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Accurate forecasting of wind power generation is essential for ensuring power safety, scheduling various energy sources, and improving energy utilization. However, the elusive nature of wind, influenced by various meteorological and geographical factors, greatly complicates the wind power forecasting task. To improve the forecasting accuracy of wind power (WP), we propose a BERT-based model for spatio-temporal forecasting (BERT4ST), which is the first approach to fine-tune a large language model for the spatio-temporal modeling of WP. To deal with the inherent characteristics of WP, BERT4ST exploits the individual spatial and temporal dependency of patches and redesigns a set of spatial and temporal encodings. By well analyzing the connection between bidirectional attention networks and WP spatio-temporal data, BERT4ST employs a pre-trained BERT encoder as the backbone network to learn the individual spatial and temporal dependency of patches of WP data. Additionally, BERT4ST fine-tunes the pre-trained backbone in a multi-stage manner, i.e., first aligning the language model with the spatio-temporal data and then fine-tuning the downstream tasks while maintaining the stability of the backbone network. Experimental results demonstrate that our BERT4ST achieves desirable performance compared to some state-of-the-art methods. • Exploit individual spatial and temporal dependency of patches with pre-trained BERT. • Redesign a set of temporal and spatial encodings tailored for the WP forecasting task. • Adopt a multi-stage fine-tuning mechanism. • Demonstrate the effectiveness of the proposed BERT4ST in regional WP forecasting. [ABSTRACT FROM AUTHOR]

In the chemical industry, materials, pharmacy and energy, hydrazine is extensively used. Meanwhile, it should be noted that it is hepatotoxicity, neurotoxicity, nephrotoxicity and mutagenic toxicity for organism and environment as a potential carcinogen. Thus, developing high sensitivity, good selectivity and short response time of hydrazine probes are vital. According to the mechanisms of detecting N 2 H 4 , this review summarizes hydrazine fluorescent bioluminescent probes from 2017 to 2024 aiming to guide for designing and constructing more outstanding properties of hydrazine probes. [Display omitted] • Hydrazine is widely used in multitudinous fields and poses a threat to environments and human health. • Fluorescent and bioluminescent probes are powerful tools for detecting hydrazine. • The recognition groups are introduced into fluorophores and bioluminescent substrates to construct probes. [ABSTRACT FROM AUTHOR]

The present work investigated the in vitro cytotoxicity of nematocyst venom (NV) from Chrysaora helvola Brandt ( C. helvola ) jellyfish against human MCF-7 and CNE-2 tumor cell lines. Potent cytotoxicity was quantified using the MTT assay (LC 50 = 12.07 ± 3.13 and 1.6 ± 0.22 μg/mL (n = 4), respectively). Apoptosis-like cell death was further confirmed using the LDH release assay and Annexin V/PI double staining-based flow cytometry analysis. However, only activation of caspase-4 was observed. It is possible that some caspase-independent pathways were activated by the NV treatment. Since no reference or antivenom is available, the effects of several commonly used antidotes on the cytotoxicity of NV were examined on more sensitive CNE-2 cells to determine the appropriate emergency measures for envenomation by C. helvola . The phospholipase A 2 (PLA 2 ) inhibitor para -bromophenacyl bromide ( p BPB) showed no protective effect, while Mg 2 + potentiated cytotoxicity. Voltage-gated L-type Ca 2 + channel blockers (verapamil, nifedipine and felodipine) and Na–Ca 2 + exchanger inhibitor KB-R7943 also showed no effect. Assays using Ca 2 + -free culture media or the intracellular Ca 2 + chelator BAPTA also could not inhibit the cytotoxicity. Taken together, these results suggest that PLA 2 and Ca 2 + are not directly involved in the cytotoxicity of NV from C. helvola . Our work also suggests caution regarding the choice for first aid for envenomation by C. helvola jellyfish. [ABSTRACT FROM AUTHOR]

Ethnopharmacological relevance Millettia pulchra Kurz var-laxior (Dunn) Z. Wei, a wild-growing plant of the family Fabaceae is known to possess multifarious medicinal properties. Yulangsan polysaccharide (YLSPS) is a chief ingredient of its root, which has been used in Chinese traditional medicine with a long history for remedy of acute or chronic hepatitis and jaundice. Aim of the study To investigate the ability of the YLSPS to protect against diclofenac-induced hepatotoxicity in mice. Materials and methods Mice were orally treated with YLSPS daily 1 h after the injection of diclofenac for 2 weeks. Dimethyl diphenyl bicarboxylate was used as a reference drug. Results YLSPS effectively reduced the elevated levels of serum alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase and enhanced the reduction of superoxide dismutase, catalase, and glutathione peroxidase activities in the liver. Moreover, the content of malondialdehyde was reduced by treatment with YLSPS, and histological findings also confirmed the anti-hepatotoxic activity. In addition, YLSPS significantly inhibited proinflammatory mediators, such as tumor necrosis factor-alpha and interleukin 1 beta. YLSPS also enhanced mitochondrial antioxidants and inhibited cell death by preventing the down-regulation of Bcl-2 and the up-regulation and release of Bax along with caspase 9 and 3 activity; thus, these findings confirm the involvement of mitochondria in diclofenac-induced apoptosis. Conclusion The results indicate that protective effects of YLSPS against diclofenac-induced acute hepatic injury may rely on its effect on reducing oxidative stress, suppressing inflammatory responses, and improving drug-metabolizing enzyme activity in the liver. [ABSTRACT FROM AUTHOR]

Background Bupivacaine causes neuronal and axonal degeneration, leading to cauda equina syndrome or permanent nerve damage. Our previous studies have shown that intrathecal or intravenous gangliosides monosialogangliosides (GM-1s) have therapeutic effects against bupivacaine-induced neurotoxicity, but we do not know what are the differences between the two methods. Methods and results Bupivacaine-induced neurotoxicity was induced in rats by three times injection of 5% bupivacaine (0.24 μl/g) to the L3 spinal cord. We observed by H&E staining that bupivacaine caused obvious neuronal injuries in the spinal cord, such as edema, vacuolation of myelin sheaths, and neuronal degeneration. Electron microscopy revealed similar pathohistological changes. Neural functions, evaluated by tail-flicking test and locomotor scaling, were also impaired. Treatment with GM-1s (30 mg/kg) repaired the neural lesions and gradually improved the neural functions. By days 14 and 28 post GM-1s, the pathohistological changes in the posterior root and posterior column had significantly recovered but not completely. Compared with intravenous routes, intrathecal application of GM-1s demonstrated faster and greater efficacies in regeneration of neural damages and in improvement of neural dysfunctions. Caspase-3, a marker of cellular apoptosis, was shown by immunohistochemistry to be suppressed in protein transcription by GM-1s application and intrathecal GM-1s had potentiated a greater reduction in caspase-3 protein than intravenous GM-1s. Conclusions Treatment with GM-1s in intrathecal routes more effectively reverses bupivacaine-induced neural injuries and improves the neural dysfunctions than intravenous routes. This may be partly attributed to that GM-1 inhibits the expression of cellular apoptosis factor caspase-3 protein. [ABSTRACT FROM AUTHOR]

Millettia pulchra Kurz var-laxior (Dunn) Z. Wei, a wild-growing plant of the family Fabaceae is known to possess multifarious medicinal properties. 17-Methoxyl-7-hydroxy-benzene-furanchalcone (MHBFC) is a flavonoid monomer extracted from its root, which has been used in traditional Chinese medicine, with a long history as a remedy of hypertension and cardiovascular remodeling. The present study was conducted to further investigate the regulatory mechanisms of MHBFC based on the endothelial nitric oxide synthase-nitric oxide (eNOS-NO) signaling pathway. The abdominal aorta of the male Sprague–Dawley rats was narrowed to induce cardiac remodeling, and the rats were given corresponding drugs for 6 weeks after operation. At the end of the experiment, the relevant indexes were detected. The results showed that Nω-nitro-L-arginine methyl ester (L-NAME) could increase the myocardial cell cross-section area, myocardial fibrosis, and the cardiac collagen volume fraction. The serum NO and eNOS levels and the expression of p-eNOS, p-PI 3 K and p-Akt protein were decreased, and myocardial microvascular endothelial cell (MMVEC) apoptosis increased. However, the above changes were reversed after treatment with MHBFC. These results indicated that MHBFC could increase eNOS protein phosphorylation by increasing PI 3 K and Akt protein phosphorylation, and activated the eNOS-NO signaling pathway, increased eNOS enzyme activity, catalyzed the generation of protective NO, and counteracted MMVEC apoptosis induced by cardiac remodeling, thereby protecting against myocardial damage and reversing cardiac remodeling. [ABSTRACT FROM AUTHOR]