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T Sakakura

Publications and source records attributed to T Sakakura.

At least 73 records · Page 4Linked to original sources
PubMed1994

[Transurethral hyperthermic treatment in patients with benign prostatic hypertrophy].

Transurethral hyperthermic treatment was performed on 30 patients with benign prostatic hypertrophy (BPH). Two patients had a urethral catheter because of urinary retention. The prostate was heated transurethrally. The treatment consisted of 3-8 sessions of 60 min. each. To evaluate this treatment, the following parameters were determined before and 1-5 weeks after the last hyperthermia session; subjective symptoms score, and as objective data residual urine volume and uroflowmetry. The symptoms score improved in 25 (83%) patients. Of 2 patients with a catheter, the catheter could be removed from 1 patient. Although there was no change in prostatic volume, significant decreases in residual urine volume, and increases of maximum flow rate and mean flow rate were observed. No adverse reactions were seen. Judging from the above results, this treatment is considered to be useful for patients with BPH.

Aged↗
PubMed1994

Tenascin expression and postnatal development of the human prostate.

We investigated the distribution of tenascin during postnatal development of the human prostate. Monoclonal antibody specific to human tenascin was applied to paraffin sections by the avidin-biotin-complex method to examine its localization. Infantile prostates showed two distinct zones. The inner zone had sparse acini with fibromuscular bundles. The peripheral zone had similar acini and lighter stroma as compared with inner zone. Tenascin was found diffusely but weakly. The periglandular area occasionally showed immunoreactivity. The prostates from 9- to 13-year-old subjects had a morphology similar to that of the infantile gland. The difference was increased density of the acini. Immunoreactivity was low. In the prostates from 14- to 21-year-old subjects, the acini distribution was more crowded, and the epithelial lining had become taller in both zones. Tenascin distributed preferentially in the peripheral zone during this period. Simultaneously, the percent of glandular area in the peripheral zone rose abruptly. The dynamics of tenascin expression are closely associated with the development and maturation of the gland. The distribution of tenascin during the post-puberal period may suggest its participation in the preferential of prostatic carcinoma in the peripheral zone.

Adolescent↗
PubMed1994

Can tenascin be redundant in cancer development?

Histological and biochemical analyses of tenascin in various human tumors have indicated that tenascin is expressed in various cancer stroma and increased in the serum, getting strong with advancement of its malignancy. Of interest, the prognostic analysis of breast and colon cancers revealed favorable survival and no lymphogenous metastasis in patients whose cancer expressed tenascin strongly. Injection of tenascin nonproducing A431 human epidermoid cancer cells into nude mice resulted in tenascin production by these cells, suggesting cancer cells can make tenascin if necessary. Thus, both carcinoma and adjacent stroma cells may produce tenascin to coordinate the microenvironment surrounding the cancer tissues. Several tenascin variants have been clearly demonstrated to date. With these findings in mind, we would propose that epithelial tenascin supports the carcinoma cell outgrowth, whereas stromal tenascin may block cancer invasion by covering the cancer nest. No obvious phenotype in tenascin gene knockout mice would indicate that tenascin is functionally redundant in developmental processes, yet it may well be very important in progression of cancer.

Animals↗
PubMed1994

[A case of uterine prolapse with hydroureter].

We report a case of complete uterine prolapse with bilateral hydroureter. The patient was a 81-year-old woman with complete uterine prolapse suffering from dysuria and urinary incontinence. Bilateral moderate hydroureter happened to be revealed by drip infusion pyelography (DIP) but blood creatinine was normal. Hydroureter was ameliorated by vaginal hysterectomy. A brief discussion and review of the literature are given.

Aged↗
PubMed1993

Structure and organization of the gene encoding a mouse mitochondrial stress-70 protein.

We have previously found that an antigenic protein specific for C3H strain mouse (C3H strain-specific antigen, CSA) is identical to peptide-binding protein 74 (PBP74). PBP74/CSA is a novel member of the stress-70 protein family in mitochondria. In this study, mouse genomic clones encoding PBP74/CSA, including the 5'- and 3'-flanking regions of the gene, have been isolated and sequenced. The PBP74/CSA gene contained 17 exons interrupted by 16 introns. Two dimeric repeats of the consensus sequence of the heat-shock element are present in the 5'-flanking region of the PBP74/CSA gene. Moreover, the first intron is interrupted within the amino-terminal leader sequence, the pattern of which is similar to that of cytochrome c1 located in the mitochondria.

Amino Acid Sequence↗
PubMed1993

Antigenic protein specific for C3H strain mouse is a mitochondrial stress-70 protein.

Cells derived from C3H strain mouse produce an antigenic protein (CSA) specific for this strain [Kusakabe, M., et al. (1988) J. Cell Biol. 107, 257-265]. To examine the molecular basis of CSA, cDNA cloning of the antigenic protein was carried out. The deduced amino acid sequence demonstrates that CSA is the same protein as peptide-binding protein 74 (PBP74), a novel member of the stress-70 family. However, comparison of the PBP74/CSA sequences between C3H/HeN and BALB/c strain mice reveals the substitution of two amino acids in the substrate-recognition domain of the stress-70 protein. Western blot analysis indicates that one out of these two residues, arginine at residue 578 in the PBP74/CSA sequence of C3H mouse, contributes to the immunogenicity of CSA. Moreover, the subcellular localization of PBP74/CSA in mitochondria is also demonstrated by immunohistochemical analysis using anti-CSA monoclonal antibody. Thus, it is interesting that a genetic marker sequence in mice is located on the gene encoding a mitochondrial stress-70 protein.

Amino Acid Sequence↗
PubMed1993

Reconstruction of neural tube-like structures in vitro from primary neural precursor cells.

Vertebrate central nervous system develops from a neural tube derived from the embryonic ectoderm. In mouse, the neural tube around embryonic day 10 primarily consists of neural precursor cells (NPCs). During the development of embryonic central nervous system, NPCs proliferate and migrate outward; thus later stages show NPCs toward the lumen of the neural tube and neurofilament-positive differentiated cells toward the periphery. In conventional liquid culture, NPCs isolated from mouse on embryonic day 10 proliferate and differentiate into neurofilament-positive neurons. In the present communication, we show that fragments of neural tubes and aggregates of NPCs, when placed into collagen gel matrix, form three-dimensional structures which resemble the neural tube formed in vivo in the developing embryos. Even dissociated NPCs form the three-dimensional structures in the collagen gel matrix. Our results indicate that individual NPCs or fragments of neural tubes carry morphogenetic information which allows them to reconstruct neural tube-like structures in vitro.

Animals↗
PubMed1993

Tenascin expression in vitro and in vivo: comparison between epithelial and nonepithelial rat cell lines.

Tenascin is a novel six-armed extracellular-matrix glycoprotein expressed in association with mesenchymal-epithelial interactions, and its expression is temporally and spatially restricted during organogenesis and carcinogenesis. The distribution and alterations in the expression of fibronectin, laminin, and especially of tenascin, were compared between in vitro and in vivo studies with rat epithelial (hepatocyte-derived) and nonepithelial (sarcoma-derived) cell lines. Immunoprecipitation studies revealed that the production of extracellular-matrix glycoproteins varied among the cell lines. Two ascites-hepatoma-derived cell lines and one sarcoma-derived line were found to synthesize tenascin in vitro. Their major tenascin isoform yielded a molecular weight of 220 kDa under reducing conditions. The other cell lines examined, including all of those derived from normal hepatocytes, were negative for the expression of tenascin. Coculture studies were performed between epithelial and nonepithelial cell lines. No drastic change in tenascin expression was found after coculturing the cells. As an in vivo study, cell lines were transplanted into nude mice. All xenografts of the epithelial lines were associated with a strong positive reaction for extracellular-matrix glycoproteins, and especially for tenascin, in the mouse fibrous stroma adjacent to them. This represents the epithelial induction of stromal tenascin. Whether or not they produced tenascin in vitro, after transplantation none of the epithelial cell lines themselves produced tenascin, whereas both of the nonepithelial cell lines prominently produced tenascin. These findings suggest that, in the process of interactions between epithelial and nonepithelial cells, the expression of tenascin depends on the switch from in vitro to in vivo.

Animals↗
PubMed1993

Specific expression of tenascin in human colonic neoplasms.

Tenascin, a novel six-armed extracellular matrix glycoprotein, was immunohistochemically examined in the human normal adult colon, and colonic neoplasms such as tubular adenomas, primary and metastatic adenocarcinomas. In contrast to previous reports, tenascin was hardly detectable in the normal adult colons, being predominantly localised in the fibrous stroma surrounding the glandular epithelia of the neoplastic lesions. The neoplastic cells themselves were totally negative for tenascin expression. Both the tubular adenoma tissues and the superficial layer of well-differentiated adenocarcinomas in general were intensely reactive to tenascin antibody, and the staining intensity increased as the adenoma became more atypical in cases of tubular adenomas. By pretreatment of the paraffin-embedded tissue sections with pepsin, the distribution of tenascin was often intensified considerably and distinct localisation was more clearly demonstrated in the colonic tumour tissues. Tenascin was also biochemically purified from human invasive colonic carcinomas, and this cancerous tissue tenascin was compared with that extracted from a human umbilical cord fibroblast cell line in terms of molecular heterogeneity. Two major isoforms of the purified tenascin from colonic cancer tissues were found to have relative molecular masses of 250 kD and 190 kD, which were almost identical to those of human foetal fibroblast tenascin glycoproteins. In addition, several lower molecular weight isoforms were frequently detectable in the cancerous tissues, which might represent immuno-reactive tenascin isoforms proteolytically digested in human colonic carcinomas in vivo.

Adenocarcinoma↗
PubMed1993

Distribution of tenascin in normal cycling human ovary.

Tenascin is an extracellular matrix glycoprotein, which has been reported to be involved in parenchymal-mesenchymal interactions during morphogenesis, wound healing, and carcinogenesis. Tenascin immunolocalization was performed in 51 specimens of morphologically normal human ovaries by using a specific monoclonal antibody against purified human fibroblast tenascin. In preovulatory follicles, no significant immunoreactivity was detected. In functioning corpora lutea, immunoreactivity was present as a fine border around the periphery. In association with the involution of the corpora lutea, marked diffuse tenascin immunostaining in the intercellular space was observed. These data raise the question of whether tenascin may be involved in luteolysis and may play an important role in the ovarian cycle by regulating the involution of corpora lutea.

Cell Adhesion Molecules, Neuronal↗
PubMed1993

Relationships among tenascin expression, DNA ploidy patterns, and multidrug resistance gene product (P-glycoprotein) in human colon carcinoma.

Relationships among tenascin expression, DNA ploidy, and P-glycoprotein were examined in 81 primary human colon cancers and 61 metastatic lymph nodes. First, the DNA ploidy patterns of colon cancerous tissue surrounded (TN+) and not surrounded (TN-) by tenascin immunoreactivity were investigated. Then the expression of P-glycoprotein, one of two multidrug resistance gene products, was examined in TN+ and TN- colon cancer tissues by immunohistochemistry. Aneuploid DNA patterns were observed at high frequency in TN- colon cancer tissues (37/61) and metastatic lymph nodes (44/52). In contrast, diploid DNA patterns were observed predominantly in TN+ colon cancer tissues (50/56). Although P-glycoprotein expression was observed in primary TN+ and TN- colon cancer (9/81), the level of P-glycoprotein expression was not correlated with DNA aneuploidy in TN- colon cancer tissues. Overall, reduced tenascin expression was correlated well with DNA aneuploidy, but no significant correlation was found between DNA aneuploidy and P-glycoprotein appearing when cancer cells become resistant to several anti-cancer drugs. Thus, tenascin may play an important role in preventing colon cancer cells from invading surrounding tissues.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1993

The mouse chimera during intrauterine stages: immunohistochemical analysis with the C3H strain-specific antibody.

Our objective was to establish an immunohistological method for analysis of chimerism in mouse chimeras at embryonic stages with an anti-C3H strain-specific antigen (CSA) antibody. We developed an effective new method to retain CSA antigenicity with good morphology of embryonic tissues by using microwave irradiation (MWI) for pre-fixation, 95% ethanol/1% acetic acid as post-fixative solution, and polyester wax as embedding material. We used a biotinylated mouse monoclonal anti-CSA antibody, peroxidase-avidin, and silver amplification. These procedures were successful in demonstrating the chimerisms in various tissues of C3H<-->Balb/c chimeras at different embryonic stages and postnatal days. In chimeras at Days 7 and 7.5 post coitum (p.c.), both genotypes were clearly identified and well intermingling in every embryonic tissue (embryonic ectoderm, mesoderm, extra-embryonic ectoderm, ectoplacental cone, amnion, and chorion). Chimerisms at Day 14.5 p.c. were also clearly observed in mesencephalon, neural retina, spinal cord, lung, kidney, and liver. We concluded that the present immunohistological procedures for analysis of chimerism during embryonic periods will give us insightful information about dynamic histological changes such as cell proliferation, migration, selection, and death during organogenesis.

Amnion↗
PubMed1993

Induction of tenascin in cancer cells by interactions with embryonic mesenchyme mediated by a diffusible factor.

Human cancer cell lines A431 and MCF7, which do not produce tenascin (TN) in vitro, were found to produce TN when injected into nude mice or co-cultured with the embryonic mesenchyme. The TN expression in the developing A431 solid tumor was demonstrated by immunohistochemistry and by in situ hybridization. Human TN was detected in culture media by western blot analysis using human specific monoclonal antibody (RCB-1). During tumorigenesis, in the early stage, mouse TN was actively induced and deposited in the peri- and intertumor spaces surrounding the developing tumor. Two days later, TN derived from human epithelial cancer cells was induced and mainly deposited in the intertumor basement membrane. After this stage, tumor cells were actively producing TN. On the other hand, TN induction in non TN-producing cells, such as A431 and MCF7 cell lines, was also observed in vitro. Although cell lines such as NIH-3T3, phi 2, STO, 2H6, 3E5 and CMT315, had no effect on the TN induction, primary cultured embryonic mesenchyme effectively stimulated the TN expression in the cancer cell lines. This mesenchymal effect decreased with age and was entirely lost postnatally. Furthermore, conditioned media from these embryonic mesenchymes could reproduce the same effects on TN induction as observed in the co-culture study. In conclusion, these findings suggest that TN induction in epithelial cancer cells may depend on interactions with the surrounding environment, that these interactions may be mediated by a soluble factor(s) derived from the surrounding mesenchyme and that the TN induction observed in the tumorigenesis may reflect histogenesis during the embryonic period.

Animals↗
PubMed1993

Mapping of the 70 kDa, 34 kDa, and 11 kDa subunit genes of the human multimeric single-stranded DNA binding protein (hSSB/RPA) to chromosome bands 17p13, 1p35-p36.1, and 7p21-p22.

Human single-stranded DNA binding protein (hSSB/RPA) is a multimeric single-stranded DNA binding protein consisting of three subunits of 70 kDa, 34 kDa, and 11 kDa. Human SSB was isolated from HeLa cells as an essential factor for the in vitro replication of simian virus 40 DNA. We and others have isolated and sequenced cDNAs for each subunit of the SSB. The chromosome on which each gene is located was determined through the analysis of a panel of human/hamster somatic cell hybrids using the polymerase chain reaction with pairs of synthetic oligonucleotide primers from the 3'-untranslated sequences of the genes. Genomic clones for each gene were isolated from a genomic cosmid library prepared from human lymphoblastoid cells. Using those clones as probes, we have carried out fluorescence in situ hybridization to human metaphase chromosomes and have mapped the 70 kDa subunit gene to 17p13, the 34 kDa subunit gene to 1p35-p36.1, and the 11 kDa subunit gene to 7p21-p22. Since hSSB participates in replication, recombination and repair of DNA, the physical mapping of hSSB genes may aid in the identification of human hereditary diseases associated with aberrant DNA reactions caused by genetic alterations of the hSSB.

Animals↗
PubMed1993

[Clinical evaluation of pressure-flow test to male patients with micturition disturbance].

We examined pressure-flow test results in 28 male patients with micturition disturbance in whom it is difficult to determine whether bladder outlet obstruction or impaired detrusor contractility is the cause. One reason that some patients do not improve after prostatectomy is that detrusor contractility was not estimated before preoperatively. The degree of infravesical obstruction and of detrusor function were assessed by the method of Griffiths' diagram (maximum flow rate versus corresponding detrusor pressure). Three patients showed infravesical obstruction, 11 equivocal obstruction, and 14 no obstruction. No patients showed strong detrusor function, 14 normal function, and 14 weak function. Eleven patients underwent TU-procedure. Two patients with normal detrusor function and infravesical obstruction showed good postoperative improvement of uroflowmetry results, but 4 patients with weak detrusor function and no infravesical obstruction showed no improvement. Preoperative assessment of the degree of infravesical obstruction and of detrusor function by pressure-flow testing is therefore considered useful. We emphasize that preoperative evaluation of detrusor function is an important aspect of treatment of male micturition disturbance.

Adult↗
PubMed1993

[Relationship of an extracellular matrix protein, tenascin and breast diseases].

Tenascin is an extracellular matrix glycoprotein consisting of six disulfide-linked subunits with molecular masses of 190-250 kDa. Molecular analysis of the tenascin gene revealed that it contains a region homologous to epidermal growth factor genes, repetitive sequences of the type III fibronectin and the fibrinogen gene. Culture studies have shown that tenascin has multiple functions including cell attachment and detachment, promotion and inhibition of neural crest cell migration, cell growth stimulation and hemagglutination. Immunohistochemically, tenascin shows a characteristic and spatially restricted distribution. In mouse mammary glands, tenascin protein is demonstrated in the dense mesenchyme present around growing epithelia during embryogenesis and oncogenesis. Tenascin is expressed in normal human adult breast tissue and benign conditions, although it is expressed more abundantly in breast cancer tissue. Prominent tenascin staining is found in dense cancer-mesenchymal junctions. The staining positivity is significantly correlated with metastasis to regional lymph nodes and tumor grade. Tenascin positive patients have a significantly poorer prognosis compared with tenascin-negative patients. Although the biological functions of tenascin in breast cancer tissue have not yet been clearly elucidated, tenascin staining in surgical tissue specimens might be useful when applied to detect a subgroup of breast cancer patients who have a poorer prognosis.

Animals↗
PubMed1993

Tenascin expression in normal and abnormal human endometrium.

Tenascin has been recently characterized as an extracellular matrix glycoprotein involved in tissue interactions during fetal development and oncogenesis. In order to study the possible involvement of tenascin in epithelial growth of the human endometrium, we evaluated the expression of tenascin in 84 cases of normal, hyperplastic, or neoplastic human edometrium. The specimens were obtained by curettage and/or biopsy and analyzed by immunohistochemistry utilizing a newly developed monoclonal antibody against human tenascin. Weak periglandular immunoreactivity was observed in 50% of proliferative phase, but not in secretory endometrium. Approximately 60% of endometrial hyperplasia specimens had weak periglandular tenascin immunoreactivity, but its distribution was irregular and not necessarily correlated with degree of cell atypia. Invasive endometrial carcinomas displayed intense and diffuse staining around the carcinoma cells, in addition to thin periglandular immunoreactivity similar to that seen in hyperplasia. The intensity of tenascin staining in endometrial carcinoma was not related to the degree of tumor differentiation. These results suggest that tenascin appears as a result of interactions between neoplastic epithelium and stroma in tumor development and that diffuse and intense staining could be a stromal marker for the invading capacity of human endometrial malignancies.

Cell Adhesion Molecules, Neuronal↗