19 research outputs found

    SNR improvement by variation of recording and media parameters for a HAMR exchange coupled composite media

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    An exchange coupled composite media structure proposed previously seems to address both the issue of Tc variation in FePt as well as poor SNR/User Density during the HAMR process. Here we examine a thinner 3-6 nm structure that is likely easier to fabricate than the previous 13.5 nm thick structure. We find that increasing the damping within the write (superparamagnetic) layer and introducing intergranular exchange within the grains in the write layer are both successful approaches to improve the recorded SNR. Ensemble waveform analysis that allows the breakdown of the total SNR into transition SNR (due to AC noise) and remanence SNR (due to DC noise) helps identify the leading causes for this SNR improvement. Further studies indicate that varying the peak heat spot temperature in the HAMR write process is also a successful approach for improving the recorded SNR. This lends credence to the idea that a thinner composite media may still be used successfully to realize significant enhancements of SNR and the corresponding user density

    In vivo

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    Patterns of fetal growth in a rural Indian cohort and a comparison with a western European population: data from the Pune Maternal Nutrition Study

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    The purpose of this study was to describe fetal size on sonography in a rural Indian population and compare it with those in European and urban Indian populations. Methods. Participants were from the Pune Maternal Nutrition Study of India. Fetal growth curves were constructed from serial ultrasound scans at approximately 18, 30, and 36 weeks’ gestation in 653 singleton pregnancies. Measurements included femur length (FL), abdominal circumference (AC), biparietal diameter (BPD), and occipitofrontal diameter, from which head circumference (HC) was estimated. Measurements were compared with data from a large population-based study in France and a study of urban mothers in Vellore, south India. Results. Fetal AC and BPD were smaller than the French reference at 18 weeks’ gestation (–1.38 and –1.30 SD, respectively), whereas FL and HC were more comparable (–0.77 and –0.59 SD). The deficit remained similar at 36 weeks for AC (–0.97 SD), FL (–0.43 SD), and HC (–0.52 SD) and increased for BPD (–2.3 SD). Sonography at 18 weeks underestimated gestational age compared with the last menstrual period date by a median of –1.4 (interquartile range, –4.6, 1.8) days. The Pune fetuses were smaller, even at the first scan, than the urban Vellore sample. Conclusions. Fetal size was smaller in a rural Indian population than in European and urban Indian populations, even in mid pregnancy. The deficit varied for different fetal measurements; it was greatest for AC and BPD and least for FL and H

    SARS-CoV-2 Infects Primary Neurons from Human ACE2 Expressing Mice and Upregulates Genes Involved in the Inflammatory and Necroptotic Pathways

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    Transgenic mice expressing human angiotensin-converting enzyme 2 under the cytokeratin 18 promoter (K18-hACE2) have been extensively used to investigate the pathogenesis and tissue tropism of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection. Neuroinvasion and the replication of SARS-CoV-2 within the central nervous system (CNS) of K18-hACE2 mice is associated with increased mortality; although, the mechanisms by which this occurs remain unclear. In this study, we generated primary neuronal cultures from K18-hACE2 mice to investigate the effects of a SARS-CoV-2 infection. We also evaluated the immunological response to SARS-CoV-2 infection in the CNS of K18-hACE2 mice and mouse neuronal cultures. Our data show that neuronal cultures obtained from K18-hACE2 mice are permissive to SARS-CoV-2 infection and support productive virus replication. Furthermore, SARS-CoV-2 infection upregulated the expression of genes involved in innate immunity and inflammation, including IFN-α, ISG-15, CXCL10, CCL2, IL-6 and TNF-α, in the neurons and mouse brains. In addition, we found that SARS-CoV-2 infection of neurons and mouse brains activates the ZBP1/pMLKL-regulated necroptosis pathway. Together, our data provide insights into the neuropathogenesis of SARS-CoV-2 infection in K18-hACE2 mice
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