Biomedical subjects

N Terada

Publications and source records attributed to N Terada.

At least 307 records · Page 17Linked to original sources

PubMed1990

Impaired development of mammary glands in scorbutic rats unable to synthesize ascorbic acid.

The effects of ascorbic acid (AsA)-deficiency on the development of mammary glands were investigated using mutant rats (osteogenic disorder syndrome rats; ODS rats) with hereditary inability to synthesize AsA. Female ODS rats of 21 days old were castrated and divided into two groups. One group was given AsA in their drinking water, and the other was not. All the rats received a daily injection of oestradiol-17 beta and progesterone (EP) from day 28 to day 49 of age. After EP treatment, the concentrations of AsA in the mammary glands of rats not given AsA were less than one tenth of those of rats given AsA and the contents of hydroxyproline in the mammary glands of the former rats were about half of those in the latter. Furthermore, the concentration of serum prolactin in rats not given AsA was reduced to about one third of that in rats given AsA. After EP treatment, whole mounts of mammary glands showed that in rats not given AsA the development of ducts was impaired and there was extensive accumulation of endbuds. Consistent with this finding, EP injections did not increase the area of parenchyma in the mammary glands of rats not given AsA, whereas they increased it about 2-fold in rats given AsA. Moreover, after EP treatment the amount of alpha-lactalbumin was significantly less in the mammary parenchyma of rats not given AsA than in that of rats given AsA. On the other hand, AsA deficiency did not impair the response of the mammary cells to insulin or prolactin in terms of DNA synthesis and alpha-lactalbumin production. These findings indicate that AsA deficiency impaired the development of mammary glands. This effect may be partly attributable to a defect in collagen synthesis in the mammary glands and a decrease in the concentration of serum prolactin.

Animals↗

PubMed1990

Marked nitrosation by stimulation with lipopolysaccharide in ascorbic acid-deficient rats.

Marked formation of N-nitrosothioproline (N-nitrosothiazolidine-4-carboxylic acid) by stimulation with Escherichia coli lipopolysaccharide (LPS) was demonstrated in ascorbic acid-deficient mutant rats (osteogenic disorder syndrome rats; ODS rats) unable to synthesize ascorbic acid. The amounts of urinary nitrate and N-nitrosothioproline excretion after thioproline administration was measured in ODS rats with and without ascorbic acid supplement before and after the injection of LPS. LPS caused marked increase of urinary nitrate excretion in both groups. Urinary N-nitrosothioproline excretion increased 6-fold after LPS injection in ODS rats not supplied with ascorbic acid, but supplement with ascorbic acid markedly decreased the excretion of N-nitrosothioproline.

Adrenal Glands↗

PubMed1990

Squamous cell carcinoma of the esophagus with cartilaginous metaplasia at metastatic lesions.

Subdermal metastatic nodules in a 62-year old male patient with esophageal carcinoma contained both carcinomatous and chondroid areas. The carcinomatous areas showed the histology of poorly differentiated squamous cell carcinoma, and light microscopically an apparent transition could be traced from carcinomatous cells to chondroid cells. In the chondroid cells, the characteristics of chondrocytes were demonstrated by light microscopic, electron microscopic, histochemical and immunohistochemical studies, although nuclear atypism was evident, suggesting their malignancy. Furthermore, immunohistochemical studies showed that some chondroid cells contained both keratin proteins and squamous cell carcinoma antigen, which were also found in the carcinomatous cells. These findings together with the light microscopic observations suggest that chondroid cells are derived from squamous cell carcinoma cells.

Carcinoma, Squamous Cell↗

PubMed1990

The effects of salicylate on ketogenesis, gluconeogenesis and urea production in rat liver perfusion.

In order to elucidate the relation between the hepatotoxicity of salicylate (SA) and the pathogenesis of Reye's syndrome (RS), urea production, gluconeogenesis and ketogenesis were investigated in isolated perfused rat livers in the presence of salicylate (SA) and oleate. Although urea formation from 0.5 mM NH4Cl, 2 mM ornithine and 0.3 mM oleate was not inhibited by infusion of SA, 3 mM SA caused a 26% decrease of ketogenesis, 85% decrease of 3-hydroxybutyrate/acetoacetate ratio (30HB/AcAc) and 45% increase of oxygen consumption. Glucose production from 2 mM pyruvate in the presence of 0.3 mM oleate decreased by 33% after administration of 3 mM SA, and 30HB/AcAc ratio also decreased by 33%. The decrement of gluconeogenesis and that of the 30HB/AcAc ratio were very close. These results suggested that ATP production was maintained but that the intra-mitochondrial redox state was changed to a more oxidized state after SA administration in perfused rat livers. This change in redox state could be responsible for the decrease of gluconeogenesis. Metabolic characteristics found in RS were not obtained by infusion of 3 mM SA and 0.3 mM oleate in rat livers. Therefore, some other factors in addition to SA seem necessary to establish an animal model of RS.

Animals↗

PubMed1990

Compensatory adjustment in blood flow of the rabbit cerebral cortex during graded cerebral ischemia.

The role of the bilateral internal carotid and vertebral arteries in supplying cerebral cortex tissue blood flow (CTF) and the compensatory adjustment in CTF during graded cerebral ischemia were studied to determine the relationship to the increase in systemic arterial pressure (SAP) in anesthetized rabbits. CTF was recorded continuously by using Peltier stacks placed on both sides of the surface of the cerebral parietal cortex. Occlusion of the bilateral internal carotid arteries caused a decrease in CTF to 81.9% of the control value for the right hemisphere, and 83.5% of that for the left. Occlusion of the bilateral vertebral arteries produced no appreciable change in CTF. Compensatory adjustment in CTF was incomplete, i.e., CTF was reduced to a lower level, in the range of internal carotid flow (ICF) from 2 to 6 ml/min, and was severely reduced at 1 and 0 ml/min. The relationships between ICF and SAP, and ICF and CTF formed rectangular hyperbolic curves. No significant difference was observed between the decreases in CTF obtained before and after bilateral sectioning of the cervical sympathetic trunks. The relationship between SAP and CTF was described by a linear regression equation. These results indicate that the internal carotid arteries play a much more important role in supplying CTF than the vertebral arteries, that SAP rises in inverse proportion to the decrease in CTF, and that the cervical sympathetic trunks do not influence the compensatory adjustment in CTF caused by cerebral ischemia.

Animals↗

PubMed1990

[An inflammatory pseudotumor of the appendix].

A 41-year-old male, complaining of an abdominal pain and suspected of having acute appendicitis, underwent examination on hospitalization. Ultrasonography revealed a tumorous lesion of the appendix. Thus, a laparotomy was performed and mass lesions were found in the mid and distal parts of the appendix. A subsequent histological examination revealed an inflammatory pseudotumor consisting of remarkable eosinophilic cell and fibroblastic infiltrations, similar to that seen in a inflammatory fibroid polyp (Helwig). Although such lesions, polypoid in appearance, have been found to occur in the stomach and intestines, to find them in the appendix is extremely rare. In this instance, as the growth of this mass of lesions was more predominant in the wall rather than in intraluminal area, it was decided that pseudotumor was the appropriate term to describe this case.

Adult↗

PubMed1990

Long-term survival after brain metastasis from endometrial cancer.

A case is reported of prolonged survival after radical hysterectomy for poorly differentiated adenocarcinoma of the endometrium and resection of metastatic carcinoma of the brain followed by radiation therapy. The 43-year-old patient has survived for seven years after hysterectomy and six years 10 months after excision of the brain metastasis. Our results show that the surgical excision of a single metastatic lesion of the brain with postoperative irradiation offers hope of prolonged survival in patients with a solitary brain metastasis and no evident systemic disease.

Adenocarcinoma↗

PubMed1989

Analysis of molecular events in leukemic cells arrested at an early stage of T-cell differentiation.

We analyzed the rearrangement and expression of T-cell receptor (TCR) genes, including the recently identified TCR delta gene, in 21 patients with T-lineage leukemia/lymphoma. Among 8 patients with CD3-, CD4-, and CD8- (group I), 2 patients showed germline configuration of the TCR delta, gamma, beta, and alpha genes and 1 patient demonstrated only TCR delta gene rearrangement. All nine patients with CD3-, CD4+, and/or CD8+ (group II) showed concomitant rearrangements of the TCR delta, gamma, and beta genes. TCR alpha gene rearrangement was also observed in two patients. Three of four patients with CD3+ (group III) showed rearrangement of the TCR alpha gene with deletion of both alleles or of a single allele of the TCR delta gene. With Northern blot analysis, full-length transcripts of the TCR delta gene were detected in 3 of 15 examined patients. All were restricted to group I or group II. In contrast, full-length transcripts of TCR beta and alpha were observed mainly in samples from groups II and III. Based on these findings, rearrangement of the TCR delta gene may be the earliest event in T-cell differentiation, preceding rearrangements of the other TCR genes.

Antigens, CD↗

PubMed1989

Androgen dependency of a tumor produced by a cell line derived from androgen-responsive Shionogi carcinoma 115.

An androgen-dependent tumor (SCC8 tumor) was obtained by inoculating an androgen-responsive cell line derived from the androgen-responsive Shionogi carcinoma 115 (SC115) into mice and then treating the mice with testosterone propionate (TP) at a pharmacological dose (400 micrograms/day). The SCC8 tumor differed in histological appearance from the SC115 tumor and its growth was less stimulated by androgen than that of the SC115 tumor. However, its growth was completely androgen dependent; SCC8 tumors did not develop in castrated mice and regressed when TP treatment was discontinued. The decreased sensitivity of the SCC8 tumor seemed to be attributable in part to its rapid metabolism of testosterone to metabolites with lower androgenic actions. The effects of TP at doses of 0, 100, 200, and 400 micrograms/day on cell division and cell death in SCC8 tumors of medium size were examined by measurements of the mitotic index and the retention of 5-[125I]iodo-2'-deoxyuridine incorporated into the whole tumor. TP increased the mitotic index dose dependently and at all doses reduced the decrease in the retention of 5-[125I]iodo-2'-deoxyuridine. These results suggest that steroids may not only stimulate cell division but also reduce cell death in steroid-dependent tumors.

Androgens↗

PubMed1989

Central vasomotor control of the rabbit portal vein.

Contractile responses of the portal vein of the anesthetized rabbit were measured quantitatively by plethysmography during transmural electrical field stimulation (TES, 0.8 ms and 15 V) and during the cerebral ischemic pressor response at various volemic states. To evoke the cerebral ischemic response, the route of blood supply to the brain was surgically restricted to the right internal carotid artery, the artery was then compressed in a stepwise fashion by a micrometer device. The maximum contractile response of the portal vein segment that could be evoked by cerebral ischemia corresponded in magnitude to that produced by TES of 10-11 Hz. The contractile response began when the internal carotid blood flow was reduced to 4 ml/min from its normal value of 13.8 +/- 1.2 (mean +/- SE) ml/min and reached a maximum at 0 ml/min. The maximum contractile response was an increase of 26% from control value under normovolemic condition, 20% after hemorrhage and 31% after volume loading. It was estimated that the contractile response in normovolemia was 95% neurogenic, the rest was thought to be of humoral origin.

Animals↗

PubMed1989

Effect of androgen pretreatments at adulthood on androgen-induced proliferative response of seminal vesicles in neonatally castrated mice.

Male mice were castrated on days 0 and 60 after birth. The majority of the neonatally castrated mice were pretreated with androgen; the mice were given daily injections of testosterone propionate (TP; 4 or 8 micrograms/g body wt) for 20 or 30 days starting from day 60. Daily injections of TP (4 micrograms/g body wt) to examine androgen-induced proliferation were started from day 30 or 60 after the end of TP pretreatments or from day 60 after castration; on various days after starting TP injections, the weight and the incorporation of 5-[125I]iodo-2'-deoxyuridine into the whole seminal vesicles were determined as indices for proliferation. The seminal vesicles of neonatally castrated adult mice were characterized by long duration of androgen-induced proliferation (greater than 20 days) with a low peak (neonatal castration type), whereas the seminal vesicles of adult castrated mice were characterized by short duration of proliferation (10 days) with a high peak (adult castration type). In neonatally castrated adult mice, the neonatal castration type of androgen-induced proliferation was changed largely to the adult castration type when pretreatment with 8 micrograms/g body wt of TP had been given for 30 days. However, this effect gradually disappeared when the mice had been pretreated with decreasing amounts of TP for a shorter period. The present findings suggest that the defect in the androgen-induced proliferative response of mouse seminal vesicles induced by the absence of neonatal and prepubertal testicular androgens can be compensated by androgens given in adulthood, if enough androgen is given for a sufficiently long time.

Animals↗

PubMed1989

Inhibitory effect of progesterone on cell death of mouse uterine epithelium.

The protective effect of progesterone against cell death of mouse uterine epithelium was evaluated by examining the retention of 5'-[125I]iodo-2'-deoxyuridine [( 125I]IdUrd) incorporated into the whole uterus and the apoptotic index (percentage of apoptotic cells in total cells), which is a good index of physiological cell death. Castrated adult female mice were given a daily injection of oestradiol-17 beta for 3 days, and then an injection of [125I]IdUrd. They were then divided into 4 groups, which received a daily injection of vehicle only, oestradiol-17 beta (E), progesterone (P), or both oestradiol-17 beta and progesterone (EP), and were killed at intervals during these treatments for determination of 125I radioactivity retained in the whole uterus. On treatment with vehicle only, the 125I radioactivity retained in the uterus decreased rapidly, but treatment with E, P or EP reduced the loss of 125I radioactivity significantly. Progesterone did not antagonize the effect of oestradiol-17 beta on the 125I radioactivity retained in the uterus. The apoptotic index of uterine cells was examined by a similar experimental protocol, but without injection of [125I]IdUrd. In the group treated with vehicle only, the apoptotic indices of both luminal and glandular epithelia increased markedly, but the injection of E, P or EP suppressed these increases significantly. Progesterone did not antagonize the effect of oestradiol-17 beta on the apoptotic index. The apoptotic index of stroma was not affected by the injection of E, P or EP. On the other hand, progesterone completely inhibited the increase in the mitotic index of uterine epithelia induced by oestradiol-17 beta. These results show that progesterone alone or in combination with oestrogen reduced cell death in mouse uterine epithelium and that the effects of oestrogen and progesterone on uterine cell death were independent of their actions on cell division.

Animals↗

PubMed1989

Increase in epithelial cell growth by hyperprolactinemia induces delay of castration-induced involution of mouse seminal vesicle.

Male (C57BL/6 x DBA)F1 hybrid mice were castrated on day 60 after birth; two pituitaries from 60-day-old female mice were immediately grafted under the capsule of the left kidney in half of the castrated mice to induce hyperprolactinemia. The seminal vesicles in the absence of androgen treatment were examined 15, 22, 30 and 60 days after castration with or without grafting. Significant increases in the weight (1.3-1.4-fold), DNA content (1.2-1.3-fold) and labeling index of epithelial cells (4-10-fold) of the seminal vesicles were found in mice with pituitary grafts compared to mice without grafts on days 15-30 after castration but not on day 60 after castration. Such stimulatory effects of hyperprolactinemia on mouse seminal vesicle cells were also observed on day 15 after castration plus adrenalectomy. Cell loss from the seminal vesicles was found to be similar in castrated mice with and without the grafts. The present findings demonstrate that hyperprolactinemia induces an increase in DNA synthesis of epithelial cells in the seminal vesicles until 30 days after castration and results in a significant delay of castration-induced involution of the weight and DNA content of the seminal vesicles for 1 month. However, the delay with increased epithelial cell growth by hyperprolactinemia disappeared 60 days after castration.

Adrenalectomy↗

PubMed1989

Aromatase activity in cultured ovaries from fetal and neonatal golden hamsters.

The production of oestrogen from androstenedione by ovaries of hamsters on day 14 of pregnancy and on days 0 and 3 after birth was investigated by culturing these ovaries for 48 h in serum-free medium containing insulin and [3H]androstenedione. Both oestrone and oestradiol-17 beta were produced in culture of ovaries on day 14 of pregnancy. The production of oestrogen increased about 2-fold in culture of ovaries on days 0 and 3. Dibutyryladenosine 3':5'-cyclic monophosphate stimulated the oestrogen production by ovaries on day 14 of pregnancy and on days 0 and 3. The present results indicate that the ovaries of fetal and neonatal hamsters have an aromatase activity and that these aromatase activities are responsive to adenosine 3':5'-cyclic monophosphate.

Animals↗

PubMed1989

Clinicopathological study of livers from brain-dead patients treated with a combination of vasopressin and epinephrine.

Studies were made on the pathological lesions and biochemical indices of the livers of 22 patients in whom normal hemodynamics was maintained for 0-48 days after brain death by administration of vasopressin and epinephrine. Thirty-one specimens of liver tissues were obtained by percutaneous biopsy or at autopsy. The degrees of central venous congestion, central fibrosis, focal fibrosis, fatty metamorphosis, piecemeal necrosis, periportal fibrosis, and intrahepatic cholangitis in livers on various days after brain death were compared with those on the day of brain death (day 0). Central venous congestion was extensive on days 0-4, significantly less on days 5-14, and then again extensive on days 15-48. Central fibrosis and focal fibrosis showed no remarkable change during the 48-day period. Fatty metamorphosis, piecemeal necrosis, and periportal fibrosis showed no significant changes until day 16, but spread extensively on days 40-48. Intrahepatic cholangitis was scarcely observed on day 0 but began to increase after day 3, and spread extensively after day 5. The level of serum glutamic pyruvic transaminase did not increase in most patients until day 15. The mean value of prothrombin activity also did not decrease until day 15. However, the mean value of serum alkaline phosphatase increased gradually after day 3, and was correlated with cholangitis. The present study showed that during prolonged hemodynamic maintenance of brain-dead patients, pathological lesions did not spread or diminished and that biochemical indices did not become worse, or improved, in the first 2 weeks, except for increases in cholangitis and the serum alkaline phosphatase level.

Adult↗

PubMed1989

Opioid receptor modulation of neural transmission in the rabbit coeliac ganglion and ganglionic opioid receptor activation by bunitrolol.

1. We examined the preganglionic splanchnic nerve activity and postganglionic renal nerve activity before and after a local injection of naloxone (20 micrograms/kg) into the coeliac ganglion of anaesthetized rabbits. This was done during graded hypertension, induced by the administration of phenylephrine (0.5-10 micrograms/kg, i.v.) and with selective intraganglionic injection of methionine-enkephalin (ME) and bunitrolol, which is a beta-blocker. 2. During hypertension both pre- and postganglionic discharge decreased, but only postganglionic discharge was inhibited by naloxone treatment into the ganglion. 3. Local injection of ME (0.1-10 micrograms/kg) into the coeliac ganglion decreased postganglionic activity by 9.0 +/- 1.0 to 41.2 +/- 4.7% from control, and this decrease was inhibited by naloxone. 4. Administration of bunitrolol (1-300 micrograms/kg) decreased postganglionic discharge by 3.9 +/- 1.4 to 39.7 +/- 2.4% of the control and this decrease was also inhibited by naloxone. 5. These results suggest that opioid receptors in the coeliac ganglion play an inhibitory role in neural ganglionic transmission and that this inhibitory action reduces postganglionic sympathetic discharge.

Adrenergic beta-Antagonists↗

PubMed1989

Roles of prepubertal androgen, estrogen or androgen plus prolactin on androgen-induced proliferative response of seminal vesicles in adult mice.

Male mice castrated on day 0 after birth were pretreated daily with testosterone propionate (TP, 4 micrograms/g body weight), 17 beta-estradiol (E2, 0.2 micrograms/g body weight) or vehicle for 21 days starting from day 20. In another experiment, male mice were castrated on day 25; two pituitaries from 60-day-old females were immediately grafted under the capsule of the left kidney in one group. The castrated mice with or without grafts were pretreated daily with TP (4 or 20 micrograms/g body weight) for 36 days starting from day 25, and the left kidney was removed on day 60. Daily TP injections (4 micrograms/g body weight) were started again at 30 days after the end of pretreatments to examine androgen-induced proliferation, and incorporation of 5-[125I]iodo-2'-deoxyuridine into the whole seminal vesicles was used as an index of proliferation. In the neonatally castrated mice, both TP and E2 pretreatments given during the prepubertal period significantly increased seminal vesicle weight even long after the end of the pretreatments. However, androgen-induced proliferative response found in the neonatally castrated adult mice (poor response; long duration with a low peak) was changed to that found in mice castrated at adulthood (good response; short duration with a high peak) by the TP pretreatment only but not at all by the E2 pretreatment. In the mice castrated on day 25, a pharmacological dose of TP or TP plus hyperprolactin could not enhance or change the adult castration type of androgen-induced proliferation induced by physiological prepubertal androgens, although both treatments significantly enhanced the prepubertal growth of the seminal vesicles.

Animals↗

PubMed1989

Ovarian aromatase activity in scorbutic mutant rats unable to synthesize ascorbic acid.

Osteogenic disorder syndrome rats are unable to synthesize ascorbic acid owing to the lack of l-gulonolactone oxidase, and become scorbutic within a few weeks without the supply of ascorbic acid. We studied effects of ascorbic acid deficiency on the ovarian aromatase activity in vivo using osteogenic disorder syndrome rats. The ovarian aromatase activity in ascorbic acid-deficient osteogenic disorder syndrome rats was significantly higher than that in normal or ascorbic acid-supplied osteogenic disorder syndrome rats. The activity in hypophysectomized immature rats was extremely low, but increased after treatment with pregnant mare serum gonadotropin, regardless of the presence or absence of ascorbic acid. The extent of the increase was the same among experimental groups. The present results indicate that ascorbic acid at physiological level lowers the ovarian aromatase activity, whereas it does not impair the responsiveness of the aromatase activity to gonadotropins.

Animals↗