Camposkilic2026

The potential mechanism involved in the release of arsenic from CFA, vacuum sulfurization, evaporation, and condensation was proposed. The kinetic analysis indicated that the apparent activation energy (Eα) was 31.24 kJ mol-1. Those results encourage further exploration of vacuum separation technology to environmentally friendly recycle CFA.Lithium-rich manganese-based materials are currently considered to be highly promising cathode materials for next-generation lithium-ion batteries due to their high specific capacity (>250 mA h g-1) and low cost. A key challenge for the commercialization of these lithium-rich manganese-based materials is their poor rate performance, which is caused by the low electronic conductivity and increasing interface charge transfer resistance produced by the side reaction during the cycling procedure. In this work, we try to improve the rate performance of a lithium-rich manganese-based material Li1.2Mn0.54Co0.13Ni0.13O2 using a collaborative approach with Co-doping and Na x CoO2-coating methods. Cobalt doping can improve the electronic conductivity, and Na x CoO2 coating provides a convenient lithium-ion diffusion channel and moderately alleviates the inevitable decrease in cycling stability caused by cobalt doping. Under the synergistic effect of these two modification strategies, the surface and internal dynamics of the Li1.2Mn0.54Co0.13Ni0.13O2 material are enhanced and its rate performance is considerably improved without decay of the cycle stability.A current theory in environmental science states that dissolved anxiolytics (oxazepam) from wastewater effluents can reduce anti-predator behavior in fish with potentially negative impacts on prey fish populations. Here, we hypothesize that European perch (Perca fluviatilis) populations being exposed to oxazepam in situ show reduced anti-predator behavior, which has previously been observed for exposed isolated fish in laboratory studies. We tested our hypothesis by exposing a whole-lake ecosystem, containing both perch (prey) and northern pike (Esox lucius; predator), to oxazepam while tracking fish behavior before and after exposure in the exposed lake as well as in an unexposed nearby lake (control). Oxazepam concentrations in the exposed lake ranged between 11 and 24 μg L-1, which is >200 times higher than concentrations reported for European rivers. In contrast to our hypothesis, we did not observe an oxazepam-induced reduction in anti-predator behavior, inferred from perch swimming activity, distance to predators, distance to conspecifics, home-range size, and habitat use. In fact, exposure to oxazepam instead stimulated anti-predator behavior (decreased activity, decreased distance to conspecifics, and increased littoral habitat use) when using behavior in the control lake as a reference. Shoal dynamics and temperature changes may have masked modest reductions in anti-predator behavior due to oxazepam. Although we cannot fully resolve the mechanism(s) behind our observations, our results indicate that the effects of oxazepam on perch behavior in a familiar natural ecosystem are negligible in comparison to the effects of other environmental conditions.Colon cancer is an aggressive malignancy with very limited therapeutic approaches. The available therapeutic agents for colon cancer show strong adverse effects and poor effectiveness, indicating the urgent need to identify new therapeutic drugs for this malignancy. Kaempferol, a flavonoid found in a variety of natural foods, exhibits significant inhibitory effects on colon cancer. Here, it was found that kaempferol inhibited the proliferation of human colon cancer cells HCT116 and DLD1 in a dose-dependent manner, and the IC50 values were 63.0 ± 12.9 and 98.3 ± 15.9 μM, respectively. Cathepsin Inhibitor 1 in vitro Also, kaempferol treatment delayed G1 phase progression of cell cycle and induced apoptosis. Aerobic glycolysis is the major energy source for various tumor growths, including colon cancer. Indeed, kaempferol treatment impaired glucose consumption, which subsequently led to reduced lactic acid accumulation and ATP production. Mechanistically, kaempferol promoted the expression of miR-339-5p. Further studies identified hnRNPA1 and PTBP1 as two direct targets of miR-339-5p. By directly targeting hnRNPA1 and PTBP1, miR-339-5p reduced the expression of M2-type pyruvate kinase (PKM2) but induced that of PKM1. In conclusion, these data demonstrate that by modulating miR-339-5p-hnRNPA1/PTBP1-PKM2 axis, kaempferol inhibits glycolysis and colon cancer growth, which reveals a new explanation for the molecular mechanism underlying kaempferol anti-tumor.Microtubule-associated protein tau is abnormally phosphorylated and forms the aggregates of paired helical filaments in Alzheimer's disease (AD) and other tauopathies. So far, the relationship and mechanism between the abnormal phosphorylation of tau and fibril formation is still unclear. Therefore, studying the effect of phosphorylation on the structure of tau protein is helpful to elucidate the pathogenic mechanism of tauopathies. It has been shown that pS202/pT205/pS208 triple phosphorylations located in the proline-rich region can promote tau aggregation. In this work, the effect of triple phosphorylations on tau structure was investigated by molecular dynamics simulations combined with multiple analytical methods of trajectories. The results showed that the conformational diversity of G192-T212 fragments decreased after phosphorylation compared with that of the wild-type. Moreover, the dynamic network and hydrogen bond analyses showed that the addition of pS208 phosphorylation can destroy the key hydrogen bonds and the network structure formed centered on pT205 at the C-terminal of the pS202/pT205 double phosphorylated peptide and then destroy the turn structure formed in the region of G207-R211. The destruction of this turn structure is considered to be the main reason for the aggregation of pS202/pT205/pS208 triple phosphorylations. For the pS202/pT205/pS208 triple phosphorylated system, the G207-R211 region is a coil structure, which is more extended and prone to aggregation. In a word, our results reveal the mechanism that pS202/pT205/pS208 triple phosphorylations promote tau aggregation at the atomic level, which can provide useful theoretical guidance for the rational design of effective therapeutic drugs against AD and other tauopathies.