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Monitoring grassland productivity dynamics is essential for understanding the impacts of climate variation and human activities. Solar-induced chlorophyll fluorescence (SIF) has been validated as an effective indicator of gross primary productivity. Satellite-derived vegetation indices (VIs) have long been used as key proxies for vegetation productivity. However, the ability of different VIs to represent grassland productivity in relation to SIF, as well as their spatiotemporal consistency with SIF at various scales, remains unclear. In this study, we systematically compared the performance of the Normalized Difference Vegetation Index (NDVI), the Enhanced Vegetation Index (EVI), and the Near-Infrared Reflectance of Vegetation (NIRv), using SIF as a benchmark in grassland areas of China. Utilizing TROPOMI SIF and MODIS VI datasets from 2018 to 2021, we analyzed the spatial and temporal consistency between VIs and SIF at a monthly scale and 0.05-degree resolution, employing Pearson correlation coefficients, paired-sample t-tests, and two-way Analysis of Variance (ANOVA). The results indicate that NIRv consistently demonstrates a higher capacity to capture variations in SIF compared to EVI and NDVI. In low-elevation areas with high-productivity grasslands, all three vegetation indices exhibit a stronger ability to represent vegetation productivity than in high-elevation areas with low-productivity vegetation types. These findings suggest that, at a monthly and regional spatiotemporal scale, NIRv can serve as a robust complement to SIF in monitoring vegetation productivity dynamics, particularly given the challenges in acquiring high-quality, long-term SIF data. [ABSTRACT FROM AUTHOR]

Background: Lung cancer is the leading cause of cancer morbidity and mortality worldwide, however, the individualized treatment is still unsatisfactory. DNA methylation can affect gene regulation and may be one of the most valuable biomarkers in predicting the prognosis of lung adenocarcinoma. This study was aimed to identify methylation CpG sites that may be used to predict lung adenocarcinoma prognosis. Methods: The Cancer Genome Atlas (TCGA) database was used to detect methylation CpG sites associated with lung adenocarcinoma prognosis and construct a methylation signature model. Then, a Chinese cohort was carried out to estimate the association between methylation and lung adenocarcinoma prognosis. Biological function studies, including demethylation treatment, cell proliferative capacity, and gene expression changes in lung adenocarcinoma cell lines, were further performed. Results: In the TCGA set, three methylation CpG sites were selected that were associated with lung adenocarcinoma prognosis (cg14517217, cg15386964, and cg18878992). The risk of mortality was increased in lung adenocarcinoma patients with the gradual increase level of methylation signature based on three methylation sites levels (HR = 45.30, 95% CI = 26.69–66.83; p < 0.001). The C‐statistic value increased to 0.77 when age, gender, and other clinical variables were added to the signature to prediction model. A similar situation was confirmed in Chinese lung adenocarcinoma cohort. In the biological function studies, the proliferative capacity of cell lines was inhibited when the cells were demethylated with 5‐aza‐2'‐deoxycytidine (5‐aza‐2dC). The mRNA and protein expression levels of SEPT9 and HIST1H2BH (cg14517217 and cg15386964) were downregulated with different concentrations of 5‐aza‐2dC treatment, while cg18878992 showed the opposite result. Conclusion: This study is the first to develop a three‐CpG‐based model for lung adenocarcinoma, which is a practical and useful tool for prognostic prediction that has been validated in a Chinese population. [ABSTRACT FROM AUTHOR]

Purpose: ERCC1 and ERCC2 play critical roles in the nucleotide excision repair pathway that effectively repairs DNA damage induced by chemotherapeutic agents. Therefore, functional single nucleotide polymorphisms (SNPs) in these genes could have an impact on clinical outcomes in cancer patients who received chemotherapy. However, few studies have simultaneously investigated the roles of ERCC1 and ERCC2 SNPs in clinical outcomes in gastric cancer patients. Experimental Design: We genotyped by the TaqMan assay three common, potentially functional ERCC1 (rs3212986) and ERCC2 SNPs (rs13181 and rs1799793) in 360 gastric cancer patients. We used both Kaplan-Meier tests and Cox proportional hazards models to evaluate the effects of ERCC1 and ERCC2 genotypes and haplotypes on clinical outcomes. Results: We found that, compared with ERCC2 rs1799793 GG+AG genotypes, the homozygous variant AA genotype was associated with significantly poorer overall survival (OS) (AA vs. GG+AG, log-rank P = 0.012) and significantly higher risk of death (AA vs. GG+AG, Adjusted hazards ratio [HR] 2.13; 95% CI, 1.28 to 3.56; P = 0.004). In combined analyses, patients with any one of the three unfavorable genotypes (i.e. ERCC1 rs3212986 TT, ERCC2 rs13181 GG and rs1799793 AA) had statistically significant hazards of poor prognosis (Adjusted HR, 1.54; 95% CI, 1.06 to 2.25; P = 0.025), compared with those without any unfavorable genotypes. Furthermore, the haplotype A-G-G (rs1799793/rs13181/rs3212986) had a significant impact on OS (Adjusted HR, 1.57; 95% CI, 1.11 to 2.21; P = 0.011), compared with the common haplotype G-T-G. Conclusion: ERCC1 and ERCC2 functional SNPs may jointly affect OS in Caucasian gastric cancer patients. Additional large prospective studies are essential to confirm our findings. [ABSTRACT FROM AUTHOR]

Background and Objective: Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are the primary treatment for advanced non-small cell lung cancer (NSCLC) patients with EGFR mutations, significantly enhancing patient prognosis. Despite the efficacy of EGFR-TKIs, monotherapy faces challenges such as variability among individuals and early drug resistance. This article aims to explore the treatment strategies and influencing factors for advanced NSCLC patients treated with EGFR-TKIs, optimize treatment plans, and improve the prognosis of patients with advanced NSCLC., Methods: We undertook a comprehensive, narrative review of the latest literature to define the current application and progress of EGFR-TKIs in treating patients with advanced NSCLC., Key Content and Findings: The efficacy and promise of EGFR-TKIs, both as monotherapy and combined with other agents, for treating patients with advanced NSCLC are outlined. The study delves into the mechanisms of resistance and the ongoing development of EGFR-TKIs. Various factors influencing the treatment of advanced NSCLC patients with EGFR-TKIs are also examined., Conclusions: EGFR-TKIs alone improve survival in patients with advanced NSCLC. Combined with other agents, some regimens have shown improved benefits in overcoming drug resistance and prolonging patient survival. It is imperative to focus on developing novel EGFR-TKIs and investigate innovative combination therapies to maximize patient benefit., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tcr.amegroups.com/article/view/10.21037/tcr-24-637/coif). The authors have no conflicts of interest to declare., (2024 AME Publishing Company. All rights reserved.)

Abnormalities of methyl-CpG binding protein 2 (Mecp2) cause neurological disorders with metabolic dysfunction; however, its role in adipose tissues remains unclear. Here, we report upregulated Mecp2 in white adipose tissues (WAT) of obese humans, as well as in obese mice and during in vitro adipogenesis. Normal chow-fed adipocyte-specific Mecp2 knockout mice ( Mecp2 Adi KO mice) showed a lean phenotype, with downregulated lipogenic genes and upregulated thermogenic genes that were identified using RNA sequencing. Consistently, the deficiency of Mecp2 in adipocytes protected mice from high-fat diet (HFD)-induced obesity and inhibited in vitro adipogenesis. Furthermore, Mecp2 Adi KO mice showed increased browning under different stimuli, including cold treatment. Mechanistically, Mecp2 bound to the promoter of secretory leukocyte protease inhibitor ( Slpi ) and negatively regulated its expression. Knockdown of Slpi in inguinal WAT of Mecp2 Adi KO mice prevented cold-induced browning. Moreover, recombinant SLPI treatment reduced the HFD-induced obesity via enhancing browning. Together, our results suggest a novel non-central nervous system function of Mecp2 in obesity by suppressing browning, at least partially, through regulating adipokine Slpi., (© 2019 by the American Diabetes Association.)

Thymidylate synthase (TYMS) is involved in the folate metabolism and provision of nucleotides needed for DNA synthesis and repair. Thus, functional genetic variants in TYMS may alter cancer risk. In the study, we evaluated associations of three germline variants (rs2790 A > G, rs16430 6 bp > 0 bp, and rs1059394 C > T) in the predicted miRNA-binding sites of TYMS with risk of sporadic breast cancer in non-Hispanic white women aged ≤ 55. We found that carriers of the rs16430 0 bp variant allele had an increased risk of breast cancer [adjusted odd ratio (OR) = 1.37, 95% confidence interval (CI): 1.08-1.73; P = 0.010], compared with carriers of the 6 bp/6 bp genotype. This increased risk was more evident in older subjects (OR = 1.47, 95% CI = 1.06-2.03, P = 0.022), never smokers (OR = 1.67, 95% CI = 1.23-2.25, P < 0.001), never drinkers (OR = 1.44, 95% CI = 1.01-2.05, P = 0.043), and estrogen receptor-positive patients (OR = 1.46, 95% CI = 1.11-1.92, P = 0.006), regardless of tumor stages. The results are consistent with the functional analyses of rs16430 as previously reported, which showed that the 0 bp allele had a decrease in both luciferase activity by ∼ 70% and mRNA levels by ∼ 50% compared with the 6bp allele. Additionally, the rs16430 variant was predicted to influence the binding activity of miR-561. Taken together, these findings indicate that the TYMS rs16430 may contribute to the etiology of sporadic breast cancer in non-Hispanic white women aged ≤ 55 yr. Further validation in large population-based or cohort studies is needed., (© 2013 Wiley Periodicals, Inc.)

Background and Objective: Patient whose carina is involved by carcinoma is difficult to treat by surgery. The aim of this study is to evaluate the safety and effectiveness of left main bronchus root prolongation to cure these patients., Methods: Three patients with lung carcinoma received tumor, right upper lung and carina excision. And then the trachea and the carina was rebuilt by continuous suture, so that the left main bronchus root was extended by 3 cm, then the middle and lower lobe bronchus were sutured to the right lateral wall of the moved up eminence., Results: All the patients left hospital successfully after three-week treatment, without anastomotic stoma fistula. And they got good quality of life after 30, 21 and 11 months' follow-up, no recurrence or metabasis was found., Conclusions: The left main bronchus root prolongation can preserve the left lateral wall, however, part of the tracheal mucous membrane and arteria trachealis can be protected without injury. It's benifit for making productive cough and lowering complications after operation. The new carinal reconstruction process has definite indication, which refer to patient with normal left main bronchus root and the right inferior segment trachea involved by carcinoma.