Background Dysregulated inflammation is central to COVID-19 pathogenesis. Mast cells (MCs) and their protease tryptase are implicated in tissue injury and vascular dysfunction, but the prognostic value of circulating tryptase in COVID-19 remains uncertain. Methods We conducted a prospective cohort study including 82 patients with laboratory-confirmed COVID-19 admitted between January and March 2021. On admission, serum tryptase, C-reactive protein (CRP), procalcitonin (PCT), lactate dehydrogenase (LDH), and lymphocyte counts were measured. The objective of this study was to assess whether serum tryptase levels measured upon hospital admission are associated with COVID-19 severity and in-hospital mortality. Statistical analyses comprised t-tests, Mann–Whitney U tests, χ 2 tests, receiver operating characteristic (ROC) curve analysis, and logistic regression. Results Serum tryptase levels at admission did not differ significantly between patients requiring oxygen and those who did not (mean 5.45 vs. 4.97 μg/L; p = 0.2906) or between survivors and non-survivors (mean 5.24 vs. 5.60 μg/L; p = 0.6486). ROC analysis confirmed limited prognostic performance for tryptase regarding oxygen requirement (AUC = 0.580; p = 0.2972) and mortality (AUC = 0.538; p = 0.6103). By contrast, CRP, PCT, and LDH correlated strongly with disease severity. Elevated PCT (p = 0.0016) and LDH (p = 0.0360) were significantly associated with mortality. Logistic regression showed no independent association between tryptase and adverse outcomes. Conclusion In this prospective cohort, serum tryptase measured at admission was not associated with COVID-19 severity or mortality, suggesting limited utility as a prognostic biomarker. Established markers, particularly PCT and LDH, outperformed tryptase in predicting adverse clinical outcomes. The negative findings are clinically relevant as they demonstrate that tryptase does not contribute to prognostic risk stratification in COVID-19, and its measurement does not provide added value beyond standard inflammatory biomarkers.

In most vertebrates, hemoglobin’s primary function is to transport oxygen and carbon dioxide. Hemoglobin is also expressed in cells such as dopaminergic neurons and chondrocytes, as well as in organelles such as mitochondria. Depending on its location, hemoglobin subunits can interact with proteins involved in various functions, including anion exchange, nitric oxide synthesis, and ATP synthesis. These interactions suggest that hemoglobin has diverse regulatory roles beyond gas transport. During hypoxia and an excess of nitrite and protons, deoxygenated hemoglobin exhibits nitrite reductase activity and produces nitric oxide, a gaseous signaling molecule. Hemoglobin-derived nitric oxide is associated with vasodilation in mammals and the inhibition of mitochondrial respiration in cell cultures. This raises the question of whether hemoglobin functions as a gasoreceptor in these cells or organelles. The HIF1α/PHD2 pathway in mammals and cysteine oxidases in plants are largely responsible for sensing hypoxia, but the identity of oxygen gasoreceptors analogous to the mammalian nitric oxide gasoreceptor soluble guanylate cyclase and the plant ethylene gasoreceptor kinases remains unknown. Since the heme-based dual oxygen-binding and catalytic domain emerged earlier than the allosteric regions, I propose hemoglobin as an oxygen proto-gasoreceptor derivative. Furthermore, since hemoglobin interacts with and regulates proteins depending on its oxygen binding state, I propose that hemoglobin functions as an oxygen gasoreceptor in split-component signal transduction systems. Recognizing hemoglobin as a gasoreceptor will expand the emerging field of gasocrinology to encompass gases that were previously considered primarily metabolic substrates.

Biology textbooks lack precise terms to describe oxygen-based inter-organismal signaling between oxygen-producing and aerobic organisms. To address this gap, I recently proposed the concept of gasocrine signaling, which encompasses all signaling mediated by gaseous molecules and gasoreceptors within and between cells, organisms, and even abiotic factors. Given the fundamental importance of gaseous molecules for life, I propose the gasocrine hypothesis: all cells require gasocrine signaling. This hypothesis can be divided into three sub-hypotheses: First, all living organisms composed of one or more cells require gasocrine signaling to sense, communicate, grow, and propagate. Second, gasocrine signaling mediated via gasoreceptor proteins (or yet to be identified gas-sensing riboceptors) is the most essential cellular and inter-organismal signaling. Third, acellular entities arising from or replicating in pre-existing cells require gasocrine signaling. I propose several potential experiments to falsify these hypotheses. If they withstand falsification, the gasocrine hypothesis would supplement cell theory. It would also provide a novel framework for understanding fundamental biological principles, cellular and organismal communication, and the role of abiotic factors. Furthermore, it establishes the foundation for the emerging field of gasocrinology, which is critical in the context of a changing environment.

Fatty acids play important, yet different roles in bacterial physiology, specifically their growth, either stimulating or inhibiting this parameter which are of biotechnological importance. Here, we present results showing to what degree short- and medium-chain fatty acids (butyric acid (butanoic acid, C4:0); caproic acid (hexanoic acid, C6:0); caprylic acid (octanoic acid, C8:0)), used at relatively low concentrations (in a range of μg/mL, contrary to previously reported mg/mL which revealed inhibitory effects on bacterial growth) affect growth of Escherichia coli K-12 (MG1655 laboratory strain) depending on various conditions. In rich medium (LB) positive effects of all tested fatty acids on E. coli growth were observed, while temperature of incubation (growth at 25 °C and 37 °C was assessed) modulated these effects. In contrast, a slight but significant growth inhibition by fatty acids was observed in a minimal medium (M9) supplemented with glucose. Nonetheless, in minimal medium containing acetate, the effects of these compounds varied, being either positive or negative depending on their concentrations. No measurable bacterial growth was observed in the case of the presence of any tested fatty acids when primary carbon source (glucose or acetate) was removed from a minimal medium before addition of butyric acid, caproic acid or caprylic acid. Our results indicated that effects of low concentrations of fatty acids on E. coli cells depend on growth conditions of bacterial cultures. This may be of biotechnological importance, especially for modulating E. coli growth by using different compositions of media and incubation temperatures.

Studies have identified specific salivary biomarkers associated with different types of cancer, including oral, lung, and pancreatic cancers. These biomarkers can be proteins, DNA fragments, or other molecules that indicate the presence or progression of the disease. Saliva-based cancer detection offers the potential for earlier diagnosis, leading to better treatment outcomes. Additionally, salivary biomarkers can help tailor treatment plans to individual patients, improving their chances of successful recovery.

Research aimed to examine the effects of β-blockers on cytokine release in Jurkat cells under basal conditions and during oxidative stress. Oxidative stress was induced in Jurkat cells through the application of hydrogen peroxide (H2O2). Subsequently, β-blockers were administered to the incubation medium for 24 h, encompassing both intact and oxidatively stressed cell conditions. For β-blocker toxicity screening, the viability of Jurkat cells was determined using the MTT (3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide) test. The IL-6, IL-17, and TNF-α content were measured in the supernatant of Jurkat cells incubated under different conditions. The study results show that propranolol, metoprolol, carvedilol, but not nebivolol, revealed toxic effects on the intact Jurkat cells (pc-p = 0.0001; pc-m > 0.0001; pc-c = 0.0003; pc-n = 0.0525). Under oxidative stress conditions, the viability of Jurkat cells decreased significantly (pc-H2O2 = 0.0001). Propranolol and metoprolol did not affect ((pc-p = 0.0001; pc-m > 0.0001), while nebivolol and carvedilol improved the viability of Jurkat cells incubated under oxidative stress conditions (pc-n = 0.002; pc-c = 0.0002). Oxidative stress significantly increased the cytokines (IL-6, TNF-α, IL-17) expression levels (pc-H2O2 < 0.0001; pc-H2O2 < 0.0001; pc-H2O2 < 0.0001) in Jurkat cells. Propranolol, carvedilol, nebivolol, and metoprolol did not significantly affect the expression levels of IL-6, TNF-α, and IL-17 in intact Jurkat cells, but decreased IL-6, TNF-α, and did not change IL-17 expression levels in Jurkat cells incubated under oxidative stress conditions. This study demonstrates that β-blockers can influence redox-sensitive cytokine pathways in Jurkat T lymphocytes when they are under oxidative stress. All the agents tested inhibited the production of IL-6 and TNF-α, but nebivolol and carvedilol showed the strongest protective and anti-inflammatory effects. These effects likely result from their combined properties, including antioxidant effects, nitric oxide modulation, and the regulation of NF-κB/MAPK pathways. In contrast, propranolol and metoprolol exhibited more limited activity. These findings suggest that third-generation β-blockers may offer both cardiovascular and immunomodulatory benefits, although further validation in primary immune cells and in vivo models is still required.

In recent years, cannabinoids and their derivatives have been tested for efficacy in epilepsy therapy and related disorders. Many of them may help alleviate ailments associated with seizures. An in-depth study of cannabinoid derivatives and the receptors on which they operate give us a chance for more effective use of these substances in epilepsy therapy. Many studies point to the beneficial synergy of cannabinoids with chemotherapeutics and the increase in effectiveness of the latter. As a result, both alternatives to drug treatment and support for the pharmacotherapy are being developed. In this review, we focused on compounds such as Δ9-THC, CBDV, Δ9-THCA, Δ9-THCV, H2CBD and their receptors as well as on CBD’s actions, and the enzymes, ion channels, and transporters engaged in the fundamental causes of epileptic seizures. Treating epilepsy and drug-resistant epilepsy are the two common medical uses of cannabinoids. We looked at approximately 150 current scientific articles from peer-reviewed journals to explore the molecular effects of cannabinoids in these applications. Our goal was to improve physician awareness of factors influencing treatment decisions and potential adverse reactions to minimize medical errors and optimize patient care.

Glioblastoma remains one of the most aggressive and treatment-resistant malignancies. Current treatment options, such as radio- and chemotherapy, induce oxidative stress-mediated DNA damage leading to cancer cell death, but are also neurotoxic and not efficient in long term. Our study investigated the effects of cannabidiol, celecoxib and 2,5-dimethylcelecoxib, individually and in combinations, on U-138 MG glioblastoma cell survival, oxidative stress, canonical and non-canonical Nrf2 pathway activation, cell migration and apoptosis. Using the MTT and flow cytometry assay we found that the analyzed compounds and their combinations induce dose-dependent, synergistic, and oxidative stress-related cytotoxicity, with minimal impact (at the concentrations exhibiting anti-cancer effects) on non-cancerous human astrocyte (HA) cell line. The Nrf2 ELISA assay was used for the analysis of the nuclear binding of the nuclear factor-2 erythroid related factor-2 (Nrf2), which followed by the RT-qPCR and Western blot analysis, confirmed the antioxidant response of cells to the applied treatments. Diminished migratory potential, and increase of the autophagy-related p62, LC3 and apoptosis-related caspase-3 protein levels were also observed in response to the treatment with the analyzed compounds. Overall, our study provides evidence that cannabidiol combined with celecoxib or 2,5-dimethylcelecoxib may represent a promising strategy for glioblastoma treatment.

Human and mouse incisors are both primarily composed of dentin and enamel, which meet at an interface called the dentin-enamel junction (DEJ). However, incisors in the two species have very different growth patterns, structures, and loading requirements. Since the DEJ is responsible for minimizing cracking at this at-risk interface between mechanically dissimilar dentin and enamel, its structure is expected to be significantly different between humans and mice. Here, structural and compositional gradients across human and murine incisors DEJs were measured via microcomputed tomography and Raman spectroscopy. Density gradients across the DEJ were significantly larger in humans compared to murine teeth, likely due to the larger size of the mantle dentin. Multiple gradients in mineral content and crystallinity were found at the murine DEJ, while the human DEJ only exhibited gradients in mineral content. Models predicting the modulus across the DEJ according to compositional results show that mineral crystallinity is critical in regulating gradients in tissue stiffness across the murine DEJ. Together, these results show the multiple ways in which the DEJ can adapt to variations in the loading environment.

During the rearing period, fish may be exposed to fasting due to low or high temperatures, transportation, handling, and other stressors, while they may catch-up the growth differently after supplying the feed. The aim of this study was to investigate the compensatory growth (CG) response of juvenile Siberian sturgeon Acipenser baerii after restricted feeding. In the first phase (60 days), triplicate groups of fish were subjected to feed restriction (25%, 50%, and 75% of the amount needed to reach satiation, respectively) or satiation feeding (control) and in the second phase all treatment groups were fed to satiation for an additional 60 days. Growth performance was measured during the two phases and blood samples were collected at the end of the second phase to measure blood biochemical indices. At the end of the first phase of the experiment, as expected, the control group showed the highest mean body weight, followed by the 75%, 50% and 25% satiation fed groups (P < 0.05). However, at the end of the second phase, the final body weights were not significantly different between the groups (P > 0.05), while some of the growth performance improved in the 25% satiation fed group (P < 0.05). At the end of the second phase, serum metabolites except for glucose and cholesterol were significantly different among treatment groups, with the highest levels in the control group. Feed restriction significantly lowered hematocrit, total protein and triglyceride levels especially in the 25% satiation fed group (P < 0.05). The results showed that juvenile Siberian sturgeon could tolerate feed restriction without any significant negative impacts on the majority of growth and metabolite indices. In conclusion, using an appropriate feeding regime helps to improve feed efficiency with no physiological impacts on Siberian sturgeon rearing.