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Biomedical subjects

T Endo

Publications and source records attributed to T Endo.

At least 667 records · Page 37Linked to original sources
PubMed1993

Cadmium uptake by primary cultures of rat renal cortical epithelial cells: influence of cell density and other metal ions.

The uptake and accumulation of 1-5 microM cadmium (Cd) was studied in primary cultures of rat renal cortical epithelial cells under protein-free conditions at 4 or 37 degrees C for up to 30 min. The cells were isolated from female rats by collagenase digestion and cultured for 3-7 days. Confluency of the culture, monitored morphologically as well as by total protein content, was achieved on Day 5. Cd accumulation at 1 microM concentration demonstrated an inverse relationship to the cell density; the Cd level in Day 5 culture was only 45% of that in Day 3 culture. In subconfluent cultures (Days 3 and 4) the Cd accumulation was temperature sensitive; on Day 3 the cells accumulated one-third less Cd at 4 degrees C than at 37 degrees C. In comparison, the confluent cells (Day 5) had the same Cd accumulation regardless of the incubation temperature. In these cells, preincubation with cyanide also had no significant effect on Cd accumulation, implying a lack of energy requirement for Cd uptake. As the transport of Cd may involve processes that exist for the essential metal ions, the effect of 30 microM zinc (Zn) and copper (Cu) on the accumulation of 1 microM Cd was studied in Day 5 cultures. Coincubation with Zn caused a 16% reduction in Cd levels at 37 degrees C and even greater reduction (44% of control) at 4 degrees C. Similarly, Cu inhibited Cd accumulation by 26 and 45% at 37 and 4 degrees C, respectively, as compared to the temperature-matched controls. The Vmax for the initial Cd uptake (1 min) was 125 pmol/mg protein/min and the Km was 7 microM. Both Zn and Cu exhibited competitive inhibition kinetics and doubled the Km for Cd uptake. The Ki for Zn and Cu was 23 and 30 microM, respectively. Mercury (Hg) and lead (Pb) were also tested for their ability to affect Cd accumulation. As compared to the controls, 1 microM Hg caused an 11% reduction in Cd level at 37 degrees C. In contrast, 1 microM Pb enhanced Cd accumulation by 20%. However, neither Hg nor Pb had any significant effect on Cd accumulation at 4 degrees C. All four metals had no significant effect on the efflux of Cd from the cells. Thus, these metals affected Cd accumulation by changing its uptake rather than its efflux.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Histologic examination of peripheral nerves elongated by tissue expanders.

Histological changes induced by the slow stretch of peripheral nerves using a tissue expander were studied using a rat sciatic model. Tissue expanders were adapted to elongate the sciatic nerve in vivo. Nerves elongated over an eight week period using this method achieved an average increase in length of 88%. Light microscopic examination revealed that individual axons were separated but each axon and the myelin sheaths were stained well. Electron microscopic examination showed that the convoluted contour of the axons appeared and some loss of myelin was also observed, but the intraneural cytoskeleton elements were kept intact.

Animals↗
PubMed1993

Gonadotropin-induced ovarian carbonyl reductase in mice and hamsters: comparison with carbonyl reductase in rats.

We investigated the effects of pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotropin (hCG) on ovarian carbonyl reductase activities towards 13,14-dihydro-15-ketoprostaglandin F2 alpha (15KD-PGF2 alpha), p-nitroacetophenone (PNAP) and p-nitrobenzaldehyde (PNBA) in mice and hamsters, and compared with their effects on those we observed previously in rats. The treatment with PMSG and hCG caused a significant increase in ovarian weights and superovulation in both mice and hamsters. Hamster ovary possessed appreciable carbonyl reductase activities towards all three substrates, whereas the activities were lower than those in rat ovary. The reductase activities were not increased by the treatment with gonadotropins, differing from rat ovarian carbonyl reductase. In untreated mice, carbonyl reductase activity towards 15KD-PGF2 alpha was not detected, whereas the activities towards PNAP and PNBA were detected, which activities were lower than those in rats and hamsters. The PNAP and PNBA reductase activities in mouse ovary were significantly increased up to 7.1- and 1.7-fold, respectively, by the treatment with gonadotropins. These results show that there are species differences in ovarian carbonyl reductase and response of the enzyme to gonadotropins.

Alcohol Oxidoreductases↗
PubMed1993

Acidic regions of cytochrome c1 are essential for ubiquinol-cytochrome c reductase activity in yeast cells lacking the acidic QCR6 protein.

It has been suggested that the two acidic regions around residue 70 and residue 170 in yeast cytochrome c1, a subunit of ubiquinol-cytochrome c reductase (complex III), interact with cytochrome c in the electron transfer reaction and that the QCR6 protein, the acidic subunit of yeast complex III, enhances this interaction. In order to determine the roles of the acidic regions of cytochrome c1 more precisely, we introduced several mutations in the two acidic regions and examined their effects on the ability of modified cytochrome c1 to complement the respiration deficiency of yeast cells lacking only cytochrome c1 or both cytochrome c1 and the QCR6 protein. The mutant cytochrome c1 with the deletion of the first acidic region (delta 68-80) was still functional in the cytochrome c1-deficient strain. Mutant cytochrome c1 with the deletion of the second acidic region (delta 168-179) caused a decrease in the complementing ability, but this is probably due to failure in its proteolytic maturation and/or correct assembly into complex III. Mutant cytochrome c1 with altered charge distribution in the acidic regions (Asp170Asp171-->Asn170Asn171 or Asp170Asp171-->Asn170Lys171) made the cytochrome c1-deficient cells respiration-competent. On the other hand, mutant cytochrome c1 with the deletion of the first acidic region (delta 68-80) or altered charge distribution in the second region (Asp170Asp171-->Asn170Lys171) did not restore the respiration deficiency of the cells lacking not only cytochrome c1 but also the QCR6 protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1993

Surgical treatment of axillary osmidrosis.

Various types of surgical procedures have been developed for treatment of axillary hyperhidrosis and osmidrosis. However, Asian people tend to seek treatment for osmidrosis rather than hyperhidrosis. In this article, we report a new modified surgical method concerning axillary osmidrosis. At first we make four transverse parallel incisions; two incisions in the center are large (approximately 4 cm in length) and the lateral ones are small (approximately 1.5 cm in length). Then, we do enough undermining from the four wound edges to make a wide subcutaneous tunnel, and the adipose tissue beneath the skin is removed with scissors through each incision. Finally, two pieces of Penrose drain are inserted through the small lateral incisions. With this method we have operated on 21 patients in the past 3 years; 19 patients were female, and only 2 were male. Patients were followed for a minimum of 3 months and a maximum of 22 months, with an average follow-up of 7 months. In terms of results, 14 were good, 5 fair, and 2 poor. Minor complications such as partial epidermal necrosis occurred in only 2 patients, but healed with conservative treatment, and other complications such as hematoma formation or infection did not occur. In this article, we emphasize two merits of our procedure. One is that adding small incisions at both lateral margins makes it possible to perform the further excision of the apocrine glands. The other merit is that drainage from the small incisions is very effective. We believe this procedure is a viable option for treatment of axillary hyperhidrosis and osmidrosis.

Adolescent↗
PubMed1993

Effects of a thromboxane synthetase inhibitor, Y-20811, on infarct size, neutrophil accumulation, and arrhythmias after coronary artery occlusion and reperfusion in dogs.

To examine effects of a new thromboxane synthetase inhibitor, Y-20811, on infarct size, neutrophil accumulation, and arrhythmias, coronary artery was occluded for 90 min and reperfused for 6 h in anesthetized dogs. Y-20811 administered intravenously (i.v.) 30 min before occlusion decreased serum thromboxane B2 (TBX2) formation by 98% 30 min later and by 79% at 6 h after reperfusion. Ventricular fibrillation (VF) developed in 1 of 15 control and 3 of 10 treated dogs during occlusion (p = NS), whereas after reperfusion it occurred in 7 of 14 control and none of seven treated dogs (p < 0.05). The number of arrhythmias during the first hour of reperfusion was significantly reduced in treated dogs (134 +/- 74 beats/min in control vs. 14 +/- 4 beats/min in treated dogs, p < 0.05). Hemodynamics, area at risk, and collateral flow to the ischemic region were similar for the two groups. The extent of myocardial necrosis was 28.0 +/- 10.0% (n = 7) of the area at risk in control dogs and 27.6 +/- 6.2% (n = 7) in treated dogs (p = NS). The relation between the ratio of myocardial necrosis to area at risk and collateral flow was similar. The degree of neutrophil accumulation did not differ but correlated with infarct size (r = 0.85). Thus, Y-20811 reduced reperfusion arrhythmias but failed to limit infarct size and neutrophil accumulation after coronary artery occlusion/reperfusion in dogs.

Animals↗
PubMed1993

15-Deoxyspergualin "rescue therapy" for methylprednisolone-resistant rejection of renal transplants as compared with anti-T cell monoclonal antibody (OKT3).

A randomized trial with OKT3, an anti-T cell monoclonal antibody or with 15-deoxyspergualin against methylprednisolone-resistant rejection crisis was performed in 25 posttransplant patients immunosuppressed with prednisolone and cyclosporine. At least temporary reversal of rejection was observed in 58.3% of patients treated with 15-deoxyspergualin. This reversal rate may be quite comparable to 61.5% seen in patients treated with OKT3. Adverse effects with 15-deoxyspergualin were related to bone marrow suppression, while those with OKT3 were pyrexia, gastrointestinal symptoms, and herpes infection. In contrast to OKT3, which may act by modulating T cell surface antigen, 15-deoxyspergualin may be effective somewhere in the later stages of the rejection cascade.

Adult↗
PubMed1993

Involvement of opioid receptors in shaking behaviour induced by paraquat in rats.

Paraquat (30-70 mg/kg intraperitoneally) caused typical shaking behaviour in rats in a dose-dependent manner. Myoclonus also appeared after the shaking behaviour in several rats treated with the highest dose of paraquat. Morphine (5 mg/kg intraperitoneally, 30 min. before paraquat) significantly reduced the frequency of shaking behaviour. The alleviation by morphine disappeared when naloxone (1.5 mg/kg intraperitoneally 15 min. after morphine) was coadministered. Although there was no histological change in brain slices of paraquat-treated rats (70 mg/kg intraperitoneally), the fluorescein uptake into brain was increased by the treatment. Morphine prevented the increase of fluorescein uptake, but naloxone failed to antagonize this effect. On the other hand, intracerebroventricularly administered paraquat (25.7 micrograms/rat) caused tremor in all rats, but not shaking behaviour nor myoclonus. These findings suggest that paraquat administered systemically as well as centrally may be toxic to the brain. Although the actions of paraquat on the brain seem to be complicated, opioid receptors may play a role in the actions.

Animals↗
PubMed1993

Vasodilatory effect of arginine vasopressin is mediated by nitric oxide in human forearm vessels.

Arginine vasopressin (AVP) causes biphasic changes in vascular resistance in human forearms; vasoconstriction at lower doses and vasodilation at higher doses. Vasoconstriction is mediated by the V1 receptor. However, the mechanism of AVP-induced vasodilation is not known. We investigated whether AVP-induced vasodilation is mediated by nitric oxide (NO) in human forearms by examining the effects of L-arginine (a precursor of NO) and NG-monomethyl-L-arginine (L-NMMA, a blocker of NO synthase) on AVP-induced vasodilation. AVP was infused intraarterially at doses of 0.05, 0.1, 0.2, 0.5, and 1.0 ng/kg per min (n = 8). The lower doses of AVP (< or = 0.1 ng/kg per min) increased, whereas the higher doses of AVP (> or = 0.5 ng/kg per min) decreased forearm vascular resistance (FVR) (P < 0.01). Intraarterially infused L-arginine at 10 mg/min did not alter arterial pressure, baseline FVR, or heart rate. L-arginine did not alter the magnitude of AVP-induced vasoconstriction at the lower doses, but L-arginine augmented the magnitude of AVP-induced vasodilation at doses of 0.2 (P < 0.05), 0.5 (P < 0.01), and 1.0 (P < 0.05) ng/kg per min. In another group (n = 6), intraarterially infused L-NMMA (4 mumol/min for 5 min) increased baseline FVR without systemic effects, and inhibited acetylcholine-induced vasodilation (P < 0.01). L-NMMA at this dose inhibited AVP-induced vasodilation (P < 0.01) but did not affect vasoconstriction. L-arginine reversed the inhibitory effect of L-NMMA. Our results suggest that the vasodilatory effect of AVP may be mediated by NO in human forearms.

Adult↗
PubMed1993

Coordinate induction and activation of metalloproteinase and ascorbate depletion in structural luteolysis.

Structural luteolysis was found decades ago to be induced by PRL in the hypophysectomized rat, but the mechanisms of this process are unknown. To gain information on mechanisms of luteal involution, we developed an animal model that circumvented complex surgery and provided ample tissue for analyses. Gonadotropin-synchronized ovulation and luteinization were induced in immature rats, followed by treatment with ergot alkaloid and PRL. PRL-induced structural luteolysis, as shown by loss of luteal weight, protein, and DNA after pretreatment with ergot alkaloid, was evident after 36 h. Ascorbic acid depletion was rapid, severe, and lasting in luteal tissue during structural luteolysis, but lipid peroxidation or depletion of vitamin E was not evident. PRL treatment of animals with functional corpora lutea did not induce luteal involution. Significantly, after natural functional luteolysis occurred, PRL was highly effective in inducing structural luteolysis. Thus, either natural or ergot-induced functional luteolysis permitted the luteolytic expression of PRL. A greater depletion of protein than DNA was seen during PRL-induced structural luteolysis and was associated with a significant increase in neutral caseinase activity in luteal extracts. Caseinase activity was markedly reduced by calcium chelators and profoundly inhibited by the chelator orthophenanthroline; only slightly reduced activity was seen with serine, aspartate, or cysteine proteinase inhibitors. These findings implicate metalloproteinase (MMP) as the relevant caseinase that was increased during structural luteolysis. The major proteinase identified by zymography had apparent sizes of 72 and 66 kilodaltons (kDa), and slight but detectable activity was also seen at 92 and 84 kDa. Organomercurial treatment caused a major shift of the 72-kDa band to 66 kDa and the 92-kDa band to 84 kDa, confirming MMP-2 and MMP-9 by activation of latent activity of each MMP, respectively. Structural luteolysis caused a significant increase in the activated 66-kDa form and the latent 72-kDa form of MMP-2, which occurred before a loss of luteal weight or protein. As MMP-2 degrades collagen (type IV) in basement membranes, we conclude that an early event in PRL-induced structural luteolysis is the degradation of extracellular matrix. This conclusion is further emphasized by the marked and lasting depletion of ascorbic acid, a vitamin long known to serve an essential role in collagen synthesis.

Animals↗
PubMed1993

Hydrogen peroxide evokes antisteroidogenic and antigonadotropic actions in human granulosa luteal cells.

The nature of the luteolysin in humans is unknown. Hydrogen peroxide (H2O2), notably released by activated leukocytes, is generated in the rat corpus luteum at luteolysis and evokes luteolytic-like effects in rat luteal cells. We, therefore, evaluated the actions of H2O2 in human luteinized granulosa cells. After 2 days of preculture with low levels of hCG, human granulosa luteal cells were placed in suspension culture for 1 h in the presence of isobutylmethylxanthine (100 microM). A 60-min challenge with hCG evoked dose-dependent stimulation of cAMP and progesterone production. H2O2 dose-dependently inhibited progesterone production (ED50, 50-100 microM) in the absence or presence of hCG and blocked hCG-stimulated cAMP accumulation. Inhibition of progesterone synthesis by H2O2 was near maximal within 5 min, whereas inhibition of cAMP accumulation was not evident until 60 min. Cell viability was unaffected by H2O2, and inhibition of cAMP was reversible, but inhibition of steroidogenesis was long-lasting. Progesterone production stimulated by 8-bromo-cAMP, 22-hydroxycholesterol, and pregnenolone was inhibited by H2O2 as was androstenedione-dependent estradiol production. These findings indicate that H2O2 blocked progesterone synthesis by inhibition of cholesterol side-chain cleavage cytochrome P450, 3 beta-hydroxysteroid dehydrogenase, aromatase, and/or 17 beta-hydroxysteroid dehydrogenase. While H2O2 blocked stimulation of cAMP accumulation in response to hCG and cholera toxin, this same response produced by forskolin or aluminum fluoride was unaffected by H2O2. Thus, H2O2 appears to uncouple LH (hCG) receptors by interruption of G-protein-dependent activation of adenylate cyclase. In summary, H2O2 evokes effects in isolated human granulosa luteal cells that are associated with luteal regression, which raises the interesting possibility that H2O2 may serve a role as a mediator of this process like that in the rat.

1-Methyl-3-isobutylxanthine↗
PubMed1993

Dermatomyositis-polymyositis and malignancy. Is there a direct relation?

An association between dermatomyositis-polymyositis and malignancy has been reported. However, controversy exists regarding a direct causal relationship between the two diseases. We describe a patient who had the concurrent onset and parallel clinical course of dermatomyositis and malignancy, and discuss the possible mechanisms for the association of the two disorders.

Adenocarcinoma↗
PubMed1993

Immunodetection of TSH receptor antibodies in sera of patients with autoimmune thyroid disease by ELISA (enzyme-linked immunosorbent assay).

An ELISA system has been developed for detecting antibodies to TSH receptor peptides. It has been used to study antibodies against peptides corresponding to four different extracellular domains of human TSH receptor in the sera of patients with Graves' disease (N = 10, TBII positive) and Hashimoto's disease (N = 10, TBII negative). Two peptides, N (amino acid residues nos. 29-57) and P3 (nos. 359-371) are specific for TSH receptor, and two, C (nos 172-202) and P1 (nos. 398-417) are homologous with the corresponding portions of the LH/CG receptor. All of the peptides were recognized by sera from patients with Graves' disease but individual sera recognized different numbers and combinations of these peptides. Sera from patients with Hashimoto's disease did not bind to any of these peptides. These results suggest that antibodies to the TSH receptor in patients with Graves' disease recognize various regions of extracellular domain of TSH receptor in addition to TSH receptor-specific regions.

Amino Acid Sequence↗
PubMed1993

Thyrotrophin-dependent desensitization by Chinese hamster ovary cells that express the recombinant human thyrotrophin receptor.

To determine whether thyrotrophin (TSH)-induced desensitization requires a thyroid-specific factor(s), the human TSH (hTSH) receptor was expressed in Chinese hamster ovary cells. The first incubation of the cells with TSH decreased the subsequent response of adenosine 3',5'-cyclic monophosphate to freshly added TSH in the second incubation. This homologous desensitization was observed as early as after 3 h of the first incubation. The lowest dose of TSH that elicited desensitization was 0.1 nmol/l. The desensitization was not overcome by adding higher doses of TSH in the second incubation. A 125I-labelled TSH-binding study revealed a decrease in the number of high-affinity binding sites but not in that of low-affinity binding sites. The data suggest that TSH-induced desensitization in hTSH receptor-transfected cells is caused, at least in part, by a decrease in the number of TSH receptors on the cell surface. The evidence demonstrates, contrary to an earlier report, that a thyroid-specific factor(s) is not required for hTSH receptor desensitization.

Animals↗