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A. CANIGGIA, F. LORÉ, R. NUTI, G. MARTINI, B. FREDIANI, G.Di CA ...
1992 年 38 巻 Special 号 p.
232-235
発行日: 1992年
公開日: 2010/11/26
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M. F. HOLICK, Z. Lu, T. C. CHEN
1992 年 38 巻 Special 号 p.
236-239
発行日: 1992年
公開日: 2010/11/26
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M. TANAKA, A. SOTOMATSU, S. HIRAI
1992 年 38 巻 Special 号 p.
240-243
発行日: 1992年
公開日: 2010/11/26
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Using a recently-developed membrane lipid peroxidation (MLP) system, we demonstrated the important role of vitamin E in the prevention of MLP and the possible relationship between MLP and pathogenesis of Parkinson's disease.
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E.J. VANDAMME
1992 年 38 巻 Special 号 p.
244-247
発行日: 1992年
公開日: 2010/11/26
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L. J. BOROWITZKA
1992 年 38 巻 Special 号 p.
248-250
発行日: 1992年
公開日: 2010/11/26
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Y. TANI
1992 年 38 巻 Special 号 p.
251-254
発行日: 1992年
公開日: 2010/11/26
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H. YAMADA, S. SHIMIZU, Y. SHINMEN, K. AKIMOTO, H. KAWASHIMA
1992 年 38 巻 Special 号 p.
255-258
発行日: 1992年
公開日: 2010/11/26
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M. T. ÖZBAS
1992 年 38 巻 Special 号 p.
259-262
発行日: 1992年
公開日: 2010/11/26
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O. IFUKU, S. HAZE, J. KISHIMOTO, M. YANAGI
1992 年 38 巻 Special 号 p.
263-266
発行日: 1992年
公開日: 2010/11/26
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K. UEDA, M. BANASIK, L. SAITO, T. KIDO, B. R. DAS, N. A. N. ABED, H. K ...
1992 年 38 巻 Special 号 p.
267-270
発行日: 1992年
公開日: 2010/11/26
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Biological roles of mono- and poly (ADP-ribosyl) ation reactions are reviewed, along with analysis of functional sequences of poly(ADP-ribose) synthetase and inhibitors of the synthetase compared with mono (ADP-ribosyl) transferase.
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M. SHIMOYAMA, M. TSUCHIYA
1992 年 38 巻 Special 号 p.
271-274
発行日: 1992年
公開日: 2010/11/26
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We investigated vertebrate arginine-specific ADP-ribosyltransferases and target proteins for the enzyme. ADP-ribosyltransferase found in each organelle ADP-ribosylated preferentially an endogenous acceptor protein co-localized with the enzyme. We propose that the ADP-ribosylation of tissue-specific target protein by the endogenous ADP-ribosyltransferase may participate in the regulation of cellular processes, including signal transduction.
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K. KAIBUCHI, A. KIKUCHI, M. KAWATA, Y. TAKAI
1992 年 38 巻 Special 号 p.
275-278
発行日: 1992年
公開日: 2010/11/26
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H. KIDO, N. KATUNUMA
1992 年 38 巻 Special 号 p.
279-282
発行日: 1992年
公開日: 2010/11/26
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We have found several compounds that specifically modulte the action of glucocorticoid
in vivo and
in vitro without themselves having any glucocorticoid-like action and have proposed the concept of “Glucocorticoid Action Biomodulators”. These biomodulators consist of “Glucocorticoid Sensitivity Amplifier” (GSA), “Glucocorticoid Potency Amplifiers” (GPAs), and supressors of glucocorticoid action. GSA increased the incorporation of glucocorticoid into the liver and its binding to cytosol receptor without changing the total receptor concentration in liver cytosol and the equilibrium constant of the glucocorticoid binding reaction. GPAs, potent activators of protein kinase C, markedly enhanced the glucocorticoid action and the glucocorticoid action was inhibited by the inhibitors of protein kinase C. H-7, an inhibitor of protein kinase C, inhibited the translocation of glucocorticoid-receptor complex into nuclei without affecting the extent of phosphorylation of glucocorticoid recetor. These findings suggest that GPA(s) and the suppressors modulate some protein(s) which regulates the translocation of glucocorticoid receptor into nuclei.
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H.L. SEGAL
1992 年 38 巻 Special 号 p.
283-286
発行日: 1992年
公開日: 2011/06/02
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H. HOLZER, C. GUBLER
1992 年 38 巻 Special 号 p.
287-291
発行日: 1992年
公開日: 2010/11/26
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V. TURK
1992 年 38 巻 Special 号 p.
292-297
発行日: 1992年
公開日: 2010/11/26
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C.-N. JOO
1992 年 38 巻 Special 号 p.
298-301
発行日: 1992年
公開日: 2010/11/26
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H. OKUDA, H. NINOMIYA, C. MORIMOTO, T. TSUJITA
1992 年 38 巻 Special 号 p.
302-305
発行日: 1992年
公開日: 2010/11/26
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K. TAMURA, M. YAMAMURA, S. FUKUI, M. SATOMI, T. SHIMOYAMA
1992 年 38 巻 Special 号 p.
306-308
発行日: 1992年
公開日: 2010/11/26
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R. OGURA
1992 年 38 巻 Special 号 p.
309-312
発行日: 1992年
公開日: 2010/11/26
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The hydroxyl radicals are known to be a biologically active oxygen species. A remarkable enhancement of hydroxyl radical generation was observed in the mitochondria obtained from ischemic myocardium. The hydroxyl radicals are the primary reactive species leading to cellular damages, such as membrane damages, DNA damages, enzyme inactivation, protein denaturation and so forth. The origin of the hydroxyl radicals appeared in mitochondria was discussed.
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R.E. OLSON
1992 年 38 巻 Special 号 p.
313-316
発行日: 1992年
公開日: 2010/11/26
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The pathophysiology of carcinogenesis as a multistage process has been reviewed and the rationale for the action of vitamins and biofactors has been presented. This overview will now be followed by presentations of the actions of retinoids, carotenoids, vitamin D and marine natural products by other members of this Symposium.
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H. MORIWAKI, T. MUTO
1992 年 38 巻 Special 号 p.
317-320
発行日: 1992年
公開日: 2010/11/26
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L. SANTAMARIA, A. BIANCHI-SANTAMARIA
1992 年 38 巻 Special 号 p.
321-326
発行日: 1992年
公開日: 2011/06/02
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Carotenoid (CARs: beta-carotene BC and/or canthaxanthin CX) supplementation have been shown to be chemopreventive in animals, since 1980, against direct or indirect chemical carcinogenesis/photo-carcinogenesis of the skin, breast, stomach, salivary glands, colon-rectum, urinary bladder, and against transplanted tumors. This action could be either independent of or dependent on pro-vitamin A activity of BC.
In vitro, both BC and CX proved to be antimutagenic and to have anti-malignant transformation properties in cell cultures. Preliminary interventions in humans with BC ± CX prevented the onset of second primary tumors in lung, colon, urinary bladder, and head and neck. The powerful antioxidant properties of CARs, possibly associated with their retinoid potential, played a role in all the above observations, producing free-radical quenching and immunostimulation.
The current development of the above investigations on CARs in the Pavia University Tumor Center has so far achieved the following data: 1) the anticlastogenic action of CARs in humans was demonstrated by the reduction of the micronuclei induced by bleomycin in cultured lymphocytes from subjects supplemented with CARs; 2) the immunoresponse modulated by BC augmented in mice, thus lengthening survivals after transplantation of ascites tumors along with a dramatic increase in liver mastocytes; 3) a synergism between BC and retinol, previously shown in pre-menstrual mastalgia (with BBD or otherwise), was confirmed as a relevant tool to obtain marked relief and/or complete recovery from breast pain only in cyclical mastalgia with no side effects at all in 20-42 aged women; 4) finally, a tentative trial with BC 80 mg/day in nonsurgically treatable human lung cancer cases performing high K. I. on admission, achieved a S. D. status as monitored by X-ray and high K.I. for one year, leading to an increase (1.5-3 times more) in overall survival with respect to expected median survival. The latter was consistent with a therapeutic rather than a preventive effect by BC.
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R. Blomhoff, H. Senoo, S. Smeland, T. Bjerknes, K.R. NORUM
1992 年 38 巻 Special 号 p.
327-330
発行日: 1992年
公開日: 2010/11/26
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A. KAWAURA, T. TANIDA, K. SAWADA, M. ODA, T. SHIMOYAMA
1992 年 38 巻 Special 号 p.
331-332
発行日: 1992年
公開日: 2010/11/26
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J. YATSUNAMI, H. FUJIKI, A. KOMORI, M. SUGANUMA, S. NISHIWAKI, S. OKAB ...
1992 年 38 巻 Special 号 p.
333-336
発行日: 1992年
公開日: 2010/11/26
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This review article dealed with significant effects of marine natural products in carcinogenesis, namely as chemical probes to understand the process of carcinogenesis and as possible cancer preventive agents in humans.
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M. ONO, M. OH-EDA, S. KAMACHI, M. KATO, Y. ENDO, N. OCHI
1992 年 38 巻 Special 号 p.
337-340
発行日: 1992年
公開日: 2010/11/26
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1. The carbohydrate chain protects rhG-CSF from polymerization and/or conformational alterations associated with physicochemical changes, elevation of pH or temperature fluctuations.
2. The carbohydrate chain of rhG-CSF prevents loss of its biological activity in normal human serum by inhibiting proteinase activity.
3. These facts indicate that the carbohydrate chain of rhG-CSF has a markedly important role in maintaining the stability of the protein itself as well as in effecting the exertion of its biological activity.
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S. NAGATA, R. FUKUNAGA
1992 年 38 巻 Special 号 p.
341-344
発行日: 1992年
公開日: 2010/11/26
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K. OZAWA, K. WATARI, T. TSURUTA, S. TAKAHASHI, H. OGURA, T. YOSHIKUBO, ...
1992 年 38 巻 Special 号 p.
345-348
発行日: 1992年
公開日: 2010/11/26
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G-CSF is produced by a variety of cells. In situ hybridization showed that only a small proportion of stromal cells expressed G-CSF after stimulation with LPS or IL-1. The measurement of serum G-CSF level by enzyme immunoassay provided valuable information as to the pathophysiological roles of G-CSF. In aplastic anemia, there was an inverse correlation between blood neutrophil count and serum G-CSF level. Similarly, the G-CSF level rose during the neutropenic phase of cyclic neutropenia. These findings suggest that the serum G-CSF level is regulated by a feedback mechanism. In some cases, the reduced G-CSF production by stromal cells may underlie the pathogenesis of neutropenia. On the other hand, infections and cancers sometimes caused high serum G-CSF levels in association with increased blood neutrophils, presumably reflecting reactive and aberrant production of G-CSF, respectively. Expression of G-CSF by myeloid leukemia cells may partly contribute to their abnormal growth through the autocrine mechanism.
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Y. YOSHIDA, S. ASANO, K. HIRASHIMA, F. TAKAKU
1992 年 38 巻 Special 号 p.
349-352
発行日: 1992年
公開日: 2010/11/26
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N. CLUMECK, S. D. WIT, P. HERMANS, P. FRANCHIOLY, B. SOMMEREIJNS
1992 年 38 巻 Special 号 p.
353-356
発行日: 1992年
公開日: 2010/11/26
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F. -D. GOEBEL, J. R. BOGNER, A. MATUSCHKE, B. HEINRICH, U. KRONAWITTER
1992 年 38 巻 Special 号 p.
357-360
発行日: 1992年
公開日: 2010/11/26
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A. OYAMA, H. SUZUKI, M. OGURA, Y. ARIYOSHI, S. ASANO
1992 年 38 巻 Special 号 p.
361-364
発行日: 1992年
公開日: 2010/11/26
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J. H. SCARFFE
1992 年 38 巻 Special 号 p.
365-367
発行日: 1992年
公開日: 2010/11/26
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IN VITRO and IN VIVO Aspects
C. G. BEGLEY, E. DELUCA, P. A. ROWLINGS, J. SZER, D. WATSON, C. JUTTNE ...
1992 年 38 巻 Special 号 p.
368-371
発行日: 1992年
公開日: 2010/11/26
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G-CSF administration leads to significant elevation in the levels of circulating progenitor cells. Infusion of these cells after high-dose chemotherapy is associated with accelerated platelet engraftment that has a considerable impact in shortening thrombocytopenia and reducing need for platelet transfusions.
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C. J. GUBLER
1992 年 38 巻 Special 号 p.
372-374
発行日: 1992年
公開日: 2010/11/26
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A. IWASHIMA, Y. KAWASAKI, K. NOSAKA, H. NISHIMURA
1992 年 38 巻 Special 号 p.
375-378
発行日: 1992年
公開日: 2010/11/26
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G. RINDI
1992 年 38 巻 Special 号 p.
379-382
発行日: 1992年
公開日: 2010/11/26
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T. KAWASAKI
1992 年 38 巻 Special 号 p.
383-386
発行日: 1992年
公開日: 2010/11/26
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フリー
All the evidence obtained indicates that the synthesis of TTP in vitro and in vivo is catalyzed by cytosolic adenylate kinase. Further studies should explore whether adenylate kinase is the only enzyme involved in TTP synthesis, together with physiological roles of TTP in living organisms.
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E. SCHOFFENIELS
1992 年 38 巻 Special 号 p.
387-391
発行日: 1992年
公開日: 2010/11/26
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A. SCHELLENBERGER
1992 年 38 巻 Special 号 p.
392-396
発行日: 1992年
公開日: 2010/11/26
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Besides the pyrophosphate group, acting as the essential and primary binding function of TPP the N1-atom of the aminopyrimidine component functions as a second and also essential anchor to the protein component. Only if both of the contacts are formed the productive conformation of TPP within the active site of TPP enzymes is realized. A mechanism is proposed, which explains the results of our experiments with TPP-analogs.
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K. KOIKE, Y. URATA, S. GOTO
1992 年 38 巻 Special 号 p.
397-400
発行日: 1992年
公開日: 2010/11/26
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Genomic clones encompassing the entire genes for the human pyruvate dehydrogenase α and β subunits (PDHα or β) have been isolated by screening the leukocyte genomic libraries with a nick-translated human foreskin fibroblast PDHα or β cDNA probe. These genomic clones were characterized by restriction enzyme analysis, extensive DNA sequencing and primer extension analysis. The PDHα gene spans 17.08 kilobases and is composed of 11 exons and 10 introns within its coding region. The 18-kilobase clone of PDHβ gene is composed of 10 exons and 9 introns. All intron-exon splice junctions of two genes follow the GT/ AG rule. A total of seven
Alu repeats in the PDHα gene were found in five introns and two
Alu family in the PDHβ gene were found in intron 2 and 8. The 5'-flanking region of the PDHα gene contains typical CCAAT and TATA-like consensus promoter sequence and two Sp1 binding sequences. That of the PDHβ gene contains a TCAAT sequence but no TATA sequence. Primer extension analyses indicated that the PDHα and β genes transcription start sites are thymine and adenine residues located 124 and 132 bases upstream from initiation codon in exon 1, respectively.
Genomic DNA of patient, died 93 hours after birth with acidemia and defect of PDH activity, was isolated and all of the exons of PDHα and β genes were amplified by PCR. Two single mutations in PDHα gene, TGT to TTT at codon 116 of Exon 5 and CTG to CCG at codon 162 of Exon 6, were identified by sequence analysis and resulted in a Cys to Phe and Leu to Prosubstitution in PDHα protein. The mutation causes the loss of PDH activity and missing two subunit protein bands revealed by immunoblot analysis.
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J. P. BLASS, K.-F. R. SHEU, A. J. L. COOPER, E. H. JUNG, G. E. GIBSON
1992 年 38 巻 Special 号 p.
401-404
発行日: 1992年
公開日: 2010/11/26
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Because of Clinical and neuropathological overlap between The Characteristics of dementia of The Alzheimer type (DAT) and of a Human thiamin deficiency syndrome (Wernicke-Korsakoff syndrome), Thiamin pyrophosphate (TPP) dependent processes have been studied in DAT brain and other tissues. The activities of 3 TPP-dependent enzymes are reduced in DAT brain: Transketolase (TK), The Pyruvate dehydrogenase Complex (PDHC), and The α-ketoglutarate dehydrogenase Complex (KGDHC). Quantitatively, The most marked reductions are in KGDHC (to less Than 20% of normal). In cultured skin fibroblasts, KGDHC activity is reduced To 50-60% of normal, TK activity To 80-90% of normal, and PDHC is normal. Structural and molecular studies of The DAT and non-DAT enzymes are in Process. A lesion of KGDHC may be related To The pathogenesis of DAT. Treatment with large doses of Thiamin Has not been beneficial, but The data are not totally negative. Further studies of Thiamin-dependent mechanisms in DAT seem justified.
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J. W. SUTTIE, C. P GROSSMAN, M. E. BENTON
1992 年 38 巻 Special 号 p.
405-408
発行日: 1992年
公開日: 2010/11/26
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A. SHIRAHATA, N. ARIYOSHI
1992 年 38 巻 Special 号 p.
409-412
発行日: 1992年
公開日: 2010/11/26
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M. J. SHEARER, R. V. KRIES, J. SAUPE
1992 年 38 巻 Special 号 p.
413-416
発行日: 1992年
公開日: 2010/11/26
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H. Tanimura, T. Tsuji
1992 年 38 巻 Special 号 p.
417-420
発行日: 1992年
公開日: 2010/11/26
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H. OBATA, B. JIZUKA, K. UCHIDA
1992 年 38 巻 Special 号 p.
421-424
発行日: 1992年
公開日: 2011/06/02
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S. KIMURA, H. SATOH, M. KOMAI
1992 年 38 巻 Special 号 p.
425-428
発行日: 1992年
公開日: 2010/11/26
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M. MINO, A. MURATA, K. YASUDA, Y. ITOKAWA
1992 年 38 巻 Special 号 p.
429-433
発行日: 1992年
公開日: 2010/11/26
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