The morphology of occlusion stump for endovascular recanalization in non-acute vertebral ostial occlusion.

PURPOSE: Non-acute vertebral ostial occlusion (VOO) is a debilitating condition with significant mortality and morbidity rates. However, currently, there is no consensus on the optimal treatment strategy for VOO. This study aims to examine the feasibility, effectiveness, and safety of endovascular recanalization in patients with VOO. METHODS: We conducted a retrospective review of data from 21 consecutive patients with VOO who underwent endovascular recanalization between May 2018 and August 2023. The patients were divided into two groups based on a new angiographic classification proposed by Gao et al. Type I (tapered stump group) included patients with non-acute extracranial vertebral artery ostial occlusion presenting a tapered occlusion stump. Type II (nontapered stump group) consisted of patients with a nontapered occlusion stump. We collected data on recanalization rates, perioperative complications, and follow-up outcomes. RESULTS: Our analysis included data from a total of 21 patients (22 lesions) with a mean age of 64.6 ± 10.6 years. The technical success rate was 66.7 % (14/21), and the rate of periprocedural complications was 14.3 % (3/21). The success rate of transitioning from the tapered stump group to the nontapered stump group was 90.9 % (10/11) and 40 % (4/10), respectively (P = 0.024). The perioperative complication rate for type I and type II patients was 18.2 % (2/11) and 10 % (1/10), respectively. Among these patients, 18 cases underwent endovascular recanalization using transfemoral access, while 3 patients underwent transradial access after failed transfemoral access, with successful outcomes for two patients. CONCLUSIONS: This study suggests that endovascular recanalization may offer a safe, effective, and feasible treatment option for VOO patients. Additionally, the proposed angiographic classification may serve as a useful guide in selecting suitable candidates for surgery.

Identification of Survival-Associated Hub Genes in Pancreatic Adenocarcinoma Based on WGCNA.

Pancreatic adenocarcinoma is one of the leading causes of cancer-related death worldwide. Since little clinical symptoms were shown in the early period of pancreatic adenocarcinoma, most patients were found to carry metastases when diagnosis. The lack of effective diagnosis biomarkers and therapeutic targets makes pancreatic adenocarcinoma difficult to screen and cure. The fundamental problem is we know very little about the regulatory mechanisms during carcinogenesis. Here, we employed weighted gene co-expression network analysis (WGCNA) to build gene interaction network using expression profile of pancreatic adenocarcinoma from The Cancer Genome Atlas (TCGA). STRING was used for the construction and visualization of biological networks. A total of 22 modules were detected in the network, among which yellow and pink modules showed the most significant associations with pancreatic adenocarcinoma. Dozens of new genes including PKMYT1, WDHD1, ASF1B, and RAD18 were identified. Further survival analysis yielded their valuable effects on the diagnosis and treatment of pancreatic adenocarcinoma. Our study pioneered network-based algorithm in the application of tumor etiology and discovered several promising regulators for pancreatic adenocarcinoma detection and therapy.

Fractalkine/CX3CR1 axis modulated the development of pancreatic ductal adenocarcinoma via JAK/STAT signaling pathway.

Pancreatic ductal adenocarcinoma (PDAC) is a fatal malignancy with an estimated 5 year survival rate of approximately 5% of all stages combined. High potential of PDAC metastasis is a leading cause for high mortality and poor prognosis. The majority of patients present with distant metastasis at diagnosis. Fractalkine (FKN) is recognized as a chemokine and a specific ligand of CX3CR1. It has been reported that FKN/CX3CR1 system was upregulated in many types of solid tumors. However, role of FKN/CX3CR1 in PDAC development remains unclear. In the current investigation, we found that FKN and CX3CR1 expression was significantly increased in PDAC tissues, especially in the metastatic samples, and was highly-correlated with severity of PDAC. Ectopic expression of FKN promoted the proliferation and migration of PDAC, while knockdown of CX3CR1 reversed the function of FKN. In addition, PDAC cells with FKN-deficiency showed impaired proliferation and migration activity. The underlying mechanism is that FKN/CX3CR1 activated JAK/STAT signaling, which in turn regulated cell growth. Consistently, in vivo tumorigenesis assay validated the regulatory role of FKN/CX3CR1 in PDAC growth. Our investigation helped understanding the pathogenesis of PDAC occurrence, and demonstrated critical role of FKN/CX3CR1 in PDAC development.

Electrocardiographic, cardiac enzymes, and magnesium in patients with severe acute pancreatitis.

Severe acute pancreatitis (SAP) can lead to multiple-organ dysfunction syndrome (MODS). Electrocardiographic (ECG), cardiac enzyme, and serum magnesium abnormalities occur after SAP. Electrocardiographic and cardiac enzyme abnormalities are described as variables in SAP patients, which contribute to the effects of MODS. Hypomagnesium is also closely associated with ECG abnormalities; therefore, hypomagnesium was also considered to be a variable in this study. A consecutive series of 54 patients admitted within 72 hours after SAP occurred was studied. A standard 12-lead ECG, cardiac enzyme, and serum magnesium measurement were routinely performed at admission. Linear correlation was used to analyze the relationship between hypomagnesemia and sinus tachycardia. The nonparametic binomial test was used to analyze dichotomized dependent variables (premature beat, atrial fibrillation, ST-segment depression, abnormal T wave, and long QT interval). Hypomagnesemia was present in 15 patients (28%), who subsequently had sinus tachycardia. There was a significant negative relationship (-1 < r <0) between hypomagnesemia and sinus tachycardia (p < .05). There were 14 (17%) premature beat, 7 (8%) atrial fibrillation, 21 (25%) ST-segment depression, 18 (21%) abnormal T wave, and 17 (31%) long QT-interval events in 54 SAP patients. Hypomagnesemia is a reason for ECG abnormalities. Electrocardiographic and cardiac enzyme abnormalities are considered to be transitory variables that are present in patients with SAP.