The Third Affiliated Hospital of Southern Medical University

To identify the prognostic value of C-reactive protein to albumin ratio (CRP/ALB, CAR) and Glasgow Coma Scale (GCS) score in the weaning outcomes of mechanical ventilation (MV) in patients with traumatic brain injury (TBI).

Medical records of patients with TBI who were hospitalized at The Third Affiliated Hospital of Southern Medical University between January 2018 and September 2023 were collected and analysed. The patients were divided into the weaning success group and the weaning failure group. Data from the two groups were analysed to assess the predictive value of CAR and GCS score on weaning outcomes.

CAR was an independent risk factor for weaning failure (p = .001, adjusted OR = 1.878, 95% CI: 1.283-2.750), while GCS score was a protective factor for weaning success (p = .006, adjusted OR = 0.629, 95% CI: 0.452-0.873). In the receiver operating characteristic (ROC) curve analysis, the area under the curve (AUC) of CAR predicted the weaning failure was 0.780 (p < .001), and predicted the weaning success by GCS score was 0.727 (p = .003). Moreover, the combination of the two predicted better with an AUC of 0.849 (p < .001).

TBI patients with higher CAR and lower GCS score were more likely to experience weaning failure, which can provide reliable guidance for patients with TBI to leave the ventilator.

We previously described the enrichment of plasma exosome metabolites in CRPC, PCa, and TFC cohorts, and found significant differences in pyrimidine metabolites. The PMGs is associated with the clinical prognosis of several cancers, but its biological role in PCa is still unclear.

This study extracted 98 reliable PMGs, and analyzed their somatic mutations, expression levels, and prognostic significance. Unsupervised clustering was applied to classify patients with PCa into clusters based on six PMGs that were related to the prognosis of PCa. The TME, gene mutations, and immune escape ability were compared among the clusters. A scoring algorithm based on prognostic PMGs, referred to as the PMGscore, was developed. TK1 was identified and the biological functions of TK1 were determined using loss-of-function experiments. RNA sequencing was subsequently performed to determine the molecules associated with the underlying mechanisms of TK1 function.

In total, six out of 98 PMGs simultaneously exhibited differential expression in PCa and were correlated with BCR. Patients were clustered into two clusters according to the expression levels of these six PMGs, which reflected distinct clinical outcomes and immune cell infiltration characteristics. Clinical features, tumor prognosis, and functional annotation were analyzed. Subsequently, we constructed a prognostic signature using these six PMGs. In combination with other clinical traits, we found that the six PMGs' prognostic signature was an independent prognostic factor for patients with PCa. Finally, we found that the expression of TK1 was higher in CRPC tissues than in PCa tissues in three GEO datasets. The results indicated that TK1 promotes the growth and metastasis of PCa cells.

We provide evidence for a PMG signature for PCa patients to accurately predict clinical prognosis. TK1 plays crucial roles in the progression of PCa cells and can be used as a potential therapeutic target for CRPC.

Liver steatosis and fibrosis increase the predicted 10-year atherosclerotic cardiovascular disease (ASCVD) risk, though the roles of chronic inflammation and metabolic dysregulation remain unclear. This cross-sectional study quantitatively assesses this association and evaluates the mediating effects of metabolic dysregulation and chronic inflammation.

In this study, we enrolled 6110 adults from ten communities in Canton, China. Hepatic steatosis and fibrosis were assessed using vibration-controlled transient elastography (VCTE) through controlled attenuation parameter (CAP) and liver stiffness measurement (LSM), while predicted 10-year ASCVD risk was calculated using the China-PAR project model. Associations between CAP/LSM values and predicted 10-year ASCVD risk were analyzed. Mediation analysis quantified the effects of high-sensitivity C-reactive protein (hs-CRP), homeostasis model assessment of insulin resistance (HOMA-IR), remnant cholesterol (RC), and non-high-density lipoprotein cholesterol (non-HDL-C). The main statistical methods used included logistic regression, restricted cubic splines (RCS) analysis, interaction calculations, and mediation analysis to examine the relationships and mediators.

The study population had a mean age of 50.1 years (SD = 9.7), with 3927 females (64.3%) and 2183 males (35.7%). Additionally, 808 participants (13.2%) had type 2 diabetes, and 1911 participants (31.3%) had hypertension. Compared to the first CAP quartile (Q1), higher CAP quartiles showed increased odds ratios (OR) for predicted moderate to high 10-year ASCVD risk: 1.14 (0.89, 1.45), 1.37 (1.08, 1.73), and 2.44 (1.93, 3.10). Mediation analysis showed hs-CRP and HOMA-IR mediated CAP's link to ASCVD risk, with mediation proportions of 15.40% and 27.37%. RC and non-HDL-C mediated this association at 7.12% and 6.26%. Among patients with hepatic steatosis (CAP ≥ 248 dB/m), LSM Q4 participants had a significantly higher predicted 10-year ASCVD risk than those in LSM Q1 (OR 2.22, [1.52, 3.25]), with hs-CRP and HOMA-IR mediating 2.62% and 13.75%, respectively.

Liver steatosis and fibrosis were associated with the increased predicted ASCVD risk, with mediation effects from hs-CRP, HOMA-IR, RC, and non-HDL-C.