Biomedical subjects
Publications and source records attributed to N Seki.
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Connectin was isolated from fish dorsal myofibrils by an SDS-gel filtration method and estimated to account for approximately 13% of the total myofibrillar proteins. There was no significant difference in the amount of connectin among seven fish species but rabbit skeletal myofibrils contained a slightly higher content (16%) of connectin. The high molecular weight connectins from carp and rabbit both showed a doublet band, consisting of bands 1 and 2, on SDS-polyacrylamide gel electrophoresis using a large-pore gel. However, rabbit band 1 (a component of the connectin doublet) was found to migrate more slowly than carp band 1. During post-mortem ageing of the muscles, it was observed that the band 1 component rapidly disappeared with a concomitant increase in band 2 component and then the band 2 component was transformed slowly into faster migrating components. These results suggest that post-mortem ageing has qualitatively similar effects on the submolecular compositions of carp and rabbit connectins. However, the apparent rate of disappearance of the band 1 component was considerably higher in carp muscle than that in rabbit muscle.
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The aim of this study was to investigate the relationship between heparanase expression and prognostic factors in endometrial cancer, as well as the relationship between heparanase expression during phases of the normal endometrial cycle. Immunohistochemical analysis of 166 endometrial cancers and 34 normal endometria in various phases of growth was performed. The heparanase expression in the late-proliferative phase of normal endometria was found to be significantly higher than in either the early-proliferative or the secretory phases (P= .012 and P= .044, respectively). Heparanase expression was also significantly higher in endometrial cancer patients with tumors of an advanced FIGO stage (P= .0003) and high FIGO grade (P= .004) and with cancers showing either deep myometrial invasion (P= .023), lymph node metastasis (P= .006), lymphvascular space involvement (P= .048), or positive peritoneal cytology (P= .010). The disease-free and overall survival rates of patients with intense heparanase expression were significantly lower than those of patients with absent or moderate heparanase expression (P= .004 and P= .002, respectively). Heparanase may participate in normal endometrial remodeling and can serve as an indicator of the aggressive potential and poor prognosis of endometrial cancers.
The pathogenesis of Sjögren's syndrome (SS) is poorly understood. In this study we used an in-house mouse spleen cDNA microarray to analyse genes in spleens from MRL/lpr (an SS mouse model) mice. We have previously demonstrated that GRAP genes were up-regulated in salivary glands of the same mice. The microarray analysis showed that seven out of 2304 genes were highly expressed in spleens from the MRL/lpr mice, one of which was the GRAP gene. In other words, the GRAP gene is highly expressed in the salivary glands and spleen of MRL/lpr mice. We also carried out immunohistochemical studies. Mouse and human Grb-2-related adaptor protein (GRAP) antigens were expressed on ductal cells and infiltrating lymphocytes in salivary glands of MRL/lpr mice and SS patients, but only weakly in controls (MRL/+ mice and individuals with salivary cysts). These results suggest that the GRAP gene might have a role in the pathogenesis of SS.
We examined the expression of platelet-derived endothelial cell growth factor (PD-ECGF) mRNAs in 47 invasive cervical cancer tissues by semi-quantitative RT-PCR and addressed its association with clinicopathological features including microvessel density. Squamous cell carcinomas expressed higher levels of PD-ECGF mRNA than non-squamous cell carcinomas (P=0.014). We found no association between FIGO stage and levels of PD-ECGF mRNA. A subset of 31 patients with stage Ib-II cervical cancer underwent radical hysterectomy and pelvic lymphadenectomy. There were no significant differences in PD-ECGF mRNA levels with respect to tumor size, degree of stromal invasion, lymphvascular space involvement, parametrial involvement, vaginal involvement or lymph node metastasis among these patients. There was no correlation between microvessel density and the levels of PD-ECGF mRNA. These findings suggest that PD-ECGF expression is not associated with progression and metastasis of cervical cancer.
The aim of this study was to determine whether tumor-associated macrophages (TAMs) infiltration correlates with clinicopathological factors including microvessel, counts and clinical outcome in endometrial cancer. Overall 56 out of the 109 endometrial cancers (51.4%) expressed distinct tumor-associated macrophages infiltration in their tumor stroma. Tumor-associated macrophages infiltration was significantly high in tumors with deep myometrial invasion, high grade and elderly patients. Microvessel counts strongly correlated with tumor-associated macrophages infiltration in tumor stroma (p = 0.0002). However, tumor-associated macrophages infiltration was not a prognostic factor. In conclusion, tumor-associated macrophages may play a crucial role in the promotion of angiogenesis, but can not be used to prodict prognosis of patients with endometrial cancer.
BACKGROUND: The role of thrombospondin (TSP) in tumor progression remains controversial. The association of TSP with clinicopathological features regarding prognostic significance was examined in patients with epithelial ovarian tumor. MATERIALS AND METHODS: Gene expression of TSP-1 and TSP-2 was assessed by reverse transcriptase-polymerase chain reaction in 6 borderline and 29 malignant epithelial ovarian tumors. RESULTS: TSP-1 mRNA expression was detected in 14 out of the 29 malignant epithelial ovarian tumors (48.3%), whereas TSP-2 mRNA expression was detected in 7 malignant epithelial ovarian tumors (24.1%). In contrast, no specimen from the borderline epithelial ovarian tumors expressed TSP mRNA. TSP-1 expression was significantly higher in tumors with advanced stage, massive ascites, positive peritoneal cytology and high grade. TSP-2 expression was significantly higher in tumors with massive ascites. Patients exhibiting TSP-1 and -2 mRNA expression demonstrated a markedly poorer prognosis than those lacking TSP-1 and -2 mRNA expression. CONCLUSION: These findings provide evidence that TSP expression may be associated with an aggressive phenotype in this class of neoplasm.
The present study investigates the cellular and molecular mechanisms responsible for expressing genetic control of type II collagen-induced murine chronic arthritis. Analyses were made for both humoral and cellular immune responses, since the induction of arthritis required synergy between both types of immunities. Immunization of high (DBA/1) and low (C57BL/6, C3H/He, BALB/c) responder mice with native bovine type II collagen resulted in the production of the respective high and low levels of anti-collagen antibody. However, polyclonal in vitro stimulation of normal spleen cells from high or low responder mice with lipopolysaccharide (LPS) induced a comparable magnitude of anti-collagen antibody responses, indicating the localization of the genetic defect at cellular levels other than B cells themselves. In contrast to immunization with native collagen, sensitization of DBA/1 mice with heat-denatured collagen failed to stimulate B cells, but resulted in selective generation of L3T4+ T cell-mediated immunity. These included anti-collagen delayed-type-hypersensitivity (DTH) responses and the generation of various interleukins (IL) responsible for antibody production as well as DTH responses. It was demonstrated that there was appreciable difference in the magnitudes of these responses between lymphoid cells from high and low responder mice. Differential effects of sensitization with heat-denatured collagen in high versus low responders were reflected on the genetic difference in the development of chronic arthritis. A typical arthritis was induced neither in denatured collagen-sensitized DBA/1 mice nor in unsensitized mice transferred with anti-collagen antiserum. However, the antiserum transfer into denatured collagen-sensitized DBA/1 mice induced chronic perpetuating arthritis. This sharply contrasted with the failure of the same aliquot of the antiserum to induce a chronic arthritis when inoculated into denatured collagen-sensitized low responder mice. These results indicate that the genetic control of the induction of arthritis is expressed on L3T4+ T cells which are required for generating anti-collagen humoral as well as cell-mediated immunities as assessed by DTH responses in vivo or lymphokine productions in vitro.