Protective effect of OPC-6535, a superoxide anion production inhibitor, on liver grafts subjected to warm ischemia during porcine liver transplantation.
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Animals↗
Biomedical subjects
Y Eguchi
Publications and source records attributed to Y Eguchi.
Amino acid sequences of hemoglobin from guinea fowl (Numida meleagri) and California quail (Lophortyx californica) with phylogenetic analysis of major groups of Galliformes.
We determined the complete amino acid sequences of the hemoglobin of two species, guinea fowl and California quail, in Galliformes from intact globin chain and chemical cleavage fragments in order to analyze the molecular evolution of hemoglobin for the classification of Galliformes. Galliformes have two types of hemoglobin components, HbA and HbD, which consist of identical beta chain and different alpha chains. The sequences are similar to globin chains of Galliformes reported previously. These sequences were compared with those of other Galliformes (Phasianidae, Meleagrididae) using duck and goshawk as out-groups. The phylogenetic tree of major groups of Galliformes based on hemoglobin was similar to the tree model produced based on the amino acid sequence of lysozyme c.
Amino Acid Sequence↗
Regions essential for the interaction between Bcl-2 and SMN, the spinal muscular atrophy disease gene product.
The SMN gene is implicated in spinal muscular atrophy (SMA), and its product has been shown to interact with Bcl-2 protein to enhance its anti-apoptotic activity. In this study, we determined the regions that were essential for the interaction of Bcl-2 and SMN by co-immunoprecipitation of deletion mutants. Bcl-2 lacking its amino-terminal 20 amino acid residues or its carboxyl-terminal membrane-anchoring domain showed no or greatly reduced binding with SMN, respectively. However, Bcl-2 lacking other regions could still bind to SMN. Because Bcl-2 lacking the membrane-anchoring domain could bind to SMN in a yeast two-hybrid system, the amino-terminal region of Bcl-2 seems to be the most important domain for binding with SMN. A fragment of SMN encoded by exon 6 could bind to Bcl-2, but SMN lacking this region could not. From these results, we concluded that Bcl-2 and SMN proteins bound with each other at the amino-terminal region near the BH4 domain of Bcl-2 and the region encoded by exon 6 of SMN, both regions known to be important for their function.
Amino Acid Sequence↗
Isolated pericardial effusion and transient abnormal myelopoiesis in a fetus with Down's syndrome.
Isolated pericardial effusion was detected in a fetus at 34 weeks of gestation. A male infant weighing 2,044 g was born by cesarean section because of a non-assuring fetal heart rate pattern at 35 weeks of gestation. Transient leukocytosis (36,100/microl) with 49% blast cells was seen in this neonate. The infant's karyotype was 47, XY + 21. The pericardial effusion disappeared after treatment with prednisolone at a dose of 2 mg/kg/day. Hypothyroidism was subsequently found. Thus, the subject patient with Down's syndrome developed isolated pericardial effusion, transient abnormal myelopoiesis (TAM), and hypothyroidism. Because more than 20% of the infants with TAM and Down's syndrome develop acute nonlymphocytic leukemia in early childhood, he is being closely observed.
Adult↗
Effect of follicle-stimulating hormone on sertoli cell division in cultures of fetal rat testes.
The present study was performed to determine when follicle-stimulating hormone (FSH) begins to promote Sertoli cell division in fetal rats, and to determine whether the effect of FSH is mediated by cAMP-dependent protein kinase (PKA). When testes from 15- to 17-day fetuses were cultured with or without FSH for 48 h, FSH did not promote Sertoli cell division in 15-day testes, but did in 16- and 17-day testes. Anti-rat FSH was injected into 16-day fetuses in utero. Twenty-four hours later, the testes of the injected fetuses and those of their intact littermates were cultured with or without FSH for 48 h. Without FSH, the Sertoli cell division index was significantly lower in anti-FSH-treated fetuses than in intact fetuses. With FSH, however, the index increased. When PKA inhibitor was added to cultures of 16-day testes with FSH, the promotion of Sertoli cell division by FSH was inhibited. We conclude that between 16 and 17 days of gestation, fetal pituitary FSH stimulates the division of Sertoli cells by activating the PKA activity.
Animals↗
Necrotizing myopathy in a patient with chronic hepatitis C virus infection: a case report and a review of the literature.
We describe a 61-year-old man presenting with necrotizing myopathy associated with chronic active hepatitis due to hepatitis C virus (HCV) infection. Thirteen patients with HCV-associated myopathy have been reported previously. In most of these cases, varying degrees of inflammatory changes were observed in the muscle tissue. In 2 patients, myopathy developed after initiation of interferon therapy for chronic HCV hepatitis. Our case was unusual due to long-standing elevation of creatine kinase values which improved following interferon therapy and the non-inflammatory features of the muscle tissue where the HCV RNA minus strand, a marker for replicative intermediates of the virus, was undetectable. The association of myopathy with HCV infection might represent a unique clinical entity, although the underlying pathological mechanisms remain unknown.
Biopsy↗
Influence of chorioamnionitis on survival and morbidity in singletons live-born at < 32 weeks of gestation.
BACKGROUND: Chorioamnionitis (CAM) may accelerate lung maturation in fetuses. It is possible that CAM prevents infant death after live birth. METHODS: A retrospective study of live-born singletons at < 32 weeks of gestation between 1993 and 1997. Perinatal risk factors for adverse outcomes were analyzed using a logistic regression model, with special reference to the presence of histologically confirmed CAM. Adverse outcomes included infant death before 1 year of age, and survival with cerebral palsy and/or mental retardation. RESULTS: A total of 81 infants, weighing 1181 +/- 426 g, were born at 28.1 +/- 2.3 weeks of gestation. Of those, 15 (19%) died before 1 year of age, while 16 (20%) infants developed major handicaps by 1.5 years of age (six with cerebral palsy, eight with mental retardation, and two with both cerebral palsy and mental retardation). CAM, present in 44 women, was significantly associated with a reduced risk of death after live birth, with an odds ratio of 0.11 (p = 0.01). Only the presence of such intracranial lesions as periventricular leukomalacia and intraventricular hemorrhage were significantly associated with an increased risk of major handicaps (odds ratio of 11.0, p = 0.04). Adverse outcomes occurred in a similar proportion of infants in groups without CAM (14/37) and with CAM (17/44). However, among infants with adverse outcomes, the number of deaths was significantly higher in the group without CAM (10/14) vs. with CAM (5/12) (p < 0.05). CONCLUSIONS: The presence of CAM may somehow prevent infant death after live birth. Larger studies are required to confirm this phenomenon.
Adult↗
Acinus is a caspase-3-activated protein required for apoptotic chromatin condensation.
Apoptosis is defined by several unique morphological nuclear changes, such as chromatin condensation and nuclear fragmentation. These changes are triggered by the activation of a family of cysteine proteases called caspases, and caspase-activated DNase (CAD/DFF40) and lamin protease (caspase-6) have been implicated in some of these changes. CAD/DFF40 induces chromatin condensation in purified nuclei, but distinct caspase-activated factor(s) may be responsible for chromatin condensation. Here we use an in vitro system to identify a new nuclear factor, designated Acinus, which induces apoptotic chromatin condensation after cleavage by caspase-3 without inducing DNA fragmentation. Immunodepletion experiments showed that Acinus is essential for apoptotic chromatin condensation in vitro, and an antisense study revealed that Acinus is also important in the induction of apoptotic chromatin condensation in cells.
Amino Acid Sequence↗
ATP-dependent steps in apoptotic signal transduction.
Apoptotic changes of the nucleus induced by Fas (Apo1/CD95) stimulation are completely blocked by reducing intracellular ATP level. In this study, we examined the ATP-dependent step(s) of Fas-mediated apoptotic signal transduction using two cell lines. In SKW6.4 (type I) cells characterized by rapid formation of the death-inducing signaling complex on Fas treatment, the activation of caspases 8, 9, and 3, cleavage of DFF45 (ICAD), and release of cytochrome c from the mitochondria to the cytoplasm were not affected by reduction of intracellular ATP, although chromatin condensation and nuclear fragmentation were inhibited. On the other hand, in the Fas-mediated apoptosis of Jurkat (type II) cells, which is characterized by involvement of mitochondria and, thus, shares signal transduction mechanisms with apoptosis induced by other stimuli such as genotoxins, activation of the three caspases, cleavage of DFF45 (ICAD), and nuclear changes were blocked by reduction of intracellular ATP, whereas release of cytochrome c was not affected. These results suggested that the ATP-dependent step(s) of Fas-mediated apoptotic signal transduction in type I cells are only located downstream of caspase 3 activation, whereas the activation of caspase 9 by released cytochrome c is the most upstream ATP-dependent step in type II cells. These observations also confirm the existence of two pathways for Fas-mediated apoptotic signal transduction and suggest that the Apaf-1 (Ced-4 homologue) system for caspase 9 activation operates in an ATP-dependent manner in vivo.
Adenosine Triphosphate↗
150-kDa oxygen-regulated protein (ORP150) suppresses hypoxia-induced apoptotic cell death.
To determine the contribution of 150-kDa oxygen-regulated protein (ORP150) to cellular processes underlying adaptation to hypoxia, a cell line stably transfected to overexpress ORP150 antisense RNA was created. In human embryonic kidney (HEK) cells stably overexpressing ORP150 antisense RNA, ORP150 antigen and transcripts were suppressed to low levels in normoxia and hypoxia, whereas wild-type cells showed induction of ORP150 with oxygen deprivation. Inhibition of ORP150 in antisense transfectants was selective, as hypoxia-mediated enhancement of glucose-regulated protein (GRP) 78 and GRP94 was maintained. However, antisense ORP150 transfectants displayed reduced viability when subjected to hypoxia, compared with wild-type and sense-transfected HEK cells. In contrast, diminished levels of ORP150 had no effect on cytotoxicity induced by other stimuli, including oxygen-free radicals and sodium arsenate. Although cellular ATP content was similar in hypoxia, compared with ORP150 antisense transfectants and wild-type HEK cells, suppression of ORP150 expression was associated with accelerated apoptosis. Hypoxia-mediated cell death in antisense HEK transfectants did not cause an increase in caspase activity or in cytoplasmic cytochrome c antigen. A well recognized inducer of apoptosis in HEK cells, staurosporine, caused increased caspase activity and cytoplasmic cytochrome c levels in both wild-type and antisense cells. These data indicate that ORP150 has an important cytoprotective role in hypoxia-induced cellular perturbation and that ORP150-associated inhibition of apoptosis may involve mechanisms distinct from those triggered by other apoptotic stimuli.
Apoptosis↗
Fetus with long QT syndrome manifested by tachyarrhythmia: a case report.
We encountered a fetus who exhibited transient (at most 30 s), repeated episodes of tachyarrhythmia (240 bpm). This female neonate was born at 36 weeks of gestation and showed a markedly prolonged QT interval and transient, repeated episodes of polymorphic ventricular tachycardia. Congenital long QT syndrome was diagnosed. Retrospective analysis of the videotape showing fetal cardiac movement revealed that atrio-ventricular dissociation was present prenatally and thus, the fetal tachyarrhythmia was due to ventricular tachycardia. To our knowledge, there are few reports of a fetus with the long QT syndrome who exhibited ventricular tachycardia in utero. In the presence of unexplained fetal tachyarrhythmia, long QT syndrome should be considered as a possible underlying cause disorder. The presence of atrio-ventricular dissociation may be useful in prenatal diagnosis of long QT syndrome.
Adult↗
Secretion of lipocalin-type prostaglandin D synthase (beta-trace) from human heart to plasma during coronary circulation.
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Animals↗
Alterations of protein kinase C, 8-hydroxydeoxyguanosine, and K-ras oncogene in rat lungs exposed to passive smoking.
To investigate the effects of exposure to sidestream cigarette smoke (CS) on the initiation and promotion of lung cancer, two groups of 8 or 10 rats were exposed to CS for a 1 h period twice a day for 8, 12, or 20 weeks. The protein kinase C (PKC) activity of the lung exhibited significant changes of 120, 86 and 81% in the CS groups, compared with the respective control group values in the three exposure periods. The in vitro activation of PKC by the active oxygens was efficiently eliminated by hydroxyl radical scavengers, indicating that hydroxyl radicals are responsible for the PKC activation. For the alterations in the lung nucleus caused by passive smoking, the 12- and 20-week exposure CS groups showed significant increases in the accumulation of 8-hydroxydeoxyguanosine. One rat with K-ras activation by G:C transversion (GGT-->GCT) at codon 12 was found among 26 rats of the CS groups in the three exposure periods. These results show that active oxygens introduced by passive smoking may contribute to K-ras activation as an initiator of a tumor model, possibly through the oxygen-induced DNA damage, and may also contribute to an initial activation and the subsequent down-regulation of PKC as a promoter.
8-Hydroxy-2'-Deoxyguanosine↗
Divergence of the regulation of alpha-amylase activity in Drosophila melanogaster, Drosophila funebris, and Drosophila saltans.
The regulation of amylase activity in three Drosophila species, D. melanogaster, D. funebris and D. saltans, was analyzed by measuring the specific activity levels in four dietary environments, cornmeal, glucose, 5% starch, and 10% starch, at three developmental stages, i.e., the third-instar larval, pupal, and 2-day-old adult stages. The developmental profiles of amylase activity for the three Drosophila species showed that the level of activity was high at the larval and adult stages but substantially low at the pupal stage, suggesting that Drosophila does not utilize starch at the pupal stage. Divergence in the regulation of amylase was observed among the three Drosophila species on the following points. (1) The order of amylase specific activity was D. melanogaster > D. funebris > D. saltans. (2) The response pattern to the dietary environment varied among the species and changed during development. (3) The timing of the switch in the response pattern to the dietary environment during development was before pupation in D. funebris and D. saltans but after pupation in D. melanogaster. The significance of the divergence in the regulation of amylase activity for adaptation to a starch environment in Drosophila is discussed.
Animals↗
Adaptation to a starch environment and regulation of alpha-amylase in Drosophila.
The adaptation to glucose and starch foods in six species, D. melanogaster, D. virilis, D. saltans, D. funebris, D. levanonensis and D. americana, was studied by measuring productivity. D. melanogaster and D. virilis adapted more to the starch environment than to the glucose environment, while D. saltans adapted more to the glucose environment than to the starch environment. D. funebris, D. levanonensis, and D. americana did not distinctly adapt to either environment. In addition, the regulation of amylase in the six species was investigated by measuring the levels of amylase activity with glucose and starch food environments. The levels of amylase activity in D. levanonensis and D. saltans were substantially low, indicating that these species cannot utilize starch as a carbon source. The starch-adapted species, D. melanogaster and D. virilis, showed higher levels of amylase activity with the starch environment and higher inducibility. These results suggest that changing the regulation of amylase is important for the adaptation to a starch environment in Drosophila.
Adaptation, Physiological↗
Relation between hemoglobin discordance and adverse outcome in monochorionic twins.
BACKGROUND: The effects of discrepancies in the birth weight and hemoglobin concentration ([Hb]) at the birth on infant outcome have not been fully investigated in monochorionic (MC) and dichorionic (DC) twins. METHODS: A retrospective study of 95 twin pregnancies. All 190 neonates (68 MC twins and 122 DC twins) were admitted to the neonatal intensive care unit, and the [Hb] was determined soon after birth. The [Hb] discordance represents the [Hb] of the smaller twin expressed as a percentage of the [Hb] of the larger twin. Infants were followed-up until 1 year of corrected age and their psychomotor development was evaluated between 12 and 18 months. RESULTS: One DC infant died by 1 year of age. Twelve MC infants and eight DC infants had disabilities by 1.5 year of age. In the MC group, 11 infants (28%) of 20 pairs with an intertwin [Hb] discordance >100 had disabilities compared with one (3.6%) of 14 pairs with an [Hb] discordance < or = 100 (p<0.05). A similar trend was observed in the DC group, but the difference was not significant. The incidence of disabled infants increased as the intertwin birth weight discordance increased in MC twins. CONCLUSIONS: An adverse outcome at 1 year of age in MC twins was associated with a greater birth weight discordance and an [Hb] disordance that indicated polycythemia in the smaller twin.
Adult↗
[Apoptotic signal transduction from cytosol to nucleus].
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Animals↗
Dose-dependent doxycycline-mediated adrenocorticotropic hormone secretion from encapsulated Tet-on proopiomelanocortin Neuro2A cells in the subarachnoid space.
We previously reported that polymer-encapsulated mouse neuroblastoma cells that are capable of secreting beta-endorphin may reduce pain sensitivity in rats after capsule implantation into the cerebrospinal fluid (CSF)-filled subarachnoid space of the spinal cord. The neuroblastoma cells carry the proopiomelanocortin (POMC) gene that encodes the precursor of adrenocorticotropic hormone (ACTH) and beta-endorphin. To control the expression of these hormones in the present study, a promoter that is inducible by administration of tetracycline derivatives such as doxycycline (Dox) was linked to the POMC gene. Encapsulated cells in the CSF space of rats stimulated by four intraperitoneal doses of Dox responded with ACTH expression as determined in a subsequence 36-hr in vitro incubation. The amount of ACTH released was dependent on the in vivo Dox dose. These findings indicate that gene expression in xenogeneic cells in the CSF space can be manipulated by injection of a relatively innocuous drug, and suggest that this system may be applicable to cell transplantation therapy in patients with central nervous system diseases that require temporary control of ligand delivery.
Adrenocorticotropic Hormone↗