Irradiation-energy Dependence on the Spectral Changes of Hydrous C-Type Asteroids Based on 4kev and 20kev He Exposure Experiments of Murchison Cm Chondrite

C-type asteroid 162173 Ryugu was observed by remote sensing apparatus onboard Hayabusa2 spacecraft and found to be very dark object whose reflectance is (1.60 0.15) % at 0.55m and showed a small 2.7m absorption band indicative of phyllosilicates. The optical navigation camera detected color variations of Ryugus surface in the wavelength range from 0.4 to 0.95m: Bluer spectra are ob-served at both poles and on the equatorial ridge, both of which are topographic highs and thus may be fresh material exposed by gradual erosion. On the other hand, many locations at middle-latitude areas exhibit redder and darker colors. Similar color variations are also detected in the near-infrared wavelength range. These observations suggest that a surface-correlated process is responsible for the color variation, most prob-ably from blue to red, but the mechanism for the change is not yet identified. Space weathering is one possible mechanism responsible for the color variation, but the spectral changes of C-type asteroids from space weathering are far from being fully understood. Past experimental studies using hydrous carbonaceous chondrites such as Murchison and Tagish Lake show that He exposure (simulating solar wind irradiation) changes spectra to bluer and brighter. Recently our He exposure experiments indicate that spectral changes depend on physical properties such as porosity of exposed material. In this study, we per-formed further He exposure experiments using Murchison CM chondrite in order to understand energy dependence on the spectral changes. We found that He energy is a critical parameter, as well as physical properties of the samples, that affects spectral changes of space weathering of hydrated C-type asteroids

Diamond Blackfan anemia is mediated by hyperactive Nemo-like kinase

Diamond Blackfan Anemia (DBA) is a congenital bone marrow failure syndrome associated with ribosomal gene mutations that lead to ribosomal insufficiency. DBA is characterized by anemia, congenital anomalies, and cancer predisposition. Treatment for DBA is associated with significant morbidity. Here, we report the identification of Nemo-like kinase (NLK) as a potential target for DBA therapy. To identify new DBA targets, we screen for small molecules that increase erythroid expansion in mouse models of DBA. This screen identified a compound that inhibits NLK. Chemical and genetic inhibition of NLK increases erythroid expansion in mouse and human progenitors, including bone marrow cells from DBA patients. In DBA models and patient samples, aberrant NLK activation is initiated at the Megakaryocyte/Erythroid Progenitor (MEP) stage of differentiation and is not observed in non-erythroid hematopoietic lineages or healthy erythroblasts. We propose that NLK mediates aberrant erythropoiesis in DBA and is a potential target for therapy

Biharmonic PNMC Submanifolds in Spheres

We obtain several rigidity results for biharmonic submanifolds in $\mathbb{S}^{n}$ with parallel normalized mean curvature vector field. We classify biharmonic submanifolds in $\mathbb{S}^{n}$ with parallel normalized mean curvature vector field and with at most two distinct principal curvatures. In particular, we determine all biharmonic surfaces with parallel normalized mean curvature vector field in $\mathbb{S}^n$. Then we investigate, for (not necessarily compact) proper biharmonic submanifolds in $\mathbb{S}^n$, their type in the sense of B-Y. Chen. We prove: (i) a proper biharmonic submanifold in $\mathbb{S}^n$ is of 1-type or 2-type if and only if it has constant mean curvature {\mcf}=1 or {\mcf}\in(0,1), respectively; (ii) there are no proper biharmonic 3-type submanifolds with parallel normalized mean curvature vector field in $\mathbb{S}^n$.Comment: 17 page

Sample collection from asteroid (162173) Ryugu by Hayabusa2: Implications for surface evolution

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Generation of Germline-Competent Rat Induced Pluripotent Stem Cells

Recent progress in rat pluripotent stem cell technology has been remarkable. Particularly salient is the demonstration that embryonic stem cells (ESCs) in the rat (rESCs) can contribute to germline transmission, permitting generation of gene-modified rats as is now done using mouse ESCs (mESCs) or mouse induced pluripotent stem cells (iPSCs; miPSCs). However, determinations of whether rat iPSCs (riPSCs) can contribute to germ cells are not published. Here we report the germline competency of riPSCs.We generated riPSCs by transducing three mouse reprogramming factors (Oct3/4, Klf4, and Sox2) into rat somatic cells, followed by culture in the presence of exogenous rat leukemia inhibitory factor (rLIF) and small molecules that specifically inhibit GSK3, MEK, and FGF receptor tyrosine kinases. We found that, like rESCs, our riPSCs can contribute to germline transmission. Furthermore we found, by immunostaining of testis from mouse-rat interspecific chimeras with antibody against mouse vasa homolog, that riPSCs can contribute to embryonic development with chimera formation in mice (rat-mouse interspecific chimeras) and to interspecific germlines.Our data clearly demonstrate that using only three reprogramming factors (Oct3/4, Klf4, and Sox2) rat somatic cells can be reprogrammed into a ground state. Our generated riPSCs exhibited germline transmission in either rat-rat intraspecific or mouse-rat interspecific chimeras

Dysregulated lipid synthesis by oncogenic IDH1 mutation is a targetable synthetic lethal vulnerability

Isocitrate dehydrogenase 1 and 2 (IDH) are mutated in multiple cancers and drive production of (R)-2-hydroxyglutarate (2HG). We identified a lipid synthesis enzyme (acetyl CoA carboxylase 1, ACC1) as a synthetic lethal target in mutant IDH1 (mIDH1), but not mIDH2, cancers. Here, we analyzed the metabolome of primary acute myeloid leukemia (AML) blasts and identified a mIDH1-specific reduction in fatty acids. mIDH1 also induced a switch to beta-oxidation indicating reprogramming of metabolism towards a reliance on fatty acids. Compared to mIDH2, mIDH1 AML displayed depletion of NADPH with defective reductive carboxylation that was not rescued by the mIDH1-specific inhibitor ivosidenib. In xenograft models, a lipid-free diet markedly slowed the growth of mIDH1 AML, but not healthy CD34+ HSPCs or mIDH2 AML. Genetic and pharmacologic targeting of ACC1 resulted in growth inhibition of mIDH1 cancers, not reversible by ivosidenib. Critically, pharmacologic targeting of ACC1 improved sensitivity of mIDH1 AML to venetoclax.Daniel Thomas, Manhong Wu, Yusuke Nakauchi, Ming Zheng, Chloe A.L. Thompson-Peach, Kelly Lim, Niklas Landberg, Thomas Köhnke, Nirmal Robinson, Satinder Kaur, Monika Kutyna, Melissa Stafford, Devendra Hiwase, Andreas Reinisch, Gary Peltz, Ravindra Majet