The multiple responses of Mytilus galloprovincialis in the multi-stressor scenario: Impacts of low pH, low dissolved oxygen, and microplastics.

Global metabolomic responses of dogwhelk and mussel during different stages of predation.

Histological methods to quantify changes of white and brown adipose tissue in response to a high content fat diet in mice.

Differential metabolic reprogramming due to nitrogen starvation leads to remobilization of storage metabolites in microalgal strains.

Ginsenoside Re exerts neuroprotective in MPTP mice: potential links to gut microbiota and serum metabolism.

Quantitative lipidomics for three-dimensional cell culture using deuterium oxide metabolic labeling.

Fangji Huangqi Tang alleviated chronic kidney disease by regulating intestinal bacteria to inhibit the AHR/ROS pathway.

Association between MR-derived oxygen extraction fraction and neurological improvement at 24-72 h after successful reperfusion.

Integrated metabolomics and lipidomics for in-depth understanding of dynamic metabolic changes in passion fruit with different ripeness.

Metabolic changes explain how training mitigates the reduction in strength caused by sleep restriction.

Large consortia link variants in SLC22A1 , SLC47A1 , and GLP1R to antidiabetic response, yet few data confirm these effects in small real-world cohorts. We tested whether three common polymorphisms translate into measurable 3-month metabolic changes. Twenty-seven Bulgarian adults with type 2 diabetes [BMI ≥ 25 kg/m²; mean glycated hemoglobin (HbA1c): 8.3 ± 0.9%] received metformin XR 2000 mg ( n = 17) or oral semaglutide 14 mg ( n = 10). Sanger sequencing identified SLC22A1 rs628031, SLC47A1 rs2252281, and GLP1R rs6923761. Primary endpoints were 3-month changes (Δ) in weight and HbA1c; analysis of variance and ordinary least squares regression assessed genotype and treatment effects, as well as covariate-adjusted linear models of 3-month change (Δ). Semaglutide produced greater weight loss than metformin [-6.5 ± 3.6 vs. -1.6 ± 2.5 kg; 95% confidence interval (CI) -7.6 to -2.2; P = 0.001] and larger BMI reduction (-2.0 ± 1.2 vs. -0.3 ± 0.9 kg/m²; P = 0.001). At an exploratory 10% FDR, only OCT1 rs34130495 dosage was associated with high-density lipoprotein (HDL) change in metformin-treated participants ( β = +0.340 mmol/L per minor allele; P = 0.0026; q = 0.063; N = 16). GLP1R rs6923761 showed nominal trends for weight and BMI change in semaglutide users that did not survive FDR ( P ≈ 0.06-0.07; q ≈ 0.29; N = 10). Semaglutide outperformed metformin for short-term weight loss. An HDL signal for OCT1 rs34130495 at an exploratory 10% FDR warrants replication. These hypothesis-generating data support the feasibility of genotype-guided studies in local clinical settings.

Discovering metabolic pathways associated with immune activation in people living with HIV following ChAdOx1 nCoV-19 vaccination using mass spectrometry.

Metabolic reprogramming represents a targetable mechanism to overcome acquired resistance to venetoclax in acute myeloid leukemia.

Raman spectroscopic characterization of liver steatosis and fibrosis in a 2D and 3D in vitro thyroxine-treated hypothyroid cellular model.

Metformin-mediated modulation of gut microbiota-derived trimethylamine N-oxide (TMAO) in myocardial infarction: Insights from in vivo, metabolomics, and in silico studies.

Changing trends of non-volatile metabolites during industrial broad bean paste production via untargeted metabolomics.

Rationale: Rechallenge peptide receptor radionuclide therapy (PRRT) is a valid therapeutic option for patients with advanced/metastatic neuroendocrine tumors (NETs) who previously benefited from initial PRRT. In this context, [18F]FDG PET may serve as a prognostic marker. This multicenter 10-year survival study aims to evaluate the prognostic implications of [18F]FDG PET and PRRT-induced changes in NET patients undergoing rechallenge PRRT. Methods: This retrospective multicenter study included 100 patients (median age: 54 years, range: 29-83) treated with rechallenge PRRT. All patients underwent [68Ga]Ga-DOTA-TOC/TATE/NOC and [18F]FDG PET/CT prior to the first PRRT period, 3-4 months after PRRT, and every 6-9 months thereafter. Metabolic status and its changes (no change vs. FDG+/FDG- vs. FDG-/FDG+) before the first PRRT period and at each restaging were recorded and correlated to baseline characteristics, time to progression (TTP), and overall survival (OS). Results: In 43 out of 100 patients, the primary tumor site was the pancreas; the liver was involved in more than 90% of patients. Biopsies revealed G1 NET in 16%, G2 NET in 66%, and G3 NET in 18% of cases. Before the first PRRT period, 50% of patients were FDG-positive. Following the first PRRT period, 27 patients exhibited a change in metabolic status: 20 converted to FDG-negative, whereas 7 became FDG-positive. After the second PRRT period, metabolic status changed in 41 patients, with 25 converting to FDG-negative and 16 to FDG-positive. Metabolic status after the first period was significantly correlated with NET grade (p = 0.009). The correlation persisted also after rechallenge (p < 0.001), suggesting that FDG positivity increased progressively in G3 NET patients (p = 0.020). The presence of bone metastases statistically correlated with FDG positivity before (p < 0.001) and after (p = 0.001) the first PRRT period. Multivariate Cox regression analysis revealed NET G3 and FDG status after the first PRRT course as independent factors for shorter TTP. After a median follow-up time of 117.6 months (range: 38.4-180 months), 37 patients had died. Multivariate Cox regression analysis revealed FDG positivity after the first (p < 0.001) and second (p < 0.001) periods of PRRT as independent predictors of poor OS. Conclusions: Assessing [18F]FDG status before PRRT and during follow-up after treatment enables prediction of TTP and OS, even in patients considered for rechallenge PRRT. Standardizing the use of dual-tracer imaging in patients receiving PRRT seems a valuable approach to improve clinical decision-making in NET patients.

HIF-1α silencing downregulates SLC37A2, SLC37A3, and G6PC3 gene expression and impacts glioblastoma stemness features in 3D neurospheres.

Fecal microbiota transplantation alleviates chronic cerebral hypoperfusion-induced axonal hypomyelination by regulating gut microbiota-derived metabolism and oligodendrogenesis.

Microbiota-gut-brain axis dysregulation in Alzheimer's disease and its modulation through probiotic supplementation.