ObjectiveTo investigate the protective effect of artemitin against ozone (O₃)-induced pulmonary inflammation in mice and to explore its underlying mechanism. MethodsThirty-two specific pathogen-free (SPF) male C57BL/6 mice were randomly divided into a blank control group, an artemitin-only control group, an O₃-induced model group, and an artemitin-treated group, with 8 mice in each group. In the artemitin-treated group, animals were injected intraperitoneally with artemitin (20 mg/kg) daily, followed by a 1 h exposure to 0.000 25% O₃. The artemitin-only control group received the same artemitin injection but was exposed to clean air. The O₃-induced model group was injected intraperitoneally with an equal volume of normal saline daily, followed by a 1-h exposure to 0.000 25% O₃. The blank control group received the saline injection and was exposed to clean air. All treatments were administered for 7 consecutive days. Pulmonary function indices of the mice in each group were measured using a whole-body plethysmography system. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in bronchoalveolar lavage fluid (BALF) were detected by enzyme-linked immunosorbent assay (ELISA). Hematoxylin-eosin (HE) staining was used to observe the histopathological changes in the lung tissue, and ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) was employed for untargeted metabolomic analysis to examine the changes in overall metabolic pathways in plasma. ResultsCompared with the O₃-induced model group, artemitin treatment significantly improved O₃-induced lung function impairments (P<0.05), lowered the levels of TNF-α and IL-1β in BALF (P<0.05) and alleviated inflammatory cell infiltration and structural damage in lung tissues. Metabolomics results indicated that artemitin treatment compensatorily enhanced energy supply and oxidized lipid signaling, while inhibiting purine metabolism and tryptophan-derived pathways. ConclusionArtemitin exhibits a significant protective effect against O₃-induced pulmonary inflammation in mice. It corrects upstream metabolic disorders by synergistically modulating tryptophan metabolism, energy metabolism, and lipid inflammatory mediators, thereby inhibiting downstream inflammatory responses and airway hyperresponsiveness. This study not only reveals the pleiotropic mechanism of artemitin in treating airway inflammation but also provides potential metabolic biomarkers and a theoretical basis for its clinical translation.

Objective To explore the diagnostic value of full-field digital mammography (FFDM) combined with digital breast tomosynthesis (DBT) in breast diseases.Methods 506 patients receiving mammary gland molybdenum target inspection from January 1, 2014 to December 31, 2014 were selected.The images from FFDM and DBT were analyzed, respectively.The breast imaging reports and pathological results were compared to investigate the sensitivity, specificity and accuracy of FFDM, DBT alone and combined use of DBT and FFDM.Results The results of preoperative mammography in the 506 women (bilateral breast) were as follows: FFDM combined with DBT detected 202 benign cases (39.9%) and 304 malignant cases (60.1%);FFDM alone detected 194 benign cases (38.3%) and 312 malignant cases (61.7%);DBT alone detected 187 benign cases (37.0%) and 319 malignant cases (63.0%).Pathologically, 214 benign cases (42.3%) were detected and 292 malignant cases (57.7%).In terms of the sensitivity, specificity and accuracy, The combined use of DBT combined with FFDM was the best, followed by FFDM alone and DBT alone.Conclusion The sensitivity, specificity and accuracy of FFDM combined with DBT for diagnosis are better than those of FFDM alone or DBT alone.

0.05);the persons with hypersexuality from 25 to 31 age had the highest infection percentage and it taken 75% of all the NGU.The minocycline and doxycycline were sensitive and ciprofloxacin was a resistant drug.CONCLUSIONS In our hospital,the Uu is still a main pathogen,and the minocycline and doxycycline are the fist choice to treat it.At the same time,the NGU survey and the antibacterial susceptibility tests are very important.

Background and purpose:Anticancer mechanism of epigallocatechin-3-gallate(EGCG)remains unclear.This study investigated the role of reactive oxygen species(ROS)in epigallocatechin-3-gallate(EGCG)-induced apoptosis in human gastric cancer MGC803 cells.Methods:The inhibition of MGC803 cells growth was measured by MTT assay.Apoptosis of MGC803 cells was studied by using the AO/EB fluorescence stain.Flow cytometry was used to detect the intracellular ROS level and the rate of apoptosis.Results:EGCG could induce apoptosis of MGC803 cells and increased in the intracellular ROS level.However,after treatment with N-acetyl-L-cystein and an athiol-containing antioxidant,the inhibitory effect of EGCG on MGC803 cells was significantly weakened.The apoptotic rate of the cells and the activity of the intracellular ROS level also decreased dramatically.Conclusion:EGCG can induce apoptosis of MGC803 cells.In turn,the ROS inhibitor can significantly inhibit the apoptosis induced by EGCG in MGC803 cells.These results suggest that the cellular generation of ROS plays a role in initiating EGCG-mediated apoptosis of MGC803 cells.