Lifeboat Foundation

Gating—controlling the state of one qubit conditioned on the state of another—is a key procedure in all quantum information processors. As the scale of quantum processors increases, the qubits will need to interact over larger and larger distances, which presents an experimental challenge in solid-state architectures. Wan et al. implemented the 20-year-old theoretical proposal of quantum gate teleportation that allows separated qubits to interact effectively. They deterministically teleported a controlled-NOT gate between two computational qubits in spatially separated zones in a segmented ion trap, demonstrating a feasible route toward scalable quantum information processors.

Science, this issue p. 875

Large-scale quantum computers will require quantum gate operations between widely separated qubits. A method for implementing such operations, known as quantum gate teleportation (QGT), requires only local operations, classical communication, and shared entanglement. We demonstrate QGT in a scalable architecture by deterministically teleporting a controlled-NOT (CNOT) gate between two qubits in spatially separated locations in an ion trap. The entanglement fidelity of our teleported CNOT is in the interval (0.845, 0.872) at the 95% confidence level. The implementation combines ion shuttling with individually addressed single-qubit rotations and detections, same- and mixed-species two-qubit gates, and real-time conditional operations, thereby demonstrating essential tools for scaling trapped-ion quantum computers combined in a single device.

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Repeated error correction creates a logical qubit encoded in the hybrid state of a superconducting circuit and a bosonic cavity, which is shown to be fully controllable under a universal single-qubit gate set.

Circa 2015

ETH researchers have found an error-free way to store information in the form of DNA, potentially preserving it for millions of years: encapsulate the information-bearing segments of DNA in silica (glass), using an error-correcting information-encoding scheme.

Scrolls thousands of years old provide us with a glimpse into long-forgotten cultures and the knowledge of our ancestors. In this digital era, in contrast, a large part of our knowledge is located on servers and hard drives, which may not survive 50 years, let alone thousands of years. So researchers are searching for new ways to store large volumes of data over the long term.

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A 120-sided dice is not an original idea, says mathematician Henry Segerman. “We were just the people crazy enough to actually do it.”

Elon Musk says adding two to four Raptor Engines to the Starship will let it go sub-orbital for 6000 miles at mach 20. This would mean trips like San Francisco to Shanghai or New York to Berlin. Many world cities are within 6000 miles of each other.

Boeing extended range 767s can reach 6000 miles and the newer 777 and 787 have longer ranges.

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Is up at Cosmoquest.

Some antidepressants could potentially be used to treat a wide range of diseases caused by bacteria living within cells, according to work by researchers in the Virginia Commonwealth University School of Medicine and collaborators at other institutions.

Research published in the April print edition of the journal Life Science Alliance, shows that antidepressant drugs called FIASMAs, including desipramine, amitriptyline, and nortriptyline, halt the growth or kill four different intracellular bacterial pathogens in tissue cell culture and animal models.

“Antibiotic options for diseases caused by intracellular bacteria are limited because many of these drugs cannot penetrate our cell membranes. In essence, the bacteria are protected,” said Jason Carlyon, Ph.D., leader of the study and professor in the VCU Department of Microbiology and Immunology.

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The cells of most patients’ cancers are resistant to a class of drugs, called proteasome inhibitors, that should kill them. When studied in the lab, these drugs are highly effective, yet hundreds of clinical trials testing proteasome inhibitors have failed. Now scientists may have solved the mystery of these cells’ surprising hardiness. The key: Resistant cancer cells have shifted how and where they generate their energy. Using this new insight, researchers have identified a drug that resensitizes cancer cells to proteasome inhibitors and pinpointed a gene that is crucial for that susceptibility.

As cancer cells develop, they accrue multiple genetic alterations that allow the cells to quickly reproduce, spread and survive in distant parts of the body, and recruit surrounding cells and tissues to support the growing tumor. To perform these functions, cancer cells must produce high volumes of the proteins that support these processes. The increased protein production and numerous mutated proteins of cancer cells make them particularly dependent on the proteasome, which is the cell’s protein degradation machine. These huge protein complexes act as recycling machines, gobbling up unwanted proteins and dicing them into their amino acid building blocks, which can be reused for the production of other proteins.

Previously, researchers exploited cancer cells’ increased dependency on their proteasomes to develop anti-cancer therapies that inhibit the proteasomes’ function. Several distinct proteasome inhibitors have been developed, and when used in the lab, these proteasome inhibitor drugs are indeed highly effective at eradicating tumor cells. However, when administered to animal models or patients with cancer, such as multiple myeloma, proteasome inhibitors have limited efficacy and even initially vulnerable cancer cells quickly develop resistance to them. How do cancer cells so adroitly sidestep drugs that should kill them?

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