| 1 | Pathol. Res. Pract. 2006 -1 202: 541-8 |
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| PMID | 16564140 |
| Title | Follicular dendritic cell tumor of the gastrointestinal tract: Report of a rare neoplasm and literature review. |
| Abstract | Follicular dendritic cell (FDC) tumor is a rare neoplasm of the accessory immune system showing FDC differentiation. Histologically, a conventional type and an inflammatory pseudotumor (IPT-like) type are recognized. The etiology of FDC tumor is unknown. While rare FDC tumors were associated with hyaline-vascular Castleman's disease (HVCD), hepatosplenic IPT-like FDC tumors consistently harbor EBV infection. FDC tumors of the gastrointestinal (GI) tract and mesentery/omentum are exceedingly rare, with only 17 cases reported so far. We report an additional case of an IPT-like FDC tumor of the ileum and mesentery in a 52-year-old schizophrenic man. The tumor consisted of highly atypical multinucleated giant cells in a background of intense lymphoid infiltrate with prominent eosinophilia reminiscent of Hodgkin's lymphoma. Tumor cells were immunoreactive for vimentin, CD21, CD35, fascin, smooth muscle actin and CD68, but were negative for all lineage-specific lymphoreticular, myeloid, mesenchymal and epithelial markers. Immunostaining for HHV-8 and in situ hybridization for EBV-encoded RNA (EBER) were negative. Some mesenteric lymph nodes showed HVCD-like changes. The differential diagnostic considerations of this unusual and rare neoplasm, mainly lymphocyte-rich GI stromal tumor (GIST), malignant lymphoma and inflammatory neoplasia of diverse histogenetic types, will be discussed together with a literature review on gastrointestinal FDC tumors. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 2 | Schizophr. Res. 2010 Jun 119: 164-74 |
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| PMID | 20346631 |
| Title | Haloperidol activates quiescent oligodendroglia precursor cells in the adult mouse brain. |
| Abstract | Recent human studies suggest that abnormal development of oligodendrocytes (OLs) is an important component in the pathophysiology of schizophrenia. However, less information is available regarding effects of antipsychotics on OLs' development. In the present study, young adult C57BL/6 mice were given haloperidol (HAL; 2mg/kg/day) in their drinking water for three or six weeks. At the conclusion of the drug treatment, mice were sacrificed and the numbers of NG2- and Olig2-expressing cells in the brain regions of the corpus callosum, hippocampus and cerebral cortex were quantified. NG2 is a specific marker for oligodendroglia precursor cells (OPCs); Olig2 marks glial progenitors. HAL treatment for three weeks increased the number of NG2-expressing cells in the corpus callosum; HAL treatment for three and six weeks increased the numbers of Olig2-expressing cells in all three brain regions and increased the levels of Olig2 expression in the same brain regions. These results suggest that HAL treatment activates adult OPCs, which divide infrequently under normal conditions but respond to a variety of insulting factors by proliferation and differentiation. However, our further observations showed no changes in the number of mature OLs and the amount of myelin basic protein in HAL-treated mice, suggesting the drug treatment has no effect on the maturation of OLs. In addition, HAL treatment did not increase the numbers of GFAP- and CD68-expressing cells, suggesting that no gliosis and inflammatory responses occurred while the drug activated the quiescent OPCs in adult brain. These results suggest that HAL treatment may target the development of OLs. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 3 | Behav. Brain Res. 2014 Jan 258: 179-86 |
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| PMID | 24129217 |
| Title | Hypolocomotive behaviour associated with increased microglia in a prenatal immune activation model with relevance to schizophrenia. |
| Abstract | Over the past decade a neurodevelopmental animal model with high validity for schizophrenia has been developed based on the environmental risk factor known as maternal immune activation (MIA). The immunological basis of this model, together with extensive data from clinical and preclinical context, suggests the involvement of an aberrant neuro-immune system in the pathophysiology of schizophrenia. The goal of this study was to examine microglia activation in adult behaviourally phenotyped MIA offspring. MIA was induced in pregnant rats using viral mimetic Poly I:C at gestational day 15. Adult offspring were behaviourally phenotyped at postnatal days (PND) 56, 90 and 180 through the evaluation of prepulse inhibition (PPI) of the acoustic startle and spontaneous locomotion. Finally, the presence of activated microglia in brain regions associated with schizophrenia was evaluated using post-mortem immunohistochemistry against OX-42 (CD11b) and ED-1 (CD68). Although a deficit in PPI could not be replicated despite the high number of animals tested, we found an overall decrease in basal startle response and spontaneous locomotion in offspring born to Poly I:C- compared to saline-treated dams, accompanied by increased microglial density with characteristics of non-reactive activation in the chronic stage of the model. These findings provide additional evidence for a role played by microglial activation in schizophrenia-related pathology in general and psychomotor slowing in particular, and warrant extensive research on the underlying mechanism in order to establish new drug targets for the treatment of schizophrenia patients with an inflammatory component. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 4 | Schizophr. Res. 2015 Feb 161: 215-21 |
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| PMID | 25487697 |
| Title | Innate immune response is differentially dysregulated between bipolar disease and schizophrenia. |
| Abstract | schizophrenia (SZ) and bipolar disorder (BD) are severe psychiatric conditions with a neurodevelopmental component. Genetic findings indicate the existence of an overlap in genetic susceptibility across the disorders. Also, image studies provide evidence for a shared neurobiological basis, contributing to a dimensional diagnostic approach. This study aimed to identify the molecular mechanisms that differentiate SZ and BD patients from health controls but also that distinguish both from health individuals. Comparison of gene expression profiling in post-mortem brains of both disorders and health controls (30 cases), followed by a further comparison between 29 BD and 29 SZ revealed 28 differentially expressed genes. These genes were used in co-expression analysesthat revealed the pairs CCR1/SERPINA1, CCR5/HCST, C1QA/CD68, CCR5/S100A11 and SERPINA1/TLR1 as presenting the most significant difference in co-expression between SZ and BD. Next, a protein-protein interaction (PPI) network using the 28 differentially expressed genes as seeds revealed CASP4, TYROBP, CCR1, SERPINA1, CCR5 and C1QA as having a central role in the diseases manifestation. Both co-expression and network topological analyses pointed to genes related to microglia functions. Based on this data, we suggest that differences between SZ and BP are due to genes involved with response to stimulus, defense response, immune system process and response to stress biological processes, all having a role in the communication of environmental factors to the cells and associated to microglia. |
| SCZ Keywords | schizophrenia, schizophrenic |