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1.
Neurology Asia ; : 69-75, 2018.
Article in English | WPRIM | ID: wpr-732260

ABSTRACT

@#Metastatic brain lymphomas, which belong to secondary central nervous system lymphomas, usually originate from primary tumors of the bone marrow, testis, or orbit. Gastrointestinal lymphomas commonly metastasize to the lung or heart. We report here a case of brain hemorrhage due to metastasis from primary gastrointestinal diffuse large B-cell lymphoma (DLBCL). A 30-year-old male presented with headache. He was diagnosed to have gastrointestinal lymphoma 6 months earlier, and treated with gastrointestinal surgery. Pathological diagnosis was DLBCL. A PET-CT scan immediately after gastrointestinal surgery demonstrated no brain metastasis. On admission to the ward, imaging of the brain showed right temporoparietal hematoma. In the ward, the patient deteriorated with impaired consciousness. Repeat brain imaging showed enlargement of the hematoma. He underwent right temporoparietal craniotomy for the removal of a hematoma, and tumor nodules adherent to the cortex was found. Pathology confirmed a metastatic DLBCL in the brain. Literature review showed that this was the first reported case of brain hemorrhage from metastatic lymphoma. Metastatic central nervous system lymphoma should be considered as a differential diagnosis in patients with a history of gastrointestinal lymphoma presenting with neurological symptoms.

2.
Neurology Asia ; : 357-362, 2017.
Article in English | WPRIM | ID: wpr-732048

ABSTRACT

Microvascular decompression is an effective treatment for hemifacial spasm. Hemorrhage is oneof the complications of microvascular decompression. However, delayed hemorrhage is very rare.Here, we report a case of ipsilateral cerebellar hemorrhage at day seven following microvasculardecompression. A 45-year-old woman presented with left HFS for the previous two years. Diagnostictesting demonstrated the presence of neurosyphilis. Brain magnetic resonance image was unremarkableon presentation. She received microvascular decompression and her hemifacial spasm completelyresolved after surgery. At day seven post-operatively, the patient presented with a sudden onsetheadache. Emergency computed tomography scan showed a cerebellar hemorrhage. A suboccipitalcraniotomy was performed and a cerebellar hematoma was evacuated. The delayed hemorrhage wasattributed to possible microaneurysm from syphilis.

3.
International Journal of Radiation Research. 2017; 15 (2): 141-148
in English | IMEMR | ID: emr-191371

ABSTRACT

Background: Radiotherapy is an effective and important therapeutic method for breast cancer, but at the same time it has a radiation-induced bystander effect on normal tissue around the tumor. Repair of double-strand breaks [DSBs] by normal cells can reduce the extent of damage caused by this effect. Caveolin-1 [Cav-1] is an important regulatory molecule in cell signal transduction. However, the response of normal human mammary epithelial cells following low dose radiation [LDR]- induced DSBs and the role of Cav-1 in the repair of the DSBs are not clear. The present study examined the DNA damage repair mechanism triggered by LDR in human mammary epithelial cells


Materials and Methods: Human mammary epithelial [MCF10A] and Cav-1 haplo-insufficiency [MCF10A-ST1] cells were irradiated with LDR gamma rays and the effect of this radiation on cell proliferation was determined by cytometric method. Western blot analysis was then used to measure the expression levels of different proteins associated with cell proliferation and DNA repair


Results: LDR enhanced the radiation responsiveness of MCF10A cells in a dose- and time-dependent manner. At a dose of 100 cGy, LDR increased the expression levels of several proteins involved in DNA repair pathways, such as ATM, p53, DNA-PKcs and also activated Cav-1-mediated cell proliferation and survival pathways, such as the MAPK and AKT pathways. The expression of the various DNA repair related proteins was changed after down-regulating the Cav-1 expression


Conclusion: LDR could increase the radiation responsiveness of human mammary epithelial cells through activating the DNA repair pathways, including both HR and NHEJ pathways, as well as triggering the cell proliferation and survival pathways, both of which required Cav-1

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