Tumor microenvironment (TME) plays a crucial role in the initiation and progression of lung adenocarcinoma (LUAD); however, there is still a challenge in understanding the dynamic modulation of the immune and stromal components in TME. In the presented study, we applied CIBERSORT and ESTIMATE computational methods to calculate the proportion of tumor-infiltrating immune cell (TIC) and the amount of immune and stromal components in 551 LUAD cases from The Cancer Genome Atlas (TCGA) database. The differentially expressed genes (DEGs) were analyzed by COX regression analysis and protein-protein interaction (PPI) network construction. Then, Bruton tyrosine kinase (BTK) was determined as a predictive factor by the intersection analysis of univariate COX and PPI. Further analysis revealed that BTK expression was negatively correlated with the clinical pathologic characteristics (clinical stage, distant metastasis) and positively correlated with the survival of LUAD patients. Gene Set Enrichment Analysis (GSEA) showed that the genes in the high-expression BTK group were mainly enriched in immune-related activities. In the low-expression BTK group, the genes were enriched in metabolic pathways. CIBERSORT analysis for the proportion of TICs revealed that B-cell memory and CD8+ T cells were positively correlated with BTK expression, suggesting that BTK might be responsible for the preservation of immune-dominant status for TME. Thus, the levels of BTK might be useful for outlining the prognosis of LUAD patients and especially be a clue that the status of TME transition from immune-dominant to metabolic activity, which offered an extra insight for therapeutics of LUAD.

The genus Vibrio contains some enteropathogenic species including V. cholerae, V. parahaemolyticus, V. fluvialis and V. mimicus. V. cholerae is responsible for severe cholera epidemics in many parts of the world, especially developing countries (4,12). V. mimicus has been recognized as a biotype of V. cholerae, but was reclassified as an independent species because of differences in some biochemical characteristics including negative sucrose fermentation in 1981 (5). Therefore V. mimicus and V. cholerae are quite similar to each other and they share some pathogenic factors such as enterotoxins or hemolysins (15,19,24). Although V. mimicus has not been reported to produce severe epidemic of diarrhea like V. cholerae, it is often isolated from patients of sporadic diarrheal cases (14).Successful infection by pathogenic bacteria is established by coordinate expression of various virulence factors in addition to actual toxic factors. In V. cholerae, ToxR ToxS, ToxT and toxin co-regulated pilus (TCP) are known to coordinate the action of the major toxic factor, cholera toxin (CT) (8,13,21). Production of these virulence factors is regulated at the transcriptional level by ToxR (6, 7). Meanwhile, ToxS is known to enhance ToxR-mediated transcriptional activation (10). Moreover, ToxR is conjugated with another transmembrane transcriptional activator, and TcpP positively controls the expression of ToxT (6, 9). ToxT can directly activate expression of the genes encoding CT, TCP (21) and other virulence determinants (6, 7). TCP, the product of the tcpA gene, plays an important role in the colonization of V. cholerae O1/O139, and also acts as a receptor for the acquisition of the CTXΦ genetic element (23). Recent studies have demonstrated the presence of the tcpA gene, as well as the ctxA gene encoding CT, in certain non-O1/non-O139 V. cholerae strains (8,14). A hypothesis on horizontal transfer of the virulence genes among Vibrio species has been proposed (23). Distribution of these virulence-associated genetical elements in V. mimicus is also possible because of its taxonomical relatedness with V. cholerae (3).We have surveyed the existence of virulence-associated genes by the polymerase chain reaction (PCR) method (2,15,16 Shinjuku-ku, Tokyo 162-8640, Japan Received February 23, 2004. Accepted April 13, 2004 Abstract: Distribution of virulence-associated genes in Vibrio mimicus was studied including the toxin genes ctxA, tdh, st and vmh and the genes necessary for regulation of toxin production, toxR, toxS, toxT, tcpA and tcpP. Approximately half of clinical V. mimicus isolates possessed one or more genes encoding V. cholerae enterotoxic factors such as ctxA, tdh and st. All of the clinical and environmental isolates possessed vmh encoding V. mimicus hemolysin (VMH). The ctxA encoding cholera toxin was detected in only 2 strains, 5% of the clinical isolates. Furthermore, there were very few strains possessing tcpP and toxT needed for the expression of ctxA. These results may suggest that VMH is a more important pathog...

: Allergic asthma is a chronic inflammatory disease, which involves many cellular and cellular components. Cataract is a condition that affects the transparency of the lens, which the opacity of the lens caused by any innate or acquired factor degrades its transparency or changes in color. Both of them belong to diseases induced by immune disorders or inflammation. We want to confirm the signaling pathways involved in the regulation of asthma and cataract simultaneously, and provide reference for the later related experiments. So we conducted a scoping review of many databases and searched for studies (Academic research published in Wiley, Springer and Bentham from 2000 to 2019) about the possible relationship between asthma and cataract. It was found that during the onset of asthma and cataract, Rho/Rock signaling pathway, Notch signaling pathway, Wnt/β-catenin signaling pathway, PI3K/AKT signaling pathway, JAK/STAT signaling pathway, MAPK signaling pathway, TGF-β1/Smad signaling pathway and NF-κB signaling pathway are all active, so they may have a certain correlation in pathogenesis. Asthma may be associated with cataract through the eight signaling pathways, causing inflammation or immune imbalance based on allergy that can lead to cataract. According to these studies, we speculated that the three most likely signaling pathway are PI3K/AKT, MAPK and NF-κB signaling pathway.

A total of 42 clinical strains of Vibrio mimicus were examined for the presence of virulence associated genes toxR, toxS, toxT, tcpP, ctx and tcpA by PCR assay. Ahnost all strains were shown to have the toxR gene, while the toxS gene was found in 27 strains. On the other hand, five strains possessed both toxT and tcpP genes, but others had neither. Only two strains were positive for amplification of the ctx gene, whereas no PCR product with tcpA primers was detected. The results indicate the incomplete copies of virulence cascade in V. mimicus strains. The pathogenesis and epidemic potential of this species is also discussed.

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