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To determine the effects of drying methods on the volatile compounds and explore the key aroma compounds in Chrysanthemum nankingense leaves, head-space solid phase micro-extraction combined with gas chromatography mass spectrometry (HS-SPME-GC-MS) was employed for quantitative and qualitative analysis of the volatile compounds in C. nankingense leaves dried by hot air drying, vacuum-freeze drying or microwave-hot air drying. The result showed that a total of 140 compounds belonging to six classes (terpenes, esters, aldehydes, alcohols, aromatic compounds and other substances) were identified in all samples. Of these, 112, 86, 83 and 85 were detected in fresh and dried C. nankingense obtained by hot air drying, microwave-hot air drying, and vacuum-freeze drying, respectively. Among these compounds, terpenes were the most abundant, with contents of 229 474.33, 64 629.68, 56 469.88 and 70 832.87 μg/kg in fresh, hot air dried, microwave-hot air dried, and vacuum-freeze dried samples, respectively. Compared with the other drying methods, vacuum-freeze drying gave better retention of the abundance of volatile compounds. Vacuum-freeze dried C. nankingense had similar flavor to fresh samples, showing camphor-like, turpentine-like, flowery and grassy aromas. GC-MS combined with odor activity values (OAVs) confirmed that β-ocimene, caryophyllene and trans-β-farnesene were the major aroma components. GC-MS combined with E-nose can represent an efficient nondestructive method for the detection of volatile compounds in C. nankingense leaves and allow the discrimination of dried C. nankingense obtained by different drying methods. These results provide a theoretical basis for choosing drying methods and understanding the difference in volatiles components in dried C. nankingense obtained by different drying methods.

Oncogenic KRAS is a major driver in lung adenocarcinoma (LUAD) that has yet to be therapeutically conquered. Here we report that the SLC7A11/glutathione axis displays metabolic synthetic lethality with oncogenic KRAS. Through metabolomics approaches, we found that mutationally activated KRAS strikingly increased intracellular cystine levels and glutathione biosynthesis. SLC7A11, a cystine/glutamate antiporter conferring specificity for cystine uptake, was overexpressed in patients with KRAS-mutant LUAD and showed positive association with tumor progression. Furthermore, SLC7A11 inhibition by either genetic depletion or pharmacological inhibition with sulfasalazine resulted in selective killing across a panel of KRASmutant cancer cells in vitro and tumor growth inhibition in vivo, suggesting the functionality and specificity of SLC7A11 as a therapeutic target. Importantly, we further identified a potent SLC7A11 inhibitor, HG106, that markedly decreased cystine uptake and intracellular glutathione biosynthesis. Furthermore, HG106 exhibited selective cytotoxicity toward KRAS- mutant cells by increasing oxidative stress- and ER stress-mediated cell apoptosis. Of note, treatment of KRAS-mutant LUAD with HG106 in several preclinical lung cancer mouse models led to marked tumor suppression and prolonged survival. Overall, our findings reveal that KRAS-mutant LUAD cells are vulnerable to SLC7A11 inhibition, offering potential therapeutic approaches for this currently incurable disease., Introduction Lung cancer is the leading cause of global cancer-related mortality, and lung adenocarcinoma (LUAD) represents the most common histological subtype of this disease. Approximately two-thirds of LUADs have activated [...]

The original article can be found online at https://doi.org/10.1007/s10853-023-08180-5.Correction to: J Mater Sci (2023) 58:3551–3567https://doi.org/10.1007/s10853-023-08180-5There are errors in Fig. 3. The corrected figure follows:Graph: Figure 3 XRD patterns of CTO and CTM.Publisher's NoteSpringer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.By Xia Yang; Songrui Wei; Xilong Ma; Zhuwei Gao; Wei Huang; Dun Wang; Zhongxin Liu and Jieqiong WangReported by Author; Author; Author; Author; Author; Author; Author; Author [Extracted from the article]