Catálogo de publicaciones - revistas

<jats:p>The assembly and activation of a mitochondrial channel is triggered by direct interaction with signaling molecules that promote cell death.</jats:p>

<jats:p>Rats with a damaged perirhinal cortex exhibit false memory, raising questions about brain organization.</jats:p>

<jats:p>A mixture of carbon nanotubes creates a material that can recover its shape after deformation over a wide temperature range.</jats:p>

<jats:p>Precise localization of switchable fluorescent molecules facilitates nanoscale biological imaging.</jats:p>

<jats:p>Studies on a variety of interesting biological problems, ranging from circadian rhythm to cancer cell growth to longevity, have begun to give evidence that the physiological state of cells and tissues reflects both the cell’s regulatory systems and its state of intermediary metabolism. It is appreciated that the regulatory state of a cell or tissue, as driven by transcription factors and signaling pathways, can impose itself upon the dynamics of metabolic state. It follows that the reciprocal must also be the case, that metabolic state will feed back to impose itself on regulatory state. An appreciation and understanding of this reciprocity may be required to crack open problems in biological research that have heretofore been insoluble.</jats:p>

<jats:p>Cells from some tumors use an altered metabolic pattern compared with that of normal differentiated adult cells in the body. Tumor cells take up much more glucose and mainly process it through aerobic glycolysis, producing large quantities of secreted lactate with a lower use of oxidative phosphorylation that would generate more adenosine triphosphate (ATP), water, and carbon dioxide. This is the Warburg effect, which provides substrates for cell growth and division and free energy (ATP) from enhanced glucose use. This metabolic switch places the emphasis on producing intermediates for cell growth and division, and it is regulated by both oncogenes and tumor suppressor genes in a number of key cancer-producing pathways. Blocking these metabolic pathways or restoring these altered pathways could lead to a new approach in cancer treatments.</jats:p>

<jats:p>Autophagy is a process of self-cannibalization. Cells capture their own cytoplasm and organelles and consume them in lysosomes. The resulting breakdown products are inputs to cellular metabolism, through which they are used to generate energy and to build new proteins and membranes. Autophagy preserves the health of cells and tissues by replacing outdated and damaged cellular components with fresh ones. In starvation, it provides an internal source of nutrients for energy generation and, thus, survival. A powerful promoter of metabolic homeostasis at both the cellular and whole-animal level, autophagy prevents degenerative diseases. It does have a downside, however—cancer cells exploit it to survive in nutrient-poor tumors.</jats:p>

<jats:p>Circadian clocks align behavioral and biochemical processes with the day/night cycle. Nearly all vertebrate cells possess self-sustained clocks that couple endogenous rhythms with changes in cellular environment. Genetic disruption of clock genes in mice perturbs metabolic functions of specific tissues at distinct phases of the sleep/wake cycle. Circadian desynchrony, a characteristic of shift work and sleep disruption in humans, also leads to metabolic pathologies. Here, we review advances in understanding the interrelationship among circadian disruption, sleep deprivation, obesity, and diabetes and implications for rational therapeutics for these conditions.</jats:p>