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Late embryogenesis abundant (LEA) proteins are a class of proteins associated with osmotic regulation and plant tolerance to abiotic stress. However, studies on the LEA gene family in the alpine cold-tolerant herb are still limited, and the phylogenetic evolution and biological functions of its family members remain unclear. In this study, we conducted genome-wide identification, phylogenetic evolution, and abiotic stress response analyses of LEA family genes in Notopterygium species, alpine cold-tolerant medicinal herbs in the Qinghai–Tibet Plateau and adjacent regions. The gene family identification analysis showed that 23, 20, and 20 LEA genes were identified in three Notopterygium species, N. franchetii, N. incisum, and N. forrestii, respectively. All of these genes can be classified into six LEA subfamilies: LEA_1, LEA_2, LEA_5, LEA_6, DHN (Dehydrin), and SMP (seed maturation protein). The LEA proteins in the three Notopterygium species exhibited significant variations in the number of amino acids, physical and chemical properties, subcellular localization, and secondary structure characteristics, primarily demonstrating high hydrophilicity, different stability, and specific subcellular distribution patterns. Meanwhile, we found that the members of the same LEA subfamily shared similar exon–intron structures and conserved motifs. Interestingly, the chromosome distributions of LEA genes in Notopterygium species were scattered. The results of the collinearity analysis indicate that the expansion of the LEA gene family is primarily driven by gene duplication. A Ka/Ks analysis showed that paralogous gene pairs were under negative selection in Notopterygium species. A promoter cis-acting element analysis showed that most LEA genes possessed multiple cis-elements connected to plant growth and development, stress response, and plant hormone signal transduction. An expression pattern analysis demonstrated the species-specific and tissue-specific expression of NinLEAs. Experiments on abiotic stress responses indicated that the NinLEAs play a crucial role in the response to high-temperature and drought stresses in N. franchetii leaves and roots. These results provide novel insights for further understanding the functions of the LEA gene family in the alpine cold-tolerant Notopterygium species and also offer a scientific basis for in-depth research on the abiotic stress response mechanisms and stress-resistant breeding. [ABSTRACT FROM AUTHOR]

To measure the correlation and agreement between arterial and peripheral venous blood lactate in the emergency room and to assess the predictive value of lactate for the occurrence of cardiac arrest. This was a retrospective cohort study involving 784 patients from January 1, 2020, to July 31, 2021, in the Emergency Room of the First Affiliated Hospital of Xinjiang Medical University. General information, vital signs, clinical symptoms, and laboratory findings of the patient were collected. Linear regression was used to analyze the correlation between arterial and venous blood lactate, Bland-Altman plots were drawn to assess the concordance of (arterial-venous) serum lactate concentrations, and the predictive value of arterial and venous lactate for the occurrence of cardiac arrest was assessed by using the receiver operating characteristic curve (ROC). A total of 784 emergency room patients were included in the study, of whom 384 experienced cardiac arrest and 400 had no cardiac arrest. Arterial and venous lactate univariate linear regression analysis, correlation coefficient r = 0.80, linear equation Y (venous blood lactate)  = 0.729 + 0.960*X (arterial blood lactate) , and had statistical significance (P < 0.001); arterial blood (lactate) and venous blood (lactate) were -0.548 (95%CI -0.774 ~ -0.322 mmol/L), and the upper and lower limits of the 95% limits of agreement (LoA) were 5.777 (95%CI 5.390 ~ 6.163 mmol/L) and -6.872 (-7.2590 ~ -6.4855 mmol/L), indicating that the consistency of arterial blood lactate and venous blood lactate is poor and statistically significant (P < 0.001). The results of this study show that venous and arterial blood lactate levels are not identical, but are highly correlated and are important predictors of cardiac arrest in emergency room patients., Competing Interests: Declarations. Competing interests: The authors declare no competing interests. Ethical statement: This study was approved by the Medical Ethics Committee of the First Affiliated Hospital of Xinjiang Medical University (Approval No. K202301-27) without the need for written informed consent., (© 2025. The Author(s).)

Sepsis-induced acute lung injury (ALI) is a complex and life-threatening condition characterized by excessive inflammatory responses, ferroptosis, and oxidative stress. A comprehensive investigation and effective therapeutic strategies are crucial for managing this condition. In this study, we established in vivo sepsis models using lipopolysaccharide (LPS) in wild-type (WT) mice and triggering receptor expressed on myeloid cells 2 (TREM2) knockout (TREM2-KO) mice to assess lung morphology, oxidative stress, and ferroptosis. In vitro, RAW264.7 cells with TREM2 overexpression (TREM2-OE) or knockdown (TREM2-SiRNA) were utilized to assess oxidative stress and ferroptosis. RNA sequencing of LPS-stimulated cells transfected with either vector or TREM2-OE revealed significant differences in inflammation- and ferroptosis-related pathways. LPS-induced lung injury and ferroptosis were exacerbated in TREM2-KO mice and TREM2-SiRNA cells but alleviated by the ferroptosis inhibitor ferrostatin-1 (Fer-1). Mechanistically, TREM2-KO led to SHP1 downregulation and STAT3-P upregulation, which were reversed by the SHP1 agonist SC-43. These findings highlight the role of TREM2 in the SHP1/STAT3 signaling pathway and its regulatory effects on ferroptosis. Our study demonstrates that TREM2, via the SHP1/STAT3 pathway, suppresses oxidative stress and ferroptosis, thereby significantly mitigating sepsis-induced ALI. These results underscore the pivotal role of TREM2 in modulating inflammatory responses and immunity, providing a theoretical foundation for developing therapeutic strategies., Competing Interests: Declaration of Competing Interest The authors declare no conflict of interest., (Copyright © 2025. Published by Elsevier Inc.)