Open Medicine最新文献

[This corrects the article DOI: 10.1515/med-2024-0986.].

Objective: To investigate the relationship between the expression levels of serum forkhead box protein M1(FOXM1) and insulin-like growth factor 2 (IGF2) mRNA in patients with acute respiratory distress syndrome (ARDS) condition and prognosis.

Methods: Ninety patients with ARDS admitted to our hospital were regarded as the ARDS group, according to the prognosis, they were grouped into death group (n = 64) and survival group (n = 126); the control group consisted of 190 healthy individuals.

Results: Compared with the control group, the level of serum FOXM1 mRNA in ARDS group was obviously lower, and the level of IGF2 mRNA was higher. The serum IGF2 mRNA, serum creatinine, inhaled oxygen concentration (FiO₂), and mechanical ventilation time in the death group were higher than those in the control group, and the arterial oxygen partial pressure (PaO₂), FOXM1 mRNA, and oxygenation index (PaO₂/FiO₂) were lower than those in control group. Logistic regression analysis indicated that FOXM1, IGF2, and PaO₂/FiO₂ were significant factors influencing the prognosis and mortality in ARDS patients. Correlation analysis showed that there was a negative correlation between serum FOXM1 and IGF2 mRNA levels in patients with ARDS.

Conclusion: Serum FOXM1 and IGF2 mRNA in patients with ARDS are correlated with the severity and prognosis of ARDS.

Background: Postoperative cognitive dysfunction (POCD) frequently occurs following endovascular therapy for acute ischemic stroke (AIS). Given the complexity of predicting AIS clinically, there is a pressing need to develop a preemptive prediction model and investigate the impact of anesthesia depth on AIS.

Methods: A total of 333 patients diagnosed with AIS were included in the study, comprising individuals with non-POCD (n = 232) or POCD (n = 101). Univariate and multivariate logistic regression analyses were utilized to examine the independent risk factors associated with POCD. A calibration, decision curve analysis, and precision-recall curves were employed to assess the model's goodness of fit.

Results: Multivariate regression analysis identified two inflammatory indicators, high-sensitivity C reactive protein (hs-CRP) and systemic immune inflammatory index (SII), and three brain injury indicators, National Institute of Health Stroke Scale (NIHSS) score, N-terminal pro-brain natriuretic peptide (NT-proBNP), and soluble protein-100 β (S100-β), which were used to construct a nomogram model.

Conclusion: The composite predictive model incorporating NIHSS score, hs-CRP, SII, NT-proBNP, and S100-β demonstrated efficacy in predicting POCD following AIS. Additionally, our results suggest a potential association between depth of anesthesia, cognitive impairment, and inflammatory response in AIS patients.

Selective serotonin reuptake inhibitor correlates with decreased bone mineral density and impedes orthodontic tooth movement. The present study aimed to examine the effects of fluoxetine on osteoclast differentiation and function. Human peripheral blood mononuclear cells (hPBMCs) and murine RAW264.7 cells were cultured with RANKL to stimulate osteoclast differentiation. The resulting multinucleated cells displayed characteristics of mature osteoclasts. Fluoxetine at 0.01-1 μM did not impact cellular viability or oxidative stress. However, 10 μM fluoxetine significantly reduced clonal growth, cell viability, and increased cytotoxicity and lipid peroxidation in RAW 264.7 cells. Further, application of 0.1 μM fluoxetine potently suppressed osteoclast differentiation of both RAW264.7 and hPBMCs, with reduced osteoclast numbers and downregulation of osteoclastic genes matrix metalloproteinase-9, cathepsin K, and integrin β3 at mRNA and protein levels. Fluoxetine also disrupted F-actin ring formation essential for osteoclast resorptive function. Mechanistically, fluoxetine inhibited NF-kB signaling by reducing phosphorylation of pathway members IκBα and p65, preventing IκBα degradation and blocking p65 nuclear translocation. In conclusion, this study demonstrates fluoxetine suppressing osteoclast differentiation in association with disrupting NF-kB activation, providing insight into orthodontic treatment planning for patients taking fluoxetine.

Purpose: This study compared the efficacy and safety of carboplatin combined with arsenic trioxide versus carboplatin combined with docetaxel in treating locally advanced cervical cancer (LACC).

Methods: A total of 48 patients were enrolled between January 2019 and December 2022 and randomly assigned to the experimental group (carboplatin + arsenic trioxide, n = 24) or control group (carboplatin + docetaxel, n = 24). The clinical efficacy, adverse reactions, and serological markers were analyzed.

Results: There was no significant difference in baseline characteristics or total effective rates between the two groups (72.22% vs 68.42%, P > 0.05). Both groups showed significant reductions in serum squamous cell carcinoma antigen levels after chemotherapy (P < 0.05), but no significant difference was observed between groups (6.00 ± 11.36 ng/mL vs 8.42 ± 12.17 ng/mL, P > 0.05). Additionally, there was no significant difference in the incidence of adverse reactions (P > 0.05).

Conclusion: Arsenic trioxide combined with carboplatin as a preoperative neoadjuvant chemotherapy for LACC is not worse than docetaxel combined with carboplatin in terms of short-term efficacy and safety during the treatment of LACC.

Background: Post-myocardial infarction (MI) complications, including ventricular remodeling (VR) and left ventricular aneurysm (LVA) formation, significantly affect patient prognosis and quality of life. Both iron overload and deficiency play critical roles in these pathological processes.

Objectives: This review aims to explore the mechanisms linking abnormal iron metabolism with post-MI VR and LVA formation and to highlight therapeutic strategies that regulate iron levels to mitigate adverse cardiac remodeling.

Methods: The review analyzes existing clinical and experimental research on the role of iron metabolism in post-MI complications. It focuses on iron overload, oxidative stress, ferroptosis, and the impact of iron deficiency on mitochondrial function, energy metabolism, and cardiomyocyte repair.

Results: Iron overload exacerbates myocardial injury through oxidative stress, ferroptosis, and inflammation, leading to fibrosis and ventricular dilation. In contrast, iron-deficiency impairs mitochondrial function, energy metabolism, and cardiomyocyte repair, further contributing to adverse remodeling outcomes. Therapeutic strategies such as iron chelators, ferroptosis inhibitors, and iron supplementation are potential interventions for mitigating adverse remodeling.

Conclusion: Abnormal iron metabolism, both overload and deficiency, plays a critical role in post-MI complications. Therapeutic strategies targeting iron levels hold promise for reducing adverse cardiac remodeling and improving patient outcomes after MI.

Background: We aimed to assess whether neuron-specific enolase (NSE) and S100-β levels are associated with early neurological deterioration (END) in patients with acute ischemic stroke (AIS).

Methods: We conducted a prospective study between March 2022 and October 2023 in 286 patients with AIS. Serum NSE and S100-β levels on admission and at 24 and 48 h after stroke onset were measured using electrochemiluminescence immunoassays. Outcomes included END events within 48 h of admission and unfavorable neurological outcomes at 3 months.

Results: Patients with END had higher serum NSE and S100-β levels. Patients with poor prognosis had higher serum NSE and S100-β levels. Serum NSE (on admission) was an independent biomarker for END in AIS patients and for unfavorable recovery at 3 months. In addition, serum S100-β was an independent biomarker of unfavorable recovery after 3 months in patients with AIS.

Conclusion: Serum NSE on admission and S100-β at 48 h of stroke onset may serve as biomarkers of short-term clinical outcome in patients with AIS. Elevated serum NSE and S100-β levels may be useful tools to predict prognosis in patients with AIS.

Purpose: To investigate the risk factors associated with progressive kyphosis (PK) after percutaneous kyphoplasty (PKP) in osteoporotic vertebral compression fractures (OVCFs).

Methods: A single-center retrospective study (January 2020 to December 2022) analyzed 129 OVCF patients treated with PKP. Patients were divided into a PK group and a non-progressive kyphosis group. Clinical and radiological data were compared, and univariate and multivariate regression analyses identified independent risk factors for PK. A nomogram was then developed to predict the risk factors for PK after PKP.

Results: Of 129 patients, 47 (36.4%) experienced PK after PKP. Multivariate analysis identified independent risk factors for PK as preoperative kyphosis angle (OR = 1.26, P = 0.008), Type D magnetic resonance image (MRI) signal change on T2-weighted images (T2WI) (OR = 18.49, P = 0.003), black line signal (OR = 44.00, P < 0.001), intervertebral disc endplate complex (IDEC) injury (OR = 7.86, P = 0.021), and postoperative Oswestry Disability Index (ODI) score (OR = 1.18, P = 0.004). The nomogram, based on these factors, demonstrated strong discriminative performance (area under the curve = 0.953) and good calibration.

Conclusions: Preoperative kyphosis angle, Type D MRI signal change on T2WI, black line signal, IDEC injury, and higher postoperative ODI score are independent risk factors for PK after PKP. A nomogram based on these factors accurately predicts PK risk.

Background: This study aims to evaluate the correlation between miRNAs and known nerve injury markers neuron-specific enolase (NSE) and S100β in ischemic stroke (IS) patients, exploring its efficacy.

Methods: We retrospectively analyzed 86 IS patients and 32 healthy controls. Clinical and neurological examinations were performed in the admitted patients and the severity of neurological deficits was assessed by National Institutes of Health Stroke Scale (NIHSS). Plasma extraction and serum isolation were performed on all subjects before and 2 weeks after admission. miR-142-5p in serum, and NSE and S100β contents were measured by RT-qPCR and ELISA.

Results: Ischemic lesions were more severe in IS patients, and NSE and S100β were abnormally elevated. miR-142-5p in the serum of IS patients was 2.85 times higher. After 2 weeks of treatment, serum miR-142-5, NSE, and S100β decreased. Patients' serum levels of miR-142-5p were 57.5% lower. Serum miR-142-5, NSE, and S100β were lower in patients with disease improvement than in patients with poor recovery. Additionally, miR-142-5 was positively correlated with NSE (P < 0.0001) and S100β (P = 0.0147), and also with the NIHSS score (P = 0.0004).

Conclusions: miR-142-5p, NSE, and S100β in peripheral blood (PB) of IS patients are elevated, and miR-142-5p is positively correlated with NSE and S100β.

To investigate the correlation between blood stasis syndrome and arteriopathy in immunoglobulin A nephropathy (IgAN). Wall thickness/outer vessel diameter, intimal thickness/outer vessel diameter, and medial thickness/outer vessel diameter were measured using ImageJ software. Vascular endothelial-derived growth factor (VEGF), matrix metalloproteinase-9 (MMP-9), proliferating cell nuclear antigen (PCNA), extracellular signal-regulated kinase (ERK) 1/2, and nuclear factor kappa B (NF-κB) were detected by immunohistochemical staining. Twenty-four-hour urine protein quantification, serum creatinine, urea nitrogen, and uric acid were collected. Blood stasis syndrome and vessel scores were calculated based on Katafuchi's grade. Intimal thickness/outer vessel diameter (0.2725 ± 0.0932 μm), medial thickness/outer vessel diameter (0.2747 ± 0.1139 μm), and wall thickness/outer vessel diameter (0.6136 ± 0.1120 μm) were the largest in IgAN with arteriopathy group. VEGF (0.35 ± 0.90), MMP-9 (0.38 ± 0.12), PCNA (0.43 ± 0.12), ERK1/2 (0.31 ± 0.11), and NF-κB (0.37 ± 0.14) were the highest in IgAN with arteriopathy group. Intimal thickening of IgAN was moderately positively correlated with VEGF, MMP-9, PCNA, ERK1/2, and NF-κB (0.5 < r < 0.8). Medial thickening of IgAN was moderately positively correlated with PCNA and NF-κB (0.5 < r < 0.8). Wall thickening of IgAN was lowly positively correlated with VEGF and MMP-9 (0.3 < r < 0.5). Blood stasis syndrome score was associated with vessel score in IgAN with arteriopathy (P < 0.05). Blood stasis syndrome score can assess the degree of pathological changes.