Biomedical subjects

Y Kanda

Publications and source records attributed to Y Kanda.

296 records · Page 17Linked to original sources

PubMedDate not supplied

Interferon-induced sudden hearing loss.

With the increasing long-term use of interferon (IFN), several new adverse effects have been recognized. Very little attention, however, has been paid to auditory acuity. We encountered 3 cases of sudden hearing loss associated with IFN. We then conducted a prospective study to assess the auditory function of 73 patients receiving IFN. Auditory disability (tinnitus and/or hearing loss) occurred in 32 patients (43.8%) during IFN therapy, among which audiometry documented sensorineural hearing loss in 27 cases (36.9%); 17 (48.6%) of the 35 patients receiving IFN-beta had auditory disability, including hearing loss in 13 cases (37.1%), and 15 (39.5%) of 38 patients receiving IFN-alpha suffered from auditory disability. There was not much difference between the influences of IFN-alpha and -beta. Auditory disability frequently developed in the later stages of treatment, and most patients recovered 7-14 days after the discontinuation of IFN. The results demonstrate that sudden hearing loss can occur as a side effect of treatment with IFN. This may reveal the association between autoimmunity and sudden hearing loss.

Adult↗

PubMedDate not supplied

Induction of apoptosis by dopamine in human oral tumor cell lines.

Dopamine dose-dependently reduced the viable cell number of both human salivary gland tumor HSG and oral squamous cell carcinoma HSC-2, HSC-4, and NA cells. CoCl2 significantly reduced both the cytotoxic activity and radical intensity of dopamine (determined by ESR spectroscopy). Dopamine produced DNA fragments (demonstrated by TUNEL method) and induced degradation of cytokeratin by activated caspase in HSG cells (detected by an immunocytochemical method, using a specific M30 monoclonal antibody). FACS analysis demonstrated that dopamine induced DNA fragmentation, a biochemical hallmark of apoptosis, in human promyelocytic leukemia HL-60 cells. The addition of catalase did not prevent the apoptosis-inducing activity of dopamine, reducing the possibility of the involvement of H2O2 for dopamine-induced apoptosis. Dopamine transiently induced p38 mitogen-activated protein kinase (MAP kinase) phosphorylation. However, an inhibitor of p38 MAP kinase phosphorylation, SB203680, failed to inhibit the dopamine-induced apoptosis. These data suggest that p38 phosphorylation at an early stage may not be a causative event for apoptosis.

Apoptosis↗

PubMedDate not supplied

Postoperative changes in vaginal smears after vaginal reconstruction with a free skin graft.

Surgical vaginal reconstruction was performed by a free skin graft in two patients without a vagina. The postoperative changes in vaginal smears collected from the artificial vaginas were observed for about two years. Marked operation-induced inflammatory changes were observed until the second postoperative month. After the third postoperative month, the background became relatively clear. Cyanophilic and eosinophilic superficial cells, intermediate cells and Döderlein bacilli were observed occasionally in addition to keratotic cells. Six to 12 months after surgery, the vaginal smears showed little abnormality, except for the presence of keratotic cells. The changes in the vaginal smears after the third month show that the artificial vaginal epithelium changed cytologically to an almost normal vaginal mucosa that, although not histologically complete, responded to hormones. The presence of Döderlein bacilli suggests that the regional environment of the artificial vagina was almost the same as that of the normal vagina.

Adolescent↗

PubMedDate not supplied

Cervicovaginal and endometrial cytology in ovarian cancer.

The clinical significance of cytologic examination was studied in 114 patients with ovarian cancer who had received preoperative cytologic examinations. The overall positive rate of the cytologic examinations was 26.3% (30 of 114): 22 (19.3%) of the 114 cases had positive cervicovaginal smears while 13 of 31 endometrial aspiration smears (41.9%) were positive. The positive rate was not related to the volume of ascites but rather to its presence or absence. Thus, if ascites was observed, the positive rate was about 2.1 times higher than if it was absent. In two of four cases of ovarian cancer with no endometrial invasion but a positive cytologic examination of ascitic fluid, fallopian tube specimens contained cancer cells; this suggests that ovarian cancer cells may reach the cervix and/or vagina by passing through the fallopian tube, particularly if ascites is present. Since cytologic examination, especially of endometrial aspiration smears, shows a high positive rate if ovarian cancer cells are observed in the abdominal cavity, cytology should be used as an important ancillary method for the assessment of ovarian cancer.

Adenocarcinoma↗

PubMedDate not supplied

Adrenal metastasis from hepatocellular carcinoma--report of a case.

A 66-year-old man presented with an epigastric tumor demonstrated by both ultrasonography and computed tomography as hepatocellular carcinoma. He referred himself to a specialist at another hospital who performed transarterial embolization (TAE) of the hepatic artery. But the serum alpha fetoprotein (AFP) concentration gradually rose after the procedure. A right adrenal metastasis was discovered by computed tomography 9 months after his presentation, 8 months after first embolization. When TAE was performed for this metastasis, there was transverse palsy of the lower limb secondary to spinal artery embolization. He returned to our hospital where a right adrenectomy was performed 14 months after his first presentation. The operation was successful and he was discharged 6 weeks later. But he was readmitted in 8 months with an elevated serum AFP concentration and died within 2 weeks. The details of this case are presented, and the indications for resection of adrenal metastasis from hepatocellular carcinoma are discussed.

Adrenal Gland Neoplasms↗

PubMedDate not supplied

Effects of prolactin and estrogen on cell proliferation of the mouse liver induced by partial hepatectomy.

Estrogen or prolactin suppresses mouse hepatocellular tumorigenesis induced by carcinogens through inhibition of the growth of preneoplastic hepatocytes. In the present study, we investigated whether estrogen or prolactin inhibits proliferation of normal hepatocytes as well as preneoplastic hepatocytes in mice. The proliferation of mouse hepatocytes was induced by partial hepatectomy, and DNA synthesis of the liver was evaluated by measurement of 5-[125I]iododeoxyuridine ([125I]IdUrd) uptake/mg liver DNA after an injection of [125I]IdUrd into mice. For acute treatment with estrogen or prolactin, estradiol-17 beta (E2) (1 micrograms) or ovine prolactin (140 micrograms) was injected into ovariectomized mice twice a day from the day of partial hepatectomy. For chronic treatment with estrogen, ovariectomized mice received implants of E2 pellets containing 100 micrograms E2 40 days before partial hepatectomy, and for chronic treatment with prolactin, hyperprolactinemia was induced by pituitary graft under the renal capsule of ovariectomized mice 40 days before partial hepatectomy or by daily injections of perphenazine (150 micrograms/day) beginning 40 days before partial hepatectomy. The acute treatment with either estrogen or prolactin did not affect the hepatocyte proliferation induced by partial hepatectomy. Chronic hyperprolactinemia induced by the pituitary graft or by injections of perphenazine, and the chronic treatment with E2 pellets did not suppress either basal or partial hepatectomy-induced proliferation of hepatocytes. The present results show that acute and chronic treatments with estrogen or prolactin do not inhibit proliferation of mouse normal hepatocytes, and suggest that the effects of estrogen and prolactin on proliferation of mouse hepatocytes are different from those on proliferation of preneoplastic hepatocytes.

Animals↗

PubMedDate not supplied

Role of hydrogen peroxide for cell death induction by sodium 5,6-benzylidene-L-ascorbate.

The role of hydrogen peroxide in the induction of cell death in human promyelocytic leukemic HL-60 cells by sodium 5,6-benzylidene-L-ascorbate (SBA) and its degradation product, ascorbic acid, was investigated. Millimolar concentrations of these compounds induced cell death, characterized by cell shrinkage, nuclear and internucleosomal DNA fragmentation, disappearance of microvilli and condensation of chromatin near the nuclear membrane. Catalase significantly reduced the cytotoxic activity of these compounds, whereas superoxide dismutase, nitric oxide (NO) generator, NO scavenger and NO synthase inhibitor were inactive, suggesting the possible role of H2O2. Determination of H2O2 with the peroxyoxalate chemiluminescence demonstrated that sodium ascorbate and SBA produced H2O2 in amounts necessary for cell death induction.

Antineoplastic Agents↗

PubMedDate not supplied

Induction of apoptosis by cooperative action of vitamins C and E.

Millimolar concentrations of sodium ascorbate (vitamin C) induced apoptotic cell death in human promyelocytic leukemic HL-60 cells. The apoptotic cells displayed a smaller cell volume, disappearance of cell surface microvilli, appearance of cytoplasmic vacuoles, chromatin condensation, nuclear fragmentation and production of apoptotic bodies. The apoptosis-inducing activity of sodium ascorbate was significantly enhanced by noncytotoxic concentrations of CuCl2, but was almost completely eliminated by FeCl3. CuCl2 transiently stimulated the hydrogen peroxide (H2O2) production by sodium ascorbate, whereas FeCl3 slightly reduced the H2O2 production. alpha-Tocopherol (vitamin E) slightly enhanced the radical and H2O2 productions, and apoptosis induction by sodium ascorbate. The effect of alpha-tocopherol seems to be rather specific for ascorbic acid, since alpha-tocopherol did not significantly affect the cytotoxic activity of CuCl2, FeCl3 nor gallic acid. The present study demonstrated the cooperative action of vitamins C and E.

Antioxidants↗