Evolving data on cardiovascular complications in cancer.

Cancer and cardiovascular disease are leading causes of mortality and morbidity worldwide. Scientific studies show that patients with cancer are at increased risk of developing cardiovascular events, leading to the novel cardio-oncology research field. Growing evidence suggests that cancer and cardiovascular disease are not separate entities but are connected through shared risk factors, pathological mechanisms, and genetic predispositions. Moreover, anticancer therapies such as radiotherapy have been known to further increase the cardiovascular risk in patients with cancer. Due to the significant advances in oncological diagnostics and therapy, the number of cancer survivors has been growing substantially. Nowadays, the majority of patients with cancer dies from non-cancer causes. Cardiovascular disease substantially contributes to mortality and morbidity in cancer survivors. For some cancers, such as breast, prostate, endometrial and thyroid cancer, about half of the patients dies from cardiovascular disease. This raises an urge for effective strategies in preventing and treating cardiovascular events in patients living with and surviving cancer. In this review, we address the evolving data on cardiovascular disease in patients with cancer, with a special focus on atherothrombotic manifestations including myocardial infarction and ischemic stroke.

Co-administration of Anti microRNA-124 and -137 Oligonucleotides Prevents Hippocampal Neural Stem Cell Loss Upon Non-convulsive Seizures.

Convulsive seizures promote adult hippocampal neurogenesis (AHN) through a transient activation of neural stem/progenitor cells (NSPCs) in the subgranular zone (SGZ) of the dentate gyrus (DG). However, in a significant population of epilepsy patients, non-convulsive seizures (ncSZ) are observed. The response of NSPCs to non-convulsive seizure induction has not been characterized before. We here studied first the short-term effects of controlled seizure induction on NSPCs fate and identity. We induced seizures of controlled intensity by intrahippocampally injecting increasing doses of the chemoconvulsant kainic acid (KA) and analyzed their effect on subdural EEG recordings, hippocampal structure, NSPC proliferation and the number and location of immature neurons shortly after seizure onset. After establishing a KA dose that elicits ncSZ, we then analyzed the effects of ncSZ on NSPC proliferation and NSC identity in the hippocampus. ncSZ specifically triggered neuroblast proliferation, but did not induce proliferation of NSPCs in the SGZ, 3 days post seizure onset. However, ncSZ induced significant changes in NSPC composition in the hippocampus, including the generation of reactive NSCs. Interestingly, intrahippocampal injection of a combination of two anti microRNA oligonucleotides targeting microRNA-124 and -137 normalized neuroblast proliferation and prevented NSC loss in the DG upon ncSZ. Our results show for the first time that ncSZ induce significant changes in neuroblast proliferation and NSC composition. Simultaneous antagonism of both microRNA-124 and -137 rescued seizure-induced alterations in NSPC, supporting their coordinated action in the regulation of NSC fate and proliferation and their potential for future seizure therapies.