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Abstract Background Myocardial infarction (MI) poses a global public health challenge, often associated with elevated mortality rates and a grim prognosis. A crucial aspect of the inflammatory injury and healing process post-MI involves the dynamic differentiation of macrophages. A promising strategy to alleviate myocardial damage after MI is by modulating the inflammatory response and orchestrating the shift from pro-inflammatory (M1) to anti-inflammatory (M2) macrophages, aiming to achieve a reduced M1/M2 ratio. Nuanxinkang (NXK), a simplified herbal decoction, has demonstrated noteworthy cardioprotective, inflammation-regulating, and myocardial energy metabolism-regulating properties. Methods In this study, we constructed an MI model by ligating coronary arteries to investigate the efficacy of NXK in improving ventricular remodeling and cardiac function. Mice were administered NXK (1.65 g/kg/d) or an equivalent volume of regular saline via gavage for 28 consecutive days, commencing the day after surgery. Then, we conducted echocardiography to assess the cardiac function, Masson staining to illustrate the extent of myocardial fibrosis, TUNEL staining to reveal myocardial apoptosis, and flow cytometry to analyze the polarization of M1 and M2 macrophages in the hearts. Besides, a lipopolysaccharide (LPS)-induced pro-inflammatory macrophage (M1) polarization model was implemented in RAW264.7 cells to elucidate the underlying mechanism of NXK in regulating macrophage polarization. RAW264.7 cells were pre-treated with or without NXK-containing serum. Oxidative stress was detected by MitoSox staining, followed by Seahorse energy metabolism assay to evaluate alterations in mitochondrial metabolic patterns and ATP production. Both In vivo and in vitro, HIF-1α and PDK1 were detected by fluorescent quantitative PCR and Western blotting. Results In vivo, MI mice exhibited a decline in cardiac function, adverse ventricular remodeling, and an increase in glycolysis, coupled with M1-dominant polarization mediated by the HIF-1α/PDK1 axis. Notably, robust responses were evident with high-dose NXK treatment (1.65 g/kg/day), leading to a significant enhancement in cardiac function, inhibition of cardiac remodeling, and partial suppression of macrophage glycolysis and the inflammatory phenotype in MI mice. This effect was achieved through the modulation of the HIF-1α/PDK1 axis. In vitro, elevated levels of mitochondrial ROS production and glycolysis were observed in LPS-induced macrophages. Conversely, treatment with NXK notably reduced the oxidative stress damage induced by LPS and enhanced oxidative phosphorylation (OXPHOS). Furthermore, NXK demonstrated the ability to modify the energy metabolism and inflammatory characteristics of macrophages by modulating the HIF-1α/PDK1 axis. The influence of NXK on this axis was partially counteracted by the HIF-1α agonist DMOG. And NXK downregulated PDK1 expression, curtailed glycolysis, and reversed LPS-induced M1 polarization in macrophages, similar to the PDK1 inhibitor DCA. Conclusion In conclusion, NXK protects against MI-induced cardiac remodeling by inducing metabolic reprogramming and phenotypic differentiation of macrophages, achieved through the modulation of the HIF-1α/PDK1 axis. This provides a novel and promising strategy for the treatment of MI.

A novel 3D metal/semiconductor nanostructured surface‐enhanced Raman scattering (SERS)‐active substrate is constructed through Ag nanoparticles decoration of flower‐like ZnO nanorods (fZnOs) on a buckled substrate. A thermal treatment is applied to induce substrate buckling and is followed by ZnO hydrothermal synthesis and Ag reduction, resulting in the production of a buckled Ag/fZnOs SERS‐active device. In addition to providing a high areal density of hotspots, surface buckling enhanced the hydrophilicity of the Ag/fZnO composite surface, which aided the adsorption of probe molecules. Buckling also facilitated the formation of eddies in the depressions on the surface, promoting the capture and accumulation of chemicals. Compared with flat Ag/fZnOs, the buckle‐enhanced SERS effects can increase their enhancement factor by over 103 times. The buckled Ag/fZnOs SERS‐active device is recyclable, stable, and inexpensive and is found to be highly sensitive for the detection of Rhodamine 6G and commercial pesticides, achieving a low detection limit of 10−9 m and a high enhancement factor of 2.43 × 108. [ABSTRACT FROM AUTHOR]

Brown root rot disease (BRRD), caused by Phellinus noxius , is an important tree disease in tropical and subtropical areas. To improve chemical control of BRRD and deter emergence of fungicide resistance in P . noxius , this study investigated control efficacies and systemic activities of fungicides with different modes of action. Fourteen fungicides with 11 different modes of action were tested for inhibitory effects in vitro on 39 P. noxius isolates from Taiwan, Hong Kong, Malaysia, Australia, and Pacific Islands. Cyproconazole, epoxiconazole, and tebuconazole (Fungicide Resistance Action Committee [FRAC] 3, target-site G1) inhibited colony growth of P. noxius by 99.9 to 100% at 10 ppm and 97.7 to 99.8% at 1 ppm. The other effective fungicide was cyprodinil + fludioxonil (FRAC 9 + 12, target-site D1 + E2), which showed growth inhibition of 96.9% at 10 ppm and 88.6% at 1 ppm. Acropetal translocation of six selected fungicides was evaluated in bishop wood ( Bischofia javanica ) seedlings by immersion of the root tips in each fungicide at 100 ppm, followed by liquid or gas chromatography tandem mass spectrometry analyses of consecutive segments of root, stem, and leaf tissues at 7 and 21 days posttreatment. Bidirectional translocation of the fungicides was also evaluated by stem injection of fungicide stock solutions. Cyproconazole and tebuconazole were the most readily absorbed by roots and efficiently transported acropetally. Greenhouse experiments suggested that cyproconazole, tebuconazole, and epoxiconazole have a slightly higher potential for controlling BRRD than mepronil, prochloraz, and cyprodinil + fludioxonil. Because all tested fungicides lacked basipetal translocation, soil drenching should be considered instead of trunk injection for their use in BRRD control., Competing Interests: The author(s) declare no conflict of interest.

Fusarium wilt of Luffa , caused by Fusarium oxysporum f. sp. luffae , causes great losses in Luffa plants worldwide. In this study, 45 accessions of Luffa germplasm were used to determine their resistance to F. oxysporum f. sp. luffae isolates (FOLUST, FOLUSC, Fomh16, and Fol114) in two independent trials. In the first trial, only FOLUST was used to preliminarily identify resistant accessions. Nine accessions of Luffa acutangula and five of L. aegyptiaca were resistant to the FOLUST isolate. In the second trial, the other three isolates were then used to reevaluate the 14 resistant accessions. The results indicated that the 14 accessions were resistant to FOLUSC but exhibited variable resistance to the Fomh16 and Fol114 isolates. Eight accessions of L. acutangula and one accession of L. aegyptiaca were resistant to Fol114. Seven accessions of L. acutangula and one accession of L. aegyptiaca were resistant to Fomh16. Despite the lack of any symptoms, the F. oxysporum f. sp. luffae isolates were recovered from the hypocotyls of all resistant accessions at 28 days postinoculation, except for isolates FOLUSC and FOLUST on one accession (LA140). A high percentage (87.5%) of accessions collected from Bangladesh were identified as resistant, highlighting the effect of local adaptation on resistance. These results provide potentially valuable genetic resources for breeding programs to develop new varieties or rootstocks that could be beneficial for controlling soilborne diseases in different cucurbit crops and further investigating the mechanisms of resistance to F. oxysporum f. sp. luffae in Luffa plants., Competing Interests: The author(s) declare no conflict of interest.