Preliminary study of the transition of sea ice during the melting process

In order to understand the transition in sea ice, snow transformation, and temperature variations, we carried out tank experiments in a cold room. In the melting experiment of bare ice, the transition of the condition of the ice surface was observed through visual observations and reflectance measurements. The first change was manifested in the surface becoming wet and acquiring a rough texture. Subsequently, a porous layer was formed under the ice surface. Since this layer scattered the incident light, it appeared as a bright surface. The reflectance of this surface was high as compared with that measured during the initial stages of melting. However, this thin scattering layer disappeared as the melting progressed. As a result, the reflectance was reduced to its value during the initial stage of melting. In the melting experiments on snow covered sea ice, the structure of snow-ice became porous and mechanically weak before the thickness reduction commenced. The temperature gradients of bare ice and snow covered ice were small during the melting process compared to those during the growth period

Synthesis of diblock copolymers with cellulose derivatives 4. Self-assembled nanoparticles of amphiphilic cellulose derivatives carrying a single pyrene group at the reducing-end

Self-assembled cellulose-pyrene nanoparticles were prepared from amphiphilic cellulose derivatives carrying a single pyrene group at the reducing-end, N-(1-pyrenebutyloyl)-β-cellulosylamine (CELL13Py and CELL30Py, the number average degrees of polymerization (DPn) of 13 and 30, respectively) and N-(15-(1-pyrenebutyloylamino)-pentadecanoyl)-β-cellulosylamine (CELL13C15Py and CELL30C15Py, DPn of 13 and 30, respectively). Transmission electron microscopy (TEM) observation revealed that CELL13C15Py and CELL30C15Py formed self-assembled nanoparticles with the average diameters of 108.8 and 40.0 nm, respectively. The average radius of CELL30C15Py nanoparticles (20.0 nm) agreed well with the molecular length of its cellulose chain (19.2 nm). CELL30C15Py nanoparticles were expected to have monolayered structure, consisting of cellulose shell with radial orientation and hydrophobic core of 15-(1-pyrenebutyloylamino)-pentadecanoyl groups. The fluorescent spectrum of CELL30C15Py nanoparticles showed an excimer emission due to dimerized pyrene groups, indicating that the pyrene groups at the reducing-end of cellulose are associating in the particles. The balance of hydrophilic and hydrophobic parts of the cellulose derivatives controlled their self-assembled nanostructures. X-ray diffraction measurements revealed that radially oriented cellulose chains of CELL30C15Py nanoparticles were mostly amorphous, and at the same time exhibited weak reflection pattern of cellulose II, which is believed to have anti-parallel orientation

Electrochemical Dy-Alloying Behaviors of Ni-Based Alloys in Molten LiF–CaF2–DyF3: Effects of Constituent Elements

The electrochemical Dy-alloying behaviors of Ni–Cr and Ni–Mo alloys were compared with those of Ni–Cr–Mo alloy and pure Ni in a molten LiF–CaF2–DyF3 (0.30 mol%) system at 1123 K. The effects of chromium and molybdenum as constituent elements of the Ni-based alloys were investigated. Cyclic voltammetry and open-circuit potentiometry indicated the formations of Dy–Ni alloys for all the Ni-based electrodes, as well as for the pure Ni electrode. XRD analysis confirmed the formation of DyNi2 and DyNi3 phases for all the electrodes electrolyzed at 0.20 V (vs. Li+/Li) for 60 min. SEM/TEM-EDX analysis of the sample prepared from Ni–Cr–Mo alloy revealed that the Dy-alloyed layer consists of Cr-rich Cr–Mo and Mo-rich Mo–Cr phases, as well as a Dy–Ni(–Fe) matrix phase. The shear stress measurements of the Dy-alloyed samples showed that the Ni–Cr–Mo alloy is the most suitable substrate to improve mechanical strength, which is explained by precipitation strengthening by both the Cr–Mo and Mo–Cr phases

Artemin, a Novel Member of the GDNF Ligand Family, Supports Peripheral and Central Neurons and Signals through the GFRα3–RET Receptor Complex

AbstractThe glial cell line–derived neurotrophic factor (GDNF) ligands (GDNF, Neurturin [NTN], and Persephin [PSP]) signal through a multicomponent receptor system composed of a high-affinity binding component (GFRα1–GFRα4) and a common signaling component (RET). Here, we report the identification of Artemin, a novel member of the GDNF family, and demonstrate that it is the ligand for the former orphan receptor GFRα3–RET. Artemin is a survival factor for sensory and sympathetic neurons in culture, and its expression pattern suggests that it also influences these neurons in vivo. Artemin can also activate the GFRα1–RET complex and supports the survival of dopaminergic midbrain neurons in culture, indicating that like GDNF (GFRα1–RET) and NTN (GFRα2–RET), Artemin has a preferred receptor (GFRα3–RET) but that alternative receptor interactions also occur

The Wnt Antagonist Frzb-1 Regulates Chondrocyte Maturation and Long Bone Development during Limb Skeletogenesis

AbstractThe Wnt antagonist Frzb-1 is expressed during limb skeletogenesis, but its roles in this complex multistep process are not fully understood. To address this issue, we determined Frzb-1 gene expression patterns during chick long bone development and carried out gain- and loss-of-function studies by misexpression of Frzb-1, Wnt-8 (a known Frzb-1 target), or different forms of the intracellular Wnt mediator LEF-1 in developing limbs and cultured chondrocytes. Frzb-1 expression was quite strong in mesenchymal prechondrogenic condensations and then characterized epiphyseal articular chondrocytes and prehypertrophic chondrocytes in growth plates. Virally driven Frzb-1 misexpression caused shortening of skeletal elements, joint fusion, and delayed chondrocyte maturation, with consequent inhibition of matrix mineralization, metalloprotease expression, and marrow/bone formation. In good agreement, misexpression of Frzb-1 or a dominant-negative form of LEF-1 in cultured chondrocytes maintained the cells at an immature stage. Instead, misexpression of Wnt-8 or a constitutively active LEF-1 strongly promoted chondrocyte maturation, hypertrophy, and calcification. Immunostaining revealed that the distribution of endogenous Wnt mediator β-catenin changes dramatically in vivo and in vitro, from largely cytoplasmic in immature proliferating and prehypertrophic chondrocytes to nuclear in hypertrophic mineralizing chondrocytes. Misexpression of Frzb-1 prevented β-catenin nuclear relocalization in chondrocytes in vivo or in vitro. The data demonstrate that Frzb-1 exerts a strong influence on limb skeletogenesis and is a powerful and direct modulator of chondrocyte maturation, phenotype, and function. Phases of skeletogenesis, such as terminal chondrocyte maturation and joint formation, appear to be particularly dependent on Wnt signaling and thus very sensitive to Frzb-1 antagonistic action

Single nucleotide polymorphism-based genome-wide linkage analysis in Japanese atopic dermatitis families

<p>Abstract</p> <p>Background</p> <p>Atopic dermatitis develops as a result of complex interactions between several genetic and environmental factors. To date, 4 genome-wide linkage studies of atopic dermatitis have been performed in Caucasian populations, however, similar studies have not been done in Asian populations. The aim of this study was to identify chromosome regions linked to atopic dermatitis in a Japanese population.</p> <p>Methods</p> <p>We used a high-density, single nucleotide polymorphism genotyping assay, the Illumina BeadArray Linkage Mapping Panel (version 4) comprising 5,861 single nucleotide polymorphisms, to perform a genome-wide linkage analysis of 77 Japanese families with 111 affected sib-pairs with atopic dermatitis.</p> <p>Results</p> <p>We found suggestive evidence for linkage with 15q21 (LOD = 2.01, NPL = 2.87, <it>P </it>= .0012) and weak linkage to 1q24 (LOD = 1.26, NPL = 2.44, <it>P </it>= .008).</p> <p>Conclusion</p> <p>We report the first genome-wide linkage study of atopic dermatitis in an Asian population, and novel loci on chromosomes 15q21 and 1q24 linked to atopic dermatitis. Identification of novel causative genes for atopic dermatitis will advance our understanding of the pathogenesis of atopic dermatitis.</p

The whole blood transcriptional regulation landscape in 465 COVID-19 infected samples from Japan COVID-19 Task Force

「コロナ制圧タスクフォース」COVID-19患者由来の血液細胞における遺伝子発現の網羅的解析 --重症度に応じた遺伝子発現の変化には、ヒトゲノム配列の個人差が影響する--. 京都大学プレスリリース. 2022-08-23.Coronavirus disease 2019 (COVID-19) is a recently-emerged infectious disease that has caused millions of deaths, where comprehensive understanding of disease mechanisms is still unestablished. In particular, studies of gene expression dynamics and regulation landscape in COVID-19 infected individuals are limited. Here, we report on a thorough analysis of whole blood RNA-seq data from 465 genotyped samples from the Japan COVID-19 Task Force, including 359 severe and 106 non-severe COVID-19 cases. We discover 1169 putative causal expression quantitative trait loci (eQTLs) including 34 possible colocalizations with biobank fine-mapping results of hematopoietic traits in a Japanese population, 1549 putative causal splice QTLs (sQTLs; e.g. two independent sQTLs at TOR1AIP1), as well as biologically interpretable trans-eQTL examples (e.g., REST and STING1), all fine-mapped at single variant resolution. We perform differential gene expression analysis to elucidate 198 genes with increased expression in severe COVID-19 cases and enriched for innate immune-related functions. Finally, we evaluate the limited but non-zero effect of COVID-19 phenotype on eQTL discovery, and highlight the presence of COVID-19 severity-interaction eQTLs (ieQTLs; e.g., CLEC4C and MYBL2). Our study provides a comprehensive catalog of whole blood regulatory variants in Japanese, as well as a reference for transcriptional landscapes in response to COVID-19 infection

DOCK2 is involved in the host genetics and biology of severe COVID-19

「コロナ制圧タスクフォース」COVID-19疾患感受性遺伝子DOCK2の重症化機序を解明 --アジア最大のバイオレポジトリーでCOVID-19の治療標的を発見--. 京都大学プレスリリース. 2022-08-10.Identifying the host genetic factors underlying severe COVID-19 is an emerging challenge. Here we conducted a genome-wide association study (GWAS) involving 2, 393 cases of COVID-19 in a cohort of Japanese individuals collected during the initial waves of the pandemic, with 3, 289 unaffected controls. We identified a variant on chromosome 5 at 5q35 (rs60200309-A), close to the dedicator of cytokinesis 2 gene (DOCK2), which was associated with severe COVID-19 in patients less than 65 years of age. This risk allele was prevalent in East Asian individuals but rare in Europeans, highlighting the value of genome-wide association studies in non-European populations. RNA-sequencing analysis of 473 bulk peripheral blood samples identified decreased expression of DOCK2 associated with the risk allele in these younger patients. DOCK2 expression was suppressed in patients with severe cases of COVID-19. Single-cell RNA-sequencing analysis (n = 61 individuals) identified cell-type-specific downregulation of DOCK2 and a COVID-19-specific decreasing effect of the risk allele on DOCK2 expression in non-classical monocytes. Immunohistochemistry of lung specimens from patients with severe COVID-19 pneumonia showed suppressed DOCK2 expression. Moreover, inhibition of DOCK2 function with CPYPP increased the severity of pneumonia in a Syrian hamster model of SARS-CoV-2 infection, characterized by weight loss, lung oedema, enhanced viral loads, impaired macrophage recruitment and dysregulated type I interferon responses. We conclude that DOCK2 has an important role in the host immune response to SARS-CoV-2 infection and the development of severe COVID-19, and could be further explored as a potential biomarker and/or therapeutic target

The Constrained Maximal Expression Level Owing to Haploidy Shapes Gene Content on the Mammalian X Chromosome.

X chromosomes are unusual in many regards, not least of which is their nonrandom gene content. The causes of this bias are commonly discussed in the context of sexual antagonism and the avoidance of activity in the male germline. Here, we examine the notion that, at least in some taxa, functionally biased gene content may more profoundly be shaped by limits imposed on gene expression owing to haploid expression of the X chromosome. Notably, if the X, as in primates, is transcribed at rates comparable to the ancestral rate (per promoter) prior to the X chromosome formation, then the X is not a tolerable environment for genes with very high maximal net levels of expression, owing to transcriptional traffic jams. We test this hypothesis using The Encyclopedia of DNA Elements (ENCODE) and data from the Functional Annotation of the Mammalian Genome (FANTOM5) project. As predicted, the maximal expression of human X-linked genes is much lower than that of genes on autosomes: on average, maximal expression is three times lower on the X chromosome than on autosomes. Similarly, autosome-to-X retroposition events are associated with lower maximal expression of retrogenes on the X than seen for X-to-autosome retrogenes on autosomes. Also as expected, X-linked genes have a lesser degree of increase in gene expression than autosomal ones (compared to the human/Chimpanzee common ancestor) if highly expressed, but not if lowly expressed. The traffic jam model also explains the known lower breadth of expression for genes on the X (and the Z of birds), as genes with broad expression are, on average, those with high maximal expression. As then further predicted, highly expressed tissue-specific genes are also rare on the X and broadly expressed genes on the X tend to be lowly expressed, both indicating that the trend is shaped by the maximal expression level not the breadth of expression per se. Importantly, a limit to the maximal expression level explains biased tissue of expression profiles of X-linked genes. Tissues whose tissue-specific genes are very highly expressed (e.g., secretory tissues, tissues abundant in structural proteins) are also tissues in which gene expression is relatively rare on the X chromosome. These trends cannot be fully accounted for in terms of alternative models of biased expression. In conclusion, the notion that it is hard for genes on the Therian X to be highly expressed, owing to transcriptional traffic jams, provides a simple yet robustly supported rationale of many peculiar features of X's gene content, gene expression, and evolution