Spinal cord injury (SCI) significantly impacts the central nervous system, with limited effective treatments available. Brain-derived neurotrophic factor (BDNF) plays a crucial role in neuronal growth, survival, and regeneration after SCI. MicroRNAs, particularly miR-124-3p, have been implicated in SCI pathophysiology. However, the relationship between miR-124-3p and BDNF in the context of SCI remains unclear. This study aimed to investigate the correlation between miR-124-3p expression and BDNF levels in a rat model of spinal cord injury and to assess how the timing of injury affects this relationship.

This study included 72 male Wistar rats divided into three groups: intact (n = 8), sham (n = 32), and SCI (n = 32). SCI diagnosis was confirmed through behavioral-motor function analysis using the Basso, Beattie & Brenham score and histological examination with crystal violet staining. The expression levels of miR-124-3p and BDNF were assessed using real-time polymerase chain reaction in all groups at four time points (one hour, one day, three days, and seven days post-injury).

In the SCI group, a marked reduction in miR-124-3p expression was observed relative to both the sham and intact groups. Conversely, there was a substantial elevation in BDNF expression within the SCI group in comparison to the sham and intact groups. The findings underscore a negative association between miR-124-3p expression and BDNF messenger RNA levels.

The downregulation of miR-124-3p and concurrent upregulation of BDNF suggest a potential regulatory role of miR-124-3p in modulating BDNF expression during SCI. These findings provide new insights into the molecular mechanisms underlying SCI and suggest that miR-124-3p and BDNF could serve as potential therapeutic targets. Further research is needed to explore the translational potential of these findings for developing novel diagnostic and therapeutic strategies for SCI.

Endometrial cancer is a common malignant tumor of the female reproductive system, and its incidence is increasing worldwide. The underlying causes of endometrial cancer are multifactorial. In recent years, the role of diet and lifestyle has received considerable attention and has become a key area of research for cancer prevention. Available literature suggests that different dietary patterns, such as the Mediterranean diet or a plant-based diet, along with moderate physical activity, are associated with a reduced risk of this cancer. Despite these findings, significant gaps in knowledge remain, particularly regarding the specific foods, lifestyle choices, and mechanisms of action that can help mitigate the risk of cancer. Furthermore, the effects of cultural and genetic differences among subpopulations make this issue even more complex. In this context, this review aimed to assess the existing literature on the potential role of diet and lifestyle factors in preventing endometrial cancer, evaluate the available data, and highlight areas that require further investigation to provide concrete evidence and recommendations for prevention.

There are no intraepithelial eosinophils present in the normal esophageal mucosa. It is well established that gastroesophageal reflux disease (GERD) and eosinophilic esophagitis (EoE) individually can result in esophageal eosinophilia and that the two disorders frequently coexist in the same patient. Nevertheless, the first step in the diagnostic algorithm for patients with esophageal symptoms associated with esophageal eosinophilia is to exclude non-EoE disorders that can cause esophageal eosinophilia, including GERD. While it is clear that GERD without EoE can cause low-level esophageal eosinophilia, it is less clear whether GERD alone can induce EoE-level esophageal eosinophilia (i.e., ≥15 eosinophils per high-power field). In this report, we have reviewed mechanisms by which reflux might induce eosinophilia in the esophagus and assessed studies suggesting that GERD alone can induce EoE-level esophageal eosinophilia. Studies on the latter issue have suffered from numerous shortcomings, including the use of outmoded or dubious methods for identifying GERD. Many of these studies were published prior to the realization that EoE can respond to proton pump inhibitor treatment. Our review of these studies suggests that GERD alone rarely, if ever, causes EoE-level eosinophilia (perhaps <1% of cases). For patients with definitive evidence of GERD associated with EoE-level esophageal eosinophilia but without endoscopic or clinical features of EoE, it is impossible to determine whether the eosinophilia is caused solely by GERD, by underlying but unrelated EoE that does not manifest typical features, or by EoE driven by GERD-induced defects, such as impaired esophageal barrier function. Until better diagnostic tests for EoE become available, this situation will remain a clinical conundrum.

Fat mass and obesity-associated protein (FTO) has been linked to various cancers, though its role in hepatocellular carcinoma (HCC) remains unclear. This study aimed to investigate FTO expression, its clinical relevance, functional role in HCC progression, and the underlying molecular mechanisms.

Quantitative reverse-transcription polymerase chain reaction and immunohistochemical analysis were used to assess FTO expression in HCC. Functional assays, including proliferation, invasion, and epithelial-mesenchymal transition studies, were conducted using HCC cell lines with FTO knockdown. N6-methyladenosine (m6A) RNA immunoprecipitation and RNA stability assays further elucidated the role of FTO in BUB1 mRNA methylation and stability. Co-immunoprecipitation studies were employed to confirm the interaction between BUB1 and TGF-βR1. In vivo studies in nude mice were conducted to evaluate tumor growth following FTO knockdown.

FTO was significantly upregulated in HCC tissues compared to normal liver tissues, with higher expression observed in advanced tumor-node-metastasis stages and metastatic HCC. Elevated FTO correlated with poor overall survival in patients. Silencing FTO decreased HCC cell proliferation, colony formation, invasion, epithelial-mesenchymal transition, and tumor growth in nude mice. Mechanistically, FTO downregulation led to increased m6A modification of BUB1 mRNA, thereby promoting its degradation via the YTH domain family 2-dependent pathway and reducing BUB1 protein levels. Additionally, BUB1 physically interacted with TGF-βR1, activating downstream TGF-β signaling.

FTO is overexpressed in HCC and is associated with poor clinical outcomes. Mechanistically, FTO promotes HCC progression by stabilizing BUB1 mRNA through an m6A-YTH domain family 2–dependent pathway, which activates TGF-β signaling. Targeting the FTO–BUB1–TGF-βR1 regulatory network may offer a promising therapeutic strategy for HCC.

Ectopic or heterotopic pancreases are normal pancreatic tissues located outside the pancreas. The ectopic pancreas has its own vascular and ductal systems and does not communicate with the normal pancreas. The prevalence of ectopic pancreas ranges from 0.6% to 15% among all autopsies. Many types of tumors, including intraductal papillary mucinous neoplasms (IPMNs), have been reported in the ectopic pancreas. However, little is known about the synchronous occurrence of IPMNs in both ectopic and orthotopic pancreas. In this study, we report, for the first time, two cases of concurrent IPMNs in an ectopic pancreas and an orthotopic pancreas. One patient had IPMNs both in the pancreas and in ectopic pancreatic tissue in the jejunum. Another patient had IPMNs in both the pancreas and ectopic pancreatic tissue in the duodenum. These cases may provide valuable insights into the etiological factors of IPMNs.

Human papillomavirus (HPV) infection is the primary cause of cervical, anogenital, and oropharyngeal cancers in the United States. These cancers are preventable through HPV vaccination. Research is critically needed to identify effective strategies for promoting HPV vaccination among high-risk groups. This study develops a risk prediction model to identify patients who are unlikely to complete HPV vaccination, with the goal of using the model to direct resources and increase vaccination rates.

We assessed vaccination status along with patient, provider, and clinic characteristics that predict vaccination completion. We then developed a predictive model to assess the likelihood of completing HPV vaccination, which can be used to target interventions based on patient needs. We used a retrospective cohort from a large integrated delivery system in Oregon. Using logistic regression with data available in the electronic health record, we created a risk model to determine the likelihood of vaccination completion among patients aged 11–17 years.

In a cohort of 61,788 patients, 40,570 (65.7%) had received at least one dose of the HPV vaccine. The full model included 17 demographic, clinical, provider, and community characteristics, achieving a bootstrap-corrected C-statistic of 0.67 with adequate calibration. The reduced model, which retained five demographic and clinical characteristics (age, language, race, ethnicity, and prior vaccinations), had a bootstrap-corrected C-statistic of 0.65 and adequate calibration.

Our findings suggest that a risk prediction model can guide the implementation of targeted interventions and the intensity of those interventions based on the likelihood of vaccination completion.

Extrahepatic portosystemic shunts (EPS) are abnormal connections between the portal and systemic circulations. Acquired EPS occur most commonly in adults and are usually associated with portal hypertension due to cirrhosis. Acquired EPS cases can be further subdivided into two types: variceal (pre-existing) EPS and non-variceal EPS (NVEPS). Variceal EPS arise from originally small vessels with pre-existing dual portal and systemic drainage. Due to elevated portal pressure, these vessels dilate and undergo a reversal of flow, sending blood back to the systemic circulation. A much less common and, therefore, underappreciated subset of acquired EPS is NVEPS, which consists of aberrant connections that did not previously exist between the portal vein and large systemic vessels, usually in the presence of portal hypertension. Neoangiogenesis results in the development of abnormal anastomoses between the portal vein and other large veins, resulting in splenorenal, gastrorenal, portocaval, and mesocaval shunts. While not uncommon, they are frequently overlooked in the diagnosis and treatment of portal hypertension and can pose significant diagnostic and therapeutic challenges. Because the treatment of variceal EPS and NVEPS can differ markedly, it is important to correctly diagnose NVEPS and institute appropriate management. The aim of this article was to review acquired EPS, with particular attention to NVEPS, updating the pathogenesis, diagnosis, and treatment.

Prostate cancer is the second most diagnosed cancer in men worldwide and a significant cause of cancer-related death. Proteogenomic analysis offers insights into how genomic mutations influence protein expression and can identify novel biomarkers. This study aimed to investigate the impact of missense mutations on protein abundance in prostate cancer versus healthy tissues using SILAC-based quantitative proteomics.

Mass spectrometry data from prostate tumors and adjacent healthy tissues were analyzed using stable isotope labeling. Peptides were classified based on their abundance into RefSeq and Variant Abundant groups. Missense mutations were mapped via RefSeq and dbPepVar databases. Protein intensity metrics were compared, and Spearman’s correlation was used to evaluate the relationship between mutation presence and protein abundance.

Functional enrichment revealed that RefSeq Abundant proteins are involved in normal metabolic and structural functions, while Variant Abundant proteins are enriched in tumor-related pathways such as immune evasion and apoptosis suppression. A significant negative correlation was found between protein intensity difference and ratio (p < 0.05), indicating that missense mutations contribute to altered protein expression. Mutation hotspot analysis identified recurrent alterations in genes such as PPIF and ACTB. PROVEAN was used to evaluate the functional impact of variants, identifying several as deleterious to protein stability and function.

Missense mutations are associated with altered protein abundance and may promote oncogenic processes in prostate cancer. These findings enhance the understanding of genome-proteome interactions and could support the development of targeted biomarkers and therapies.