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High-resolution ‘before and after’ imaging of the Moon is used to quantify the rate of crater production and provide insights into the cratering process. Current cratering rates on the Moon Emerson Speyerer and co-authors use 14,092 temporal ('before and after') image pairs obtained by NASA's Lunar Reconnaissance Orbiter to quantify the contemporary crater-production rate on the Moon. They identify broad reflectance zones associated with the new craters that they interpret as evidence of a surface-bound jetting process, and estimate that this secondary cratering process is churning the top of the regolith much faster than previously thought. Random bombardment by comets, asteroids and associated fragments form and alter the lunar regolith and other rocky surfaces. The accumulation of impact craters over time is of fundamental use in evaluating the relative ages of geologic units. Crater counts and radiometric ages from returned samples provide constraints with which to derive absolute model ages for unsampled units on the Moon and other Solar System objects 1 , 2 , 3 , 4 . However, although studies of existing craters and returned samples offer insight into the process of crater formation and the past cratering rate, questions still remain about the present rate of crater production, the effect of early-stage jetting during impacts and the influence that distal ejecta have on the regolith. Here we use Lunar Reconnaissance Orbiter Camera (LROC) Narrow Angle Camera (NAC) temporal (‘before and after’) image pairs to quantify the contemporary rate of crater production on the Moon, to reveal previously unknown details of impact-induced jetting, and to identify a secondary impact process that is rapidly churning the regolith. From this temporal dataset, we detected 222 new impact craters and found 33 per cent more craters (with diameters of at least ten metres) than predicted by the standard Neukum production and chronology functions for the Moon 2 . We identified broad reflectance zones associated with the new craters that we interpret as evidence of a surface-bound jetting process. We also observe a secondary cratering process that we estimate churns the top two centimetres of regolith on a timescale of 81,000 years—more than a hundred times faster than previous models estimated from meteoritic impacts (ten million years) 5 .

When a genetic test was used to assess prognosis, women with midrange scores were found to have similar outcomes after adjuvant treatment with either endocrine therapy alone or chemotherapy plus endocrine therapy.

Patients with early-stage estrogen-receptor–positive, node-negative breast cancer whose 21-gene Oncotype DX profile suggested a low risk of recurrence were safely treated with endocrine therapy alone and were spared exposure to adjuvant chemotherapy. Breast cancer is the most common cancer in women worldwide and in the United States, and it is the leading cause of death from cancer in women worldwide. 1 Prognostic factors for the recurrence of breast cancer at a distant site regardless of treatment include clinicopathologic features such as tumor size and grade and the number of axillary lymph nodes with metastasis. 2 Predictive factors that identify a benefit from specific therapies include the expression of the estrogen receptor and the progesterone receptor, which identifies patients who benefit from adjuvant endocrine therapy, 3 and overexpression of the human epidermal growth factor receptor 2 . . .

One of the most challenging obstacles to realizing exascale computing is minimizing the energy consumption of L2 cache, main memory, and interconnects to that memory. For promising cryogenic computing schemes utilizing Josephson junction superconducting logic, this obstacle is exacerbated by the cryogenic system requirements that expose the technology’s lack of high-density, high-speed and power-efficient memory. Here we demonstrate an array of cryogenic memory cells consisting of a non-volatile three-terminal magnetic tunnel junction element driven by the spin Hall effect, combined with a superconducting heater-cryotron bit-select element. The write energy of these memory elements is roughly 8 pJ with a bit-select element, designed to achieve a minimum overhead power consumption of about 30%. Individual magnetic memory cells measured at 4 K show reliable switching with write error rates below 10 −6 , and a 4 × 4 array can be fully addressed with bit select error rates of 10 −6 . This demonstration is a first step towards a full cryogenic memory architecture targeting energy and performance specifications appropriate for applications in superconducting high performance and quantum computing control systems, which require significant memory resources operating at 4 K.

Myocardial mitochondrial Ca ²⁺ entry enables physiological stress responses but in excess promotes injury and death. However, tissue-specific in vivo systems for testing the role of mitochondrial Ca ²⁺ are lacking. We developed a mouse model with myocardial delimited transgenic expression of a dominant negative (DN) form of the mitochondrial Ca ²⁺ uniporter (MCU). DN-MCU mice lack MCU-mediated mitochondrial Ca ²⁺ entry in myocardium, but, surprisingly, isolated perfused hearts exhibited higher O ₂ consumption rates (OCR) and impaired pacing induced mechanical performance compared with wild-type (WT) littermate controls. In contrast, OCR in DN-MCU–permeabilized myocardial fibers or isolated mitochondria in low Ca ²⁺ were not increased compared with WT, suggesting that DN-MCU expression increased OCR by enhanced energetic demands related to extramitochondrial Ca ²⁺ homeostasis. Consistent with this, we found that DN-MCU ventricular cardiomyocytes exhibited elevated cytoplasmic [Ca ²⁺] that was partially reversed by ATP dialysis, suggesting that metabolic defects arising from loss of MCU function impaired physiological intracellular Ca ²⁺ homeostasis. Mitochondrial Ca ²⁺ overload is thought to dissipate the inner mitochondrial membrane potential (ΔΨm) and enhance formation of reactive oxygen species (ROS) as a consequence of ischemia-reperfusion injury. Our data show that DN-MCU hearts had preserved ΔΨm and reduced ROS during ischemia reperfusion but were not protected from myocardial death compared with WT. Taken together, our findings show that chronic myocardial MCU inhibition leads to previously unanticipated compensatory changes that affect cytoplasmic Ca ²⁺ homeostasis, reprogram transcription, increase OCR, reduce performance, and prevent anticipated therapeutic responses to ischemia-reperfusion injury. Mitochondrial Ca ²⁺ is a fundamental signal that allows for adaptation to physiological stress but a liability during ischemia-reperfusion injury in heart. On one hand, mitochondrial Ca ²⁺ entry coordinates energy supply and demand in myocardium by increasing the activity of matrix dehydrogenases to augment ATP production by oxidative phosphorylation. On the other hand, inhibiting mitochondrial Ca ²⁺ overload is promulgated as a therapeutic approach to preserve myocardial tissue following ischemia-reperfusion injury. We developed a new mouse model of myocardial-targeted transgenic dominant-negative mitochondrial Ca ²⁺ uniporter (MCU) expression to test consequences of chronic loss of MCU-mediated Ca ²⁺ entry in heart. Here we show that MCU inhibition has unanticipated consequences on extramitochondrial pathways affecting oxygen utilization, cytoplasmic Ca ²⁺ homeostasis, physiologic responses to stress, and pathologic responses to ischemia-reperfusion injury.

While South Americans are underrepresented in human genomic diversity studies, Brazil has been a classical model for population genetics studies on admixture. We present the results of the EPIGEN Brazil Initiative, the most comprehensive up-to-date genomic analysis of any Latin-American population. A population-based genome-wide analysis of 6,487 individuals was performed in the context of worldwide genomic diversity to elucidate how ancestry, kinship, and inbreeding interact in three populations with different histories from the Northeast (African ancestry: 50%), Southeast, and South (both with European ancestry >70%) of Brazil. We showed that ancestry-positive assortative mating permeated Brazilian history. We traced European ancestry in the Southeast/South to a wider European/Middle Eastern region with respect to the Northeast, where ancestry seems restricted to Iberia. By developing an approximate Bayesian computation framework, we infer more recent European immigration to the Southeast/South than to the Northeast. Also, the observed low Native-American ancestry (6–8%) was mostly introduced in different regions of Brazil soon after the European Conquest. We broadened our understanding of the African diaspora, the major destination of which was Brazil, by revealing that Brazilians display two within-Africa ancestry components: one associated with non-Bantu/western Africans (more evident in the Northeast and African Americans) and one associated with Bantu/eastern Africans (more present in the Southeast/South). Furthermore, the whole-genome analysis of 30 individuals (42-fold deep coverage) shows that continental admixture rather than local post-Columbian history is the main and complex determinant of the individual amount of deleterious genotypes.