The Outcome of Sac Filling With Fibrin Sealant and Gentamicin After Endovascular Aortic Repair of Brucella-Related Aorto-Iliac Artery Aneurysms: A Retrospective Single-Center Study.

PURPOSE: This study aimed to analyze the experience of our center and assess the efficacy of sac filling with fibrin sealant (FS) and gentamicin after endovascular aortic repair (EVAR) in patients with Brucella-related aorto-iliac artery aneurysms. MATERIALS AND METHODS: All patients who received sac filling with FS and gentamicin after EVAR for Brucella-related aorto-iliac artery aneurysms between March 2019 and September 2022 were reviewed. Before and after sac filling with FS and gentamicin, aneurysm sac thrombosis and endoleak were evaluated using a preloaded catheter to monitor immediate repair outcome. Short- to mid-term outcomes were assessed by the incidence of vascular graft infection (VGI), all-cause mortality, maximum aneurysm diameter, aneurysm sac thrombosis, and other adverse events. RESULTS: There were 14 patients with Brucella-related aorto-iliac artery aneurysms who underwent sac filling with FS and gentamicin after EVAR. Perioperative death due to myocardial infarction in 1 patient resulted in a postoperative all-cause mortality rate of 7.1% (1/14). All patients received anti-Brucella drugs for a median of 6.0 (range: 3-12) months postoperatively. During a median follow-up period of 15.0 (range 0.5-36) months, the absolute and sagittal maximum diameters of the aorto-iliac aneurysm sac were significantly smaller than preoperation (from 46.3 ± 17.0 to 27.2 ± 16.3 mm, P<.001, and from 39.2 ± 13.1 to 24.0 ± 13.8 mm, P<.001). Two of these patients had a postoperative disappearance of the pseudoaneurysm. One patient was reintervened for bilateral femoral artery bypass surgery. Except for sac filling with gentamicin, all patients received anti-brucella medication for a median of 6.0 (range: 3-12) months. There were no allergic reactions, nephrotoxicity, endoleak, recurrence, VGI, aorta-related or infection-related deaths during the perioperative period and follow-up. CONCLUSIONS: Sac filling with FS and gentamicin adjunctive to EVAR, with targeted drug delivery to the sites of Brucella-related aorto-iliac artery aneurysm infection lesions, may be an effective solution to control pseudoaneurysm infection and rupture. CLINICAL IMPACT: Previous Brucella-associated aorto-iliac artery aneurysms have been limited to case reports. This study significantly increased the number of Brucella-associated aorto-iliac aneurysms by 19.7% (14/71) and extended the follow-up to 3 years. In this retrospective study of 14 patients with Brucella-associated aorto-iliac aneurysms treated endovascularly with fibrin sealant and gentamicin for sac filling and targeted administration to infection-related aneurysms, there were no aneurysm-related deaths or infection-related complications and may be an effective solution for controlling aneurysm infection and rupture. And, this approach is an attractive treatment for moving away from long-term dependence on antibiotics but still needs further evaluation.

Oxidative stress mediates hippocampal neuronal apoptosis through ROS/JNK/P53 pathway in rats with PTSD triggered by high-voltage electrical burn.

BACKGROUND: The pathogenesis of post-traumatic stress disorder (PTSD) triggered by high-voltage electrical burn (HVEB) remains unclear and the oxidative stress plays a role in this process. The purpose of this study is to investigate the underlying mechanism of oxidative stress mediates hippocampal neuronal apoptosis in rats with PTSD triggered by HVEB. MATERIALS AND METHODS: The PTSD rat model was developed by stimulating with high voltage electricity and screened using behavioral performance including Morris water maze (MWM), elevated plus-maze (EPM) and open-field test (OFT). The reactive oxygen species (ROS) generation was measured by DHE fluorescence staining or flow cytometry. Western blotting assay was used to detect the proteins of p-JNK, JNK, P53, PUMA, Bcl-2 and Bax in hippocampal tissue or HT22 cells treated with electrical stimulation. RESULTS: The serum MDA and 8-OHdG levels were increased (P < 0.001), while the activities of SOD and CAT were decreased (P < 0.001) significantly in patients with HVEB. Behavioral test results showed that high-voltage electric stimulation induced the PTSD-like symptoms and the ROS-JNK-P53 pathway was involved in the neuronal apoptosis in rats with PTSD induced by HVEB. In vitro experiments further confirmed the electrical stimulation induced neuronal apoptosis through ROS/JNK/P53 signaling pathway and the antioxidant NAC could rescued the ROS generation, activation of JNK/P53 proteins and improved the cell apoptosis rate in HT22 cells. Finally, the JNK inhibitor SP600125 could significantly inhibited the percentage of HT22 cell apoptosis induced by electrical stimulation (P < 0.001). CONCLUSIONS: These results indicated that oxidative stress mediates hippocampal neuronal apoptosis through ROS/JNK/P53 pathway in rats with PTSD triggered by HVEB.

Incidence and Clinical Features of Venous Thromboembolism in Inpatients with Mental Illness.

AIMS: We investigated the incidence and clinical features of venous thromboembolism (VTE) in inpatients with mental illnesses. METHODS: We retrospectively analyzed records of inpatients with mental illnesses and confirmed VTE at The First Hospital of Hebei Medical University between August 2018 and July 2022. We recorded demographic characteristics, psychosis-related conditions, and thrombus distribution. RESULTS: Among 12939 patients diagnosed with mental illness, 156 (1.21%) presented with VTE at the first visit or during the disease course. Crude VTE incidence varied significantly across mental illnesses, being highest in patients with organic mental disorders (5.20%), followed by emotional disorders (1.10%), and others (P < 0.001). Distal and proximal deep venous thromboses (DVT) occurred in 79.17% and 20.84% of patients, respectively. The Hamilton Depression Scale (HAMD) score was higher in patients with proximal DVT than in those with distal DVT (P < 0.001). On multivariate analysis, the HAMD score (odds ratio [OR] 1.173, confidence interval [CI] 1.100-1.251, P＜0.001) was a risk factor and the Hamilton Anxiety Scale (HAMA) (OR 0.862, CI 0.796-0.934, P＜0.001), a protective factor against DVT progression. CONCLUSION: VTE is not rare in patients with mental illnesses and is most commonly associated with organic mental disorders. Psychosis-related DVT typically shows a significantly high incidence of distal DVT. Prevention and early treatment in patients with severe depression and distal DVT can prevent DVT aggravation.

Crocin ameliorates atherosclerosis by promoting the reverse cholesterol transport and inhibiting the foam cell formation via regulating PPARγ/LXR-α.

Crocin (CRO) is feasible in alleviating atherosclerosis (AS), the mechanism of which was therefore explored in the study. High-fat diet (HFD)-induced apolipoprotein E-deficient (ApoE-/-) mice and lysophosphatidic acid (LPA)-treated macrophages received CRO treatment. Treated macrophage viability was determined via MTT assay. In both murine and macrophage, the lipid level and total Cholesterol/Cholesteryl l Ester (TC/CE) levels were quantified by oil-red-O staining and ELISA, respectively. Lipid droplet, aortic plaque formation and collagen deposition were detected via Oil-red-O staining, hematoxylin-eosin staining and Masson staining, respectively. Liver X Receptor-α (LXR-α), Peroxisome Proliferator-Activated Receptor γ (PPARγ), CD68, PCSK9, CD36, ATP Binding Cassette Subfamily A Member 1 (ABCA1), phosphorylated (p)-AKT, and AKT expressions were detected via Western blot, the former three also being detected using Immunohistochemistry and the first being measured by qRT-PCR. CRO decreased HFD-induced weight gain, ameliorated the abnormal serum lipid levels of HFD-treated mice, and inhibited aortic plaque formation and lipid deposition, and increased collagen fibers, with upregulated high-density lipoprotein-cholesterol (HDL-C) and downregulated TC and low-density lipoprotein-cholesterol (LDL-C). CRO alleviated the HFD-induced upregulations of CD68, PCSK9 and CD36 as well as downregulations of PPARγ/LXR-α, ABCA1 and AKT phosphorylation. In LPA-treated macrophages, CRO alone exerted no effect on the viability yet inhibited the lipid droplets formation and downregulated TC/CE levels. Silent LXR-α reversed the effect of CRO on the lipid droplets formation and levels of lipid metabolism-related factors. CRO ameliorated AS by inhibiting foam cells formation and promoting reverse cholesterol transport via PPARγ/LXR-α.

CA19-9 as a predictor of resectability in patients with borderline resectable pancreatic cancer.

BACKGROUND/AIMS: The aim of the present study was to evaluate whether CA19-9 level related to the curative resection and prevented unnecessary laparotomy in patients with borderline resectable pancreatic cancer. METHODOLOGY: Retrospectively, logistic multivariate regression analysis was used to analyze data from 207 patients who underwent laparotomy for planned surgical resection at West China Hospital, during a 5-year period, and performed to identify CA19-9 levels contributing significantly to surgical resection. Inoperable patients were excluded. RESULTS: Patients with CA19-9 >150U/mL had a frequency of surgical resection 11.7% (14/120) vs. 34.5% (30/87) in those patients with a lower level of CA19-9 (p<0.001). Patients with larger tumor size had a 1.98-fold increased risk of unresectability compared to those with smaller tumor size (p=0.046). Using multivariate analysis adjusted the effects of other factors, high level of CA19-9 and larger tumor size were both considered to be an important risk factor for influencing surgical resection. CONCLUSIONS: CA19-9 should be a good predictor of surgical resection possibility in patients with borderline resectable pancreatic cancer. Furthermore, it is useful in prognosis and optimizing surgical strategy.

[The expressions and correlation of bcl-2 and Beclin-1 in pancreatic cancer].

OBJECTIVE: To investigate the expressions of Bcl-2 and Beclin-1 in pancreatic cancer and analyze the correlation between them. METHODS: The pancreatic tissue samples were collected from each 6 cases of pancreatic cancer, pancreatic exocrine benign tumor, chronic pancreatitis and normal pancreas and marked as group A, group B, group C and group D, respectively. The mRNA expression levels of Bcl-2 and Beclin-1 were detected by real-time fluorescence quantitative PCR and the protein expression levels of Bcl-2 and Beclin-1 were detected through immunohistochemistry. RESULTS: The expression levels of Bcl-2 mRNA and protein, were the lowest in group D and the highest in group A (P < 0.05). The expression levels of Beclin-1 mRNA and protein in group A were significantly lower than those in group B and group D (P < 0.05). However, the expression levels of Beclin-1 between group A and group C were not significantly different (P > 0.05). The correlation coefficient between Bcl-2 and Beclin-1 protein expression in pancreatic cancer is--0.827 (P = 0. 042). CONCLUSION: Compared with normal pancreatic tissue, pancreatic cancer had Bcl-2 expression upregulated and Beclin-1 expression downregulated. The increased anti-apoptotic effect of Bcl-2 and the decreased autophagic effect of Beclin-1 may collaboratively contribute to the occurrence of pancreatic cancer.