Publications by authors named "Toshiyuki Kobayashi"

ApcMin/+ mouse was a model mouse for human familial adenomatous polyposis, and irradiation at an early age increases tumors in the small and large intestine. To study the effects of antioxidant administration on tumor incidence after continuous whole-body exposure to gamma rays, ApcMin/+ mice were exposed to a medium-dose-rate, 200 mGy/d, from postnatal Day 0 to 21 of age or a high-dose-rate of 0.65 Gy/min (total dose 4.

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The present work investigates the long-term effects of continuous low dose-rate (20 mGy/day to total doses of 1-8 Gy) gamma-ray exposure on the hematopoietic cells of specific pathogen-free C3H/HeN mice. Peripheral white blood cell (WBC) counts decreased on days 206, 471, and 486, with no significant changes in red blood cell (RBC) and platelet (PLT) counts. The number of colony forming units (CFU-S and CFU-GM) in the bone marrow and spleen from irradiated mice decreased with increasing total dose on day-12 and day-7.

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Article Synopsis
  • - The Institute for Radiological Science, QST, and IES have conducted significant animal experiments to analyze radiation risks related to life expectancy and cancer rates.
  • - Due to economic, practical, and ethical challenges, there's a need to store data and biological samples from these experiments for future research and sharing.
  • - QST/NIRS has created J-SHARE, an archive to store and promote collaboration on radiation biology research, and aims to integrate data and tissue specimens from IES to enhance knowledge on radiation risk assessment and protection.
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Background: Along with the improved prognosis of patients with congenital heart disease, the associated diverse complications are under scrutiny. Due to various medical restrictions on their upbringing, patients with congenital heart disease often have coexisting mental disorders. However, reports on patients with congenital heart disease and coexisting eating disorders are rare.

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In the 1960s and 1970s, there was widespread discussion in Japan about the pathological experience of "unpleasant odors emanating from one's body." This symptom is called "Jikoshu," and this term was used in combination with various words, such as "Genkaku" (hallucination) and "Moso" (delusion), reflecting its symptomatological ambiguity. The best-known term in the English-language literature is ( phobia).

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Recently, there has been a high demand for elucidating kinetics and visualizing reaction processes under extreme dynamic conditions, such as chemical reactions under meteorite impact conditions, structural changes under nonequilibrium conditions, and in situ observations of dynamic changes. To accelerate material science studies and Earth science fields under dynamic conditions, a submillisecond in situ X-ray diffraction measurement system has been developed using a diamond anvil cell to observe reaction processes under rapidly changing pressure and temperature conditions replicating extreme dynamic conditions. The development and measurements were performed at the high-pressure beamline BL10XU/SPring-8 by synchronizing a high-speed hybrid pixel array detector, laser heating and temperature measurement system, and gas-pressure control system that enables remote and rapid pressure changes using the diamond anvil cell.

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Tuberous sclerosis complex (TSC) is an intractable inherited disease caused by a germline mutation in either the TSC complex subunit 1 () or tumor suppressor genes. Recent progress in the treatment of TSC with rapamycin has provided benefits to patients with TSC. However, the complete elimination of tumors is difficult to achieve as regrowth often occurs after a drug is suspended; thus, more efficient medication and novel therapeutic targets are required.

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Objectives: ERC/mesothelin is a glycosylphosphatidylinositol (GPI)-anchor protein expressed in mesothelioma. A precursor protein is cleaved by proteases and an N-terminal fragment (N-ERC) is extracellularly secreted. A remaining C-terminal fragment (C-ERC) is tethered on cellular membranes by the GPI-anchor, but C-ERC is also released after cleavage by proteases.

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The tuberous sclerosis complex (TSC) gene products (TSC1/TSC2) negatively regulate mTORC1. Although mTORC1 inhibitors are used for the treatment of TSC, incomplete tumor elimination and the adverse effects from long-term administration are problems that need to be solved. Branched-chain amino acid (BCAA) metabolism is involved in the growth of many tumor cells via the mTORC1 pathway.

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Background: Tuberous sclerosis complex (TSC) is an autosomal dominant disorder that is associated with neurological symptoms, including autism spectrum disorder. Tuberous sclerosis complex is caused by pathogenic germline mutations of either the TSC1 or TSC2 gene, but somatic mutations were identified in both genes, and the combined effects of TSC1 and TSC2 mutations have been unknown.

Methods: The present study investigated social behaviors by the social interaction test and three-chambered sociability tests, effects of rapamycin treatment, and gene expression profiles with a gene expression microarray in Tsc1 and Tsc2 double heterozygous mutant (TscD) mice.

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This article introduces the concept proposed by the eminent second-generation Japanese psychopathologist Tadao Miyamoto in 1992 that the manic-depressive mixed state is the basic psychopathology of manic-depressive illness. When Kraepelin first established the dichotomy between schizophrenia and manic-depressive illness, mania and depression were placed in a symmetrical relationship. Now, in Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), manic-depressive illness is divided into two distinct categories: bipolar and related disorders, and depressive disorders.

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Objective: Electroconvulsive therapy (ECT) is an effective treatment of major depressive disorder (MDD). However, high relapse rates after ECT represent clinical problems. To date, influence of number of ECT sessions on relapse rate remains to be elucidated.

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Tuberous sclerosis complex (TSC) is caused by mutations in or , whose gene products inhibit the small G-protein Rheb1. Rheb1 activates mTORC1, which may cause refractory epilepsy, intellectual disability, and autism. The mTORC1 inhibitors have been used for TSC patients with intractable epilepsy.

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Background: In transmediastinal esophagectomy (TME) with equivalent lymphadenectomy to transthoracic procedure, an understanding of surgical anatomy in the deep mediastinum near the aortic arch or tracheal bifurcation is essential for the safe procedure. The present study aimed to evaluate the bronchial arteries (BAs) with preoperative 3D-CT in TME.

Methods: Seventy-nine patients with thoracic esophageal cancer undergoing TME were examined by preoperative 3D-CT to evaluate BA variations in the number, branching pattern, and mediastinal course.

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A 59-year-old woman's father and paternal grandmother died of colorectal cancer and her paternal uncle died of pancreatic cancer. She was positive for fecal occult blood and underwent colonoscopy. The colonoscopy revealed a type 0-Ⅱa+ Ⅱc lesion in the transverse colon suspected to be submucosal deep invasion, and the biopsy revealed poorly differentiated adenocarcinoma.

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Malignant mesothelioma (MM) is an aggressive tumor that typically develops after a long latency following asbestos exposure. Although mechanistic target of rapamycin complex 1 (mTORC1) activation enhances MM cell growth, the mTORC1 inhibitor everolimus has shown limited efficacy in clinical trials of MM patients. We explored the mechanism underlying mTORC1 activation in MM cells and its effects on cell proliferation and progression.

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Article Synopsis
  • A case involving a 77-year-old man with type 2 diabetes showed that after starting suvorexant for insomnia, he developed hyponatremia that met SIADH criteria.
  • After discontinuing suvorexant, his hyponatremia improved within six days, highlighting the need for clinicians to monitor for SIADH as a possible side effect of this medication.
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Malignant mesothelioma (MM) is an aggressive malignant neoplasm which rapidly invades pleural tissues and has a poor prognosis. Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM. The level of CES2 mRNA was greatly increased on treatment with nutlin-3a.

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Ionizing radiation can damage DNA and, therefore, is a risk factor for cancer. Eker rats, which carry a heterozygous germline mutation in the tumor-suppressor gene tuberous sclerosis complex 2 (Tsc2), are susceptible to radiation-induced renal carcinogenesis. However, the molecular mechanisms involved in Tsc2 inactivation are unclear.

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Article Synopsis
  • - Lupus nephritis (LN) is a type of kidney inflammation linked to systemic lupus erythematosus (SLE) and is associated with immune complex issues, while antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis (AAV) leads to serious conditions like lung hemorrhage and kidney failure.
  • - Research has identified specific genetic factors related to AAV using a mouse model (SCG/Kj) that mimics human AAV, by creating congenic mice to study the roles of these genetic traits.
  • - The study found that B6/lpr mice, a kind of congenic model, displayed symptoms of glomerulonephritis and vasculitis
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Case 1 was that of a 65-year-old woman. Radical esophagectomy was performed after neoadjuvant chemotherapy(NAC) for lower thoracic esophageal cancer. Nineteen months after surgery, local recurrence was indicated on the dorsal side of the descending aorta.

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A 68-year-old man was diagnosed with esophagogastric junction adenocarcinoma, cT4a(SE)N3aM0, cStage Ⅲ. Because "bulky N" was present, he was administered 2 courses of preoperative chemotherapy containing S-1 plus oxaliplatin(SOX). Both the primary tumor and enlarged lymph nodes had greatly decreased in size following chemotherapy, and total gastrectomy and lower esophagectomy with D2 lymphadenectomy were then performed.

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The mammalian target of rapamycin (mTOR) signaling pathway plays a crucial role in cell metabolism, growth, and proliferation. The overactivation of mTOR has been implicated in the pathogenesis of syndromic autism spectrum disorder (ASD), such as tuberous sclerosis complex (TSC). Treatment with the mTOR inhibitor rapamycin improved social interaction deficits in mouse models of TSC.

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