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Biomedical subjects

Y Takami

Publications and source records attributed to Y Takami.

At least 109 records · Page 6Linked to original sources
PubMed1992

Determination of the functional difference between human papillomavirus type 6 and 16 E7 proteins by their 30 N-terminal amino acid residues.

Human papillomavirus type 16 (HPV 16) is often found in cervical carcinomas, while HPV 6 is frequently associated with benign genital lesions. We have compared the abilities of the E7 transforming proteins of HPV 6 and 16 to transform various established and primary rodent cells by using the same heterologous promoter system. HPV 16 E7 efficiently induced anchorage-independent growth of all the rodent cell lines tested and immortalized or cooperated with ras in transforming primary rat cells. On the other hand, the transforming activity of HPV 6 E7 was lower and was restricted. By construction of chimeras of HPV 6 and 16 E7, we found that the difference in transforming activity between the two E7 proteins was mainly determined by the difference in their 30 N-terminal amino acid residues, although some activities seem to be slightly affected by differences in their residual C-terminal portions.

3T3 Cells↗
PubMed1992

Penile reconstruction with de-epithelized superficial external pudendal artery flap.

Complete loss of skin, Buck's fascia and tunica albuginea of the corpus cavernosum occurred on both sides of the penile shaft after placement of a penile prosthesis for the treatment of Peyronie's disease. We describe this unusual complication and surgical reconstruction of the penis with a de-epithelized superficial external pudendal artery axial pattern flap (January 1988). A good result was obtained.

Humans↗
PubMed1992

[A case of subaortic stenosis due to parashute accessory mitral valve tissue].

An 11-year-old boy with subaortic stenosis due to parashute accessory mitral valve tissue was treated successfully with surgery. He had a mild left ventricular-aortic pressure gradient associated with mild aortic regurgitation. The abnormal subaortic tissue was attached to the anterior leaflet of the mitral valve and was complicated with discrete subaortic stenosis. This tissue had five chordae connecting to the anterior papillary muscle and the anterior leaflet of the mitral valve. By resection of this accessory tissue and the part of the septal discrete stenotic tissue, stenosis of the left ventricular outflow tract was relieved completely.

Aortic Stenosis, Subvalvular↗
PubMed1992

[A case of post infarction true left ventricular aneurysm which showed pseudoaneurysm-like shape in left ventriculography].

A 69-year-old man who had a post-infarction left ventricular aneurysm underwent surgical repair. Preoperative left ventriculography showed a small aneurysm, 3.0 x 3.0 x 2.5 cm in size, with a narrow neck at the inferior wall suggesting a typical "false" aneurysm. But intraoperative and pathological examination revealed that this was a "true" aneurysm which contains coronary artery and myocardial cells in its wall. Left ventriculography is not necessarily the definite standard to differentiate between true and false left ventricular aneurysm.

Aged↗
PubMed1991

Cloning and characterization of human papillomavirus type 52 from cervical carcinoma in Indonesia.

Human papillomavirus (HPV) type 52 from a cervical carcinoma in Indonesia was molecularly cloned and characterized. By hybridization with cervical carcinoma DNAs from Indonesian patients, HPV 52 was detected in 3 of 52 cases (6%), whereas HPV 16 and 18 were detected in 8 and 7 cases, respectively (15% and 13%). Sequence analysis revealed that the E6-E7 ORFs contained several DNA binding motifs (Cys-X-X-Cys) like previously sequenced HPVs. The E6 ORF also contained splice donor and acceptor signals, which may allow the expression of E6* protein. The E7 ORF encoded an amino acid sequence that is conserved in some DNA tumor viruses and is involved in binding to Rb protein and in cellular transformation. Transfection of a subgenomic fragment of HPV 52 under the control of a heterologous promoter showed that the E7 ORF alone induced anchorage-independent growth of established rodent cells and immortalized primary rat embryo fibroblasts (REF), and that in cooperation with activated ras, it induced malignant transformation of REF. The E6 ORF also induced, less efficiently, anchorage-independent growth. These results strongly suggest that HPV 52, like HPV 16 and 18, has oncogenic potential.

Amino Acid Sequence↗
PubMed1991

Rat primary embryo fibroblast cells suppress transformation by the E6 and E7 genes of human papillomavirus type 16 in somatic hybrid cells.

The E6 and E7 genes of human papillomavirus type 16 (HPV-16) transform established lines of rat cells but not rat cells in primary culture irrespective of the expression of the two genes. The reason for this difference between the susceptibilities of cell lines and primary cells was examined by using hybrid cells obtained by somatic cell fusion of rat cell lines transformed by the E6 and E7 genes of HPV-16 and freshly isolated rat embryo fibroblast cells. In these hybrid cells, transformed phenotypes, including colony formation in soft agar, saturation density, and tumorigenicity in nude mice, were suppressed, whereas hybrid cells between E6/E7-transformed cell lines and normal rat cell lines retained these transformed phenotypes. RNA analysis showed that the E6 and E7 genes were transcribed in both types of hybrid cells. These results suggest that primary rat cells possess intracellular functions that cause posttranscriptional suppression of induction of the transformed phenotypes by the E6 and E7 genes of HPV-16.

Animals↗
PubMed1990

[Expression of gamma-glutamyl transpeptidase related to the tumor differentiation on squamous cell carcinoma of human skin].

gamma-Glutamyl transpeptidase (gamma-GTP) has been noticed as one of the useful markers for malignant transformation of the skin. But the role and mechanism of the induction of gamma-GTP in skin carcinogenesis had not yet been studied. In this report, the authors studied the relationship between gamma-GTP activity and tumor differentiation in squamous cell carcinoma of human skin (SCC). Ten cases of SCC were examined on intensity and localization of the activity of gamma-GTP histochemically by the method of Rutenberg. gamma-GTP activity was found to be more intense in well differentiated SCC than in poorly differentiated SCC. On the other hand, localization pattern of gamma-GTP activity in SCC was not always related to the tumor grade. We concluded that expression of gamma-GTP activity in SCC may reflects the modulating cell differentiation rather than cell proliferation in malignant transformation of the skin. And some of the typical cases were presented.

Aged↗
PubMed1989

Possible involvement of microfilaments in protein kinase C translocation.

We investigated the role of microfilaments in stimulus-induced translocation of protein kinase C (PKC) in polymorphonuclear leukocytes (PMNs) from C57BL/6 mice. Cytochalasin B and dihydrocytochalasin B almost completely inhibited PKC translocation induced by either TPA or Ca2+ ionophore after pretreatment of cells for 30 min. In addition, ML-9, a potent inhibitor of Ca2+/calmodulin-dependent myosin light chain kinase which regulate microfilament contraction, and a calmodulin antagonist W-7, also inhibited PKC translocation. These findings suggest the possibility that microfilaments are involved in the translocation of PKC.

Actin Cytoskeleton↗
PubMed1989

The thiol proteinase inhibitors improve the abnormal rapid down-regulation of protein kinase C and the impaired natural killer cell activity in (Chediak-Higashi syndrome) beige mouse.

Protein kinase C (PKC) is essential in intracellular signal transduction for various cell functions including natural killer (NK) cell activity. This enzyme is hydrolysed by calpain, which is Ca2+-dependent thiol proteinase. We showed here that in NK activity-deficient beige (bg/bg) mouse, the model of Chediak-Higashi syndrome, the translocated membrane-bound PKC activity declined rapidly in NK cell-enriched lymphocytes after TPA stimulation. However, the rapid decline was abolished by the pretreatment of cells with leupeptin (a thiol and serine proteinase inhibitor) or E64 (a thiol proteinase inhibitor). Furthermore, these reagents improved the impaired NK cell activity in beige mouse whereas they did not affect NK cell activity in C57BL/6 (+/+) and the heterozygous (+/bg) mice. Meanwhile, TPA stimulation induced only low levels in NK cytotoxic factors (NKCF) release from beige NK cells, but these reagents augmented the lowered NKCF release. These results suggest that the improvement of impaired NK cell activity in beige mouse by the thiol proteinase inhibitors may be due to the elimination of abnormal rapid down-regulation of PKC, resulting in the augmentation of the lowered PKC activity.

Animals↗
PubMed1989

Inhibition of natural killer cell-mediated cytotoxicity by ML-9, a selective inhibitor of myosin light chain kinase.

To investigate the role of microfilaments in natural killer (NK) cell-mediated cytotoxicity, general microfilament inhibitors, cytochalasins B,D and dihydrocytochalasin B, and a selective inhibitor of myosin light chain kinase (MLCK) which regulates microfilament contraction, i.e. 1-(5-chloronaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine hydrochloride (ML-9) were examined in an NK assay system. ML-9 inhibited NK cell activity in a dose-dependent manner without affecting target cell binding, whereas cytochalasins suppressed the binding. The dextran suspension method revealed that ML-9 inhibits the programming for the lysis stage of the lytic process. In the single cell assay, the addition of ML-9 after target cell binding had occurred inhibited the lysis of bound target cells, whereas the addition of cytochalasins in a similar manner did not affect it. Thus, these results suggest the possibility that microfilament contraction is involved in the lytic mechanism of NK cell-mediated cytolysis. However, the mechanism whereby cytochalasins inhibit target cell binding remains unclear.

Actin Cytoskeleton↗
PubMed1989

[An autopsied case of an aged patient with advanced gastric cancer that showed a complete response to immunochemotherapy].

Described is the case of an 88-year-old male suffering from advanced hemorrhagic gastric cancer who, because of surgical risk factors, was conservatively treated with immuno-chemotherapy in the form of suppositories containing ftorafur (FT-207) and Picibanil (OK-432). The patient showed marked clinical improvement from this therapy. However, his advanced age and other associated complications kept us from performing further examinations, such as an upper-G-I series and a gastrofiberscopy. A year and 4-months later, the patients died of pneumonia and subsequently was autopsied. Macroscopically, his gastric tumor was found to have completely disappeared and had been replaced by a yellowish-white scar tissue. Microscopically, no cancer cells were found in the examined specimens or in the regional lymph nodes.

Adenocarcinoma↗
PubMed1989

[Oncogene of human papillomavirus].

Although certain types of human papillomavirus (HPV) have been supposed to be associated with carcinogenesis of cervix, a definitive conclusion has not yet been reported. To show that HPV is a causative agent of cervical cancer, we performed several lines of experiments and obtained the results described below. 1) In attempting to identify an activated oncogene(s), we showed that cellular DNAs from 8 cervical carcinomas induced transformation of NIH 3 T 3 cells and, in all cases, HPV sequences were retained in the secondary transformants. 2) Using a retrovirus vector system, we showed that HPV-16 had transforming activity for mouse or rat established cells. The transforming genes are located in the E6 and E7 ORF: the former governs tumorigenicity in nude mice and the latter influences cell growth properties such as saturation density, colony formation in soft ager and immortalization. These results strongly suggest that specific types of HPV are involved in carcinogenesis of the cervix. However, HPV only may not be sufficient to induce carcinomas, because even the E6 and E7 ORFs of HPV-16 could not transform rat primary cells immediately after infection, but could do so after a long latency. Evaluation of the change during the latency is very important to clarify the mechanism of cervical carcinogenesis.

Animals↗
PubMed1988

Rapid down-regulation of protein kinase C in (Chediak-Higashi syndrome) beige mouse by phorbol ester.

Protein kinase C(PKC) activity in macrophages and polymorphonuclear leukocytes was assayed in beige mouse, the model of Chediak-Higashi syndrome, control C57BL/6 and the heterozygous (+/bg) mice. Regarding enzyme activity in the cytosolic and membrane fractions of these cells, there was no difference between beige mouse and the control. After short-term activation by TPA, the translocated membrane-bound PKC activity in beige mouse decreased rapidly compared with that in control mouse. However, the cytosolic PKC activity decreased at just the same pace as the control. The change in [3H] PDBu binding paralleled the changes in PKC activity. An increase in Ca2+/phospholipid-independent protein kinase by TPA was notable in the membrane fraction of beige mouse. The increase in the kinase activity was abolished and the PKC activity recovered to normal level by the addition of calpain inhibitor, leupeptin, to the incubation of cells along with TPA. Therefore, these findings suggest that a rapid decrease in membrane-bound PKC activity in beige mouse by TPA stimulation is associated with calpain.

Animals↗
PubMed1988

Modulation of protein kinase C activity during inhibition of tumor cell growth by IFN-beta and -gamma.

We investigated the effects of human interferon(IFN)-beta and -gamma on protein kinase C activity in human HEp-2 and KHm-14 tumor cells during IFN-induced inhibition of cell growth. Cytosolic protein kinase C activity in both cell lines was strikingly decreased following treatment with either IFN-beta or -gamma. In the particulate fraction, IFN-gamma decreased protein kinase C activity within 1 hr but it reappeared after 24 hr, whereas IFN-beta decreased the activity during the inhibition of cell growth. Furthermore, phorbol-12,13-dibutyrate(PDBu)-binding activity was altered in parallel with the changes in protein kinase C activity induced by the IFNs. In summary, we showed that IFN-beta and -gamma cause long-term modulation of protein kinase C activity in these cultured tumor cells.

Cell Division↗
PubMed1988

A potent inhibitor of protein kinase C inhibits natural killer activity.

A potent inhibitor of protein kinase C(PKC), 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7), dose-dependently inhibited natural killer (NK) activity in large granular lymphocytes (LGL) pretreated at 37 degrees C for 30 min. However, neither N-(2-aminoethyl)-5-isoquinolinesulfonamide dihydrochloride (H-9), which inhibits more effectively cyclic nucleotide-dependent protein kinases than other kinases, nor N-(2-guanidinoethyl)-5-isoquinolinesulfonamide hydrochloride (HA1004), which was used as a control for H-7, reduced NK activity. The inhibitor effect of H-7 was not due to changes in effector cell viability or target cell binding. We also found that H-7 suppresses PKC activity in both the cytosol and membrane fractions of LGL. From these findings, PKC is considered to play an essential role in the lytic mechanism of NK cell-mediated cytolysis.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗