Balkan Medical Journal最新文献

Background: The association between the glucose-to-lymphocyte ratio (GLR) and adverse outcomes in intensive care unit patients receiving mechanical ventilation (MV) has not been clearly established.

Aims: To examine the link between GLR and 28-day mortality in MV patients and to develop an interpretable machine learning model to predict mortality risk.

Study design: A retrospective study.

Methods: Data were obtained from the Medical Information Mart for Intensive Care IV (MIMIC-IV, version 3.1) database. Receiver operating characteristic (ROC) and restricted cubic spline (RCS) curves were employed to assess the relationship between GLR and mortality. Patients were categorized into high and low GLR groups for Kaplan-Meier survival analysis. Subgroup analyses were performed to evaluate the association across different patient populations. Selected variables were used to construct eXtreme Gradient Boosting (XGBoost), support vector machine, Naive Bayes, and k-nearest neighbors models. Model interpretability was assessed using SHapley Additive exPlanations (SHAP) values.

Results: A total of 5,738 patients met the inclusion criteria. RCS analysis indicated a nonlinear relationship between GLR and 28-day mortality. Patients with elevated GLR had significantly higher 28-day mortality rates (hazard ratio > 1, p < 0.05). Among the models, XGBoost demonstrated the best performance, achieving an area under the ROC curve of 0.969 and an F1-score of 0.963. SHAP analysis identified Acute Physiology Score III, GLR, and lactate as the three most important predictors.

Conclusion: GLR is nonlinearly associated with 28-day mortality in patients undergoing MV and may serve as a valuable prognostic marker. The interpretable XGBoost model confirmed the significant association between GLR and short-term mortality.

Background: The accumulation of proteins such as amyloid-beta and tau, which disrupt normal cellular processes, characterizes Alzheimer's disease (AD). Cognitive decline is strongly linked to tau pathology, which initially manifests in the medial temporal lobe (MTL).

Aims: To investigated the association between cognitive performance and regional tau accumulation, as measured by positron emission tomography (PET) imaging, in cognitively normal older adults. Understanding this relationship is critical for early intervention before noticeable cognitive decline emerges.

Study design: Retrospective study.

Methods: Tau PET scans were conducted on 440 participants enrolled in the anti-amyloid treatment in asymptomatic Alzheimer's (A4) study. The participants, aged 65-85, were cognitively unimpaired and had complete demographic and genetic profiles. Tau levels in the MTL and temporal neocortex (NEO) was quantified using composite metrics. Cognitive function was evaluated using the preclinical Alzheimer's cognitive composite (PACC) and its individual components. Multiple linear regression models were applied to determine the associations between tau burden and cognitive outcomes, including interaction terms to evaluate the moderating roles of sex and apolipoprotein E (APOE)-ε4 genotype.

Results: The average participant age was 71.8 years (standard deviation = 4.84), with females comprising 58% of the sample. Greater tau accumulation in both tauMTL and tauNEO regions was significantly associated with lower cognitive scores. Specifically, reduced PACC scores (p < 0.001) corresponded with higher tau levels in both regions, primarily influenced by declines in Delayed Logical Memory and Free and Cued Selective Reminding test scores. Additionally, tauNEO levels were modestly linked to Mini-Mental State Examination scores. The effects of sex and APOE-ε4 status were minimal.

Conclusion: Elevated tau deposition in the MTL and NEO is associated with diminished cognitive function, particularly in memory and processing speed domains. Notably, tau accumulation in the MTL showed a strong association with poorer outcomes on memory-related cognitive measures. The limited influence of sex and APOE-ε4 genotype highlights tau pathology as a key contributor to early cognitive decline in preclinical AD.