European review for medical and pharmacological sciences最新文献

Objective: This study aimed to investigate the effect of psoralidin, a natural phenolic coumarin compound, on MK-801-induced neurotoxicity that may cause Alzheimer's disease and to determine the phosphodiesterase (PDE)-related molecular mechanism of action.

Materials and methods: In this study, neurotoxicity was performed using the MK-801 in the HT-22 cell line. The effects of compounds on the proliferation of HT-22 cells were determined by Real-Time Cell Analysis (RTCA). After measuring the total protein concentration, the PDE4A protein level was determined using the Western blot method.

Results: Psoralidin (100, 200, 400 µM) has been shown to have a neuroprotective effect against MK-801-induced neurotoxicity, as indicated by Real-Time Cell Analysis. In HT-22 cells, the half maximal effective concentration (EC50) value of psoralidin was calculated to be 230.4 µM, IC50 value of MK-801 was calculated to be 62.4 µM at 24 hours. It has been determined that psoralidin (200, 400 µM) inhibits PDE4A by using the Western blot method.

Conclusions: This research uncovers that psoralidin has neuroprotective effects in MK801-associated accumulation of the excitatory amino acid glutamate neurodegeneration and Alzheimer's disease.

The article "Aldose reductase inhibitor Epalrestat alleviates high glucose-induced cardiomyocyte apoptosis via ROS" by X. Wang, F. Yu, W.-Q. Zheng, published in Eur Rev Med Pharmacol Sci 2019; 23 (3 Suppl): 294-303-DOI: 10.26355/eurrev_201908_18660-PMID: 31389594 has been retracted by the Editor in Chief. The authors contacted the journal in June 2024, requesting to withdraw the article. Following this request, the journal discovered that the article was commented on PubPeer (link: https://pubpeer.com/publications/DE4E22B2B9E506EDC2E650C58152E0). The journal started an investigation and asked the authors to provide answers to the concerns raised as well as to send the raw data. Following the journal's requests, the authors neither responded nor provided the raw data. The journal's investigation revealed duplications between panels Blank, HG+1 umol/l, and HG+10 umol/l of Figure 4A. Consequently, the Editor in Chief mistrusts the results presented and has decided to retract the article. This article has been retracted. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18660.

Objective: This study aimed to investigate the expression levels of the MKNK2 gene in pan-cancer, its prognostic significance, and its relationship with the tumor immune microenvironment, as well as to assess its potential as an immunological and prognostic biomarker.

Materials and methods: The research utilized data from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and Cancer Cell Line Encyclopedia (CCLE), including clinical and mutational information. Bioinformatic tools were employed to analyze the association of MKNK2 with carcinogenesis, including its links to prognosis, immune cell infiltration, tumor immune microenvironment, gene mutation, and the stemness of various tumor cells. A variety of statistical software and analytical tools were applied, including R software, SPSS 27.0, TIMER, CIBERSORT algorithm, and EPIC algorithm.

Results: The study found that MKNK2 is abnormally expressed in pan-cancer and is associated with a poor prognosis. The levels of MKNK2 are highly related to immune cell infiltration and tumor stemness. Notably, in liver hepatocellular carcinoma, glioblastoma multiforme, low-grade gliomas, and acute myeloid leukemia, MKNK2 expression shows a strong correlation with clinical outcomes and immune infiltration. Furthermore, the expression of MKNK2 shows significant correlations with immune cell infiltration, immune checkpoints, tumor mutational burden (TMB), microsatellite instability (MSI), and stemness scores across various cancers.

Conclusions: The abnormal expression of MKNK2 is associated with tumor progression, immune checkpoint genes, immune cell infiltration, microsatellite instability (MSI), tumor mutational burden (TMB), and stemness in a variety of tumors, especially in glioblastoma multiforme low-grade gliomas (GBMLGG). Therefore, MKNK2 may serve as a potent prognostic physiological marker and provide new avenues for the development of tumor mechanisms and therapeutic strategies targeting MKNK2 to enhance the efficacy of immunotherapy.

The Editor in Chief and the Publisher are issuing an expression of concern to alert readers that the following article is under investigation due to a potential ethical breach regarding lack of transparency in the transplantation procedure as outlined in the article published by Rogers W et al (DOI: 10.1136/bmjopen-2018-024473): - Chen J, Zhong L. Clinical significance of serum hepcidin-25 levels in predicting invasive fungal disease in patients after transplantation. Eur Rev Med Pharmacol Sci 2013; 17 (13): 1769-1773-PMID: 23852902. Further updates will be provided once the investigation is completed. The authors have been notified about the ongoing investigation and the publication of this expression of concern.

Objective: Next-generation sequencing (NGS) has been offered as a large-scale and effective genomic analyzing tool. In this research, we seek to examine the possible benefits of an actionable mutation panel in association with clinical and pathological features in the treatment of esophageal cancer.

Patients and methods: In our study, 85 cases whose diagnosis of carcinoma was confirmed histopathologically either by endoscopic biopsy or esophageal surgery between 2010 and 2020 were identified from the hospital database. In formalin-fixed, paraffin-embedded tumor samples, a total of 20 genes of AKT1, ALK, BRAF, DDR, EGFR, ERBB2, ERBB3, ESR1, FGFR1, KIT, KRAS, MAP2K1, MET, NRAS, NTRK, PDGFRA, PIK3CA, PTEN, RICTOR and ROS1 were analyzed via NGS for actionable mutations.

Results: Of 85 cases, 47 patients (55.3%) were men and 38 (44.7%) were women, and the mean age of the patients was 58.01±11.45 years. There were substantial distinctions in the variables of pathogenicity of variant, operation type, stage, and both lymphovascular and perineural invasion (p<0.05). Most of the primary tumors were situated in the lower thoracic esophagus (n=23; 27%). PIK3CA variant was the highest in number among the variant types (n=17) and was detected in 41.2% of the lower thoracic tumors. The increases in mutation numbers of >2 were especially concentrated in the lower thoracic esophageal carcinomas.

Conclusions: The utility of an actionable multigene panel revealed the value of a well-designed NGS workflow in the practical use of clinical outcomes via the prediction of responsiveness to therapeutic agents or indications for novel treatment modalities in addition to the estimation of prognosis.

Objective: Standard treatment for adults with acute myeloid leukemia (AML) involves anthracycline and cytarabine, while alternative regimens are necessary for elderly and frail patients. This study aims to compare the effectiveness and safety of various induction regimens in AML patients.

Patients and methods: The retrospective study included 130 adult AML patients treated at a tertiary care center from January 2014 to December 2022. Patients received one of the following induction regimens: anthracycline and cytarabine (n = 82), azacitidine and venetoclax (n = 11), etoposide and cytarabine (n = 22), or reduced-dose anthracycline and cytarabine (n = 15). Data on demographics, clinical characteristics, treatment-related toxicities, and infectious complications were collected. Outcomes included overall survival and remission rates.

Results: The anthracycline and cytarabine regimen demonstrated the highest overall survival rate, although remission rates did not significantly differ among the treatment groups. Patients receiving azacitidine and venetoclax experienced a significantly longer duration of neutropenia. The use of antiviral prophylaxis increased over the study period, reflecting improved management strategies. Infection remained the leading cause of mortality.

Conclusions: Effective management of prolonged neutropenia and infections is crucial for improving patient outcomes. Future research should focus on optimizing prophylactic and infection treatment strategies to further enhance survival in AML.

Objective: End-stage renal disease (ESRD) commonly manifests with disrupted calcium balance, leading to renal osteodystrophy. We posited that variations in the genetic makeup of vitamin D and calcium-sensing receptors, specifically single nucleotide polymorphisms (SNPs), could affect calcium homeostasis. This study aimed to identify the genetic predictors related to vitamin D and calcium-sensing receptors on calcium metabolism using machine learning algorithm analysis in ESRD.

Patients and methods: We conducted a cross-sectional analysis on adults with ESRD. We gathered comprehensive demographic data and medical history. Blood samples were collected to measure SNPs, and a panel of calcium metabolism biomarkers associated with the calcium-sensing receptor and vitamin D receptor. The biomarkers included calcium, phosphate, vitamin D, parathyroid hormone (PTH), sclerostin, procollagen type 1 alpha 1, osteocalcin, and bone-specific alkaline phosphatase. We utilized machine learning algorithms to pinpoint genetic markers predictive of vitamin D deficiency.

Results: We found a notable decrease in serum procollagen type 1 alpha 1 levels among individuals with the CC of rs10190 (related to the calcium-sensing receptor) compared to those with the TT genotype and in those with the TT of rs739837 (pertaining to the vitamin D receptor) compared to the GG genotype. Similarly, the TT genotype of rs10190 was associated with significantly lower serum phosphate levels compared to CC and CT genotypes. Additionally, a lower serum PTH level was noted in individuals with the CT of rs1802757 (calcium-sensing receptor) compared to those with the CC genotype. Our machine learning analysis identified rs2221266 and rs1042636 as the most significant SNPs linked to vitamin D deficiency, demonstrating considerable predictive accuracy.

Conclusions: Our findings indicate that specific single nucleotide polymorphisms in the vitamin D and calcium-sensing receptors significantly influence calcium metabolism biomarkers in ESRD patients. Assessing the clinical implications of these genetic variations is crucial for advancing personalized medicine in renal care.

The article "MiR-299-3p inhibits proliferation and invasion of cervical cancer cell via targeting TCF4" by Y. Yu, J.-D. Zhao, H. Yang published in Eur Rev Med Pharmacol Sci 2019; 23 (13): 5621-5627-DOI: 10.26355/eurrev_201907_18296-PMID: 31298314 has been retracted by the Editor in Chief. Following some concerns raised on PubPeer (link: https://pubpeer.com/publications/4275612B2FA-7C9A9CD7255B791D3A6), the Editor in Chief has started an investigation to assess the validity of the results as well as possible figure manipulation. The journal's investigation revealed data fabrication and several figure manipulations. Specifically, duplications were found within Figures 2C, 2F, 3C, 4A, and 4E. Moreover, Figure 2 (C, D, E), Figure 3C, and Figure 4 (C-D) contained duplications from previously published articles. The authors have been informed about the journal's investigation but remained unresponsive and have not provided the study's raw data. Consequently, the Editor in Chief decided to retract the article. This article has been retracted. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18296.

Objective:   Acute respiratory distress syndrome (ARDS) is a systemic disease with high morbidity and mortality. Dead space fraction (Vd/Vt) represents the volume of air that does not participate in gas exchange and accurately depicts the pathophysiology of ARDS due to ventilation and perfusion mismatch. In this study, we aim to conduct a systematic review and meta-analysis regarding its usefulness for predicting mortality.

Materials and methods: We performed a systematic literature search identifying comparative studies meeting the above criteria from four databases: MEDLINE, clinicaltrials.gov, CENTRAL, and Google Scholar. A statistical meta-analysis was conducted utilizing the "meta" package in R software, with the included studies assessed based on the Newcastle-Ottawa scale.

Results: A total of twelve studies were included and data from over 1,700 patients was collected. Patients with higher levels of Vd/Vt were more likely to not survive with an OR=1.27 [95% CI (1.09, 1.48), I2=93%, p<0.01]. In addition, non-survivors of ARDS had higher mean value levels of Vd/Vt than survivors with an MD=0.07 [95% CI (0.02, 0.11), I2=82%, p<0.01]. Furthermore, a leave-one-out meta-analysis was performed in order to assess the effect of each individual study on the overall outcome, which led to the lowering of heterogeneity to 0.

Conclusions: The Vd/Vt ratio is an accurate index for determining the mortality of ARDS, reflecting the severity of the disease.

Objective: The recently discovered protein adropin is a highly conserved polypeptide that plays critical functions in energy homeostasis, metabolic processes, fat metabolism, and insulin resistance. On the other hand, non-alcoholic fatty liver disease (NAFLD) is a medical condition that causes the buildup of fat in the liver cells in individuals who consume little or no alcohol. The frequency of NAFLD is rising globally, and it is frequently linked to obesity, insulin resistance, type 2 diabetes, and metabolic syndrome. Therefore, this study evaluates the association between adropin levels and insulin resistance in individuals with and without NAFLD.

Materials and methods: Data from Scopus, Science Direct, and PubMed were searched between January 1, 2012, and February 18, 2024, using precise terms and stated criteria. Comprehensive Meta-Analysis V. 2 (Biostat, Englewood, NJ, USA) was used for data analysis, and Random-effect models were used to estimate the pooled mean differences with 95% CIs of adropin level, insulin level, and homeostatic model assessment for insulin resistance (HOMA-IR) associated with the exposures of interest.

Results: Our results revealed that adropin blood levels are significantly reduced in NAFLD patients compared to control individuals. The mean difference in adropin blood levels was 2.391 ng/ml with a 95% CI of 1.127 to 3.656 with I2 99.6. on the other hand, insulin resistance was significantly higher in NAFLD compared to controls (MD: -1.668, 95% CI: -2.333 to -1.002, I2=86%).

Conclusions: Our findings reveal that adropin levels are significantly greater in healthy controls than in NAFLD patients, suggesting that adropin may have a preventative effect on NAFLD. This meta-analysis highlights how closely adropin and insulin resistance interact in non-alcoholic fatty liver disease. Also, it may open the door to new diagnostic tools and therapeutic modalities.