β-cryptoxanthin suppresses oxidative stress via activation of the Nrf2/HO-1 signaling pathway in diabetic kidney disease.

Objectives: This study aims to explore the role and investigate mechanisms of β-Cryptoxanthin (BCX) in high glucose (HG)-induced podocyte injury and renal dysfunction.

Methods: In this study, db/db mice were orally treated with BCX. Blood glucose, body weight, urinary albumin creatinine ratio (ACR) were recorded to evaluate the mice renal function.

Synaptotagmin-1 antagonizes paraquat intracellular accumulation and nephrocyte toxicity by up-regulating SERBP1/GLUT2 expression.

Acute kidney injury (AKI) is common and an independent risk factor for mortality in patients with paraquat (PQ) poisoning. Currently, no specific antidote is available. Synaptotagmin-1 (SYT1) has been identified as a key protein that facilitates PQ efflux in PQ-resistant A549 cells, thereby preventing PQ-induced lung injury.

Hypoxia-Inducible Factor-1 Regulates High Phosphate-Induced Vascular Calcification via Type III Sodium-Dependent Phosphate Cotransporter 1.

Vascular calcification (VC) has a high incidence in patients with chronic kidney disease, which is a worldwide public health problem and presents a heavy burden to society. Hypoxia-inducible factor (HIF)-1, the active subunit of HIF-1, has been reported to play a vital role in high phosphate-induced VC. However, the underlying mechanism is still undetermined, and effective treatment is unavailable.

Paraquat-induced ferroptosis suppression via NRF2 expression regulation.

Paraquat (PQ) is an environmentally friendly and efficient herbicide, but PQ misuse or intentional self-use can cause death through multiple organ damage and can cause acute lung injury. Existing clinical treatments alleviate symptoms but do not significantly improve the mortality rate. Ferroptosis is a type of necrosis that presents in a manner very similar to the cell damage induced by high doses of PQ, but the role of ferroptosis in paraquat-induced lung injury remains unclear.

ETI signaling nodes are involved in resistance of Hawaii 7996 to bacterial wilt disease in tomato.

Bacterial wilt caused by the soil-borne pathogen is a destructive disease of tomato. Tomato cultivar Hawaii 7996 is well-known for its stable resistance against . However, the resistance mechanism of Hawaii 7996 has not yet been revealed.

Duality of immune recognition by tomato and virulence activity of the Ralstonia solanacearum exo-polygalacturonase PehC.

Ralstonia solanacearum is a devastating soil-borne bacterial pathogen capable of infecting many plant species, including tomato (Solanum lycopersicum). However, the perception of Ralstonia by the tomato immune system and the pathogen's counter-defense strategy remain largely unknown. Here, we show that PehC, a specific exo-polygalacturonase secreted by Ralstonia, acts as an elicitor that triggers typical immune responses in tomato and other Solanaceous plants.

Treatment with paraquat affects the expression of ferroptosis-related genes.

Objective: We aimed to explore the mechanisms underlying paraquat (PQ)-induced damage using cell lines (NCTC1469, TC-1, TCMK-1) and bioinformatic analysis of the GSE153959 dataset. Assessment of changes in the expression of ferroptosis-related genes in cellular damage due to paraquat poisoning and the important value of these genes in the pathogenesis.

Methods: Data were retrieved from the Gene Expression Omnibus database.

A bioartificial transgenic porcine whole liver expressing human proteins alleviates acute liver failure in pigs.

Background: Preventing heterologous protein influx in patients is important when using xenogeneic bioartificial livers (BALs) to treat liver failure. The development of transgenic porcine livers synthesizing human proteins is a promising approach in this regard. Here, we evaluated the safety and efficacy of a transgenic porcine liver synthesizing human albumin (hALB) and coagulation factor VII (hFVII) within a bioartificial system.

Chromatin Remodeling Induced by ARID1A Loss in Lung Cancer Promotes Glycolysis and Confers JQ1 Vulnerability.

Unlabelled: ARID1A is a key mammalian SWI/SNF complex subunit that is mutated in 5% to 11% of lung cancers. Although recent studies have elucidated the mechanism underlying dysregulation of the switch/sucrose non-fermentable (SWI/SNF) complexes in cancers, the significance of ARID1A loss and its implications in lung cancers remain poorly defined. This study investigates how ARID1A loss affects initiation and progression of lung cancer.

Hyperbaric Oxygen Therapy Represses the Warburg Effect and Epithelial-Mesenchymal Transition in Hypoxic NSCLC Cells the HIF-1α/PFKP Axis.

Background: Tumor cells initiate hypoxia-induced mechanisms to fuel cell proliferation, invasion, and metastasis, largely mediated by low O-responsive Hypoxia-Inducible Factor 1 Alpha (HIF-1α). Therefore, hyperbaric oxygen therapy (HBO) is now being studied in cancer patients, but its impact upon non-small-cell lung cancer (NSCLC) cell metabolism remains uncharacterized.

Methods: We employed the NSCLC cell lines A549 and H1299 for studies.