Background and purpose Aneurysmal wall enhancement (AWE) has emerged as a new possible biomarker for depicting inflammation of the intracranial aneurysm (IA). However, the relationships of AWE with other risk factors are still unclear for unruptured IA. The purpose of this study was to investigate the association between AWE and other risk metrics. Methods Forty-eight patients with unruptured saccular IAs diagnosed by digital subtraction angiography were recruited to undergo magnetic resonance (MR) black-blood imaging. AWE was evaluated using the pre- and post-contrast black-blood MR images. Univariate and multivariate logistic regression analysis was performed to investigate the association of AWE with other risk factors, including size, maximal neck width, parent vessel diameter, location, multiplicity, daughter sacs and other clinical factors. The prevalence of AWE in each ISUIA grade was reported and compared by Wilcoxon rank sum test. Results In total, 61 aneurysms were detected in 48 patients. Aneurysm size was found to be an independent risk factor associated with AWE (OR 2.46 per mm increase, 95% CI 1.34–4.51; p = 0.004). Patient age was independently and inversely associated with AWE (OR 0.898 per year increase, 95% CI 0.812–0.994; p = 0.037). Higher prevalence of AWE was observed in larger aneurysms (12%, 71.4%, 100%, and 100% of ISUIA grade 1–4 IAs have AWE, respectively). Notably, 12% of small IAs (size <7 mm) exhibited AWE. The IAs with AWE had significant higher ISUIA grade than the IAs without ( p < 0.001, Wilcoxon rank sum test). Conclusions The wall enhancement in contrast-enhanced black-blood MR images was independently associated with aneurysm size in unruptured IAs. However, some small unruptured aneurysms did exhibit wall enhancement, suggesting that AWE may provide additional aneurysm instability information to improve current size-based rupture risk evaluation metrics.

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Modest clinical outcomes of dendritic cell (DC) vaccine trials call for novel strategies. In this study, we have created a chimeric CD40 molecule that incorporates a single chain Fv (scFv) molecule specific for human ErbB2 antigen and fusing to the membrane spanning and cytosolic domains of murine CD40. After adenoviral transfer to bone marrow-derived DC, this chimeric receptor (CR) induced nuclear factor-KB (NF-KB)-dependent DC activation and effector function when cultured with immobilized ErbB2 protein or ErbB2-positive tumor cells in vitro. In vivo migration assays showed that f40% injected CR-modified DC (scFv-CD40-DC) effectively migrated to ErbB2-positive tumors, where they were activated after ErbB2 antigen stimulation, and sequentially homed into the draining lymph nodes. In murine ErbB2-positive D2F2/E2 breast tumor (BALB/c) and EL4/E2 thymoma (C57BL/6) models, i.v. injection of 1 Â 10 6 scFv-CD40-DC significantly inhibited tumor growth and cured established tumors. Importantly, the cured mice treated by injection of scFv-CD40-DC were effective in preventing both ErbB2-positive and parental ErbB2-negative tumor rechallenge. Analysis of the underlying mechanism revealed that i.v. infusion of scFv-CD40-DC elicited tumor-specific CTL responses, and the transfer of CTLs from scFv-CD40-DC-treated mice protected naive mice against a subsequent tumor challenge. These results support the concept that genetic modification of DC with tumor-associated antigen-specific CD40 chimeric receptor might be a useful strategy for treatment of human cancers.

Hepatoid adenocarcinoma is a rare and unusual tumor in the female genital tract. Hepatoid adenocarcinoma resembles hepatocellular carcinoma morphologically but develops in extrahepatic organs, and usually demonstrates foci of adenocarcinoma of the primary organ. Tumor cells often stain positive for anti-α-fetoprotein antibody, and may be associated with elevated serum α-fetoprotein, which may be useful as a tumor marker to guide treatment. There is little reliable information to guide clinical management of these unusual tumors and prognosis is poor despite multi-modal treatment. This report describes the diagnosis and treatment of this tumor in a postmenopausal woman.

Circulating progenitor cells and stromal-derived factor-1alpha (SDF-1α) have been suggested to participate in tissue repair following ischemic injury. However, the predictive role of circulating CD133+CD34+ progenitors and plasma SDF-1α in ischemic stroke (IS) patients remains unknown. In this study, we recruited 95 acute IS patients, 40 at-risk subjects and 30 normal subjects. The NIH stroke scale (NIHSS), infarct volume and carotid intima-media thickness (IMT) were determined at day 1 and the modified rankin scale (mRS) of functional outcome was assessed at day 21. The levels of circulating CD133+CD34+ cells and plasma SDF-1α were determined by flow cytometry and enzyme-linked immunosorbent assay, respectively. Our data showed that: 1) The levels of CD133+CD34+ cells were lower in at-risk subjects and IS patients at admission (day 1) when compared to normal controls. 2) The day 1 level of CD133+CD34+ cells varied in IS subgroups and inversely correlated with NIHSS and carotid IMT. The level of SDF-1α inversely correlated with NIHSS and infarct volume. 3) The increment rates of circulating CD133+CD34+ cells and plasma SDF-1α within the first week were correlated. 4) Patients with a higher level of CD133+CD34+ cells at day 7 had a low mRS. The increase rate of CD133+CD34+ cells in the first week was inversely associated with mRS. In conclusion, our findings demonstrate that the circulating CD133+CD34+ progenitor cells and plasma SDF-1α can be used as predictive parameters for IS severity and outcome.