The impact of hyperoxia-induced brain injury in preterm infants is being increasingly investigated. However, the parameters and protocols used to study this condition in animal models lack consistency. Research is further hampered by the fact that hyperoxia exerts both direct and indirect effects on oligodendrocytes and neurons, with the precise underlying mechanisms remaining unclear. In this article, we aim to provide a comprehensive overview of the conditions used to induce hyperoxia in animal models of immature brain injury. We discuss what is known regarding the mechanisms underlying hyperoxia-induced immature brain injury, focusing on the effects on oligodendrocytes and neurons, and briefly describe therapies that may counteract the effects of hyperoxia. We also identify further studies required to fully elucidate the effects of hyperoxia on the immature brain as well as discuss the leading therapeutic options.

Primary aldosteronism (PA) is the most frequent form of secondary endocrine hypertension, which is characterized by excessive aldosterone secretion and suppressed renin. The currently recommended diagnostic algorithm is very clear, and the plasma aldosterone-to-renin ratio (ARR) is considered the first-line screening test. However, this indicator is influenced by many factors, some of which may cause false-negative results, consequently leading to underdiagnosed PA. Here, we report the rare case of a 38-year-old man who presented with bilateral accessory renal arteries and aldosterone-producing adenoma but had a negative ARR test result.

Objective: To determine the risk factors for plastic bronchitis (PB) in children diagnosed with Mycoplasma Pneumoniae Pneumonia (RMPP) and facilitate early intervention. Methods: A retrospective study of 205 hospitalized children diagnosed with RMPP in two tertiary hospitals was conducted from January 2023 to May 2025. The children were divided into the PB group and non-PB group. Clinical characteristics, laboratory indices, pulmonary imaging findings, and treatment approaches were compared between the two groups. A nomogram model was established based on logistic regression to assess the risk of PB in children infected with RMPP. Results: A total of 52 patients (25.4%) were included in the PB group. The nomogram model constructed in this study indicated that three risk factors- C-reactive protein (CRP) > 20 mg/L, pleural effusion, and high Lactate Dehydrogenase (LDH) levels- could be used for the early identification of PB in children with RMPP. The area under the receiver operating characteristic curve of the prediction model was 0.783 (95%CI: 0.71–0.86). The Hosmer–Lemeshow goodness-of-fit test demonstrated the good calibration of the nomogram [( P = 0.408, R ² = 8.269)]. Decision curve analysis showed that the model had clinical value. Conclusions: Early identification of these risk factors (CRP > 20 mg/L, pleural effusion, and elevated LDH) may facilitate timely bronchoscopic examination in children with RMPP at high risk of PB, potentially contributing to improved clinical management.

The impact of the difference between cystatin C- and creatinine-based estimated glomerular filtration rate (eGFRdiff) on hypertension remains unknown. We investigated the association of eGFRdiff and the risk of developing hypertension. A total of 3628 participants without hypertension at baseline in 2011 from the China Health and Retirement Longitudinal Study were enrolled. The eGFRdiff was calculated using both absolute difference (eGFRabdiff = eGFRcys–eGFRcr) and the ratio (eGFRrediff = eGFRcys/eGFRcr) between cystatin C- and creatinine-based estimated glomerular filtration rate. The association between eGFRdiff and hypertension risk was examined using restricted cubic spline (RCS) and multivariable logistic regression analysis. The mean (± SD) for eGFRabdiff and eGFRrediff were − 16.3 ± 16.5 mL/min/1.73 m2, and 0.83 ± 0.17, respectively. During 4 years of follow-up, 605 incident hypertension cases were identified. Participants in the third quantile of eGFRabdiff had a lower risk of hypertension than participants in the first quantile of eGFRabdiff (OR 0.72, 95% CI 0.57–0.92, P = 0.01), adjusting for potential confounders. RCS showed an inversely linear relationship between eGFRabdiff and hypertension risk. In the fully adjusted model, each standard deviation increase in eGFRabdiff was associated with a 0.85-fold decrease in the risk of incident hypertension (OR 0.85, 95% CI 0.77–0.94, P = 0.002). Sensitivity analysis also confirmed the results. In exploratory analyses, the proportional effect of eGFRabdiff on hypertension risk was consistent across the six pre-specified subgroups (all P for interaction > 0.05). Similar results were observed for eGFRrediff. A large negative difference in cystatin C-based and creatinine-based eGFR was significantly associated with the risk of hypertension. Our findings suggested that monitoring eGFRdiff could be clinically useful in identifying high-risk people for hypertension.

Objective: The Apolipoprotein B/Apolipoprotein A-I (ApoB/ApoA-I) ratio has been strongly associated with the risk of cardiovascular disease. However, its association with in-stent restenosis (ISR) after drug-eluting stent (DES) implantation in patients with coronary heart disease (CHD) remains unclear. Methods: This retrospective study enrolled CHD patients who underwent follow-up coronary angiography 6–24 months after successful DES-based percutaneous coronary intervention (PCI). The ApoB/ApoA-I ratio was calculated, and participants were grouped by quartiles of the ratio. Multivariable logistic regression and restricted spline cubic (RCS) models assessed the association between the ApoB/ApoA-I ratio and ISR risk. Subgroup and sensitivity analyses were also conducted. Results: A total of 1,004 CHD patients (mean age 67.32 ± 10.63 years, 63.65% male) were included. 176 (17.5%) patients developed ISR over a median 12-month follow-up. The prevalence of ISR rose stepwise with increasing quartiles of the ApoB/ApoA-I ratio (5.6% vs. 11.2% vs. 20.3% vs. 32.6%, P < 0.001), and the ratio was higher in the ISR group than in the non-ISR group (0.86 ± 0.28 vs. 0.67 ± 0.21, P < 0.001). After full adjustment for confounders, the ApoB/ApoA-I ratio remained positively associated with ISR risk [per 1-SD increase: odds ratios (OR) = 2.39, 95% CI: 1.81–3.15, P < 0.001]. Using the first quartile as reference, the OR for the third and fourth quartiles were 3.48 (95% CI: 1.67–7.22, P = 0.001) and 6.09 (95% CI: 2.66–13.93, P < 0.001), respectively. Sensitivity analyses supported these findings. RCS analysis indicated a linear dose-response relationship between the ApoB/ApoA-I ratio and ISR risk ( P for overall 0.05). Moreover, adding ApoB/ApoA-I ratio to the predictive model for ISR could contribute to an increase in C-statistics (0.732 vs. 0.768, P = 0.001), categorical net reclassifcation improvement (0.128, P = 0.001), and integrated discrimination improvement (0.053, P < 0.001). Conclusions: An elevated ApoB/ApoA-I ratio was significantly associated with an increased risk for ISR after DES-based PCI in CHD patients. Our findings suggested that the ApoB/ApoA-I ratio might serve as a useful predictor for ISR risk in this population.