Synergetic sludge conditioning by US enhanced Fe2+ activated sodium persulfate: Physicochemical properties and mechanisms.

Efficient dewatering of sewage sludge is an energy- and carbon-saving procedure for sludge treatment in wastewater treatment facilities. The ultrasound-coupled divalent iron ion activated persulfate process can effectively promote sludge dewatering and improve organic substance content. Under the action of ultrasound (US 50 w/L), divalent iron ions (Fe2+) 200 mg/g (TS), and persulfate (PDS) 200 mg/g (TS) for 60 min, the capillary suction time (CST) was reduced by 79.74%, and the moisture content of the dewatered sludge cake reached 56.51 wt%. The organic carbon content of treated sludge was also four times higher than the original sludge and types were richer in short-chain volatile species in US/Fe2+/PDS. Moreover, the correlation analysis found that the relationship of between CST and SV30, Zeta and lactate dehydrogenase (LDH) were positive correlation, and the relationship of SCOD and TC were positively correlated with the PN (SB-EPS). Mechanistic studies showed that the US/Fe2+/PDS system could produce oxygen activators by US coupling Fe2+ to strengthen the effect of activated PDS strongly, while the sulfate radicals (SO4·-) radical was a dominant role. The cracking mechanism is divided into two pathways effectively degraded the macromolecule EPS into a small-molecule acid and further reduced the water-holding interfacial affinity as follow: (1) the radical path dominated by hydroxyl radicals (·OH), SO4·-, and superoxide radical (O2·-); (2) the non-radicals dominated by monoclinic oxygen (1O2). Afterwards, the electrostatic force and interfacial free energy were reduced, resulting in enhanced self-flocculation and mobility to enhanced dewaterability. These findings demonstrated the US/Fe2+/PDS system had significant advantages in sludge cracking and provided theoretical support for its practical application.

Secure cross-chain interaction solution in multi-blockchain environment.

In the context of the increasingly diversified blockchain technology, interoperability among heterogeneous blockchains has become key to further advancing this field. Existing cross-chain technologies, while facilitating data and asset exchange between different blockchains to some extent, have exposed issues such as insufficient security, low efficiency, and inconsistent standards. Consequently, these issues give rise to significant obstacles in terms of both scalability and seamless communication among blockchains within a multi-chain framework. To address this, this paper proposes an efficient method for cross-chain interaction in a multi-chain environment. Building upon the traditional sidechain model, this method employs smart contracts and hash time-locked contracts (HTLCs) to design a cross-chain interaction scheme. This approach decentralizes the execution of locking, verifying, and unlocking stages in cross-chain transactions, effectively avoiding centralization risks associated with third-party entities in the process. It also greatly enhances the efficiency of fund transfers between the main chain and sidechains, while ensuring the security of cross-chain transactions to some extent. Additionally, this paper innovatively proposes a cross-chain data interaction strategy. Through smart contracts on the main chain, data from sidechains can be uploaded, verified, and stored on the main chain, achieving convenient and efficient cross-chain data sharing. The contribution of this paper is the development of a decentralized protocol that coordinates the execution of cross-chain interactions without the need to trust external parties, thereby reducing the risk of centralization and enhancing security. Experimental results validate the effectiveness of our solution in increasing transaction security and efficiency, with significant improvements over existing models. Our experiments emphasize the system's ability to handle a variety of transaction scenarios with improved throughput and reduced latency, highlighting the practical applicability and scalability of our approach.

Dual blockchain-based data sharing mechanism with privacy protection for medical internet of things.

In the period of big data, the Medical Internet of Things (MIoT) serves as a critical technology for modern medical data collection. Through medical devices and sensors, it enables real-time collection of a large amount of patients' physiological parameters and health data. However, these data are often generated in a high-speed, large-scale, and diverse manner, requiring integration with traditional medical systems, which further exacerbates the phenomenon of scattered and heterogeneous medical data. Additionally, the privacy and security requirements for the devices and sensor data involved in the MIoT are more stringent. Therefore, when designing a medical data sharing mechanism, the data privacy protection capability of the mechanism must be fully considered. This paper proposes an alliance chain medical data sharing mechanism based on a dual-chain structure to achieve secure sharing of medical data among entities such as medical institutions, research institutions, and cloud privacy centers, and at the same time provide privacy protection functions to achieve a balanced combination of privacy protection capability and data accessibility of medical data. First, a knowledge technology based on ciphertext policy attribute encryption with zero-knowledge concise non-interactive argumentation is used, combined with the data sharing structure of the federation chain, to ensure the integrity and privacy-protecting capability of medical data. Second, the approach employs certificate-based signing and proxy re-encryption technology, ensuring that entities can decrypt and verify medical data at the cloud privacy center using this methodology, consequently addressing the confidentiality concerns surrounding medical data. Third, an efficient and secure key identity-based encryption protocol is used to ensure the legitimacy of user identity and improve the security of medical data. Finally, the theoretical and practical performance analysis proves that the mechanism is feasible and efficient compared with other existing mechanisms.

Discovery of zolinium TSG1180 as a novel agonist of transgelin-2 for treating asthma.

Asthma is a complex and heterogeneous respiratory disease that causes serious social and economic burdens. Current drugs such as ß2-agonists cannot fully control asthma. Our previous study found that Transgelin-2 is a potential target for treating asthmatic pulmonary resistance. Herein, we discovered a zolinium compound, TSG1180, that showed a strong interaction with Transgelin-2. The equilibrium dissociation constants (KD) of TSG1180 to Transgelin-2 were determined to be 5.363 × 10-6 and 9.81 × 10-6 M by surface plasmon resonance (SPR) and isothermal titration calorimetry (ITC). Cellular thermal shift assay (CETSA) results showed that the thermal stability of Transgelin-2 increased after coincubation of TSG1180 with lysates of airway smooth muscle cells (ASMCs). Molecular docking showed that Arg39 may be the key residue for the binding. Then, the SPR result showed that the binding affinity of TSG1180 to Transgelin-2 mutant (R39E) was decreased by 1.69-fold. Real time cell analysis (RTCA) showed that TSG1180 treatment could relax ASMCs by 19 % (P < 0.05). Once Transgelin-2 was inhibited, TSG1180 cannot induce a relaxation effect, suggesting that the relaxation effect was specifically mediated by Transgelin-2. In vivo study showed TSG1180 effectively reduced pulmonary resistance by 64 % in methacholine-induced mice model (P < 0.05). Furthermore, the phosphorylation of Ezrin at T567 was increased by 8.06-fold, the phosphorylation of ROCK at Y722 was reduced by 38 % and the phosphorylation of RhoA at S188 was increased by 52 % after TSG1180 treatment. These results suggested that TSG1180 could be a Transgelin-2 agonist for further optimization and development as an anti-asthma drug.

Experimental and Numerical Calculation Study on the Slope Stability of the Yellow River Floodplain from Wantan Town to Liuyuankou.

More than two million people live on the floodplains along the middle and lower streams of the Yellow River. The rapid development of industry and agriculture on both sides of the Yellow River has caused serious pollution of the floodplain soil. Erosion by water has led to the destruction of the floodplain which has not only compressed people's living space but also resulted in a large amount of sediment containing heavy metals entering the river, aggravating water pollution. To further study the law governing the release of pollutants in soil, this work, based on field surveys of the Yellow River floodplain slopes from Wantan town to Liuyuankou, was focused on determining the failure mechanism and laws for the floodplain slope through the combination of a flume experiment and numerical calculations. The results showed that the floodplain slopes, composed of clay and silty sand, presented an interactive structure. Under the action of water erosion, the slope was first scoured to form a curved, suspended layer structure, and then the upper suspended layer toppled. The bank stability coefficient decreased by about 65% when the scour width increased from 0.07 m to 0.42 m, and the water content increased from 20% to 40%. For the failure characteristics, the angle of the failure surface was negatively correlated with the scour width, and the distance from the top failure surface to the bank edge was about 2.5 times that of the scour width.

The Effects of a Transgelin-2 Agonist Administered at Different Times in a Mouse Model of Airway Hyperresponsiveness.

Airway hyperresponsiveness (AHR) is one of the most important features of asthma. Our previous study showed that inhaled transgelin-2 agonist, TSG12, effectively reduced pulmonary resistance in a mouse model of asthma in a dose-dependent manner. However, the optimal administration time of TSG12 to reduce AHR and the pharmacological effects are still unclear. In this study, the effects of TSG12 inhalation before and during AHR occurrence were examined. The results showed that the pulmonary resistance was reduced by 57% and the dynamic compliance was increased by 46% in the TSG12 Mch group (atomize TSG12 10 min before methacholine, p < 0.05 vs. model). The pulmonary resistance was reduced by 61% and the dynamic compliance was increased by 47% in the TSG12 + Mch group (atomize TSG12 and methacholine together, p < 0.05 vs. model). Quantitative real-time PCR showed that the gene expression levels of transgelin-2, myosin phosphatase target subunit-1, and myosin light chain were up-regulated by 6.4-, 1.9-, and 2.8-fold, respectively, in the TSG12 Mch group. The gene expression levels of transgelin-2, myosin phosphatase target subunit-1, and myosin light chain were up-regulated by 3.2-, 1.4-, and 1.9-fold, respectively, in the TSG12 + Mch group. The results suggested that TSG12 effectively reduces pulmonary resistance when TSG12 inhalation occurred both before and during AHR occurrence. Gene expression levels of transgelin-2 and myosin light chain were significantly up-regulated when TSG12 inhalation occurred before AHR occurrence. This study may provide a basis for the administration time of TSG12 for asthma treatment in the future.

Electroacupuncture at ST36 (Zusanli) Prevents T-Cell Lymphopenia and Improves Survival in Septic Mice.

Purpose: Sepsis is the main cause of death in intensive care unit. Maladaptive cytokine storm and T-cell lymphopenia are critical prognosis predictors of sepsis. Electroacupuncture (EA) is expected to be an effective intervention to prevent sepsis. This study aims to determine the potential of EA at ST36 (Zusanli) to prevent experimental septic mice. Methods: Mice were randomly assigned into PBS, LPS, or EA+LPS group. EA (0.1 mA, continuous wave, 10 Hz) was performed stimulating the ST36 for 30 min, once a day for 3 days. After the third day, all mice were challenged with PBS or LPS (4 mg/kg) simultaneously. Mice were evaluated for survival, ear temperature, and other clinical symptoms. Lung and small intestine tissue injuries were analyzed by hematoxylin and eosin staining. Bio-Plex cytokine assay was used to analyze the concentration of cytokines. T lymphocytes were analyzed by flow cytometry and Western blot assays. The role of T cells in preventing sepsis by EA was analyzed by using nude mice lacking T lymphocytes. Results: EA at ST36 improved survival, symptom scores, and ear temperature of endotoxemic mice. EA also improved dramatically pulmonary and intestinal injury by over 50% as compared to untreated mice. EA blunted the inflammatory cytokine storm by inducing a lasting inhibition of the production of major inflammatory factors (TNF-α, IL-1ß, IL-5, IL-6, IL-10, IL-17A, eotaxin, IFN-γ, MIP-1ß and KC). Flow cytometry and Western blot analyses showed EA significantly reduced T-lymphocyte apoptosis and pyroptosis. Furthermore, T lymphocytes were critical for the effects of EA at ST36 stimulation blunted serum TNF-α levels in wild-type but not in nude mice. Conclusion: EA halted systemic inflammation and improved survival in endotoxemic mice. These effects are associated with the protective effect of EA on T lymphocytes, and T cells are required in the anti-inflammatory effects of EA in sepsis.

Role of Purinergic Signaling in Acupuncture Therapeutics.

Acupuncture is a therapeutic treatment that is well recognized in many countries. However, the initiation mechanisms of acupuncture are not well understood. Purinergic signaling has been considered a key signaling pathway in acupuncture in recent years. Acupuncture-induced ATP is mainly produced by mast cells and fibroblasts, and ATP is gradually hydrolyzed into adenosine. ATP and adenosine further participate in the process of acupuncture information transmission to the nervous and immune systems through specific purine receptors. Acupuncture initiates analgesia via the down-regulation of the expression of P2 receptors or up-regulation of the expression of adenosine A1 receptors on nerve fibers. ATP also promotes the proliferation of immune cells through P2 receptors and A3 receptors, causing inflammation. In contrast, adenosine activates A2 receptors, promotes the production and infiltration of immunosuppressive cells, and causes an anti-inflammatory response. In summary, we described the role of purinergic signaling as a general signaling pathway in the initiation of acupuncture and the influence of purinergic signaling on the neuroimmune network to lay the foundation for future systematic research on the mechanisms of acupuncture therapeutics.

Luminescent Thermochromic Silver Iodides as Wavelength-Dependent Thermometers.

Luminescent thermochromic materials with a dramatic shift of emission band under different temperatures are highly desirable in temperature sensing fields. However, the design of the synthesis of such compounds remains a great challenge. In this work, two new luminescent thermochromic silver iodides, (emIm)Ag3I4 (1) and (emIm)Ag2I3 (2) (emIm = 1-ethyl-3-methyl imidazole), have been synthesized under solvothermal conditions. Compound 1 features a [Ag3I4]- anionic layer, while compound 2 possesses an infinite [Ag2I3]- chain structure, both of which are charge balanced by emIm+ cations. Particularly, they display luminescent thermochromism with a significant wavelength shift of emission maximum with temperature change. They represent rare examples of infinite layered or chain silver iodides that show luminescent thermochromism. Furthermore, the results indicate that compounds 1 and 2 are promising wavelength-dependent luminescent thermometers.