This product is freeze dried. All water molecules have been removed.
Every lot is tried & tested in a relevant biological assay.
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- Olianas, M.C. et al. (2000) Br. J. Pharmacol. 131, 447.
- Alomone Labs Muscarinic Toxin 7 inhibits Carbachol-evoked [Ca2+]in increase in M1R-expressing C6 cells.Cells were loaded with Fluo-3 AM and pre-incubated for 20 min with control or with 25 nM and 100 nM Muscarinic Toxin 7 (#STM-200), as indicated, and stimulated with 100 µM Carbachol (arrow). Changes in intracellular Ca2+ were detected as changes in Fluo-3 emission following stimulation.
- 1. Felder, C.C. et al. (2000) J. Med. Chem. 43, 4333.
- 2. Forsythe, S.M. et al. (2002) Am. J. Respir. Cell. Mol. Biol. 26, 298.
- 3. Ferreira, A.R. et al. (2003) Pharmacol. Biochem. Behav. 74, 411.
- 4. Van der Zee, E.A. et al. (1999) Prog. Neurol. 58, 409.
- 5. Adem, A. and Karlsson, E. (1997) Life Sci. 60, 1069.
- 6. Olianas, M.C. et al. (2000) Br. J. Pharmacol. 131, 447.
- 7. Kukkonen, A. et al. (2004) J. Biol. Chem. 279, 50923.
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The action of the neurotransmitter acetylcholine (Ach) is mediated through two types of receptors, the ionotropic nicotinic receptors and the metabotropic muscarinic receptors. The muscarinic receptors belong to the superfamily of G-protein coupled receptors. Five subtypes of muscarinic receptors have been cloned: m1-m51,2.
The muscarinic receptors are widely distributed throughout the body, but are predominantly expressed within the parasympathetic nervous system and exert both excitatory and inhibitory control over central and peripheral tissues1,2.
Muscarinic receptors participate in a number of physiological functions such as regulation of heart rate, muscle contraction, cognition, sensory processing and motor control1. They also participate in learning and memory processing3,4.
Muscarinic Toxin 7 is a 65 amino acid peptide toxin isolated from the Dendroaspis angusticeps (Eastern green mamba)5. It was first found to inhibit M1 muscarinic receptors stably transfected in CHO cells at very low concentrations (1-30 nM)6 and acts as a non-competitive antagonist by binding to an allosteric site6.
Muscarinic Toxin 7 binding studies using a M1 and M3 chimera demonstrated that the high affinity of Muscarinic Toxin 7 towards M1 receptor is due to only three residues located in the 2nd and 3rd extracellular loops of the receptor7.
Muscarinic Toxin 7 (#STM-200) is a highly pure, synthetic, and biologically active peptide toxin.
ebiomall.com
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1.若都为正常,那么并未有太大问题,只要定期复查就可以了。
2.如果TGAb、TMAb、甲状腺功能均高,那么就是桥本氏甲状腺炎并甲亢,需要抗甲亢治疗。
3.如果TGAb、TMAb高,甲状腺功能下降,那么就是桥本氏甲状腺炎并甲减,需要进行甲减治疗。
4.如果TGAb、TMAb高,甲状腺功能正常,那么就是桥本氏甲状腺炎,无需特殊治疗,只要定期复查甲状腺功能就可能以了,不过这种情况有可能以后演变成甲减或者甲亢。
1.若都为正常,那么并未有太大问题,只要定期复查就可以了。
2.如果TGAb、TMAb、甲状腺功能均高,那么就是桥本氏甲状腺炎并甲亢,需要抗甲亢治疗。
3.如果TGAb、TMAb高,甲状腺功能下降,那么就是桥本氏甲状腺炎并甲减,需要进行甲减治疗。
4.如果TGAb、TMAb高,甲状腺功能正常,那么就是桥本氏甲状腺炎,无需特殊治疗,只要定期复查甲状腺功能就可能以了,不过这种情况有可能以后演变成甲减或者甲亢。
请问这个图是怎么做出来的?
辣根过氧化物酶+DAB显色和免疫荧光染色可以同时在一张脑片里面做吗?
具体是先DAB显色还是先染荧光一抗二抗呢,具体实验步骤是怎样的呢?
第一张图是往血管里打入辣根过氧化物酶,后DAB显色,DIC成像
第二张图是萤光图
1.若都为正常,那么并未有太大问题,只要定期复查就可以了。
2.如果TGAb、TMAb、甲状腺功能均高,那么就是桥本氏甲状腺炎并甲亢,需要抗甲亢治疗。
3.如果TGAb、TMAb高,甲状腺功能下降,那么就是桥本氏甲状腺炎并甲减,需要进行甲减治疗。
4.如果TGAb、TMAb高,甲状腺功能正常,那么就是桥本氏甲状腺炎,无需特殊治疗,只要定期复查甲状腺功能就可能以了,不过这种情况有可能以后演变成甲减或者甲亢。
(Hypertension,2004,43:297-305)
2月5日 过氧化物酶体增生物激活受体γ(PPARγ)是一种属于核激素受体超家族的配体激活转录因子。在巨噬细胞、内皮细胞和血管平滑肌细胞中均有表达。它调节与脂质代谢、血管炎症和促成动脉粥样硬化及血管成形术后再狭窄的增生有关的主要蛋白的基因表达。PPARγ合成配体的发现加深了人们对其配体依赖性激活和之后的生物效应机制的认识,特别是有关PPARγ在血管病理生理学中作用的认识。噻唑烷二酮PPARγ激动剂不仅改善了2型糖尿病患者的胰岛素耐药性,而且在离体情况下或动脉粥样硬化动物模型中均有广谱的抗动脉粥样硬化效应。
美国加州大学洛杉矶分校的Willa A. Hsueh博士及其同事总结了PPARγ作为噻唑烷二酮分子靶点的重要作用以及在控制血管炎症和心血管系统增生方面的意义。
Peroxisome Proliferator-Activated Receptor: Implications for Cardiovascular Disease
Willa A. Hsueh; Dennis Bruemmer
From Division of Endocrinology, Diabetes, and Hypertension, David Geffen School of Medicine, University of California, Los Angeles.
Correspondence to Willa A. Hsueh, Division of Endocrinology, Diabetes, and Hypertension, David Geffen School of Medicine, University of California, Los Angeles Warren Hall, Suite 24–130, 900 Veteran Avenue, Los Angeles, CA 90095. E-mail whsueh@mednet.ucla.edu
Abstract
Peroxisome proliferator-activated receptor(PPAR ) is a ligand-activated transcription factor belonging to the nuclear hormone receptor superfamily. PPARis expressed by macrophages, endothelial cells, and vascular smooth muscle cells. It regulates gene expression of key proteins involved in lipid metabolism, vascular inflammation, and proliferation contributing to atherogenesis and postangioplasty restenosis. The discovery of synthetic ligands for PPARhas led to significant enhancement of our understanding of the mechanism of their ligand-dependent activation and subsequent biological effects, particularly with respect to the role of PPARin vascular pathophysiology. The thiazolidinedione PPARagonists not only improve insulin resistance in patients with type II diabetes but also exert a broad spectrum of antiatherogenic effects in vitro and in animal models of atherosclerosis. In this review, we summarize the important role of PPARas a molecular target for thiazolidinediones and its implications for the control of vascular inflammation and proliferation for the cardiovascular system.
Key Words: atherosclerosis • diabetes mellitus • peroxisome proliferator-activated receptor • angiotensin • inflammation
相关链接:http://hyper.ahajournals.org/cgi/content/abstract/43/2/297?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=PPAR&searchid=1076561399333_3746&stored_search=&FIRSTINDEX=0&volume=43&issue=2&search_url=http%3A%2F%2Fhyper.ahajournals.org%2Fcgi%2Fsearch&journalcode=hypertensionaha
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