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Biomedical subjects

J M Powers

Publications and source records attributed to J M Powers.

At least 19 recordsLinked to original sources
PubMed1992

Immunohistochemistry and proliferative activity in Lhermitte-Duclos disease.

We have evaluated a recurrence of Lhermitte-Duclos disease by immunohistochemistry for Purkinje cell markers and proliferative activity (proliferating cell nuclear antigen), by electron microscopy and for DNA ploidy (image analysis). While most of the abnormal neurons in the lesion appear to be derived from granule cells, several Purkinje cell specific polyclonal and monoclonal antibodies, including L7, PEP 19 and calbindin, labeled a minor subpopulation. Staining with monoclonal antibodies to proliferating cell nuclear antigen and measuring cell DNA index and ploidy with a cell image analyzer revealed no proliferative activity. Electron microscopy findings were similar to those previously reported. In spite of its recurrence, our findings support the notion that Lhermitte-Duclos disease is malformative, not neoplastic, and that the characteristic neurons are derived predominantly but not exclusively from a non-Purkinje cell source, probably the granule cell.

Brain↗
PubMed1992

Phospholipids in X-linked adrenoleukodystrophy white matter: fatty acid abnormalities before the onset of demyelination.

Changes in fatty acid composition of complex lipids were analyzed in postmortem white matter from a patient with late onset adrenoleukodystrophy (ALD). The specimen showed three regions with progressive myelin breakdown: morphologically normal white matter; areas with active demyelination and perivascular lymphocyte and macrophage infiltration; and areas with marked gliosis. In the morphologically intact region, cholesterol esters were similar in amount and fatty acid composition to those in control tissue, although marked changes were observed in the actively demyelinating area. Galactolipids in these areas were also similar to those in controls. In contrast, glycerophospholipids were increased in amount and in very long chain fatty acids (VLCFA), which are the hallmark of ALD, at the active edge of the demyelinative lesion and even in the apparently intact sample. Further fractionation of the glycerophospholipids by high performance liquid chromatography showed a significant (up to 39-fold) accumulation of hexacosanoic acid (C26:0) in phosphatidylcholine, but not in other phosphatidyl derivatives. The consistent increases in phosphatidylcholine VLCFA in all samples from the ALD brain, which are postulated to represent progressive stages in the development of the disorder, suggest that phosphatidylcholine may be involved in antigen formation and may underlie an immunological basis for the pathogenesis of ALD.

Adrenoleukodystrophy↗
PubMed1992

Progressive multifocal leukoencephalopathy in patients with human immunodeficiency virus.

Lesions of progressive multifocal leukoencephalopathy (PML) in patients infected with the human immunodeficiency virus (HIV) often have mononuclear cell infiltrates so intense that they obscure the nature of the lesion. This response may be especially prominent in stereotactic biopsies of contrast-enhancing areas. Of 10 consecutive PML lesions biopsied stereotactically, three were markedly, two were moderately, and five were mildly inflamed. There were few to no enlarged oligodendrocytic nuclei with inclusions in the markedly and moderately inflamed lesions. We investigated all biopsies with immunoperoxidase, DNA in situ hybridization, polymerase chain reaction, and Southern immunoblot methodologies for toxoplasmosis and the following viruses: JC, cytomegalovirus, herpes simplex viruses I and II, and human T-cell lymphotropic viruses I, II, and III. We confirmed the presence of JC virus in each lesion; polymerase chain reaction revealed HIV genome only in one. Inflammatory PML lesions in HIV+ patients do not reflect co-infection with toxoplasmosis or viruses commonly seen in these patients. The mononuclear cells are primarily T lymphocytes. Patients with severely inflamed PML lesions, whether HIV+ or not, often show stabilization of symptoms with or without antiviral treatment and have longer lengths of survival than patients with less inflamed lesions.

Adult↗
PubMed1992

Bond strength of composite to porcelain treated with new porcelain repair agents.

In vitro tensile bond strengths of composite to porcelain were evaluated using three pretreatments (HF etching, sandblasting, diamond abrasion) of the porcelain, four bonding agents (Clearfil Porcelain Bond, Porcelain Liner M, Porcelain Liner M with Super-Bond C&B, and Scotchprime) and two storage conditions (24 h and thermocycling). The overall coefficient of variation was 27%. Significant differences among bond strengths were observed, with storage condition being the most important factor, followed by bonding agent and then pretreatment. Thermocycling decreased the bond strength of all samples, but samples treated with Scotchprime were affected least. For 24 h storage, Clearfil Porcelain Bond and Scotchprime had bond strengths above 23 MN/m2 to sandblasted porcelain.

Analysis of Variance↗
PubMed1992

Bond strength of composites to etched and silica-coated porcelain fusing alloys.

In vitro bond strengths of two composite veneering materials to two porcelain fusing alloys were measured utilizing two storage conditions. The alloys were etched or treated with silica applied by blasted, thermal or pyrogenic techniques and then silanated. Bond strengths were higher for the Ni-Cr-Be than the Au-Pd alloy with most values greater than 18 MPa. Bond strengths to etched and silanated Au-Pd alloy were low (less than 6.5 MPa), whereas samples treated with silica and silanated had significantly higher values. Bond strengths to the Ni-Cr-Be alloy were highest with the thermal and pyrogenic silica treatments. After thermocycling, most bond strengths to the Au-Pd alloy decreased, but were the same or higher to the Ni-Cr-Be alloy. Cohesive failures of the opaquers were observed.

Analysis of Variance↗
PubMed1992

The inflammatory myelinopathy of adreno-leukodystrophy: cells, effector molecules, and pathogenetic implications.

Prominent inflammation in the demyelinative lesion of adreno-leukodystrophy (ALD) has suggested an immune-mediated pathogenetic component. Commercially available antibodies to T cells, B cells, macrophages, class I and II molecules, complement, IgG, IgM, IgA, interleukin-1 (IL-1), intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-alpha (TNF) were applied to paraffin sections of formaldehyde-fixed postmortem samples. Twenty-five primary demyelinative lesions from five juvenile ALD, three adult ALD, and three adrenomyeloneuropathic patients were evaluated with appropriate positive and negative controls. Macrophages and astrocytes were the predominant cells detected at the active edge; T lymphocytes, including T4 and CD45R subsets, were nearly as numerous but usually located around vessels within the lesion. B cells and plasma cells, usually containing IgG, were uncommon. The expression of class II molecules, restricted to one adult, was problematic; class I expression was increased in microvascular and other cells. Degraded myelin was labeled with antibodies to C3d and IL-1; IL-1 and ICAM-1 immunoreactivity was seen on microvessels and astrocytes. Tumor necrosis factor-alpha immunoreactivity was detected in macrophages, but more prominently in astrocytes. These data support a natural immune response in the demyelinative lesion of ALD, consisting predominantly of reactive astrocytes, macrophages, T cells and cytokines. A two-stage pathogenetic theory is discussed. The postulated roles of TNF and reactive astrocytes, in concert with a fundamental myelinolytic biochemical defect, suggest a different pathogenetic mechanism and raise novel therapeutic possibilities.

Adrenoleukodystrophy↗
PubMed1992

The in vivo wear resistance of 12 composite resins.

PURPOSE: The in vivo wear resistance of 12 composite resins were compared with an amalgam control using the Latin Square experimental design. Sixteen edentulous patients wearing specially designed complete dentures formed the experimental population. MATERIALS AND METHODS: The Michigan Computer Graphics Measurement System was used to digitize the surface of the control and composite resin samples before and after 3-month test periods to obtain wear data. The 12 composite resins selected for this investigation based on their published composite classification types were seven fine particle composites, three blends, and two microfilled composite resins. The Latin Square experimental design was found to be valid with the factor of material being statistically different at the 5% level of significance. Wear was computed as volume loss (mm3/mm2), and all of the composites studied had more wear than the amalgam control (P = .001). RESULTS: After 3 months, the mean (error) of wear of the amalgam was 0.028 (0.006). Means (error) of wear for the 12 composites were ranked from most to least wear by mean wear volume loss. CONCLUSION: The absence of any relationship between mean wear volume loss and the volume percentage filler was confirmed by the correlation coefficient r = -0.158.

Analysis of Variance↗
PubMed1992

Relative fit of new denture resins polymerized by heat, light and microwave energy.

This study compared in vitro the relative fit of seven denture resins polymerized by different methods to their gypsum casts. Relative fit in the molar-to-molar region of the resin bases on their stone casts was evaluated independently by five evaluators at three times (after processing, after polishing and after storage in water) and ranked using non-parametric statistics. The denture resins polymerized by microwave energy, (Acron MC), low heat, (Perform, 45 degrees C), and visible light, (Triad) fit better after polishing and after storage in water than those resins polymerized at higher temperatures (Lucitone 199, 74 degrees C and Accelar 20, Compak and Permacryl 20, 100 degrees C). The traditional heat-polymerized resin (Lucitone) had an average fit after storage in water.

Acrylic Resins↗
PubMed1992

Cellular tropism and localization in the rodent nervous system of a neuropathogenic variant of Friend murine leukemia virus.

BACKGROUND: We studied PVC-211 murine leukemia virus (MuLV) (1), a neuropathogenic variant of Friend MuLV, to determine its cellular tropism and distribution in the nervous system of infected rats and the factors that affected disease expression. EXPERIMENTAL DESIGN: Rats from five different strains and mice from 3 strains were inoculated intracerebrally or intraperitoneally from birth to 10 days of age and observed for signs of neurologic disease and tumors for 24 weeks. Nervous system pathology, MuLV gp70 expression, and virus production were evaluated weekly for 4 weeks after perinatal infection of Fisher (F344) rats. Blood-brain-barrier integrity and ultrastructure were evaluated in 21-day-old symptomatic infected rats. Microvessel and mixed glial cell cultures were prepared from brains of infected and uninfected 21-day-old F344 rats and evaluated for virus production, MuLV gp70 expression, and the presence of PVC-211 MuLV DNA. RESULTS: Tremor, ataxia, spasticity, and hindlimb weakness occurred in rats and mice as early as 3 weeks after neonatal infection. Severity, latency, and progression varied among mouse and rat strains but exposure to PVC-211 MuLV before 6 days of age was required for disease expression. Rapid PVC-211 MuLV replication in brain capillary endothelial cells (BCEC) early in the perinatal period was followed by widespread astrogliosis, neuropil vacuolation, and finally, neuronal degeneration in the spinal cord, brainstem, cerebellum, and subcortex. MuLV gp70 expression in vivo increased during infection, was restricted to BCEC, but was not associated with perivascular inflammatory infiltrates. BCEC cultured from microvessel preparations but not astrocytes or microglia in mixed glial cell cultures isolated from infected rats contained PVC-211 MuLV DNA, expressed MuLV gp70, and produced infectious virus. CONCLUSIONS: The rapid replication of PVC-211 MuLV that occurs in the nervous system of infected rodents is restricted to BCEC. These infected BCEC appear to play a critical role in initiating the astroglial response in this neurodegenerative process through mechanisms that remain to be defined.

Animals↗
PubMed1991

Intracerebral Hodgkin's disease in a human immunodeficiency virus-seropositive patient.

Intracerebral involvement of Hodgkin's disease (HD) is rarely described, with only 42 cases in the literature. Since the outbreak of the acquired immune deficiency syndrome (AIDS) epidemic, there has been an increasing number of human immunodeficiency virus (HIV)-infected (HIV+) persons who have diffuse non-Hodgkin's lymphoma and, more recently, atypical aggressive HD. The authors report the case of a patient with a history of intravenous drug abuse (IVDA) and Stage IVB HD who, after a drug-induced clinical remission, had intracerebral mixed-cellularity HD. This appears to be the first report of intracerebral HD in a person who is HIV+.

Adult↗
PubMed1991

Concomitant Creutzfeldt-Jakob and Alzheimer diseases.

We report a 69-year-old female with cerebral and cerebellar symptomatology of 15-month duration. At autopsy, both panencephalopathic Creutzfeldt-Jakob and plaque-predominant Alzheimer diseases were found. Plaque amyloid was exclusively of the beta/A4 type, but abundant abnormal protease-resistant protein was identified by Western blot analysis of brain extracts.

Aged↗
PubMed1991

Spreading of oligomers on polymers.

The successful repair of a composite restoration may depend on the ability of a repair composite to spread on the restoration to be repaired. The purpose of this study was to measure the spreading of four oligomers on their polymers. The oligomers were: ethoxylated bisphenol A dimethacrylate (EB), BisGMA/3EDMA:70/30 (ED), BisGMA-Nupol (NU), and urethane dimethacrylate (UD). Polymer strips were made from these oligomers by light-curing. Spreading was calculated from measurements of the contact angle of the oligomers on the polymers, the surface tension of the oligomers, and the viscosity of the oligomers. In this model system, values of spreading of EB, ED, UD, and NU on oligomer ED were: 2.8, 1.4, 0.24, and 0.0009 cm/s, respectively. The spreading by oligomers EB, ED, and UD on polymer ED was slightly higher than that on polymer UD.

Analysis of Variance↗
PubMed1991

The metabolic landscape of cortico-basal ganglionic degeneration: regional asymmetries studied with positron emission tomography.

Regional metabolic rate for glucose (rCMRGlc) was estimated using [18F]fluorodeoxyglucose (FDG) and positron emission tomography (PET) in five patients (four men, one woman; mean age 68; mean disease duration 2.4 years) with clinical findings consistent with the syndrome of cortico-basal ganglionic degeneration (CBGD). Left-right rCMRGlc asymmetry, (L-R)/(L + R) x 100, was calculated for 13 grey matter regions and compared with regional metabolic data from 18 normal volunteers and nine patients with asymmetrical Parkinson's disease (PD). In the CBGD group mean metabolic asymmetry values in the thalamus, inferior parietal lobule and hippocampus were greater than those measured in normal control subjects and patients with asymmetrical PD (p less than 0.02). Parietal lobe asymmetry of 5% or more was evident in all CBGD patients, whereas in PD patients and normal controls, all regional asymmetry measures were less than 5% in absolute value. Measures of frontal, parietal and hemispheric metabolic asymmetry were found to be positively correlated with asymmetries in thalamic rCMRGlc (p less than 0.05). The presence of cortico-thalamic metabolic asymmetry is consistent with the focal neuropathological changes reported in CBGD brains. Our findings suggest that metabolic asymmetries detected with FDG/PET may support a diagnosis of CBGD in life.

Aged↗
PubMed1991

Non-neoplastic pineal cysts.

We identified 53 patients with non-neoplastic cysts of the pineal gland. In contrast to patients with pineal neoplasms, pineal cysts are usually asymptomatic. They infrequently obstruct the aqueduct to cause hydrocephalus or compress the tectum to produce the neuro-ophthalmologic signs of dorsal midbrain dysfunction. Obstructive hydrocephalus was present in only five patients (9.4%); three of them showed clinical signs of Parinaud's syndrome. CT and MRI typically reveal a cystic mass that averages 1.6 cm in anteroposterior (A-P) diameter with calcification at the periphery and faint rim-like contrast enhancement. Sagittal MRI is the most useful diagnostic test because it shows the anatomic relationship of the cyst to the aqueduct. The mass may compress the tectum and distort the proximal aqueduct; occasionally a large cyst may occlude the aqueduct. All patients with obstructive hydrocephalus had cysts greater than 2.0 cm in A-P diameter. Nine patients had suboccipital craniotomy. In all of them, the cysts contained clear fluid and were easily removed. We advocate conservative management with clinical observation of these benign lesions that may be developmental variants of normal pineal gland.

Adolescent↗
PubMed1991

Bond strength of repaired glass ionomer core materials.

Chelon Silver (C), Ketac-Silver Aplicap (K), Miracle Mix (M) silver-reinforced glass ionomers, and Valiant PH.D were evaluated as in vitro repair materials for cores. The core materials were placed in a 6 x 3 mm mold and stored at 37 degrees C at 100% RH for 24 hours. The cores were roughened with a coarse diamond. Five samples were conditioned (T) with Dentin Conditioner for 20 seconds, whereas another 5 samples were untreated (U). The cores were then repaired with C, K and M and subsequently tested after additional storage for 24 hours. Bond strength (MN/m2) was measured in tension using an inverted cone bond test at a crosshead speed of 0.05 cm/min. Mean bond strengths (S.D.) for the three repair materials when averaged over the three glass ionomer cores were: K, 5.0 (1.2); M, 3.4 (1.2) and C, 2.7 (1.5) for condition U; and M, 4.2 (1.1); K, 3.4 (1.2); and C, 3.1 (1.0) for condition T, where M, K and C were the repair materials. The Tukey intervals at the 95% level were 0.7 among materials and 0.5 between treatments. Bond strength of repaired amalgam was only successful with M, 0.9 MN/m2. Bond strengths to untreated silver-reinforced glass ionomer cores were higher with K used as a repair material.

Cermet Cements↗
PubMed1990

Sporadic cerebral amyloid angiopathy with giant cell reaction.

We report a case of intracerebral hemorrhages due to sporadic cerebral amyloid angiopathy in a 43-year-old male with a luxuriant giant cell reaction. The amyloid was resistant to potassium permanganate-sulfuric acid oxidation and reacted with an antiserum to synthetic beta-protein. The distribution and histologic characteristics of the multinucleated giant cell reaction suggest that it represents a foreign-body reaction rather than giant cell arteritis.

Adult↗