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Handling the massive quantities of by‐products from metallurgical processes has become a major concern in recent decades. Efforts to develop sustainable alternatives for these secondary resources are ongoing to achieve the transition to climate neutrality. This study has investigated the potential of employing vanadium‐bearing slag as a new value‐added binder in refractories, aiming to replace virgin raw materials. Two types of vanadium‐bearing slags from BOF, each containing <2 wt.% vanadium were studied. Low‐cement vanadium slag‐based castables were prepared by gradually substituting 0, 2.5, and 5 wt.% of the commercial calcium aluminate cements (Secar71 and CMA72) by the slags. The flow values of the mixes containing 5 wt.% of slag decrease significantly from about 90% to 30% after 30 min, showing poor ability to flow and thus are not considered as self‐flow castables. Castables containing 2.5 wt.% of slag present a cold crushing strength value, in the range of 71–116 MPa while values for castables containing 5 wt.% of slag fall into the range of 53–68 MPa due to the lower packing properties leading to higher porosity and reduce in strength. Similar observation was concluded for cold modulus of rupture. The micrographs of the samples containing both slag and cement show promising compatibility between the binder and aggregates after sintering at 1500°C. Overall, characteristics obtained with the samples containing slag show promising alternatives as a refractory lining. This study investigated the use of vanadium‐bearing slag as an alternative to calcium aluminate cement in high‐alumina refractory castables, with the aim to support decarbonization by reducing reliance on natural raw materials.

Discovering that metals are essential for the structure and function of biomolecules has given a completely new perspective on the role of metal ions in living organisms. Nowadays, the design and synthesis of new metal-based compounds, as well as metal ion binding components, for the treatment of human diseases is one of the main aims of bioinorganic chemistry. One of the areas in vanadium-based compound research is their potential anticancer activity. In this review, we summarize recent molecular and cellular mechanisms in the cytotoxic activity of many different synthetic vanadium complexes as well as inorganic salts. Such mechanisms shall include DNA binding, oxidative stress, cell cycle regulation and programed cell death. We focus mainly on cellular studies involving many type of cancer cell lines trying to highlight some new significant advances.

Vanadium is the 21st most abundant element in the Earth’s crust and the 2nd-to-most abundant transition metal in sea water. The element is ubiquitous also in freshwater and nutrients. The average body load of a human individual amounts to 1 mg. The omnipresence of vanadium hampers checks directed towards its essentiality. However, since vanadate can be considered a close blueprint of phosphate with respect to its built-up, vanadate likely takes over a regulatory function in metabolic processes depending on phosphate. At common concentrations, vanadium is non-toxic. The main source for potentially toxic effects caused by vanadium is exposure to high loads of vanadium oxides in the breathing air of vanadium processing industrial enterprises. Vanadium can enter the body via the lungs or, more commonly, the stomach. Most of the dietary vanadium is excreted. The amount of vanadium resorbed in the gastrointestinal tract is a function of its oxidation state (VV or VIV) and the coordination environment. Vanadium compounds that enter the blood stream are subjected to speciation. The predominant vanadium species in blood are vanadate and vanadyl bound to transferrin. From the blood stream, vanadium becomes distributed to the body tissues and bones. Bones act as storage pool for vanadate. The aqueous chemistry of vanadium(V) at concentration <10 μM is dominated by vanadate. At higher concentrations, oligovanadates come in, decavanadate in particular, which is thermodynamically stable in the pH range 2.3–6.3, and can further be stabilized at higher pH by interaction with proteins. The similarity between vanadate and phosphate accounts for the interplay between vanadate and phosphate-dependent enzymes: phosphatases can be inhibited, kinases activated. As far as medicinal applications of vanadium compounds are concerned, vanadium’s mode of action appears to be related to the phosphate-vanadate antagonism, to the direct interaction of vanadium compounds or fragments thereof with DNA, and to vanadium’s contribution to a balanced tissue level of reactive oxygen species. So far vanadium compounds have not yet found approval for medicinal applications. The antidiabetic (insulin-enhancing) effect, however, of a singular vanadium complex, bis(ethylmaltolato)oxidovanadium(IV) (BEOV), has revealed encouraging results in phase IIa clinical tests. In addition, in vitro studies with cell cultures and parasites, as well as in vivo studies with animals, have revealed a broad potential spectrum for the application of vanadium coordination compounds in the treatment of cardiac and neuronal disorders, malignant tumors, viral and bacterial infections (such as influenza, HIV, and tuberculosis), and tropical diseases caused by parasites, e.g., Chagas’ disease, leishmaniasis, and amoebiasis.

Secondary damage following primary spinal cord injury extends pathology beyond the site of initial trauma, and effective management is imperative for maximizing anatomical and functional recovery. Bisperoxovanadium compounds have proven neuroprotective effects in several central nervous system injury/disease models, however, no mechanism has been linked to such neuroprotection from bisperoxovanadium treatment following spinal trauma. The goal of this study was to assess acute bisperoxovanadium treatment effects on neuroprotection and functional recovery following cervical unilateral contusive spinal cord injury, and investigate a potential mechanism of the compound's action. Two experimental groups of rats were established to 1) assess twice-daily 7 day treatment of the compound, potassium bisperoxo (picolinato) vanadium, on long-term recovery of skilled forelimb activity using a novel food manipulation test, and neuroprotection 6 weeks following injury and 2) elucidate an acute mechanistic link for the action of the drug post-injury. Immunofluorescence and Western blotting were performed to assess cellular signaling 1 day following SCI, and histochemistry and forelimb functional analysis were utilized to assess neuroprotection and recovery 6 weeks after injury. Bisperoxovanadium promoted significant neuroprotection through reduced motorneuron death, increased tissue sparing, and minimized cavity formation in rats. Enhanced forelimb functional ability during a treat-eating assessment was also observed. Additionally, bisperoxovanadium significantly enhanced downstream Akt and mammalian target of rapamycin signaling and reduced autophagic activity, suggesting inhibition of the phosphatase and tensin homologue deleted on chromosome ten as a potential mechanism of bisperoxovanadium action following traumatic spinal cord injury. Overall, this study demonstrates the efficacy of a clinically applicable pharmacological therapy for rapid initiation of neuroprotection post-spinal cord injury, and sheds light on the signaling involved in its action.

Vanadium dioxide (VO 2 ) is a Mott phase transition compound that can be applied as a thermochromic smart material for energy saving and comfort and titanium dioxide (TiO 2 ) is a well-known photocatalyst for self-cleaning coatings. In this paper, we report a VO 2 @TiO 2 core-shell structure, in which the VO 2 nanorod core exhibits a remarkable modulation ability for solar infrared light and the TiO 2 anatase shell exhibits significant photocatalytic degradation of organic dye. In addition, the TiO 2 overcoating not only increased the luminous transmittance of VO 2 based on an antireflection effect, but also modified the intrinsic colour of VO 2 films from yellow to light blue. The TiO 2 also enhanced the chemical stability of VO 2 against oxidation. This is the first report of such a single nanoparticle structure with both thermochromic and photocatalytic properties that offer significant potential for creating a multifunctional smart coating.

Multidrug resistant (MDR) bacterial infections, particularly those involving methicillin-resistant Staphylococcus aureus (MRSA), pose a grave threat to global population health, necessitating novel therapeutic approaches capable of circumventing existing resistance mechanisms. Biomimetic enzymes, which generate bactericidal reactive oxygen species (ROS) by mimicking natural enzyme activity, represent a highly promising solution. This study reports a straightforward one-step synthesis method for vanadium dioxide (VO₂) nanoparticles, which function as potent biomimetic enzymes exhibiting both oxidase-like and peroxidase-like activities. When combined with near-infrared laser irradiation (808 nm, 1 W/cm²) for photothermal therapy (PTT), these VO₂ nanoparticles not only mediate local hyperthermia with a photothermal conversion rate of up to 36.9%, but also significantly enhance ROS generation through biomimetic catalysis. This achieves potent synergistic effects between photothermal therapy and chemodynamic therapy (CDT). This combined therapy exhibits potent antibacterial activity against suspended methicillin-resistant Staphylococcus aureus (MRSA) and effectively disrupts preformed biofilms. Furthermore, in a subcutaneous abscess mouse model, VO₂-mediated PTT-CDT treatment efficiently eradicated bacteria, alleviated local inflammation, promoted tissue repair and angiogenesis. In summary, this readily synthesised VO₂ nanozyme system offers an efficient and translatable therapeutic strategy for tackling challenging multidrug-resistant bacterial infections. Graphical Abstract

Vanadium-based compounds with various crystal structures are highly promising cathode materials for aqueous zinc-based batteries. However, their further development is limited due to the low electrical conductivity, slow zinc ion diffusion, and weak structural stability. It is a feasible strategy to resolve above mentioned issues through surface modification. Herein, we design bi-phase coexisting CaV2O6/NaV6O15 nanobelt structures with abundant interfaces, which provide more reactive sites than single-phase ones. The samples as the electrode materials deliver a specific capacity of 312 mAh g−1 at 5 A g−1 after 2000 cycles. They still keep a capacity of 231 mAh g−1 at 10 A g−1 with a cycle life of 6500 times.

Osteoblastogenesis plays a critical role in bone repair. Insulin and insulin-mimetic compounds, such as vanadium (IV) oxide acetylacetonate (VAC), have been reported to enhance bone healing in various models. This study aimed to evaluate the effects of vanadium compounds, VAC and vanadium (IV) oxide sulfate (VOSO4), on osteoblast proliferation and function. MC3T3-E1 pre-osteoblast cells were treated with insulin, ascorbic acid, and varying concentrations of VAC or VOSO4, and samples were collected at multiple time points over 21 days. We assessed cell proliferation, functional markers, and gene and protein expression. Our findings demonstrate that both VAC and VOSO4 stimulate MC3T3-E1 proliferation, increase calcium and proteoglycan deposition, and enhance phosphorylation of Protein Kinase B (Akt) over time. Gene expression analysis revealed that VAC treatment upregulated RUNX2, BGLAP, and TWIST2 at Day 7 compared to controls, with sustained expression patterns observed at Day 10. These results align with existing literature, supporting that VAC and VOSO4 promote osteoblastogenesis and may serve as effective adjuvants to accelerate bone regeneration during fracture healing.

Oncolytic viruses rewire the immune system and can lead to long-lasting antitumor defenses against primary and metastatic tumors. However, results from clinical studies have shown heterogeneity in responses suggesting that multiplexed approaches may be necessary to consistently generate positive outcomes in patients. To this end, we explored the combination of oncolytic rhabdovirus VSV∆51 with vanadium(V) dipicolinate derivatives, which have already been explored for their antidiabetic properties in animal models. The combination of vanadium-based dipicolinate compounds with VSV∆51 significantly increased viral replication and cytotoxicity in the human renal cell carcinoma cell line 786-0. The effects of three vanadium(V)-dipicolinate coordination complexes ([VO2dipic]−, [VO2dipic-OH]− and [VO2dipic-Cl]− with –OH or –Cl in the para position) were compared to that of the simple salts using spectroscopy and speciation profiles. Like the vanadate salts and the vanadyl cation, all dioxovanadium(V) dipicolinate complexes tested were found to increase viral infection and cytotoxicity when used in combination with VSV∆51. Viral sensitization is dependent on the vanadium since free dipicolinate ligands exerted no effect on viral infection and viability. The ability of these complexes to interact with interfaces and the stability of the complexes were evaluated under physiological conditions. Results indicate that these complexes undergo hydrolysis in cell culture media thereby generating vanadate. The vanadium dipicolinate derivatives in the context of immunovirotherapy shares similarities with previous studies exploring the antidiabetic properties of the compounds. The synergy between vanadium compounds and the oncolytic virus suggests that these compounds may be valuable in the development of novel and effective pharmaco-viral therapies.

Studies have shown that the inhibition of phosphatase and tensin homolog deleted on chromosome 10 (PTEN)was neuroprotective against ischemia/reperfusion(I/R) injury. Bisperoxovanadium (bpV), a derivative of vanadate, is a well-established inhibitor of PTEN. However, its function islimited due to its general inadequacy in penetrating cell membranes. Mxene(Ti 3 C 2 T x ) is a novel two-dimensional lamellar nanomaterial with an excellent ability to penetrate the cell membrane. Yet, the effects of this nanomaterial on nervous system diseases have yet to be scrutinized. Here, Mxene(Ti 3 C 2 T x ) was used for the first time to carry bpV(HOpic), creating a new nanocomposite Mxene-bpV that was probed in a cerebral I/R injury model. The findings showed that this synthetic Mxene-bpV was adequately stable and can cross the cell membraneeasily. We observed that Mxene-bpV treatment significantly increased the survival rate of oxygen glucose deprivation/reperfusion(OGD/R)--insulted neurons, reduced infarct sizes and promoted the recovery of brain function after mice cerebral I/R injury. Crucially, Mxene-bpV treatment was more therapeutically efficient than bpV(HOpic) treatment alone over the same period. Mechanistically, Mxene-bpV inhibited the enzyme activity of PTEN in vitro and in vivo. It also promoted the expression of phospho-Akt (Ser 473 ) by repressing PTEN and then activated the Akt pathway to boost cell survival. Additionally, in PTEN transgenic mice, Mxene-bpV suppressed I/R-induced inflammatory response by promoting M2 microglial polarization through PTEN inhibition. Collectively, the nanosynthetic Mxene-bpV inhibited PTEN’ enzymatic activity by activating Akt pathway and promoting M2 microglial polarization, and finally exerted neuroprotection against cerebral I/R injury. Graphical Abstract