Lifeboat Foundation

Humans are not the only species facing a potential threat from SARS-CoV-2, the novel coronavirus that causes COVID-19, according to a new study from the University of California, Davis.

An international team of scientists used genomic analysis to compare the main cellular receptor for the virus in humans—angiotensin converting enzyme-2, or ACE2—in 410 different species of vertebrates, including birds, fish, amphibians, reptiles and mammals.

ACE2 is normally found on many different types of cells and tissues, including epithelial cells in the nose, mouth and lungs. In humans, 25 amino acids of the ACE2 protein are important for the virus to bind and gain entry into cells.

Metabolic plasticity allows cancer cells to adjust their metabolic phenotypes to adapt in hostile environments. There is an urgent need to understand the cross-talk between gene regulation and metabolic pathways underlying cancer metabolic plasticity. We establish a theoretical framework to decode the coupling of gene regulation and metabolic pathways. Our work characterizes a hybrid metabolic state where cells can use both glycolysis and oxidative phosphorylation (OXPHOS) and a possible metabolically inactive state where cells have low activity of both glycolysis and OXPHOS. We show that targeting both OXPHOS and glycolysis may be necessary to eliminate cancer aggressiveness. Our work serves as a platform to target abnormal metabolism in cancer by modulating both genes and metabolic pathways.

Metabolic plasticity enables cancer cells to switch their metabolism phenotypes between glycolysis and oxidative phosphorylation (OXPHOS) during tumorigenesis and metastasis. However, it is still largely unknown how cancer cells orchestrate gene regulation to balance their glycolysis and OXPHOS activities. Previously, by modeling the gene regulation of cancer metabolism we have reported that cancer cells can acquire a stable hybrid metabolic state in which both glycolysis and OXPHOS can be used. Here, to comprehensively characterize cancer metabolic activity, we establish a theoretical framework by coupling gene regulation with metabolic pathways. Our modeling results demonstrate a direct association between the activities of AMPK and HIF-1, master regulators of OXPHOS and glycolysis, respectively, with the activities of three major metabolic pathways: glucose oxidation, glycolysis, and fatty acid oxidation.

Purpose: This was an open-label phase 1a study assessing the maximum tolerated dose (MTD), safety, and tolerability of CXCR4 peptide antagonist, LY2510924, administered in combination with durvalumab in patients with advanced refractory solid tumors.

Methods: Patients received LY2510924 at 20, 30, or 40 mg subcutaneous (SC) once daily in combination with durvalumab at 1500 mg intravenously (IV) on day 1 of each 28-day cycle. The primary objective was to assess the MTD and safety of LY2510924 SC daily in combination with durvalumab in patients with advanced (metastatic and/or unresectable) solid tumors. Secondary objectives included pharmacokinetics (PK) and the antitumor activity of LY2510924 in combination with durvalumab. Exploratory objectives were biomarker analysis, including pharmacodynamic markers, relevant to LY2510924 and durvalumab, including immune functioning, drug targets, cancer-related pathways, and the disease state.

Results: Nine patients (three each at 20, 30, and 40 mg) were enrolled in the study (eight patients with pancreatic cancer and one patient with rectal cancer). The majority of patients completed one or two cycles (100.0% ≥ 1 cycle; 88.9% ≥ 2 cycles) of LY2510924 and durvalumab. No dose limiting toxicities were reported. Most common (10%) treatment-emergent adverse events were injection-site reaction (44.4%), fatigue (33.3%), and increased white blood cell count (33.3%). PK parameters for combination were similar to those reported in previous studies when given as monotherapy. Best overall response of stable disease was observed in four (44.4%) patients and one patient had unconfirmed partial response.

Researchers have fashioned ultrathin silicon nanoantennas that trap and redirect light, for applications in quantum computing, LIDAR and even the detection of viruses.

Light is notoriously fast. Its speed is crucial for rapid information exchange, but as light zips through materials, its chances of interacting and exciting atoms and molecules can become very small. If scientists can put the brakes on light particles, or photons, it would open the door to a host of new technology applications.

Now, in a paper published on August 17, 2020, in Nature Nanotechnology, Stanford scientists demonstrate a new approach to slow light significantly, much like an echo chamber holds onto sound, and to direct it at will. Researchers in the lab of Jennifer Dionne, associate professor of materials science and engineering at Stanford, structured ultrathin silicon chips into nanoscale bars to resonantly trap light and then release or redirect it later. These “high-quality-factor” or “high-Q” resonators could lead to novel ways of manipulating and using light, including new applications for quantum computing, virtual reality and augmented reality; light-based WiFi; and even the detection of viruses like SARS-CoV-2.

Amid a pandemic, civil unrest and a divisive US election season, we now have an asteroid zooming toward us.

On the day before the presidential vote, no less.

Yep. The celestial object known as 2018VP1 is projected to come close to Earth on November 2, according to the Center for Near Earth Objects Studies at NASA’s Jet Propulsion Laboratory.

Continue reading “NASA: An Asteroid Will Come Close To Earth Right Before Election Day” »

Salk Institute scientists have harnessed stem cell technology to generate the first human insulin-producing pancreatic cell clusters that can evade the immune system. Generated from induced pluripotent stem cells (iPSCs), these “immune shielded” human islet-like organoids (HILOs) controlled blood glucose following transplantation into a mouse model of diabetes, without the use of immunosuppressive drugs. The researchers suggest the achievement represents a major advance in the quest for a safe and effective treatment for type 1 diabetes (T1D), which impacts an estimated 1.6 million people in the United States, at a cost of $14.4 billion annually.

“Most type 1 diabetics are children and teenagers,” said Salk professor Ronald Evans, PhD, holder of the March of Dimes chair in molecular and developmental biology. Evans is senior author of the team’s paper, which is published in Nature. “This is a disease that is historically hard to manage with drugs. We hope that regenerative medicine in combination with immune shielding can make a real difference in the field by replacing damaged cells with lab-generated human islet-like cell clusters that produce normal amounts of insulin on demand.”

Continue reading “Diabetes Controlled in Mice Using First Immune-Evading Human Islet Cell Organoids” »

The coronavirus has wreaked havoc on our world’s economy, and many scientists and nations are scrambling to get a vaccine out. In today’s video, I will talk about what will happen when that vaccine actually appears:

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If artificial intelligence can replace some highly specialized medical doctors, is any job safe? It appears the biomedical profession is ripe for an overhaul.

“We have for the first time used deep learning to find disease-related genes. This is a very powerful method in the analysis of huge amounts of biological information, or ‘big data’,” said Sanjiv Dwivedi, first author of the newly published research.