We investigated the immune response mechanisms under systemic and local inflammation using mouse models whereby lipopolysaccharide (LPS) was administered intraperitoneally to induce systemic inflammation, and epicutaneous sensitization with ovalbumin was used to induce local inflammation. LPS increased the immune cell infiltration in the cardiac muscle near the aorta, alveoli, hepatic sinusoid, renal interstitium, and the submucosal layer of the duodenum. Similarly, ovalbumin increased the abundance of macrophages in the skin. Both LPS and ovalbumin induced NF-κB p65 and IκBα phosphorylation, as well as the expression of NF-κB target genes (TLR4, IL6, and TNFα). Additionally, both LPS and ovalbumin led to an increase in the absolute IL-1β, IL-6, and TNFα serum levels and cytokine-related janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) phosphorylation. Moreover, the activated JAK2/STAT3 signaling increased the number of Ki67-positive cells (proliferating cells) and development pathway target gene expression (regeneration) in the inflammation models. In conclusion, LPS and ovalbumin increase immune cell infiltration in tissues, NF-κB activation, cytokine levels in serum, cytokine-stimulated JAK2/STAT3 signaling, and tissue regeneration.

The Wnt signaling pathway is important for cell growth and development in the central nervous system and its associated vasculature. Thus, it is an interesting factor for establishing anti-brain cancer therapy. However, simply inhibiting the Wnt signaling pathway in patients with brain tumors is not an effective anti-cancer therapy. Due to their complex microenvironment, which comprises various cell types and signaling molecules, brain tumors pose significant challenges. It is important to understand the interplay between tumor cells and the microenvironment for developing effective therapeutic strategies for both benign and malignant brain tumors. Thus, this research focused on the role of the tumor microenvironment (TME) in brain tumor progression, particularly the involvement of Wnt-dependent signaling pathways. The brain parenchyma comprises neurons, glia, endothelial cells, and other extracellular matrix elements that can contribute to the TME. The TME components can secrete Wnt ligands or associated molecules, resulting in the aberrant activation of the Wnt signaling pathway, followed by tumor progression and therapeutic resistance. Therefore, it is essential to understand the intricate crosstalk between the Wnt signaling pathway and the TME in developing targeted therapies. This review aimed to elucidate the complexities of the brain TME and its interactions with the Wnt signaling pathways to improve treatment outcomes and our understanding of brain tumor biology.

Polypyrrole (Ppy) is a biologically compatible polymer that is used as a matrix, in which drugs and enzymes can be incorporated by doping. Here, we suggest an inventive application of Ppy as a biorecognition film encapsulated with an antibody (Ab) as an alternative strategy for the on-site multistep functionalization of thiol-based self-assembled monolayers. The fabrication steps of the recognition films were followed by dropping pyrrole and Ab mixed solutions onto the electrode and obtaining a thin film by direct current electropolymerization. The efficiency of Ab immobilization was studied by using fluorescence microscopy and electrochemical (EC) methods. Finally, the Ab density was increased and immobilized in 1 min, and the sensing performance as an EC immunosensor was demonstrated using α-fetoprotein with a limit of detection of 3.13 pg/mL and sensing range from 1 pg/mL to 100 ng/mL. This study demonstrates the potential for electrochemical functionalization of biomolecules with high affinity and rapidity.

Nicotinamide adenine dinucleotide (NADH) is an important cofactor involved in metabolic redox reactions in living cells. The detection of NADH in living animal cells is a challenge. We developed a one-step monitoring method for NADH via an electrocatalytic reaction that uses a surface-modified, screen-printed electrode (SPE) having a redox active monolayer 4′-mercapto-N-phenlyquinone diamine (NPQD) formed by a self-assembled monolayer (SAM) of an aromatic thiol, 4-aminothiophenol (4-ATP). This electrode has a limit of detection (LOD) of 0.49 μM and a sensitivity of 0.0076 ± 0.0006 μM/μA in cell culture media, which indicates that it retains its selectivity. The applicability of this NADH sensor was demonstrated for the first time by cell viability monitoring via NADH-sensing in cell culture supernatants.

Introduction: Because minipig skin is similar to human skin in anatomy and physiology, establishing an atopic dermatitis (AD) minipig model seems meaningful. Material and Methods: We applied 1-fluoro-2,4-dinitrobenzene (DNFB) or ovalbumin onto the back skin of five Yucatan minipigs aged 8–10 months and 19 kg in median weight. Two minipigs with the same parameters served as controls. Results: Both DNFB and ovalbumin mediated epithelial hyperplasia, spongiosis, and immune cell infiltration in the dermis, which is a typical histopathological feature of AD. Moreover, AD upregulated the Th1- and Th2-related cytokine expressions in DNFB- or in ovalbumin-treated skin. Notably, AD-induced minipigs exhibited greater cytokine serum concentrations. Conclusion: Histopathological finding and cytokine analysis revealed that DNFB or ovalbumin mediates AD. However, ovalbumin-treated minipig is a more reliable and precise AD model owing to the DNFB-induced severe skin damage. In summary, ovalbumin-treated skin shows similar AD as human in histopathological and molecular analysis.

Gold (Au) is of considerable interest for electrochemically active surfaces because thiol-modified chemicals and biomolecules can be easily immobilized through a simple procedure. However, most Au surfaces are damaged after repetitive measurements, making them difficult to reuse. Here, we present a novel electrochemical (EC) etching method for Au surfaces that enables electrode reuse through a simple, nontoxic, and straightforward protocol. This process, referred to as double-step EC etching (DSEE), consists of two sequential steps: (i) a cyclic voltammetry (CV) sweep in a very low concentration of H₂SO₄, followed by (ii) a CV sweep in K₃Fe-(CN)₆. For comparison, alternative etching methods were also evaluated. After the assembly and subsequent desorption of cells and antigens, changes in the performance of the Au electrode as both an immunosensor and a cytosensor were examined using EC impedance spectroscopy and CV. Repetitive measurements were found to be feasible for up to five cycles while maintaining reproducibility. We believe that this Au electrode reuse method can be applied to long-term, cost-effective, and accurate monitoring of biological effects.