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Article: [Biological Effects of Neutron Radiation: An Overview].

Imaoka, Tatsuhiko

Igaku butsuri : Nihon Igaku Butsuri Gakkai kikanshi = Japanese journal of medical physics : an official journal of Japan Society of Medical Physics

2021 Volume 42, Issue 2, Page(s) 73–79

Abstract: Exposure of human body to neutrons occurs in radiotherapy using high-energy radiations. This review summarizes knowledges related to biological effects of neutrons, including those obtained in recent projects in Japan and Europe. A study of Japanese ... ...

Abstract	Exposure of human body to neutrons occurs in radiotherapy using high-energy radiations. This review summarizes knowledges related to biological effects of neutrons, including those obtained in recent projects in Japan and Europe. A study of Japanese atomic bomb survivors with recently revised dosimetry indicated very high relative biological effectiveness (RBE) of 25-80 (as point estimates) regarding cancer risk. Animal studies indicate RBE of 2-100 or even higher regarding cancer induction, which seem to have a peak around ～1 MeV. Evidence suggests that these values depend on the age and sex. Reported RBE regarding the effects on the lens of the eye is in a similar range and sometimes very high. Regarding other tissue reactions, reported RBE values range from 2-10. Experiments at the cellular level have reported RBE of 1-5 regarding cell killing, 2-20 regarding induction of mutations (with a peak at ～1 MeV), and ～1 regarding induction of DNA double strand breaks. A simulation study predicted that the RBE of induction of complex DNA breaks peaks at ～1 MeV with a value of ～17. The complex breaks produced are likely to be far less in amount than simple DNA breaks, leading to a subtle increase in the yield of total DNA breaks; however, these complex damages may be very efficient in inducing mutations and cancer. Thus, the combination of the yield of complex DNA damage and its efficacy in inducing cancer is considered to underlie the high RBE of neutrons regarding cancer risk.
MeSH term(s)	Animals ; Neoplasms ; Neutrons ; Radiometry ; Relative Biological Effectiveness ; Risk
Language	Japanese
Publishing date	2021-06-24
Publishing country	Japan
Document type	Journal Article ; Review
ISSN	1345-5354
ISSN	1345-5354
DOI	10.11323/jjmp.42.2_73
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Article ; Online: Modifiers of radiation effects on breast cancer incidence revealed by a reanalysis of archival data of rat experiments.

Imaoka, Tatsuhiko / Nishimura, Mayumi / Daino, Kazuhiro / Kakinuma, Shizuko

Journal of radiation research

2023 Volume 64, Issue 2, Page(s) 273–283

Abstract: Cancer risk after exposure to ionizing radiation can vary between individuals and populations, but the impact of factors governing those variations is not well understood. We previously conducted a series of carcinogenesis experiments using a rat model ... ...

Abstract	Cancer risk after exposure to ionizing radiation can vary between individuals and populations, but the impact of factors governing those variations is not well understood. We previously conducted a series of carcinogenesis experiments using a rat model of breast cancer, in which 1654 rats born in 2002-2012 were exposed to γ rays at various doses and ages with or without non-radiation factors including high-fat diet, parity and chemical carcinogens. We herein reanalyze the incidence data from these archival experiments to clarify the effect of age at exposure, attained age, radiation dose and non-radiation factors (i.e. fat, parity, chemicals and birth cohorts) on radiation-related mammary cancer incidence. The analysis used excess relative risk (ERR) and excess absolute risk (EAR) models as well as generalized interaction models. Age-at-exposure dependence displayed a peak of susceptibility at puberty in both the ERR and EAR models. Attained age decreased ERR and increased EAR per unit radiation dose. The dose response was concordant with a linear model. Dietary fat exhibited a supra-multiplicative interaction, chemicals represented a multiplicative interaction, and parity and birth cohorts displayed interactions that did not significantly depart from additivity or multiplicativity. Treated as one entity, the four non-radiation factors gave a multiplicative interaction, but separation of the four factors significantly improved the fit of the model. Thus, the present study supports age and dose dependence observed in epidemiology, indicates heterogenous interactions between radiation and various non-radiation factors, and suggests the potential use of more flexible interaction modeling in radiological protection.
MeSH term(s)	Rats ; Animals ; Incidence ; Neoplasms, Radiation-Induced/epidemiology ; Neoplasms, Radiation-Induced/etiology ; Risk ; Carcinogenesis ; Carcinogens
Chemical Substances	Carcinogens
Language	English
Publishing date	2023-01-09
Publishing country	England
Document type	Journal Article
ZDB-ID	603983-2
ISSN	1349-9157 ; 0449-3060
ISSN (online)	1349-9157
ISSN	0449-3060
DOI	10.1093/jrr/rrac090
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Article ; Online: Arsenite-induced Radiosensitization of Glioma Cells Is Dependent on p53 Deficiency.

Ninomiya, Yasuharu / Imaoka, Tatsuhiko / Daino, Kazuhiro / Kakinuma, Shizuko / Nakajima, Tetsuo

Anticancer research

2023 Volume 43, Issue 6, Page(s) 2551–2559

Abstract: Background/aim: Arsenite is a radiosensitizer of glioma cells both in vitro and in vivo; however, the underlying mechanism of action is unclear. Radiosensitizers specific for p53-deficient tumors are a promising adjunct to radiotherapy because, unlike ... ...

Abstract	Background/aim: Arsenite is a radiosensitizer of glioma cells both in vitro and in vivo; however, the underlying mechanism of action is unclear. Radiosensitizers specific for p53-deficient tumors are a promising adjunct to radiotherapy because, unlike normal cells, many tumor cells lack p53. Previously, we demonstrated that arsenite sensitizes the p53-deficient glioma cell line U87MG-E6 to X-rays. Materials and methods: Using flowcytometry, we expand these findings to p53-proficient U87MG cells exposed to heavy ion beams, including carbon and iron ions. Results: Arsenite sensitized U87MG-E6, but not U87MG, cells to heavy ion beams and X-rays. Cell cycle analysis indicated that sensitization of U87MG-E6 was related to an increase in the percentage of cells in the late S/G Conclusion: Arsenite sensitizes cells by increasing the percentage of cells in the late S/G
MeSH term(s)	Humans ; Arsenites/pharmacology ; Carbon ; Carmustine ; Cell Line, Tumor ; Cell Survival ; Glioma/pathology ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	arsenite (N5509X556J) ; Arsenites ; Carbon (7440-44-0) ; Carmustine (U68WG3173Y) ; Tumor Suppressor Protein p53
Language	English
Publishing date	2023-05-27
Publishing country	Greece
Document type	Journal Article
ZDB-ID	604549-2
ISSN	1791-7530 ; 0250-7005
ISSN (online)	1791-7530
ISSN	0250-7005
DOI	10.21873/anticanres.16422
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Article ; Online: Combined effects of radiation and simulated microgravity on intestinal tumorigenesis in C3B6F1 Apc

Suzuki, Kenshi / Tsuruoka, Chizuru / Morioka, Takamitsu / Seo, Hitomi / Ogawa, Mari / Kambe, Ryosuke / Imaoka, Tatsuhiko / Kakinuma, Shizuko / Takahashi, Akihisa

Life sciences in space research

2024 Volume 41, Page(s) 202–209

Abstract: Explorations of the Moon and Mars are planned as future manned space missions, during which humans will be exposed to both radiation and microgravity. We do not, however, know the health effects for such combined exposures. In a ground-based experiment, ... ...

Abstract	Explorations of the Moon and Mars are planned as future manned space missions, during which humans will be exposed to both radiation and microgravity. We do not, however, know the health effects for such combined exposures. In a ground-based experiment, we evaluated the combined effects of radiation and simulated microgravity on tumorigenesis by performing X-irradiation and tail suspension in C3B6F1 Apc
MeSH term(s)	Animals ; Mice ; Weightlessness Simulation ; Intestinal Neoplasms/pathology ; Intestinal Neoplasms/etiology ; Carcinogenesis/radiation effects ; Mice, Inbred C57BL ; Hindlimb Suspension ; Male ; X-Rays ; Disease Models, Animal ; Female ; Intestine, Small/radiation effects ; Intestine, Small/pathology ; Thymus Gland/radiation effects ; Thymus Gland/pathology ; Neoplasms, Radiation-Induced/pathology ; Neoplasms, Radiation-Induced/etiology
Language	English
Publishing date	2024-03-30
Publishing country	Netherlands
Document type	Journal Article
ISSN	2214-5532
ISSN (online)	2214-5532
DOI	10.1016/j.lssr.2024.03.005
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Article ; Online: Molecular and cellular basis of the dose-rate-dependent adverse effects of radiation exposure in animal models. Part I: Mammary gland and digestive tract.

Suzuki, Keiji / Imaoka, Tatsuhiko / Tomita, Masanori / Sasatani, Megumi / Doi, Kazutaka / Tanaka, Satoshi / Kai, Michiaki / Yamada, Yutaka / Kakinuma, Shizuko

Journal of radiation research

2023 Volume 64, Issue 2, Page(s) 210–227

Abstract: While epidemiological data are available for the dose and dose-rate effectiveness factor (DDREF) for human populations, animal models have contributed significantly to providing quantitative data with mechanistic insights. The aim of the current review ... ...

Abstract	While epidemiological data are available for the dose and dose-rate effectiveness factor (DDREF) for human populations, animal models have contributed significantly to providing quantitative data with mechanistic insights. The aim of the current review is to compile both the in vitro experiments with reference to the dose-rate effects of DNA damage and repair, and the animal studies, specific to rodents, with reference to the dose-rate effects of cancer development. In particular, the review focuses especially on the results pertaining to underlying biological mechanisms and discusses their possible involvement in the process of radiation-induced carcinogenesis. Because the concept of adverse outcome pathway (AOP) together with the key events has been considered as a clue to estimate radiation risks at low doses and low dose-rates, the review scrutinized the dose-rate dependency of the key events related to carcinogenesis, which enables us to unify the underlying critical mechanisms to establish a connection between animal experimental studies with human epidemiological studies.
MeSH term(s)	Animals ; Humans ; Dose-Response Relationship, Radiation ; Neoplasms, Radiation-Induced/etiology ; Mammary Glands, Human ; Risk Assessment/methods ; Radiation Exposure/adverse effects ; Carcinogenesis ; Models, Animal ; Gastrointestinal Tract
Language	English
Publishing date	2023-02-10
Publishing country	England
Document type	Review ; Journal Article
ZDB-ID	603983-2
ISSN	1349-9157 ; 0449-3060
ISSN (online)	1349-9157
ISSN	0449-3060
DOI	10.1093/jrr/rrad002
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Article ; Online: Molecular and cellular basis of the dose-rate-dependent adverse effects of radiation exposure in animal models. Part II: Hematopoietic system, lung and liver.

Suzuki, Keiji / Imaoka, Tatsuhiko / Tomita, Masanori / Sasatani, Megumi / Doi, Kazutaka / Tanaka, Satoshi / Kai, Michiaki / Yamada, Yutaka / Kakinuma, Shizuko

Journal of radiation research

2023 Volume 64, Issue 2, Page(s) 228–249

Abstract: While epidemiological data have greatly contributed to the estimation of the dose and dose-rate effectiveness factor (DDREF) for human populations, studies using animal models have made significant contributions to provide quantitative data with ... ...

Abstract	While epidemiological data have greatly contributed to the estimation of the dose and dose-rate effectiveness factor (DDREF) for human populations, studies using animal models have made significant contributions to provide quantitative data with mechanistic insights. The current article aims at compiling the animal studies, specific to rodents, with reference to the dose-rate effects of cancer development. This review focuses specifically on the results that explain the biological mechanisms underlying dose-rate effects and their potential involvement in radiation-induced carcinogenic processes. Since the adverse outcome pathway (AOP) concept together with the key events holds promise for improving the estimation of radiation risk at low doses and low dose-rates, the review intends to scrutinize dose-rate dependency of the key events in animal models and to consider novel key events involved in the dose-rate effects, which enables identification of important underlying mechanisms for linking animal experimental and human epidemiological studies in a unified manner.
MeSH term(s)	Animals ; Humans ; Radiation Dosage ; Neoplasms, Radiation-Induced ; Risk Assessment/methods ; Radiation Exposure/adverse effects ; Models, Animal ; Liver ; Lung ; Hematopoietic System ; Dose-Response Relationship, Radiation
Language	English
Publishing date	2023-01-13
Publishing country	England
Document type	Review ; Journal Article
ZDB-ID	603983-2
ISSN	1349-9157 ; 0449-3060
ISSN (online)	1349-9157
ISSN	0449-3060
DOI	10.1093/jrr/rrad003
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Article ; Online: BRCA1 haploinsufficiency impairs iron metabolism to promote chrysotile-induced mesothelioma via ferroptosis resistance.

Luo, Yaguang / Akatsuka, Shinya / Motooka, Yashiro / Kong, Yingyi / Zheng, Hao / Mashimo, Tomoji / Imaoka, Tatsuhiko / Toyokuni, Shinya

Cancer science

2023 Volume 114, Issue 4, Page(s) 1423–1436

Abstract: Malignant mesothelioma (MM) is still a social burden associated with asbestos exposure. Local iron accumulation thereby represents the major pathogenesis, followed by oxidative DNA strand breaks and genomic alterations in the mesothelium. BRCA1 is a ... ...

Abstract	Malignant mesothelioma (MM) is still a social burden associated with asbestos exposure. Local iron accumulation thereby represents the major pathogenesis, followed by oxidative DNA strand breaks and genomic alterations in the mesothelium. BRCA1 is a critical component of homologous recombination repair directed to DNA double-stranded breaks, whereas BRCA1 germline mutation is an established risk for breast/ovarian cancer, its role in MM development remains to be elucidated. Murine Brca1 mutant models so far have not reproduced human phenotypes. However, a rat Brca1 mutant model (Mut; L63X/+ ) recently reproduced them at least partially. Here we describe the differential induction of MM in Brca1 mutant rats by intraperitoneal injection of chrysotile or crocidolite. Only Mut males injected with chrysotile revealed a promotional effect on mesothelial carcinogenesis in comparison with wild-type and/or females, with all the MMs Brca1 haploinsufficient. Array-based comparative genomic hybridization of MMs disclosed a greater extent of chromosomal deletions in Brca1 mutants, including Cdkn2a/2b accompanied by Tfr2 amplification, in comparison with wild-type tumors. Mutant MMs indicated iron metabolism dysregulation, such as an increase in catalytic Fe(II) and Ki67-index as well as a decrease in Fe(III) and ferritin expression. Simultaneously, mutant MMs revealed ferroptosis resistance by upregulation of Slc7A11 and Gpx4. At an early carcinogenic stage of 4 weeks, induced Brca1 expression in mesothelial cells was significantly suppressed in chrysotile/Mut in comparison with crocidolite/Mut, whereas significant preference to iron with a decrease in Fe(III) has been already established. In conclusion, chrysotile exposure can be a higher risk for MM in BRCA1 mutant males, considering the rat results.
MeSH term(s)	Animals ; Female ; Male ; Rats ; Asbestos/toxicity ; Asbestos, Crocidolite/toxicity ; Asbestos, Serpentine/toxicity ; BRCA1 Protein/genetics ; Carcinogenesis/genetics ; Comparative Genomic Hybridization ; DNA ; Ferric Compounds/metabolism ; Ferroptosis/genetics ; Haploinsufficiency ; Iron/metabolism ; Lung Neoplasms/chemically induced ; Lung Neoplasms/genetics ; Mesothelioma, Malignant/chemically induced ; Mesothelioma, Malignant/genetics
Chemical Substances	Asbestos (1332-21-4) ; Asbestos, Crocidolite (12001-28-4) ; Asbestos, Serpentine ; BRCA1 Protein ; DNA (9007-49-2) ; Ferric Compounds ; Iron (E1UOL152H7)
Language	English
Publishing date	2023-02-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2115647-5
ISSN	1349-7006 ; 1349-7006
ISSN (online)	1349-7006
ISSN	1349-7006
DOI	10.1111/cas.15705
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Article ; Online: Corrigendum to "Azithromycin induces read-through of the nonsense Apc allele and prevents intestinal tumorigenesis in C3B6F1 Apc

Semba, Ryoko / Morioka, Takamitsu / Yanagihara, Hiromi / Suzuki, Kenshi / Tachibana, Hirotaka / Hamoya, Takahiro / Horimoto, Yoshiya / Imaoka, Tatsuhiko / Saito, Mitsue / Kakinuma, Shizuko / Arai, Masami

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2023 Volume 165, Page(s) 115082

Language	English
Publishing date	2023-06-28
Publishing country	France
Document type	Published Erratum
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2023.115082
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Article ; Online: Differential expression of DNA-dependent protein kinase catalytic subunit in the brain of neonatal mice and young adult mice.

Okawa, Aoi / Morioka, Takamitsu / Imaoka, Tatsuhiko / Kakinuma, Shizuko / Matsumoto, Yoshihisa

Proceedings of the Japan Academy. Series B, Physical and biological sciences

2020 Volume 96, Issue 5, Page(s) 171–179

Abstract: It is generally thought that younger people are more susceptible to cancer development after exposure to ionizing radiation in reference to epidemiological studies and animal experiments. However, little is known about the age-dependent alteration in DNA ...

Abstract	It is generally thought that younger people are more susceptible to cancer development after exposure to ionizing radiation in reference to epidemiological studies and animal experiments. However, little is known about the age-dependent alteration in DNA repair ability. In the present study, we examined the expression levels of proteins involved in the repair of DNA double-strand breaks through non-homologous end joining (NHEJ), i.e., DNA-dependent protein kinase catalytic subunit (DNA-PKcs), X-ray repair cross-complementing 4 (XRCC4) and XRCC4-like factor (XLF). We found that the expression of DNA-PKcs in brain tissues was higher in neonatal mice (1 week after birth) than in young adult mice (7 weeks after birth). In association with this, DNA double-strand breaks were repaired more rapidly in the brain tissues of neonatal mice than in those of young adult mice. The current results suggested a possible role for DNA-PKcs protecting developing brain tissues from DNA double-strand breaks.
MeSH term(s)	Animals ; Animals, Newborn ; Brain/metabolism ; Catalytic Domain ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; DNA Repair ; DNA-Activated Protein Kinase/chemistry ; DNA-Activated Protein Kinase/metabolism ; Gene Expression Regulation, Enzymologic ; Mice
Chemical Substances	DNA-Activated Protein Kinase (EC 2.7.11.1)
Language	English
Publishing date	2020-04-23
Publishing country	Japan
Document type	Journal Article
ZDB-ID	161781-3
ISSN	1349-2896 ; 0386-2208
ISSN (online)	1349-2896
ISSN	0386-2208
DOI	10.2183/pjab.96.014
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Article ; Online: Copenhagen Rats Display Dominantly Inherited Yet Non-uniform Resistance to Spontaneous, Radiation-induced, and Chemically-induced Mammary Carcinogenesis.

Nishimura, Mayumi / Imaoka, Tatsuhiko / Daino, Kazuhiro / Nishimura, Yukiko / Kokubo, Toshiaki / Takabatake, Masaru / Kakinuma, Shizuko / Shimada, Yoshiya

Anticancer research

2022 Volume 42, Issue 5, Page(s) 2415–2423

Abstract: Background/aim: Genetic and environmental factors interact to dictate the risk of cancer, and animal models are expected to provide avenues for identifying such interactions. The aim of the study was to clarify the genetic susceptibility of Copenhagen ... ...

Abstract	Background/aim: Genetic and environmental factors interact to dictate the risk of cancer, and animal models are expected to provide avenues for identifying such interactions. The aim of the study was to clarify the genetic susceptibility of Copenhagen rats to spontaneous, radiation-induced, and chemically-induced mammary carcinogenesis. Materials and methods: Female Copenhagen and Sprague- Dawley rats and their F Results: Radiation and 1-methyl-1-nitrosourea both significantly increased the incidence of mammary cancer in all strains. Copenhagen and F Conclusion: Copenhagen rats display non-uniform resistance to spontaneous, radiation-induced, and chemically-induced mammary carcinogenesis with dominant inheritance over Sprague-Dawley rats.
MeSH term(s)	Animals ; Breast Neoplasms ; Cell Transformation, Neoplastic ; Female ; Humans ; Mammary Neoplasms, Experimental/chemically induced ; Mammary Neoplasms, Experimental/genetics ; Methylnitrosourea/toxicity ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Methylnitrosourea (684-93-5)
Language	English
Publishing date	2022-04-27
Publishing country	Greece
Document type	Journal Article
ZDB-ID	604549-2
ISSN	1791-7530 ; 0250-7005
ISSN (online)	1791-7530
ISSN	0250-7005
DOI	10.21873/anticanres.15720
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