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

Solid and Cystic Tumor (SCT) of the Pancreas in an Adult Man

Solid and cystic tumor (SCT) of the pancreas predominantly Occurs in women, and the occurrence in men is extremely rare. We experienced a male case of SCT. A 38-year-old man was admitted with the complaint of upper abdominal pain. CT scan showed the presence of a mass in the head of the pancreas. The mass was composed of high density areas and low density areas. Ultrasonograms revealed the mass being composed of high echoic areas and low echoic areas. The mass .was hypovascular on angiography. SCT was suspected and pancreaticoduodenectomy was performed. The cut surface of the tumor showed mainly cystic degenerative areas containing dark red hemorrhagic materials. Microscopically, there were solid areas in the periphery and pseudopapillary areas in the center. No metastasis was found in the removed lymph nodes. The tumor cells were not stained by Grimelius' silver stain. The tumor cells were positive for alpha-l-antitrypsin (AAT) and neuron-specific enolase (NSE). Pancreatic hormones such as insulin, glucagon, and somatostatin were all negative. Electron micrograph showed that tumor cells were rich in mitochondria. Zymogen granules and neurosecretory granules were not detected. Estrogen receptor (ER) and progesterone receptor (PR) were both negative

Acute Cholecystitis and Cholelithiasis Developed after Esophagectomy

BACKGROUND: Although the prevalence of gallstone disease after gastrectomy is reported to be high, its prevalence after esophagectomy is scarcely reported.MATERIALS AND METHODS: Gallbladder disease following an esophagectomy was prospectively evaluated in 237 patients with esophageal cancer by abdominal ultrasonography twice a year up to five years postoperatively. The median follow-up period was 18.6 months.,RESULTS: One patient (0.4%) developed acute acalculous cholecystitis postoperatively, and 13 patients (5.5%) developed gallstone disease during the follow-up period. Nine (69%) of these 13 patients developed gallstone disease within two years, and another two patients developed the disease three years after esophagectomy. Another patient developed gallbladder debris at 35 months postoperatively, and one developed gallbladder polyps at 33 months. Seven of the 13 patients with gallstone disease underwent cholecystectomy between 13 and 125 months after esophagectomy: two developed acute cholecystitis; two had associated common bile duct stones; the remaining three patients had upper abdominal pain. Nine of the 13 patients who developed gallstone disease showed a history of alcoholism, whereas only 81 of 224 patients without gallstone disease had a similar history (P<0.05).CONCLUSION: A certain number of patients with esophageal carcinoma and a history of alcoholism develop cholelithiasis within three years after esophagectomy, and subsequently undergo cholecystectomy during the follow-up period

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

Expression of peroxisome proliferator-activated receptor (PPAR)γ in gastric cancer and inhibitory effects of PPARγ agonists

Peroxisome proliferator-activated receptor (PPAR) γ is expressed in human colon cancer, prostate cancer and breast cancer cells, and PPARγ activation induces growth inhibition in these cells. PPARγ expression in human gastric cancer cells, however, has not been fully investigated. We report the PPARγ expression in human gastric cancer, and the effect of PPARγ ligands on proliferation of gastric carcinoma cell lines. Immunohistochemistry was used to demonstrate the presence of PPARγ protein in surgically resected specimens from well differentiated, moderately differentiated and poorly differentiated adenocarcinoma. We used reverse transcription-polymerase chain reaction and Northern and Western blot analyses to demonstrate PPARγ expression in four human gastric cancer cell lines. PPARγ agonists (troglitazone and 15-deoxy-Δ12,14-prostaglandin J2) showed dose-dependent inhibitory effects on the proliferation of the gastric cancer cells, and their effect was augmented by the simultaneous addition of 9-cis retinoic acid, a ligand of RXRα. Flow cytometry demonstrated G1 cell cycle arrest and a significant increase of annexin V-positive cells after treatment with troglitazone. These results suggest that induction of apoptosis together with G1 cell cycle arrest may be one of the mechanisms of the antiproliferative effect of PPARγ activation in human gastric cancer cells. © 2000 Cancer ResearchCampaig

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

A phase II study of the vitamin D analogue Seocalcitol in patients with inoperable hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is a common malignant tumour, which has a poor prognosis. Surgical resection can be curative but most patients are inoperable and most chemotherapy agents have minimal activity in this disease. Seocalcitol, a vitamin D analogue, induces differentiation and inhibits growth in cancer cell lines and in vivo. The vitamin D receptor is expressed in hepatocytes and more abundantly in HCC cells. In total, 56 patients with inoperable advanced HCC were included in an uncontrolled study of oral Seocalcitol treatment for up to 1 year ( with possible extension for responders). The dose was titrated according to serum calcium levels. The treatment effect was evaluated by regular CT scans. Out of 33 patients evaluable for tumour response, two had complete response (CR), 12 stable disease and 19 progressive disease. The CRs appeared after 6 and 24 months of treatment, and lasted for 29 and at least 36 months ( patient still in remission when data censored). Seocalcitol was well tolerated; the most frequent toxicity was hypercalcaemia and related symptoms. Most patients tolerated a daily dose of 10 mug of Seocalcitol. This is the first study showing activity, by reduction in tumour dimensions, of a differentiating agent in patients with an advanced bulky, solid tumour. Seocalcitol may have an effect in the treatment of HCC, especially in early disease when a prolonged treatment can be instituted. The survival benefit with or without tumour response should be determined in controlled studies