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W Tourtellotte

Publications and source records attributed to W Tourtellotte.

13 recordsLinked to original sources
PubMed2004

Transforming growth factor beta and monocyte chemotactic protein-1 are elevated in cerebrospinal fluid of immunocompromised patients with HIV-1 infection.

Monocyte infiltration of the brain is central to the pathogenesis of HIV-1 encephalitis. The cytokines promoting recruitment of monocytes into the central nervous system during HIV-1 infection are not established. In this study, we evaluated human cerebrospinal fluid from patients with HIV-1 infection for transforming growth factor beta1 (TGFbeta1) and monocyte chemotactic protein-1 (MCP-1) using a quantitative sandwich enzyme-linked immunoassays. Cytokine levels were compared to those from patients with multiple sclerosis and normal controls. In cerebrospinal fluid of patients with HIV-1 infection and CD4<500 cells/mm3, both TGFbeta1 and MCP-1 were significantly elevated compared to those with CD4>500 cells/mm3, multiple sclerosis, and controls.

CD4 Lymphocyte Count↗
PubMed2001

Phenylethanolamine N-methyltransferase (PNMT) gene and early-onset Alzheimer disease.

The activity of human phenylethanolamine N-methyltransferase (PNMT) is reduced in the neurons of those cells in many subcortical areas of the brain that are known to undergo neurodegeneration in Alzheimer disease (AD). Others have reported that PNMT is decreased in brains of persons with AD and that the decrease in enzymatic activity is due to a reduced amount of the enzyme protein. We have previously described two polymorphisms, G-353A and G-148A, in the promoter region of the gene coding for PNMT. These markers were tested for their association with the occurrence of sporadic AD. Genotyping of 131 necropsy confirmed AD cases, and 947 adult nondemented controls were completed. We observed a significant association between both of the PNMT gene polymorphisms and early-onset AD (EOAD) (P < or = 0.007), but not in late-onset AD (LOAD). These data suggest that genetic variation in the promoter of the PNMT gene is associated with increased susceptibility to the sporadic form of EOAD.

Adult↗
PubMed1998

Association between the gamma-aminobutyric acid A3 receptor gene and multiple sclerosis.

BACKGROUND: In a prior study we observed an association between the dopamine D2 receptor gene (DRD2) and the age of onset and/or diagnosis of multiple sclerosis (MS). We hypothesized that this effect was mediated through the dopaminergic control of the release of prolactin, a modulator of immune response. Since gamma-aminobutyric acid also modulates the release of prolactin, we examined the possible association between alleles of the GABRA3 (gamma-aminobutyric acid A3 receptor) gene and MS. DESIGN: We examined the GABRA3 alleles of 189 subjects with MS who died of their disease. They were divided into test group 1 (n=64) and retest group 2 (n=56). Each group had a separate set of controls (group 1, n=109; group 2, n=430). All subjects were white. All were tested at a dinucleotide cytosine-adenosine repeat polymorphism with 6 alleles representing 11 to 16 repeats. RESULTS: In the first group there was a significant difference in the frequency of the GABRA3 alleles (P<.002), with the most notable difference being an increase in the frequency of the 16-repeat allele in subjects with MS and a relative decrease in the other alleles. In the replication group there was again a significant difference in the distribution of the GABRA3 alleles (P<.001), and again the greatest difference was an increase in the frequency of the 16-repeat allele in subjects with MS. For both groups combined, a significant difference in the frequency of the 16-repeat allele was noted (chi2=46.30; P<.001). CONCLUSIONS: These results suggest the GABRA3 gene may be a risk factor for MS. As with the DRD2 gene, the effect may be mediated through its regulation of prolactin release.

Alleles↗
PubMed1985

Natural history of restricted synthesis and expression of measles virus genes in subacute sclerosing panencephalitis.

Subacute sclerosing panencephalitis (SSPE) is a slow infection caused by measles virus in which several years separate recovery from typical acute measles and the development of a slowly progressive neurological disease. We have investigated replication of measles virus in brain tissue obtained after the onset of neurological disease and in the terminal phase. With a hybridization tomographic technique that combines in situ hybridization with macroradioautographic screening of large areas of tissue, we analyzed the spatial and temporal distribution of virus genes in vivo, using region- and strand-specific probes for the nucleocapsid and matrix genes. We show that early in the course of SSPE there is a global repression in the synthesis and expression of the genome. In the final stage of SSPE most infected cells still have depressed levels of plus- and minus-strand viral RNA and contain nucleocapsid protein but lack matrix protein. These findings provide further evidence for a unified view of slow infections of the nervous system, where the general constraints on virus gene expression provide an explanation for persistence of virus in the face of the host's immune response, and the slow evolution of pathological change. In the final phases of SSPE the more specific block in virus replication accounts for the cell-associated state of the virus and the difficulty in virus isolation.

Brain↗
PubMed1983

Oxygen radical dependent lung damage following thermal injury of rat skin.

Acute thermal injury (70 degrees C, 30 sec) to rat skin results in progressive consumptive depletion of the complement system. Individual complement components (C3, C4, C6) each show reductions in hemolytic activity. Crossed immunoelectrophoresis analysis of serum from thermally injured rats reveals conversion of C3 compatible with activation of the complement system. During the first hour following thermal injury, C5a-related chemotactic activity appears in the serum and is temporally related to the development of neutropenia. Lung injury, as revealed by increases in lung permeability, develops progressively during a 6-hour period and parallels changes in complement levels. Morphologically, lung changes include leukoaggregates within pulmonary capillaries and the presence of intra-alveolar hemorrhage. Protection from lung injury following remote thermal injury to skin is afforded by depleting animals of complement or neutrophils, or by systemic treatment of animals with a combination of catalase and superoxide dismutase. Antihistamine drugs have no protective effect. These data suggest that acute thermal injury leads to systemic complement activation, neutrophil activation, and acute lung injury that is related to production of toxic oxygen products by activated blood neutrophils.

Animals↗
PubMedDate not supplied

Cytoskeletal neurofilament gene expression in brain tissue from Alzheimer's disease patients. I. Decrease in NF-L and NF-M message.

The cytoskeletal changes seen in brains of patients with Alzheimer's disease include neurofibrillary tangles, neuritic plaques, Hirano bodies, and granulovacuolar degeneration. Northern and slot blot analyses were used to investigate the expression of the genes coding for actin, tubulin, neurofilaments, and histone in brain tissue from Alzheimer's disease patients and normal aged controls. We found a marked decrease of 94% in the expression of the neurofilament gene coding for the medium size subunit (150 kDa) and a 73% decrease in the expression of the gene coding for the small subunit (68 kDa) in Alzheimer's disease patients as compared to controls. Expression of the other genes, such as actin and histone, did not show any significant difference. Expression of the gene coding for medium size, neurofilament gene was not decreased in other neurodegenerative diseases, such as amyotrophic lateral sclerosis and Parkinson's disease. This abnormality in neurofilament gene expression may explain some of the pathologic features found in Alzheimer's disease patients.

Aged↗