32 results on '"Maezono K"'
Search Results
2. Effect of alanine on ?-galactosamine-induced acute liver failure in rats
- Author
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Maezono, K, primary
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- 1996
- Full Text
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3. Epitaxial MgO buffer layers for YBCO thin films onR-plane
- Author
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Hakuraku, Y, primary, Maezono, K, additional, and Ueda, H, additional
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- 1996
- Full Text
- View/download PDF
4. Alanine protects liver from injury caused by ?-galactosamine and CCl4
- Author
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Maezono, K, primary
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- 1996
- Full Text
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5. Skeletal muscle insulin resistance in normoglycemic subjects with a strong family history of type 2 diabetes is associated with decreased insulin-stimulated insulin receptor substrate-1 tyrosine phosphorylation.
- Author
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Pratipanawatr, Wilailak, Pratipanawatr, Thongchai, Cusi, Kenneth, Berria, Rachele, Adams, John M., Jenkinson, Christopher P., Maezono, Katsumi, DeFronzo, Ralph A., Mandarino, Lawrence J., Pratipanawatr, W, Pratipanawatr, T, Cusi, K, Berria, R, Adams, J M, Jenkinson, C P, Maezono, K, DeFronzo, R A, and Mandarino, L J
- Subjects
INSULIN resistance ,MUSCLES - Abstract
Normoglycemic subjects with a strong family history of type 2 diabetes are insulin resistant, but the mechanism of insulin resistance in skeletal muscle of such individuals is unknown. The present study was undertaken to determine whether abnormalities in insulin-signaling events are present in normoglycemic, nonobese subjects with a strong family history of type 2 diabetes. Hyperinsulinemic-euglycemic clamps with percutaneous muscle biopsies were performed in eight normoglycemic relatives of type 2 diabetic patients (FH(+)) and eight control subjects who had no family history of diabetes (FH(-)), with each group matched for age, sex, body composition, and ethnicity. The FH(+) group had decreased insulin-stimulated glucose disposal (6.64 +/- 0.52 vs. 8.45 +/- 0.54 mg. kg(-1) fat-free mass. min(-1); P < 0.05 vs. FH(-)). In skeletal muscle, the FH(+) and FH(-) groups had equivalent insulin stimulation of insulin receptor tyrosine phosphorylation. In contrast, the FH(+) group had decreased insulin stimulation of insulin receptor substrate (IRS)-1 tyrosine phosphorylation (0.522 +/- 0.077 vs. 1.328 +/- 0.115 density units; P < 0.01) and association of PI 3-kinase activity with IRS-1 (0.299 +/- 0.053 vs. 0.466 +/- 0.098 activity units; P < 0.05). PI 3-kinase activity was correlated with the glucose disposal rate (r = 0.567, P = 0.02). In five subjects with sufficient biopsy material for further study, phosphorylation of Akt was 0.266 +/- 0.061 vs. 0.404 +/- 0.078 density units (P < 0.10) and glycogen synthase activity was 0.31 +/- 0.06 vs. 0.50 +/- 0.12 ng. min(-1). mg(-1) (P < 0.10) for FH(+) and FH(-) subjects, respectively. Therefore, despite normal insulin receptor phosphorylation, postreceptor signaling was reduced and was correlated with glucose disposal in muscle of individuals with a strong genetic background for type 2 diabetes. [ABSTRACT FROM AUTHOR]
- Published
- 2001
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6. Effects of exercise and insulin on insulin signaling proteins in human skeletal muscle.
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Koval JA, Maezono K, Patti ME, Pendergrass M, DeFronzo RA, and Mandarino LJ
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- 1999
7. Effect of alanine on D-galactosamine-induced acute liver failure in rats.
- Author
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Maezono, K, Mawatari, K, Kajiwara, K, Shinkai, A, and Maki, T
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- 1996
- Full Text
- View/download PDF
8. Alanine protects liver from injury caused by D-galactosamine and CCl4.
- Author
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Maezono, K, Kajiwara, K, Mawatari, K, Shinkai, A, Torii, K, and Maki, T
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- 1996
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9. Regulation of hexokinase II expression in human skeletal muscle in vivo
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Vogt, C., Ardehali, H., Iozzo, P., Yki-Jarvinen, H., Koval, J., Maezono, K., Pendergrass, M., Printz, R., Granner, D., DeFronzo, R., and Mandarino, L.
- Abstract
The phosphorylation of glucose to glucose-6-phosphate (G-6-P) is the first committed step in glucose uptake in skeletal muscle. This reaction is catalyzed by hexokinase (HK). Two HK isoforms, HKI and HKII, are expressed in human skeletal muscle, but only HKII is regulated by insulin. The present study was undertaken to determine the time course for the regulation of HK activity and expression by physiological plasma insulin concentrations in human skeletal muscle in vivo. A hyperinsulinemiceuglycemic glucose clamp and percutaneous muscle biopsy were performed in separate groups of healthy subjects after 60, 120, 180, and 360 minutes of euglycemic hyperinsulinemia. Muscle biopsies were subfractionated into soluble and particulate fractions to determine HKI and HKII activities. RNA was extracted from a separate portion of the muscle biopsy, and HKI and HKII mRNA content was determined using an RNase protection assay. Glycogen synthase (GS) activity and fractional velocity were also determined. HKII mRNA was increased 2-fold by 120 minutes and remained high versus the basal value for up to 360 minutes. HKI mRNA was unchanged throughout the study. HKII activity increased after 360 minutes of insulin infusion, and this increase was limited to the soluble fraction. In contrast, insulin induced a 1.5- to 2-fold increase in GS fractional velocity that was sustained for 360 minutes. The time course of the ability of hyperinsulinemia to increase HKII mRNA indicates that insulin is likely a physiological regulator of HKII expression in human skeletal muscle in vivo.
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- 2000
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10. ラマ属家畜の血液タンパク質および酵素の多型
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Luis K. MAEZONO, Enrique Flores MARIAZZA, Gustavo A. Gutierrez REYNOSO, Jorge A. Gamarra BOJORQUES, Yutaka, Yoshida, Hanzawa Kei, Kuwayama Takehito, Sukemori Seizi, Ikeda Shuhei, Sato Mitsuo, Monji Yasunori, Watanabe Tadao, Ohmi Hiroaki, Kurihara Yoshio, Domeki Ikuo, Ito Sumimaro, Maezono K. Luis, Mariazza Flores Enrique, Reynoso Gustavo A. Gutierrez, Bojorques Jorge A. Gamarra, and Watanabe Seiki
- Subjects
alpacas ,enzyme ,酵素 ,blood protein ,llamas ,electrophoretic polymorphisms ,アルパカ ,血液蛋白質 ,電気泳動的多型 ,リャマ - Abstract
ペルーおよび日本国内で採取したラマ47頭,アルパカ27頭および両者の交雑種1頭とそのアルパカへの戻し交雑種1頭の計76頭の血液を用いて,19座位の血液タンパク質・酵素型を電気泳動学的に解析し,以下に示す成績を得た。1)血漿タンパク質 : Albumin, Haptoglobin,血漿酵素 : Alanine aminotransferase, Aspartate aminotransferase, γ-Glutamyltranspeptidase,赤血球タンパク質 : Haemoglobin,ならびに赤血球酵素 : Acid phosphatase, Catarase, Glucose-6-phosphate dehydrogenase, Phosphoglucomutase, Phosphohexose isomeraseの計11座位では多型は認められなかった。2)血漿タンパク質4座位 : Post-albumin(Po),Gc-protein(Gc),Transferrin(Tf)およびγ-globurin field protein(γG),血漿酵素3座位 : Amylase(Amy),Creatine kinase(CK)およびLeucine aminopeptidase(LAP),ならびに赤血球酵素1座位 : EsteraseD(EsD)の計8座位に多型が認められた。これら8座位のうちTfでは6型,PoおよびGcでは4型,γ-G, AmyおよびEsDでは3型,LAPおよびCKでは2型が認められた。ラマおよびアルパカにおけるこれら8座位の総合的な父権否定率は,0.931および0.867であった。3)ラマとアルパカとの間で血液タンパク質・酵素型を比較したところ,Gc, AmyおよびEsDにおいて種間差が認められた。すなわち,GcおよびAmyでは両種で共通な易動度を示すバンド以外に各々種特有の易動度を示すバンドが存在し,またEsDでは両種間でバンドの易動度が異なっていた。4)ラマとアルパカの交雑種,ならびにアルパカへの戻し交雑種の血液タンパク質・酵素型はラマあるいはアルパカと共通であった。5)CKおよびEsDを除く,17座位の遺伝子頻度に基づいて算出したラマとアルパカとの間の遺伝的距離は0.035であった。以上の成績から,血液タンパク質・酵素型の解析はラマおよびアルパカの集団の遺伝子構成を推定する上で有力な指標となることが明確となった。一方,ラマとアルパカが遺伝的に極めて近縁な関係にあることを裏付けるものと判断された。, Blood samples of llamas and alpacas were classified by using electrophoretic procedures in the polymorphism at 19 loci. Electrophoretic variation was found for 8 loci, namely plasma proteins : post albumin (Po), Gc protein (Gc) and transferrin (Tf) and γ-globurin zone protein (γG), for plasma enzymes : amylase (Amy), creatine kinase (CK) and leucine aminopeptidase (LAP), and for red cell enzyme : esteraseD (EsD). Synthetic probabilityes of paternity exclusion about the 8 loci for llamas and alpacas were 0.931 and 0.867, respectively. No variants were found for plasma proteins : albumin and haptoglobin, for plasma enzymes : alanine aminotransferase, aspartate aminotransferase and γ-glutamyltranspeptidase, for red cell haemoglobin, and for red cell enzymes : acid phosphatase, catarase, glucose-6-phosphate dehydrogenase, phosphoglucomutase and phosphohexose isomerase. Nei's genetic distance between llamas and alpacas on the 17 loci (except CK and EsD) was 0.035. Preliminary estimate of the genetic distance measure may suggest that llamas and alpacas are more likely related as subspecies than as separate species.
11. Epitaxial MgO buffer layers for YBCO thin films on R-plane.
- Author
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Hakuraku, Y., Maezono, K., and Ueda, H.
- Published
- 1996
- Full Text
- View/download PDF
12. Molecular evolution of Hokkaido virus, a genotype of Orthohantavirus puumalaense, among Myodes rodents.
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Thuy DTN, Sasaki M, Orba Y, Thammahakin P, Maezono K, Kobayashi S, and Kariwa H
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- Animals, Japan, Arvicolinae virology, RNA, Viral genetics, Rodent Diseases virology, Hantavirus Infections virology, Hantavirus Infections veterinary, Orthohantavirus genetics, Orthohantavirus classification, Phylogeny, Evolution, Molecular, Genome, Viral, Genotype, Puumala virus genetics, Puumala virus classification
- Abstract
Viruses in the genus Orthohantavirus within the family Hantaviridae cause human hantavirus infections and represent a threat to public health. Hokkaido virus (HOKV), a genotype of Orthohantavirus puumalaense (Puumala virus; PUUV), was first identified in Tobetsu, Hokkaido, Japan. Although it is genetically related to the prototype of PUUV, the evolutionary pathway of HOKV is unclear. We conducted a field survey in a forest in Tobetsu in 2022 and captured 44 rodents. Complete coding genome sequences of HOKVs were obtained from five viral-RNA-positive rodents (four Myodes rufocanus bedfordiae and one Apodemus speciosus). Phylogenetic analysis revealed a close relationship between the phylogenies and geographical origins of M. rufocanus-related orthohantaviruses. Comparison of the phylogenetic trees of the S segments of orthohantaviruses and the cytochrome b genes of Myodes species suggested that Myodes-related orthohantaviruses evolved in Myodes rodent species as a result of genetic isolation and host switching., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)
- Published
- 2024
- Full Text
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13. Rab27a promotes degradation of West Nile virus E protein in the lysosome.
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Kobayashi S, Kawai S, Fukuda Y, Eguchi H, Maezono K, Thammahakin P, Sawa H, and Kariwa H
- Abstract
Rab27a, a Rab family small GTPases, plays an important role in the trafficking and secretion of the intracellular proteins and has been reported to promote various viral multiplication. However, whether Rab27a is involved in West Nile virus (WNV) multiplication is unknown. This study examined the ability of Rab27a to suppress WNV multiplication. The inhibition of Rab27a expression increased viral multiplication and the intracellular levels of WNV structural proteins, E and prM proteins. Rab27a partially colocalized with E protein, mainly in the perinuclear region, while inhibition of Rab27a expression resulted in diffuse subcellular localization of E protein. In addition, some of the perinuclear E protein colocalized with the lysosomal marker LAMP1, and inhibition of lysosomal acidification increased intracellular levels of Rab27a and E proteins. These observations suggested that Rab27a inhibits WNV multiplication by inducing the degradation of viral protein in lysosomes., Competing Interests: The authors declare that they have no conflicts of interest with the contents of this article., (© 2024 The Authors.)
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- 2024
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14. D-Dimer Trends Predict Recurrent Stroke in Patients with Cancer-Related Hypercoagulability.
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Fujinami J, Nagakane Y, Fujikawa K, Murata S, Maezono K, Ohara T, and Mizuno T
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- Humans, Retrospective Studies, Risk Factors, Fibrin Fibrinogen Degradation Products analysis, Cerebral Infarction, Anticoagulants adverse effects, Ischemic Stroke complications, Stroke diagnosis, Stroke epidemiology, Stroke complications, Thrombophilia diagnosis, Thrombophilia drug therapy, Thrombophilia complications, Neoplasms complications, Neoplasms diagnosis, Neoplasms drug therapy
- Abstract
Introduction: In patients with cancer-associated hypercoagulability (CAH)-related stroke, D-dimer trends after anticoagulant therapy may offer a biomarker of treatment efficacy. The purpose of this study was to clarify the association between D-dimer trends and recurrent stroke after anticoagulant therapy in patients with CAH-related stroke., Methods: We performed retrospective cohort study of consecutive patients with CAH-related stroke at two stroke centers from 2011 to 2020. The ratio of posttreatment to pretreatment D-dimer levels (post/pre ratio) was used as an indicator of D-dimer trends after anticoagulant therapy. Fine-Gray models were used to evaluate the association between post/pre ratio and recurrent stroke., Results: Among 360 acute ischemic stroke patients with active cancer, 73 patients with CAH-related stroke were included in this study. Recurrent stroke occurred in 13 patients (18%) during a median follow-up time of 28 days (interquartile range, 11-65 days). Multivariate analysis revealed that high post/pre ratio was independently associated with recurrent stroke (per 0.1 increase: hazard ratio 2.20, 95% confidence interval 1.61-3.01, p = 0.012)., Conclusion: D-dimer levels after anticoagulant therapy were associated with recurrent stroke in CAH-related stroke patients. Patients with neutral trends in high D-dimer levels after anticoagulant therapy were at high risk of recurrent stroke., (© 2023 The Author(s). Published by S. Karger AG, Basel.)
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- 2024
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15. Ubiquitin accumulation induced by the finger and palm sub-domains of NS5 modulates the replication of West Nile virus.
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Kobayashi S, Kawakami R, Takeda C, Maezono K, Thammahakin P, Eguchi H, Hang'ombe BM, Orba Y, Sawa H, Yoshii K, and Kariwa H
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- Humans, Animals, Mice, Ubiquitin, Brain, Virus Replication genetics, West Nile virus genetics, West Nile Fever
- Abstract
West Nile virus (WNV) causes encephalitis in human and animals. WNV is phylogenetically classified into at least five distinct genetic lineages with different pathogenicity. The pathogenesis of West Nile encephalitis is affected by ubiquitin accumulation in infected cells, but the mechanism is unknown. In this study, the association between ubiquitin accumulation and WNV pathogenicity was investigated. Ubiquitin accumulation was detected in cells infected with NY99 strain belonging to lineage-1, but not FCG and Zmq16 strains belonging to lineage-2. Substitution of the Finger and Palm sub-domains of NS5 from lineage-1 to -2 decreased ubiquitin accumulation and viral replication. Furthermore, the survival rate was increased, and viral replication and ubiquitin accumulation in the brain were attenuated, in mice inoculated with the substituted WNV compared with lineage-1 WNV. Therefore, the intracellular ubiquitin accumulation induced by the Finger and Palm sub-domains of NS5 is linked to the differences in pathogenicity among WNV lineages., Competing Interests: Declaration of competing interest The authors have no conflicts of interest to declare., (Copyright © 2023 Elsevier Inc. All rights reserved.)
- Published
- 2023
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16. Detection of disease-associated microglia among various microglia phenotypes induced by West Nile virus infection in mice.
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Thammahakin P, Maezono K, Maekawa N, Kariwa H, and Kobayashi S
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- Mice, Animals, Humans, Horses, Microglia, Brain, Phenotype, West Nile Fever, West Nile virus
- Abstract
West Nile virus (WNV) has emerged as a significant cause of viral encephalitis in humans and horses. However, the pathogenesis of the West Nile encephalitis remains unclear. Microglia are activated by WNV infection, and the pathogenic involvement of their phenotypes is controversial. In this study, we examined the diversity of microglia phenotypes caused by WNV infection by assessing various microglia markers and identified disease-associated microglia in WNV-infected mouse brain tissue. Cells positive for general microglia markers such as Iba1, P2RY12, or TMEM119 were detected in the control and WNV-infected brain tissue. The morphology of the positive cells in brain tissue infected by WNV was different from that of control brain tissue, indicating that WNV infection induced activation of microglia. The activated microglia were classified into various phenotypes by investigation of specific marker expression. Among the activated microglia, disease-associated microglia that were positive for CD11c and weakly positive for TMEM119 were detected close to the WNV-infected cells. These results indicate that WNV infection induces activation of diverse microglia phenotypes and that disease-associated microglia may be associated with the pathogenicity of WNV infection in the mouse brain., (© 2023. The Author(s) under exclusive licence to The Journal of NeuroVirology, Inc.)
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- 2023
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17. Development of recombinant West Nile virus expressing mCherry reporter protein.
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Kobayashi S, Fukuda Y, Yoshii K, Thammahakin P, Maezono K, Eyer L, Růžek D, and Kariwa H
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- Humans, Mice, Animals, Recombinant Proteins genetics, West Nile virus genetics, West Nile Fever veterinary
- Abstract
West Nile virus (WNV) is transmitted to humans and animals by a mosquito and enters the central nervous system, leading to lethal encephalitis. Reporter viruses expressing fluorescent proteins enable detection of infected cells in vitro and in vivo, facilitating evaluation of the dynamics of viral infection, and the development of diagnostic or therapeutic methods. In this study, we developed a method for production of a recombinant replication-competent WNV expressing mCherry fluorescent protein. The expression of mCherry was observed in viral antigen-positive cells in vitro and in vivo, but the growth of the reporter WNV was reduced as compared to the parental WNV. The expression of mCherry was stable during 5 passages in reporter WNV-infected culture cells. Neurological symptoms were observed in mice inoculated intracranially with the reporter WNV. The reporter WNV expressing mCherry will facilitate research into WNV replication in mouse brains., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)
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- 2023
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18. [Brain infarction and cerebral venous thrombosis in paroxysmal nocturnal hemoglobinuria: case report].
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Maezono K, Tanaka E, Ashida S, Ogura S, Nakahara Y, and Nagakane Y
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- Aged, Brain Infarction, Female, Heparin, Humans, Hemoglobinuria, Paroxysmal complications, Intracranial Thrombosis diagnostic imaging, Intracranial Thrombosis etiology, Venous Thrombosis diagnostic imaging, Venous Thrombosis etiology
- Abstract
A 65-year-old woman with a six-year history of paroxysmal nocturnal hemoglobinuria (PNH) was admitted due to weakness in the right leg following a seven-day history of fever and upper respiratory infection. MRI revealed several high-intensity areas in bilateral frontal lobe cortices and the left cerebellum on diffusion-weighted imaging, and signal hypointensity along the course of the cortical vein in the left frontal lobe on T
2 *-weighted imaging. We diagnosed cerebral venous thrombosis and brain infarction, and commenced heparin infusion. She developed right-sided dens hemiparesis on hospital day 6, when brain CT showed subcortical hemorrhage in the left frontal lobe. Despite eculizumab administration and decompressive craniectomy for hematoma, she died on hospital day 26. Thrombosis in PNH has been recognized as a life-threating complication, and intensive treatment including emergent administration of eculizumab is warranted if this situation arises.- Published
- 2022
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19. Development of a highly specific serodiagnostic ELISA for West Nile virus infection using subviral particles.
- Author
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Maezono K, Kobayashi S, Tabata K, Yoshii K, and Kariwa H
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- Animals, Female, Mice, Mice, Inbred BALB C, Neutralization Tests, West Nile Fever immunology, Antibodies, Viral immunology, Enzyme-Linked Immunosorbent Assay methods, Serologic Tests methods, Virion immunology, West Nile Fever diagnosis, West Nile virus immunology
- Abstract
West Nile virus (WNV), a member of the Japanese encephalitis virus (JEV) serocomplex group, causes lethal encephalitis in humans and horses. Because serodiagnosis of WNV and JEV is hampered by cross-reactivity, the development of a simple, secure, and WNV-specific serodiagnostic system is required. The coexpression of prM protein and E protein leads to the secretion of subviral particles (SPs). Deletion of the C-terminal region of E protein is reported to affect the production of SPs by some flaviviruses. However, the influence of such a deletion on the properties and antigenicity of WNV E protein is unclear. We analyzed the properties of full-length E protein and E proteins lacking the C-terminal region as novel serodiagnostics for WNV infection. Deletion of the C-terminal region of E protein suppressed the formation of SPs but did not affect the production of E protein. The sensitivity of an enzyme-linked immunosorbent assay (ELISA) using the full-length E protein was higher than that using the truncated E proteins. Furthermore, in the ELISA using full-length E protein, there was little cross-reactivity with anti-JEV antibodies, and the sensitivity was similar to that of the neutralization test.
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- 2021
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20. Attack Interval Is the Key to the Likely Pathogenesis of Multiple Transient Ischemic Attacks.
- Author
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Nagakane Y, Ohara T, Tanaka E, Yamada T, Ashida S, Kojima Y, Maezono K, Ogura S, Nakashima D, Kitaoji T, and Yamamoto Y
- Subjects
- Diffusion Magnetic Resonance Imaging, Female, Humans, Male, Ischemic Attack, Transient diagnostic imaging, Ischemic Attack, Transient epidemiology, Stroke diagnostic imaging, Stroke epidemiology
- Abstract
Introduction: The aim of this study was to test the hypothesis that the attack interval of multiple transient ischemic attacks (TIAs) is correlated with the underlying pathogenesis of ischemia., Methods: Patients with multiple TIAs, defined as 2 or more motor deficits within 7 days, were studied. The attack interval between the last 2 episodes was classified into 3 groups: 2 episodes within an hour (Hour group), over hours within a day (Day group), and over days within a week (Week group). Patients with a lacunar syndrome, no cortical lesions, and no embolic sources were recognized as having a small vessel disease (SVD) etiology for their multiple events., Results: Of 312 TIA patients admitted over a 9-year period, 50 (37 males, 13 females, mean 67.6 years) had multiple TIAs. Twelve patients were classified as being within the Hour group, 23 within the Day group, and 15 within the Week group. Lacunar syndromes were observed in 30 (75%, 35%, and 67%), embolic sources were detected in 28 (25%, 65%, and 67%), and a high signal lesion on diffusion-weighted imaging was depicted in 30 (75%, 48%, and 67%) patients (18 cortical, 11 subcortical, and one cerebellar). Patients in the Hour group had a significantly higher prevalence of SVD etiology (75%) than those in the Day and Week groups (30%, p = 0.0165; 27%, p = 0.0213, respectively). Four patients had a subsequent stroke within 7 days., Conclusion: Attack intervals of multiple TIAs may be correlated with the underlying pathogenesis of ischemia. Two motor deficits within an hour are more likely to suggest a SVD etiology., (© 2021 The Author(s) Published by S. Karger AG, Basel.)
- Published
- 2021
- Full Text
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21. [A case of hypertrophic pachymeningitis associated with probable sarcoidosis with increased serum IgG4].
- Author
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Fujino Y, Saito K, Maezono K, Kasai T, and Mizuno T
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- Brain diagnostic imaging, Brain pathology, Diagnosis, Differential, Humans, Hypertrophy, Magnetic Resonance Imaging, Male, Meningitis diagnosis, Meningitis pathology, Sarcoidosis pathology, Submandibular Gland diagnostic imaging, Submandibular Gland pathology, Hypergammaglobulinemia blood, Hypergammaglobulinemia etiology, Immunoglobulin G blood, Meningitis etiology, Sarcoidosis complications, Sarcoidosis diagnosis
- Abstract
We report a 54-year-old man, who presented with an acute onset of diplopia and ptosis on the left side. On admission, neurological examination showed left oculomotor and abducens nerve palsy. Brain MRI showed thickening of the left parieto-temporal dura mater with gadolinium enhancement. Whole-body CT revealed a mass lesion in the right submandibular gland, diffuse goiter, and bilateral hilar lymph node enlargement. Initially, IgG4-related disease was considered because of an elevated serum IgG4 level (240 mg/dl); however, biopsy of the submandibular gland showed non-caseating epithelioid cell granulomas that suggested sarcoidosis, which could be associated with the intracranial lesions causing his neurological manifestation. In cases of hypertrophic pachymeningitis, especially with increased serum IgG4 including our case, a careful assessment with pathological examination is critical for identifying various underlying conditions.
- Published
- 2019
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22. [Vertebrobasilar territory embolisms due to the ununited fracture of the right clavicle from 35 years ago].
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Ogura S, Tanaka E, Ashida S, Maezono K, and Nagakane Y
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- Arterial Occlusive Diseases diagnostic imaging, Brain diagnostic imaging, Cerebral Infarction diagnostic imaging, Cerebral Infarction etiology, Diffusion Magnetic Resonance Imaging, Fractures, Bone diagnostic imaging, Fractures, Ununited diagnostic imaging, Humans, Magnetic Resonance Angiography, Male, Middle Aged, Posterior Cerebral Artery diagnostic imaging, Thrombosis diagnostic imaging, Time Factors, Ultrasonography, Vertebrobasilar Insufficiency diagnostic imaging, Arterial Occlusive Diseases etiology, Clavicle injuries, Fractures, Bone complications, Fractures, Ununited complications, Pseudarthrosis etiology, Subclavian Artery diagnostic imaging, Thrombosis etiology, Vertebrobasilar Insufficiency etiology
- Abstract
A 61-year-old man, with a history of right clavicular fracture 35 years prior, visited our hospital due to the sudden onset of vertigo and tinnitus following weakness and numbness in his left arm and leg. He also had a 6-month history of right arm pain with overuse. Brain MRI showed acute brain infarcts in the right posterior cerebral artery territory. Intravenous alteplase was administered 188 minutes after onset. Although heparin infusion was commenced on day 2, he had vertigo again on day 9, and MRI showed a recurrent brain infarct in the right posterior inferior cerebellar artery territory. Ultrasound examination revealed occlusion of his right subclavian artery beneath the old right clavicular fracture as well as mobile thrombus in the proximal portion of the right subclavian artery. We speculated that a pseudarthrosis at the site of the old right clavicular fracture had repetitively pressed the right subclavian artery. Subsequently, we considered thrombi, which had developed in the proximal portion of the right subclavian artery, migrated into the right vertebral artery, causing recurrent emboli in the vertebrobasilar artery territory.
- Published
- 2018
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23. [Safety of Dual Antiplatelet Therapy with Argatroban in Patients with Acute Ischemic Stroke].
- Author
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Nagakane Y, Tanaka E, Ashida S, Kojima Y, Ogura S, Maezono K, and Yamamoto Y
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- Arginine analogs & derivatives, Drug Therapy, Combination, Humans, Pipecolic Acids, Platelet Aggregation Inhibitors, Retrospective Studies, Sulfonamides, Brain Ischemia, Ischemic Attack, Transient, Stroke
- Abstract
To prevent early neurological worsening or recurrence in stroke patients with intracranial arterial stenosis or branch atheromatous disease, aggressive antithrombotic therapy, such as dual antiplatelet therapy (DAPT) with or without anticoagulant therapy, is warranted. Such an aggressive antithrombotic therapy, however, may increase the bleeding risk. We studied the risks of DAPT with the anticoagulant argatroban in patients with acute ischemic stroke or transient ischemic attack (TIA). Between October 2011 and September 2015, 341 patients with stroke or TIA, who received DAPT with argatroban within 48 hours after onset, were retrospectively studied. The endpoint was any bleeding event during hospitalization or 30 days after admission. Median duration of DAPT was 12 days, and 66% of the patients received intravenous heparin (median duration, 5 days) following argatroban. No symptomatic intracerebral hemorrhages were observed, while severe, moderate, and mild extracranial hemorrhages occured in one (0.3%), three (0.9%), and four (1.2%) patients, respectively. In conclusion, DAPT with argatroban can be safely administered to patients with acute ischemic stroke or TIA. (Received July 24, 2017; Accepted January 15, 2018; Published May 1, 2018).
- Published
- 2018
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24. Acute and chronic treatment of L-isoleucine ameliorates glucose metabolism in glucose-intolerant and diabetic mice.
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Ikehara O, Kawasaki N, Maezono K, Komatsu M, and Konishi A
- Subjects
- Animals, Blood Glucose analysis, Diabetes Mellitus, Experimental blood, Diabetes Mellitus, Experimental metabolism, Diabetes Mellitus, Type 2 blood, Diabetes Mellitus, Type 2 metabolism, Dietary Fats administration & dosage, Drug Administration Schedule, Female, Glucose Tolerance Test, Hypoglycemic Agents administration & dosage, Insulin blood, Isoleucine administration & dosage, Male, Mice, Mice, Inbred C57BL, Sucrose administration & dosage, Diabetes Mellitus, Experimental drug therapy, Diabetes Mellitus, Type 2 drug therapy, Glucose metabolism, Hypoglycemic Agents therapeutic use, Isoleucine therapeutic use
- Abstract
The administration of L-isoleucine (isoleucine) has been shown to induce hypoglycemia in normal rats. However, it remains to be elucidated whether isoleucine can improve the blood glucose level in glucose-intolerant or diabetic animals. In the present study, oral isoleucine significantly reduced the blood glucose level after an oral glucose challenge in normal mice, as well as in glucose-intolerant mice fed a high-fat diet (HFD) and db/db mice, a model of severe type 2 diabetes. Isoleucine treatment significantly augmented the blood insulin level after an oral glucose load in HFD mice, but not in normal or db/db mice, suggesting that its hypoglycemic activity was attributable to both insulinotropic and non-insulinotropic mechanisms. Chronic supplementation of isoleucine in mice on a high-fat/high-sucrose diet significantly reduced insulin release after an oral glucose challenge without any change in glucose tolerance curve, suggesting that isoleucine might have an insulin-sensitizing effect along with its acute hypoglycemic effect. These results indicate that both acute and chronic treatment with isoleucine is beneficial for glucose metabolism in glucose-intolerant and diabetic animals.
- Published
- 2008
- Full Text
- View/download PDF
25. Pyrazole-O-glucosides as novel Na(+)-glucose cotransporter (SGLT) inhibitors.
- Author
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Ohsumi K, Matsueda H, Hatanaka T, Hirama R, Umemura T, Oonuki A, Ishida N, Kageyama Y, Maezono K, and Kondo N
- Subjects
- Animals, Enzyme Inhibitors administration & dosage, Glucose metabolism, Glucosides administration & dosage, Glycosuria chemically induced, Glycosuria metabolism, Hypoglycemic Agents administration & dosage, Indicators and Reagents, Injections, Intravenous, Kidney drug effects, Microvilli drug effects, Microvilli metabolism, Pyrazoles chemical synthesis, Pyrazoles pharmacology, Rats, Rats, Wistar, Sodium-Glucose Transporter 1, Structure-Activity Relationship, Enzyme Inhibitors chemical synthesis, Enzyme Inhibitors pharmacology, Glucosides chemical synthesis, Glucosides pharmacology, Hypoglycemic Agents chemical synthesis, Hypoglycemic Agents pharmacology, Kidney metabolism, Membrane Glycoproteins antagonists & inhibitors, Monosaccharide Transport Proteins antagonists & inhibitors
- Abstract
O-glucuronides and O-glucosides of a series of pyrazoles analogues were synthesized and evaluated for their SGLT inhibitory activity in brush border membrane vehicles (BBMVs) of rat kidney. O-glucosides of certain pyrazole analogues inhibited the transport of [(14)C]-glucose in BBMVs, and induced glucosuria in Wistar rats by intravenous injection.
- Published
- 2003
- Full Text
- View/download PDF
26. Regulation of MAP kinase pathway activity in vivo in human skeletal muscle.
- Author
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Osman AA, Pendergrass M, Koval J, Maezono K, Cusi K, Pratipanawatr T, and Mandarino LJ
- Subjects
- Adult, Blood Glucose metabolism, Enzyme Activation, Female, Glucose Clamp Technique, Glycogen Synthase metabolism, Humans, Kinetics, MAP Kinase Kinase 1, Male, Mitogen-Activated Protein Kinase 3, Mitogen-Activated Protein Kinase Kinases metabolism, Phosphorylation, Protein Serine-Threonine Kinases metabolism, Exercise physiology, Insulin blood, Mitogen-Activated Protein Kinase 1 metabolism, Mitogen-Activated Protein Kinases metabolism, Muscle, Skeletal enzymology
- Abstract
Insulin and exercise potently stimulate glucose metabolism and gene transcription in vivo in skeletal muscle. A single bout of exercise increases the rate of insulin-stimulated glucose uptake and metabolism in skeletal muscle in the postexercise period. The nature of the intracellular signaling mechanisms that control responses to exercise is not known. In mammalian tissues, numerous reports have established the existence of the mitogen-activated protein (MAP) kinase signaling pathway that is activated by a variety of growth factors and hormones. This study was undertaken to determine how a single bout of exercise and physiological hyperinsulinemia activate the MAP kinase pathway. The euglycemic-hyperinsulinemic clamp and cycle ergometer exercise techniques combined with percutaneous muscle biopsies were used to answer this question. In healthy subjects, within 30 min, insulin significantly increased MAP kinase [isoforms p42(MAPK) and p44(MAPK) (ERK1 and ERK2)] phosphorylation (141 +/- 2%, P < 0.05) and activity (177 +/- 5%, P < 0.05), and the activity of its upstream activator MEK1 (161 +/- 16%, P < 0.05). Insulin also increased the activity of the MAP kinase downstream substrate, the p90 ribosomal S6 kinase 2 (RSK2) almost twofold (198 +/- 45%, P < 0.05). In contrast, a single 30-min bout of moderate-intensity exercise had no effect on the MAP kinase pathway activation from MEK to RSK2 in muscle of healthy subjects. However, 60 min of exercise did increase extracellular signal-related kinase activity. Therefore, despite similar effects on glucose metabolism after 30 min, insulin and exercise regulate the MAP kinase pathway differently. Insulin more rapidly activates the MAP kinase pathway.
- Published
- 2000
- Full Text
- View/download PDF
27. Insulin resistance differentially affects the PI 3-kinase- and MAP kinase-mediated signaling in human muscle.
- Author
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Cusi K, Maezono K, Osman A, Pendergrass M, Patti ME, Pratipanawatr T, DeFronzo RA, Kahn CR, and Mandarino LJ
- Subjects
- Adult, Diabetes Mellitus, Type 2 physiopathology, Female, Humans, Insulin Receptor Substrate Proteins, Male, Muscle, Skeletal physiopathology, Phosphoproteins metabolism, Receptor, Insulin metabolism, Diabetes Mellitus, Type 2 metabolism, Insulin Resistance, Mitogen-Activated Protein Kinases metabolism, Muscle, Skeletal metabolism, Phosphatidylinositol 3-Kinases metabolism, Signal Transduction
- Abstract
The broad nature of insulin resistant glucose metabolism in skeletal muscle of patients with type 2 diabetes suggests a defect in the proximal part of the insulin signaling network. We sought to identify the pathways compromised in insulin resistance and to test the effect of moderate exercise on whole-body and cellular insulin action. We conducted euglycemic clamps and muscle biopsies on type 2 diabetic patients, obese nondiabetics and lean controls, with and without a single bout of exercise. Insulin stimulation of the phosphatidylinositol 3-kinase (PI 3-kinase) pathway, as measured by phosphorylation of the insulin receptor and IRS-1 and by IRS protein association with p85 and with PI 3-kinase, was dramatically reduced in obese nondiabetics and virtually absent in type 2 diabetic patients. Insulin stimulation of the MAP kinase pathway was normal in obese and diabetic subjects. Insulin stimulation of glucose-disposal correlated with association of p85 with IRS-1. Exercise 24 hours before the euglycemic clamp increased phosphorylation of insulin receptor and IRS-1 in obese and diabetic subjects but did not increase glucose uptake or PI 3-kinase association with IRS-1 upon insulin stimulation. Thus, insulin resistance differentially affects the PI 3-kinase and MAP kinase signaling pathways, and insulin-stimulated IRS-1-association with PI 3-kinase defines a key step in insulin resistance.
- Published
- 2000
- Full Text
- View/download PDF
28. Alanine protects liver from injury caused by F-galactosamine and CCl4.
- Author
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Maezono K, Kajiwara K, Mawatari K, Shinkai A, Torii K, and Maki T
- Subjects
- Adenosine Triphosphate metabolism, Alanine Transaminase blood, Amino Acids pharmacology, Animals, Aspartate Aminotransferases blood, Bilirubin blood, Carbon Tetrachloride antagonists & inhibitors, Cells, Cultured, Galactosamine antagonists & inhibitors, Kinetics, L-Lactate Dehydrogenase, Liver metabolism, Liver pathology, Male, Rats, Rats, Sprague-Dawley, Rats, Wistar, Time Factors, Alanine pharmacology, Carbon Tetrachloride toxicity, Carbon Tetrachloride Poisoning prevention & control, Galactosamine toxicity, Liver drug effects
- Abstract
The liver is the main organ involved in amino acid metabolism, and it utilizes glucogenic amino acids as substrates for glucose or adenosine triphosphate (ATP), but this process is impaired in clinical and experimental liver diseases. In this study, we administered high doses of amino acids in rats or cultured hepatocytes with experimental models of liver injury to examine whether such supplementation could attenuate liver damage. We found that the addition of alanine reduced enzyme leakage from primary cultured rat hepatocytes treated with D-galactosamine (D-gal), while other amino acids did not. A significant decrease of lactate dehydrogenase (LDH) leakage was observed when cells were cultured with >6 from mmol/L alanine. Alanine also reduced enzyme leakage from normal hepatocytes that were not treated with D-gal. In D-gal-treated rats, constant infusion of a high dose of alanine significantly reduced the plasma transaminase and total bilirubin levels when compared with infusion of an amino acid mixture. Bolus administration of alanine significantly prevented the elevation of plasma transaminase levels and histological liver damage in CCl4-treated rats, while fructose-1,6 bisphosphate (FDP) had little effect. Alanine might promote the restoration of damaged liver in hepatotoxicant-treated rats, because significant effect was found after the elevation in plasma transaminase levels. Alanine also prevented the decrease of cellular ATP caused by D-gal and appeared to promote ATP production in primary cultured rat hepatocytes. These results indicate that alanine reduces experimental liver damage by a direct effect on hepatocytes.
- Published
- 1996
- Full Text
- View/download PDF
29. Effect of combined alanine and glutamine administration on the inhibition of liver regeneration caused by long-term administration of alcohol.
- Author
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Tanaka T, Imano M, Yamashita T, Monna T, Nishiguchi S, Kuroki T, Otani S, Maezono K, and Mawatari K
- Subjects
- Animals, Male, Ornithine Decarboxylase metabolism, Rats, Rats, Wistar, Spermine metabolism, Alanine metabolism, Alanine pharmacology, Ethanol pharmacology, Glutamine metabolism, Glutamine pharmacology, Liver drug effects, Liver metabolism, Liver Regeneration
- Abstract
We studied the effect of administration of a mixture of alanine and glutamine on the inhibition of liver regeneration caused by alcohol in rats undergoing partial hepatectomy 6 weeks after the start of alcohol administration. DNA synthesis was inhibited 24 hr after partial hepatectomy in rats given alcohol, but treatment with alanine and glutamine partially prevented this inhibition. To identify the mechanism of this effect, polyamine metabolism was studied. Administration of alcohol or alanine plus glutamine had no effect on the activity of ornithine decarboxylase, a rate-limiting enzyme of polyamine metabolism. In the liver, of the three polyamines, only the spermine concentration changed significantly. It decreased during long-term administration of alcohol, and this decrease was prevented by treatment with alanine and glutamine. The level of N(1)-acetylspermidine, the acetylated product of spermidine, was increased by alcohol, and its elevation was significantly less when alanine and glutamine were given. Hepatic spermidine/spermine N(1)-acetyltransferase, the key enzyme of polyamine acetylation, was induced by long-term administration of alcohol, and this induction was suppressed by alanine plus glutamine. The results suggest that treatment with alanine and glutamine can help to prevent the inhibition of liver regeneration caused by alcohol by maintaining the spermine level and suppressing the acetylation of spermidine.
- Published
- 1994
30. Ethanol and hydrazine sulfate induced chronic hepatic injury in rats: the curative effect of administration of glucogenic amino acids.
- Author
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Suzuki H, Tominaga T, Mizuno H, Kouno M, Suzuki M, Kato Y, Sato A, Okabe K, Uchikoshi T, and Maezono K
- Subjects
- Alanine Transaminase blood, Animals, Antineoplastic Agents toxicity, Aspartate Aminotransferases blood, Body Weight drug effects, Energy Intake, Fatty Liver pathology, Fatty Liver, Alcoholic pathology, L-Lactate Dehydrogenase blood, Liver drug effects, Liver metabolism, Liver Function Tests, Male, Rats, Rats, Sprague-Dawley, gamma-Glutamyltransferase blood, Ethanol toxicity, Fatty Liver chemically induced, Gluconeogenesis drug effects, Hydrazines toxicity, Liver pathology
- Abstract
There is a widespread belief that when ethanol is fed to rats for a long time, it produces only fatty degeneration without necrosis or fibrosis. In this study, hydrazine sulfate, an inhibitor of low Km ALDH and gluconeogenetic enzymes, was fed with ethanol to rats, and produced more serious pathological changes compared with those found in Lieber's model. Male Sprague-Dawley rats were fed with a low fat liquid diet as a basal diet with ethanol (4%, w/v) and hydrazine sulfate for 4 weeks. At the end of the experiment, plasma aminotransferase levels were found to be elevated. Histological examination showed not only fatty degeneration but also pericellular fibrosis. Therefore, we have evaluated the curative effect of glucogenic amino acids, alanine and glutamine, on this hepatic injury model and found them to be partially protective.
- Published
- 1993
- Full Text
- View/download PDF
31. Effects of alanine and glutamine administration on the inhibition of liver regeneration by acute ethanol treatment.
- Author
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Tanaka T, Ando M, Yamashita T, Toda T, Monna T, Nishiguchi S, Matsui T, Kuroki T, Otani S, and Maezono K
- Subjects
- Alcoholic Intoxication pathology, Animals, Culture Techniques, DNA Replication drug effects, Ethanol pharmacokinetics, Liver drug effects, Liver pathology, Male, Organ Size drug effects, Ornithine Decarboxylase metabolism, Polyamines metabolism, Rats, Rats, Wistar, Alanine pharmacology, Ethanol toxicity, Glutamine pharmacology, Liver Regeneration drug effects
- Abstract
We studied the effects of alanine and glutamine administration on the inhibition of liver regeneration by acute ethanol treatment after partial hepatectomy (PH) in rats. When rats were dosed i.p. with ethanol at 2 g/kg at the time of PH, DNA synthesis 48 hr after PH was significantly inhibited, but it was completely reversed by the combined use of alanine and glutamine. Although hepatic ornithine decarboxylase (ODC) activity in the alcohol-treated group 4 hr after PH was significantly inhibited, there was a tendency towards recovery of the ODC inhibition in the alanine and glutamine-treated group. The putrescine (PUT) level in liver which was decreased by ethanol was also increased by the administration of alanine and glutamine. However, the levels of spermidine (SPD) and spermine (SPM) in liver were unaffected either by ethanol or by alanine and glutamine. These results suggest that alanine and glutamine show a protective effect on the inhibition of liver regeneration caused by acute ethanol treatment by improving polyamine metabolism, particularly by increasing hepatic PUT levels.
- Published
- 1993
- Full Text
- View/download PDF
32. Deduced primary structure of rat tryptophan-2,3-dioxygenase.
- Author
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Maezono K, Tashiro K, and Nakamura T
- Subjects
- Amino Acid Sequence, Animals, Base Sequence, Cloning, Molecular, DNA, Recombinant analysis, Molecular Sequence Data, Rats, Tryptophan Oxygenase genetics, Liver enzymology, Tryptophan Oxygenase analysis
- Abstract
The complete amino acid sequence of the tryptophan 2,3-dioxygenase (TO) of rat liver was determined from the nucleotide sequence of a full length TO cDNA isolated from a rat liver cDNA library and determined its primary structure. TO was encoded in a mRNA of about 1.7 kb containing an open reading frame of 1218 bp. According to the deduced amino acid sequence, the monomeric polypeptide of TO consisted of 406 amino acid residues with a calculated molecular weight of 47,796 daltons. It has twelve histidine residues around its hydrophobic region, which has homology with some heme proteins and oxygenase, suggesting that this hydrophobic region might to be the core of TO for the activity.
- Published
- 1990
- Full Text
- View/download PDF
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