Herein, the phosphorylation profiles of shrimp muscle proteins after chilling storage at 4 °C for 120 h were investigated by phosphoproteomics. A total of 1255 differential abundance phosphopeptides (DAPPs), encompassing 2128 phosphorylated sites in 608 phosphoproteins, were identified, and they were dominantly enriched in ultrastructure assembly and myofilament contraction of sarcomere architecture, mTOR signaling, autophagy, and energy metabolism pathways. Meanwhile, the dephosphorylations of kinases, phosphatases, and assembly-regulating factors were revealed through SP and R/KxxS motifs. Moreover, the predominant nodes in the protein-protein interaction (PPI) network included mitogen-activated protein kinase 14, ubiquitin-ribosomal protein eL40 fusion protein, cAMP-dependent protein kinase catalytic subunit, heat shock protein, and myosin light chain kinase; meanwhile, these proteins significantly correlated with texture deterioration. Subsequently, the associated protein MAPK was verified by Western blotting. Collectively, this study deciphered the undefined mechanisms governing muscle softening of L. vannamei during refrigeration from a phosphoproteomics perspective and provided valuable targets against softening.

Increased heat levels can affect follicle development, oocyte maturation, and bovine fertility by disrupting amino acid (AA) metabolism and oocyte competence. This study aimed to explore the effect of heat shock on AA metabolism in bovine cumulus cells (CCs) or denuded oocytes (DOs). CCs and DOs were separately cultured for 24 h in vitro at 38.5 °C (control group), 39.5 °C (moderate heat shock-CC, MHS-CC group), or 40.5 °C (high heat shock-CC, HHS-CC group). AA levels were analyzed in 24-h in vitro maturation media using high-performance liquid chromatography. The findings indicated that the HHS-CC group consumed more AAs than the control (p = 0.04) or MHS-CC group (p = 0.03). Compared with the control and HHS-CC groups, the MHS-CC group exhibited elevated alanine levels (p = 0.02). The MHS-CC (p = 0.03) and HHS-CC (p = 0.03) groups exhibited significantly greater glutamine depletion than the control group. The HHS-DO group exhibited significant lysine depletion (p < 0.01) but produced more tryptophan than the control and MHS-DO groups (p = 0.02). In contrast to the control and MHS-DO groups, the HHS-DO group displayed a notably elevated level of appearance (p = 0.005) and net balance (p = 0.005) for all AAs. The findings imply that heat shock may alter the metabolism of certain AAs in CCs and DOs, thereby affecting the developmental competence of bovine oocytes.

The neuropeptides vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) have emerged as potent modulators of immune responses during sepsis, yet their roles remain complex, alternating between protective and permissive depending on timing, tissue compartment, and inflammatory context. This review presents a historical assessment of VIP and PACAP in sepsis research, highlighting the evolution of conceptual advances across five decades. Starting in the 1980s, early studies revealed that VIP levels rise during endotoxemia and correlated with hypotension and mortality, suggesting a deleterious role. By the 1990s, research pivoted toward understanding gut-derived VIP and its interaction with nitric oxide, culminating in the classification of VIP and PACAP as "macrophage deactivating factors" that downregulate TNFα and IL-6. The 2000s further clarified their cell-specific actions through VPAC1/2 and PAC1 receptors, showing anti-inflammatory effects on both innate and adaptive immune cells, while illuminating delivery challenges overcome by liposomal encapsulation. The 2010s expanded this narrative by dissecting receptor dynamics, gut barrier regulation, and VIP's role in neuroimmune crosstalk and thrombo-inflammation. Most recently, studies in the 2020s provide a nuanced view of how VIP suppresses inflammatory damage but also enables pathogen persistence during live bacterial infection, implicating VIP signaling in trade-offs between tolerance and clearance. Across this chronological framework, VIP and PACAP have oscillated between friend, foe, and frenemy, underscoring the importance of context in leveraging their therapeutic potential in sepsis.

Tinnitus is a serious medical and social problem of our time for many people, leading to significant psycho-emotional shock in some cases, disruption of social and professional adaptation. To date, there are several methods of treating tinnitus, the principle of which is based on pathogenetic concepts of brain neuroplasticity. The purpose of this work is to review existing tinnitus treatment methods from the point of view of modern neurophysiological concepts. Materials and methods: A keyword search and analysis of the works found in Russian and foreign databases (elibrary, CyberLeninka, PubMed, Scopus, Google Academic) over the past 5 years was carried out. A total of 387 keyword publications were found, and after eliminating duplicates and those that did not match the subject of the article, 21 papers were selected. Results. The use of non-medicinal tinnitus therapies such as sound therapy, transcranial magnetic stimulation, bimodal stimulation, and psychotherapeutic methods has shown statistically significant effectiveness in a number of systematic reviews and meta-analyses, both as part of monotherapy and as part of complex therapy aimed at retraining in tinnitus, which has shown the best results. The effectiveness of these methods has a neurophysiological explanation based on the neuroplasticity of the brain and the fact that changes occurring during the development of tinnitus can regress with certain measures. Thus, these options can be considered effective pathogenetic methods of treating tinnitus from the point of view of the principles of evidence-based medicine.

Sepsis-induced cardiomyopathy represents a life-threatening complication arising from severe sepsis and septic shock. Hydroxysafflor yellow A (HSYA), a major quinone chalcone constituent, protects cardiac function in this disease. This study explored the detailed mechanisms of HSYA in mitigating sepsis-related cardiomyopathy. Potential targets of HSYA against sepsis-induced cardiomyopathy were identified by integrating sepsis-related genes (GSE131761), genes associated with myocardial damage (GeneCards), and potential targets of HSYA (CTD, GeneCards, SwissTargetPrediction). GO and KEGG pathway enrichment analyses were performed, and a protein-protein interaction (PPI) network was constructed. Hub genes were identified by machine learning and WGCNA. An in vitro cellular model was generated by stimulating AC16 cardiomyocytes with LPS. Cell viability and apoptosis were determined by CCK-8 assay and flow cytometry, respectively. KEGG pathway enrichment analysis revealed the potential involvement of NF-κB, TNF, IL-17, and MAPK signaling pathways in the protective role of HSYA against sepsis-induced cardiomyopathy. HSYA attenuated LPS-induced pro-inflammatory cytokine expression, ROS generation, and cell apoptosis in AC16 cardiomyocytes. Mechanistically, HSYA upregulated GATA3 expression in LPS-stimulated AC16 cardiomyocytes. Moreover, downregulation of GATA3 enhanced pro-inflammatory cytokine expression, ROS generation, and cell apoptosis in HSYA-treated AC16 cardiomyocytes under LPS. Our in vitro findings suggest that GATA3 may serve as a potential mediator through which HSYA attenuates LPS‑induced cardiomyocyte injury by concurrently dampening inflammation, oxidative stress, and apoptosis.