A new Einsteinian equation, ER=EPR, may be the clue physicists need to merge quantum mechanics with general relativity.
We were unsure if wormholes could exist long enough to allow a person through. Now calculations indicate they are extremely rare, but could last the age of the universe.
O.o.
This paper describes a new and efficient method of defining an annular region of a curl-free magnetic field with specific physics and coil properties that can be used in stellarator design. Three statements define the importance:
Codes can follow an optimized curl-free initial state to a final full-pressure equilibrium. The large size of the optimization space of stellarators.
Approximately fifty externally-produced distributions of magnetic field, makes success in finding a global optimum largely determined by the starting point.
Continue reading “Curl-free magnetic fields for stellarator optimization” »
O.o.
Laser weapons can strike at the speed of light, and they’re quickly deploying to every possible fighting domain, whether on land, in the air, and at sea. But what about under the sea?
Open-source budget documents, the earliest of which date back to 2011, show the Navy’s plans to arm Virginia-class nuclear subs with high-energy laser weapons. It’s a strange idea seeing as laser weapons definitely do not work underwater. Submarines are also quiet recluses by design, rarely popping their heads above water.
Strokes cause brain cells to short-circuit and trigger a dangerous flood of fluid in the tissue.
Cancer genomes contain large numbers of somatic mutations but few of these mutations drive tumor development. Current approaches either identify driver genes on the basis of mutational recurrence or approximate the functional consequences of nonsynonymous mutations by using bioinformatic scores. Passenger mutations are enriched in characteristic nucleotide contexts, whereas driver mutations occur in functional positions, which are not necessarily surrounded by a particular nucleotide context. We observed that mutations in contexts that deviate from the characteristic contexts around passenger mutations provide a signal in favor of driver genes. We therefore developed a method that combines this feature with the signals traditionally used for driver-gene identification. We applied our method to whole-exome sequencing data from 11,873 tumor–normal pairs and identified 460 driver genes that clustered into 21 cancer-related pathways. Our study provides a resource of driver genes across 28 tumor types with additional driver genes identified according to mutations in unusual nucleotide contexts.
Researchers from SENS Research Foundation, including Matthew O’Connor and Amutha Boominathan, have published a new study showing how codons play an important role in getting copies of mitochondrial genes placed in the cellular nucleus to express themselves correctly [1].
A possible solution to mitochondrial diseases
Mitochondrial disease is not a single disease; in fact, it is a group of rare and related conditions that are thought to affect perhaps 1 in 5000 people. These are caused due to mutations in the genes involved in the process of aerobic respiration, one of the main functions of our mitochondria.
James P. Allison believed that unleashing the immune system was a way to beat cancer when almost no one else did. A Nobel Prize and a growing list of cancer survivors vindicate him.
Both genetically altered and naturally long-lived mammals are more resistant to toxic compounds that may cause cancer and age-associated diseases than their shorter-lived counterparts. The mechanisms by which this stress resistance occurs remain elusive. We found that longer-lived rodent species had markedly higher levels of signaling activity of the multifunctional regulator nuclear factor erythroid 2-related factor (Nrf2) and that this increase in cytoprotective signaling appeared to be due to species differences in Kelch-like ECH-Associated Protein 1 (Keap1) and β-transducin repeat-containing protein (βTrCP) regulation of Nrf2 activity. Both of these negative regulators of Nrf2-signaling activity are significantly lower in longer-lived species. By targeting the proteins that regulate Nrf2 rather than Nrf2 itself, we may be able to identify new therapies that impact aging and age-associated diseases such as cancer.
The preternaturally long-lived naked mole-rat, like other long-lived species and experimental models of extended longevity, is resistant to both endogenous (e.g., reactive oxygen species) and environmental stressors and also resists age-related diseases such as cancer, cardiovascular disease, and neurodegeneration. The mechanisms behind the universal resilience of longer-lived organisms to stress, however, remain elusive. We hypothesize that this resilience is linked to the activity of a highly conserved transcription factor, nuclear factor erythroid 2-related factor (Nrf2). Nrf2 regulates the transcription of several hundred cytoprotective molecules, including antioxidants, detoxicants, and molecular chaperones (heat shock proteins). Nrf2 itself is tightly regulated by mechanisms that either promote its activity or increase its degradation.
Genetic studies of mental illness have largely been conducted in people with European ancestry.
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