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This paper reports the spinning and wear comfort properties of polyethylene terephthalate (PET)/copolymer-PET (Co-PET) hollow yarns and their fabrics, as well as the effect of the wt.% of inorganic particles embedded in the core of the bicomponent yarns. The results are discussed in terms of the types and amounts of inorganic particles (titanium dioxide (TiO2) and calcium carbonate (CaCO3)) embedded in the sheath of the bi-component yarns (Kolon semi-dull (KSD), Kolon full-dull (KFD), and Kolon calcium carbonate (KCC) PET/Co-PET yarns). The three sheath/3-core bicomponent yarns developed in this study exhibited good spinnability and weavability with relatively strong tenacity and breaking strain. Their optimal spinning conditions were determined. The KCC PET/Co-PET fabric showed the greatest hollowness ratio, followed by the KFD PET/Co-PET and KSD PET/Co-PET fabrics. This might be attributed to the higher wt.% (2.5 wt.%) of CaCO3 particles embedded in the sheath of the KCC PET/Co-PET yarns and to the larger particle size (0.8 μm) of CaCO3. Regarding the wear comfort, the moisture management system (MMT) test indicated that the KFD PET/Co-PET fabric is suitable for market applications because of its good moisture absorption and rapid drying. The KFD PET/Co-PET fabric is useful for winter clothing applications because of its relatively high heat retention rate and lack of durability issues with washing. An examination of the wearing performance for fitness with a tactile hand feel showed that KFD and KCC/Co-PET fabrics imparted a softer tactile hand feel than the KSD PET/Co-PET fabric. On the other hand, the KCC PET/Co-PET fabric was assumed to have some issues with wearing durability.

Type 1 Natural Killer T-cells (NKT1 cells) play a critical role in mediating hepatic ischemia-reperfusion injury (IRI). Although hepatic steatosis is a major risk factor for preservation type injury, how NKT cells impact this is understudied. Given NKT1 cell activation by phospholipid ligands recognized presented by CD1d, we hypothesized that NKT1 cells are key modulators of hepatic IRI because of the increased frequency of activating ligands in the setting of hepatic steatosis. We first demonstrate that IRI is exacerbated by a high-fat diet (HFD) in experimental murine models of warm partial ischemia. This is evident in the evaluation of ALT levels and Phasor-Fluorescence Lifetime (Phasor-FLIM) Imaging for glycolytic stress. Polychromatic flow cytometry identified pronounced increases in CD45+CD3+NK1.1+NKT1 cells in HFD fed mice when compared to mice fed a normal diet (ND). This observation is further extended to IRI, measuring ex vivo cytokine expression in the HFD and ND. Much higher interferon-gamma (IFN-γ) expression is noted in the HFD mice after IRI. We further tested our hypothesis by performing a lipidomic analysis of hepatic tissue and compared this to Phasor-FLIM imaging using “long lifetime species”, a byproduct of lipid oxidation. There are higher levels of triacylglycerols and phospholipids in HFD mice. Since N-acetylcysteine (NAC) is able to limit hepatic steatosis, we tested how oral NAC supplementation in HFD mice impacted IRI. Interestingly, oral NAC supplementation in HFD mice results in improved hepatic enhancement using contrast-enhanced magnetic resonance imaging (MRI) compared to HFD control mice and normalization of glycolysis demonstrated by Phasor-FLIM imaging. This correlated with improved biochemical serum levels and a decrease in IFN-γ expression at a tissue level and from CD45+CD3+CD1d+ cells. Lipidomic evaluation of tissue in the HFD+NAC mice demonstrated a drastic decrease in triacylglycerol, suggesting downregulation of the PPAR-γ pathway.

ABSTRACT We have developed a new millimeter wave receiver system with input optics that support simultaneous observations in four bands of 22, 43, 86, and 129 GHz to facilitate calibrating tropospheric phase fluctuations for millimeter-wave VLBI observations. In order to make simultaneous observations in four bands pointing at the same position in sky, it is crucial that errors among the beams from any misalignments should be kept small. After doing the beam alignment in the laboratory, on-site test observations were carried out so as to evaluate the performance. The result is that the beam centers of the four bands with reference to the 86 GHz beam center were aligned within 2″ over most of the elevation range of the Korean VLBI Network (KVN) 21 m telescope. Measured telescope aperture efficiencies including the multiband receiver optics are 65% at 22 GHz, 62% at 43 GHz, 57% at 86 GHz, and 38% at 129 GHz. Through this novel optics covering wide RF bandwidth effectively, we can simultaneously observe the SiO maser transitions at 43, 86, and 129 GHz and in addition the water maser line at 22 GHz.

Innate lymphoid cells (ILCs), the most recently described family of lymphoid cells, play fundamental roles in tissue homeostasis through the production of key cytokine. Group 1 ILCs, comprised of conventional natural killer cells (cNKs) and type 1 ILCs (ILC1s), have been implicated in regulating immune-mediated inflammatory diseases. However, the role of ILC1s in nonalcoholic fatty liver disease (NAFLD) and ischemia-reperfusion injury (IRI) is unclear. Here, we investigated the role of ILC1 and cNK cells in a high-fat diet (HFD) murine model of partial warm IRI. We demonstrated that hepatic steatosis results in more severe IRI compared to non-steatotic livers. We further elicited that HFD-IRI mice show a significant increase in the ILC1 population, whereas the cNK population was unchanged. Since ILC1 and cNK are major sources of IFN-γ and TNF-α, we measured the level of ex vivo cytokine expression in normal diet (ND)-IRI and HFD-IRI conditions. We found that ILC1s in HFD-IRI mice produce significantly more IFN-γ and TNF-α when compared to ND-IRI. To further assess whether ILC1s are key proinflammatory effector cells in hepatic IRI of fatty livers, we studied both Rag1 −/− mice, which possess cNK cells, and a substantial population of ILC1s versus the newly generated Rag1 −/− Tbx21 −/− double knockout (Rag1-Tbet DKO) mice, which lack type 1 ILCs, under HFD IRI conditions. Importantly, HFD Rag1-Tbet DKO mice showed significant protection from hepatic injury upon IRI when compared to Rag1 −/− mice, suggesting that T-bet-expressing ILC1s play a role, at least in part, as proinflammatory effector cells in hepatic IRI under steatotic conditions.

The ability to coordinate carbon (C) and nitrogen (N) metabolism enables plants to regulate development and metabolic responses to different environmental conditions. The regulator(s) or sensor(s) that monitor crosstalk between biosynthetic pathways and ultimately control the flow of C or N through them have remained elusive. We used an antisense strategy to demonstrate that the putative glutamate receptor 1.1 (AtGLR1.1) functions as a regulator of C and N metabolism in Arabidopsis. Seeds from AtGLR1.1-deficient Arabidopsis (antiAtGLR1.1) lines did not germinate in the presence of an animal ionotropic glutamate receptor (iGLR) antagonist, but germination was restored upon coincubation with an iGLR agonist or the putative ligand glutamate. In antiAtGLR1.1 lines, endogenous abscisic acid (ABA) concentrations increased with iGLR antagonist treatments and decreased with coincubation with an iGLR agonist, suggesting that germination was controlled by ABA. antiAtGLR1.1 seedlings also exhibited sensitivity to increased levels of Ca2+compared with wild type, and they exhibited a conditional phenotype that was sensitive to the C:N ratio. In the presence of C, specifically sucrose, but not glucose, mannitol, or sorbitol, antiAtGLR1.1 seeds did not germinate, but germination was restored upon coincubation with NO3 -, but not NH4 +. Immunoblot, isoenzyme, and RT-PCR analyses indicate that AtGLR1.1 regulates the accumulation of distinct C- and N-metabolic enzymes, hexokinase 1 (HXK1) and zeaxanthin epoxidase (ABA1), by transcriptional control. We provide a model to describe the role of AtGLR1.1 in C/N metabolism and ABA biosynthesis, which in turn controls seed germination.

We report simultaneous multifrequency observing performance at 22 and 43 GHz of the 21 m shaped-Cassegrain radio telescopes of the Korean VLBI Network (KVN). KVN is the first millimeter-dedicated VLBI network in Korea having a maximum baseline length of 480 km. It currently operates at 22 and 43 GHz and is planned to operate in four frequency bands: 22, 43, 86, and 129 GHz. The unique quasi optics of KVN enable simultaneous multifrequency observations based on efficient beam filtering and accurate antenna-beam alignment at 22 and 43 GHz. We found that the offset of the beams is within less than 5′′ over all pointing directions of the antenna. The dual-polarization, cooled, high electron mobility transistor (HEMT) receivers at 22 and 43 GHz result in receiver noise temperatures less than 40 K at 21.25–23.25 GHz and 80 K at 42.11–44.11 GHz. The pointing accuracies have been measured to be 3′′ in azimuth and elevation for all antennas. The measured aperture efficiencies are65%(K)/67%(Q) 65 % ( K ) / 67 % ( Q ) ,62%(K)/59%(Q) 62 % ( K ) / 59 % ( Q ) , and66%(K)/60%(Q) 66 % ( K ) / 60 % ( Q ) for the three KVN antennas, KVNYS, KVNUS, and KVNTN, respectively. The main-beam efficiencies are measured to be50%(K)/52%(Q) 50 % ( K ) / 52 % ( Q ) ,48%(K)/50%(Q) 48 % ( K ) / 50 % ( Q ) , and50%(K)/47%(Q) 50 % ( K ) / 47 % ( Q ) for KVNYS, KVNUS, and KVNTN, respectively. The estimated Moon efficiencies are77%(K)/90%(Q) 77 % ( K ) / 90 % ( Q ) ,74%(K)/79%(Q) 74 % ( K ) / 79 % ( Q ) , and80%(K)/86%(Q) 80 % ( K ) / 86 % ( Q ) for KVNYS, KVNUS, and KVNTN, respectively. The elevation dependence of the aperture efficiencies is quite flat for elevations greater than 20°.

ObjectiveHepatocellular carcinoma (HCC) represents a typical inflammation-associated cancer. Tissue resident innate lymphoid cells (ILCs) have been suggested to control tumour surveillance. Here, we studied how the local cytokine milieu controls ILCs in HCC.DesignWe performed bulk RNA sequencing of HCC tissue as well as flow cytometry and single-cell RNA sequencing of enriched ILCs from non-tumour liver, margin and tumour core derived from 48 patients with HCC. Simultaneous measurement of protein and RNA expression at the single-cell level (AbSeq) identified precise signatures of ILC subgroups. In vitro culturing of ILCs was used to validate findings from in silico analysis. Analysis of RNA-sequencing data from large HCC cohorts allowed stratification and survival analysis based on transcriptomic signatures.ResultsRNA sequencing of tumour, non-tumour and margin identified tumour-dependent gradients, which were associated with poor survival and control of ILC plasticity. Single-cell RNA sequencing and flow cytometry of ILCs from HCC livers identified natural killer (NK)-like cells in the non-tumour tissue, losing their cytotoxic profile as they transitioned into tumour ILC1 and NK-like-ILC3 cells. Tumour ILC composition was mediated by cytokine gradients that directed ILC plasticity towards activated tumour ILC2s. This was liver-specific and not seen in ILCs from peripheral blood mononuclear cells. Patients with high ILC2/ILC1 ratio expressed interleukin-33 in the tumour that promoted ILC2 generation, which was associated with better survival.ConclusionOur results suggest that the tumour cytokine milieu controls ILC composition and HCC outcome. Specific changes of cytokines modify ILC composition in the tumour by inducing plasticity and alter ILC function.

A loss of large aperture quasi-optics which consist of a lens and a feed antenna is firstly measured using a radiometer receiver via the modified reference control method for a W-band imaging radiometer system. The quasi-optical loss is mainly decided by the dielectric loss of the lens with good quasi-optical transformation efficiency between the lens and the feed antenna. The quasi-optics composed of an aspheric lens and a dielectric rod antenna are designed for high resolution, low aberration, and compact size. The fabricated quasi-optics with the aperture diameter of 500 mm have the quasi-optical transformation efficiency of more than 95%. The radiometer receiver is designed applying a total power type and a direct conversion topology for simplicity, compact size and low temperature sensitivity. The manufactured receiver has the temperature sensitivity less than 1 K for both a hot source and a cold source. The calculated and measured results of the quasi-optics are very well matched by approximately 1.6dB. The expected measurement errors by the reference control method are also analyzed as the functions of the characteristic parameters of the radiometer receiver.

We report simultaneous multifrequency observing performance at 22 and 43 GHz of the 21 m shaped-Cassegrain radio telescopes of the Korean VLBI Network (KVN). KVN is the first millimeter-dedicated VLBI network in Korea having a maximum baseline length of 480 km. It currently operates at 22 and 43 GHz and is planned to operate in four frequency bands: 22, 43, 86, and 129 GHz. The unique quasi optics of KVN enable simultaneous multifrequency observations based on efficient beam filtering and accurate antenna-beam alignment at 22 and 43 GHz. We found that the offset of the beams is within less than 5'' over all pointing directions of the antenna. The dual-polarization, cooled, high electron mobility transistor (HEMT) receivers at 22 and 43 GHz result in receiver noise temperatures less than 40 K at 21.25-23.25 GHz and 80 K at 42.11-44.11 GHz. The pointing accuracies have been measured to be 3'' in azimuth and elevation for all antennas. The measured aperture efficiencies are 65%(K)/67%(Q) , 62%(K)/59%(Q) , and 66%(K)/60%(Q) for the three KVN antennas, KVNYS, KVNUS, and KVNTN, respectively. The main-beam efficiencies are measured to be 50%(K)/52%(Q) , 48%(K)/50%(Q) , and 50%(K)/47%(Q) for KVNYS, KVNUS, and KVNTN, respectively. The estimated Moon efficiencies are 77%(K)/90%(Q) , 74%(K)/79%(Q) , and 80%(K)/86%(Q) for KVNYS, KVNUS, and KVNTN, respectively. The elevation dependence of the aperture efficiencies is quite flat for elevations greater than 20 degree .

The regulators(s) or sensor(s) that monitor cross-talk between, and ultimately control the flow of C or N through the pathways have remained elusive. I used an antisense strategy to demonstrate that the putative glutamate receptor 1.1 (AtGLR1.1) functions as a regulator of C and N metabolism in Arabidopsis. Seeds from AtGLR1.1-deficient Arabidopsis (antiAtGLR1.1 ) lines did not germinate in the presence of an animal ionotropic glutamate receptor (iGLR) antagonist, but germination was restored on coincubation with an iGLR agonist or the putative ligand glutamate. AntiAtGLR1.1 also exhibited a conditional phenotype that was sensitive to the C:N ratio. In the presence of C, specifically sucrose, but not glucose, mannitol, or sorbitol, antiAtGLR1.1 seeds did not germinate, but germination was restored upon coincubation with NO3−, but not NH4+. Immunoblot, isoenzyme, and RT-PCR analysis indicate that AtGLR1.1 regulates the accumulation of distinct C- and N- metabolic enzymes such as cytosolic aspartate aminotransferase (AAT2) and cytosolic glutamine synthetase (GS 1), 6-phosphogluconate dehydrogenase (6PGDH). In addition, I investigated the role of AtGLR1.1 in the regulation of abscisic acid (ABA) biosysnthesis and signaling. The antiAtGLR1.1 lines had increased sensitivity to exogenous ABA with regard to the effect of the hormone on the inhibition of seed germination and root growth. AntiAtGLR1.1 lines exhibited altered expression of ABA biosynthetic (ABA) and signaling (ABI) genes, when compared with WT. In addition, the antiAtGLR1.1 lines had elevated ABA titers, reduced stomatal apertures, and exhibited enhanced drought tolerance due to deceased water loss compared to WT lines. Finally, to expand our understanding of the role of antiAtGLR1.1 in the regulation of distinct pathways and processes, I conducted at genome-wide analysis of mRNA accumulation in antiAtGLR1.1 mutant versus WT plants. Microarray analysis revealed that coordination of C, N and S metabolism may be regulated by AtGLR1.1, suggesting that a deprivation of one leads to a disruption of metabolism of the other. Furthermore, I demonstrate that the antiAtGLR1.1 activates or silences metabolic pathway, associated with the Asp family of amino acids and anthocyanin.