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Article: Case report: meningeal lymphangiogenesis around ependymoma forming along the dura matter.

Hino, Utaro / Tamura, Ryota / Yo, Masahiro / Kase, Yoshitaka / Tsuda, Noboru / Miyauchi, Tsubasa / Sogano, Junki / Karatsu, Kosuke / Miwa, Tomoru / Toda, Masahiro

Frontiers in oncology

2024 Volume 13, Page(s) 1340167

Abstract: Recently, there has been growing interest in the presence and function of meningeal lymphatic vessels, with no direct evidence linking these vessels to primary brain tumors. We report a unique case of recurrent ependymoma in the dura mater, showing ... ...

Abstract	Recently, there has been growing interest in the presence and function of meningeal lymphatic vessels, with no direct evidence linking these vessels to primary brain tumors. We report a unique case of recurrent ependymoma in the dura mater, showing histopathological signs of lymphatic proliferation at the tumor attachment site. The patient initially presented with a headache, and was diagnosed with
Language	English
Publishing date	2024-01-12
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2023.1340167
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Article ; Online: Age-related changes in endothelial function and blood flow regulation.

Toda, Noboru

Pharmacology & therapeutics

2012 Volume 133, Issue 2, Page(s) 159–176

Abstract: Vascular endothelial dysfunction is regarded as a primary phenotypic expression of normal human aging. This senescence-induced disorder is the likely culprit underlying the increased cardiovascular and metabolic disease risks associated with aging. The ... ...

Abstract	Vascular endothelial dysfunction is regarded as a primary phenotypic expression of normal human aging. This senescence-induced disorder is the likely culprit underlying the increased cardiovascular and metabolic disease risks associated with aging. The rate of this age-dependent deterioration is largely influenced by the poor-quality lifestyle choice, such as smoking, sedentary daily life, chronic alcohol ingestion, high salt intake, unbalanced diet, and mental stress; and it is accelerated by cardiovascular and metabolic diseases. Although minimizing these detrimental factors is the best course of action, nonetheless chronological age steadily impairs endothelial function through reduced endothelial nitric oxide synthase (eNOS) expression/action, accelerated nitric oxide (NO) degradation, increased phosphodiesterase activity, inhibition of NOS activity by endogenous NOS inhibitors, increased production of reactive oxygen species, inflammatory reactions, decreased endothelial progenitor cell number and function, and impaired telomerase activity or telomere shortening. Endothelial dysfunction in regional vasculatures results in cerebral hypoperfusion triggering cognitive dysfunction and Alzheimer's disease, coronary artery insufficiency, penile erectile dysfunction, and circulatory failures in other organs and tissues. Possible prophylactic measures to minimize age-related endothelial dysfunction are also summarized in this review.
MeSH term(s)	Adult ; Aged ; Aging/metabolism ; Aging/physiology ; Animals ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiology ; Humans ; Regional Blood Flow/physiology
Language	English
Publishing date	2012-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2011.10.004
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Article: [Nitrergic cerebrovascular regulation as affected by donepezil].

Toda, Noboru

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2011 Volume 141, Issue 3, Page(s) 150–154

MeSH term(s)	Alzheimer Disease/drug therapy ; Alzheimer Disease/physiopathology ; Cerebrovascular Circulation/drug effects ; Cholinesterase Inhibitors/pharmacology ; Cholinesterase Inhibitors/therapeutic use ; Donepezil ; Humans ; Indans/pharmacology ; Indans/therapeutic use ; Nitric Oxide/physiology ; Piperidines/pharmacology ; Piperidines/therapeutic use ; Stimulation, Chemical ; Vasodilation/drug effects
Chemical Substances	Cholinesterase Inhibitors ; Indans ; Piperidines ; Nitric Oxide (31C4KY9ESH) ; Donepezil (8SSC91326P)
Language	Japanese
Publishing date	2011-03-28
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	1097532-9
ISSN	1347-8397 ; 0015-5691
ISSN (online)	1347-8397
ISSN	0015-5691
DOI	10.1254/fpj.141.150
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Article ; Online: Cigarette smoking impairs nitric oxide-mediated cerebral blood flow increase: Implications for Alzheimer's disease.

Toda, Noboru / Okamura, Tomio

Journal of pharmacological sciences

2016 Volume 131, Issue 4, Page(s) 223–232

Abstract: Cerebral blood flow is mainly regulated by nitrergic (parasympathetic, postganglionic) nerves and nitric oxide (NO) liberated from endothelial cells in response to shear stress and stretch of vasculature, whereas sympathetic vasoconstrictor control is ... ...

Abstract	Cerebral blood flow is mainly regulated by nitrergic (parasympathetic, postganglionic) nerves and nitric oxide (NO) liberated from endothelial cells in response to shear stress and stretch of vasculature, whereas sympathetic vasoconstrictor control is quite weak. On the other hand, peripheral vascular resistance and blood flow are mainly controlled by adrenergic vasoconstrictor nerves; endothelium-derived NO and nitrergic nerves play some roles as vasodilator factors. Cigarette smoking impairs NO synthesis in cerebral vascular endothelial cells and nitrergic nerves leading to interference with cerebral blood flow and glucose metabolism in the brain. Smoking-induced cerebral hypoperfusion is induced by impairment of synthesis and actions of NO via endothelial nitric oxide synthase (eNOS)/neuronal NOS (nNOS) inhibition and by increased production of oxygen radicals, resulting in decreased actions of NO on vascular smooth muscle. Nicotine acutely and chronically impairs the action of endothelial NO and also inhibits nitrergic nerve function in chronic use. Impaired cerebral blood supply promotes the synthesis of amyloid β that accelerates blood flow decrease. This vicious cycle is thought to be one of the important factors involving in Alzheimer's disease (AD). Quitting smoking is undoubtedly one of the important ways to prevent and delay the genesis or slow the progress of impaired cognitive function and AD.
MeSH term(s)	Alzheimer Disease/metabolism ; Alzheimer Disease/physiopathology ; Cerebrovascular Circulation/physiology ; Endothelium, Vascular/metabolism ; Humans ; Models, Biological ; Muscle, Smooth, Vascular/physiology ; Nitric Oxide/metabolism ; Nitric Oxide/physiology ; Nitric Oxide Synthase Type I/metabolism ; Nitric Oxide Synthase Type III/metabolism ; Smoking/metabolism ; Smoking/physiopathology
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type I (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
Language	English
Publishing date	2016-08
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	2104264-0
ISSN	1347-8648 ; 1347-8613
ISSN (online)	1347-8648
ISSN	1347-8613
DOI	10.1016/j.jphs.2016.07.001
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Article ; Online: Hyperhomocysteinemia impairs regional blood flow: involvements of endothelial and neuronal nitric oxide.

Toda, Noboru / Okamura, Tomio

Pflugers Archiv : European journal of physiology

2016 Volume 468, Issue 9, Page(s) 1517–1525

Abstract: Increasing evidence support the idea that hyperhomocysteinemia (HHcy) is responsible for pathogenesis underlying cerebral, coronary, renal, and other vascular circulatory disorders and for hypertension. Impaired synthesis of nitric oxide (NO) in the ... ...

Abstract	Increasing evidence support the idea that hyperhomocysteinemia (HHcy) is responsible for pathogenesis underlying cerebral, coronary, renal, and other vascular circulatory disorders and for hypertension. Impaired synthesis of nitric oxide (NO) in the endothelium or increased production of asymmetric dimethylarginine and activated oxygen species are involved in the impairment of vasodilator effects of NO. Impaired circulation in the brain derived from reduced synthesis and actions of NO would be an important triggering factor to dementia and Alzheimer's disease. Reduced actions of NO and brain hypoperfusion trigger increased production of amyloid-β that inhibits endothelial function, thus establishing a vicious cycle for impairing brain circulation. HHcy is involved in the genesis of anginal attack and coronary myocardial infarction. HHcy is also involved in renal circulatory diseases. The homocysteine (Hcy)-induced circulatory failure is promoted by methionine and is prevented by increased folic acid and vitamin B6/B12. Eliminating poor life styles, such as smoking and being sedentary; keeping favorable dietary habits; and early treatment maintaining constitutive NOS functions healthy, reducing oxidative stresses would be beneficial in protecting HHcy-induced circulatory failures.
MeSH term(s)	Animals ; Cerebrovascular Circulation ; Coronary Circulation ; Humans ; Hyperhomocysteinemia/enzymology ; Hyperhomocysteinemia/metabolism ; Hyperhomocysteinemia/physiopathology ; Nitric Oxide Synthase Type I/metabolism ; Nitric Oxide Synthase Type III/metabolism
Chemical Substances	Nitric Oxide Synthase Type I (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
Language	English
Publishing date	2016-09
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-016-1849-y
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Article: Age-related changes in endothelial function and blood flow regulation

Toda, Noboru

Pharmacology and therapeutics. 2012 Feb., v. 133, no. 2

2012

Abstract	Vascular endothelial dysfunction is regarded as a primary phenotypic expression of normal human aging. This senescence-induced disorder is the likely culprit underlying the increased cardiovascular and metabolic disease risks associated with aging. The rate of this age-dependent deterioration is largely influenced by the poor-quality lifestyle choice, such as smoking, sedentary daily life, chronic alcohol ingestion, high salt intake, unbalanced diet, and mental stress; and it is accelerated by cardiovascular and metabolic diseases. Although minimizing these detrimental factors is the best course of action, nonetheless chronological age steadily impairs endothelial function through reduced endothelial nitric oxide synthase (eNOS) expression/action, accelerated nitric oxide (NO) degradation, increased phosphodiesterase activity, inhibition of NOS activity by endogenous NOS inhibitors, increased production of reactive oxygen species, inflammatory reactions, decreased endothelial progenitor cell number and function, and impaired telomerase activity or telomere shortening. Endothelial dysfunction in regional vasculatures results in cerebral hypoperfusion triggering cognitive dysfunction and Alzheimer's disease, coronary artery insufficiency, penile erectile dysfunction, and circulatory failures in other organs and tissues. Possible prophylactic measures to minimize age-related endothelial dysfunction are also summarized in this review.
Keywords	Alzheimer disease ; alcohol drinking ; blood flow ; cognition ; coronary vessels ; diet ; endothelial nitric oxide synthase ; humans ; lifestyle ; metabolic diseases ; nitric oxide ; psychological stress ; reactive oxygen species ; risk ; stem cells ; telomerase ; telomeres ; tissues
Language	English
Dates of publication	2012-02
Size	p. 159-176.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2011.10.004
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Time to Pain Relapse After Palliative Radiotherapy for Bone Metastasis: A Prospective Multi-institutional Study.

Saito, Anneyuko I / Hirai, Takahisa / Inoue, Tatsuya / Hojo, Noboru / Kawai, Satoru / Kato, Yui / Ito, Kana / Kato, Masako / Ozawa, Yukiko / Shinjo, Hidenori / Toda, Kazuma / Yoshimura, Ryo-Ichi

Anticancer research

2023 Volume 43, Issue 2, Page(s) 865–873

Abstract: Background/aim: Low risk asymptomatic bone metastasis (LRABM) without gross osteolytic changes tends to be out of indication for radiotherapy. The aim of this study was to evaluate the time between the end of palliative radiotherapy of bone metastasis ( ... ...

Abstract	Background/aim: Low risk asymptomatic bone metastasis (LRABM) without gross osteolytic changes tends to be out of indication for radiotherapy. The aim of this study was to evaluate the time between the end of palliative radiotherapy of bone metastasis (BM) until the start of new pain, in patients with painful BM. Patients and methods: Patients with BM were prospectively assessed for location and strength of pain every month for one year after radiotherapy. The correlation of pain relapse at irradiated site, and pain onset outside the irradiated site was evaluated with sex, age, primary tumor, pathology of tumor, visceral metastases, baseline scores for Eastern Cooperative Oncology Group performance status (PS), and baseline verbal rating scale (VRS). Results: A hundred and thirty-two patients were included (79 males and 53 females). Median age was 66 years. Primary sites were lung (n=60), breast (n=17), colon (n=12), prostate (n=11), and others (n=33) (one patient had two primary sites). Median follow-up was 185 days. Pain relief was observed in 92 patients (86.0%). Out of them, pain progression was observed in 69.6%. Median time to pain progression was 75.5 days. Pain onset outside the irradiated site was observed in 57 patients (43.2%). Median time to pain onset was 109 days. Out of the 57 patients, 13 (22.8%) had LRABM which existed before the start of radiotherapy. There were 54 patients with LRABM in this study and because many patients had more than one LRABM, the total LRABM sites were 123. Out of them, pain onset was observed within one year after irradiation in 44 (36%) lesions. Median time to pain onset was 67 days, which was the shortest of the three: irradiated site, out of the irradiated site, and LRABM site. Risk factors for high probability of pain onset within one year in LRABM lesions were female sex (showing a trend in univariate analysis), and pelvic, skull and spine metastasis (significant in multivariate analysis). Conclusion: Time to pain onsets in LRABM are relatively short, especially in female patients with pelvic, skull and spine metastasis. In these patients, prophylactic radiotherapy could be an option to consider.
MeSH term(s)	Male ; Humans ; Female ; Aged ; Prospective Studies ; Pain/etiology ; Pain/radiotherapy ; Palliative Care ; Bone Neoplasms/secondary ; Chronic Disease ; Recurrence
Language	English
Publishing date	2023-01-25
Publishing country	Greece
Document type	Multicenter Study ; Journal Article
ZDB-ID	604549-2
ISSN	1791-7530 ; 0250-7005
ISSN (online)	1791-7530
ISSN	0250-7005
DOI	10.21873/anticanres.16229
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Article: Prognostic Significance of Preoperative Neutrophil-to-Lymphocyte Ratio in Patients With Meningiomas.

Kuranari, Yuki / Tamura, Ryota / Tsuda, Noboru / Kosugi, Kenzo / Morimoto, Yukina / Yoshida, Kazunari / Toda, Masahiro

Frontiers in oncology

2020 Volume 10, Page(s) 592470

Abstract: Background: Meningiomas are the most common benign intracranial tumors. However, even WHO grade I meningiomas occasionally show local tumor recurrence. Prognostic factors for meningiomas have not been fully established. Neutrophil-to-lymphocyte ratio ( ... ...

Abstract	Background: Meningiomas are the most common benign intracranial tumors. However, even WHO grade I meningiomas occasionally show local tumor recurrence. Prognostic factors for meningiomas have not been fully established. Neutrophil-to-lymphocyte ratio (NLR) has been reported as a prognostic factor for several solid tumors. The prognostic value of NLR in meningiomas has been analyzed in few studies. Materials and methods: This retrospective study included 160 patients who underwent surgery for meningiomas between October 2010 and September 2017. We analyzed the associations between patients' clinical data (sex, age, primary/recurrent, WHO grade, extent of removal, tumor location, peritumoral brain edema, and preoperative laboratory data) and clinical outcomes, including recurrence and progression-free survival (PFS). Results: Forty-four meningiomas recurred within the follow-up period of 3.8 years. WHO grade II, III, subtotal removal, history of recurrence, Ki-67 labeling index ≥3.0, and preoperative NLR value ≥2.6 were significantly associated with shorter PFS ( Conclusions: NLR may be a cost-effective and novel preoperatively usable biomarker in patients with meningiomas.
Language	English
Publishing date	2020-11-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2020.592470
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Article ; Online: Recent advances in research on nitrergic nerve-mediated vasodilatation.

Toda, Noboru / Okamura, Tomio

Pflugers Archiv : European journal of physiology

2014 Volume 467, Issue 6, Page(s) 1165–1178

Abstract: Cerebral vascular resistance and blood flow were widely considered to be regulated solely by tonic innervation of vasoconstrictor adrenergic nerves. However, pieces of evidence suggesting that parasympathetic nitrergic nerve activation elicits ... ...

Abstract	Cerebral vascular resistance and blood flow were widely considered to be regulated solely by tonic innervation of vasoconstrictor adrenergic nerves. However, pieces of evidence suggesting that parasympathetic nitrergic nerve activation elicits vasodilatation in dog and monkey cerebral arteries were found in 1990. Nitric oxide (NO) as a neurotransmitter liberated from parasympathetic postganglionic neurons decreases cerebral vascular tone and resistance and increases cerebral blood flow, which overcome vasoconstrictor responses to norepinephrine liberated from adrenergic nerves. Functional roles of nitrergic vasodilator nerves are found also in peripheral vasculature, including pulmonary, renal, mesenteric, hepatic, ocular, uterine, nasal, skeletal muscle, and cutaneous arteries and veins; however, adrenergic nerve-induced vasoconstriction is evidently greater than nitrergic vasodilatation in these vasculatures. In coronary arteries, neurogenic NO-mediated vasodilatation is not clearly noted; however, vasodilatation is induced by norepinephrine released from adrenergic nerves that activates β1-adrenoceptors. Impaired actions of NO liberated from the endothelium and nitrergic neurons are suggested to participate in cerebral hypoperfusion, leading to brain dysfunction, like that in Alzheimer's disease. Nitrergic neural dysfunction participates in impaired circulation in peripheral organs and tissues and also in systemic blood pressure increase. NO and vasodilator peptides, as sensory neuromediators, are involved in neurogenic vasodilatation in the skin. Functioning of nitrergic vasodilator nerves is evidenced not only in a variety of mammals, including humans and monkeys, but also in non-mammals. The present review article includes recent advances in research on the functional importance of nitrergic nerves concerning the control of cerebral blood flow, as well as other regions, and vascular resistance. Although information is still insufficient, the nitrergic nerve histology and function in vasculatures of non-mammals are also summarized.
MeSH term(s)	Animals ; Humans ; Muscle, Smooth, Vascular/innervation ; Muscle, Smooth, Vascular/metabolism ; Muscle, Smooth, Vascular/physiology ; Nitrergic Neurons/metabolism ; Nitrergic Neurons/physiology ; Nitric Oxide/metabolism ; Vasodilation
Chemical Substances	Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2014-10-23
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-014-1621-0
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Article ; Online: How mental stress affects endothelial function.

Toda, Noboru / Nakanishi-Toda, Megumi

Pflugers Archiv : European journal of physiology

2011 Volume 462, Issue 6, Page(s) 779–794

Abstract: Mental stress is an important factor contributing to recognized mechanisms underlying cardiovascular events. Among these, stress-related endothelial dysfunction is an early risk factor that predicts future development of severe cardiovascular disorders. ... ...

Abstract	Mental stress is an important factor contributing to recognized mechanisms underlying cardiovascular events. Among these, stress-related endothelial dysfunction is an early risk factor that predicts future development of severe cardiovascular disorders. Acute mental stress by a variety of tests impairs endothelial function in humans, although the opposite results have been reported by some investigators. Chronic stress always deteriorates endothelial function in humans and experimental animals. Stress hormones, such as glucocorticoids and pro-inflammatory cytokines, and endothelin-1 liberated in response to mental stress participate in endothelial dysfunction possibly via downregulation of endothelial nitric oxide synthase (eNOS) expression, eNOS inactivation, decreased nitric oxide (NO) actions, and increased NO degradation, together with vasoconstriction counteracting against NO-induced vasodilatation. Catecholamines do not directly affect endothelial function but impair its function when blood pressure elevation by the amines is sustained. Endogenous opioids favorably affect endothelial function, which counteract deteriorating effects of other stress hormones and mediators. Inhibition of cortisol and endothelin-1 production, prevention of pro-inflammatory mediator accumulation, hypnotics, mirthful laughter, humor orientation, and lifestyle modification would contribute to the prevention and treatment for stress-related endothelial dysfunction and future serious cardiovascular disease.
MeSH term(s)	Animals ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/physiopathology ; Catecholamines/metabolism ; Cytokines/metabolism ; Endothelin-1/metabolism ; Endothelium, Vascular/physiology ; Humans ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type III/metabolism ; Opioid Peptides/metabolism ; Risk Factors ; Stress, Psychological/complications
Chemical Substances	Catecholamines ; Cytokines ; Endothelin-1 ; Opioid Peptides ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
Language	English
Publishing date	2011-09-23
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-011-1022-6
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