Study of nuclear correlation effects via 12C(p,n)12N(g.s.,1+) at 296 MeV

We report measurements of the cross section and a complete set of polarization observables for the Gamow--Teller ${}^{12}{\rm C}(\vec{p},\vec{n}){}^{12}{\rm N}({\rm g.s.},1^+)$ reaction at a bombarding energy of 296 MeV. The data are compared with distorted wave impulse approximation calculations employing transition form factors normalized to reproduce the observed beta-decay $ft$ value. The cross section is significantly under-predicted by the calculations at momentum transfers $q \gtrsim$ 0.5 ${\rm fm^{-1}}$. The discrepancy is partly resolved by considering the non-locality of the nuclear mean field. However, the calculations still under-predict the cross section at large momentum transfers of $q$ $\simeq$ 1.6 ${\rm fm^{-1}}$. We also performed calculations employing random phase approximation response functions and found that the observed enhancement can be attributed in part to pionic correlations in nuclei.Comment: 5 figures, submitted to Phys. Lett.

Isovector effective NN interaction in 28Si(p,n)28P(6-) at 198 MeV

We report measurements of the cross section and a complete set of polarization observables for the View the MathML source reaction at a bombarding energy of 198 MeV. The data are compared with distorted wave impulse approximation calculations employing response functions normalized to inelastic electron scattering. The spin-longitudinal polarized cross section IDq is slightly over-predicted by the calculations, while the normal spin-transverse polarized cross section IDn is significantly under-predicted. The calculated in-plane spin-transverse IDp and spin-scalar ID0 polarized cross sections agree well with the experimental data. These results are consistent with those for View the MathML source scattering at the same energy, and thus it is concluded that isospin-mixing effects are not responsible for the discrepancy between theory and experiment in the View the MathML source case. Energy half-off-shell effects as medium effects on the effective nucleon?nucleon interaction are also investigated and found to be too small to be responsible for the discrepancy

Peroxisome proliferator-activated receptor γ ligand-induced growth inhibition of human hepatocellular carcinoma

Peroxisome proliferator-activated receptor γ (PPARγ) ligands have been implicated in the growth inhibition and differentiation of certain human cancers with diverse tissue origin. In this study, expression of PPARγ in human hepatocellular carcinoma (HCC) and the effect of PPARγ ligands on HCC cells were investigated in vitro using Hep G2, HuH-7, KYN-1 and KYN-2 cell lines. All cell lines were found to express functionally active PPARγ and a marked growth inhibition was induced by thiazolidinedione ligands troglitazone, and pioglitazone as well as with its natural ligand 15-deoxy-Δ12,14-prostaglandin J 2. The growth inhibitory effect was associated with a dose-dependent inhibition of DNA synthesis, cell cycle progression and α fetoprotein expression. © 2001 Cancer Research Campaign http://www.bjcancer.co

Polarization transfer measurements for 12C(p⃗,n⃗)12N(g.s.,1+)^{12}{\rm C}(\vec{p},\vec{n})^{12}{\rm N (g.s.},1^+) at 296 MeV and nuclear correlation effects

Differential cross sections and complete sets of polarization observables are presented for the Gamow-Teller $^{12}{\rm C}(\vec{p},\vec{n})^{12}{\rm N}({\rm g.s.},1^+)$ reaction at a bombarding energy of 296 MeV with momentum transfers $q$ of 0.1 to $2.2{\rm fm}^{-1}$. The polarization transfer observables are used to deduce the spin-longitudinal cross section, $ID_q$, and spin-transverse cross sections, $ID_p$ and $ID_n$. The data are compared with calculations based on the distorted wave impulse approximation (DWIA) using shell-model wave functions. Significant differences between the experimental and theoretical results are observed for all three spin-dependent $ID_i$ at momentum transfers of $q \gtrsim 0.5{\rm fm}^{-1}$, suggesting the existence of nuclear correlations beyond the shell model. We also performed DWIA calculations employing random phase approximation (RPA) response functions and found that the observed discrepancy is partly resolved by the pionic and rho-mesonic correlation effects.Comment: accepted for publication in Phys. Rev.

Evaluation of macrophage migration inhibitory factor as an imaging marker for hepatocellular carcinoma in murine models

Objective. Macrophage migration inhibitory factor (MIF) is considered as an important mediator in the pathogenesis of neoplasia. The aim of the present study was to evaluate whether MIF could be used as a marker for hepatocellular carcinoma (HCC) detection. Material and methods. Biodistribution and whole-body autoradiography studies of 131I-labeled anti-MIF monoclonal antibody (McAb) and 131I-labeled control IgG were performed. The HCC-bearing mice were injected with 3.7 MBq of each agent and killed at 24, 48, and 72 h postinjection (p.i.). The organs, blood, and HCC tissues were removed from model mice, weighed, and counted using a gamma-counter. The expression of MIF mRNA and protein within HCC tissues was confirmed by RT-PCR and immunohistochemistry. Results. HCCs in model mice could be adequately visualized at 24 h p.i. The target-to-non-target (T/NT) ratios were 6.72 ± 1.09 (24 h), 9.85 ± 0.81 (48 h), and 12.31 ± 0.57 (72 h) for 131I-labeled anti-MIF McAb group, whereas in the control group of 131I-IgG, T/NT ratios were 4.65 ± 0.63 (24 h), 6.12 ± 0.60 (48 h), and 8.23 ± 0.35 (72 h) (p < 0.05). MIF mRNA expression was twofold higher in the HCC tissues than in the healthy liver tissues. MIF protein expression was much higher in the HCC tissues than in controls. Conclusions. Our findings suggested that 131I-anti-MIF McAb could be rapidly and specifically localized in tumors. Thus, MIF could be used as a marker for HCC tumor detection

Genetic and epigenetic characteristics of human multiple hepatocellular carcinoma

<p>Abstract</p> <p>Background</p> <p>Multiple carcinogenesis is one of the major characteristics of human hepatocellular carcinoma (HCC). The history of multiple tumors, that is, whether they derive from a common precancerous or cancerous ancestor or individually from hepatocytes, is a major clinical issue. Multiple HCC is clinically classified as either intratumor metastasis (IM) or multicentric carcinogenesis (MC). Molecular markers that differentiate IM and MC are of interest to clinical practitioners because the clinical diagnoses of IM and MC often lead to different therapies.</p> <p>Methods</p> <p>We analyzed 30 multiple tumors from 15 patients for somatic mutations of cancer-related genes, chromosomal aberrations, and promoter methylation of tumor suppressor genes using techniques such as high-resolution melting, array-comparative genomic hybridization (CGH), and quantitative methylation-specific PCR.</p> <p>Results</p> <p>Somatic mutations were found in <it>TP53 </it>and <it>CTNNB1 </it>but not in <it>CDKN2A </it>or <it>KRAS</it>. Tumors from the same patient did not share the same mutations. Array-CGH analysis revealed variations in the number of chromosomal aberrations, and the detection of common aberrations in tumors from the same patient was found to depend on the total number of chromosomal aberrations. A promoter methylation analysis of genes revealed dense methylation in HCC but not in the adjacent non-tumor tissue. The correlation coefficients (<it>r</it>) of methylation patterns between tumors from the same patient were more similar than those between tumors from different patients. In total, 47% of tumor samples from the same patients had an <it>r </it>≥ 0.8, whereas, in contrast, only 18% of tumor samples from different patients had an <it>r </it>≥ 0.8 (p = 0.01). All IM cases were highly similar; that is, <it>r </it>≥ 0.8 (<it>p </it>= 0.025).</p> <p>Conclusions</p> <p>The overall scarcity of common somatic mutations and chromosomal aberrations suggests that biological IM is likely to be rare. Tumors from the same patient had a methylation pattern that was more similar than those from different patients. As all clinical IM cases exhibited high similarity, the methylation pattern may be applicable to support the clinical diagnosis of IM and MC.</p

Metallothionein expression correlates with metastatic and proliferative potential in squamous cell carcinoma of the oesophagus

The goal of this study is to clarify whether the expression of metallothionein (MT) could affect the prognosis and the metastatic potential of squamous cell carcinoma (SCC) of the oesophagus. In paraffin-embedded specimens resected from 57 patients, MT mRNA and protein expressions were detected by in situ hybridization and immunohistochemistry respectively. The expression of MT was evaluated in respect of clinicopathologic variables and patients' survival. MT mRNA expression was significantly associated with the proportion of lymph node metastasis (71% in MT mRNA-positive tumours vs 42% in MT mRNA-negative tumours; P = 0.0343) and that of distant metastasis (29% in MT mRNA-positive tumours vs 5% in MT mRNA-negative tumours; P = 0.0452). In respect of MT protein expression, the frequency of distant metastasis was more common in MT-positive tumours than in MT-negative tumours (30% in MT-positive tumours vs 8% in MT-negative tumours; P = 0.0446). The survival rate of the patients with MT protein-negative tumours was significantly better than that of the patients with MT protein-positive tumours (P = 0.0340). There was a positive correlation between the expression of MT protein and that of proliferating cell nuclear antigen (P = 0.0018). Therefore, we conclude that MT expression, both at the mRNA and protein levels, may be a potential marker predicting metastatic and proliferative activities of oesophageal SCC. © 1999 Cancer Research Campaig