Dysphagia is considered to be a significant barrier for recovery after lateral medullary infarction (LMI). However, there is still no gold standard treatment for dysphagia. The aim of this study was to explore an effect of an early treatment options for swallowing dysfunction after acute LMI. Medical records of acute LMI patients who had been admitted to the department of rehabilitation medicine from January 2014 to December 2017 were reviewed retrospectively. We compared the clinical efficacy of conventional dysphagia rehabilitation to early endoscopic intervention using either botulinum toxin injection into cricopharyngeal muscle or endoscopic balloon dilatation of the muscle. Outcomes, such as duration of parental feeding, albumin level at diet transition to enteral feeding, and complications, were analyzed. A total of 18 patients with LMI were included. While eight patients (8/9, 88.89%) in the endoscopic group were capable of orally ingesting their diet after intervention, the conversion from tube feeding to an oral diet was possible in only five patients (5/9, 55.56%) of the conventional group during hospitalization. However, the difference between the two groups was not significant (p-value ≤ 0.147, chi-square test). Only the final dietary level at the time of discharge was higher level in endoscopic group. The conversion interval from tube feeding to oral diet was also comparable between groups. There was no re-conversion from the oral diet to tube feeding in patients of either group during the median follow-up period of 20 months. Early endoscopic intervention may be a better option for dysphagia with LMI, compared to conventional dysphagia rehabilitation. However, a larger and prospective trial may be needed to confirm our observations.

Although the roles of erythroblastic leukemia viral oncogene homolog 2 (ERBB2), neuregulin 4 (NRG4), and mitogen-inducible gene 6 (MIG6) in epidermal growth factor receptor signaling in hepatocellular carcinoma (HCC) and other malignancies have been previously investigated, the prognostic value of their serum levels in HCC remains undetermined. In the present study, correlations between serum levels and tumor characteristics, overall survival, and tumor recurrence were analyzed. Furthermore, the prognostic potential of the serum levels of these biomarkers was evaluated relative to that of alpha-fetoprotein. Both ERBB2 and NRG4 correlated with the Barcelona Clinic Liver Cancer stage, ERBB2 correlated with the tumor-maximal diameter, and NRG4 correlated with a tumor number. Cox proportional hazards regression analysis revealed that ERBB2 (hazard ratio [HR], 2.719; p = 0.007) was an independent prognostic factor for overall survival. Furthermore, ERBB2 (HR, 2.338; p = 0.002) and NRG4 (HR, 431.763; p = 0.001) were independent prognostic factors for tumor recurrence. The products of ERBB2 and NRG4 had a better area under the curve than alpha-fetoprotein for predicting 6-month, 1-year, 3-year, and 5-year mortality. Therefore, these factors could be used to evaluate prognosis and monitor treatment response in patients with HCC.

Background: Pancreatic ductal adenocarcinoma (PDAC), a challenging and malignant cancer, primarily originates from the exocrine cells of the pancreas. The superfamily of solute carrier (SLC) transporters, consisting of more than 450 proteins divided into 65 families, is integral to various cellular processes and represents a promising target in precision oncology. As therapeutic targets, SLC transporters are explored through an integrative analysis. Materials and Methods: The expression profiles of SLCs were systematically analyzed using mRNA data from The Cancer Genome Atlas (TCGA) and protein data from the Human Protein Atlas (HPA). Survival analysis was examined to evaluate the prognostic significance of SLC transporters for overall survival (OS) and disease-specific survival (DSS). Genetic alterations were examined using cBioPortal, while structural studies were performed with AlphaFold and AlphaMissense to predict functional impacts. Furthermore, Gene Set Enrichment Analysis (GSEA) was carried out to identify oncogenic pathways linked to SLC transporter expression. Results: SLC transporters were significantly upregulated in tumors relative to normal tissues. Higher expression levels of SLC39A10 (HR = 1.89, p = 0.0026), SLC22B5 (HR = 1.84, p = 0.0042), SLC55A2 (HR = 2.15, p = 0.00023), and SLC30A6 (HR = 1.90, p = 0.003) were strongly associated with unfavorable OS, highlighting their connection to poor prognosis in PDAC. GSEA highlighted that these four transporters are significantly involved in key oncogenic pathways, such as epithelial–mesenchymal transition (EMT), TNF-α signaling, and angiogenesis. Conclusions: The study identifies four SLCs as therapeutic targets in PDAC, highlighting their crucial role in essential metabolic pathways. These findings lay the groundwork for developing next-generation metabolic anti-cancer treatment to improve survival for PDAC patients.