Browsing by Author "Guerrero, Julia"
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Publication Association between phase angle and daily creatinine excretion changes in critically ill patients: an approach to muscle mass(2025) Vargas, Patricio; Dreyse, Natalia; López, René; Cano, Marcelo; Jerónimo Graf; Graf, Jerónimo; Guerrero, JuliaAssessing muscle mass in critically ill patients remains challenging. This retrospective cohort study explores the potential of phase angle (PA°) derived from bioelectrical impedance analysis (BIA) as a surrogate marker for muscle mass monitoring by associating it with daily creatinine excretion (DCE), a structural and metabolic muscle mass marker. In 20 ICU patients, we observed a linear relationship between PA° and DCE at initial (S1) and follow-up (S2) points, with Rho values of 0.78 and 0.65, respectively, as well as between their percentage changes (Rho = 0.80). Multivariate analysis confirmed a strong association between changes in PA° and DCE (adjusted R2 of 0.73), while changes in the extracellular water to total body water (ECW/TBW) ratio showed no significant association. This study establishes a relationship between a BIA-derived independent-weight parameter and DCE, highlighting the potential of PA° for muscle mass monitoring during acute changes, such as those seen in ICU settings. Integrating PA° into clinical practice could provide a non-invasive and reliable tool to enhance muscle assessment and support targeted interventions in critically ill patients.Publication Enhanced mTORC1 Signaling in Inflammatory Monocytes Links Systemic Inflammation to Cardiovascular Disease in Rheumatoid Arthritis(2025) Karsulovic, Claudio; Tempio, Fabian; Lopez, Mercedes; Guerrero, Julia; Joo, Ka Wei KattyBackground/Objectives: Cardiovascular disease (CVD) is the leading cause of mortality in patients with rheumatoid arthritis (RA), not fully explained by traditional risk factors and disease activity alone. This study explored the relationship between circulating monocyte subsets, inflammatory cytokine profiles, and Mammalian Target of Rapamycin Complex (mTORC) signaling in RA patients with and without a history of CVD. Methods: Peripheral blood mononuclear cells from 9 RA patients with prior CVD, 9 carefully matched RA controls without CVD, and 6 healthy controls were analyzed by flow cytometry. Matching was rigorously conducted across clinically relevant variables, including age, sex, blood pressure, lipid profile, smoking status, RA duration, disease activity, Disease-Modifying Anti-Rheumatic Drug (DMARD) failures, and steroid use. Monocyte subsets were classified as inflammatory (CD14+HLA-DR+CCR2+) and non-inflammatory (CD14+CD163+CCR2-). Results: RA-CVD+ patients exhibited higher frequencies of inflammatory monocytes and elevated intracellular levels of Interleukin 1 β (IL-1β) and Interleukin 6 (IL-6) compared to RA-CVD- patients and healthy controls. mTORC activation, assessed by phosphorylation of S6 Ribosomal Protein (S6Rp), was significantly increased in inflammatory monocytes from RA-CVD+ patients. Conclusions: S6Rp correlated with IL-1β and IL-6 levels only in the RA-CVD+ group, suggesting a link between mTORC activity and inflammatory monocyte function. Notably, these inflammatory features did not correlate with disease activity scores or disease duration. We observed increased mTORC1 signaling in inflammatory monocytes in RA-CVD+ patients, suggesting a potential association with cardiovascular comorbidity.Item Glucocorticoid Receptor-α and MKP-1 as Candidate Biomarkers for Treatment Response and Disease Activity in Vogt-Koyanagi-Harada Disease(Elsevier Inc, 2019) Urzúa, Cristhian; Chen, Ping; Chaigne-Delalande, Benjamin; Liu, Baoying; Anguita, Rodrigo; Guerrero, Julia; Sabat, Pablo; Velásquez, Víctor; Sen, Nida; Lee, Richard; Goecke, AnnelisePurpose To investigate the potential of utilizing the expression of genes for glucocorticoid receptor (GR) and mitogen-activated protein kinase phosphatase-1 (MKP-1) as biomarkers of corticosteroid (CS) refractoriness and disease activity in patients with Vogt-Koyanagi-Harada (VKH) disease. Design Prospective cohort study. Methods Twenty VKH patients receiving their first cycle of CS treatment in the absence of additional systemic immunosuppressive therapy and a control group of fifteen healthy volunteers were recruited from the University of Chile (Santiago, Chile) and US National Institutes of Health (Bethesda, United States). Intraocular inflammation was clinically quantified at enrolment and all follow-up visits. CS refractoriness was defined as an ocular reactivation of VKH upon CS withdrawal at a daily oral prednisone dose of 10 mg or more. Quantitative Reverse transcription polymerase chain reaction (qRT-PCR) was performed to measure the mRNA levels of the alpha (α) and beta (β) isoforms of GR and MKP-1 in peripheral blood mononuclear cells (PBMC) after in vitro stimulation with either anti-CD3/anti-CD28 antibodies, lipopolysaccharide (LPS), or phytohemagglutinin (PHA), in the presence or absence of dexamethasone (Dex). Results After 6 hours of stimulation in the presence of Dex, PBMC from CS-refractory VKH patients had an impaired elevation in GRα expression (P = .03). Furthermore, inactive patients showed a significant Dex-induced upregulation of MKP-1 (P = .005). Conclusions In this pilot study, the expression of GR isoforms and MKP-1 corresponded with patients' clinical response to systemic CS treatment and disease activity, respectively. Hence, these candidate biomarkers have potential clinical utility in the early identification of CS refractoriness and subclinical inflammation in patients with VKH disease.Item Para entender la acción del cortisol en inflamación aguda: una mirada desde la glándula suprarrenal hasta la célula blanco(Sociedad Medica de Santiago, 2017) Guerrero, JuliaGlucocorticoids (cortisol in humans) are essential for numerous biological functions. Among critically ill patients, therapy with cortisol has gained strength in recent years, but clinical results have been mixed. A series of events, that may explain the diversity of clinical responses, occur from the synthesis of cortisol in the adrenal gland to the activation of the cortisol receptor by the hormone when it enters the nucleus of the target cell. Some of these events are revised; a proposition for identifying critically ill patients who may benefit with this therapy is suggested.