Serum autoantibodies that react with tumor-associated antigens (TAAs) can be used as potential biomarkers for diagnosis of cancer. This study aims to evaluate the immunodiagnostic value of 11 anti-TAAs autoantibodies for detection of breast cancer (BC) and establish a diagnostic model for distinguishing BC from normal human controls (NHC) and benign breast diseases (BBD). Sera from 10 BC patients and 10 NHC were used to detect 11 anti-TAAs autoantibodies by western blotting. The 11 anti-TAAs autoantibodies were further assessed in 983 sera by relative quantitative enzyme-linked immunosorbent assay (ELISA). Binary logistic regression and Fisher linear discriminant analysis were conducted to establish a prediction model by using 184 BC and 184 NHC (training cohort, n = 568) and validated by leave-one-out cross-validation. Logistic regression model was selected to establish the prediction model. Results were validated using an independent validation cohort (n = 415). The five anti-TAAs (p53, cyclinB1, p16, p62, 14-3-3ξ) autoantibodies were selected to construct the model with the area under the curve (AUC) of 0.943 (95% CI, 0.919-0.967) in training cohort and 0.916 (95% CI, 0.886-0.947) in the validation cohort. In the identification of BC and BBD, AUCs were 0.881 (95% CI, 0.848-0.914) and 0.849 (95% CI, 0.803-0.894) in training and validation cohort, respectively. In summary, our study indicates that the immunodiagnostic model can distinguish BC from NHC and BC from BBD and this model may have a potential application in immunodiagnosis of breast cancer.
BACKGROUND AND PURPOSE: Comprehensive imaging characterization of the morphology and luminal patency of cerebral aneurysms are cornerstones of their successful treatment and subsequent appropriate management. Giant cerebral aneurysms (GCAs), a distinct subgroup of aneurysms, are defined by large size (ࣙ 25 mm in greatest diameter), complex blood flow dynamics, and a high risk of rupture. The purpose of this study is to explore compare multiple imaging modalities in the assessment of GCAs. METHODS: This study retrospectively evaluated CT angiography (CTA), 3D time-of-flight (TOF) MR angiography (MRA), contrastenhanced MRA (CEMRA), and digital subtraction angiography (DSA) in characterizing GCAs in 21 patients. RESULTS: Aneurysm size ranged from 26 to 58 mm (mean 31.3 ± 12.2) and 18/21 (85.7%) had intraluminal thrombus. No significant difference was found between the aneurysmal sizes of any two modalities regarding comparisons of CTA, 3D TOFMRA, and CEMRA. However, there were significant differences in the aneurysmal patency visibility grade between CTA versus TOFMRA and CTA versus CEMRA. Moreover, the patent luminal size measured on CTA was significantly larger than DSA. CONCLUSIONS: CTA, 3D TOFMRA, and CEMRA are equivalent in the delineation of size of GCAs. Nevertheless, 3D TOFMRA and CEMRA seem to be inferior to CTA in demonstrating luminal size/patency, likely because of the signal loss resulting from the presence of intraluminal thrombus and flow turbulence. Moreover, CTA is superior to DSA in determining lumen patency in GCAs, probably due to CTA's multipass-related luminal enhancement while DSA general fills the lesion via the first pass of enhancement or soon thereafter. In addition, CTA may also better demonstrate intraluminal thrombus, adjacent anatomical structures, and calcified rims.
The purpose of this study was to investigate the dosimetric properties and the lowest detectable dose of fingernails from their electron paramagnetic resonance signal. Fingernail clippings from 50 healthy individuals were collected, rinsed in water, and irradiated with (137)Cs gamma rays. Next, their electron paramagnetic resonance spectra were measured before and after exposure. The radiation-induced signal from the irradiated fingernails was relatively stable even after 68 d. Further, the intensity of the radiation-induced signal increased with progressive increases in the dose until saturation, while the background signal from the irradiated fingernails increased only gradually with time. The lowest detectable dose of the irradiated fingernails was 2 Gy. On the basis of these results, it can be concluded that the effect of the intrinsic signal must be taken into account during dose reconstruction. This electron paramagnetic resonance assessment method should be useful for the rapid screening of irradiated populations after nuclear accidents.
BackgroundRadiotherapy is among the commonly applied treatment options for glioma, which is one of the most common types of primary brain tumor. To evaluate the effect of radiotherapy noninvasively, it is vital for oncologists to monitor the effects of X-ray irradiation on glioma cells. Preliminary research had showed that PKC-ι expression correlates with tumor cell apoptosis induced by X-ray irradiation. It is also believed that the lactate-to-creatine (Lac/Cr) ratio can be used as a biomarker to evaluate apoptosis in glioma cells after X-ray irradiation. In this study, we evaluated the relationships between the Lac/Cr ratio, apoptotic rate, and protein kinase C iota (PKC-ι) expression in glioma cells.MethodsCells of the glioma cell lines C6 and U251 were randomly divided into 4 groups, with every group exposed to X-ray irradiation at 0, 1, 5, 10 and 15 Gy. Single cell gel electrophoresis (SCGE) was conducted to evaluate the DNA damage. Flow cytometry was performed to measure the cell cycle blockage and apoptotic rates. Western blot analysis was used to detect the phosphorylated PKC-ι (p-PKC-ι) level. 1H NMR spectroscopy was employed to determine the Lac/Cr ratio.ResultsThe DNA damage increased in a radiation dose-dependent manner (p < 0.05). With the increase in X-ray irradiation, the apoptotic rate also increased (C6, p < 0.01; U251, p < 0.05), and the p-PKC-ι level decreased (C6, p < 0.01; U251, p < 0.05). The p-PKC-ι level negatively correlated with apoptosis, whereas the Lac/Cr ratio positively correlated with the p-PKC-ι level.ConclusionThe Lac/Cr ratio decreases with an increase in X-ray irradiation and thus can be used as a biomarker to reflect the effects of X-ray irradiation in glioma cells.
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