Bioscience hypotheses最新文献

Glial response to polyglutamine-mediated stress 神经胶质对多谷氨酰胺介导的应激反应

Bioscience hypotheses Pub Date : 2009-01-01 DOI: 10.1016/j.bihy.2008.12.006

Parminder J.S. Vig, Qingmei Shao, Maripar E. Lopez

引用次数: 1

Regional health and function in the hippocampus: Evolutionary compromises for a critical brain region 海马体的区域健康和功能:一个关键大脑区域的进化妥协

Bioscience hypotheses Pub Date : 2009-01-01 DOI: 10.1016/j.bihy.2009.02.013

Travis C. Jackson, Thomas C. Foster

引用次数: 15

May astrocyte-elevated gene-1 is a novel predictor of poor prognosis for cancer patients? 星形胶质细胞升高基因-1可能是癌症患者预后不良的新预测因子吗?

Bioscience hypotheses Pub Date : 2009-01-01 DOI: 10.1016/j.bihy.2008.10.016

Haiyan Liu , Li Xie , Ruopeng Sun

{"title":"May astrocyte-elevated gene-1 is a novel predictor of poor prognosis for cancer patients?","authors":"Haiyan Liu , Li Xie , Ruopeng Sun","doi":"10.1016/j.bihy.2008.10.016","DOIUrl":"10.1016/j.bihy.2008.10.016","url":null,"abstract":"<div>Astrocyte-elevated gene-1 was cloned as a human immunodeficiency virus-1-inducible and tumor necrosis factor-α-inducible transcript in primary human fetal astrocytes by a rapid subtraction hybridization approach. Astrocyte-elevated gene-1 down-regulates the expression of the glutamate transporter excitatory amino acid transporter 2, thus, it is implicated in glutamate-induced excitotoxic damage to neurons as evident in human immunodeficiency virus-associated neurodegeneration. However, accumulating evidences imply that astrocyte-elevated gene-1 might play a pivotal role in the pathogenesis, progression and metastasis of diverse cancers. Astrocyte-elevated gene-1 expression is elevated in diverse cancers, overexpression of astrocyte-elevated gene-1 increases while siRNA inhibition of astrocyte-elevated gene-1 decreases migration and invasion of cancer cells, respectively. Astrocyte-elevated gene-1 exerts its effects by activating the nuclear factor kappa B pathway, the oncogenic Ha-ras could up-regulate astrocyte-elevated gene-1 expression by inducing the binding of c-Myc to the astrocyte-elevated gene-1 promoter and astrocyte-elevated gene-1 inhibited prostate cancer progression through up-regulation of FOXO3a activity. These provocative findings are intensifying interest in astrocyte-elevated gene-1 as a crucial regulator of tumor progression and metastasis and as a potential mediator of neurodegeneration. The evidences to show the expression of astrocyte-elevated gene-1 in breast cancer and its correlation with clinicopathologic features, including the survival of patients with breast cancer confirm the hypotheses that astrocyte-elevated gene-1 is a novel predictor of poor prognosis for cancer patients.</div>","PeriodicalId":87894,"journal":{"name":"Bioscience hypotheses","volume":"2 2","pages":"Pages 78-80"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.bihy.2008.10.016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72466374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The involvement of Nrf2-mediated antioxidant defense in neurovascular protection by activated protein C Nrf2介导的抗氧化防御在活化蛋白C保护神经血管中的作用

Bioscience hypotheses Pub Date : 2009-01-01 DOI: 10.1016/j.bihy.2008.09.007

Kursad Genc

引用次数: 0

Disorder of Cytochrome P450 expression is inducible by gold nanoparticles? 金纳米粒子可诱导细胞色素P450表达紊乱？

Bioscience hypotheses Pub Date : 2009-01-01 DOI: 10.1016/j.bihy.2009.03.006

Warangkana Warisnoicharoen , Ladear Wangcharoenrung

引用次数: 0

Do free fatty acids induce insulin resistance in alpha cells? 游离脂肪酸诱导α细胞胰岛素抵抗吗?

Bioscience hypotheses Pub Date : 2009-01-01 DOI: 10.1016/j.bihy.2008.02.015

Li Hong-Liang, Yang Wen-Ying, Xiao Jian-Zhong, Du Rui-Qin, Hong Jing, Pan Lin, Li Guang-Wei

{"title":"Do free fatty acids induce insulin resistance in alpha cells?","authors":"Li Hong-Liang, Yang Wen-Ying, Xiao Jian-Zhong, Du Rui-Qin, Hong Jing, Pan Lin, Li Guang-Wei","doi":"10.1016/j.bihy.2008.02.015","DOIUrl":"10.1016/j.bihy.2008.02.015","url":null,"abstract":"<div>Thirty years ago, Unger and Orci proposed the bihormonal-abnormality hypothesis, which highlighted that both deficient insulin secretion and excessive glucagon levels contributed to the hyperglycemic state in type 2 diabetes. The plasma free fatty acid (FFAs) concentrations are higher in patients with diabetes and prediabetes, suggesting that FFAs may be involved in the pathophysiology of diabetes. In type 2 diabetes, at least in the obese form, insulin does not seem to correct the exaggerated alpha cell responses. This phenomenon suggests that the inability of insulin to suppress the glucagon level could be caused by alpha cell insulin resistance. However, it has remained unclear whether alpha cell insulin resistance is caused by FFAs. Recent studies have demonstrated that long-term exposure to elevated FFA levels leads to hypersecretion of glucagon and accumulation of triglycerides (TG) in clonal alpha-TC1-6 cells, but the mechanism of FFA-induced alpha cell insulin resistance is unclear. We hypothesize that long-term exposure to FFAs reduces AMP-activated protein kinase (AMPK) activity and increases TG accumulation in alpha cells, leading to impaired insulin signaling of alpha cells and hypersecretion of glucagon. This hypothesis provides the first detailed examination of the effects of FFAs on alpha cells with glucagon hypersecretion. It potentially suggests that improving alpha cell insulin resistance as well as reversing lipotoxicity will normalize alpha cell function and may benefit glucose control. Consequently, AMPK and insulin-related pathways in alpha cells could be potential targets for controlling glucagon secretion and glucose counter-regulation.</div>","PeriodicalId":87894,"journal":{"name":"Bioscience hypotheses","volume":"2 1","pages":"Pages 19-23"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.bihy.2008.02.015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84580788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

BMP-7: Therapeutic target for ocular fibrotic disorders BMP-7:眼部纤维化疾病的治疗靶点

Bioscience hypotheses Pub Date : 2009-01-01 DOI: 10.1016/j.bihy.2009.02.012

Jun-Yi Wang, Guo-ge Han, Jing Wang, Hai-Feng Mei, An-Huai Yang

{"title":"BMP-7: Therapeutic target for ocular fibrotic disorders","authors":"Jun-Yi Wang, Guo-ge Han, Jing Wang, Hai-Feng Mei, An-Huai Yang","doi":"10.1016/j.bihy.2009.02.012","DOIUrl":"10.1016/j.bihy.2009.02.012","url":null,"abstract":"<div>Scarring of cornea, glaucoma, after-cataract and also proliferative vitreoretinopathy(PVR) related tractional retina detachment, age related macular degeneration and diabetic retinopathy etc., which are the major and seriously impair vision diseases in eyes, with various appearance and different therapy method, but maybe they have the similar pathogenesis—fibrosis, and all the above ocular diseases can be regarded as fibrotic disorders. Thus inhibition of the fibrotic process may provide a potentially novel therapeutic approach to the treatment of these ocular diseases mentioned above. Now numerous studies have proved that BMP-7 significantly reversed renal, hepatic, pulmonary fibrosis, including inhibition of Transforming growth factor-β (TGF-β) production, suppression of epithelial-to-mesenchymal transition (EMT), and repair of severely damaged epithelial cells. So it is reasonable to refer that BMP-7 may have the same preventive effect in these ocular fibrotic disorders. A potential clinical therapy can be developed by using the anti-fibrosis effect of BMP-7.</div>","PeriodicalId":87894,"journal":{"name":"Bioscience hypotheses","volume":"2 6","pages":"Pages 413-416"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.bihy.2009.02.012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86051656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Double effects of red light on the development of myopia 红光对近视发展的双重影响

Bioscience hypotheses Pub Date : 2009-01-01 DOI: 10.1016/j.bihy.2009.06.003

Jia Huang , Bai-chuan Jiang , Ren-yuan Chu , Xiao-mei Qu

引用次数: 0

The progression of type 2 diabetes: Partly caused by deficiency of ASP-C5L2 pathway? 2型糖尿病的进展:部分原因是ASP-C5L2通路缺乏?

Bioscience hypotheses Pub Date : 2009-01-01 DOI: 10.1016/j.bihy.2009.05.003

Wenlong Li, Rutai Hui

引用次数: 0

Why homocysteine-lowering therapy does not have beneficial effects on patients with cardiovascular disease? 为什么降低同型半胱氨酸治疗对心血管疾病患者没有有益效果?

Bioscience hypotheses Pub Date : 2009-01-01 DOI: 10.1016/j.bihy.2008.10.007

Jamal Shamsara , Mohammad Ramezani , Amir Hooshang Mohammadpoor

{"title":"Why homocysteine-lowering therapy does not have beneficial effects on patients with cardiovascular disease?","authors":"Jamal Shamsara , Mohammad Ramezani , Amir Hooshang Mohammadpoor","doi":"10.1016/j.bihy.2008.10.007","DOIUrl":"10.1016/j.bihy.2008.10.007","url":null,"abstract":"<div>Homocysteine is a sulfur-containing amino acid produced during the metabolism of methionine and elevated plasma levels of homocysteine have been linked to an increased risk of atherosclerosis and cardiovascular ischemic events by numerous authors. Several mechanisms by which elevated homocysteine impairs vascular function have been proposed including impairment of endothelial function and at least some of those mechanisms are induced via homocysteine-associated DNA hypomethylation. Oral administration of folic acid and B vitamins, required for remethylation of homocysteine to methionine, decreased plasma total homocysteine levels but clinical trials using folic acid and B vitamins did not confirm that the decreased plasma levels of homocysteine through diet or drugs may be paralleled by a reduction in cardiovascular risk. In our view a plausible explanation for the discordance between the epidemiologic studies and the results of the clinical trials may be related to the homocysteine-associated global DNA hypomethylation which cannot easily be reversed by homocysteine-lowering therapy.</div>","PeriodicalId":87894,"journal":{"name":"Bioscience hypotheses","volume":"2 1","pages":"Pages 13-15"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.bihy.2008.10.007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83866684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2