Computed tomographic features of colorectal carcinoma liver metastases predict posthepatectomy patient survival

PURPOSE: The gross appearance of colorectal carcinoma liver metastases reflects the biologic behavior of the tumor, yielding prognostic information. The aims of this retrospective study were to determine whether preoperative computed tomographic features of colorectal carcinoma liver metastases reflect the gross appearance of resected specimens and whether these computed tomographic hepatic features predict survival after hepatectomy. METHODS: Eighty-five patients underwent curative partial hepatectomy for colorectal carcinoma liver metastases. Preoperative computed tomographic features of the largest hepatic deposit were classified by the contour of advancing margin of the tumor into two types: lobular tumors with indentations with an acute angle and nonlobular tumors without such indentations. The correlation between computed tomographic features and 18 other clinicopathologic factors was examined. RESULTS: The overall five-year survival rate was 34.1 percent. Of 85 hepatic tumors examined, 49 were lobular and 36 were nonlobular. Computed tomographic features correlated significantly with gross appearance (P = 0.007). Univariate analysis revealed that computed tomographic features (P < 0.0001), gross appearance (P = 0.0063), size of the largest hepatic deposit (P = 0.0075), age (P = 0.0140), and satellite lesions (P = 0.0443) were significant prognosticators. The five-year survival rates in patients with lobular and nonlobular tumors were 10.4 and 66.1 percent, respectively. By multivariate analysis, computed tomographic features (P < 0.0001) and size of the largest hepatic deposit (P = 0.0419) were independently significant. CONCLUSIONS: Computed tomographic features of colorectal carcinoma liver metastases correlate with their gross appearance. The computed tomographic characterization of liver metastases is the most important independent prognostic factor in patients undergoing curative hepatectomy.     

An esophageal cancer case unresectable due to tuberculous fibrosing mediastinitis: report of a case

We present a case of esophageal carcinoma in which esophagectomy was not possible because of tuberculous fibrosing mediastinitis. A 77-year-old man was diagnosed with carcinoma of the thoracic esophagus and admitted to our hospital. Chest radiography on admission revealed no abnormality except pleural thickening of the pulmonary apices, suggesting a history of subclinical infection of tuberculous pleurisy. The patient underwent surgery with a curative intent. Thoracotomy revealed that the mediastinum had been replaced with dense fibrous tissues and was widely encased with laminar calcification. Esophagectomy was not performed because it was considered impossible to do so safely. Although diagnosis of fibrous mediastinitis was not made preoperatively, review of the preoperative computed tomographic scans revealed proliferation of mediastinal soft tissues that were associated with patchy and laminar calcifications. Tuberculous fibrosing mediastinitis is an uncommon but clinically important disease for physicians who are involved in the diagnosis and treatment of esophageal cancer.     

A potential peptide vaccine against two different strains of influenza virus isolated at intervals of about 10 years.

We have developed a strategy for making synthetic peptide vaccines, in which a peptide, HA127-133, derived from the hemagglutinin (HA) of A/Aichi/2/68(H3N2) influenza virus (Aichi/68) is introduced into the Ab binding component consisting of 43-46 and 54-58 residues of a pigeon cytochrome c analogue peptide, 46F50V54A. Indeed, this hybrid peptide, 46F/HA127-133/54A, induced impressive T-cell responses and antibody production neutralizing infectivity of Aichi/68 in vitro. In a subsequent study we found that 46F/HA127-133/54A(18mer) peptide antigen, which had been prepared by substitution at the central five residues of 46F50V54A with HA127-133, generated T-cell responses and neutralizing antibody responses as well. On the basis of these prior findings, in the present study we analyzed immunopotency of 46F/HA127-133/54A(18mer) in vivo administered in several ways to I-Ab mice. We show herein that this peptide vaccine loaded in multilamellar liposomes without adjuvant protects the mice against infection with Aichi/68 within 2 weeks after final immunization. Further, this peptide vaccine was shown to be effective in preventing infection with a naturally occurring antigenic variant, A/Texas/1/77(H3N2), carrying the same sequence at 127-133 of the HA as Aichi/68 virus. Since this part of the HA is relatively conserved among H3 subtype influenza viruses, our peptide vaccine may become the basis for a new strategy to prepare effective vaccines that will overcome the ineffectiveness of classical vaccines attributable to antigenic drift of influenza viruses.     

Case Report: Determination of Primary Foci of Metastatic Tumors by p53 Mutational Analysis in Intraesophageal Multiple Carcinomas

It is well known that squamous carcinomasfrequently develop multifocally, either synchronously ormetachronously, in the upper aerodigestive tract (1).Such phenomena were first reported by Slaughter et al in 1953, and they were named fieldcancerization (2). Using recent molecular biologytechniques, these multiple carcinomas have been revealedto arise from independent origins (3). Esophagealcarcinomas have been reported to frequently metastasize tothe lymph nodes even at the early stage of tumorextension (4). Furthermore, simultaneous multifocalcancer development is not rare in the esophagus (5). In cases of intraesophageal multiple carcinomaswith lymph node metastases, the primary focus of themetastatic tumors cannot be identified by conventionalhistologic examination. Here we report a case of intraesophageal multiple carcinomas in whichthe attributed foci of lymph nodal metastases could beclearly identified by analyzing the p53 gene mutationalstatus used as a clonal marker.     

Relationship between the ability to perform the sit-to-stand movement and the maximum pelvic anteversion and retroversion angles in patients with stroke

[Purpose] The purpose of this study was to investigate the relationship between the ability to perform the sit-to-stand movement and the maximum pelvic anteversion and retroversion angles of patients. [Subjects] Thirty-two stroke patients (66.7±7.6 years) (>3 months post-stroke) who were able to sit unsupported and 50 age-matched healthy subjects participated in this study. The stroke patients were classified into two groups according to the sit-to-stand movement test: the group that was able to stand up (the stand-able group) (18 persons) and the group that was unable to stand up (the stand-unable group) (14 persons). [Methods] Pelvic anteversion and retroversion maximum angles were measured by a manual goniometer attached to an inclinometer. [Results] The maximum pelvic anteversion angles were −1.6 ± 5.0°, 1.2 ± 2.8°, and −12.4 ± 6.1° in the control group, the stand-able stroke group, and the stand-unable stroke group, respectively. A significant main effect of group was found. An angle discriminating between the two stroke groups was found: the maximum anteversion angles in the stand-able group were distributed above −5°. [Conclusion] The maximum pelvic anteversion angle was significantly smaller in the stand-unable group than in the stand-able and control groups.Key words: Stroke, Pelvis, Sit-to-stand     

Antifibrotic effect of adrenomedullin on coronary adventitia in angiotensin II-induced hypertensive rats

OBJECTIVE: The extracellular matrix (ECM) determines the structural integrity of the heart and vasculature, participating in cardiovascular remodeling. We previously reported that adrenomedullin (AM) inhibited cellular proliferation and protein synthesis of cardiac fibroblasts; however, the precise mechanisms of AM actions as an antifibrotic factor remain unknown. The purpose of this study was to examine the biological actions of AM against the profibrotic factor angiotensin II (Ang II) in coronary adventitia. METHODS AND RESULTS: Rats with hypertension induced by Ang II infusion were administered 0.06 mug/kg/min recombinant human AM subcutaneously for 14 days. The AM infusion significantly (p<0.05) reduced the Ang II-induced increase of coronary adventitial fibroblasts expressing Ki-67 and alpha-smooth muscle actin (alpha-SMA) in the left ventricle, by 65%, and 62%, respectively, without affecting systolic blood pressure, left ventricle/body weight, or cross-sectional area of myocardial fibers. Collagen deposition of coronary arteries was reduced by the AM infusion (-24%, p<0.01), and these effects of AM were accompanied by significant reductions in gene expression of type 1 collagen (-49%, p<0.05) and transforming growth factor-beta1 (TGF-beta1) (-55%, p<0.01). In cultured cardiac fibroblasts, 10(-7) mol/L AM exerted an inhibitory effect on TGF-beta1-induced alpha-SMA expression (p<0.01) that was mimicked by 8-bromo-cAMP and attenuated by the protein kinase A inhibitor H-89. CONCLUSION: AM decreased Ang II-induced collagen deposition surrounding the coronary arteries, inhibiting myofibroblast differentiation and expressions of ECM-related genes in rats. The present findings further support the biological action of AM as an antifibrotic factor in vascular remodeling.     

Roles of phosphatidylinositol 3-kinase-Akt and NADPH oxidase in adenosine 5'-triphosphate-sensitive K+ channel function impaired by high glucose in the human artery

The present study was designed to examine roles of the phosphatidylinositol 3-kinase-Akt pathway and reduced nicotinamide-adenine dinucleotide phosphate oxidases in the reduced ATP-sensitive K(+) channel function via superoxide produced by high glucose in the human artery. We evaluated the activity of the phosphatidylinositol 3-kinase-Akt pathway, as well as reduced nicotinamide-adenine dinucleotide phosphate oxidases, the intracellular levels of superoxide and ATP-sensitive K(+) channel function in the human omental artery without endothelium. Levels of the p85-alpha subunit and reduced nicotinamide-adenine dinucleotide phosphate oxidase subunits, including p47phox, p22phox, and Rac-1, increased in the membrane fraction from arteries treated with D-glucose (20 mmol/L) accompanied by increased intracellular superoxide production. High glucose simultaneously augmented Akt phosphorylation at Ser 473, as well as Thr 308 in the human vascular smooth muscle cells. A phosphatidylinositol 3-kinase inhibitor LY294002, as well as tiron and apocynin, restored vasorelaxation and hyperpolarization in response to an ATP-sensitive K(+) channel opener levcromakalim. Therefore, it can be concluded that the activation of the phosphatidylinositol 3-kinase-Akt pathway, in combination with the translocation of p47phox, p22phox, and Rac-1, contributes to the superoxide production induced by high glucose, resulting in the impairment of ATP-sensitive K(+) channel function in the human visceral artery.