ABSTRACT
Primary and secondary traumatic brain injury (TBI) can cause tissue damage by inducing cell death pathways including apoptosis, necroptosis, and autophagy. However, similar pathways can also lead to senescence. Senescent cells secrete senescence-associated secretory phenotype proteins following persistent DNA damage response signaling, leading to cell disorders. TBI initially activates the cell cycle followed by the subsequent triggering of senescence. This study aims to clarify how the mRNA and protein expression of different markers of cell cycle and senescence are modulated and switched over time after TBI. We performed senescence-associated-ß-galactosidase (SA-ß-gal) staining, immunohistochemical analysis, and real-time PCR to examine the time-dependent changes in expression levels of proteins and mRNA, related to cell cycle and cellular senescence markers, in the cerebrum during the initial 14 days after TBI using a mouse model of controlled cortical impact (CCI). Within the area adjacent to the cerebral contusion after TBI, the protein and/or mRNA expression levels of cell cycle markers were increased significantly until 4 days after injury and senescence markers were significantly increased at 4, 7, and 14 days after injury. Our findings suggested that TBI initially activated the cell cycle in neurons, astrocytes, and microglia within the area adjacent to the hemicerebrum contusion in TBI, whereas after 4 days, such cells could undergo senescence in a cell-type-dependent manner.
Subject(s)
Brain Injuries, Traumatic/enzymology , Brain Injuries, Traumatic/physiopathology , Cellular Senescence , Cerebrum/enzymology , beta-Galactosidase/metabolism , Animals , Apoptosis , Autophagy , Cerebrum/physiopathology , Cyclin D1/metabolism , Disease Models, Animal , Gene Expression Profiling , Male , Mice , Mice, Inbred C57BL , Neurons/metabolism , Proliferating Cell Nuclear Antigen/metabolism , Signal TransductionABSTRACT
BACKGROUND: We came across a rare case of recurrent hemorrhage from a meningioma. Here, we describe this case and discuss the treatment strategies for recurrent hemorrhage from a meningioma using a literature review. CASE DESCRIPTION: A 61-year-old woman with a history of 2 episodes of hemorrhage from a meningioma originating from the left falx cerebri presented to our outpatient clinic. She was asymptomatic, and magnetic resonance imaging revealed a small tumor along the falx cerebri. However, we decided to remove the hemorrhagic meningioma. No abnormal vascular structures were recognized on preoperative angiography and intraoperative evaluation. The tumor was easily removed along the falx cerebri (Simpson grade I). The pathologic diagnosis was transitional meningioma, World Health Organization grade I. The patient experienced no recurrence of tumor or hemorrhage for up to 15 months after surgery. CONCLUSIONS: The incidence of repeated bleeding from meningiomas is very rare and is seldom reported because the mortality associated with hemorrhage in meningiomas is high (28%-50%). Immediate diagnosis and surgical treatment with both hematoma evacuation and tumor removal are crucial to avoid inadequate and delayed treatment that may cause mortality.
ABSTRACT
Bilateral traumatic carotid-cavernous fistula(CCF)is rare. It is most commonly caused by a direct head or face injury involving the cavernous sinus and develops immediately after trauma. We report a case of bilateral traumatic CCF that occurred as an intracerebral hematoma(ICH)mimicking apoplexy 5 months later. We treated the patient with point occlusion of venous reflux causing an ICH using coil embolization to remove the hematoma. Three days after we performed trans-venous occlusion of the intercavernous connection and right cavernous sinus using coil embolization through the right inferior petrosal vein, it was identified that the left CCF was occluded after first embolization into the left sylvian vein. The mechanism of delayed development of traumatic CCF and spontaneous disappearance of CCF after occlusion of venous reflux are discussed.
