The diagnosis of acute ischemic stroke (AIS) can be challenging when neuroimaging findings are normal or equivo‑ cal. Neutrophil extracellular traps (NETs), particularly histone H3.1, have potential as biomarkers for AIS. This study evaluated NETs, specifically histone H3.1, as diagnostic biomarkers for AIS. This prospective study included 89 patients with AIS and 20 healthy controls. Plasma histone H3.1 levels were measured using the Nu.Q® H3.1 enzyme-linked immunosorbent assay (ELISA). Seven cytokines were analyzed using a bead-based immunoassay. Statistical analy‑ ses were used to compare histone H3.1 levels between groups and evaluate correlations with clinical parameters and cytokines. Histone H3.1 levels were significantly higher in patients with AIS (271.05 ± 33.40 ng/mL) versus controls (95.33 ± 12.86 ng/mL, p < 0.001). Multivariable logistic regression identified H3.1 as an independent risk factor for AIS (p = 0.006), with an area under the curve of 0.907. Significant correlations were found between H3.1, interleukin-6 (0.290, p = 0.013) and vascular cell adhesion molecule 1 (0.297, p = 0.011). In conclusion, the NETs H3.1 ELISA test is a reliable new diagnostic option that supports the diagnosis of AIS.

The diagnosis of acute ischemic stroke (AIS) can be challenging when neuroimaging findings are normal or equivo‑ cal. Neutrophil extracellular traps (NETs), particularly histone H3.1, have potential as biomarkers for AIS. This study evaluated NETs, specifically histone H3.1, as diagnostic biomarkers for AIS. This prospective study included 89 patients with AIS and 20 healthy controls. Plasma histone H3.1 levels were measured using the Nu.Q® H3.1 enzyme-linked immunosorbent assay (ELISA). Seven cytokines were analyzed using a bead-based immunoassay. Statistical analy‑ ses were used to compare histone H3.1 levels between groups and evaluate correlations with clinical parameters and cytokines. Histone H3.1 levels were significantly higher in patients with AIS (271.05 ± 33.40 ng/mL) versus controls (95.33 ± 12.86 ng/mL, p < 0.001). Multivariable logistic regression identified H3.1 as an independent risk factor for AIS (p = 0.006), with an area under the curve of 0.907. Significant correlations were found between H3.1, interleukin-6 (0.290, p = 0.013) and vascular cell adhesion molecule 1 (0.297, p = 0.011). In conclusion, the NETs H3.1 ELISA test is a reliable new diagnostic option that supports the diagnosis of AIS.

The diagnosis of acute ischemic stroke (AIS) can be challenging when neuroimaging findings are normal or equivo‑ cal. Neutrophil extracellular traps (NETs), particularly histone H3.1, have potential as biomarkers for AIS. This study evaluated NETs, specifically histone H3.1, as diagnostic biomarkers for AIS. This prospective study included 89 patients with AIS and 20 healthy controls. Plasma histone H3.1 levels were measured using the Nu.Q® H3.1 enzyme-linked immunosorbent assay (ELISA). Seven cytokines were analyzed using a bead-based immunoassay. Statistical analy‑ ses were used to compare histone H3.1 levels between groups and evaluate correlations with clinical parameters and cytokines. Histone H3.1 levels were significantly higher in patients with AIS (271.05 ± 33.40 ng/mL) versus controls (95.33 ± 12.86 ng/mL, p < 0.001). Multivariable logistic regression identified H3.1 as an independent risk factor for AIS (p = 0.006), with an area under the curve of 0.907. Significant correlations were found between H3.1, interleukin-6 (0.290, p = 0.013) and vascular cell adhesion molecule 1 (0.297, p = 0.011). In conclusion, the NETs H3.1 ELISA test is a reliable new diagnostic option that supports the diagnosis of AIS.

Traumatic neuroma (TN), also known as amputation neuroma, is a reactive hyperplasia of nerve fibers and connective tissue arising from Schwann cells after trauma or surgery. TN of the bile duct is usually asymptomatic, but rarely can lead to right upper quadrant pain, biliary obstruction, and acute cholangitis. It is very difficult to discriminate TN from malignancy before surgery, although doing so could avoid an unnecessary radical resection of the lesion. In the course of surgery, TN can be caused by unintentional injury of a nerve fiber near the common bile duct (CBD) and heat damage to an artery, complete ligation of an artery, and excessive manipulation of the CBD. Therefore, to prevent TN after cholecystectomy, surgery should be performed carefully with appropriate consideration of anatomic variations, and a cystic duct should not be resected too close to the CBD. The possibility of TN should be considered if a patient who has undergone CBD resection with hepaticojejunostomy or cholecystectomy long ago experiences symptoms of jaundice, cholangitis, or obliteration of the CBD. In this report, we present a case of TN mimicking cholangiocarcinoma that emerged from a cystic duct stump after cholecystectomy.