Keystone microalgae species determine the removal efficiency of sulfamethoxazole: a case study of Chlorella pyrenoidosa and microalgae consortia.

In recent years, antibiotics pollution has caused serious harm to the aquatic environment, and microalgae mediated degradation of antibiotics has attracted increasing attention. However, the potential toxicity of antibiotics to keystone microalgae species or their microalgae consortia, and the impact of microalgal diversity on antibiotic removal need to be further studied. In this study, we investigated the removal efficiency and tolerance of five freshwater microalgae (Chlorella pyrenoidosa, Scenedesmus quadricauda, Dictyosphaerium sp., Haematoccocus pluvialis, and Botryococcus braunii) and their microalgae consortia to sulfamethoxazole (SMX). We found that the removal efficiency of SMX by C. pyrenoidosa reached 49%, while the other four microalgae ranged between 9% and 16%. In addition, C. pyrenoidosa, S. quadricauda, and Dictyosphaerium sp. had better tolerance to SMX than H. pluvialis, and their growth and photosynthesis were less affected. At 10 and 50 mg/L SMX, the removal capacity of SMX by mixed microalgae consortia was lower than that of C. pyrenoidos except for the consortium with C. pyrenoidos and S. quadricauda. The consortia generally showed higher sensitivity towards SMX than the individual species, and the biochemical characteristics (photosynthetic pigment, chlorophyll fluorescence parameters, superoxide anion (O2 -), superoxide dismutase activity (SOD), malondialdehyde (MDA) and extracellular enzymes) were significantly influenced by SMX stress. Therefore, the removal of antibiotics by microalgae consortia did not increase with the number of microalgae species. Our study provides a new perspective for the selection of microalgal consortia to degrade antibiotics.

Savolitinib monotherapy exerted significant benefit in a non-small cell lung cancer patient with osimertinib resistance harboring primary EGFR L858R mutation and MET amplification: a case report.

Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have significantly improved response in all stages of patients with EGFR positive mutations in nonsmall cell lung cancer. However, the primary resistance mechanism of EGFR-TKIs has not been thoroughly revealed. Here, we described a case of a 64-year-old male with lung adenocarcinoma presented primary resistance on osimertinib combined with bevacizumab and platinum-based chemotherapy, next-generation sequencing revealed EGFR exon 21 L858R mutation and MET gene amplification. Afterward, savolitinib monotherapy was started until now, and the treatment was temporarily successful, the last follow-up clinical evaluation was near complete response, the progression-free survival has over 7 months. Our case highlights that EGFR-TKIs may be not the optimal choice for lung adenocarcinoma with primary EGFR -sensitive mutation with MET amplification simultaneously, whereas MET inhibitor alone may be an effective treatment option. In clinical practice, we should fully consider the possibility of primary resistance in EGFR-TKIs administration.