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MXenes are the newest class of two-dimensional nanomaterials characterized by large surface area, high conductivity, and hydrophilicity. To further improve their performance for use in energy storage devices, heteroatoms or functional groups can be inserted into the Mxenes’ structure increasing their stability. This work proposes insertion of lanthanum atoms into niobium-MXene (Nb-MX/La) that was characterized in terms of morphogy, structure, and electrochemical behavior. The addition of La to the Nb-MXene structure was essential to increase the spacing between the layers, improving the interaction with the electrolyte and enabling charge/discharge cycling in a higher potential window and at higher current densities. Nb-MX/La achieved a specific capacitance of up to 157 mF cm–2, a specific capacity of 42 mAh cm–2at 250 mV s–1, a specific power of 37.5 mW cm–2, and a specific energy of 14.1 mWh cm–2after 1000 charge/discharge cycles at 50 mA cm–2.

Obesity is the best described risk factor for the development of non-alcoholic fatty liver disease (NAFLD)/metabolic dysfunction associated steatotic liver disease (MASLD) and polycystic ovary syndrome (PCOS) while the major pathogenic mechanism linking these entities is insulin resistance (IR). IR is primarily caused by increased secretion of proinflammatory cytokines, adipokines, and lipids from visceral adipose tissue. Increased fatty acid mobilization results in ectopic fat deposition in the liver which causes endoplasmic reticulum stress, mitochondrial dysfunction, and oxidative stress resulting in increased cytokine production and subsequent inflammation. Similarly, IR with hyperinsulinemia cause hyperandrogenism, the hallmark of PCOS, and inflammation in the ovaries. Proinflammatory cytokines from both liver and ovaries aggravate IR thus providing a complex interaction between adipose tissue, liver, and ovaries in inducing metabolic abnormalities in obese subjects. Although many pathogenic mechanisms of IR, NAFLD/MASLD, and PCOS are known, there is still no effective therapy for these entities suggesting the need for further evaluation of their pathogenesis. Extracellular vesicles (EVs) represent a novel cross-talk mechanism between organs and include membrane-bound vesicles containing proteins, lipids, and nucleic acids that may change the phenotype and function of target cells. Adipose tissue releases EVs that promote IR, the development of all stages of NAFLD/MASLD and PCOS, while mesenchymal stem cell-derived AVs may alleviate metabolic abnormalities and may represent a novel therapeutic device in NAFLD/MASLD, and PCOS. The purpose of this review is to summarize the current knowledge on the role of adipose tissue-derived EVs in the pathogenesis of IR, NAFLD/MASLD, and PCOS.

Background: Macrophage migration inhibitory factor (MIF) is a multipotent cytokine that contributes to the inflammatory response to chemical liver injury. This cytokine exhibits pro- and anti-inflammatory effects depending on the etiology and stage of liver disease. Objective: Our study aimed to investigate the role of MIF in oxidative stress and inflammation in the liver, and modulatory effects of betaine on MIF in thioacetamide (TAA)-induced chronic hepatic damage in mice. Methods: The experiment was performed on wild type and knockout MIF-/- C57BL/6 mice. They were divided into the following groups: control; Bet-group that received betaine (2% wt/v dissolved in drinking water); MIF-/- mice group; MIF-/-+Bet; TAA-group that received TAA (200 mg/kg b.w.), intraperitoneally, 3x/week/8 weeks); TAA+Bet; MIF-/-+TAA, and MIF-/-+TAA+Bet. In TAA- and Bet-treated groups, animals received the same doses. After eight weeks of treatment, blood samples were collected for biochemical analysis, and liver specimens were prepared for the assessment of parameters of oxidative stress and inflammation. Results: In MIF-/-mice, TAA reduced transaminases, γ-glutamyltranspeptidase, bilirubin, malondialdehyde (MDA), oxidative protein products (AOPP), total oxidant status (TOS), C-reactive protein (CRP), IL-6, IFN-γ, and increased thiols and total antioxidant status (TAS). Betaine attenuated the mechanism of MIF and mediated effects in TAA-induced liver injury, reducing transaminases, γ-glutamyltranspeptidase, bilirubin, MDA, AOPP, TOS, CRP, IL-6, IFN-g, and increasing thiols. Conclusion: MIF is a mediator in hepatotoxic, pro-oxidative, and proinflammatoryeffects of TAA-induced liver injury. MIF-targeted therapy can potentially mitigate oxidative stress and inflammation in the liver, but the exact mechanism of its action requires further investigation. Betaine increases anti-oxidative defense and attenuates hepatotoxic effects of MIF, suggesting that betaine can be used for the prevention and treatment of liver damage.

Dysfunction of the endocannabinoid system (ES) has been identified in nonalcoholic fatty liver disease (NAFLD) and associated metabolic disorders. Cannabinoid receptor type 1 (CB1) expression is largely dependent on nutritional status. Thus, individuals suffering from NAFLD and metabolic syndrome (MS) have a significant increase in ES activity. Furthermore, oxidative/ nitrosative stress and inflammatory process modulation in the liver are highly influenced by the ES. Numerous experimental studies indicate that oxidative and nitrosative stress in the liver is associated with steatosis and portal inflammation during NAFLD. On the other hand, inflammation itself may also contribute to reactive oxygen species (ROS) production due to Kupffer cell activation and increased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity. The pathways by which endocannabinoids and their lipid-related mediators modulate oxidative stress and lipid peroxidation represent a significant area of research that could yield novel pharmaceutical strategies for the treatment of NAFLD. Cumulative evidence suggested that the ES, particularly CB1 receptors, may also play a role in inflammation and disease progression toward steatohepatitis. Pharmacological inactivation of CB1 receptors in NAFLD exerts multiple beneficial effects, particularly due to the attenuation of hepatic oxidative/nitrosative stress parameters and significant reduction of proinflammatory cytokine production. However, further investigations regarding precise mechanisms by which CB1 blockade influences the reduction of hepatic oxidative/nitrosative stress and inflammation are required before moving toward the clinical phase of the investigation.

Galectin-3 (Gal-3) has increasingly been recognized as a modulator of inflammation, oxidative/nitrosative stress, fibrogenesis, and tissue remodeling. The objective of the current pilot study was to investigate the influence of Gal-3 on cardiac and renal antioxidant capacity using biochemical and histopathological examinations. Two groups (n=7 each) of male mice were tested: 1. control (CON) group (wild type of C57BL/6 mice) and 2. GAL-3-/-group (galectin-3-/-knockout mice). After overnight fasting, mice were sacrificed by exsanguination in ketamine (100mg/kg intraperitoneally). Then, cardiac and renal tissue samples were taken to determine the parameters of oxidative/nitrosative stress and antioxidant capacity. The levels of malondialdehyde and nitrites+nitrates was not significantly different in the GAL-3-/-group vs. the CON group. The total superoxide dismutase activity in the renal tissue of the GAL-3-/-mice was significantly lower compared to the CON group. Cardiac and renal catalase and glutathione S-transferase activity was significantly reduced in the GAL-3-/-group vs. the CON group, respectively. A significant decrease in glutathione level was also registered in hearts of the GAL-3-/-group vs. the CON group. Our findings indicate that Gal-3 deficiency does not lead to lipid peroxidation and nitrosative stress in cardiac and renal tissue in mice. However, the lack of this beta-galactoside-binding lectin does reduce antioxidant capacity in both of the investigated tissues.

Methionine is an essential sulphur-containing amino acid involved in protein synthesis, regulation of protein function and methylation reactions. Dietary methionine restriction (0.12–0.17% methionine in food) extends the life span of various animal species and delays the onset of aging-associated diseases and cancers. In the liver, methionine restriction attenuates steatosis and delays the development of non-alcoholic steatohepatitis due to antioxidative action and metabolic reprogramming. The limited intake of methionine stimulates the fatty acid oxidation in the liver and the export of lipoproteins as well as inhibits de novolipogenesis. These effects are mediated by various signaling pathways and effector molecules, including sirtuins, growth hormone/insulin-like growth factor-1 axis, sterol regulatory element binding proteins, adenosine monophosphate-dependent kinase and general control nonderepressible 2 pathway. Additionally, methionine restriction stimulates the synthesis of fibroblast growth factor-21 in the liver, which increases the insulin sensitivity of peripheral tissues. In the brain, methionine restriction delays the onset of neurodegenerative diseases and increases the resistance to various forms of stress through antioxidative effects and alterations in lipid composition. This review aimed to summarize the morphological, functional and molecular changes in the liver and brain caused by the methionine restriction, with possible implications in the prolongation of maximal life span.

Gold-silver (AuAg) nanoparticles were deposited on reduced graphene oxide (rGO), with Au wt% varying from 34.6 to 46.2 and Ag wt% ranging from 31.7 to 35.3. Three AuAg/rGO samples were characterized by inductively coupled plasma optical emission spectroscopy, transmission and scanning electron microscopy with energy-dispersive X-ray spectroscopy, and X-ray diffraction analysis. Subsequently, AuAg/rGO materials were studied using the rotating disk electrode as electrocatalysts for oxygen reduction reaction (ORR) for potential application in alkaline fuel cells. AuAg/rGO-3 (with ca. 34.6 wt% Au and 35.3 wt% Ag) showed the most promising performance, with high ORR activity and good stability, as evidenced by the highest current density (−4.45 mA cm−2at 0.5 V), the lowest Tafel slope (103 mV dec−1), and the highest number of electrons exchanged (4.1).

The basic problem in the operation of automotive brakes is the unpredictable nature of the tribological processes that occur at the contact of the friction pair. The stochastic nature of the tribological contact of the disc brake is affected differently by the complex interaction between the brake disc and the friction material under different conditions because of the influences of the applied pressure, the speed and the brake interface temperature. Owing to the highly dynamic non-linear change in the braking torque induced by the complex situation at the contact of the disc brake, the braking torque could not be modelled, predicted and controlled using classical mathematical methods. This is related, in particular, to the dynamic change in the braking torque in a braking cycle. Dynamic modelling and prediction of the braking torque is very important for further improvement in the performance of the brakes of motor vehicles through more precise control of their performance with respect to the driver demands and the change in the adhesion between the tyre and the road. Recurrent dynamic neural networks were employed in this paper for modelling, prediction and control of the dynamic change in the braking torque during a braking cycle. The dynamic functional relationship between the changes in the applied pressure, the sliding speed, the brake interface temperature and the braking torque of the disc brake was established. The dynamic model developed was used to predict and control the braking torque during a braking cycle under different disc brake operation conditions.