Notes

Balancing Genetic fix in order to avoid getting older along with cancers.
Epilepsy affects about 1% of the general population. Frontal lobe epilepsy is the second most common focal epilepsy accounting for nearly 25% of medically refractory epilepsies. CQ inhibitor This paper reviews frontal lobe epilepsy from a perspective of a network disease that may help us to understand epilepsy from the microscale of genes, to local neuronal circuits, to the macrolevel of a whole-brain network. Surgical interventions, such as ablation and resection act by removing the active target nodes in the network, while responsive neurostimulation and vagus nerve stimulation act by modulating networks at the local neuronal circuit level and whole-brain level.Temporal lobe epilepsy (TLE) is the most common type of drug-resistant focal epilepsy. Epilepsy can be conceptualized as a network disorder with the epileptogenic zone a critical node of the network. Temporal lobe networks can be identified on the microscale and macroscale, both during the interictal and ictal periods. This review summarizes the current understanding of TLE networks as studied by neurophysiological and imaging techniques discussing both functional and structural connectivity.We provide a history and overview of the network approach to epilepsy surgery. Models of the epileptogenic zone (EZ) have evolved considerably over the years with more recent models accounting for the connectivity and network properties of epileptic foci. Next, we describe several examples of network phenotypes of focal epilepsy and how these have the potential to influence surgical decision-making and patient outcome. Future research will provide new insight into how network models of the EZ can determine optimal surgical interventions that improve seizure outcomes and optimize cognitive outcomes.Background Binge drinking is associated with poor academic behaviors and performance. Excessive alcohol drinking induces molecular changes and neurobehaviors that support use of other substances and alter cognitive functions. The purpose of this study was to compare neurobehaviors and academic effort among college students with low alcohol use with those of high alcohol consumption and build conceptual models that represent the integration of the different variables. Method College students from several U.S colleges were assessed through an anonymous online survey for alcohol use, academic performance, lifestyle factors and mental distress. Results Our results depicted common neurobehaviors and differential responses to high alcohol use. Conclusion The common responses in young men and women with high alcohol use are reflective of a hyperactive limbic system. The different responses involve cognitive aptitudes, typically controlled by cortical regions and affected by levels of brain connectivity known to be dissimilar between men and women.Background Generating questions by learners might be a potent learning technique but previous research yielded several shortcomings and underlying mechanisms are not well understood. Methods Students (N = 231) first read an expository text including bold keywords and then generated questions and answers referring to these keywords in three conditions (1) open-book (i.e., text accessible), (2) closed-book (i.e., text inaccessible), and (3) cued closed-book (i.e., only keywords provided). Results In a test after one week, students in the open-book and in the cued closed-book conditions performed better than students in the restudying condition. The number of generated questions and answers was largest in the open-book condition, smaller in the cued closed-book condition and smallest in the closed-book condition and predicted final test performance. Conclusions Generating questions and answers is an effective tool to boost retention in university learning when (at least part of) the learning material remains accessible.Autophagy is a highly conserved catabolic process in which cytoplasmic material is recycled under various conditions of cellular stress, preventing cell damage and promoting survival in the event of energy or nutrient shortage, or in response to various cytotoxic insults. Autophagy is also responsible for the removal of aggregated proteins and damaged organelles, playing a vital role in the quality control of proteins and organelles. Impairment of autophagy has been linked to various diseases, including cancer and neurodegenerative disorders, making it a very interesting process for further research. Recent research highlighted that autophagy is not random and can be selective, making it even more important to understand the molecular mechanisms of selectivity at the organismal level. Drosophila has been demonstrated to be an excellent animal model for studying selective autophagy, as the autophagic machinery is highly conserved, although much is still left to be explored. In this review, an overview of autophagy and its selectivity in Drosophila will be presented.Vascular calcification (VC), characterized by different mineral deposits (i.e., carbonate apatite, whitlockite and hydroxyapatite) accumulating in blood vessels and valves, represents a relevant pathological process for the aging population and a life-threatening complication in acquired and in genetic diseases. Similarly to bone remodeling, VC is an actively regulated process in which many cells and molecules play a pivotal role. This review aims at (i) describing the role of resident and circulating cells, of the extracellular environment and of positive and negative factors in driving the mineralization process; (ii) detailing the types of VC (i.e., intimal, medial and cardiac valve calcification); (iii) analyzing rare genetic diseases underlining the importance of altered pyrophosphate-dependent regulatory mechanisms; (iv) providing therapeutic options and perspectives.Dietary interventions combined with cancer drugs represent a clinically valid polytherapy. In particular nutrient restriction (NR) in the form of varied fasting or caloric restriction regimens holds great clinical promise, conceptually due to the voracious anabolic appetite of cancer cells. This metabolic dependency is driven by a strong selective pressure to increasingly acquire biomass of a proliferating tumor and can be therapeutically exploited as vulnerability. A host of preclinical data suggest that NR can potentiate the efficacy of, or alleviate resistance to, cancer drugs. However, complicating clinical implementation are the many variables involved, such as host biology, cancer stage and type, oncogenic mutation landscape, tumor heterogeneity, variations in treatment modalities, and patient compliance to NR protocols. This calls for systematic preclinical screens and co-clinical studies to predict effective combinations of NR with cancer drugs and to allow for patient stratification regarding responsiveness to polytherapy.
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