Analysis of enhanced CT imaging signs and clinicopathological prognostic factors in hepatoid adenocarcinoma of stomach patients with radical surgery: a retrospective study.

BACKGROUND: To investigate the association between CT signs and clinicopathological features and disease recurrence in patients with hepatoid adenocarcinoma of stomach (HAS). METHODS: Forty nine HAS patients undergoing radical surgery were retrospectively collected. Association between CT and clinicopathological features and disease recurrence was analyzed. Multivariate logistic model was constructed and evaluated for predicting recurrence by using receiver operating characteristic (ROC) curve. Survival curves between model-defined risk groups was compared using Kaplan-Meier method. RESULTS: 24(49.0%) patients developed disease recurrence. Multivariate logistic analysis results showed elevated serum CEA level, peritumoral fatty space invasion and positive pathological vascular tumor thrombus were independent factors for disease recurrence. Odds ratios were 10.87 (95%CI, 1.14-103.66), 6.83 (95%CI, 1.08-43.08) and 42.67 (95%CI, 3.66-496.85), respectively. The constructed model showed an area under ROC of 0.912 (95%CI,0.825-0.999). The model-defined high-risk group showed poorer overall survival and recurrence-free survival than the low-risk group (both P < 0.001). CONCLUSIONS: Preoperative CT appearance of peritumoral fatty space invasion, elevated serum CEA level, and pathological vascular tumor thrombus indicated poor prognosis of HAS patients.

Fused monochromatic imaging acquired by single source dual energy CT in hepatocellular carcinoma during arterial phase: an initial experience.

OBJECTIVE: To explore whether single and fused monochromatic images can improve liver tumor detection and delineation by single source dual energy CT (ssDECT) in patients with hepatocellular carcinoma (HCC) during arterial phase. METHODS: Fifty-seven patients with HCC who underwent ssDECT scanning at Beijing Cancer Hospital were enrolled retrospectively. Twenty-one sets of monochromatic images from 40 to 140 keV were reconstructed at 5 keV intervals in arterial phase. The optimal contrast-noise ratio (CNR) monochromatic images of the liver tumor and the lowest-noise monochromatic images were selected for image fusion. We evaluated the image quality of the optimal-CNR monochromatic images, the lowest-noise monochromatic images and the fused monochromatic images, respectively. The evaluation indicators included the spatial resolution of the anatomical structure, the noise level, the contrast and CNR of the tumor. RESULTS: In arterial phase, the anatomical structure of the liver can be displayed most clearly in the 65-keV monochromatic images, with the lowest image noise. The optimal-CNR monochromatic images of HCC tumor were 50-keV monochromatic images in which the internal structural features of the liver tumors were displayed most clearly and meticulously. For tumor detection, the fused monochromatic images and the 50-keV monochromatic images had similar performances, and were more sensitive than 65-keV monochromatic images. CONCLUSIONS: We achieved good arterial phase images by fusing the optimal-CNR monochromatic images of the HCC tumor and the lowest-noise monochromatic images. The fused images displayed liver tumors and anatomical structures more clearly, which is potentially helpful for identifying more and smaller HCC tumors.

Spectral CT in the demonstration of the gastrocolic ligament: a comparison study.

PURPOSE: To investigate the performance of spectral CT in the depiction of the gastrocolic ligament (GCL) compared to conventional polychromatic CT. METHODS: Gemstone spectral CT and conventionally polychromatic CT examinations were randomly allocated to be performed on 62 consecutive patients. A total of 11 groups of monochromatic images were generated on energy levels ranging from 40 to 140 keV at an interval of 10 keV. A five-score classification system was used to evaluate the performances of CT images in the demonstration of GCL. The inter-observer agreement between two radiologists in their evaluation of the GCL by each method was evaluated using kappa statistics. RESULTS: There were statistically significant differences between the spectral CT and polychromatic CT in their abilities to highlight the GCL (observer 1: χ(2) = 18.310, P < 0.001; observer 2: χ(2) = 19.780, P < 0.001). The distinct display (score ≥ 3) rates of the GCL by integrated monochromatic images were higher than that of polychromatic images (P < 0.001). The best energy level for displaying the GCL by spectral CT was 50-70 keV. The kappa value for the image scores on the integrated keV images between the two radiologists was higher than that for polychromatic CT images (P < 0.01). CONCLUSIONS: Spectral CT can improve the visualisation of the GCL compared to polychromatic CT.

Efficacy evaluation of different measurement methods for target lesions after neoadjuvant chemotherapy and radical radiotherapy in locally advanced hypopharyngeal carcinoma.

AIM: To assess the diagnostic efficacy in response evaluation of hypopharyngeal carcinoma (HPC) using different CT measurement methods. METHODS AND MATERIALS: One hundred and three patients with locally advanced HPC receiving neoadjuvant chemotherapy (NACT) and radical radiotherapy (RT) were retrospectively enrolled. The long diameter, short diameter and largest axial area of the tumors and the largest metastatic cervical lymph node (LN) were measured before and after NACT, at the end of RT and 1 month after RT. Tumor regression ratios of the sum of the tumor's long diameter and LN's short diameter (LDTSDL), the sum of tumor and LN's short diameter (TTSDL), the sum of tumor and LN's largest axial area (AATML) were calculated. Analysis was conducted for overall survival (OS), metastasis-free survival, regional recurrence-free survival (RRFS), and local recurrence-free survival (LRFS). RESULTS: Note that 35, 28, 23, and 16 patients suffered death, local recurrence, regional recurrence and distant metastasis, respectively. TTSDL-defined effective group demonstrated better LRFS (p = .039) and RRFS (p = .047) after NACT and better OS since the end of RT (p = .037); AATML-defined effective groups demonstrated better OS, LRFS, and RRFS since the end of RT (p = .015, .008, and .005). While LDTSDL-defined groups showed differences in OS and LRFS until 1 month after RT (p = .013 and .014). CONCLUSIONS: The regression rate of TTSDL and AATML can distinguish prognosis at an earlier time and demonstrated better reliability compared with LDTSDL. They were recommended for response evaluation in HPC.

Hepatocyte proliferation during liver regeneration is impaired in mice with methionine diet-induced hyperhomocysteinemia.

Elevated homocysteine levels are defined as hyperhomocysteinemia (HHcy), a disorder that is associated with cardiovascular and neurodegenerative diseases as well as with hepatic fibrosis. Recent studies have shown that HHcy promotes hepatic injury by increasing oxidative stress. Although homocysteine induces cell cycle arrest in a variety of different cell types, it is not known whether HHcy has a definitive role in hepatocyte proliferation during liver regeneration. In this report, we investigated the effect of homocysteine on liver regeneration. Our results demonstrated that mice with HHcy exhibited an impairment in liver regeneration after partial hepatectomy, as measured by immunohistochemical staining of proliferation cell nuclear antigen and bromodeoxyuridine incorporation. Impaired proliferation was also correlated with reduced cyclin D1 induction and elevated expression levels of both p53 and p21Cip1. In addition, the phosphorylation of Akt, which plays an essential role in normal regeneration responses, was attenuated during the early phases of liver regeneration in HHcy mice. Our results also indicated that the cAMP/protein kinase A pathway mediated the inhibitory effect of homocysteine on liver regeneration. These findings provide evidence that impairment of liver regeneration by HHcy may result in delayed recovery from liver injury induced by homocysteine itself.

Enhancement of green-light photoluminescence of Ta2O5 nanoblock stacks.

In this study we have explored the structural, electronic, and photoluminescence (PL) properties of Ta(2)O(5) nanoblock stacks. The Ta(2)O(5) nanoblocks were synthesized by the hot filament metal-oxide vapor deposition (HFMOVD) technique and randomly arranged in large-area stacks. Field-emission scanning electron microscopy (FESEM) showed most of the stacking Ta(2)O(5) nanoblocks to be 21 nm wide. Energy dispersive spectroscopy (EDS) analysis verified the presence of only the elements Ta and O. X-Ray photoemission spectroscopy (XPS) not only revealed the electronic structures and chemical properties of the stacking Ta(2)O(5) nanoblocks but also their stoichiometric Ta/O ratio of ∼0.416 (i.e. Ta:O = 2.08 : 5). Photoluminescence (PL) spectroscopy showed very strong green-light emissions, which emerged from the trap-levels of the oxygen vacancies within the Ta(2)O(5) bandgap. The PL intensities were linearly enhanced by increasing the laser power and the excitation time. The PL results suggest that the nanoblocks are excellent visible-light emitters.

Scanning photoemission spectromicroscopic study of 4-nm ultrathin SiO(3.4) protrusions probe-induced on the native SiO(2) layer.

Atomic force microscopy probe-induced large-area ultrathin SiO(x) (x ≡ O/Si content ratio and x > 2) protrusions only a few nanometers high on a SiO(2) layer were characterized by scanning photoemission microscopy (SPEM) and X-ray photoemission spectroscopy (XPS). SPEM images of the large-area ultrathin SiO(x) protrusions directly showed the surface chemical distribution and chemical state specifications. The peak intensity ratios of the XPS spectra of the large-area ultrathin SiO(x) protrusions provided the elemental quantification of the Si 2p core levels and Si oxidation states (such as the Si(4+), Si(3+), Si(2+), and Si(1+) species). The O/Si content ratio (x) was evidently determined by the height of the large-area ultrathin SiO(x) protrusions.

Homocysteine enhances cell proliferation in hepatic myofibroblastic stellate cells.

Homocysteine is an intermediate in sulfur amino acid metabolism, which takes place mainly in the liver. Recent studies have shown that hyperhomocysteinemia in patients and murine models develop hepatic fibrosis. To define mechanisms underlying homocysteine-induced hepatic fibrosis, the effect of homocysteine on hepatic stellate cell (HSC) proliferation was examined. In the present study, homocysteine promoted proliferation in myofibroblastic HSCs. Homocysteine elicited a transient formation of reactive oxygen species (ROS). The initial ROS activated extracellular signal-regulated kinase and p38 mitogen-activated protein kinase, which were involved in the activation of NAD(P)H oxidases and the generation of more ROS. The activation of NAD(P)H oxidases resulted from upregulation of the expression of p22(phox) and the phosphorylation of p47(phox). The ROS derived from NAD(P)H oxidases activated the PI3K/Akt pathway, thus promoting cellular proliferation in HSCs. These findings provide a mechanistic explanation for the development and progression of hepatic fibrosis in hyperhomocysteinemia.

Creation and manipulation of surface magnetic domains in an alternating up-and-down pattern.

According to Lenz's law, the magnetic field from the oscillating magnetic probe will induce out-of-plane surface magnetic domains (SMDs) from the in-plane magnetization at the locally tapped points on a ferromagnetic La(0.7)Sr(0.3)MnO3 (LSMO) thin film. It was possible to control and manipulate the out-of-plane SMDs by varying the tapping intervals and changing the scanning direction. We also found that the anisotropic stresses from the out-of-plane SMDs caused the appearance of large-area straight striped domain structures on the order of several micrometers. Smaller oscillating magnetic probe tapping intervals produced larger periods (or widths) of the straight striped domain structure.

The molecular mechanism of endoplasmic reticulum stress-induced apoptosis in PC-12 neuronal cells: the protective effect of insulin-like growth factor I.

Endoplasmic reticulum (ER) stress has been implicated in several neurodegenerative diseases. Although CCAAT/enhancer-binding protein homologous protein (CHOP) has been shown to play a critical role in ER stress, the precise apoptosis cascade downstream of CHOP is unknown. In this report, we investigated the mechanism of ER stress-mediated apoptosis as well as the action of IGF-I in PC-12 neuronal cells. Our results demonstrated that tribbles-related protein 3 (TRB3), which is a target gene of CHOP, was responsible for tunicamycin (an ER stress inducer)-induced apoptosis. TRB3 could promote dephosphorylation of Akt in PC-12 cells. IGF-I inhibited ER stress-induced apoptosis by restoring the phosphorylation level of Akt. Both wortmannin (a phosphatidylinositide 3-kinase inhibitor) and SB 212090 (a p38 MAPK inhibitor) suppressed the protective effect of IGF-I on ER stress-induced apoptosis. Interestingly, IGF-I attenuated ER stress-mediated expression of TRB3 but not CHOP. This action of IGF-I was abolished by SB 212090 but not by wortmannin. Immunoprecipitation analysis revealed that IGF-I promoted the phosphorylation of CHOP by activating p38 MAPK, probably leading to a decrease in the transcriptional activity of CHOP. The dephosphorylation of Akt resulted in increased expression of a proapoptotic protein, p53 up-regulated modulator of apoptosis (PUMA), in a forkhead box O3a-dependent manner. Knockdown of PUMA by short hairpin RNA attenuated ER stress-mediated apoptosis. Thus, our current study indicates that both TRB3 and PUMA are critical molecules in ER stress-induced apoptosis. IGF-I effectively protects PC-12 neuronal cells against ER stress-induced apoptosis through the phosphatidylinositide 3-kinase/Akt and p38 MAPK pathways.

Dynamic enhanced CT: is there a difference between liver metastases of gastroenteropancreatic neuroendocrine tumor and adenocarcinoma.

This study proposed to evaluate the feasibility of dynamic enhanced CT in differentiation of liver metastases of gastroenteropancreatic well-differentiated neuroendocrine tumors (GEP NETs) from GEP adenocarcinomas based on their characteristic features. CT images of 23 well-differentiated (G1 or G2) GEP NETs and 23 GEP adenocarcinomas patients with liver metastases were retrospectively reviewed. The distribution type, shape, intra-tumoral neovascularity, enhancement on hepatic artery phase, dynamic enhancement pattern and lymphadenopathy were subjective analyzed. Meanwhile, the size, number, CT value of tumor and adjacent normal liver parenchyma were measured and the metastasis-to-liver ratios were calculated objectively. Compared with GEP adenocarcinomas, the liver metastases of GEP NETs more frequently demonstrated a hyper enhancement on hepatic artery phase, washout dynamic enhancement pattern, absence of lymphadenopathy and higher metastasis-to-liver ratios on both hepatic artery phase and portal venous phase (P=0.017, P<0.001, P =0.038, P <0.001 and P =0.008, respectively). Logistic regression analysis showed that the dynamic enhancement pattern (P=0.012), and the metastasis-to-liver ratios on hepatic artery phase (P=0.009) were independent CT predictors for liver metastases of GEP NETs. The sensitivity and specificity of combing the two predictors in differentiation of liver metastases of GEP adenocarcinomas from GEP NET were 82.6% (19 of 23) and 91.3% (21 of 23), respectively. CT features are helpful in differentiating liver metastases of well-differentiated GEP NETs from that of GEP adenocarcinomas.

Identification of benign and malignant thyroid nodules by in vivo iodine concentration measurement using single-source dual energy CT: A retrospective diagnostic accuracy study.

This study proposed to determine whether in vivo iodine concentration measurement by single-source dual energy (SSDE) CT can improve differentiation between benign and malignant thyroid nodules. In total, 53 patients presenting with thyroid nodules underwent SSDE CT scanning. Iodine concentrations were measured for each nodule and normal thyroid tissue using the GSI-viewer image analysis software. A total of 26 thyroid nodules were malignant in 26 patients and confirmed by surgery; 33 nodules from 27 patients were benign, with 10 confirmed by surgery and others after follow-up. Iodine concentrations with plain CT were significantly lower in malignant than benign nodules (0.47 ±â€Š0.20 vs 1.17 ±â€Š0.38 mg/mL, P = 0.00). Receiver operating characteristic (ROC) curve showed an area under the curve (AUC) of 0.93; with a cutoff of 0.67, iodine concentration showed 92.3% sensitivity and 88.5% specificity in diagnosing malignancy. Iodine concentration obtained by enhanced and plain CT were significantly higher in malignant than benign nodules (9.05 ±â€Š3.35 vs 3.46 ±â€Š2.24 mg/mL, P = 0.00). ROC curve analysis showed an AUC of 0.93; with a cutoff value of 3.37, iodine concentration displayed 78% sensitivity, 95% specificity in diagnosing malignancy. Combining unenhanced with enhanced iodine concentrations, the diagnostic equation was: Y = -8.641 × unenhanced iodine concentration + 0.663 × iodine concentration. ROC curve showed an AUC of 0.98 (95% CI, 0.94, 1.00). With Y ≥ -2 considered malignancy, diagnostic sensitivity and specificity were 96%, 96.3%, respectively. This study concluded that SSDE CT can detect the differences in iodine uptake and blood supply between benign and malignant thyroid lesions.

Homocysteine promotes proliferation and activation of microglia.

Epidemiological and experimental studies have correlated hyperhomocysteinemia to a range of neurodegenerative conditions, including Alzheimer's disease, stroke, and Parkinson's disease. Although homocysteine-induced apoptosis in neurons has been extensively studied, little information is available regarding the effect of homocysteine on microglia. In this report, we demonstrated that homocysteine promoted proliferation and up-regulated the expression of CD11b (a marker of microglial activation). Consistent with our in vitro results, a significant increase in the number of CD11b-positive microglia was also observed in brain sections of mice with hyperhomocysteinemia. Homocysteine promoted the activity of NAD(P)H oxidases, resulting in the generation of reactive oxygen species. Up-regulation of NAD(P)H oxidase activity by homocysteine appears to be due to its ability to induce the phosphorylation of p47phox through the p38 MAPK pathway. Furthermore, inhibition of reactive oxygen species significantly blocked cellular proliferation and activation in microglia. Since microglial proliferation and activation play an important role in the development of several neurodegenerative disorders, our results reveal a novel role of homocysteine in the pathogenesis of neurodegenerative diseases.