Search PubMed⌕ Search

Biomedical subjects

P Morin

Publications and source records attributed to P Morin.

At least 73 records · Page 4Linked to original sources
PubMed1992

Right motor neglect associated with dynamic aphasia, loss of drive and amnesia: case report and cerebral blood flow study.

A 30-year-old right-handed man had right motor neglect, amnesia, aphasia and loss of drive following bilateral thalamic and subthalamic infarctions. Serial resting cerebral blood flow (CBF) measurements with either Xenon 133 inhalation or positron emission tomography at 1, 8 and 10 months post-onset showed a widespread and long-lasting low CBF in the cortex. An additional CBF measurement, during motor tasks, showed a marked interhemispheric asymmetry in the pattern of activation: whereas left hand movement resulted in a CBF increase in contralateral superior rolandic and prerolandic areas, no significant regional CBF changes were seen during right hand movement, despite recovery from motor neglect. This loss of CBF increase in cortical motor and premotor areas during voluntary movement of the previously neglected side points to a disruption of cortico-subcortical pathways subserving motor activation. The pathophysiology of aphasia, loss of drive and amnesia as well as their relationships to motor neglect, may also be discussed on the basis of thalamo-cortical disconnections.

Adult↗
PubMed1992

[Familial parkinsonian syndrome with athymhormia and hypoventilation].

Five cases of parkinsonism with athymhormia observed in a single family are reported. Death caused by central respiratory disorders occurred after 6 to 8 years of progressive course. In 2 cases with autopsy, there was a severe neuronal loss predominant in the substantia nigra. Other brain stem nuclei (locus coeruleus, dorsal motor nucleus of the vagus nerve, nucleus of the tractus solitarius) were involved, as well as the striatum, pallidum and frontal cortex. No Lewy body was seen. In the surviving patient, positron emission tomography demonstrated, 4 years after the onset, a bilateral frontal hypometabolism. This disease is a rare variety of familial parkinsonism of dominant inheritance, already reported in 2 Canadian families by Perry et al. (1975) and Purdy et al. (1978) and in a family of West Virginia by Roy et al. (1988). The respiratory disorders can be explained by the involvement of the dorsal medullary nuclei. The peculiar neuropsychological disorder and motor slowing are best accounted for by the functional impairment of both motor and limbic striato-pallido-thalamo-frontal loops.

Cerebral Cortex↗
PubMed1991

Expression and tyrosine phosphorylation of the T cell receptor zeta-subunit in human thymocytes.

Recent evidence suggests that the zeta-subunit of the TCR complex plays a critical role in transducing signals initiated by the Ag receptor heterodimer. Because thymic maturation involves specific interactions between the TCR complex and thymic stromal cells, the zeta-subunit has been postulated to also play a role in this process. To assess the potential for zeta to contribute to thymocyte maturation, we have used an anti-zeta mAb (TIA-2) to quantitate its expression in mature (CD3bright) and immature (CD3dim and CD3-) populations of human thymocytes. Using both flow cytometric and immunoblotting analysis, we found that the relative expression of TCR-zeta varied directly with the surface expression of CD3. Importantly, TCR-zeta was detected in the majority of CD3- thymocytes, indicating that its expression precedes the surface appearance of CD3:TCR. In thymocytes, TCR-zeta was found to be constitutively phosphorylated on tyrosine residues. The relative expression of phospho-zeta varied directly with the maturational stage of the thymocyte, with the mature (CD3bright), single positive cells accounting for most of the phospho-zeta found in the human thymus. The expression of phospho-zeta could be significantly increased by activating thymocytes with mAb reactive with either CD3 or CD2. These results suggest that TCR-zeta is functionally linked to the major thymocyte activation receptors.

Cell Differentiation↗
PubMed1991

Specific gangliosides increase rapidly in rat liver following partial hepatectomy.

Rat liver gangliosides (sialic acid containing glycosphingolipids) were analyzed by HPTLC and HPLC following either partial hepatectomy or sham operation. Analysis of whole liver gangliosides by HPTLC demonstrated that within 6 h after partial (68%) hepatectomy, there was a significant increase in GM1 compared to both sham and control animals. By 48 h, GM1 was further increased and the polysialylgangliosides GD1a, GD1b and GT1b had also risen significantly, whereas changes in GM3 were negligible. Gangliosides associated with the plasma membrane were increased up to 3.5-fold in regenerating liver compared to sham-hepatectomized controls as assessed by HPLC. Although elevations in membrane gangliosides were associated with hepatocyte proliferation, they did not closely follow the growth curve. The time course of changes in ganglioside biosynthesis suggests differential upregulation of GM3 synthase and GD3 synthase in regenerating livers.

Animals↗
PubMed1991

[Aphasic disorders of written language].

After a short overview of classical neuropsychological knowledge about the disorders of written language, the authors review the data of cognitive psychology in this field. They first consider the general principles of cognitive analysis and then describe the specific syndromes of phonological and lexical routes impairment both in reading and writing. The possible correlations between these syndromes and other higher brain function impairments or anatomical localization are briefly considered. Finally an analysis of the impairments to peripheral writing processes, i.e. graphemic buffer and allographic conversion system syndromes, is given. In conclusion the contribution of cognitive psychology to daily neuropsychological practice is discussed.

Aphasia↗
PubMed1991

Tyrosine phosphorylation of the Fc gamma RIII(CD16): zeta complex in human natural killer cells. Induction by antibody-dependent cytotoxicity but not by natural killing.

NK cells are large granular lymphocytes capable of killing certain tumor cells and virally infected cells in a non-MHC-restricted manner. NK cells can also effect an antibody dependent cytotoxicity that is triggered by CD16, an FcR for IgG. In NK cells, CD16 is expressed in association with zeta, a signal transducing subunit of the TCR complex. Here we show that, just as T cell activation via the TCR complex results in tyrosine phosphorylation of zeta TCR, NK cell activation via CD16 results in tyrosine phosphorylation of zeta NK. Whereas antibody-dependent cytotoxicity also results in tyrosine phosphorylation of zeta, natural cytotoxicity does not. Our results indicate that zeta functions as a transducing element for antibody dependent, but not antibody independent killing by NK cells. Consequently, NK cells are likely to express at least two distinct receptor complexes capable of triggering cytolytic effector function.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1991

[Severe amblyopia and Alzheimer' disease].

A 69-year-old woman developed a rapid and severe visual loss and became nearly blind in a few weeks. As she also presented with memory loss and other disturbances of cognitive functions, with progressive deterioration over one year, a probable Alzheimer's disease was diagnosed. Cerebral CT scan and magnetic resonance imaging were normal. However, clinical and electrophysiological (visual evoked potentials) data indicated an impairment of the primary visual pathways rather than a degeneration of the secondary visual cortex. This case is compared with and discussed in relation to recent reports concerning retinal and optic nerve damage in Alzheimer's disease.

Aged↗
PubMed1991

[Thrombotic thrombocytopenic purpura. A case diagnosed by MRI].

A 67-years old woman developed sudden headache and transient vertigo. One week later, left arm paresis appeared and the patient became comatose. Investigations showed thrombocytopenia with hemolytic anemia and the presence of numerous irregularly contracted red cells (schizocytes). This was consistent with the diagnosis of thrombotic thrombocytopenic purpura. As focal neurological manifestations and widespread mental changes were still present when she emerged from coma, magnetic resonance imaging was performed showing numerous small infarcts in the white and grey matters.

Aged↗
PubMed1990

Administration of thyrotropin-releasing hormone into the central nucleus of the amygdala induces gastric lesions in rats.

Studies utilizing microinjections of thyrotropin-releasing hormone (TRH) were performed to determine potentially sensitive limbic brain sites to the ulcerogenic effect of TRH. Administration of TRH into the central nucleus of the amygdala (CEA) produced a high (80%) incidence of gastric lesions and also significantly stimulated acid secretion. Microinjections of TRH into other brain sites including superior colliculus, medial septum, substantia nigra and the hippocampus (CA1 area) were ineffective. Intra-CEA TRH-induced gastric lesions and acid secretion were prevented by vagotomy. These results indicate that the amygdala is of importance for mediating the ulcerogenic effect of brain TRH through peripheral vagal pathways.

Amygdala↗
PubMed1990

Brain ACTH prevents stress gastric lesions in rats.

This study evaluated the effect of ACTH and several ACTH fragments on the development of gastric glandular lesions induced by cold-restraint stress in rats. Intracerebroventricular administration of ACTH1-39 dose-dependently (0.1-10 micrograms) inhibited stress gastric lesion formation. Studies with smaller molecular weight forms of ACTH (in a dose equimolar to 10 micrograms of ACTH1-39) revealed that ACTH1-13 and ACTH1-10 were also protective. The ACTH fragments ACTH5-10, ACTH34-39 and ACTH1-17 were without effect. Immunoneutralization of endogenous brain ACTH1-39 significantly increased stress gastric lesion severity. Antisera raised against synthetic somatostatin, gonadotropin-releasing hormone, and L-enkephalin were ineffective. These results with ACTH coupled with our previous demonstration of a protective effect of beta-endorphin suggest that specific brain pro-opiomelanocortin gene products modulate gastric mucosal integrity in response to stress.

Adrenocorticotropic Hormone↗