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Biomedical subjects

T Wisniewski

Publications and source records attributed to T Wisniewski.

90 records · Page 5Linked to original sources
PubMed1992

Accumulation of alpha B-crystallin in central nervous system glia and neurons in pathologic conditions.

Alpha B-crystallin, a major protein of the vertebrate lens, is found in the central nervous system (CNS) and is a major protein component of Rosenthal fibers (RF), intracytoplasmic inclusions within astrocytes. Its level of expression in the normal CNS is low and appears to be confined to glial cells, both astrocytes and oligodendrocytes. A number of human brains displaying a variety of pathologic changes were examined by immunohistochemistry with an anti-alpha B-crystallin antiserum and increased immunoreactivity was found in astrocytes and oligodendrocytes without the formation of RFs. Furthermore, some neurons in neurodegenerative disorders were also immunolabeled with the anti-alpha B-crystallin antiserum. Thus, the accumulation of alpha B-crystallin appears to be part of the repertoire of reactive processes of CNS glial cells and some neurons in pathologic conditions.

Animals↗
PubMed1991

Peptides homologous to the amyloid protein of Alzheimer's disease containing a glutamine for glutamic acid substitution have accelerated amyloid fibril formation.

beta-Amyloid (A beta) deposition in fibril form is the central event in a number of diseases, including Alzheimer's disease (AD) and hereditary cerebral hemorrhage with amyloidosis - Dutch type (HCHWA-D). A beta is produced by degradation of a larger amyloid precursor protein (APP). Recently a mutation in the APP gene has been found in HCHWA-D causing a glutamine for glutamic acid substitution at residue 22 of A beta. The influence of this mutation on fibrillogenesis is not known, although it is clear that affected patients have accelerated cerebrovascular amyloid deposition, with disease symptoms early in life. We report the in vitro demonstration of accelerated fibril formation in a 28 residue synthetic peptide homologous to the Dutch variant A beta. Furthermore, in eight residue peptides homologous to A beta the presence of the mutation is necessary for fibril formation. These findings provide a mechanism for accelerated amyloid formation in the Dutch variant of APP.

Alzheimer Disease↗
PubMed1991

Inherited amyloids of the nervous system.

A diverse group of biochemically distinct proteins give rise to amyloids, each of which is associated with a different disease. These amyloid proteins share numerous properties and typically arise from the abnormal processing of an amyloid precursor protein. The classification, mechanisms and biochemistry of amyloid fibril formation are reviewed here, and two inherited types of amyloid affecting the nervous system are described.

Amyloid↗
PubMed1991

Lewy bodies are immunoreactive with antibodies raised to gelsolin related amyloid-Finnish type.

Lewy bodies (LB) are intraneuronal, cytoplasmic inclusion bodies. They are invariably present in Parkinson's and diffuse LB diseases. Their composition by direct biochemical methods is unknown, although LBs are immunoreactive with a number of antibodies, including anti-ubiquitin and anti-neurofilament antibodies. Familial amyloidosis, Finnish type (FAF), is an autosomal-dominant form of systemic amyloidosis. The authors have isolated and partially sequenced the amyloid. The protein has significant sequence identity with gelsolin, an actin-modulating protein. Rabbit polyclonal antibodies raised to the FAF amyloid not only immunostain the amyloid but also LBs in the cortex and substantia nigra of Parkinson's and diffuse LB disease brains. Immunoreactivity is absorbed by the purified amyloid but is unaffected by ubiquitin. This provides a link between the LB and one of the human amyloidoses, FAF.

Aged↗
PubMed1990

Pituitary hemorrhage into a Rathke's cleft cyst.

This report describes a case of symptomatic pituitary hemorrhage into a Rathke's cleft cyst in a 25-year-old woman. The literature on pituitary hemorrhage in nonadenomatous sellar tumors is reviewed.

Adult↗
PubMed1990

Intracerebral solitary plasmacytoma.

We report a rare occurrence of intraparenchymal plasmacytoma and review the literature. The clonal nature of the neoplasm is demonstrated by immunohistochemical and molecular techniques. The importance of the latter techniques in ruling out other pathological entities is stressed.

Blotting, Southern↗
PubMed1990

Clinical versus subclinical pituitary apoplexy: presentation, surgical management, and outcome in 21 patients.

A retrospective review of 16 consecutive patients with pituitary apoplexy treated over a 10-year period is reported. Eight men and 8 women (mean age, 48 years) underwent transsphenoidal decompression after an average duration of symptoms of 19 days. The diagnosis of pituitary apoplexy was made by the sudden onset of headache (88%), nausea (56%), or meningismus (13%), with or without visual disturbances (75%), in the setting of a sellar tumor on computed tomographic or magnetic resonance imaging scans. Thirteen of 16 patients showed significant improvement of symptoms after surgery (average follow-up, 2.5 years). In addition, 5 patients with clinically silent yet extensive pituitary hemorrhage were treated. Although extensive pituitary hemorrhage often produced fulminant apoplexy, it also presented insidiously over many days with few, if any, clinical signs. Rapid diagnosis, endocrine replacement, and transsphenoidal decompression constituted effective therapy. Magnetic resonance imaging (after at least 12 hours of symptoms) was superior to computed tomography in detecting hemorrhage.

Adenoma↗
PubMed1989

Isolated avulsion fracture of the anterior tubercle of the atlas.

Avulsion fracture of the tubercle of the atlas is a rare injury which is probably frequently overlooked. The fracture results from hyperextension of the neck against contraction of the long flexors. We describe two different fracture patterns and discuss the anatomical implications thereof.

Adult↗
PubMed1987

Institution-specific versus published in vitro antimicrobial susceptibility data in making formulary decisions.

The results of susceptibility testing of 549 isolates of gram-negative organisms to 17 antimicrobial agents were compared with published reports of the sensitivity of those organisms to those agents. All gram-negative bacilli isolated from cultures obtained from hospitalized patients during a three-month period were preserved for antimicrobial sensitivity testing. Standard Kirby-Bauer disk diffusion susceptibility tests were performed using 17 broad-spectrum antimicrobial agents that either were included in the hospital formulary or were being considered for inclusion. Organisms were recorded as being sensitive or resistant to each drug, and the results were compared with the published results of in vitro sensitivity studies. When the results of actual antimicrobial sensitivity testing varied from published results, the discordant results were assigned a ranking of 1 to 4 based on the percentage difference. In 34 of 77 drug-organism pairs tested, the results of susceptibility testing differed by more than 10% cumulative susceptibility from published values; 26 of these represented instances in which the results of actual testing were at least 10% less than published values. For seven of the antimicrobial agents that were being considered for inclusion in the hospital formulary, results indicating unexpectedly suboptimal activity against institutional pathogens were a determinant in eliminating the agents from further consideration. In vitro testing of antimicrobial susceptibility of local pathogens can be a better method of predicting the susceptibility of such pathogens to new antimicrobial agents than relying on published susceptibility data. Pharmacy and therapeutics committees should consider testing prevalent institutional pathogens for susceptibility to all antimicrobial agents that are proposed additions to the formulary.

Aminoglycosides↗
PubMed1984

Nurses' perceptions of early breast cancer and mastectomy, and their psychological implications, and of the role of health professionals in providing support.

The literature on the psychological precursors and outcomes of cancer and the role of the surgeon and nurse in the psychological management of early breast cancer, is briefly reviewed. A questionnaire study tapped nurses' perceptions of the disease and its treatment, patients' problems and the provision of psychological support. Their responses indicated mixed attitudes toward treatment outcomes, but a general enthusiasm for health education. Mastectomy itself was seen as posing serious social problems by half the sample, and serious sexual problems by more than three-quarters, and many felt that the support currently provided for patients is inadequate. While nurses saw themselves as having a key role in giving comfort, they were less likely to see themselves in the role of counsellor. Many of the sample felt that they had not been trained to provide psychological care at this level. Here, the skills of a specialist nurse were looked for, in the case of counselling the patient herself, or the authority of the doctor, when counselling husbands.

Breast Neoplasms↗
PubMed1981

Partial purification of neurofilament subunits from bovine brains and studies on neurofilament assembly.

The 200,000-dalton neurofilament subunit (P200) and the 160,000-dalton (P160) and 78,000-dalton (P78) neurofilament subunits were partially purified from bovine brain. Intact neurofilaments were prepared by high-speed and sucrose-zone centrifugation. The crude neurofilament was solubilized in 8 M urea solution containing pyridine, formic acid, and 2-mercaptoethanol. The solubilized neurofilament was purified by carboxymethyl (CM) cellulose column and hydroxylapatite column chromatography. The P200 was purified as separate from P160 and P78, but the P160 and P78 subunits were copurified on CM cellulose, hydroxylapatite, Bio-Gel A150m, and Sephadex G-150 column chromatography. Electron microscopy of these purified neurofilament subunits revealed the P200 subunit as a globular structure, and the P160 and P78 subunits as a rod-shaped structure extending up to 120 nm with a 8- to 12-nm width. In the presence of 200 mM KCl, 15 mM MgCl2, and 1 mM ATP, the purified subunits assembled into long filaments. Under the assembly condition, P160 and P78 subunits elongated up to 500 nm, but the longer filament formation required the presence of P200 subunits. The filaments formed in vitro were of two types: long straight filaments and intertwined knobby-type filaments. From these results, we have suggested that P160 and P78 form the neurofilament backbone structure and P200 facilitates the assembly of the backbone units into longer filaments.

Adenosine Triphosphate↗
PubMedDate not supplied

Gelsolin variant and beta-amyloid co-occur in a case of Alzheimer's with Lewy bodies.

Familial amyloidosis, Finnish type (FAF), is an autosomal dominant form of amyloidosis which is related to a point mutation in the gelsolin gene localized on chromosome 9. The mutation corresponds to codon 187 of the secreted form of gelsolin, and is expressed in the amyloid fibril at residue 15. Our original FAF patient was demented, and neuropathological analysis showed Alzheimer type brain lesions associated with both classical and cortical Lewy bodies. Furthermore, antiserum against the gelsolin-derived FAF amyloid reacted strongly with both classical and cortical Lewy bodies of this FAF patient. In preliminary experiments similar results were obtained in cases of Parkinson's disease and diffuse Lewy body disease. These observations may indicate a role for gelsolin in the pathogenesis of Parkinson's disease and related conditions.

Aged↗
PubMedDate not supplied

Alzheimer's disease and soluble A beta.

The discovery of soluble amyloid beta (sA beta) suggests that the role of amyloid in Alzheimer's disease (AD) is similar to the previously studied systemic amyloidoses and alters the notion that membrane damage is the initial event in AD. The disease state is characterized by the abnormal accumulation of a normal degradative peptide, which becomes resistant to further proteolysis due to a conformational change. Mutations in the beta PP gene have been found in a very small percentage of AD cases; hence other factors, both genetic and environmental, need to be identified. Priority needs to be given to detailed studies of the structural differences between sA beta and the A beta in amyloid deposits. This will help uncover the determining factors governing the aggregation of sA beta. These structural alterations may be critical for the possible toxic effects A beta and/or associated proteins (molecular chaperones, e.g., apolipoprotein E) have on brain cell function.

Alzheimer Disease↗