Advances in Clinical and Experimental Medicine最新文献

Background: Placenta previa, occurring when the placenta covers the cervical opening after 28 weeks, can lead to severe postpartum bleeding, especially when coupled with placenta accreta spectrum (PAS), posing risks of organ damage and necessitating hysterectomy. Accurate preoperative diagnosis of PAS in women with placenta previa is crucial to reduce adverse outcomes.

Objectives: This study aimed to develop a risk prediction model for PAS in women with placenta previa.

Material and methods: A total of 437 patients with placenta previa, delivering babies between January 2012 and December 2018, were included. Data collected encompassed clinical records, neutrophil-to-lymphocyte ratio (NLR) and sonographic findings. Utilizing univariate and multivariate logistic regression analyses, the study identified key factors correlated with PAS in expectant mothers with placenta previa. A risk prediction model was formulated and evaluated through receiver operating characteristic (ROC) analysis. External validation was performed using additional patients diagnosed with placenta previa.

Results: Independent risk factors for PAS in placenta previa included NLR, timing of cesarean section and miscarriage, placenta previa type, presence of placental lacunae, and uterovesical hypervascularity. The predictive model was established using specific coefficients. The ROC curve indicated an area under the curve (AUC) of 0.821, with a sensitivity of 80.6% and specificity of 68.9%. External validation demonstrated a diagnosis coincidence rate of 75%, and the model exhibited good calibration according to the Hosmer-Lemeshow test (p = 0.3742, >0.05).

Conclusions: The developed model showed effective potential in predicting PAS among women with placenta previa. Its application could significantly contribute to the early detection and subsequent management of PAS.

Background: Pancreaticoduodenectomy (PD), an abdominal surgery, is known for its complexity, cost and inherent risks. Recently, there has been increasing interest in enhanced recovery after surgery (ERAS) as a therapeutic approach. However, the mechanisms underlying postoperative functional recovery remain uncertain, and there are limited data on the efficacy of ERAS in postoperative physiotherapy following complex PD.

Objectives: This study aims to examine the feasibility and effectiveness of conducting a large powered randomized controlled trial (RCT) to evaluate a 2-week postoperative rehabilitation program based on the ERAS concept for patients undergoing pancreaticoduodenectomy.

Material and methods: This study is a RCT with a single treatment group. From June 2022 to June 2024, 28 PD patients will participate in the trial. Patients will be randomly assigned to either a control group receiving standard clinical care or an intervention group undergoing a 2-week postoperative rehabilitation program. Cardiopulmonary function will be assessed using the 6-minute walk test (6MWT), and gastrointestinal (GI) recovery will be evaluated using the Intake, Feeling nausea, Emesis, physical Exam, and Duration of symptoms (I-FEED) scoring system.

Results: Secondary outcomes, including changes in recovery quality post-surgery, will be evaluated using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC-QLQ-C30) and the Quality of Recovery Questionnaire (QOR-40). Additional recorded items will include time to first flatus and feces, daily volume of stomach fluid, time to gastric tube removal, length of hospital stay (LOS), and postoperative complications.

Conclusion: The study will utilize the I-FEED score, a novel tool for assessing GI function, to monitor the impact of a 2-week postoperative rehabilitation exercise program on patients. The primary outcome will focus on improvements in cardiopulmonary capacity following postoperative rehabilitation activities.

Background: Overweight and obesity are the most common high-risk conditions that increase the risk of adverse outcomes during pregnancy, childbirth, and the postpartum period. Dysfunctions in trophoblastic peroxisome proliferator-activated receptor gamma (PPARγ) contribute to a variety of related pregnancy disorders.

Objectives: This study investigated whether PPARγ influences chorionic trophoblast cell damage induced by high glucose (HG) and high lipid (HL) by regulating insulin-like growth factor-1 (IGF-1).

Material and methods: Human trophoblast HTR-8/SVneo cells were exposed to HG and HL conditions to simulate damaged trophoblasts during pregnancy in vitro. Cell Counting Kit-8 (CCK-8) was used to assess cell proliferation. The Scratch test was used to test cell migration. Cell invasion ability was assessed by Transwell assay. ELISA was used to assess the inflammatory factor levels. Glucose, lactic acid, and adenosine triphosphate (ATP) levels were measured using biochemical kits.

Results: High glucose/HL inhibited the proliferation, migration, and invasion of HTR-8/SVneo cells. High glucose and HL increased tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and IL-6 expression while decreasing IL-10 expression. High glucose and HL decreased glucose uptake and ATP levels. High glucose and HL reduced the expressiofns of PPARγ, IGF-1, insulin receptor substrate (IRS) 1, IRS2, GLUT1, and GLUT4. High PPARγ expression promoted cell proliferation, migration, and invasion induced by HG and HL, increased glucose uptake and ATP levels and inhibited inflammation. Low IGF-1 expression inhibited cell proliferation, migration, and invasion under HG and HL conditions, reduced glucose uptake and ATP levels, and increased inflammation. Low IGF-1 expression reversed the effects of PPARγ on HTR-8/SVneo cells under HG and HL conditions.

Conclusions: Peroxisome proliferator-activated receptor gamma alleviated HTR-8/SVneo cell damage induced by HG and HL by regulating IGF-1, suggesting a potentially effective approach for treating gestational obesity.

Background: The variability and disparities in the recommended targets across different international guidelines suggest the optimal oxygen saturation (SpO2) target for acute respiratory failure (ARF) patients be further explored.

Objectives: To explore the association between SpO2 and in-hospital mortality of ARF patients, as well as to determine the optimum SpO2 for ARF patients.

Material and methods: In this cohort study, 3,225 ARF patients were included at the end of the follow-up; among them, and 1,249 patients survived and 1,976 died. The restricted cubic spline (RCS) was drawn to show the nonlinear association between the median SpO2 and the risk of in-hospital mortality of ARF patients and to identify the optimal range of SpO2. Cox regression was applied to identify the association between the median SpO2 and the risk of in-hospital mortality in ARF patients. Kaplan-Meier curves were plotted to identify the in-hospital mortality of ARF patients.

Results: The in-hospital mortality rate was 61.2% in all ARF patients at the end of the follow-up. The median SpO2 was associated with decreased risk of in-hospital mortality of ARF patients after adjusting for confounders (hazard ratio (HR) = 0.95, 95% confidence interval (95% CI): 0.93-0.97). The median SpO2 was non-linearly correlated with the in-hospital mortality of ARF patients. The overall survival (OS) was higher in the 96-98% group. A median SpO2 ≤ 96% was associated with an increased risk of in-hospital mortality in ARF patients accompanied by malignant cancer (HR = 1.55, 95% CI: 1.24-1.94), renal failure (HR = 1.45, 95% CI: 1.24-1.70), chronic obstructive pulmonary disease (COPD; HR = 1.70, 95% CI: 1.27-2.28) and atrial fibrillation (AF; HR = 1.25, 95% CI: 1.02-1.53). The median SpO2 > 98% was associated with an elevated risk of in-hospital mortality in ARF patients accompanied by AF (HR = 1.22, 95% CI: 1.04-1.44).

Conclusions: The median SpO2 was linked to a decreased risk of in-hospital mortality in ARF patients.

Background: Pulmonary metastasectomy (PM) is an important procedure for the treatment of metastatic nodules in the lung. The choice of surgical approach, whether thoracotomy or video-assisted thoracoscopic surgery (VATS), remains controversial in terms of the impact on patient prognosis.

Objectives: This study aimed to evaluate the outcomes and impact on survival of patients undergoing PM with VATS compared to thoracotomy.

Material and methods: A retrospective evaluation of 136 patients who underwent PM between September 2012 and July 2020 was performed. Data on the demographics, primary tumor histopathology, metastatic features, surgical approach, surgical outcomes, and survival status were analyzed. Statistical analyses included descriptive statistics, survival analysis and Cox regression models.

Results: Of the participants, 84 underwent thoracotomy and 52 underwent VATS. The median survival time of thoracotomized patients was 86.6 months, while it was 99.6 months for VATS patients. A gender-specific analysis revealed a significantly longer survival time for female VATS patients compared to thoracotomy. Multivariate analysis showed significant independent effects of specific tumor types and the number of nodes removed on survival. Overall, no significant difference in survival was found between the 2 surgical methods.

Conclusions: Both VATS and thoracotomy are effective and safe options for PM. Video-assisted thoracoscopic surgery may offer advantages, particularly in certain patient groups and tumor types, potentially prolonging survival. Gender-specific analyses suggest a survival benefit of VATS, particularly in women. Further studies are needed to validate these results and optimize surgical decision-making in PM.

Background: Few studies have focused on the relationship between the systemic inflammation response index (SIRI) and the prognosis of elderly patients with acute coronary syndrome (ACS).

Objectives: This study aimed to evaluate the predictive value of the SIRI for predicting 3-year outcomes in patients >60 years old after stent implantation and to assess variables associated with SIRI.

Material and methods: A total of 1,758 patients with ACS who underwent percutaneous coronary intervention (PCI) were enrolled and divided into an older group (n = 960) and a younger group (n = 798) using a cutoff of >60 years. Major adverse cardiac events (MACEs) including all-cause death, nonfatal acute myocardial infarction (AMI) and nonfatal stroke were recorded.

Results: During follow-up, 165 patients experienced 1 or more MACEs. Patients in the older group had a greater incidence of recurrent MACEs and mortality than those in the younger group. The SIRIs were significantly greater in the older group. Multiple linear regression analysis revealed that the level of the SIRI was significantly associated with age, hypertension, diagnosis of AMI, number of diseased vessels, and platelet count. The SIRI was an independent predictive risk factor for MACEs in patients >60 years old. Similar relationships between the SIRI and MACEs were also observed in ACS patients with and without AMI.

Conclusions: The SIRI was an independent predictive risk factor for MACEs in patients aged >60 years with ACS and ACS with or without AMI after stent implantation during 3 years of follow-up. The SIRI can be used as an indicator for identifying high-risk patients for intensive therapy to further reduce MACEs in the PCI era.

Background: In regenerative endodontic procedures (REPs), it is crucial to find effective materials. This study introduces glycosaminoglycan (GAG) mimetic peptide amphiphile (PA, GAG-PA) and K-PA nanofibers, synthesized to emulate sulfated GAGs, aiming to enhance tissue repair within damaged pulp - an area where standardized protocols are currently lacking.

Objectives: The objective of this study was to investigate the regenerative potential of GAG-PA nanofibers in REP.

Material and methods: Heparan sulfate mimicking PAs was designed to develop a bioactive nanofibrous supramolecular system. The cavities on the mesial surfaces of the first upper molars of 8 rats (4 rats in the study group and 4 in the control group) were prepared, and the pulps were perforated. Then, the material was applied onto the dental pulp, and the cavities were closed with a self-curing glass ionomer cement filling material. Physiological saline was used in the control group. Thirty days after application, the teeth were extracted, and the formation of regenerative tissue sections in the pulp was evaluated using hematoxylin and eosin (H&E) staining and Masson's trichrome staining.

Results: After 30 days, H&E staining demonstrated robust tissue regeneration in the implanted region, with minimal neutrophil infiltration. Masson's trichrome staining confirmed reparative dentin formation. Quantitative analysis revealed a regeneration percentage of 85% in the study group, compared to 80% in the control group. Statistical analysis showed no significant difference in regeneration between the groups (p > 0.05).

Conclusions: Our comprehensive study, utilizing GAG-PA and K-PA nanofibers, demonstrated successful synthesis, characterization and formation of nanofiber networks. The in vivo experiment with rats exhibited substantial tissue regeneration with quantifiable results supporting the efficacy of the nanofiber approach. Statistical analysis confirmed the consistency between the study and control groups, emphasizing the potential of these nanofibers in endodontic tissue regeneration applications.

Background: In Poland, there are limited validated outcome measures to evaluate upper extremity function in stroke patients for clinical and research use. The Action Research Arm Test (ARAT) aims to assess functional performance of the upper extremities.

Objectives: To translate and culturally adapt the original version of ARAT into Polish, and to determine its reliability and validity.

Material and methods: A Polish version of ARAT (ARAT-PL) was developed using a forward-backward translation. The study then examined 60 patients with subacute stroke. Internal consistency (α), test-retest and inter-rater reliability (intra-class correlation (ICC), κ), standard error of measurement (SEM), minimal detectable change (MDC), and floor and ceiling effects were determined. The construct validity was evaluated using the method of hypothesis testing based on the results of correlations (rho) between subscale and total scores of the ARAT-PL and the upper and lower extremity section of the Fugl-Meyer Assessment (FMA-UE and FMA-LE).

Results: The internal consistency of the total scores and subscale was excellent (α = 0.97-0.99). Test-retest and inter-rater reliability scores were almost perfect (κ = 0.85-1.0) and excellent for the total and subscale scores (ICC = 0.99-1). The SEM and MDC for the test-retest and inter-rater reliability were 0.479, 1.327 points and 0.335, 0.930 points, respectively. The ceiling effect amounted to 48%. The validity levels with respect to FMA-UE and FMA-LE were found to be high (rho ranging from 0.70 to 0.83) and moderate (rho ranging from 0.53 to 0.68), respectively.

Conclusions: A Polish version of ARAT is a reliable and valid tool for assessing upper extremity function in subacute stroke patients in Poland. However, it appears to have a ceiling effect that limits differentiation of patients with mild upper limb impairment.

Background: The activity of proton pump inhibitors (PPIs) hinders the function of proton pumps that generate stomach acid. Nuclear factor kappa B (NF-κB) is a transcriptional factor engaged in inflammation, immunity and the formation of cancer. The farnesoid X receptor (FXR) is a nuclear receptor that governs the metabolism of bile acids and the metabolic functioning of the liver. The impact of PPIs on the signaling of FXRs and NF-κB is not well understood.

Objectives: We aimed to study the effects of esomeprazole on FXRs and NF-κB signaling in liver cells.

Material and methods: For the liver cell model, we used the human liver cell line HepaG2. Cells were treated with lipopolysaccharides (LPS) and esomeprazole, and then we assessed the effects of esomeprazole on inflammatory and carcinogenic markers, NF-κB and FXR. We applied the techniques of western blotting, reverse-transcription polymerase chain reaction (RT-PCR), confocal microscopic imaging, and electrophoretic mobility shift assay (EMSA).

Results: Lipopolysaccharides-induced FXRs and NF-κB signaling upregulated the NF-κB-associated cytokines interleukin 6 (IL-6), cyclooxygenase-2 (COX-2) and tumor necrosis factor alpha (TNF-α). Esomeprazole inhibited the upregulation of all these cytokines. Additionally, esomeprazole inhibited LPS-induced FXR expression and NF-κB signaling in HepaG2 cells. The net effect on FXRs and NF-κB signaling was the lower levels of the associated inflammatory and carcinogenic cytokines.

Conclusions: Our study provides insight into the potential therapeutic effects of esomeprazole on hepatic inflammation and carcinogenesis by inhibiting LPS-induced NF-κB and FXR expression in HepG2 cells.

Hematological malignancies encompass a diverse group of cancers affecting the blood, bone marrow and lymph nodes. The p16 gene, encoding the P16INK4A protein, plays a pivotal role in cell cycle regulation and tumor suppression. Understanding the involvement of p16 in the development and progression of hematological malignancies is crucial for advancing therapeutic strategies. This systematic review aims to elucidate the multifaceted roles of the p16 gene and P16INK4A protein in hematological malignancies, focusing on their impact on disease pathogenesis, prognostic significance and therapeutic implications. A comprehensive search was conducted across electronic databases, including PubMed, Scopus and Google Scholar, using predefined search terms related to p16, P16INK4A, hematological malignancies, and therapy. Studies published up to 2023 were included, encompassing clinical trials, observational studies, meta-analyses, and preclinical research. The review synthesizes evidence highlighting the dysregulation of the p16 pathway in various hematological cancers. Alterations in p16 expression levels, genetic mutations and epigenetic modifications contribute to disease initiation and progression. Moreover, the prognostic significance of p16 status in predicting therapeutic outcomes and patient survival is explored. The p16 gene and P16INK4A protein emerge as promising biomarkers and therapeutic targets in hematological malignancies. Integrating knowledge of p16 dysregulation into clinical practice holds the potential to optimize treatment strategies, enhance patient outcomes and pave the way for personalized medicine approaches in the management of these challenging diseases.