Bloom Science and Duke University have entered into an exclusive licensing agreement that provides the biopharmaceutical company access to the intellectual property and technology related to unique strain isolates and genetic variants of Akkermansia genus bacteria.
This type of bacteria has been demonstrated to slow disease progression and prolong survival in animal models of amyotrophic lateral sclerosis (ALS).
In a historic decision, the US Food and Drug Administration has issued emergency authorization for public use of a new test for the novel coronavirus. The exemption makes the diagnostic test available to any qualified lab in the world.
The FDA has given emergency authorization to a new test that promises to help public health labs meet a potential surge in cases.
AI cancer detection may be able to provide doctors the ability to recognize and treat the disease before it spreads.
It’s no secret that artificial intelligence (AI) has been rapidly developing over the past few years.
With Siri and Amazon Alexa, self-driving cars, targeted advertisements, chatbots, and automated customer service representatives, the infiltration of AI into our daily lives is anything but subtle.
(Reuters) — Regeneron Pharmaceuticals Inc ( REGN.O ) is working with the U.S. Department of Health and Human Services (HHS) to develop a treatment for the coronavirus outbreak that has killed more than 400 people in China, the HHS said on Tuesday.
The company will use the same technology that was used to develop an experimental drug to treat Ebola in the Democratic Republic of Congo, the agency said.
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.
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.