FABP7 expression in normal and stab-injured brain cortex and its role in astrocyte proliferation

Reactive gliosis, in which astrocytes as well as other types of glial cells undergo massive proliferation, is a common hallmark of all brain pathologies. Brain-type fatty acid-binding protein (FABP7) is abundantly expressed in neural stem cells and astrocytes of developing brain, suggesting its role in differentiation and/or proliferation of glial cells through regulation of lipid metabolism and/or signaling. However, the role of FABP7 in proliferation of glial cells during reactive gliosis is unknown. In this study, we examined the expression of FABP7 in mouse cortical stab injury model and also the phenotype of FABP7-KO mice in glial cell proliferation. Western blotting showed that FABP7 expression was increased significantly in the injured cortex compared with the contralateral side. By immunohistochemistry, FABP7 was localized to GFAP+ astrocytes (21% of FABP7+ cells) and NG2+ oligodendrocyte progenitor cells (62%) in the normal cortex. In the injured cortex there was no change in the population of FABP7+/NG2+ cells, while there was a significant increase in FABP7+/GFAP+ cells. In the stab-injured cortex of FABP7-KO mice there was decrease in the total number of reactive astrocytes and in the number of BrdU+ astrocytes compared with wild-type mice. Primary cultured astrocytes from FABP7-KO mice also showed a significant decrease in proliferation and omega-3 fatty acid incorporation compared with wild-type astrocytes. Overall, these data suggest that FABP7 is involved in the proliferation of astrocytes by controlling cellular fatty acid homeostasis

Modelling human choices: MADeM and decision‑making

Research supported by FAPESP 2015/50122-0 and DFG-GRTK 1740/2. RP and AR are also part of the Research, Innovation and Dissemination Center for Neuromathematics FAPESP grant (2013/07699-0). RP is supported by a FAPESP scholarship (2013/25667-8). ACR is partially supported by a CNPq fellowship (grant 306251/2014-0)

Cerebral infarction associated with benign mucin-producing adenomyosis: report of two cases

Abstract Background Cerebral infarction associated with a malignant tumor is widely recognized as Trousseau syndrome. In contrast, few cases of cerebral infarction associated with benign tumors have been reported. We present two cases of embolic stroke that seemed to be caused by mucin-producing adenomyosis. Case presentation The patients were women aged 42 and 50 years old. Both patients developed right hemiparesis and aphasia, and cerebral infarctions were detected in the left cerebral hemisphere. There were no other abnormal findings, except for elevation of CA125 and D-dimer. Trousseau syndrome was suspected in both cases, but whole body examinations did not reveal any malignant tumors. However, uterine adenomyosis was detected in both patients. Conclusions From our findings and a review of the literature, both mucin-producing malignant tumors and mucin-producing benign tumors such as adenomyosis may cause hypercoagulability and cerebral infarction. This mechanism should be considered in a case of a young to middle-aged woman with embolic stroke of an undetermined origin