Tomoaki Orita
Kindai University
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Featured researches published by Tomoaki Orita.
British Journal of Dermatology | 2006
Masami Yoshida; K. Fukui; Tomoaki Orita; S. Kusuda; Tadashi Tezuka; M. Hiruma
Summary We report a 7‐month‐old boy who developed vesicular lesions during the course of exanthem subitum. Human herpesvirus‐6 (HHV‐6) DNA was detected both in the skin lesions and in the throat, by polymerase chain reaction. IgG and IgM antibodies against HHV‐6 were 1:10 and <1:10, respectively on the tenth day of the illness, and >1:640 and 1:10 on the twenty‐second day, respectively. These results suggest that this was primary HHV‐6 infection.
FEBS Letters | 1991
Shunji Miki; Hidekazu Yamada; Tomoaki Orita; Masahiro Yamamoto; Yoshitsugu Miki
Renal cell carcinoma cells produced the substance(s) which killed them (suicide factor(s)) after co‐culture with mumps virus. The suicide factor(s) were heat‐sensitive and were degraded with trypsin. Furthermore, actinomycin D inhibited the production of the substance(s) by cancer cells. Considering these facts, the substance(s) were thought to be protein(s) derived from de novo synthesis in cancer cells. It was demonstrated that renal cell carcinoma cells proliferated with the autocrine loop of interleukin‐6 (IL‐6). Mumps virus almost completely inhibited the IL‐6 production in several hours. Because of these two facts, the suicide process might be initiated in renal cell carcinoma cells after encountering mumps virus, i.e. inhibition or the autocrine growth loop of IL‐6 followed by the induction of an autocrine killing loop of unknown substance(s).
Journal of Dermatology | 2001
Akira Maeda; Yoshinori Aragane; Akira Kawada; Rieko Isogai; Tomoaki Orita; Tadashi Tezuka
There is an increasing amount of evidence that melanoma cells express the ligand for CD95 (CD95L), a potent inducer of apoptosis, which contributes to creating the immune privileged circumstances of tumor sites. However, it still remains to be demonstrated whether the capacity of melanoma cells to express CD95L is acquired during the progression. We addressed this question with a case of acral lentiginous melanoma by employing immunostaining using an antibody directed against CD95L as well as by in situ TUNEL staining. H&E‐staining of tumor specimens revealed that there were two different growth patterns. The central part of the tumor showed a deeper invasion into the dermis (Breslow thickness>4‐mm). The horizontally growing edge of the tumor proliferated more superficially (Breslow thickness<3‐mm). Relatively fewer lymphocytes were observed around the melanoma nests in central areas, which expressed detectable amounts of CD95L. In contrast, more lymphocytes were observed among the melanoma cells in the peripheral lesion, where CD95L was not detected. To evaluate the relevance of the CD95L expression, in situ TUNEL staining was performed. This indicated a significant correlation of lymphocyte apoptosis with CD95L expression on melanoma cells. Together, the data suggest that expression of CD95L is turned on depending on the level of melanoma, and that it may contribute to creating immune privileged circumstances by initiating apoptosis of tumor infiltrating lymphocytes.
Skin Cancer | 1996
Atsushi Nakano; Tomoaki Orita; Akira Maeda; Hidekazu Yamada; Tadashi Tezuka
We reported a 69-year-old male case of multiple myeloma. His chief complain was a skin tumor, and it was localized on his forearm. After general examination of whole the body, atypical myeloma cells were found in the bone marrow. We selected radiation therapy, because of his age, past disease history, and so on. The tumor expressed good response, and reduced clinically. But, in a short time, it formed metastatic lesions in both thoracis vetebra and forearm arround the first lesion.Multiple myeloma is a disease, which is usually found and mainly complained chronic anemia, morbid bone fracture, and lumbago. This case that we reported was found as extramedullary plasmacytoma on the skin, and in that point, it was comparatively rare clinically.
Skin Cancer | 1994
Tomoaki Orita; Hidekazu Yamada; Kazuhiro Morikawa; Akira Maeda; Tadashi Tezuka
Skin research | 2000
Akiko Matsukura; Takehiro Noda; Tomoaki Orita; Tadashi Tezuka
Skin research | 2000
Yuri Sakamoto; Mutsuyo Asai; Kazuko Sugihara; Tomoaki Orita; Yoshinori Aragane; Akira Kawada; Tadashi Tezuka
Skin research | 2000
Yuri Sakamoto; Kazuko Sugihara; Tomoaki Orita; Yoshinori Aragane; Masami Yoshida; Akira Kawada; Tadashi Tezuka
Skin Cancer | 2000
Tomoaki Orita; Yoshinori Aragane; Akira Kawada; Tadashi Tezuka
Skin research | 1998
Yuki Mori; Atsuko Izutani; Tomoaki Orita; Hidekazu Yamada; Tadashi Tezuka