Open Medicine最新文献

Background and aim: Alcohol consumption is a major public health issue, linked to a wide range of physical, psychological, familial, and social harms, as well as increased rates of violence, accidents, and mortality. The aim of this study is to evaluate the effectiveness of a motivational interviewing program in reducing alcohol consumption patterns among Thai patients.

Methods: This quasi-experimental study included a control group (CG) and an experimental group (EG), each consisting of 30 patients. Data were collected using a structured questionnaire and analyzed with SPSS, utilizing both descriptive and inferential statistical methods.

Results: The majority of patients in the CG were aged 45-60 years, whereas the majority in the EG were aged 25-44 years. The intervention involved 4 sessions over 8 weeks motivational interviewing program (MIP). The mean AUDIT scores in the CG were 24.10 before the intervention and 22.90 after, while in the EG, scores decreased from 22.63 to 19.33. The interaction between the factors (CG and EG) before the intervention did not have a significant effect (Multivariate Analysis of Variance, MANOVA: p = 0.255), but was significant after the intervention (MANOVA: p = 0.009).

Conclusion: MIP had a significant effect on reducing alcohol consumption among patients of the EG.

We aimed to investigate the protective effect of luteolin against neuron injury induced by oxygen-glucose deprivation/reoxygenation (OGD/R), and to further elucidate the roles of NLRP3 in luteolin-mediated regulation of neuron injury. Using Schwann (SW) 10 cells, an OGD/R-induced neuron injury model was established, and six experimental groups were designated. Subsequently, cell viability and apoptosis were respectively detected by cell counting kit 8 and flow cytometry. Reactive oxygen species (ROS) levels were measured via flow cytometry with a ROS assay kit. Moreover, the expression of interleukin (IL)-6, IL-1β, NLRP3, and MMP9 was examined by real-time quantitative PCR and Western blot. Compared with control cells, OGD/R significantly reduced cell viability and increased apoptosis, ROS levels, and the mRNA levels of IL-6, IL-1β, NLRP3, and MMP9. Luteolin significantly enhanced OGD/R-induced cell viability and alleviated apoptosis in SW10 cells (P < 0.05). Additionally, luteolin suppressed ROS levels, along with the expression of IL-1β, IL-6, NLRP3, and MMP9 induced by OGD/R. Furthermore, BMS-986299 significantly decreased the cell viability and increased the expression of inflammatory factors in OGD/R-induced SW10 cells treated with luteolin. This inhibitory effect was reversed by NLRP3 knockdown. In conclusion, luteolin may exert a protective effect on OGD/R-induced nerve injury by inhibiting the NLRP3/IL-1β signaling pathway.

Background: Thyroid cancer is the most common malignancy of the endocrine system, and effective treatments for metastatic disease are still lacking. Targeting both glycolysis and oxidative phosphorylation (OXPHOS) simultaneously represents a novel approach to cancer therapy. While polyphyllin has been shown to modulate cellular metabolism in various cancers, its role in thyroid cancer remains unexplored.

Purpose: This study aimed to explore the antitumor effects and underlying mechanisms of polyphyllin in thyroid cancer.

Methods: Thyroid cancer cells were treated with varying concentrations of Polyphyllin I, II, VI, and VII. Cell viability was assessed using the CCK-8 assay to identify the most effective polyphyllin compound and its optimal dosage. Colony formation and EdU incorporation assay were performed to evaluate cell proliferation, while Transwell assays were used to assess cell invasion. Cell migration ability was examined using the wound healing assay. The effect of Polyphyllin II on OXPHOS was evaluated using an extracellular oxygen consumption rate (OCR) assay kit. Glucose uptake, lactate production, glycolysis-related protein expression, and the extracellular acidification rate (ECAR) were measured to assess the effects of Polyphyllin II on glycolysis in thyroid cancer cells. Flow cytometry and western blotting were conducted to detect apoptosis.

Results: Polyphyllin I, II, VI, and VII all inhibit the proliferation of thyroid cancer cells, with Polyphyllin II showing the most potent inhibitory effect. Polyphyllin II suppresses cell proliferation, invasion, and migration of thyroid cancer cells, while also promoting apoptosis. Mechanism studies reveal that Polyphyllin II inhibits extracellular OCR, basal respiration, maximum respiration, ATP-linked respiration, spare respiration capacity, glucose uptake, lactate production, glycolytic rate-limiting enzymes, and the ECAR in thyroid cancer cells.

Conclusion: Polyphyllin II simultaneously inhibits glycolysis and OXPHOS, thereby suppressing the invasion, migration, and proliferation of thyroid cancer cells, while also promoting apoptosis.

Background: Some observational studies have reported that sodium-glucose cotransporter 2 (SGLT2) inhibitors may have an impact on psychiatric disorders. This Mendelian randomization (MR) study aims to explore the causal relationship between SGLT2 inhibition and five types of psychiatric disorders.

Methods: Genetic variants associated with the SLC5A2 gene and glycated hemoglobin were selected from the eQTLGen Consortium and Genotype-Tissue Expression datasets. Type 2 diabetes served as a positive control in the application of MR and colocalization analyses to investigate potential causal relationships between SGLT2 inhibition and depression, anxiety disorder, schizophrenia, obsessive-compulsive disorder, and bipolar affective disorder. The impact of glycated hemoglobin on psychiatric disorders was additionally analyzed.

Results: SGLT2 inhibition was associated with an increased risk of anxiety disorder, obsessive-compulsive disorder, and bipolar affective disorder. The effect of SGLT2 inhibition on depression did not reach Bonferroni-corrected significance levels. No association was found between SGLT2 inhibition and schizophrenia.

Conclusions: This study provides genetic evidence supporting that SGLT2 inhibitors increase the risk of obsessive-compulsive disorder, anxiety disorder, and bipolar affective disorder.

[This retracts the article DOI: 10.1515/med-2023-0627.].

[This retracts the article DOI: 10.1515/med-2023-0710.].

Despite significant advances in the diagnosis and treatment of gastric cancer (GC), its incidence and mortality remain high worldwide. Therefore, finding new anticancer drugs or treatment strategies for GC is crucial. The valdien ligand, which is not soluble in water, has demonstrated potential anticancer effects on cancer. This study highlights a water-soluble derivative of the H2valdien ligand derivatives, named H2valdien3, which can inhibit the proliferation of GC by arresting the cell cycle and inducing apoptosis. Initially, the inhibitory effects and cytotoxicity of H2valdien3 on the growth of AGS and MKN45 cells were evaluated using MTT assays. Microscopic observations revealed that H2valdien3-treated AGS and MKN45 cells exhibited deteriorated morphology. Hoechst fluorescent staining and flow cytometry results further demonstrated that H2valdien3 promotes apoptosis and arrests the cell cycle in GC cells. Additionally, the anticancer mechanism of H2valdien3 was found to involve the β-catenin/c-myc pathway. In vivo experiments showed that H2valdien3 inhibited GC proliferation without significantly affecting the weight of the mice. These findings suggest that the transformed H2valdien3 has potential anticancer properties with minimal side effects for GC treatment.

Background: Papillary thyroid carcinoma (PTC) generally exhibits favorable prognosis; however, a subset of patients remains at risk for recurrence. Serine protease 2 (PRSS2) was an oncogenic factor in several solid tumors, yet its expression profile and functional role in PTC remain poorly defined. This study aimed to investigate the expression level of PRSS2 in PTC and its prognostic significance, as well as explore its potential involvement in immune regulatory mechanisms.

Methods: PTC specimens from thyroidectomy patients were analyzed by transcriptomic analysis, quantitative real-time PCR, and immunohistochemistry. Differential gene expression and survival analyses were performed by integrating data from TCGA and GEO databases. Pearson correlation analysis was utilized to evaluate associations between PRSS2 and immune-related genes.

Results: PRSS2 was upregulated in PTC tissues. High PRSS2 expression was associated with better survival (HR = 3.253; 95% CI: 1.155-9.160), especially in patients aged ≥62 and stage II/III. Patients with low PRSS2 and high BRAF expression exhibited a markedly reduced 5-year overall survival rate. PRSS2 also showed significant positive correlations with multiple immune-related genes, including a moderate to strong correlation with T-cell receptor beta variable (TRBV) region genes (R = 0.58-0.72), CD40, and transforming growth factor beta-stimulated clone 22 domain 1.

Conclusions: PRSS2 is upregulated in PTC and is associated with favorable prognosis. Its association with TRBV and other immune-related genes suggests a correlation with tumor immune microenvironment. Further studies are needed to elucidate the biological functions of PRSS2 in PTC and to assess therapeutic potential.

Background: Any variance of the normal coronary vasculature is regarded as a coronary artery anomaly (CAA). An atypical left coronary artery arising from the right aortic sinus of Valsalva has been identified as the rarest CAA and the second leading cause of sudden cardiac death (SCD) in young people. Prompt identification of the anomalous vessel is essential to mitigate early mortality risk.

Case summary: A 33-year-old male, ex-smoker presented with exertional breathlessness and retrosternal chest tightness for the past 1 year. Past history also revealed a significant decline in his exercise tolerance. His initial work-up, which included a resting electrocardiogram and echocardiogram were within normal limits. His exercise tolerance test however, was discontinued early due to the onset of symptoms, and his exercise stress echocardiogram proved positive for angina at a low workload. The cardiac computed tomography angiography revealed a common origin for the left and right coronary systems from the right ostium, with the left main stem following an inter-arterial course and showing mild, diffuse narrowing. The patient was green-lit for coronary artery bypass grafting (CABG). Post recovery and almost 2 years on, he has remained symptom-free and has regained his physical activity.

Conclusion: This case underlines the need for prompt identification and subsequent management of anomalous coronary arteries, given their association with SCD. Timely surgical intervention such as CABG can greatly mitigate the risk of grievous complications. The patient's complication-free postop recovery and resumption of physical activity, assures the reader that it is a viable and durable option with long-term quality of life improvement.

Cancer is the second biggest cause of death after cardiovascular disorders and its incidence is rising significantly. One out of every ten cancer-related deaths is caused by colon cancer. The increasing incidence calls for creating focused therapeutic strategies with fewer adverse effects than traditional clinical techniques like radiation, chemotherapy, and immunotherapy. In this study, we evaluated the anticancer effects and mechanisms of a synthesized and characterized benzofuran ring-linked 3-nitrophenyl chalcone derivative, [1-(2-benzofuranyl)-3-(3-nitrophenyl)-2-propen-1-one], on colon cancer cells (HCT-116 and HT-29) as well as healthy colon cells (CCD-18Co). Cell viability analyses using the sulforhodamine B assay demonstrated that the IC₅₀ values after 48 h of treatment were 1.71 µM for HCT-116, 7.76 µM for HT-29, and higher than 10 µM for CCD-18Co cells. These results indicate a selective cytotoxic effect on cancer cells an essential criterion for evaluating anticancer compounds. Triple fluorescence staining, flow cytometry caspase 3/7 activity, along with protein expression analyses, confirmed that the compound induces apoptosis in both cancer cell lines. At IC₅₀ values, the derivative activated DR-4-mediated apoptosis at the membrane and BCL-2-mediated apoptosis intracellularly. Moreover, treatment with 12.5 µM of the compound for 24 h, corresponding to a cell cycle time, statistically significantly arrested the cell cycle at the G0/G1 phase. In addition, it inhibited cell migration and colony formation in a dose-dependent manner, starting from values as low as 1.56 µM. Additionally, the binding affinity of the derivative with target proteins was determined using artificial intelligence-assisted molecular modeling analysis. Collectively, these findings highlight the potential of this 3-nitrophenyl chalcone derivative as a promising candidate for the development of novel therapeutic agents against colon cancer.