Phytohormone-induced changes in growth, physiology, and biochemistry of Aurantiochytrium sp. for sustainable bioproduction.

The study aimed to assess the effects of nine combinations of phytohormones, salicylic acid (SA), gibberellic acid (GA), and jasmonic acid (JA) on the growth, physiology, and biochemistry of Aurantiochytrium sp. Parameters like optical density (OD), biomass, protein content, hydrogen peroxide (H2O2), malondialdehyde (MDA), catalase activity (CAT), and gene expression (malic enzyme (ME) and acetyl-CoA carboxylase (ACCase)) were assessed at various cultivation stages (24, 48, 72, and 96 h). The research also analyzed fatty acid composition, unsaturated fatty acids (UFA), saturated fatty acids (SFA), and the UFA to SFA ratio (USS) to understand the biochemical changes induced by phytohormones. Results demonstrated that modifying phytohormone concentrations significantly affected the characteristics of the microalgae, particularly in correlation with different growth stages, emphasizing the necessity of precise control of phytohormone levels for optimizing cultivation conditions and enhancing bioactive compound production in Aurantiochytrium sp.

The Role of Innate and Adaptive Immune System in the Pathogenesis of Schizophrenia.

Schizophrenia is one of the most severely debilitating mental disorders that affects 1.1% of the world's population. The exact cause of the disease is not known, but genetics, environmental factors (such as infectious agents, season and region of birth, exposure to viruses, low birth weight, advanced paternal age, and tobacco), and immune system dysfunction can all contribute to the development of schizophrenia. Recently, the role of the immune system in schizophrenia has received much attention. Both acquired and innate immune systems are involved in the pathogenesis of schizophrenia and facilitate the disease's progression. Almost all cells of the immune system including microglia, B cells, and T cells play an important role in the blood-brain barrier damage, inflammation, and in the progression of this disease. In schizophrenia, the integrity of the blood-brain barrier is reduced and then the immune cells are recruited into the endothelium following an increase in the expression of cell adhesion molecules. The entry of immune cells and cytokines leads to inflammation and antibody production in the brain. Accordingly, the results of this study strengthen the hypothesis that the innate and acquired immune systems are involved in the pathogenesis of schizophrenia.

Purinergic signaling: decoding its role in COVID-19 pathogenesis and promising treatment strategies.

The pathogenesis of coronavirus disease (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS­CoV­2), is complex and involves dysregulated immune responses, inflammation, and coagulopathy. Purinergic signaling, mediated by extracellular nucleotides and nucleosides, has emerged as a significant player in the pathogenesis of COVID-19. Extracellular adenosine triphosphate (ATP), released from damaged or infected cells, is a danger signal triggering immune responses. It activates immune cells, releasing pro-inflammatory cytokines, contributing to the cytokine storm observed in severe COVID-19 cases. ATP also promotes platelet activation and thrombus formation, contributing to the hypercoagulability seen in COVID-19 patients. On the other hand, adenosine, an immunosuppressive nucleoside, can impair anti-viral immune responses and promote tissue damage through its anti-inflammatory effects. Modulating purinergic receptors represents a promising therapeutic strategy for COVID-19. Understanding the role of purinergic signaling in COVID-19 pathogenesis and developing targeted therapeutic approaches can potentially improve patient outcomes. This review focuses on the part of purinergic signaling in COVID-19 pathogenesis and highlights potential therapeutic approaches targeting purinergic receptors.

Role of microbiota short-chain fatty acids in the pathogenesis of autoimmune diseases.

There is emerging evidence that microbiota and its metabolites play an important role in helath and diseases. In this regard, gut microbiota has been found as a crucial component that influences immune responses as well as immune-related disorders such as autoimmune diseases. Gut bacterial dysbiosis has been shown to cause disease and altered microbiota metabolite synthesis, leading to immunological and metabolic dysregulation. Of note, microbiota in the gut produce short-chain fatty acids (SCFAs) such as acetate, butyrate, and propionate, and remodeling in these microbiota metabolites has been linked to the pathophysiology of a number of autoimmune disorders such as type 1 diabetes, multiple sclerosis, inflammatory bowel disease, rheumatoid arthritis, celiac disease, and systemic lupus erythematosus. In this review, we will address the most recent findings from the most noteworthy studies investigating the impact of microbiota SCFAs on various autoimmune diseases.

The potential targets in immunotherapy of atherosclerosis.

Cardiovascular disease is the most common cause of death, which has the highest mortality rate worldwide. Although a diverse range of inflammatory diseases can affect the cardiovascular system, however, heart failure and stroke occur due to atherosclerosis. Atherosclerosis is a chronic autoinflammatory disease of small to large vessels in which different immune mediators are involved in lipid plaque formation and inflammatory vascular remodeling process. A better understanding of the pathophysiology of atherosclerosis may lead to uncovering immunomodulatory therapies. Despite present diagnostic and therapeutic methods, the lack of immunotherapy in the prevention and treatment of atherosclerosis is perceptible. In this review, we will discuss the promising immunological-based therapeutics and novel preventive approaches for atherosclerosis. This study could provide new insights into a better perception of targeted therapeutic pathways and biological therapies. [Formula: see text].

Manganese modulates the physiological and biochemical responses of Mentha aquatica L. to ultraviolet radiation.

Ultraviolet (UV) radiation as an environmental factor alters the physiological and metabolic processes in plants. Manganese (Mn) is an essential element that is required for plant growth and development. This experiment was conducted in order to determine the effects of Mn supply and UV radiation on the physiological and metabolic responses in Mentha aquatica. With this aim, three levels of Mn and UV treatments were used as follows: basic Hoagland's nutrient solution without UV radiation (control), Mn supply (100µM), UV radiation (2h daily), and UV+100µM Mn. After three weeks of treatments, the root and shoot dry weights and the contents of photosynthetic pigments were decreased under UV radiation condition. However, the contents of flavonoids, soluble carbohydrate, anthocyanins, malonaldehyde (MDA), hydrogen peroxide (H2O2), and the activity of antioxidant enzymes (superoxide dismutase, catalase, and peroxidase) were increased. Interestingly, Mn at 100µM concentration decreased the harmful effects of UV radiation on M. aquatica. In addition, the clear differences were observed in the terpene constituents of M. aquatica after the Mn and UV treatments. In this study, 1, 8-cineole, menthofuran and ß-caryophyllene were the most abundant constituents of essential oils in both the control and treated plants. The correlation analysis between pairs of the primary and secondary metabolites showed that there were positive and negative correlations among the variables under the Mn supply and UV radiation conditions. These findings clearly display a positive effect of external Mn up to 100µM in the nutrient solution on the resistant of M. aquatica to UV radiation.