Aflatoxins in the autopsy brain tissue of children in Nigeria

1995 ◽  
Vol 132 (1) ◽  
pp. 35-38 ◽  
Author(s):  
O. A. Oyelami ◽  
S. M. Maxwell ◽  
K. A. Adelusola ◽  
T. A. Aladekoma ◽  
A. O. Oyelese
Keyword(s):  
Brain Tissue ◽  
Autopsy Brain Tissue

scholarly journals Using Autopsy Brain Tissue to Study Alcohol-Related Brain Damage in the Genomic Age

2013 ◽  
Vol 38 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Greg T. Sutherland ◽  
Donna Sheedy ◽  
Jillian J. Kril
Keyword(s):  
Brain Tissue ◽  
Brain Damage ◽  
Autopsy Brain Tissue

P1-213: Telomere length in autopsy brain tissue in dementia

2010 ◽  
Vol 6 ◽  
pp. S235-S236
Author(s):  
Lawrence S. Honig ◽  
Min-Suk Kang ◽  
Lorraine Clark ◽  
Joseph H. Lee
Keyword(s):  
Telomere Length ◽  
Brain Tissue ◽  
Autopsy Brain Tissue

Determination of mercury and lead levels in autopsy brain tissue samples

2009 ◽  
Vol 189 ◽  
pp. S220 ◽  
Author(s):  
Seda Kaya ◽  
Vugar Aliyev ◽  
Servet B. Iritas ◽  
Tülin Soylemezoglu
Keyword(s):  
Brain Tissue ◽  
Tissue Samples ◽  
Autopsy Brain Tissue ◽  
Lead Levels

scholarly journals Biochemical and molecular studies using human autopsy brain tissue

2003 ◽  
Vol 85 (3) ◽  
pp. 543-562 ◽  
Author(s):  
Matthew R. Hynd ◽  
Joanne M. Lewohl ◽  
Heather L. Scott ◽  
Peter R. Dodd
Keyword(s):  
Brain Tissue ◽  
Molecular Studies ◽  
Autopsy Brain Tissue ◽  
Human Autopsy

scholarly journals The Alzheimer Disease-Causing Presenilin-1 L435F Mutation Causes Increased Production of Soluble Aβ43 Species in Patient-Derived iPSC-Neurons, Closely Mimicking Matched Patient Brain Tissue

2020 ◽  
Vol 79 (6) ◽  
pp. 592-604 ◽  
Author(s):  
Derek H Oakley ◽  
Mirra Chung ◽  
Naomi Klickstein ◽  
Caitlin Commins ◽  
Bradley T Hyman ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Brain Tissue ◽  
Case Series ◽  
Induced Pluripotent Stem Cell ◽  
Presenilin 1 ◽  
Gamma Secretase ◽  
Severe Reduction ◽  
Autopsy Brain Tissue ◽  
Familial Alzheimer Disease ◽  
Induced Pluripotent

Abstract Familial Alzheimer disease-causing mutations in Presenilin 1 (PSEN1) are generally thought to shift the processing of APP toward longer, more amyloidogenic Aβ fragments. However, certain PSEN1 mutations cause severe reduction in gamma secretase function when expressed in the homozygous state, thus challenging the amyloid hypothesis. We sought to evaluate the effects of one such mutation, PSEN1 L435F, in more physiologic conditions and genetic contexts by using human induced pluripotent stem cell (iPSC)-derived neurons from an individual with familial AD (fAD) linked to the PSEN1 L435F mutation, and compared the biochemical phenotype of the iPS-derived neurons with brain tissue obtained at autopsy from the same patient. Our results demonstrate that in the endogenous heterozygous state, the PSEN1 L435F mutation causes a large increase in soluble Aβ43 but does not change the overall levels of soluble Aβ40 or Aβ42 when compared with control iPSC-neurons. Increased pathologically phosphorylated tau species were also observed in PSEN1-mutant iPSC-neurons. Concordant changes in Aβ species were present in autopsy brain tissue from the same patient. Finally, the feasibility of using Aβ43 immunohistochemistry of brain tissue to identify fAD cases was evaluated in a limited autopsy case series with the finding that strong Aβ43 staining occurred only in fAD cases.

scholarly journals Biological Analysis of Human Immunodeficiency Virus Type 1 R5 Envelopes Amplified from Brain and Lymph Node Tissues of AIDS Patients with Neuropathology Reveals Two Distinct Tropism Phenotypes and Identifies Envelopes in the Brain That Confer an Enhanced Tropism and Fusigenicity for Macrophages

2004 ◽  
Vol 78 (13) ◽  
pp. 6915-6926 ◽  
Author(s):  
Paul J. Peters ◽  
Jayanta Bhattacharya ◽  
Samantha Hibbitts ◽  
Matthias T. Dittmar ◽  
Graham Simmons ◽  
...  
Keyword(s):  
Lymph Node ◽  
Brain Tissue ◽  
Neurological Complications ◽  
Macrophage Tropism ◽  
Immunodeficiency Virus ◽  
Autopsy Brain Tissue ◽  
Low Levels ◽  
The Brain ◽  
Ccr5 Inhibitor

ABSTRACT Complete envelope genes were amplified from autopsy brain tissue of five individuals who had died of AIDS and had neurological complications. Lymph node samples were included for two of the patients. Nineteen different envelope clones from the five patients had distinct V1V2 sequences. Thirteen of the envelopes were functional and conferred fusigenicity and infectivity for CD4+ CCR5+ cells. Infectivity and cell-cell fusion assays showed that most envelopes used both CCR5 and CCR3. One brain-derived envelope used a broad range of coreceptors, while three other brain envelopes from one individual were restricted to CCR5. However, there was no correlation between tissue of origin and coreceptor use. Envelopes showed two very distinct phenotypes depending on their capacity to infect macrophages and to exploit low levels of CD4 and/or CCR5 for infection. Envelopes that were highly fusigenic and tropic for macrophages were identified in brain tissue from four of the five patients. The enhanced macrophage tropism correlated with reduced sensitivity to inhibition by Q4120, a CD4-specific antibody, but not with sensitivity to the CCR5 inhibitor, TAK779. The highly macrophage-tropic envelopes were able to infect cells expressing low levels of CD4 and/or CCR5. Comparison with several well-characterized macrophage-tropic envelopes showed that the four identified patient envelopes were at the top limit of macrophage tropism. In contrast, all four lymph node-derived envelopes exhibited a non-macrophage-tropic phenotype and required high levels of CD4 for infection. Our data support the presence of envelopes that are highly fusigenic and tropic for macrophages in the brains of patients with neurological complications. These envelopes are able to infect cells that express low levels of CD4 and/or CCR5 and may have adapted for replication in brain macrophages and microglia, which are known to express limited amounts of CD4.

scholarly journals Hepatitis C Virus Neuroinvasion: Identification of Infected Cells

2008 ◽  
Vol 83 (3) ◽  
pp. 1312-1319 ◽  
Author(s):  
Jeffrey Wilkinson ◽  
Marek Radkowski ◽  
Tomasz Laskus
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Brain Tissue ◽  
Nonstructural Protein ◽  
Subcortical White Matter ◽  
Hcv Infection ◽  
Cell Phenotype ◽  
Hcv Rna ◽  
Negative Strand ◽  
Autopsy Brain Tissue

ABSTRACT Hepatitis C virus (HCV) infection often is associated with cognitive dysfunction and depression. HCV sequences and replicative forms were detected in autopsy brain tissue and cerebrospinal fluid from infected patients, suggesting direct neuroinvasion. However, the phenotype of cells harboring HCV in brain remains unclear. We studied autopsy brain tissue from 12 HCV-infected patients, 6 of whom were coinfected with human immunodeficiency virus. Cryostat sections of frontal cortex and subcortical white matter were stained with monoclonal antibodies specific for microglia/macrophages (CD68), oligodendrocytes (2′,3′-cyclic nucleotide 3′-phosphodiesterase), astrocytes (glial fibrillary acidic protein [GFAP]), and neurons (neuronal-specific nuclear protein); separated by laser capture microscopy (LCM); and tested for the presence of positive- and negative-strand HCV RNA. Sections also were stained with antibodies to viral nonstructural protein 3 (NS3), separated by LCM, and phenotyped by real-time PCR. Finally, sections were double stained with antibodies specific for the cell phenotype and HCV NS3. HCV RNA was detected in CD68-positive cells in eight patients, and negative-strand HCV RNA, which is a viral replicative form, was found in three of these patients. HCV RNA also was found in astrocytes from three patients, but negative-strand RNA was not detected in these cells. In double immunostaining, 83 to 95% of cells positive for HCV NS3 also were CD68 positive, while 4 to 29% were GFAP positive. NS3-positive cells were negative for neuron and oligodendrocyte phenotypic markers. In conclusion, HCV infects brain microglia/macrophages and, to a lesser extent, astrocytes. Our findings could explain the biological basis of neurocognitive abnormalities in HCV infection.

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