Open Medicine最新文献

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.

Objective: The aim of this study was to assess the impact of the external oblique intercostal block (EOIB) on early postoperative pain in patients who underwent laparoscopic cholecystectomy.

Methods: 120 patients were divided into two groups: the EOIB group (Group E) and the control group (Group C). The assessed variables were mainly intraoperative remifentanil usage, numerical rating scale (NRS) pain scores at 0, 1, 2, 4, 6, 12, and 24 h postoperatively, cumulative fentanyl consumption within 24 h postoperatively and within the first-hour post-anesthesia care unit.

Results: Remifentanil consumption during surgery was significantly reduced in Group E compared to Group C. Postoperative fentanyl requirements were also lower in Group E at 1 and 24 h after surgery. Furthermore, Group E demonstrated significantly lower NRS scores at 0, 1, 2, 4, and 6 h postoperatively and a reduced need for rescue analgesia compared to Group C. However, at 12 h post-surgery, Group E's NRS scores were slightly higher than Group C's.

Conclusion: The EOIB is associated with reduced pain within the first 24 postoperative hours following laparoscopic cholecystectomy.

Background: Intrauterine adhesions (IUAs) are a significant clinical challenge, affecting reproductive health and leading to infertility or recurrent pregnancy loss. Understanding the molecular mechanisms underlying IUA prevention is crucial for developing effective treatment strategies.

Objective: To investigate the interaction between oviductal mucosal cells and endometrial cells and their effects on the expression of key molecules involved in embryo implantation, specifically leukemia inhibitory factor (LIF), avβ3, estrogen receptor (ER), and progesterone receptor (PR).

Methods: Tubal mucosa and endometrium specimens were collected from 22 patients undergoing surgical interventions. Cells were cultured alone and co-cultured at ratios of 1:1, 1:0.5, and 1:0.1. LIF, avβ3, ER, and PR expression levels were measured using real-time fluorescence quantitative polymerase chain reaction and enzyme-linked immunosorbent assay.

Results: Our results demonstrated that LIF expression was significantly augmented in co-culture conditions, particularly in the 1:1 ratio, compared to oviductal mucosa monoculture (P < 0.05). Although LIF expression was also elevated in 1:0.5 and 1:0.1 co-culture ratios, these increases were not statistically significant (P > 0.05). For avβ3, increased expression was observed in the 1:1 co-culture group (P < 0.05), but no significant differences were detected in 1:0.5 and 1:0.1 co-culture groups. ER expression showed a downward trend in co-culture, but without statistical significance (P > 0.05), and PR expression remained stable across all groups.

Conclusion: Co-culture modulates key molecules involved in embryo implantation, particularly LIF and avβ3. These findings highlight the potential roles of LIF and avβ3 in IUA prevention strategies and provide important insights for future clinical interventions. Tubal mucosal cells can not only grow in the endometrial cell microenvironment, but also the tolerance of tubal mucosal cells can be improved when they are co-cultured.

Background: Hyperoxia-induced injury is a well-recognized cause of bronchopulmonary dysplasia (BPD). Existing research studies have not well elucidated the exact mechanisms underlying hyperoxia-induced cellular damage. This study examines the involvement of the P2X7 receptor (P2X7R) in hyperoxia-induced damage to human pulmonary microvascular endothelial cells (HPMVECs) via the NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) pathway.

Methods: HPMVECs developing hyperoxia-induced injury were subjected to the treatment of either selective inhibitors or a P2X7R/NLRP3 agonist. Western blot analysis assisted in the quantification of the levels of P2X7R, NLRP3, caspase-1, and gasdermin D (GSDMD). Additionally, the release of TNF-α, IL-1β, and IL-18 was assessed by ELISA and qRT-PCR.

Results: Exposure to hyperoxia diminished cell viability and escalated the levels of P2X7R, caspase-1, NLRP3, GSDMD, and N-terminal-GSDMD. This exposure notably increased the release of TNF-α, IL-1β, and IL-18 in HPMVECs. Notably, the suppression of P2X7R using the inhibitor A438079 decreased pyroptosis and inflammatory responses. Conversely, stimulation of P2X7R by 3'-O-(4-benzoylbenzoyl) adenosine 5'-triphosphate (BzATP) triggered pyroptosis, while inhibition of NLRP3 with glibenclamide ameliorated the damage induced by BzATP.

Conclusions: The P2X7R/NLRP3 pathway crucially affects the hyperoxia-induced inflammation and pyroptosis in HPMVECs, hinting the potential of blocking P2X7R/NLRP3-mediated pyroptotic pathway as a valuable therapeutic strategy for BPD.

Background: Osteosarcoma, a highly malignant skeletal tumor, primarily affects children and adolescents. Autophagy plays a crucial role in osteosarcoma pathophysiology. This study utilizes bibliometric analysis to evaluate current research on autophagy in osteosarcoma and forecast future directions.

Methods: We conducted a comprehensive search of publications in the Web of Science Core Collection database from January 1, 2008, to March 15, 2024. Tools like VOSviewer, CiteSpace, R software, Excel, and Scimago were used for analysis and visualization.

Results: Publications increased steadily over 17 years, indicating rising interest. Zhang Yuan was the most influential author, with Shanghai Jiao Tong University leading. Cell Death & Disease was the top journal. "HMGB1 Promotes Drug Resistance in Osteosarcoma" was the most cited paper. Co-cited articles focused on drug resistance, therapeutic targets, autophagy in cancer, and genomic impacts on immunotherapy. Keywords highlighted invasion, migration, cell death, and breast cancer as research hotspots. Future studies will likely focus on therapeutic innovations and integrated management strategies.

Conclusion: This bibliometric analysis offers an overview of current knowledge and emerging trends in autophagy and osteosarcoma, emphasizing key areas like invasion, migration, and cell death. It serves as a valuable resource for researchers developing novel therapies for osteosarcoma.