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How soil cover types and rainfall patterns influence carbon (C) release in temperate desert ecosystems has largely been unexplored. We removed intact crusts down to 10 cm from the Shapotou region, China, and measured them in PVC mesocosms, immediately after rainfall. C release rates were measured in soils with four cover types (moss‐crusted soil, algae‐crusted soil, mixed (composed of moss, algae, and lichen)‐crusted soil, and mobile dune sand). We investigated seven different rainfall magnitudes (0–1, 1–2, 2–5, 5–10, 10–15, 15–20, and >20 mm) under natural conditions. C release from all four BSCs increased with increasing rainfall amount. With a rainfall increase from 0 to 45 mm, carbon release amounts increased from 0.13 ± 0.09 to 15.2 ± 1.35 gC m−2 in moss‐crusted soil, 0.08 ± 0.06 to 6.43 ± 1.23 gC m−2 in algae‐crusted soil, 0.11 ± 0.08 to 8.01 ± 0.51 gC m−2 in mixed‐crusted soil, and 0.06 ± 0.04 to 8.47 ± 0.51 gC m−2 in mobile dune sand, respectively. Immediately following heavy rainfall events (44.9 mm), moss‐crusted soils showed significantly higher carbon release rates than algae‐ and mixed‐crusted soils and mobile dune sands, which were 0.95 ± 0.02, 0.30 ± 0.03, 0.13 ± 0.04, and 0.51 ± 0.02 μmol CO2 m−2 s−1, respectively. Changes in rainfall patterns, especially large rain pulses (>10 mm) affect the contributions of different soil cover types to carbon release amounts; moss‐crusted soils sustain higher respiration rates than other biological crusts after short‐term extreme rainfall events.

Introduction Pemetrexed combined with platinum complexes can be used as first-line treatment for advanced non-squamous non-small cell lung cancer (NSCLC), however, the efficacy and safety is varying from individuals. There is a need to better understand the genetic variations associated with platinum response. Materials and Methods We performed next-generation sequencing (NGS) based on BGI Oseq-ctDNA panel to analyze 98 longitudinal plasma samples from 32 lung adenocarcinoma patients during platinum-based chemotherapy, and a bioinformatic pipeline was developed to detect point mutations. Results We found that mutation burden was decreased after chemotherapy, which reflected chemotherapy sensitivity, especially the frequency of C>G and C>A substitutions. Moreover, neoplastic cells carrying a specific set of somatic mutations, such as EGFR(L858R), KRAS (p.G12C) were obviously correlated with platinum treatment. In addition, the MAPK pathway was found to have a pivotal role in NSCLC and platinum based response. Finally, we found that smokers benefit less from platinum-based chemotherapy. Conclusions Collectively, this work described the dynamic changes of ctDNA mutation status during platinum-based treatment, which may contribute to advanced lung adenocarcinoma patients stratification and precision treatment.

Osimertinib is designed to target the secondary resistant EGFR T790M mutant and has shown outstanding clinical efficacy. However, the prognostic prediction of osimertinib patients is a big problem in clinical practice. The resistance mechanism of osimertinib is also not fully understood. NGS and a 1021 gene capture panel were used to analyse the somatic mutation profile of thirty‐six lung adenocarcinoma patients' serial ctDNA samples. Progression‐free survival of subgroup patients is analysed. Patients harbour TP53 mutations and patients with higher TMB value in pre‐treatment samples showed a shorter PFS. Moreover, compared to CT evaluation, ctDNA changes generally correlated with treatment responses in most patients. Novel resistance mechanisms are discovered including EGFR mutations and alternative activation pathway. Our results implied a broad potential of ctDNA as an adjuvant tool in practical clinical management of NSCLC patients. ctDNA could help with clinical practice during osimertinib treatment, regarding monitoring tumour response, detecting development of heterogeneity, identifying potential resistance mechanisms, predicting treatment efficacy and patient outcome.

We aimed to investigate the immunophenotype, differential diagnosis, and clinicopathological characteristics of signet-ring cell carcinoma (SRCC) derived from gastric foveolar epithelium.Methods: Clinical characteristics, endoscopic findings, histopathological features, and follow-up data of seven cases of SRCC derived from gastric foveolar epithelium with small intramucosal lesions were analyzed.Results: Seven patients with a mean age of 38.3 years were diagnosed with SRCC derived from gastric foveolar epithelium and small intramucosal lesions, all of them were negative for CDH-1 germline mutation. The glands proliferated and expanded, and then morphologically transformed into signet-ring cells and formed clonal hyperplastic SRCC, which expanded laterally along the gastric foveolar cells to a length of 3-6 mm. Periodic acid Schiff staining was positive, while CK7 and MUC6 were negative, in all cases. Ki-67-positive cells ranged 37%-60%. During a follow-up period of 6-30 months, no patients experienced tumor recurrence or metastasis.Conclusions: SRCC derived from gastric foveolar epithelium is originated from the proliferative region of the bottom of the gastric pit and gland neck. It is easily missed diagnosed or misdiagnosed as it grows laterally along the gastric foveolar cells. Biological behavior, genetics, and etiology of such SRCC, as well as the clinicopathological characteristics, need to be further studied.

BACKGROUND: Epidermal growth factor receptor (EGFR) mutation status is crucial in treatment selection for non–small cell lung cancer (NSCLC) patients; however, the detection materials’ availability remains challenging in clinical practice. In this study, we collected surgical resection tissues, lymph node biopsy, and cytological samples for EGFR mutation testing and investigated the associations between gene mutation and clinical characteristics. METHODS: Two hundred and seventy-six NSCLC adenocarcinoma specimens were collected, and highly sensitive amplification refractory mutation system method was implemented for EGFR mutation detection, with clinicopathologic characteristics involved in the final analysis. RESULTS: In the total of 276 samples, 96% (265/276) of tumors obtained evaluable EGFR mutation status, the frequency of mutation was 55.8% (148/265) in all specimens, and three different type samples shared a comparable successful testing rate: 97.4% (38/39) in surgical tumor tissues, 100% (108/108) in lymph node biopsy samples, and 92.2% (119/129) in cytological samples. EGFR mutation was significantly associated with sex, smoking history, lymph node metastasis status (N stage), primary tumor size, testing tissues origin, and sample type (P < .05). Multivariate analysis reconfirmed that smoking history and primary tumor size shared significant correlation with EGFR mutation after adjustment. CONCLUSIONS: Both lymph node biopsy and cytological samples were suitable surrogates for EGFR mutation detection in NSCLC compared with tumor tissues, gene status should be detected widely considering the high EGFR mutation rate, and nonsmoking history together with smaller primary tumor size was an independent indicator of EGFR mutation status.