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S Przedborski

Publications and source records attributed to S Przedborski.

120 records · Page 7Linked to original sources
PubMed1989

Nervous system manifestations and neuroradiologic findings in acquired immunodeficiency syndrome (AIDS).

We report a series of thirteen patients with nervous system complications out of a total of thirty AIDS patients admitted to our hospital over the last two years for which CT and/or MRI have been performed. Five were homosexual men and eight patients (5 men, 3 women) were of African origin (Zaïre and Rwanda) (n = 5) or had had sexual intercourse with the local African population (n = 3). The nervous system complications encountered included: toxoplasma gondii brain abscess (2 patients); cryptococcus neoformans meningitis + toxoplasmosis (1 patient); toxoplasmosis + lymphoma (2 patients); progressive multifocal leucoencephalopathy (1 patient); lymphocytic meningitis or encephalitis (3 patients); lymphoma (1 patient); polyradiculoneuritis (3 patients). Three of thirteen patients had multiple intracranial abnormalities: one had concomitant intraparenchymal toxoplasma abscess and cryptococcal meningitis; in one patient a lymphoma developed after the successful medical treatment of a toxoplasma abscess; conversely, one patient developed a toxoplasma abscess two years after mediastinal radiotherapy for a systemic non-Hodgkin lymphoma. In conclusion, in our experience, nervous system toxoplasmosis is the most frequent AIDS related CNS complication. Our series demonstrates the high frequency of a second neurological disease occurring either concomitantly or separately. In these cases, while CT may readily identify the intracranial abnormalities, it contributes little towards an etiological diagnosis. Finally, our series illustrates the importance of a central African endemic focus for AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1989

The human protooncogene product p33pim is expressed during fetal hematopoiesis and in diverse leukemias.

We measured the human pim-1 protooncogene (PIM) expression during fetal development and in hematopoietic malignancies. Our data indicate that during human fetal hematopoiesis the 33-kDa pim product, p33pim, is highly expressed in the liver and spleen. In contrast, at the adult stage it is only slightly expressed in circulating granulocytes. Out of 70 hematopoietic malignancies analyzed, 51 patients and 19 cell lines, p33pim was overexpressed in approximately 30% of the samples, particularly in myeloid and lymphoid acute leukemias. This overexpression was unrelated to any stage of cellular differentiation and was not due to gene rearrangement or amplification. These results imply a physiological role of the pim-1 protooncogene during hematopoietic development and a deregulation in various leukemias.

Adult↗
PubMed1989

Lack of efficacy of phenytoin in the syndrome of inappropriate anti-diuretic hormone secretion of neurological origin.

Phenytoin has been proposed in the management of patients with the syndrome of inappropriate secretion of anti-diuretic hormone (SIADH) of neurological origin who fail to respond to water restriction. We have conducted a prospective study in order to evaluate the role of phenytoin in the management of seven consecutive patients with SIADH of neurological origin which could not be controlled by limited water intake. Only one patient was successfully treated with chronic phenytoin regimen. This patient, like one previously reported, had suffered a basal skull fracture. It seems likely that in the majority of cases of SIADH of neurological origin phenytoin is ineffective on a long-term basis.

Adult↗
PubMed1988

Effect of HECNU in malignant supratentorial gliomas--a phase II study.

Forty adults with recurring brain gliomas were treated with HECNU 130 mg/m2, given i.v. every 5 to 6 weeks (mean 5.4) and corticosteroids. According to the response to treatment, patients were divided in 3 groups: 1. Group 1 included 8 pts (20%) with objective remission, defined as a clear-cut clinical improvement persisting at least 4 weeks after the complete discontinuation of corticosteroids. 2. Group 2 included 14 patients (35%) who improved or remained stable yet stayed corticosteroid-dependent. 3. The 18 patients (45%) of group 3 failed to respond. There was a fair correlation between clinical and radiological response. Thus sequential CT-scans showed a 50 to 100% tumour reduction in all patients of group 1, and in 5 of group 2. CT-scans remained unchanged in 8 patients of group 2 and in one of group 3, and showed tumour progression in 10 patients of group 3. Drug toxicity appeared mild, reversible and was not cumulative. The better tolerance of HECNU could represent a real advantage of this drug over the commonly used nitrosourea derivatives such as BCNU and CCNU.

Adult↗
PubMed1988

Inflammatory demyelinating polyradiculoneuropathy associated with human immunodeficiency virus infection.

Five patients infected with immunodeficiency virus who were suffering from chronic polyradiculoneuropathy were investigated during evolution of the disease. Four of them were immunodeficient. The prominent neurological feature was distal and symmetrical weakness of the legs. After 5 months only one patient had improved. All patients had an increased protein level in the cerebrospinal fluid and pleocytosis. Electrodiagnostic studies and sural nerve biopsies indicated demyelination. Sural nerve viral cultures, including human immunodeficiency virus, were negative. The presence of circulating anti-peripheral nerve antibodies and of immunoglobulin deposits in nerve biopsy specimens was investigated by immunofluorescence techniques but failed to demonstrate any immunoreactivity.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Neuropeptide Y, somatostatin, and cholecystokinin neurone preservation in anaplastic astrocytomas.

Using immunohistochemistry, well-preserved neuronal cell bodies and fibres containing neuropeptide Y, somatostatin, and cholecystokinin immunoreactivity have been identified in all seven supratentorial anaplastic astrocytomas studied. These neurones have been shown not only on the edge but also in the depth of the neoplastic tissue. These neuropeptides were not present in 18 other intracranial tumours (3 astrocytomas, 1 subependymoma, 8 glioblastoma multiformes, 1 meningioma, and 5 metastases). In all 25 intracranial tumours studied, no immunoreactivity was found for vasoactive intestinal polypeptide, substance P, methionine-enkephalin, leucine-enkephalin, synenkephalin, neurophysin I-II, and corticotropin releasing factor.

Astrocytoma↗
PubMed1988

The effect of acute hemiplegia on intercostal muscle activity.

We recorded the EMG of parasternal intercostal muscles in 25 patients with flaccid hemiplegia during quiet spontaneous breathing, voluntary hyperventilation, and CO2-induced hyperventilation. The respiratory drive was abnormal on the hemiplegic side and the function of the intercostal muscles was affected specifically during voluntary hyperventilation.

Acute Disease↗
PubMedDate not supplied

Cholecystokinin octa- and tetrapeptide degradation by synaptic membranes. III. Inactivation of CCK-8 by a phosphoramidon-sensitive endopeptidase.

Solubilization of rat synaptic membranes by Triton X-100 followed by DEAE-cellulose chromatography allowed the separation of a phosphoramidon-sensitive endopeptidase that cleaved CCK-8. This enzymatic activity revealed similar if not identical to "enkephalinase A." A major cleavage point, at the Trp30-Met31 bond, and a minor one at the Tyr27-Met28 bond were identified in the sequence of CCK-8. Replacements of the Met28 and Met31 residues by Thr and either Leu or Nle respectively, in CCK-9 analogues, did not improve the resistance of these peptides to enzymatic degradation. The regional distribution in rat brain of this CCK-8 cleaving endopeptidase displayed marked variations with the highest activity in striatal membranes; it closely followed that described for "enkephalinase" in mouse brain.

Animals↗
PubMedDate not supplied

Neurotensin high affinity binding sites and endopeptidase 24.11 are present respectively in the meningothelial and in the fibroblastic components of human meningiomas.

The presence of neurotensin receptors and endopeptidase 24.11 (E-24.11) in 16 human meningioma specimens, obtained at surgery, was assessed by measuring the binding of 125I-[tyrosyl3]neurotensin(1-13) (125I-NT) and the inhibitor 3H-N(2RS)-3-hydroxyaminocarbonyl-2-benzyl-1-oxopropyl)glycine (3H-HACBO-Gly), for the receptor and enzyme, respectively. E-24.11 activity was also measured. Autoradiography, on the 16 meningiomas, showed that specific 125I-NT labeling (nonspecific labeling was assessed in the presence of excess NT) was exclusively located in the meningothelial regions. In contrast, specific 3H-HACBO-Gly labeling (nonspecific labeling was assessed in the presence of an excess of the E-24.11 inhibitor thiorphan) was exclusively found in fibroblastic regions. No specific labeling of either ligand was found on collagen or blood vessels. In vitro binding assays were performed on membranes of 10 of the 16 meningiomas. In the 4 meningiomas rich in meningothelial cells, 125I-NT specifically bound to one population of sites with Bmax ranging from 57 to 405 fmol/mg protein and Kd around 0.3 nM. These sites share common properties with the brain NT receptor, since the carboxy terminal acetyl NT(8-13) fragment bound to the same sites but with a higher affinity. The carboxy terminal analogue of NT, neuromedin N, also bound to the same sites with a 10-fold lower affinity and the sites were bradykinin and levocabastine insensitive. In the 4 meningiomas rich in fibroblastic cells, 3H-HACBO-Gly specifically bound to one population of sites with Bmax ranging from 251 to 739 fmol/mg protein and Kd around 2.8 nM.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Brain-derived neurotrophic factor inhibits apoptosis and dopamine-induced free radical production in striatal neurons but does not prevent cell death.

In hereditary Huntington's disease, a triplet repeat disease, there is extensive loss of striatal neurons. It has been shown that brain-derived neurotrophic factor (BDNF) protects striatal neurons against a variety of insults. We confirmed that BDNF enhances survival and DARPP-32 expression in primary striatal cultures derived from postnatal mice. Furthermore, BDNF inhibited intracellular oxyradical stress triggered by dopamine, and partially blocked basal and dopamine-induced apoptosis. Nevertheless, BDNF failed to rescue striatal neurons from dopamine-induced cell death. Therefore, BDNF inhibits free radical and apoptotic pathways in medium spiny neurons, but does so downstream from the point of commitment to cell death.

Animals↗
PubMedDate not supplied

A case of late onset striatonigral degeneration.

We report the case of a 78-year-old patient who had a parkinsonian syndrome which did not respond to levodopa treatment. The duration of the illness was four years. The main clinical features were bradykinesia and rigidity. He also showed pseudobulbar and pyramidal syndromes. The prominent pathological findings were a severe neuronal loss in the depigmented substantia nigra and in the putamen, which showed a brownish discoloration. Although the late age of onset is unusual, the findings suggest striatonigral degeneration. The link of this disease to multiple system atrophy is discussed.

Aged↗