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http://dx.doi.org/10.1155/2018/9784319 | DOI Listing |
Nano Lett
September 2025
School of Chemistry and Materials Science, Hunan Agricultural University, Changsha 410128, China.
Passivating detrimental defects is essential for improving perovskite solar cells (PSCs) performance. While hydrogen interstitials are often considered harmful, their role in defect passivation remains unclear. Using nonadiabatic molecular dynamics, we uncover a self-passivation mechanism between hydrogen (H) and bromine (Br) interstitials in all-inorganic CsPbBr perovskites.
View Article and Find Full Text PDFHistol Histopathol
September 2025
Center for Experimental Teaching, School of Pharmacy, Guangzhou Medical University, Guangzhou, China.
Background: The aim of this study was to establish a rat model of premature ovarian failure (POF) with cyclophosphamide (CTX), and explore the molecular basis of POF and the mechanism of Guishen-Erxian Decoction (GSEXD) to improve POF from the perspective of oxidative stress regulation of ovarian granulosa cell (OGC) DNA fragmentation.
Method: The study utilized SD rats to establish a POF model via CTX. Rats were divided into Control, POF group, three GSEXD dosage groups (low, medium, high), and a GSEXD+PI3K agonist group to assess GSEXD's therapeutic effects on oxidative stress, DNA fragmentation and ovarian damage.
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 PDFArterioscler Thromb Vasc Biol
September 2025
Vascular Biology Program, Boston Children's Hospital and Harvard Medical School, MA (K. Cui, B.Z., B.W., S.E.-B., A.V., H.C.).
Background: Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipid-laden foam cells and plaques within the arterial wall. Dysfunctional vascular smooth muscle cells (VSMCs), fibroblasts, endothelial cells, and macrophages contribute to disease progression. Here, we report that macrophage-specific expression of epsins, highly conserved endocytic adaptor proteins involved in clathrin-mediated endocytosis, accelerates atherosclerosis in Western diet-fed mice.
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.