RESUMO
Reversible cerebral vasoconstriction syndrome (RCVS) is an essential but often unrecognized cause of intracranial haemorrhage. While there are no specific causes of the syndrome, associations with many clinical conditions and drugs have been observed, and calcium channel blockers (CCBs) are often used to relieve the symptoms. This is a case of RCVS that was triggered by the sudden withdrawal of nifedipine, a CCB.
RESUMO
We describe a previously healthy 21-year-old man who presented acutely with signs and symptoms of raised intracranial pressure (ICP). Lumbar puncture yielded an elevated opening pressure and an acellular CSF analysis. Radiological images showed bilateral flattening of the posterior eye globes and an empty sella turcica. His serum HIV antigen/antibody was reactive. We provide a review of published cases that have been labeled as idiopathic intracranial hypertension (IIH) in HIV-infected patients, addressing the appropriateness of labeling such cases as truly idiopathic. We also discuss the importance of a thorough clinical evaluation of raised ICP in those who do not fulfil the typical IIH demographic.
RESUMO
BACKGROUND/AIMS: 5-Fluorouracil (5-FU) is widely used in the treatment of patients with colorectal cancer (CRC). However, the efficacy of 5-FU as a single agent is limited, with multiple undesired side effects. Therefore, the aim of the current study was to assess the efficacy of CUDC-907 (a dual inhibitor of histone deacetylase and phosphatidylinositide 3-kinase) in combination with 5-FU against CRC cells. MATERIALS AND METHODS: Cell viability was determined using AlamarBlue and colony formation assays. Acridine orange/ethidium bromide staining and flow cytometry were used to measure apoptotic and necrotic events, as well as cell cycle progression. Immunoblotting was used to assess acetylation of histone H3 and phosphorylation of AKT. RESULTS: Our data revealed enhanced toxicity of CUDC-907 against HCT116, RKO, COLO-205, and HT-29 CRC cells when combined with 5-FU. Similarly, the colony formation capability of HCT116 cells was suppressed by the combination treatment. Cells treated with CUDC-907 and 5-FU underwent apoptosis and necrosis, and exhibited increased polyploidy. Furthermore, CRC cells treated with CUDC-907 exhibited a higher degree of histone H3 lysine 9 acetylation (H3K9ac) and reduced AKT phosphorylation (Ser473). CONCLUSION: Our data revealed, for the first time, the enhanced inhibitory effect of CUDC-907 against CRC cells when combined with 5-FU, supporting the application of this combination as a potential therapeutic strategy in CRC treatment.
