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Based on the selective quenching effect of the flavonoid rutin on the fluorescence of carbon dots prepared by asparagine pyrolysis, a method for rapid detection of rutin content in the flower buds of Sophora japonica by using chitosan-based carbon dot paper chip was developed. A filter paper was immersed in the casting solution of carbon dots and chitosan. After drying, a carbon dot chitosan film was formed on the surface of the filter paper, so that the chitosan-based carbon dot paper chip was obtained. After samples were dripped on the chip, chromogenic reaction occurred uniformly within a limited region, and pictures were taken under an ultraviolet (UV) lamp at 365 nm for analysis of the red (R), green (G), and blue (B) values of the colored spots in order to optimize the preparation conditions and detection conditions. The results showed that the optimal conditions were as follows: chitosan concentration of 20 mg/mL, carbon spot concentration of 1.0 mg/mL, 50% ethanol as sample solvent, and reaction time of 20 min. Under these conditions, the difference (ΔG) in G-value between sample and solvent spots had a linear relationship with rutin concentration (C) in the range of 4 to 120 mg/mL. Using this method, the average contents of rutin in the flower buds of S. japonica from three batches were determined to be 23.85%, 22.83% and 20.30%, the average relative standard deviations (RSDs) were 6.1%, 5.6% and 6.7%, and the recoveries were 91.27% to 107.5%, which were close to the results of high performance liquid chromatography (HPLC). The proposed method is simple and rapid, and can be used for rapid on-site determination of rutin content in the flower buds of S. japonica.

Introduction: Sepsis is characterized by an endotoxin tolerance phenotype that occurs in the stage of infection. Persistent bacterial infection can lead to immune cell exhaustion. Triad3A, an E3 ubiquitin ligase, negatively regulates its activation by TLR4. However, the effect of Triad3A on endotoxin tolerance and bactericidal ability in the state of endotoxin tolerance remains unclear. Methods: Using single dose LPS and repeated LPS stimulated macrophage cell lines at indicated times, we investigated miR‐191, Tirad3A, TRAF3, TLR4, p‐P65, TNF‐α, IL‐1β, and iNOS expression, the effect of miR‐191 on Triad3A and TRAF3, gene loss‐of‐function analyses, the effect of Triad3A on TLR4, p‐P65, cytokine, and mycobactericidal activity in endotoxin tolerant cells infected with Mycobacterium marinum. Results: Here we found that Triad3A is involved in regulating endotoxin tolerance. Our result also displayed that miR‐191 expression is downregulated in macrophages in the state of endotoxin tolerance. miR‐191 can directly bind to Triad3A and TRAF3. Additionally, knockdown of Triad3A can reverse the effect of decreasing TNF‐α and IL‐1β in endotoxin tolerant macrophages. Furthermore, we demonstrated that the TLR4‐NF‐κB‐NO pathway was associated with Triad3A and responsible for the killing of intracellular mycobacteria in a tuberculosis sepsis model. Conclusions: These results provide new insight into the mechanisms of Triad3A induced tolerogenic phenotype in macrophages, which can help the better comprehension of the pathogenesis involved in septic shock with infection of Mycobacterium tuberculosis, and suggest that Triad3A may be a potential drug target for the treatment of severe septic tuberculosis. [ABSTRACT FROM AUTHOR]

Aging is the single most significant risk factor for cancer development. However, the potential impact of aging on cancer microenvironment remains poorly understood. Here, we performed a pan‐cancer transcriptome analysis to identify aging‐specific molecular patterns across 18 cancer types. Strikingly, aging‐specific molecular features define human cancers into two types, including the strong and weak aging‐effect groups. Significant aging associated molecular signature was observed in 16 cancer types (strong aging‐effect group) such as breast invasive carcinoma and acute myeloid leukemia. In such 16 cancer types, old patients showed obvious poor survival compared to young patients, but this observation was not found in the weak aging‐effect cancers. Aging‐associated cancer‐relevant molecules significantly enriched in 23 pathways including EMT and KRAS signaling. More interestingly, in cancer microenvironment, aging significantly restrains adaptive immunity, but strikingly, increases the number of infiltrated innate immune cells. Further analysis shows that the expression of immune checkpoints including PD‐1, PD‐L1, PD‐L2 and CTLA‐4 are mostly correlated with age. In general, cancer cells in elderly patients show a more aggressive phenotype and their surrounding microenvironment is under a more immune suppression status compared to young patients. Our study provides a systematic understanding of aging‐associated molecular features in pan‐cancer and indicates a clinical requirement to develop aging‐specific therapeutic strategies in a majority of cancer types. Furthermore, aging‐altered immune cells and immune checkpoints should be considered in cancer immunotherapy. What's new? Simply getting older increases the chances of developing some form of cancer, but it is still unclear exactly why. Here, the authors sequenced transcriptomes from 18 cancer types, looking for gene expression differences between young and old patients that transcend tissue type. They found strong aging‐associated molecular changes in 16 cancer types, and in those cases, older patients had poor survival than the younger group. Older patients also had a distinctly different immune microenvironment, with higher levels of 11 immune checkpoints and reductions in adaptive immune cells. Older patients, then, may respond differently to immunotherapy. [ABSTRACT FROM AUTHOR]