression was unchanged. We then determined the influence of IFN-beta on the production of cytokines by DC. DC differentiated in the presence of IFN-beta secreted significantly less IL-12 (p40 and p70) both spontaneously and on activation by fibroblasts transfected with the CD40L gene. This effect of IFN-beta was dose dependent and selective, as it was not observed for IL-6, IL-8, and tumor necrosis factor-alpha (TNF-alpha). As a consequence, DC differentiated in the presence of IFN-beta induced significantly less IFN-gamma secretion by alloreactive T cells, whereas they were more efficient than control DC in eliciting IL-5 secretion. We conclude that the direct action of IFN-beta on DC causes inhibition of their ability to secrete IL-12 in response to CD40 ligation and to elicit Th1 type responses.

CD40 Antigens↗
PubMed1999

Interferon-beta inhibits Th1 responses at the dendritic cell level. Relevance to multiple sclerosis.

Clinical studies have demonstrated beneficial effects of interferon-beta (IFN-beta) therapy in multiple sclerosis (MS) patients. However, the mechanism of action of IFN-beta in MS remains unknown. IFN-beta has even been demonstrated to enhance isolated T cell secretion of IFN-gamma, a cytokine proven to be deleterious in MS. However, IFN-beta inhibits IFN-gamma secretion of T cells, when they are stimulated by antigen presenting cells (APC). We therefore decided to study the effects of IFN-beta on the in vitro differentiation of dendritic cells (DC), a major class of APC. First, we found that the addition of IFN-beta at the initiation of the differentiation did not modify DC morphology, but enhanced the expression of molecules involved in antigen presentation (HLA-DR, B7/1 and B7/2). However, DC, differentiated in the presence of IFN-beta, secreted less interleukin-12 (IL-12) both spontaneously and upon activation by CD40-ligand bearing cells. As a consequence, DC differentiated in the presence of IFN-beta induced less IFN-gamma secretion by alloreactive T cells. We conclude that the direct action of IFN-beta on DC results in inhibition of their ability to secrete IL-12 and to elicit Thelper-1 (Th-1) type responses. These results are of particular interest in MS, in which a critical role for IL-12 has recently been suggested by a number of clinical and experimental observations.

Blood Donors↗