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Nagoya Journal of Medical Science

Our medical research library holds 6 studies published in Nagoya Journal of Medical Science (2009–2023). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 5 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it. For 1 study PubMed has no abstract for, we give the abstract printed in the article or, where there is none, a summary we wrote from it, each labeled as such.

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About the journal

  • Publisher: Nagoya University School Of Medicine
  • Published: 1927 to the present, Japan
  • Language: English
  • ISSN: 0027-7622 (print), 2186-3326 (electronic)
  • Continues: Aichi Journal of Experimental Medicine
  • Its record in the NLM Catalog

2020s

  • Commentary on "Mechanisms of asbestos-induced carcinogenesis" published in 2009. S. Toyokuni. 2023;85(1):13-15. Comment PubMed · Publisher · Free full text

    Summary

    In this commentary, written for the journal's 100th anniversary series on highly cited articles, the author looked back on his 2009 review of the mechanisms of asbestos-induced carcinogenesis. He noted that asbestos was used in Japan until 2006 and is still used in many developing countries, although the International Agency for Research on Cancer declared all asbestos a definite human carcinogen in 1987. He restated that the review summarized the mechanism as three processes: persistent free radical generation by macrophages that scavenge fibers (frustrated phagocytosis), intense phagocytic activity of mesothelial cells, and adsorption of proteins such as hemoglobin and histone onto asbestos. The review also proposed why chrysotile, which contains no iron, can cause similar oxidative DNA damage. He then summarized later work from his group. Chrysotile-induced mesothelioma in rats showed excess iron pathology with homozygous deletion of the p16Ink4a gene. Multiwalled carbon nanotubes of about 50 nm diameter showed pathologic processes similar to asbestos. Iron removal by chelating agents or phlebotomy could work as prevention in preclinical animal models. Macrophages dying by ferroptosis released iron-loaded ferritin in exosomes, which induced oxidative DNA damage in mesothelial cells. He described this as a novel indirect mechanism of asbestos-induced mesothelial carcinogenesis.

    PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

2010s

  • Polymer coating on carbon nanotubes into Durobeads is a novel strategy for human environmental safety. F. Ito, H. Hisashi, S. Toyokuni. 2018;80(4):597-604. PubMed · Publisher · Free full text

    Abstract

    Carbon nanotubes (CNTs) have attracted much business interest in industrial applications due to their high electrical and heat conductivities while being both durable and versatile. However, multiwall CNTs (MWCNTs) of ~50 nm diameter (NT50) have been shown to cause mesothelioma in rodents after direct exposure to mesothelial cells, and thus were classified as a Group 2B carcinogen to humans, which requires considerable regulations for use. In contrast, tangled MWCNTs of ~15 nm diameter (NTtngl) are not carcinogenic to rats, indicating that the physical dimension linked with mesothelial cellular uptake is an important factor for human environmental risk. In the present study, hypothesizing that dustability is another distinct risk factor, for the first time, we evaluated the toxicity of CNT granules (Durobeads) that were generated with a polymer coating to mesothelial cells. Polymer coating induced prominent agglomeration and significantly suppressed the dustability of CNTs in a dose-dependent manner, with a 10% polymer coating resulting in 730 times less dustability. These CNT granules revealed significantly lower mesothelial uptake and cytotoxicity in comparison to NT50 in in vitro assays. Similarly, in in vivo analyses, CNT granules induced limited peritoneal inflammation 4 weeks after intraperitoneal injection, whereas NT50 caused severe fibrosing inflammation. Previously, we demonstrated that the severity of inflammation by intraperitoneal injection in the subacute studies are in agreement with the mesothelial carcinogenicity by CNTs. Therefore, we suggest that adding a polymer coating to CNTs provides another smart strategy for the safe use of CNTs.

  • Minimal inflammogenicity of pristine single-wall carbon nanotubes. S. Toyokuni, L.I. Jiang, R. Kitaura, et al. 2015;77(1-2):195-202. PubMed · Free full text

    Abstract

    Carbon nanotubes (CNTs) are a novel synthetic material comprising only carbon atoms. Based on its rigidity, its electrical and heat conductivity and its applicability to surface manufacturing, this material is expected to have numerous applications in industry. However, due to the material's dimensional similarity to asbestos fibers, its carcinogenicity was hypothesized during the last decade, and indeed, we have shown that multi-wall CNTs (MWCNTs) of 50 nm in diameter are potently carcinogenic to mesothelial cells after intraperitoneal injection. Additionally, we suggested that inflammogenicity after intraperitoneal injection can predict mesothelial carcinogenesis. However, few data have been published on the intraperitoneal inflammogenicity of single-wall CNTs (SWCNTs). Here, we conducted a series of studies on SWCNTs using both intraperitoneal injection into rats and MeT5A mesothelial cells. Intraperitoneal injection of 10 mg SWCNTs caused no remarkable inflammation in the abdominal cavity, and the exposure of MeT5A cells to up to 25 μg/cm(2) SWCNTs did not alter proliferation. MWCNTs of 50 nm in diameter were used as a positive control, and tangled MWCNTs of 15 nm in diameter were used as a negative control. The results suggest that SWCNTs are a low-risk material with respect to mesothelial carcinogenesis.

  • Gamma knife radiosurgery of brain metastasis from malignant pleural mesothelioma--report of three cases with autopsy study in a case. T. Kobayashi, T. Tsugawa, C. Hashizume, et al. 2014;76(1-2):187-93. Case report PubMed · Free full text

    Abstract

    The median survival time of malignant pleural mesothelioma (MPM) has been 9 months. Given the short survival, there have been only few cases in which brain metastases have been diagnosed and treated before death. Three cases of brain metastases treated by gamma knife radiosurgery (GKR) are reported. Case I showed a metastatic lesion in the right frontal lobe which was treated by GKR two years after diagnosis of MPM. The lesion markedly reduced and the symptoms were improved, But the patient died of progression of pleural tumor four months after GKR. A year and three months after the diagnosis, asymptomatic bifrontal lesions were treated with GKR. However, Case 2 died of abdominal mass a month after. Case 3 showed headache one and half year after the diagnosis. Three brain lesions were treated by GKR, which disappeared in 4 months. The patient died of new multiple brain metastases and periventricular dissemination seven months after. The autopsy revealed a MPM occupying the left pleural cavity. No neoplastic lesion was found in gamma knife-treated sites. The cause of death was the mass effect by new metastatic lesions. GKR was found effective also for the treatment of brain metastasis of MPM.

  • Rat model demonstrates a high risk of tremolite but a low risk of anthophyllite for mesothelial carcinogenesis. D. Aierken, Y. Okazaki, S.H. Chew, et al. 2014;76(1-2):149-60. PubMed · Free full text

    Abstract

    Asbestos was abundantly used in industry during the last century. Currently, asbestos confers a heavy social burden due to an increasing number of patients with malignant mesothelioma (MM), which develops after a long incubation period. Many studies have been conducted on the effects of the asbestos types that were most commonly used for commercial applications. However, there are few studies describing the effects of the less common types, or minor asbestos. We performed a rat carcinogenesis study using Japanese tremolite and Afghan anthophyllite. Whereas more than 50% of tremolite fibers had a diameter of < 500 nm, only a small fraction of anthophyllite fibers had a diameter of < 500 nm. We intraperitoneally injected 1 or 10 mg of asbestos into F1 Fischer-344/Brown-Norway rats. In half of the animals, repeated intraperitoneal injections of nitrilotriacetate (NTA), an iron chelator to promote Fenton reaction, were performed to evaluate the potential involvement of iron overload. Tremolite induced MM with a high incidence (96% with 10 mg; 52% with 1 mg), and males were more susceptible than females. Histology was confirmed using immunohistochemistry, and most MMs were characterized as the sarcomatoid or biphasic subtype. Unexpectedly NTA showed an inhibitory effect in females. In contrast, anthophyllite induced no MM after an observation period of 550 days. The results suggest that the carcinogenicity of anthophyllite is weaker than formerly reported, whereas that of tremolite is as potent as major asbestos as compared with our previous data.

2000s

  • Mechanisms of asbestos-induced carcinogenesis. S. Toyokuni. 2009;71(1-2):1-10. Review PubMed · Free full text

    Abstract

    Respiratory exposure to asbestos fibers has been associated with diffuse malignant mesothelioma (DMM) in humans. Despite advancements in the molecular analyses of human DMM and the development of animal models, the carcinogenic mechanisms of the disease remain unclear. There are basically three hypotheses regarding the pathogenesis of asbestos-induced DMM, which may be summarized as follows: (1) the "oxidative stress theory" is based on the fact that phagocytic cells that engulf asbestos fibers produce large amounts of free radicals due to their inability to digest the fibers, and epidemiological studies indicating that iron-containing asbestos fibers appear more carcinogenic; (2) the "chromosome tangling theory" postulates that asbestos fibers damage chromosomes when cells divide; and (3) the "theory of adsorption of many specific proteins as well as carcinogenic molecules" states that asbestos fibers in vivo concentrate proteins or chemicals including the components of cigarette smoke. Elucidation of the major mechanisms underlying DMM would be helpful for the development of novel strategies to prevent DMM induction in people who have already been exposed to asbestos.

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