Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intracranial hemorrhage associated with brain tumors is rate, but when present, it is often seen in malignant tumors such as glioblastoma and metastasis, and in meningiomas. Hemangioblastomas, benign vascular tumors, rarely develop fatal intracerebral hemorrhage. We thus documented an uncommon case of cerebellar hemangioblastoma associated with massive hemorrhage, the cause of which was thoroughly examined during autopsy. A 69-year-old man was transferred to our Service because of swallowing disturbance and dysarthria. The patient was known to have a cerebellar hemangioblastoma and hydrocephalus, for which VP shunt had been placed. Two weeks after admission he suddenly became comatose and eventually died of progressive herniation. At autopsy it was shown that the brain was edematous and covered with subarachnoid blood clots. The tumor was found involving the cerebellar vermis and the right hemisphere, protruding upward from the superior surface of the cerebellum. Horizontal sections through the cerebellum disclosed a well circumscribed tumor with adjacent hematomas involving the vermis and brain stem. The pathological diagnosis was hemangioblastoma and varix-like abnormal vessels were observed within the tumor. The sites of hematoma and tumor adjacent to the tentorial incisura and the history of VP shunting may suggest that upward herniation played a significant role in rupture of the abnormal vessels, which then led to the devastating hemorrhage in this particular case.
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PMID:[Cerebellar hemangioblastoma associated with fatal intratumoral hemorrhage: report of an autopsied case]. 801 84

Thyroid hormones (THs) are essential for brain development, where they regulate gliogenesis, myelination, cell proliferation and protein synthesis. Hypothyroidism severely affects neuronal growth and establishment of synaptic connections. Triiodothyronine (T3), the biologically active form of TH, has a central function in these activities. So, Myosin-Va (Myo-Va), a molecular motor protein involved in vesicle and RNA transport, is a good candidate as a target for T3 regulation. Here, we analyzed Myo-Va expression in euthyroid and hypothyroid adult rat brains and synaptosomes. We observed a reduction of Myo-Va expression in cultured neural cells from newborn hypothyroid rat brain, while immunocytochemical experiments showed a punctate distribution of this protein in the cytoplasm of cells. Particularly, Myo-Va co-localized with microtubules in neurites, especially in their varicosities. Myo-Va immunostaining was stronger in astrocytes and neurons of controls when compared with hypothyroid brains. In addition, supplementation of astrocyte cultures with T3 led to increased expression of Myo-Va in cells from both euthyroid and hypothyroid animals, suggesting that T3 modulates Myo-Va expression in neural cells both in vivo and in vitro. We have further analyzed Myo-Va expression in U373 cells, a human glioblastoma line, and found the same punctate cytoplasmic protein localization. As in normal neural cells, this expression was also increased by T3, suggesting that the modulatory mechanism exerted by T3 over Myo-Va remains active on astrocyte tumor cells. These data, coupled with the observation that Myo-Va is severely affected in hypothyroidism, support the hypothesis that T3 activity regulates neural motor protein expression, taking Myo-Va as a model. As a consequence, reduced T3 activity could supposedly affect axonal transport and synaptic function, and could therefore explain disturbances seen in the hypothyroid brain.
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PMID:Effect of thyroid hormone T3 on myosin-Va expression in the central nervous system. 1937 19