This study introduces a novel interface engineering strategy for high-performance cellulose/poly (vinyl alcohol) (PVA) aerogels derived from coir fiber waste. To address structural fragility, postsynthesis reinforcement was achieved through conformal liquid epoxy-acrylate infiltration. Quantitative Barrett-Joyner-Halenda (BJH) analysis confirmed the existence of a pore-wall thickening mechanism that preserved the internal mesoporous network (radius: 1.9-2.6 nm) without interstitial blockage. The functionalized scaffold demonstrated significant thermal stabilization, with the maximum degradation temperature (Tmax) shifting from 283°C to 307°C, coupled with superior mechanical resilience and a bulk density of 0.051 g/cm3. Methylene blue (MB) adsorption tests achieved 97.3% removal at pH 10, accurately modeled by pseudo-second-order kinetics and the Freundlich isotherm (R2 = 0.980, RMSE = 1.507, and Χ2 = 0.884), indicating spontaneous and endothermic multilayer physisorption. Furthermore, regeneration studies established 70% capacity retention over three cycles while maintaining full macroscopic integrity. These findings indicate that strategic resin infiltration provides a robust and sustainable pathway for the development of durable adsorbents for industrial wastewater remediation.

Methamphetamine (MA) use is a recognized risk factor for drug-associated pulmonary arterial hypertension (PAH), yet mechanisms driving methamphetamine-associated PAH (MA-PAH) remain unclear due to the lack of reproducible animal models demonstrating hemodynamic changes. This study aimed to develop a rat model of MA-PAH that reflects human patterns of MA abuse. Male Wistar rats received methamphetamine (MA, 5 mg/kg, i.p.) for 8 weeks using either a chronic daily regimen or a binge-and-crash regimen. Chronic MA administration resulted in a significant reduction in mean arterial pressure and an increase in RV systolic pressure, while ejection fraction and the Fulton index remained unchanged. In contrast, binge-crash MA exposure led to significant RV dilation, reduced RV ejection fraction, elevated RV systolic pressure, and increased RV hypertrophy. Both regimens induced pulmonary arterial medial thickening driven by smooth muscle hyperplasia; however, the binge-and-crash model exhibited more severe remodeling, including enhanced distal muscularization, sporadic endothelial proliferation, and vascular rarefaction. HMGB1 levels were significantly elevated in plasma and pulmonary microvascular endothelial cells isolated from binge-crash MA rats. In vitro, MA treatment induced HMGB1 release from endothelial cells through sigma-1 receptor signaling. Conditioned media from MA-treated endothelial cells stimulated smooth muscle cell proliferation, an effect abolished by HMGB1 neutralization. In conclusion, these findings demonstrate that binge-and-crash MA exposure produces a robust and clinically relevant PAH phenotype and identify HMGB1 as a potential mechanistic contributor linking MA exposure patterns to endothelial-smooth muscle interactions in PAH pathogenesis.

Venous grafts remain the most used conduits in coronary artery bypass grafting (CABG) but are highly susceptible to early failure due to ischemia-reperfusion injury, intimal hyperplasia, and accelerated atherosclerosis. Specialized preservation solutions such as DuraGraft and TiProtec aim to protect endothelial integrity during intraoperative storage; however, their long-term effects on venous graft adaptation remain unclear. In this study, saline, DuraGraft, and TiProtec were compared in a rat model of arterialized autologous jugular vein interposition grafting. Male Wistar rats were assigned to one of the three storage solutions or a Sham group with immediate implantation. Jugular veins were harvested, preserved for 2 h, and implanted into the infrarenal abdominal aorta using end-to-end microsurgical anastomoses. After 16 weeks, all grafts remained patent and exhibited pronounced arterial remodeling, including dilation, wall thickening, intimal hyperplasia, and loss of endothelium-dependent relaxation, while endothelium-independent relaxation was preserved. Although TiProtec-treated grafts showed slightly enhanced relaxation compared with saline-treated grafts, no preservation solution demonstrated a significant functional or structural advantage at 16 weeks. These findings suggest that long-term arterial loading is the dominant determinant of venous graft remodeling.

Slab tearing, the lateral detachment of subducting oceanic slab from continental lithosphere, is widely inferred from seismic tomography, yet its surface expressions in mountain belts and adjacent foreland basins remain ambiguous and often contradictory. Existing geodynamic models predict that slab tearing propagates at unrealistically high velocities, implying its transient signatures unlikely to be preserved in surface or stratigraphic records. In contrast, geological observations, such as lateral migration of foreland basin depocenters and systematic basin thickening in the direction of tear propagation, indicate more persistent surface responses, highlighting a long-standing disconnect between models and field evidence. Here we resolve this paradox by showing that lateral variations in passive-margin strength fundamentally control the initiation, propagation, and surface imprint of slab tearing. Using fully coupled three-dimensional thermo-mechanical and surface-process simulations, we demonstrate that accounting for passive-margin heterogeneity significantly slows tear propagation and produces long-lived tectonostratigraphic signatures consistent with natural examples from the Alps, Carpathians, Zagros, and other orogenic belts. These results bridge deep-mantle dynamics and surface geological records, providing a unified framework to identify and interpret slab tearing in orogenic systems worldwide.

Obesity-associated elevated plasma free fatty acids (FFAs) levels contribute to vascular injury and insulin resistance, but the role of CD36remains incompletely understood. This study investigated the role of CD36 in regulating high-fat diet (HFD)-induced metabolic disturbances and vascular dysfunction and its downstream signaling. In HFD-fed mice, CD36 knockdown lowered body weight, abdominal fat accumulation, and serum lipid profile without affecting blood glucose. Moreover, CD36 knockdown reversed HFD-induced increases in aortic reactive oxygen species (ROS) generation, endoplasmic reticulum (ER) stress. It also attenuated aortic wall thickening, fibrosis, and impaired endothelial-dependent vasorelaxation to insulin. In palmitic acid (PA)-treated human umbilical vein endothelial cells, CD36 silencing similarly alleviated PA-induced ROS production, ER stress, and increased expression of pro-inflammatory proteins, while restoring impaired insulin-stimulated AKT/eNOS phosphorylation. Mechanistically, the mitochondrial-targeted antioxidant MitoTEMPO attenuated PA-induced ROS generation, ER stress, and rescued insulin signaling, indicating mitochondrial ROS as an upstream mediator. Conversely, CD36 overexpression exacerbated PA-induced ROS production, ER stress, and insulin signaling impairment, all of which were reversed by the antioxidant NAC or the ER stress inhibitor TUDCA. These gain- and loss-of-function experiments establish CD36 as a critical upstream regulator coupling PA stimulation to mitochondrial ROS and subsequent ER stress. Notably, as systemic CD36 knockdown was used in vivo, the potential contribution of vascular smooth muscle CD36 cannot be excluded. In conclusion, CD36 aggravates obesity-related vascular injury by promoting ROS-dependent ER stress, leading to endothelial insulin signaling impairment. Targeting CD36 or its downstream oxidative/ER stress pathways may represent a promising therapeutic strategy for obesity-associated vascular complications.

Interlobular septal thickening (ILST) is a feature on chest computed tomography (CT) that is characterized by abnormal widening of the interlobular septa, which are thin connective tissues that separate secondary pulmonary lobules within the lung parenchyma. They contain pulmonary venules and lymphatic vessels. On CT, these septa are normally not visible in healthy patients. However, various pulmonary pathologic conditions can lead to ILST. If present, ILST can be categorized into 3 different patterns based on its morphologic appearance: smooth, nodular, and irregular/fibrotic. Each pattern occurs from different disease processes with little overlap. In this pictorial essay, we review common and rare etiologies for each type of ILST. For each disease, we discuss relevant pathophysiology, epidemiology, risk factors, symptoms, physical exam findings, labs, and management. Subsequently, we present the ILST features along with the distribution (eg, unilateral, bilateral, central, peripheral) and ancillary imaging findings that can support the diagnosis. Finally, characteristic and high-resolution figures are presented.