The aim of this study is to investigate market depth as a stock market liquidity dimension. A new methodology for market depth measurement exactly based on Shannon information entropy for high-frequency data is introduced and utilized. this website The proposed entropy-based market depth indicator is supported by an algorithm inferring the initiator of a trade. This new indicator seems to be a promising liquidity measure. Both market entropy and market liquidity can be directly measured by the new indicator. The findings of empirical experiments for real-data with a time stamp rounded to the nearest second from the Warsaw Stock Exchange (WSE) confirm that the new proxy enables us to effectively compare market depth and liquidity for different equities. Robustness tests and statistical analyses are conducted. Furthermore, an intra-day seasonality assessment is provided. Results indicate that the entropy-based approach can be considered as an auspicious market depth and liquidity proxy with an intuitive base for both theoretical and empirical analyses in financial markets.Trillions of microorganisms inhabit the mucosal membranes maintaining a symbiotic relationship with the host's immune system. B cells are key players in this relationship because activated and differentiated B cells produce secretory immunoglobulin A (sIgA), which binds commensals to preserve a healthy microbial ecosystem. Mounting evidence shows that changes in the function and composition of the gut microbiota are associated with several autoimmune diseases suggesting that an imbalanced or dysbiotic microbiota contributes to autoimmune inflammation. Bacteria within the gut mucosa may modulate autoimmune inflammation through different mechanisms from commensals ability to induce B-cell clones that cross-react with host antigens or through regulation of B-cell subsets' capacity to produce cytokines. Commensal signals in the gut instigate the differentiation of IL-10 producing B cells and IL-10 producing IgA+ plasma cells that recirculate and exert regulatory functions. While the origin of the dysbiosis in autoimmunity is unclear, compelling evidence shows that specific species have a remarkable influence in shaping the inflammatory immune response. Further insight is necessary to dissect the complex interaction between microorganisms, genes, and the immune system. In this review, we will discuss the bidirectional interaction between commensals and B-cell responses in the context of autoimmune inflammation.It has been suggested that spinach methanolic extract (SME) inhibits the formation of advanced glycation end products (AGEs), which are increased during diabetes progression, so it is important to know if SME has beneficial effects in the diabetic retina. In this study, in vitro assays showed that SME inhibits glycation, carbonyl groups formation, and reduced-thiol groups depletion in bovine serum albumin incubated either reducing sugars or methylglyoxal. The SME effect in retinas of streptozotocin-induced diabetic rats (STZ) was also studied (n = 10) in the normoglycemic group, STZ, STZ rats treated with SME, and STZ rats treated with aminoguanidine (anti-AGEs reference group) during 12 weeks. The retina was sectioned and immunostained for Nε-carboxymethyl lysine (CML), receptor RAGE, NADPH-Nox4, inducible nitric oxide synthase (iNOS), 3-nitrotyrosine (NT), nuclear NF-κB, vascular endothelial growth factor (VEGF), glial fibrillary acidic protein (GFAP), S100B protein, and TUNEL assay. Lipid peroxidation was determined in the whole retina by malondialdehyde (MDA) levels. The results showed that in the diabetic retina, SME reduced the CML-RAGE co-localization, oxidative stress (NOX4, iNOS, NT, MDA), inflammation (NF-κB, VEGF, S100B, GFAP), and apoptosis (p less then 0.05). Therefore, SME could attenuate the retinal degeneration by inhibition of CML-RAGE interaction.The cell environment plays a pivotal role in determining cellular outcome, as well as cancer initiation, progression, and dissemination. Within this environment, in addition to the structural components, such as the extracellular matrix, there are various types of cells surrounding the tumor cells. Communication among these cells and the tumor cells via signaling pathways is important for tumor growth. Originally discovered in patients with immunodeficiency X-linked gammaglobulinemia, the Bruton's tyrosine kinase (BTK) signaling pathway, known for its role in B cell maturation, is critical to cancer cell proliferation, metastasis and evasion of cancer eliminating cells. Given that BTK inhibitors have been FDA approved for chronic lymphocytic leukemia/small lymphocytic lymphoma and that the majority of BTK studies have been focused on B cells, the use of BTK inhibitors as a future treatment strategy of solid tumors has yet to be evaluated. In this review, we summarize studies analyzing BTK signaling within the cells found in the tumor microenvironment, as well as clinical trial where BTK inhibitors are currently being used to target the tumor microenvironment as a way to combat solid tumors.This study aimed to assess and compare the ultrasonographic (US) pathologic findings in patients with polymyalgia rheumatica (PMR) and bilateral frozen shoulder (FS). We included 19 patients with clinically diagnosed PMR and 19 patients with stage II bilateral FS. The US evaluation included the assessment of subacromial-subdeltoid (SASD) bursitis, long head of biceps (LHB) tenosynovitis, and posterior and inferior glenohumeral (GH) synovitis. Unilateral SASD bursitis was noted significantly more frequently in PMR patients than in bilateral FS patients (p = 0.001). There were no significant differences in the incidence of unilateral LHB tenosynovitis and posterior GH synovitis between PMR and bilateral FS patients (p = 0.108 and p = 0.304, respectively). Unilateral inferior GH synovitis was more common among bilateral FS patients than among PMR patients (p less then 0.001). Bilateral SASD bursitis and LHB tenosynovitis were noted significantly more frequently in PMR patients than in bilateral FS patients (p less then 0.001 and 0.049, respectively). Significant differences were not observed in the incidence of bilateral posterior GH synovitis between PMR and bilateral FS patients (p = 0.426). Bilateral inferior GH synovitis was more common among bilateral FS patients than among PMR patients (p = 0.044). The US evidence for bilateral inferior GH synovitis without bilateral SASD showed high specificity (94.7%) with sensitivity (78.9%) for the diagnosis of bilateral FS. SASD bursitis, representing periarticular synovial inflammation, was more common among the patients with PMR than among the patients with bilateral FS. Inferior GH synovitis without SASD bursitis suggests FS rather than PMR in patients with bilateral shoulder pain.