食物の環境効率指標の提案

The purpose of this study is to propose that the indices for the sustainability of food should be determined by the environmental efficiency which is the ratio of the Life Cycle carbon dioxide emission (environment load) of food and the total evaluation of food value. The environmental efficiency indices in the food research field are derived from dividing the evaluation of food value by the environment load. In the study, the environmental load (Life Cycle carbon dioxide emission) produced from cooking certain food and menu was compared with the food value obtained from them. The actual measurement of Life Cycle C02 emission of the food was conducted, and an ecoefficiency indices of food were calculated from quantified environmental load and food value evaluation. First, the evaluating factor of food was selected for the practical use of the environmental efficiency index. Its value was used as the numerator of the function for calculating the environmental efficiency. Next, food menu for evaluation was selected and created. Then, the environmental load was measured. The evaluating factor was assumed to be a nutritive evaluation of food. The nourishment evaluation items include energy, protein, lipid, calcium, iron, vitamin A, vitamin C, dietary fiber, salt, and vegetable. The denominator of the function for calculating the environmental efficiency is the environment load of the food. The environmental load was assumed by calculating C02 emissions per meal from the stages of producing, transporting, cooking and disposing. It became clear that the environmental efficiency indices provide important information in order to continue a sustainable food lifestyle as considering the environment without ruining health effect or taste of food

Genotoxic Stress Abrogates Renewal of Melanocyte Stem Cells by Triggering Their Differentiation

SummarySomatic stem cell depletion due to the accumulation of DNA damage has been implicated in the appearance of aging-related phenotypes. Hair graying, a typical sign of aging in mammals, is caused by the incomplete maintenance of melanocyte stem cells (MSCs) with age. Here, we report that irreparable DNA damage, as caused by ionizing radiation, abrogates renewal of MSCs in mice. Surprisingly, the DNA-damage response triggers MSC differentiation into mature melanocytes in the niche, rather than inducing their apoptosis or senescence. The resulting MSC depletion leads to irreversible hair graying. Furthermore, deficiency of Ataxia-telangiectasia mutated (ATM), a central transducer kinase of the DNA-damage response, sensitizes MSCs to ectopic differentiation, demonstrating that the kinase protects MSCs from their premature differentiation by functioning as a “stemness checkpoint” to maintain the stem cell quality and quantity

食パンのライフサイクルCO_2排出量

The purpose of this research decided to make the trial calculation of the C02 emissions in production of bread. The C02 emissions of the energy reason of the bread manufacturing process in a factory and a home were surveyed. The heat source of domestic oven has an electric formula and a gas type. Moreover, the C02 emissions of the automatic bread-baking machine UHome Bakery" were measured. As a result, C02 emissions were large when bread was baked in a domestic steam microwave oven and gas oven. It is thought that this difference is based on the size of the volume in a warehouse of oven. The C02 emissions in a factory, and in the case of a home bakery, it turned out that there is no big difference

Genotoxic stress abrogates renewal of melanocyte stem cells by triggering their differentiation.

金沢大学医薬保健研究域　医学系Somatic stem cell depletion due to the accumulation of DNA damage has been implicated in the appearance of aging-related phenotypes. Hair graying, a typical sign of aging in mammals, is caused by the incomplete maintenance of melanocyte stem cells (MSCs) with age. Here, we report that irreparable DNA damage, as caused by ionizing radiation, abrogates renewal of MSCs in mice. Surprisingly, the DNA-damage response triggers MSC differentiation into mature melanocytes in the niche, rather than inducing their apoptosis or senescence. The resulting MSC depletion leads to irreversible hair graying. Furthermore, deficiency of Ataxia-telangiectasia mutated (ATM), a central transducer kinase of the DNA-damage response, sensitizes MSCs to ectopic differentiation, demonstrating that the kinase protects MSCs from their premature differentiation by functioning as a "stemness checkpoint" to maintain the stem cell quality and quantity. © 2009 Elsevier Inc. All rights reserved

Nonbacterial thrombotic endocarditis associated with cancer of unknown origin complicated with thrombus in the left auricular appendage: case report

A 63-year-old man was admitted to our hospital with a complaint of right lateroabdominal pain. He was diagnosed with metastatic colon cancer, and then developed multiple brain embolic infarctions 7 days after admission. Transesophageal echocardiography showed that mobile, echo-dense masses were attached to the anterior and posterior mitral valve leaflet. Furthermore, there was a thrombus in the left auricular appendage despite sinus rhythm. These findings led to a diagnosis of suspected infectious endocarditis with subsequent multiple brain infarctions. The patient's general condition worsened and he died 13 days after admission. An autopsy was performed, and, while poorly differentiated cancer was observed in multiple organs, no primary tumor could be identified. Histological analysis showed that the masses of the mitral valve consisted mainly of fibrin without bacteria or oncocytes. This patient was therefore diagnosed with nonbacterial thrombotic endocarditis associated with cancer of unknown origin complicated with thrombus in the left auricular appendage

A Review of HPV-Related Head and Neck Cancer

Head and neck squamous cell carcinomas (HNSCCs) arise in the mucosal lining of the upper aerodigestive tract. Tobacco and alcohol use have been reported to be associated with HNSCC. Infection with high-risk human papillomaviruses (HPVs) has recently been implicated in the pathogenesis of HNSCCs. It is now widely accepted that high-risk HPV is a cause of almost all cervical cancers as well as some forms of HNSCCs. HPV-related HNSCCs are increasing. HPV-related HNSCCs and HPV-unrelated HNSCCs differ with respect to the molecular mechanisms underlying their oncogenic processes. HPV-related HNSCCs are known to have a better prognosis response to treatment as compared with HPV-unrelated HNSCCs. Therefore, in recent years, it has been required to accurately discriminate between HPV-related and HPV-unrelated HNSCCs. To diagnose the HPV-related HNSCCs, various methods including P16 immunohistochemistry, FISH, and genetic analyses of the HPV gene from histopathological and liquid biopsy specimens have been employed. Based on the results of the differential diagnosis, various treatments employing EGFR TKI and low-dose radiation have been employed. Here, we review the involvement of the HPV virus in HNSCCs as well as the molecular mechanism of carcinogenesis, classification, prognosis, diagnostic procedures, and therapy of the disease