PubMed HealthSearch

Biomedical subjects

H Oouchi

Publications and source records attributed to H Oouchi.

11 recordsLinked to original sources

[Complete response of lung metastasis from bladder cancer by combination chemotherapy with methotrexate, epirubicin and cisplatin: a case report].

We report a case of lung metastasis from bladder cancer effectively responding to a combination chemotherapy using methotrexate, epirubicin and cisplatin (MEC therapy). A 78-year-old man with high grade bladder cancer underwent total cystectomy on June 5, 1991. He was pointed out to have an abnormal shadow on the plain chest X-ray on August 14, 1992. Computed tomography demonstrated multiple lung metastasis. MEC combination chemotherapy was applied for this case. After 3 courses of MEC therapy, computed tomography showed marked regression of tumor. He has been alive for 12 months with no evidence of disease after chemotherapy. Toxicity of MEC therapy were moderate myelosuppression and mild anorexia and alopecia. These toxicity was adequately tolerable by the 78-year-old patient. This case suggests that MEC therapy is effective against advanced bladder cancer.

Aged

Pleural multicystic mesothelial proliferation.

We report a rare case of pleural multicystic mesothelial proliferation occurring in a 62-year-old Japanese woman. Macroscopically, the lesion consisted of multiple thin wall cysts containing clear serous fluid. Histologic studies, including hematoxin-eosin stain, as well as the immunohistochemical method, revealed that the lesion was mesothelial in origin and consistent with a reactive change.

Antigens

Formulation of pyriproxyfen, a juvenile hormone mimic, for tsetse control.

A topical dose, in 1 microliter acetone, of 0.02 microgram-2-[1-methyl-2-(4-phenoxyphenoxy) ethoxy] pyridine, the juvenile hormone mimic pyriproxyfen (S-31183, Sumitomo Chemical Co.), caused an adult female tsetse, Glossina morsitans morsitans Westwood, to produce non-viable offspring for the whole of her life. Using 14C labelled pyriproxyfen it was determined that as little as 0.001 microgram transferred to the in utero larva was sufficient to arrest development in the pupal stage. A formulation in vegetable oil was prepared for treating black cotton cloth targets which caused females to pick up 0.1 microgram active ingredient (a.i.) by tarsal contact during 1 min of exposure. Males exposed similarly for between 1 and 5 min transferred up to 0.016 microgram a.i. to females if they mated immediately after treatment. Doses as low as 0.01 micrograms in 10 microliters oil cm-2 on black cotton cloth targets caused females to produce non-viable offspring for at least two reproductive cycles following exposure. However, a dose of 0.1 microgram in 10 microliters oil cm-2 was necessary for an exposed male to cause disruption of the reproductive potential of his mate. This juvenile hormone mimic has potential to induce sterility via both sexes of tsetse using treated targets or traps under field conditions.

Animals

Juvenile hormone mimics as effective sterilants for the tsetse fly Glossina morsitans morsitans.

The development of puparia of Glossina morsitans morsitans Westwood was disrupted by topical applications of the juvenile hormone mimics S-methoprene (the resolved enantiomer of 11-methoxy-3,7,11-trimethyl-2,4-dodecadienoic acid 1-methyl ester) (Zoecon), S21149 (propionaldoxime-0-4-phenoxyphenoxyethylether) (Sumitomo), or S31183 (2-[1-methyl-2-(4-phenoxyphenoxy)ethoxy]pyridine) (Sumitomo) dissolved in acetone. Puparia so treated during the first 4 days of life suffered developmental abnormalities, the severity of which were dose-dependent. Similarly, puparia produced by adult females treated with these compounds were abnormal. Dose-response data showed that effects were greatest with S31183 and least with S-methoprene. Abnormalities in the form of abdominal lesions and wing crumpling were typical of flies emerging from puparia produced by S-methoprene-treated females. However, arrested development at the red eye and pigmented seta stage within the puparium were typical of offspring of females treated with S21149 and S31183. A dose of 2 micrograms per female of S31183 was sufficient to prevent emergence of offspring produced for the rest of the life of the fly. The same dose resulted in partial recovery of females treated with S21149 some 18 days following treatment. Treatment with 2 micrograms S-methoprene did not suppress completely the production of normal offspring and recovery was complete some 27-35 days after treatment. Exposure of males to 20 micrograms S31183 did not impair their ability to inseminate females; transfer of material during copulation was sufficient to prevent the production of viable offspring by their mates.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Prolactin directly inhibits basal as well as gonadotropin-stimulated secretion of progesterone and 17 beta-estradiol in the human ovary.

An ovarian perifusion technique was used to determine if there is a direct suppressive effect of PRL on human gonadal steroid secretion. Ovarian tissue from nine patients was examined. Ovine PRL (0.1-10 IU/ml) directly suppressed progesterone and 17 beta-estradiol secretion by human ovaries. hCG (1-10 IU/ml) stimulated both progesterone and 17 beta-estradiol secretion. Simultaneous administration of PRL (5-10 IU/ml) suppressed the stimulatory effect of hCG. The ovarian tissue obtained from a hyperprolactinemic patient did not respond to hCG. These results indicate that PRL inhibits both basal and gonadotropin-stimulated ovarian steroid secretion by human ovaries and that this may be one cause of the hypogonadism associated with hyperprolactinemia.

Adult

Placental secretion of prolactin, ACTH and immunoreactive beta-endorphin during pregnancy.

The placental secretion of Prl, ACTH and immunoreactive (IR)-beta-endorphin were examined in early and later pregnancy with a perfusion method and by determining tissue concentrations of these hormones. Prl was secreted mainly from decidual tissue during 5-6 h long perfusions. Tissue concentrations of Prl were also significantly higher in decidual than in trophoblastic tissue. In contrast, the tissue concentrations of hCG, hPL, ACTH and IR-beta-endorphin were significantly higher in decidual than in trophoblastic tissues. In contrast, the tissue concentrations of hCG, hPL, ACTH and IR-beta-endorphin were significantly higher in trophoblastic than in decidual tissues. Production of hCG and hPL was predominantly demonstrated in trophoblastic tissues by the perfusion method but ACTH and IR-beta-endorphin were too low to be detected by perfusion.

Adrenocorticotropic Hormone

[The changes of human plasma ACTH, immunoreactive-beta-endorphin and cortisol during pregnancy, labor and delivery (author's transl)].

Immunoreactive (IR)-beta-endorphin, ACTH and cortisol from the plasma of 88 pregnant women during gestation, and 28 women with spontaneous labor were measured. The concentrations of ACTH, IR-beta-endorphin and cortisol gradually increased during gestation. There were significant correlation between ACTH and IR-beta-endorphin (r = 0.79, p less than 0.0001), as well as between ACTH and cortisol (r = 0.54, p less than 0.0001) during gestation. Maternal ACTH and IR-beta-endorphin concentrations rapidly increased during the course of labor, peaked immediately after delivery at 671.3 +/- 136.1 and 513.9 +/- 85.5 pg/ml, respectively, and then decreased two hours later. There was a highly significant correlation (r = 0.89, p less than 0.0001) between ACTH and IR-beta-endorphin during labor. The levels of cortisol were elevated during labor and showed no difference during labor, or two hours later. However, there was no significant relationship between ACTH and cortisol (r = 0.24) during labor. Chromatographic analysis was performed on the pooled plasma extracts from pregnant women at the various stage of labor. In ACTH analysis, a single peak was seen at the position of native ACTH in each case. All detectable immunoreactivities eluted in two peaks at the position of beta-LPH and beta-endorphin. However, beta-LPH to beta-endorphin ratio was almost the same in each case. These results suggest that 1) ACTH and IR-beta-endorphin are secreted concomitantly, probably by the maternal pituitary gland during gestation as well as in response to the stress of labor; 2) the lack of correlation between ACTH and cortisol is due to the difference in metabolic clearance rate of these hormones during labor; 3) neither peripheral nor intrapituitary conversion of beta-LPH to beta-endorphin is seen during gestation and labor.

Adolescent

[The changes of human plasma ACTH and immunoreactive beta-endorphin during spontaneous or oxytocics induced/maintained labor and delivery (author's transl)].

To evaluate the effects of oxytocics on ACTH and Immunoreactive (IR)-beta-endorphin release, concentrations of these hormones in the plasma of 22 women during spontaneous labor, 22 women in labor who had received oxytocin and 19 women in labor who had received PG.F2 alpha at the time of vaginal delivery, were measured. Maternal ACTH and IR-beta-endorphin concentrations were elevated during spontaneous or oxytocics induced/maintained labor and peaked immediately after delivery and decreased two hours later. There were significant correlations between ACTH and IR-beta-endorphin concentrations during spontaneous labor and delivery (r = 0.921, p less than 0.0001), as well as in oxytocin or PG.F2 alpha induced/maintained labor and delivery (r = 0.833, r = 0.916, p less than 0.0001, respectively). The concentrations of ACTH and IR-beta-endorphin during PG-F2 alpha infusion were slightly higher than those seen in the other two types of labor. However, there was no significant difference in the levels of ACTH and IR-beta-endorphin among the three types of labor. Simultaneous maternal and umbilical cord plasma samples were obtained in 25 cases at delivery. However, there was no significant correlation between ACTH or IR-beta-endorphin concentrations in paired samples. These results suggest that 1) IR-beta-endorphin is secreted in parallel with ACTH, into the peripheral blood by the maternal pituitary gland in response to the stress of labor during all types of labor and delivery; 2) there is no significant difference in the response of ACTH and IR-beta-endorphin between spontaneous and oxytocics induced/maintained labor and delivery: 3) ACTH and IR-beta-endorphin in cord blood are not of maternal origin.

Adrenocorticotropic Hormone