Using commercial materials for colorimetric detection of toxic cyanide (CN-) anions can greatly improve safety and benefit society. This work discusses the colorimetric sensing properties of commercially available trans-(3-nitrostyrene analogues, including trans-(3-nitrostyrene (P1), trans-4-methoxy-(3-nitrostyrene (P2), trans-4-methyl-(3-nitrostyrene (P3), trans-4-fluoro-(3-nitrostyrene (P4), trans-4-bromo-(3-nitrostyrene (P5), trans-4-chloro-(3-nitrostyrene (P6), and trans-(3-methyl-(3-nitrostyrene (P7), in dimethyl sulfoxide (DMSO) and acetonitrile (ACN). P1-P4 show strong reddish-pink and yellowish-orange colors while detecting CN-ions in DMSO and ACN, with new UV-visible peaks appearing at 515 nm/510 nm and at 490 nm/485 nm, respectively. Conversely, P5 and P6 exhibit mild color responses to CN-in DMSO and ACN, with absorbance peaks at 505 nm/510 nm and at 490 nm/430 nm, respectively. P7 shows no selectivity for CN-ions due to steric and electronic structural effects. The high selectivity of P1-P4 for CN-is confirmed through interference studies. pH values of 6 and 7 are ideal for sensory testing. The sensor response of P1-P6 to CN-is linear across a range of 0.1 to 1000 mu M (mu M = 10-6 M), with estimated detection limits (LODs) at 10-9-10-6 M. Nuclear Magnetic Resonance (NMR), mass spectra, and density functional theory (DFT) analyses validate the Michael addition as the sensing mechanism. The test strip method demonstrates the solid-state colorimetric sensing ability of P1-P3 for CN-ions. Spiked CN-ions in water samples show the real-time sensing capability of P1-P4. These results open the door for future designs using different fluorophores with nitro (-NO2) Michael acceptor.
Inflammasomes, including NLRP3 (nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain-containing protein 3), participate in regulating immune activation and inflammation. Nonetheless, their specific roles in muscle contusion, one of the most common forms of sports injury, remain unknown. To address this, we investigated the role of NLRP3 in muscle contusion in Nlrp3-knockout (KO) mice, using a model of mass-drop injury (MDI)-induced contusion of the gastrocnemius muscle. Wild-type (WT) and Nlrp3-KO mice were assigned to four experimental groups: (1) WT-N: wild-type without MDI (control); (2) NLRP3-N: Nlrp3-KO without MDI; (3) WT-I: WT with MDI; and (4) NLRP3-I: Nlrp3-KO with MDI. Following MDI, tissue and serum samples were collected at 0, 48, 96, and 192 h. Muscle injury, recovery, and the extent of inflammation were evaluated by measuring body and muscle weight, serum biochemical markers, complete blood counts, and via histopathological immunohistochemical analysis. In the early phase following contusion, muscle weight was lower in the NLRP3-I group than in the WT-I group; however, in the later stages, it was significantly greater in the NLRP3-I group. Serum aspartate aminotransferase, lactate dehydrogenase, and creatine kinase were significantly lower in the NLRP3-I group than in the WT-I group, indicating reduced muscle damage following Nlrp3 knockout. The white blood cell and neutrophil counts were markedly higher in the WT-I group than in the NLRP3-I group. Based on histopathology, the NLRP3-I group exhibited less severe muscle injury, reduced tumor necrosis factor (TNF)-α, interleukin (IL)-6, CD68, CD206 and Caspase-3 expression, and reduced fibrosis, indicating a diminished contusion-induced inflammatory response and improved regeneration relative to the WT-I group. Nlrp3 knockout thus ameliorated contusion-induced muscle injury and inflammation. We hypothesize that NLRP3 regulates TNF-α and IL-6, with Nlrp3 downregulation reducing contusion-related muscle damage and fibrosis. NLRP3 thus represents a promising therapeutic target for treating sports injuries and for rehabilitation.
Twenty-two new monoterpene-coumarins, comprising the initial disclosure of 11 enantiomeric pairings, were isolated from the rhizomes of Luvunga scandens with the aid of LC-MS/MS based on molecular networking. Luvunscandins A-G (1-7) are dihydrofurancoumarins with a furan ring connection, and luvunscandins H-K (8-11) are dihydrofurancoumarins connected through a pyran ring. Chemical structures and absolute configurations were determined by analysis of spectroscopic data and X-ray diffraction analysis. The neuroprotective effects of all the isolates on LPS-stimulated NO production in BV2 microglia were evaluated. Compounds 6a, 7a, 7b, 8b, 9a, 9b, 11a, and 11b demonstrated more potent inhibitory effects than the positive control PDTC. Structural-activity relationship analysis revealed that neuroprotective activity was primarily associated with pyran-type dihydrofurancoumarins or compounds bearing a C3'R,6'R configuration, whereas furan-type analogs or compounds with a C3'S,6'S configuration exhibited weak or no activity. (+)-Luvunscandin I (9a) showed the most significant inhibitory activity (IC50 = 4.9 ± 0.6 μg/mL) through suppression of the inflammatory transcription factors p65NF-κB and iNOS.
Enterococcus faecalis is a significant pathogen in healthcare settings and is frequently resistant to multiple antibiotics. This resistance is compounded by its ability to form biofilms, dense bacterial communities that are challenging to eliminate via standard antibiotic therapies. As such, targeting biofilm formation is considered a viable strategy for addressing these infections. This study assessed the effectiveness of surfactin, a cyclic lipopeptide biosurfactant synthesized by Bacillus subtilis natto NTU-18, in preventing biofilm formation by E. faecalis. Analytical characterization of surfactin was performed via liquid chromatography‒mass spectrometry (LC‒MS). Additionally, transcriptomic sequencing and quantitative PCR (qPCR) were used to investigate alterations in E. faecalis gene expression following treatment with surfactin. The data revealed notable suppression of crucial virulence-related genes responsible for pilus construction and exopolysaccharide synthesis, both of which are vital for E. faecalis adhesion and biofilm structure. Functional tests confirmed that surfactin treatment substantially reduced E. faecalis attachment to Caco-2 cell monolayers and curtailed exopolysaccharide production. Moreover, confocal laser scanning microscopy revealed significant thinning of the biofilms. These observations support the potential utility of surfactin as a therapeutic agent to manage biofilm-associated infections caused by E. faecalis.
The landscape of prosthodontics and dental implantology is undergoing a transformative evolution, driven by remarkable advancements in materials science. This review explores the pivotal role of multifaceted materials, ceramics, polymers, metal alloys, and composites in revolutionizing dental restorative procedures. These materials are not only enhancing the mechanical properties and biocompatibility of dental prostheses and implants but also elevating aesthetic outcomes to meet patient expectations. Our discussion highlights how traditional materials like titanium (Ti) and cobalt-chromium (Co–Cr), alongside newer innovations such as zirconia and polymer-based composites, contribute to the restoration and enhancement of oral functions. Furthermore, this article delves into the integration of cutting-edge technologies such as 3D printing and computer-aided design/manufacturing, which synergize with these advanced materials to tailor dental solutions to individual patient needs, thereby improving both functional outcomes and patient satisfaction. As the field progresses, we anticipate future innovations to focus on increasing the sustainability of materials used, refining their properties through nanotechnology, and further personalizing dental care through digital workflows, setting a new standard in the interdisciplinary approach of modern dentistry.
