No abstract

Although ultrasound-based therapeutic strategies have achieved great success in the battle against antibiotic-resistant bacterial infections, various sonodynamic treatments still suffer from poor therapeutic efficiency, failing to completely eradicate infections. Thus, more potent strategies are urgently required. Herein, a novel ultrasound-driven treatment modality, sonoactivated chemodynamic therapy (SCDT), is proposed, which shows a robust generation of superoxide anion and destructive hydroxyl radical via sonotriggered catalytic reactions. This SCDT platform is prepared by grafting Fe 3+ onto polyethylenimine-modified bismuth oxybromide (BiOBr) nanoplates. During sonocatalysis, the introduction of Fe 3+ can effectively separate the holes (h +) and electrons (e-) of BiOBr NPs and shorten their transport path of valence electrons, resulting in the activation of multioxygen reduction and Fenton reaction to generate abundant reactive oxygen species against methicillin-resistant Staphylococcus aureus (MRSA) infection. More importantly, Fe 3+ can also serve as a magnetic resonance imaging (MRI) contrast agent to achieve the accurate diagnosis of bacterial infection. The SCDT-mediated bactericidal outcome can be monitored by in situ monitoring through MRI technique, revealing a complete elimination of MRSA myositis in mice. Collectively, its deep tissue penetration, high therapeutic efficacy, and noninvasive properties make SCDT a promising therapeutic modality for combating multidrug-resistant bacterial infection.

The dehydroxylation/dehydration and Lewis acidity of the surface of monoclinic tungsten oxide (m-WO3) powder as a function of evacuation temperature was investigated by infrared spectroscopy. At room temperature, the m-WO3 surface contains both isolated and hydrogen bonded hydroxyl groups along with equal amounts of strongly and weakly adsorbed layers of water. Most of the surface hydroxyl groups and the weakly adsorbed water layer are eliminated by evacuation at room temperature. The strongly adsorbed water is removed by evacuation above 200 °C. Adsorption of D2O shows that the surface hydroxyl groups and adsorbed water are accessible and easily exchanged. However, the removal of the strongly held water is not related to the number of Lewis or Brønsted acid sites on the surface. While there is little change in the amount of adsorbed water between a room temperature sample and a sample evacuated at 150 °C, pyridine adsorption shows that there is a corresponding 50% reduction in the number of Lewis acid sites. Furthermore, the strongly held water is eliminated by evacuation between 200 and 400 °C, whereas there is little change in the number of Brønsted or Lewis acid sites. The changes in Lewis/Brønsted acidity are not related to the dehydration but rather attributed to reduction of the oxide due to removal of lattice oxygen.

The adsorption of dimethyl methylphosphonate (DMMP), trimethyl phosphate (TMP), and methyldichlorophosphate (MDCP) on monoclinic tungsten oxide (m-WO3) evacuated at various temperatures was investigated using infrared spectroscopy. DMMP is the most common molecule used for evaluating the performance of WO3 and other semiconducting metal oxide (SMO)-based sensors to phosphonate-based nerve agents. However, toxic nerve agents such as sarin differ from DMMP in that they contain a functional group (P−F in sarin) that can be readily hydrolyzed. It is shown that the adsorption of organophosphates that contain P−Cl groups differs from nonhalogenated simulants such as DMMP and TMP on WO3 surfaces. Specifically, the non-chlorinated simulants DMMP and TMP adsorb on the surface solely through the PO functionality with the surface water layer as well as the Lewis and Brønsted acid sites. The relative number of molecules bound on Lewis and Brønsted acid surface sites depends on the initial evacuation temperature of the WO3 surface. When MDCP adsorbs on WO3 through the PO bond, it is accompanied by the hydrolysis of P−Cl groups by water vapor or the adsorbed water layer leading to additional phosphate-like species on the surface. The infrared data suggests that a halogenated phosphate like MDCP is a better simulant molecule for studies aimed at understanding the role of water and hydrolysis in the response of metal oxide-based sensors to nerve agents.

As the indispensable second cellular messenger, calcium signaling is involved in the regulation of almost all physiological processes by activating specific target proteins. The importance of calcium ions (Ca2+) makes its “Janus nature” strictly regulated by its concentration. Abnormal regulation of calcium signals may cause some diseases; however, artificial regulation of calcium homeostasis in local lesions may also play a therapeutic role. “Calcium overload,” for example, is characterized by excessive enrichment of intracellular Ca2+, which irreversibly switches calcium signaling from “positive regulation” to “reverse destruction,” leading to cell death. However, this undesirable death could be defined as “calcicoptosis” to offer a novel approach for cancer treatment. Indeed, Ca2+ is involved in various cancer diagnostic and therapeutic events, including calcium overload-induced calcium homeostasis disorder, calcium channels dysregulation, mitochondrial dysfunction, calcium-associated immunoregulation, cell/vascular/tumor calcification, and calcification-mediated CT imaging. In parallel, the development of multifunctional calcium-based nanomaterials (e.g., calcium phosphate, calcium carbonate, calcium peroxide, and hydroxyapatite) is becoming abundantly available. This review will highlight the latest insights of the calcium-based nanomaterials, explain their application, and provide novel perspective. Identifying and characterizing new patterns of calcium-dependent signaling and exploiting the disease element linkage offer additional translational opportunities for cancer theranostics.