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Biomedical subjects

Y Ando

Publications and source records attributed to Y Ando.

At least 523 records · Page 29Linked to original sources
PubMed1989

[Results of the treatment of Hodgkin's disease: the importance of establishing and executing a protocol].

A retrospective analysis was performed on 32 patients seen at Keio University Hospital and its affiliated hospitals from 1976 to 1987. Twenty-two patients were treated with our protocol, and the other 10 were not for several reasons. In this study, we compared the results of the treatment of these two groups. There were 20 males and 12 females. Age ranged from 13 to 72 years with a median value of 36 years. Histologically, six had lymphocytic predominance, 12 nodular sclerosis, 14 mixed cellularity. In the protocol group, seven were clinical stage I, 12 were CS II, two were CS III, and one was CS IV. Nine patients in the protocol group underwent staging laparotomy, and four CS II patients were upstaged to PS III. In the non-protocol group, five were CS I, four were CS II, one was CS III. According to the protocol, staging laparotomy was done excepting CS III.IV patients and some of CS I patients. In case of CS I without laparotomy, pathological stage(PS) I.II, or PS III1 with minimal splenic involvement, they were treated with radiation only. The rest of the patients were treated with chemotherapy and booster irradiation. Ten-year survival and 10-year relapse-free survival were 100%, 75%, respectively in the protocol group. In the non-protocol group, they were 31% and 32%, respectively. When picking up 17 patients treated by the authors through the whole process, 10-year survival and 10-year relapse-free survival were 100%, 92%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Enhancement of calcium sensitivity of lipocortin I in phospholipid binding induced by limited proteolysis and phosphorylation at the amino terminus as analyzed by phospholipid affinity column chromatography.

A phospholipid column was prepared by coating siliconized porous glass beads with phospholipids. The analysis of the Ca2+ requirement of lipocortin I and its derivatives in the binding to phospholipids was carried out with this column. The Ca2+ concentration required for 50% binding to the phospholipid column at room temperature was about 30 microM for lipocortin I, while that was reduced to 15 microM when lipocortin I was phosphorylated by the epidermal growth factor receptor/kinase, and a further reduction in the Ca2+ requirement was observed with proteolytic cleavage at the N-terminal region. Cathepsin D and calpain I (low calcium-requiring form of calcium-activated neutral protease) rapidly cleaved human placental lipocortin I at Trp-12 and Lys-26, respectively. These N-terminal-truncated proteins required only 5 microM Ca2+ for 50% binding to the phospholipid column. This enhancement of Ca2+ sensitivity by limited proteolysis was also observed for porcine lung lipocortin I. Essentially the same results were obtained when the Ca2+ sensitivities of the modified lipocortins I were analyzed using dispersed phospholipid vesicles instead of the phospholipid affinity column. Equilibrium dialysis indicated that the release of the N-terminal region markedly increased the affinity of lipocortin I for Ca2+ in the presence of phosphatidylserine, without any appreciable change of the number of Ca2+-binding sites. Limited proteolysis by endogenous proteases such as calpain may be an important regulatory mechanism for the Ca2+ sensitivity of lipocortin I in phospholipid binding.

Amino Acid Sequence↗
PubMed1989

Effect of a superoxide dismutase derivative on cold-induced brain edema.

Although the involvement of reactive oxygen species has been suggested in the pathogenesis of brain edema, direct evidence supporting this concept is lacking. To elucidate a critical role of oxygen radicals, effect of a superoxide dismutase (SOD) derivative that circulated bound to albumin with a half-life of 6 h on the occurrence of cold-induced brain edema was studied in the rat. When animals were challenged with brain injury by applying a liquid-nitrogen-cold probe to one side of the cerebral hemisphere over the bony skull for 20 s, the vascular permeability of the underlying tissue increased significantly and unilateral brain edema occurred as determined by the accumulation of intravenously injected Evan's blue and the increase in brain weight. Intravenous administration of the SOD derivative markedly suppressed the increase in vascular permeability and the occurrence of brain edema, particularly at their early stages. These and other results suggest that superoxide anion and/or its metabolite(s) might play a critical role in the pathogenesis of traumatic brain injury.

Animals↗
PubMed1989

Role of variant prealbumin in the pathogenesis of familial amyloidotic polyneuropathy: fate of normal and variant prealbumin in the circulation.

According to recent studies on protein chemistry and genetic engineering, replacement of the Val30 residue of prealbumin by methionine is believed to play a critical role in the formation of amyloid deposit and the pathogenesis of familial amyloidotic polyneuropathy (FAP). However, only limited information is available concerning the behavior of prealbumin in the circulation. To obtain the molecular insight into the mechanism of amyloid deposition, it is indispensable to know the fates of normal and variant prealbumin in vivo. Thus, the fates of prealbumin samples from normal and FAP patients were studied in normal rats as well as in animals that were challenged with acute inflammation induced by turpentine. The effect of in vitro photooxidation of prealbumin samples on their behavior was also examined in vivo. Kinetic analysis revealed no appreciable difference between prealbumin samples from normal and FAP patients. These results suggest that factors other than the rate of transfer of the variant form prealbumin from plasma to an extravascular compartment may play a critical role in the pathogenesis of amyloid deposition in FAP patients.

Amyloidosis↗
PubMed1989

Inhibition of stress-induced gastric injury in the rat by glutathione.

Glutathione metabolism occurs via interorgan cycles in which hepatic synthesis of reduced glutathione and its transfer to extrahepatic tissues play an important role. To elucidate the physiologic significance of the cycles and tissue thiol status during stress-induced gastric mucosal injury, dynamic aspects of glutathione metabolism were analyzed in rats that were treated with water-immersion restraint. This treatment induced gastric mucosal lesion with concomitant decrease in the levels of perchloric acid-soluble thiols in various tissues, particularly in the liver and stomach. During the treatment, glutathione levels markedly decreased in the liver but not in other tissues. Depletion of hepatic glutathione by buthionine sulfoximine, a specific inhibitor for gamma-glutamyl cysteine synthetase, markedly decreased hepatic glutathione levels and increased the gastric injury. Intraperitoneal injection of reduced glutathione significantly increased plasma levels of glutathione and inhibited the occurrence of gastric injury without affecting intracellular glutathione levels. These results indicate that extracellular glutathione and its interorgan metabolism might play a critical role in the protection of gastric mucosa particularly when animals were challenged with various stress.

Acetylcysteine↗
PubMed1989

Bottle-feeding can prevent transmission of HTLV-I from mothers to their babies.

Breast-feeding is a major factor in the vertical transmission of human T-lymphotropic virus type I (HTLV-I). We studied whether such transmission may be prevented by bottle-feeding. HTLV-I infection was detected by both HTLV-I antigen and antibody tests. Thirty bottle-fed babies were examined 24 months after birth; only one was found to be HTLV-I antigen-positive. This infection rate was lower than that for breast-fed babies in whom HTLV-I antigen was detected in 24 of the 31 24-month-old babies born to HTLV-I positive mothers in a previous study. These results suggest that most vertical transmission of HTLV-I is attributable to breast-feeding and can be prevented by bottle-feeding.

Bottle Feeding↗
PubMed1989

Relationship between periventricular hemorrhage, leukomalacia and brainstem lesions in prematurely born infants.

The brain pathology in very prematurely born infants with intraventricular hemorrhage (IVH) was studied particularly as to the severity and site of the complicated brain lesions responsible for the prognosis. A high frequency of leukomalacia, pontosubicular necrosis and/or olivocerebellar neuronal loss was found in the cases of IVH, and these non-hemorrhagic brain lesions showed an increasing frequency with the grade of IVH. However, there was marked reduction of IVH, periventricular leukomalacia and, in particular, brainstem lesions in prematurely born cases of sudden infant death. These IVH and associated conditions have different pathogenesis, but factors responsible for their occurrence may be present together in each case.

Abnormalities, Multiple↗
PubMed1989

Glucagon stimulates chloride transport independently of cyclic AMP in the rat medullary TAL.

The effect of glucagon on chloride transport was studied in the rat medullary thick ascending limb (MTAL) perfused in vitro. In the bath, 10(-6) M glucagon increased the efflux coefficient of Cl (KeCl) from 6.88 +/- 0.21 x 10(5) to 9.65 +/- 0.38 x 10(-5) cm.sec -1 (P less than 0.01) without changing the influx coefficient (KiCl; 2.87 +/- 0.54 x 10(-5) in control vs. 2.83 +/- 0.57 x 10(-5) cm.sec-1 with glucagon) or transepithelial potential difference (4.8 +/- 0.76 in control vs. 5.0 +/- 0.71 mV with glucagon). A physiological concentration of glucagon (10(-8), (10(-10) M) also increased chloride efflux significantly. Pretreatment of tubules with luminal furosemide (10(-5) M) and/or basolateral ouabain (10(-4) M) completely abolished the effect of glucagon. In isolated MTALs incubated in the same medium as that used in the microperfusion study, 10(-6) M glucagon stimulated cAMP production by 255.2 +/- 33.7% (P less than 0.01). However, neither dibutyryl cAMP (10(-3), 10(-4) M) nor forskolin (10(-4), 10(-6) M) increased the chloride efflux. It is concluded that: 1) Glucagon stimulates net Cl reabsorption by increasing Cl efflux in the rat MTAL; and 2) cyclic AMP is not responsible for this effect of glucagon.

Animals↗
PubMed1989

Ultrasonographical and morphological examination of subependymal cystic lesions in maturely born infants.

The clinical data and development of 8 cases with subependymal cysts detected on neurosonography in the neonatal period were studied, and the prognosis was found to vary. Also, clinico-pathological examination of 15 autopsied cases of congenital subependymal cysts (SEC) was performed, with immunohistochemical staining involving neuron-specific enolase in three cases, which revealed that congenital SEC are often complicated by various degrees of brain and heart anomalies, and suggested that SEC might occur in a wide gestational age range, with various causes. Therefore, it is important in the future to determine the agents which cause destruction of the subependymal germinal matrix.

Brain Diseases↗
PubMed1989

Exoribonuclease activity of purified reverse transcriptase preparations from retroviruses.

Highly purified and commercially available preparations of reverse transcriptases from retroviruses contain a 3' to 5' exoribonuclease activity capable of hydrolyzing synthetic homopolyribonucleotides having a 3'-OH end. The exoribonuclease activity of reverse transcriptase preparations from Rous associated virus-2 was further characterized. This exoribonuclease activity cleaves poly(C) and poly(U) exonucleolytically from the 3'-OH end to produce nucleoside 5'-phosphates. Poly(A), poly(G), circular polyribonucleotide, and double-stranded polyribonucleotide were not hydrolyzed by the activity. This is a novel type of exoribonuclease activity.

Buffers↗
PubMed1989

Effects of 1 alpha,25-dihydroxyvitamin D3 on the transglutaminase activity of transformed mouse epidermal cells in culture.

Induction of the transglutaminase activity of a transformed mouse epidermal cell line (PAM 212 cells) by 1 alpha,25-dihydroxyvitamin D3 (1 alpha,25-(OH)2-D3), the active form of vitamin D3, was investigated. Addition of 1 alpha,25-(OH)2-D3 to a culture medium stimulated twice the transglutaminase activity at a concentration of 10(-7) M, but vitamin D3, prostaglandin E1, E2, and F2 alpha failed to show this induction. Phorbol 12-o-tetradecanoylphorbol-13-acetate (TPA) and dexamethasone also induced an increase in transglutaminase activity. Exposure to both 1 alpha,25-(OH)2-D3 and retinoic acid caused remarkably synergistic effects on the induction of transglutaminase in the PAM 212 cells. In contrast, simultaneous addition of 1 alpha,25-(OH)2-D3 and TPA was antagonistic and resulted in less than additive induction. Vitamin D3 also showed a similar but lesser effect. These results suggest that 1 alpha,25-(OH)2-D3 induces the transglutaminase activity via mechanisms disparate from those of retinoic acid and modifies epidermal differentiation.

Animals↗
PubMed1989

Detection of HTLV-I genome in seronegative infants born to HTLV-I seropositive mothers by polymerase chain reaction.

We applied the polymerase chain reaction (PCR) method to detect gag, env and pX sequences of human T cell leukemia virus type I (HTLV-I) provirus in peripheral blood lymphocytes of seronegative infants born to HTLV-I seropositive mothers. Out of 22, five subjects were found to contain the HTLV-I provirus genome. Two of the five cases were judged to be negative for not only anti-HTLV-I antibodies but also the viral antigens on cultivated lymphocytes by the conventional antibody/antigen detection methods. These results indicate that PCR is of great use as a simple and highly sensitive method detect HTLV-I infection.

Adult↗
PubMed1989

Effect of freeze-thawing breast milk on vertical HTLV-I transmission from seropositive mothers to children.

Breast feeding is known to be a major cause of vertical transmission of HTLV-I from mothers to her children. The infectiousness of HTLV-I in breast milk was reported to be lost during freezing and thawing processes. We therefore administered frozen-and-thawed breast milk of HTLV-I carriers to their babies. Among the 13 babies given the frozen-and-thawed breast milk (now 12 months of age), no infection has been found yet. This result suggests that freezing and thawing of breast milk is a promising method for the prevention of vertical HTLV-I infection to breast-fed babies.

Breast Feeding↗
PubMed1989

Two distinct O-methyltransferases in aflatoxin biosynthesis.

The substances belonging to the sterigmatocystin group bear a close structural relationship to aflatoxins. When demethylsterigmatocystin (DMST) was fed to Aspergillus parasiticus NIAH-26, which endogenously produces neither aflatoxins nor precursors in YES medium, aflatoxins B1 and G1 were produced. When dihydrodemethylsterigmatocystin (DHDMST) was fed to this mutant, aflatoxins B2 and G2 were produced. Results of the cell-free experiment with S-adenosyl-[methyl-3H]methionine showed that first the C-6-OH groups of DMST and DHDMST are methylated to produce sterigmatocystin and dihydrosterigmatocystin (O-methyltransferase I) and then the C-7-OH groups are methylated to produce O-methylsterigmatocystin (OMST) and dihydro-O-methylsterigmatocystin (DHOMST) (O-methyltransferase II). However, no methyltransferase activity was observed when either OMST, DHOMST, 5,6-dimethoxysterigmatocystin, 5-methoxysterigmatocystin, or sterigmatin was incubated with the cell extract. Treatment of the cell extract with N-ethylmaleimide inhibited O-methyltransferase I activity but not that of O-methyltransferase II. Furthermore, these O-methyltransferases were different in their protein molecules and were involved in both the reactions from DMST to OMST and DHDMST to DHOMST. The reactions described in this paper were not observed when the same mold had been cultured in YEP medium.

Aflatoxins↗
PubMed1989

Dose-dependent heterogenous actions of vasopressin in rabbit cortical collecting ducts.

In cortical collecting ducts (CCD), arginine vasopressin (AVP) has been proposed to autoinhibit its own hydrosmotic effect through stimulation of prostaglandin (PG) synthesis or binding to a receptor coupled to phosphatidylinositol (PI) hydrolysis, the so-called V1-receptor, with resultant elevation of intracellular Ca2+ concentration [( Ca2+]i) and activation of protein kinase C (PKC). Using isolated perfused rabbit CCD, we examined whether blocking the negative feedback by a PKC inhibitor, staurosporine (SSP), or a cyclooxygenase inhibitor, indomethacin (IND), enhances AVP-induced increase in hydraulic conductivity (Lp). The Lp induced by a pharmacological concentration (23 nM) of AVP was lower than that induced by 230 pM AVP. This blunted Lp response to 23 nM AVP was significantly restored by SSP or IND pretreatment. In contrast, both SSP and IND did not affect the Lp induced by 23 pM or 230 pM AVP. Fluorescence microscopy of isolated perfused CCD using fura-2 showed a spike-like increase in [Ca2+]i only by 23 nM but not by 23 or 230 pM AVP. We conclude that 1) AVP can increase [Ca2+]i, activate PKC, and stimulate PG synthesis in CCD with resultant autoregulation of its own hydrosmotic effect and 2) importantly, however, this negative feedback occurs only with pharmacologically high concentrations of AVP. Therefore it is unlikely that circulating AVP, via binding to receptors on CCD, autoregulates water transport through activating PG synthesis and/or PI breakdown.

Alkaloids↗
PubMed1989

Phosphatidates inhibit vasopressin-induced water transport via protein kinase C activation.

Phosphatidic acid (PA), best known as an intermediate of phosphatidylinositol bisphosphate (PIP2) turnover, inhibits vasopressin (AVP)-induced increase in hydraulic conductivity (Lp) in rabbit cortical collecting ducts (CCD) perfused in vitro (Ando, Y., H. R. Jacobson, and M. D. Breyer, J. Clin. Invest. 80: 590, 1987). The present study addresses the mechanism(s) responsible for this action of PA. In control experiments, 10 microU/ml AVP (23 pM) increased Lp of CCDs from a basal of 4.9 +/- 0.4 X 10(-7) cm.atm-1.s-1 to a peak of 171.2 +/- 4.6 X 10(-7) cm.atm-1.s-1. Basolateral pretreatment of the tubule with PA (25 micrograms/ml) suppressed AVP-induced increase in peak Lp by 45.0%. This suppression was not attenuated by 5 microM indomethacin pretreatment. L-alpha-dipalmitoyl(C16) PA (DPPA, 25 micrograms/ml), an arachidonate-free synthetic PA, inhibited peak Lp by 79.0%, whereas another synthetic PA with shorter fatty acid (C12), L-alpha-dilauroyl PA (DLPA, 25 micrograms/ml), had no significant effect on AVP-induced peak Lp. In the presence of 100 nM staurosporine, a protein kinase C (PKC) inhibitor, the inhibition by PA and DPPA on AVP-induced peak Lp were abolished. Furthermore, another PKC inhibitor, 100 microM 1-(5-isoquiniline-sulfonyl)-2-methylpiperzine, also reversed the DPPA-induced inhibition of AVP action. In separate experiments using fura-2-loaded isolated perfused CCDs, however, neither PA nor DPPA caused a significant increase in intracellular free Ca2+ concentration [( Ca2+]i). Taken together, in CCD, PA-induced inhibition of AVP action is primarily mediated by PKC but not by an increased [Ca2+]i or the production of arachidonate metabolites, such as prostaglandins. Thus the PA-induced activation of PKC does not seem to involve the classic pathway for PKC activation, breakdown of PIP2.

Alkaloids↗