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At least 91 records · Page 5Linked to original sources
PubMed1991

The function of the CD2 protein is abnormal in multiple sclerosis.

In active multiple sclerosis (MS), T cell adhesion to sheep red blood cells (SRBC) is deficient. The CD2 protein mediates adhesion to SRBC. Since ligands that bind CD2 can activate T cells, we studied adhesion and activation through CD2 in leukocytes from MS patients. Mononuclear cells (MNC) from patients with MS formed markedly fewer avid T cells (TA; T cells binding greater than or equal to 10 SRBC) than MNC from controls. CD2 antigen expression as measured by FACS analysis on T cells and on T cell subsets was equivalent in MS and controls and rose to a comparable extent in both groups after cell activation; yet activated MS MNC continued to form fewer TA than control cells. Avid rosette formation may be reduced by prostaglandins (PG) secreted by monocytes. Exposure to PG in vitro decreased TA% only in controls, suggesting refractoriness to exogenous PG in MS, perhaps because endogenous PG had already acted. The finding that indomethacin increased TA in MS cells favors this formulation. MNC were activated through CD2 using mAb 9-1 paired with mAb 9.6. Proliferation was significantly diminished in MNC from MS patients compared to MNC from normal controls. Thus, even though T cell membrane expression of CD2 appeared normal in MS, adhesion to SRBC and activation through the CD2 protein were defective.

Alprostadil↗
PubMed1991

Multiple growth abnormalities in vascular smooth muscle from spontaneously hypertensive rats.

1. In tissue culture the growth characteristics of aortic smooth muscle cells isolated from spontaneously hypertensive rats (SHR) were compared with those of normotensive Wistar-Kyoto (WKY) rats. 2. Aortic smooth muscle cells from SHR exhibit enhanced proliferation when grown in the presence of low (1%) and moderate (5%) concentrations of fetal calf serum. 3. Cell quiescence in cultures of smooth muscle from SHR becomes apparent at cell densities approximately 20% higher than in cultures from WKY rats. 4. These different growth characteristics of smooth muscle between the two strains of rats may contribute to the early pre-hypertensive development of vascular hypertrophy in the SHR.

Animals↗
PubMed1979

Renal vein thrombosis: an underdiagnosed complication of multiple renal abnormalities.

Thirty-one cases of renal vein thrombosis (RVT) were reviewed retrospectively for clinical laboratory, and radiographic findings. An underlying renal disorder was present in 28 cases, absent in only 3. This supports other evidence that RVT is usually a complication of renal disease rather than a primary event, and that nephrotic syndrome may be due to renal disease rather than RVT. The findings also confirmed the large spectrum of urographic appearances in RVT, and were used as a basis for developing specific and liberal indications for renal venography.

Humans↗
PubMed1992

Structural brain correlates of neurologic abnormalities in multiple sclerosis.

We examined the relationship between cerebral magnetic resonance imaging (MRI) findings and urinary dysfunction in 70 consecutive patients with definite multiple sclerosis. MRI-weighted lesion scores for seven different brain regions were recorded according to the number and size of cerebral lesions. Thirty-two subjects (46%) had urinary symptoms and 38 (54%) were asymptomatic. Subjects with urinary symptoms exhibited greater overall functional disability and a higher midbrain MRI-weighted lesion score than asymptomatic patients. No statistically significant group differences were found for the other brain regions.

Adolescent↗
PubMed1977

Multiple leukocyte abnormalities in chronic granulomatous disease: a familial study.

A variety of leukocyte enzyme activities were studied in an 11-year-old female with chronic granulomatous disease (CGD) and several members of her family. Leukocyte glucose-6-phosphate dehydrogenase (G-6-PD) activity was 17 nmol/min/mg protein in the patient; two brothers with symptoms of recurrent bacterial infections have G-6-PD activities of 58 and 37 nmol/min/mg protein; the activites of this enzyme in both parents, maternal grandmother, and one additional brother were within normal limits. Storage at 4 degrees or heating at 37 degrees over a 120-min period revealed a marked lability of G-6-PD activity in the patient's cells which could not be stabilized by the addition of NADP and 2-mercaptoethanol; this lability was not seen in other family members tested. Activities of leukocyte glutathione reductase were reduced in both parents and the two affected male siblings with values of 18, 23, 23, and 24 nmol/min/mg protein, respectively. Activities of leukocyte glutathione peroxidase were reduced in all of the immediate family members tested, with values ranging from 11.2 to 43 nmol/min/mg protein; the activity of this enzyme in the patient was 38.5. Leukocyte NADP content in the patient, father, and two affected male siblings were 16.5, 23.4, 22.2, and 28.2 nmol/15 min/10(7) leukocytes, respectively.

Adolescent↗
PubMed1977

Anaesthetic considerations on von Recklinghausen's disease (multiple neurofibromatosis). Abnormal response to muscle relaxants.

Two cases of abnormal response to muscle relaxants in patients with von Recklinghausen's disease are reported and the literature is reviewed. A 31 year-old female showed high sensitivity to both suxamethonium and tubocurarine, and 57 year-old male showed also high sensitivity to tubocurarine. Anaesthetic problems which might be encountered in patients with von Recklinghausen's disease are concomitant phaeochromocytoma, renal hypertension, kyphoscoliosis, deformity of the spine, and intralaryngeal neurofibroma.

Adult↗
PubMed1992

[The state of the immune system in children with congenital abnormalities].

As many as 618 children with different varieties of congenital developmental abnormalities were examined for the status of the immune system. Immunologic studies were carried out in 89 patients. They included the NBT test, determination of the content of T-, B- and O-lymphocytes, IgA, IgM and IgG. Morpho-histological studies of the spleen and thymus were performed according to the data of 529 autopsies. It has been established that 3/4 of cases with congenital developmental abnormalities are characterized by morphofunctional immune deficiency, which is more pronounced in multiple abnormalities (of chromosomal etiology in particular) as well in some systemic abnormalities, largely of the CNS.

Abnormalities, Multiple↗
PubMed1979

Trisomy 8p due to the 3:1 segregation of the balanced translocation t(8;15)mat.

An additional small G-like chromosome was found in a newborn female with multiple abnormalities and hemorrhagic diathesis. G banding showed that the index patient was trisomic for the short arm of chromosome 8 and revealed the anomaly t(8;15)(q12;p11) in her mother. The relationship between chromosome 8 and multiple hemorrhages is discussed.

Abnormalities, Multiple↗
PubMed1991

Multiple sclerosis with abnormal cerebrospinal fluid--a case report.

Multiple sclerosis is an uncommon demyelinating condition in Singapore. The commonest mode of presentation here is in the form of Devic's syndrome. Although our patients here have shown classical findings with respect to clinical features, neuroimaging studies and electrophysiologic tests, abnormal cerebrospinal fluid changes have not been reported locally. We report the first case of multiple sclerosis with abnormal cerebrospinal fluid changes. We also reviewed cerebrospinal fluid changes in multiple sclerosis and recent advances in laboratory techniques of cerebrospinal fluid analyses.

Adolescent↗
PubMed1991

The evaluation of the germinal mutagenic impact of Chernobyl radiological contamination in Hungary.

The genetic consequences of radioactive fall-out deposition from the Chernobyl (USSR) accident in Hungary was evaluated as a part of the ongoing programme on the population-based Hungarian Surveillance of Germinal Mutations. The surveillance is based on three groups of indicator conditions: 15 sentinel anomalies (indicators of germinal dominant gene mutations), Down's syndrome (an indicator of germinal numerical and structural chromosomal mutations) and unidentified multiple congenital abnormalities (indicators of germinal dominant gene and chromosomal mutations). Cases with these indicator conditions were selected from the material of the Hungarian Congenital Abnormality Registry. After the diagnostic accuracies were checked, familial and sporadic cases were separated. Only the latter group was evaluated for evidence of new mutations. The analysis did not reveal any measurable germinal mutagenic effects of the Chernobyl accident. Furthermore, there were no significant differences in the rates of these three groups of indicator conditions between regions with higher and lower increased background radiation.

Abnormalities, Multiple↗
PubMed1990

[Contribution of magnetic resonance imaging in 100 cases of refractory partial epilepsy with normal CT scans].

One hundred epileptic patients were included in this study according to the following criteria: intractable partial epilepsy, normal CT scan and focal EEG abnormalities. Eighty-nine patients were suffering from complex partial seizures of temporal or frontal origin, 55 and 34 cases respectively. Eleven patients presented with only simple partial seizures. MRI was abnormal in 31 patients. The abnormalities were: focal T2 increased signal intensity (13 cases) most often temporal (10 cases), cryptic arteriovenous malformation (4 cases), focal T1 and T2 signal abnormality (4 cases), focal atrophy (2 cases) and multiple abnormal T2 signals scattered in the white matter (8 cases). The site of MRI abnormalities was consistent with electroclinical data in 22 patients, of whom 20 had a temporal lobe epilepsy. Thus MRI proved to be more often abnormal in temporal than in frontal lobe epilepsy (36 p. 100 and 5.9 p. 100 respectively) when the CT scan is normal. However MRI data, particularly focal T2 hypersignals should be confronted to electroclinical and metabolic findings whenever functional surgery is considered.

Adolescent↗
PubMed1991

Lysosomal hydrolases of different classes are abnormally distributed in brains of patients with Alzheimer disease.

beta-Amyloid formation requires multiple abnormal proteolytic cleavages of amyloid precursor protein (APP), including one within its intramembrane domain. Lysosomes, which contain a wide variety of proteases (cathepsins) and other acid hydrolases, are major sites for the turnover of membrane proteins and other cell constituents. Using immunocytochemistry, immunoelectron microscopy, and enzyme histochemistry, we studied the expression and cellular distributions of 10 lysosomal hydrolases, including 4 cathepsins, in neocortex from patients with Alzheimer disease and control (non-Alzheimer-disease) individuals. In control brains, acid hydrolases were localized exclusively to intracellular lysosome-related compartments, and 8 of the 10 enzymes predominated in neurons. In Alzheimer disease brains, strongly immunoreactive lysosomes and lipofuscin granules accumulated markedly in the perikarya and proximal dendrites of many cortical neurons, some of which were undergoing degeneration. More strikingly, these same hydrolases were present in equally high or higher levels in senile plaques in Alzheimer disease, but they were not found extracellularly in control brains, including those from Parkinson or Huntington disease patients. At the ultrastructural level, hydrolase immunoreactivity in senile plaques was localized to extracellular lipofuscin granules similar in morphology to those within degenerating neurons. Two cathepsins that were undetectable in neurons were absent from senile plaques. These results show that lysosome function is altered in cortical neurons in Alzheimer disease. The presence of a broad spectrum of acid hydrolases in senile plaques indicates that lysosomes and their contents may be liberated from cells, principally neurons and their processes, as they degenerate. Because cathepsins can cleave polypeptide sites on APP relevant for beta-amyloid formation, their abnormal extracellular localization and dysregulation in Alzheimer disease can account for the multiple hydrolytic events in beta-amyloid formation. The actions of membrane-degrading acid hydrolases could also explain how the intramembrane portion of APP containing the C terminus of beta-amyloid becomes accessible to proteases.

Aged↗