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The structure of the universe is often described as being a cosmic web of filaments, nodes, and voids, with the nodes being clusters of galaxies, the largest gravitationally bound objects known. These nodes are thought to have been seeded by small-amplitude density fluctuations like those observed in the cosmic microwave background (CMB) which grew until they collapsed into the structures seen today. While the CMB is well understood, and the details of present-day galaxy clusters are well-described, the intermediate phases of evolution lack sufficient observations to constrain the models. Traditional galaxy cluster searches assume these objects have had enough time to equilibrate so that the intergalactic gas has heated up enough to be detected in X-ray emission. To detect the more distant galaxies and protoclusters that are too faint to detect in the X-ray, astronomers use their bright infrared or submillimeter emission instead.

The supercluster SPT2349−56, discovered in the submillimeter band by the South Pole Telescope, is so distant that its light has been traveling for over twelve billion years. It hosts over thirty submillimeter-bright galaxies and dozens of other luminous and/or spectroscopically confirmed star-forming galaxies. It is one of the most active star forming complexes known, producing over ten thousand stars per year. One of its bright sources appears to be the merger of over twenty galaxies. The stellar mass of the system, however, was not known, making it impossible for example to know whether the huge burst of stars was the result of an extraordinary efficiency or simply arose because the system was so extremely large.

CfA astronomer Matthew Ashby was a member of a team that has now completed very deep observations at optical and to obtain the stellar masses through spectral energy distribution (SED) analyses. They used the Gemini and Hubble Space Telescopes to obtain optical/near infrared flux measurements and Spitzer’s IRAC camera for the infrared flux. In order to model the SEDs, the many point sources detected need to be matched to one another at all wavelengths. This is a complex undertaking, and the scientists describe the processes for doing so while also addressing the serious blending that can occur due to inadequate spatial resolution in the infrared.

Without antibiotics or any understanding of how the disease spread, The Black Death wiped out between 30 and 50% of Europe’s population. It got its name from the spots that appeared on those who were infected. The name bubonic plague refers to buboes which were painfully swollen lymph nodes that bulged. The Black Death infections included other symptoms such as delirium, high fever, and vomiting.

The key to uncovering the origin relies on evidence from three women who were buried near Lake Issyk Kul on the edge of the Tian Shan mountains. They died in 1,338 and 1,339 of what was referenced on their grave markers as a pestilence. Nearby were many more grave markers covering the decade before The Black Death arrived in Europe.

Y. Pestis was a bacterium that resided in fleas which then past it on to animals and humans through bites. Rats were seen as the likely source of Europe’s outbreak. But humans were facilitators of the spread along trade routes from Central Asia to Europe. What we do know is that the original strain of Y. Pestis mutated into four variants with one of those arriving in Europe seven years after the Kyrgyzstan outbreak.

Researchers at the University of Houston have demonstrated a new technique for helping heart cells regenerate after a heart attack, using mRNA to return the cells to a stem-cell-like state. Tests in mice showed drastic improvements to heart function a month after a heart attack.

Unlike most tissues in the body, heart cells have a limited ability to regenerate after injury. That’s a big part of why heart attacks are so deadly – afterwards, non-beating scar tissue forms instead, which can lead to further attacks and eventually heart failure.

In recent years, scientists have been investigating how to repair broken hearts by regenerating the cells, with some success seen using placental stem cells, reprogramming structural cells into ones that beat, or using stem cell messengers to induce the heart to self-repair. Others have identified transcription factors that can get heart cells to begin replicating again.