Total Reflection and Negative Refraction of Dipole-Exchange Spin Waves at Magnetic Interfaces: Micromagnetic Modeling Study

We demonstrated that dipole-exchange spin waves traveling in geometrically restricted magnetic thin films satisfy the same laws of reflection and refraction as light waves. Moreover, we found for the first time novel wave behaviors of dipole-exchange spin waves such as total reflection and negative refraction. The total reflection in laterally inhomogeneous thin films composed of two different magnetic materials is associated with the forbidden modes of refracted dipole-exchange spin waves. The negative refraction occurs at a 90 degree domain-wall magnetic interface that is introduced by a cubic magnetic anisotropy in the media, through the anisotropic dispersion of dipole-exchange spin waves.Comment: 13 pages, 5 figure

MRI Findings of Pericardial Fat Necrosis: Case Report

Pericardial fat necrosis is an infrequent cause of acute chest pain and this can mimic acute myocardial infarction and acute pericarditis. We describe here a patient with the magnetic resonance imaging (MRI) findings of pericardial fat necrosis and this was correlated with the computed tomography (CT) findings. The MRI findings may be helpful for distinguishing pericardial fat necrosis from other causes of acute chest pain and from the fat-containing tumors in the cardiophrenic space of the anterior mediastinum

Risk factors for post-contrast acute kidney injury in patients sequentially administered iodine- and gadolinium-based contrast media on the same visit to the emergency department: a retrospective study

Background This study compares the incidence of post-contrast acute kidney injury (PC-AKI) in patients who received a single administration of iodine-based contrast medium (ICM) with that in patients who received a sequential administration of ICM and gadolinium-based contrast agents (GBCA) in a single visit to an emergency department (ED) to determine the risk factors for PC-AKI. Methods Patients who received one or more contrast media in the ED from 2016 to 2021 were included in this retrospective study. They were divided into the ICM alone and ICM + GBCA groups, and the incidence of PC-AKI was compared between the groups. The risk factors were assessed using a multivariable analysis after propensity score matching (PSM). Results Overall, 6,318 patients were analyzed, of whom 139 were in the ICM + GBCA group. The incidence of PC-AKI was significantly higher in the ICM + GBCA group than in the ICM alone group (10.9% vs. 27.3%, p < 0.001). In the multivariable analysis, sequential administration was a risk factor for PC-AKI, and single administration was not (adjusted odds ratio [95% confidence interval] in the 1:1, 2:1, and 3:1 PSM cohorts: 2.38 [1.25–4.55], 2.13 [1.26–3.60], and 2.28 [1.39–3.72], respectively). In subgroup analyses of the ICM + GBCA group, osmolality (1.05 [1.01–1.10]) and estimated glomerular filtration rate (eGFR, 0.93 [0.88–0.98]) were associated with PC-AKI. Conclusion Compared with a single administration of ICM alone, sequential administration of ICM and GBCA during a single ED visit might be a risk factor for PC-AKI. Osmolality and eGFR might be associated with PC-AKI after sequential administration

Interleukin-2 induces the in vitro maturation of human pluripotent stem cell-derived intestinal organoids.

Human pluripotent stem cell (hPSC)-derived intestinal organoids (hIOs) form 3D structures organized into crypt and villus domains, making them an excellent in vitro model system for studying human intestinal development and disease. However, hPSC-derived hIOs still require in vivo maturation to fully recapitulate adult intestine, with the mechanism of maturation remaining elusive. Here, we show that the co-culture with human T lymphocytes induce the in vitro maturation of hIOs, and identify STAT3-activating interleukin-2 (IL-2) as the major factor inducing maturation. hIOs exposed to IL-2 closely mimic the adult intestinal epithelium and have comparable expression levels of mature intestinal markers, as well as increased intestine-specific functional activities. Even after in vivo engraftment, in vitro-matured hIOs retain their maturation status. The results of our study demonstrate that STAT3 signaling can induce the maturation of hIOs in vitro, thereby circumventing the need for animal models and in vivo maturation

Calcifying Aponeurotic Fibroma with Osseous Involvement of the Finger: a Case Report with Radiologic and US Findings

Calcifying aponeurotic fibroma is a rare soft tissue tumor that occurs in the distal extremities of children and adolescents. We report ultrasound and X-ray findings of a calcifying aponeurotic fibroma in the finger of a 36-year-old woman, associated with distal phalangeal bone involvement

Cordycepin promotes apoptosis by modulating the ERK-JNK signaling pathway via DUSP5 in renal cancer cells

Constitutive activation of extracellular signal regulated kinase (ERK)-Jun NH2-terminal kinase (JNK) signaling commonly occurs in tumors. The activation of ERK promotes cell proliferation, whereas that of JNK induces cell apoptosis. However, the apoptotic mechanism of ERK-JNK signaling in cancer is not well understood. Recently, we identified that apoptosis and activation of the JNK signaling pathway were induced after cordycepin treatment in human renal cancer, suggesting that JNK signaling might contribute to TK-10 cell apoptosis. We investigated the apoptotic effects of cordycepin by evaluating the activation of the ERK-JNK signaling pathway in renal cancer TK-10 cells. We found that cordycepin downregulated ERK and DUSP5, upregulated phosphorylated-JNK (p-JNK), and induced apoptosis. Moreover, we showed that siRNA-mediated inhibition of ERK downregulated DUSP5, whereas ERK overexpression upregulated DUSP5, and that DUSP5 knockdown by siRNA upregulated p-JNK. The JNK-specific inhibitor SP600125 upregulated nuclear translocation of β-catenin, and downregulated Dickkopf-1 (Dkk1), which has been shown to be a potent inhibitor of Wnt signaling. Dkk1 knockdown by siRNA upregulated nuclear β-catenin, suggesting the involvement of the Wnt/β-catenin signaling pathway. DUSP5 overexpression in TK-10 cells decreased p-JNK and increased nuclear β-catenin. The decreased Bax activation markedly protected against cordycepin-induced apoptosis. Bax subfamily proteins induced apoptosis through caspase-3. Taken together, we show that JNK signaling activation by cordycepin mediated ERK inhibition, which might have induced Bax translocation and caspase-3 activation via regulation of DUSP5 in TK-10 cells, thereby promoting the apoptosis of TK-10 cells. Targeting ERK-JNK signaling via the apoptotic effects of cordycepin could be a potential therapeutic strategy to treat renal cancer

Fatigue Prediction of the Discharge Pipe in Reciprocating Compressor

In this paper, a fatigue prediction of the line discharge tube for reciprocating compressor being installed in a refrigerator was studied. The tube usually gets plenty of the repeated loads caused by the start and stop motion of a reciprocating compressor. There are two representative methods to predict the fatigue stress. At first the stress-life can be applied to the problem which takes a lot of repeated stress within the elastic strain range. Second is the strain-life method which can be used when it comes to the problem of a small repeated stress in the plastic strain range. This paper presents the stress-life method how the design parameters of a discharge pipe relate to the fatigue prediction and analyzes the co-relation between them

The ancient phosphatidylinositol 3-kinase signaling system is a master regulator of energy and carbon metabolism in algae

Algae undergo a complete metabolic transformation under stress by arresting cell growth, inducing autophagy and hyperaccumulating biofuel precursors such as triacylglycerols and starch. However, the regulatory mechanisms behind this stress-induced transformation are still unclear. Here, we use biochemical, mutational, and “omics” approaches to demonstrate that PI3K signaling mediates the homeostasis of energy molecules and influences carbon metabolism in algae. In Chlamydomonas reinhardtii, the inhibition and knockdown (KD) of algal class III PI3K led to significantly decreased cell growth, altered cell morphology, and higher lipid and starch contents. Lipid profiling of wild-type and PI3K KD lines showed significantly reduced membrane lipid breakdown under nitrogen starvation (-N) in the KD. RNA-seq and network analyses showed that under -N conditions, the KD line carried out lipogenesis rather than lipid hydrolysis by initiating de novo fatty acid biosynthesis, which was supported by tricarboxylic acid cycle down-regulation and via acetyl-CoA synthesis from glycolysis. Remarkably, autophagic responses did not have primacy over inositide signaling in algae, unlike in mammals and vascular plants. The mutant displayed a fundamental shift in intracellular energy flux, analogous to that in tumor cells. The high free fatty acid levels and reduced mitochondrial ATP generation led to decreased cell viability. These results indicate that the PI3K signal transduction pathway is the metabolic gatekeeper restraining biofuel yields, thus maintaining fitness and viability under stress in algae. This study demonstrates the existence of homeostasis between starch and lipid synthesis controlled by lipid signaling in algae and expands our understanding of such processes, with biotechnological and evolutionary implications.Ministry of Science, ICT and Future Planning 2015M3A6A2065697Ministry of Oceans and Fisheries 2015018