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Carbon nanotubes (CNTs), typically magnetically inert, can be effectively aligned in polydimethylsiloxane (PDMS) using moderate magnetic fields when hybridized with FeO nanoparticles. We demonstrate that these CNT-FeO hybrids rapidly self-organize into aligned, bundled structures under an applied magnetic field (∼120 mT), driven by local magnetic gradients originating from FeO nanoparticles interacting with trace magnetic impurities within the CNTs. This field-induced anisotropy yields composites with significantly enhanced electrical conductivity, lower percolation thresholds, and superior piezoresistive sensitivity compared to non-aligned samples. Furthermore, we observe evidence of spontaneous local organization improving conductivity even without an external field. This simple, functionalization-free hybridization strategy offers a powerful route to control microstructure in soft composites, enabling tunable electromechanical properties for applications like soft sensors and providing insights into magnetically assisted self-assembly in hybrid materials.
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http://dx.doi.org/10.1039/d5sm00449g | DOI Listing |
Haematologica
September 2025
Department of Molecular Hematopathology, Okayama University Graduate School of Health Sciences, Okayama.
Idiopathic multicentric Castleman disease (iMCD) is a rare lymphoproliferative disorder characterized by systemic inflammation and lymphadenopathy. Two major clinical subtypes, idiopathic plasmacytic lymphadenopathy (iMCD-IPL) and iMCD with thrombocytopenia, anasarca, fever, renal dysfunction/reticulin fibrosis, and organomegaly (iMCD-TAFRO), exhibit distinct pathophysiologic mechanisms. While interleukin-6 (IL-6) is known to be elevated in iMCD, the differences in IL-6 production sources between subtypes remain unclear.
View Article and Find Full Text PDFAutophagy
September 2025
Department of Biochemistry and Molecular Biology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Macroautophagy/autophagy is an evolutionarily conserved process through which cells degrade cytoplasmic substances via autophagosomes. During the initiation of autophagosome formation, the ULK/Atg1 complex serves as a scaffold that recruits and regulates downstream ATG/Atg proteins and ATG9/Atg9-containing vesicles. Despite the essential role of the ULK/Atg1 complex, its components have changed during evolution; the ULK complex in mammals consists of ULK1 (or ULK2), RB1CC1, ATG13, and ATG101, whereas the Atg1 complex in the yeast lacks Atg101 but instead has Atg29 and Atg31 along with Atg17.
View Article and Find Full Text PDFHealth Commun
September 2025
Department of Library and Information Science, Rutgers University.
Patient portals have the potential to both improve and harm patient-clinician partnerships by reshaping how health information is exchanged and how patients and providers communicate. Patients ( = 20) and primary care clinicians ( = 11) purposively sampled from clinics serving diverse New Jersey communities were interviewed. Patients distinguished two portal functions - linear information exchange and bidirectional communication - but did so in different ways.
View Article and Find Full Text PDFACS Nano
September 2025
Department of Chemical Physics, Key Laboratory of Precision and Intelligent Chemistry, University of Science and Technology of China, Hefei, Anhui 230026, China.
The coupling between transition metal dichalcogenides (TMDCs) and SrTiO has recently emerged as a fertile platform for discovering interfacial phenomena, where particle interactions, lattice coupling, and dielectric screening give rise to interesting physical effects. These hybrid systems hold significant promise for two-dimensional (2D) electronics, ferroelectric state control, and metastable phase engineering. However, effective modulation of the interfacial electronic structure remains a critical challenge.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
September 2025
Department of Medicine/Division of Cardiology, University of California Los Angeles. (S.S., C.R.S., L.F., M.P., C.P., Z.Z., J.J.M., R.C.D., D.S., A.J.L.).
Background: In genetic studies with the Hybrid Mouse Diversity Panel, we previously identified a chromosome 9 locus for atherosclerosis. We now identify NNMT (nicotinamide -methyltransferase), an enzyme that degrades nicotinamide, as the causal gene in the locus and show that the underlying mechanism involves salvage of nicotinamide to nicotinamide adenine dinucleotide (NAD).
Methods: Gain/loss of function studies in macrophages were performed to examine the role of NAD levels in macrophage proliferation and apoptosis in atherosclerosis.