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Dissolved organic matter (DOM) in soils drives biogeochemical cycling and soil functions in different directions depending on its molecular signature. Notably, there is a distinct paucity of information concerning how the molecular signatures of soil DOM vary with different degrees of weathering across wide geographic scales. Herein, we resolved the DOM molecular signatures from 22 diverse Chinese reference soils and linked them with soil organic matter and weathering-related mineralogical properties. The mixed-effects models revealed that the yields of DOM were determined by soil organic carbon content, whereas the molecular signature of DOM was primarily constrained by the weathering-related dimension. The soil weathering index showed a positive effect on the lability and a negative effect on the aromaticity of DOM. Specifically, DOM in highly weathered acidic soils featured more amino sugars, carbohydrates, and aliphatics, as well as less O-rich polyphenols and condensed aromatics, thereby conferring a higher DOM biolability and lower DOM aromaticity. This study highlights the dominance of the weathering-related dimension in constraining the molecular signatures and potential functions of DOM in soils across a wide geographic scale.

Objective To discuss the current situation and challenge to the treatment strategy for elderly patients with advanced gastric cancer and provide reference for the exploration of ideal treatment methods. Methods Collect the clinical material of an elderly patient with advanced gastric cancer, and the relevant literatures were reviewed. Results A 79-year-old man was clinically diagnosed as adenocarcinoma on the fundus of stomach (cT4a-bN2Mx). After the third course of neo-adjuvant concurrent chemo-radiotherapy, a remarkable reduction and down-staging was achieved (cT3-4N1Mx), then followed by radical gastrectomy for gastric cancer. S1 was used alone for the postoperative chemotherapy. The patient received nutritional therapy in the full treatment course, and the physical condition was satisfactory without tumor metastasis and relapse two years and a half after the surgery. Conclusions The sequentially comprehensive therapy suggestes a treatment therapy for elderly patients with advanced gastric cancer, and deserves further verification and promotion clinically.

Flavonoids, which contain a benzo‐γ‐pyrone (C6–C3–C6) skeleton, have been reported to exhibit effective antioxidant ability. This study aimed to compare the antioxidant activities of 7,8‐dihydroxyflavone (7,8‐DHF) and 7‐hydroxyflavone (7‐HF) in H2O2, lipopolysaccharide (LPS), or tert‐butyl hydroperoxide (t‐BHP)‐induced RAW264.7 cells, respectively. The antioxidant capacities of 7,8‐DHF and 7‐HF were firstly evaluated by 2,2‐azinobis‐3‐ethyl‐benzothiazoline‐6‐sulphonic acid (ABTS), 2,2‐diphenyl‐1‐picrylhydrazyl (DPPH) and ferric reducing antioxidant power (FRAP) assays. Then, reactive oxygen species (ROS), super oxide dismutase (SOD), and malondialdehyde (MDA) productions in H2O2, LPS, or t‐BHP‐induced RAW264.7 cells were tested and compared, respectively. Finally, the antioxidant mechanisms of 7‐HF and 7,8‐DHF were initially investigated by western blot. Our results showed that 7,8‐DHF possessed stronger free‐radical scavenging capacity than 7‐HF. Both 7,8‐DHF and 7‐HF suppressed MDA production and ROS accumulation, improved the activity of SOD in H2O2, LPS, or t‐BHP‐induced RAW264.7 cells, respectively. And 7,8‐DHF exerted a better antioxidant effect than 7‐HF, especially in t‐BHP‐induced oxidative stress. Mechanically, 7,8‐DHF prevented the activation of poly ADP‐ribosepolymerase and caspase‐3, meanwhile markedly upregulated the expression of HO‐1 protein in t‐BHP‐induced oxidative stress. These results suggested that 7,8‐DHF might serve as a potential pharmaceutical drug against oxidative stress injury. [ABSTRACT FROM AUTHOR]

The effects of nuclear ubiquitous casein and cyclin-dependent kinase substrate 1 (NUCKS1) on tumor cells and the relevant mechanisms are less well defined. This study aimed to explore the role and mechanism of action of NUCKS1 in gastric cancer (GC) progression. The expression dynamics of NUCKS1 were examined using microarray-based immunohistochemistry (IHC) in a group of carcinomatous and adjacent non-tumor specimens. Various in vitro and in vivo assays were performed to clarify the function of NUCKS1 in GC and its underlying mechanisms. In our research, NUCKS1 overexpression was identified by IHC in 86/200 (43%) GC patients, was significantly related to the invasive phenotype of GC and was an indisputable predictor of shortened survival. Depleting NUCKS1 in GC cells significantly induced apoptosis and reduced cell proliferation and invasiveness in vitro and inhibited tumor growth in vivo. Additionally, ectopic overexpression of NUCKS1 in GC cells enhanced proliferation and invasion in vitro and promoted tumor growth in vivo. Importantly, PI3K/Akt/mTOR signaling pathway activity was inhibited upon downregulation of NUCKS1 expression and enhanced by ectopic overexpression of NUCKS1. Subsequently, the insulin-like growth factor 1 receptor (IGF-1R) gene was found to be a potential downstream target of NUCKS1 in GC cells, and knockdown of IGF-1R eliminated the augmentation of GC cell migration, invasion and proliferation as well as PI3K/Akt/mTOR signaling pathway activity by ectopic NUCKS1. The data suggested that NUCKS1 enhanced GC aggressiveness via the PI3K/Akt/mTOR signaling pathway in an IGF-1R-dependent manner. NUCKS1 or its respective signaling pathways could hold immense promise as potent anticancer targets for GC treatment. [ABSTRACT FROM AUTHOR]

Objective: To develop a new bioelectrical impedance analysis (BIA) model for analyzing body composition by using isotope dilution, magnetic resonance imaging (MRI), and dual-energy X-ray absorptiometry (DEXA) as the reference methods in young healthy Chinese populations.Methods: Thirty healthy participants were enrolled. Their body composition was analyzed using BIA and 3 reference methods. We established a model that uniformed data from 3 references methods (isotope, MRI, and DEXA) into 1 formula. This model was further validated with 209 participants.Results: The following BIA body composition adjustment model was developed: [Formula: see text], where X represents the impedance index; when K = 1, 2, and 3, Y represents total body water, fat mass, and bone mass, respectively. The prediction accuracy of this formula was 93.3%. By incorporating the data matrix, the protein mass was calculated using BIA: [Formula: see text]. In the verification part of this study, the lean body mass measured using DEXA and BIA was 43.02 ± 8.34 kg and 45.85 ± 8.81 kg, respectively. Analysis indicated that the model fit was extremely favorable ( R2 = .9997, P < .001).Conclusions: The accuracy of BIA measurement on body composition and protein mass is significantly improved by our work. [ABSTRACT FROM AUTHOR]

Background: An accumulation of hyperphosphorylated tau in the brain is a hallmark of Alzheimer's disease (AD). Deficits in protein phosphatase 2A (PP2A) are associated with tau hyperphosphorylation in AD. Objective: To investigate the effects of morroniside (MOR), isolated from Cornus officinalis, on tau hyperphosphorylation and its underlying mechanisms related to PP2A. Methods: SK-N-SH cells were pretreated with 50-200 μM MOR for 24 h followed by 20 nM okadaic acid (OA) for 6 h. PP2Ac siRNA was transfected into HEK293 cells to determine the direct interaction of MOR with PP2A. Western blotting was used to measure the expression of proteins and enzymes. PP2A activity was measured by molybdenum blue spectrophotometry. Results: Pretreatment with MOR improved the cellular morphological damage and inhibited tau hyperphosphorylation in SK-N-SH cells induced by OA, a PP2A inhibitor. Moreover, MOR increased PP2A activity, concurrent with a decrease in the expression of demethylated PP2A at Leu309 and phosphorylated PP2A at Tyr307. MOR decreased protein phosphatase methylesterase 1 (PME-1) expression and the ratio of PME-1/leucine carboxyl methyltransferase 1 (LCMT-1). Furthermore, MOR treatment decreased the phosphorylation of Src at Tyr416, which regulates the phosphorylation of PP2A. MOR had no effect on PP2Ac expression and tau hyperphosphorylation in PP2Ac siRNA-transfected cells. Conclusion: MOR attenuated OA-induced tau hyperphosphorylation via PP2A activation, and its mechanism might be related to the regulation of PP2Ac post-translational modification and upstream enzymes such as Src and PME-1. [ABSTRACT FROM AUTHOR]