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901.
Snake envenomation is a socio-medical problem of considerable magnitude. About 2.5 million people are bitten by snakes annually,
more than 100,000 fatally. However, although bites can be deadly, snake venom is a natural biological resource that contains
several components of potential therapeutic value. Venom has been used in the treatment of a variety of pathophysiological
conditions in Ayurveda, homeopathy and folk medicine. With the advent of biotechnology, the efficacy of such treatments has
been substantiated by purifying components of venom and delineating their therapeutic properties. This review will focus on
certain snake venom components and their applications in health and disease.
Received 6 July 2006; received after revision 14 August 2006; accepted 28 September 2006 相似文献
902.
Kramer J Böhrnsen F Lindner U Behrens P Schlenke P Rohwedel J 《Cellular and molecular life sciences : CMLS》2006,63(5):616-626
Microfracture of subchondral bone results in intrinsic repair of cartilage defects. Stem or progenitor cells from bone marrow
have been proposed to be involved in this regenerative process. Here, we demonstrate for the first time that mesenchymal stem
(MS) cells can in fact be recovered from matrix material saturated with cells from bone marrow after microfracture. This also
introduces a new technique for MS cell isolation during arthroscopic treatment. MS cells were phenotyped using specific cell
surface antibodies. Differentiation of the MS cells into the adipogenic, chondrogenic and osteogenic lineage could be demonstrated
by cultivation of MS cells as a monolayer, as micromass bodies or mesenchymal microspheres. This study demonstrates that MS
cells can be attracted to a cartilage defect by guidance of a collagenous matrix after perforating subchondral bone. Protocols
for application of MS cells in restoration of cartilage tissue include an initial invasive biopsy to obtain the MS cells and
time-wasting in vitro proliferation and possibly differentiation of the cells before implantation. The new technique already includes attraction
of MS cells to sites of cartilage defects and therefore may overcome the necessity of in vitro proliferation and differentiation of MS cells prior to transplantation.
Received 3 November 2005; received after revision 15 December 2005; accepted 4 January 2006 相似文献
903.
Myelin basic protein: a multifunctional protein 总被引:1,自引:1,他引:0
Boggs JM 《Cellular and molecular life sciences : CMLS》2006,63(17):1945-1961
Myelin basic protein (MBP), the second most abundant protein in central nervous system myelin, is responsible for adhesion
of the cytosolic surfaces of multilayered compact myelin. A member of the ‘intrinsically disordered’ or conformationally adaptable
protein family, it also appears to have several other functions. It can interact with a number of polyanionic proteins including
actin, tubulin, Ca2+-calmodulin, and clathrin, and negatively charged lipids, and acquires structure on binding to them. It may act as a membrane
actin-binding protein, which might allow it to participate in transmission of extracellular signals to the cytoskeleton in
oligodendrocytes and tight junctions in myelin. Some size isoforms of MBP are transported into the nucleus and thus they may
also bind polynucleotides. Extracellular signals received by myelin or cultured oligodendrocytes cause changes in phosphorylation
of MBP, suggesting that MBP is also involved in signaling. Further study of this very abundant protein will reveal how it
is utilized by the oligodendrocyte and myelin for different purposes.
Received 2 March 2006; received after revision 12 April 2006; accepted 16 May 2006 相似文献
904.
Phytanic acid is a branched-chain fatty acid that accumulates in a variety of metabolic disorders. High levels of phytanic
acid found in patients can exceed the millimolar range and lead to severe symptoms. Degradation of phytanic acid takes place
by α-oxidation inside the peroxisome. A deficiency of its breakdown, leading to elevated levels, can result from either a
general peroxisomal dysfunction or from a defect in one of the enzymes involved in α-oxidation. Research on Refsum disease,
belonging to the latter group of disorders and characterized by a deficiency of the first enzyme of α-oxidation, has extended
our knowledge of phytanic acid metabolism and pathology of the disease greatly over the past few decades. This review will
centre on this research on phytanic acid: its origin, the mechanism by which its α-oxidation takes place, its role in human
disease and the way it is produced from phytol.
Received 4 October 2005; received after revision 24 February 2006; accepted 26 April 2006 相似文献
905.
McTaggart SJ 《Cellular and molecular life sciences : CMLS》2006,63(3):255-267
Isoprenoids are synthesized in all living organisms and are incorporated into diverse classes of end-products that participate
in a multitude of cellular processes relating to cell growth, differentiation, cytoskeletal function and vesicle trafficking.
In humans, the non-sterol isoprenoids, farnesyl pyrophosphate and geranylgeranyl-pyrophosphate, are synthesized via the mevalonate
pathway and are covalently added to members of the small G protein superfamily. Isoprenylated proteins have key roles in membrane
attachment and protein functionality, have been shown to have a central role in some cancers and are likely also to be involved
in the pathogenesis and progression of atherosclerosis and Alzheimer disease. This review details current knowledge on the
biosynthesis of isoprenoids, their incorporation into proteins by the process known as prenylation and the complex regulatory
network that controls these proteins. An improved understanding of these processe is likely to lead to the development of
novel therapies that will have important implications for human health and disease.
Received 5 July 2005; received after revision 17 October 2005; accepted 22 October 2005 相似文献
906.
907.
Sayer JA Otto EA O'Toole JF Nurnberg G Kennedy MA Becker C Hennies HC Helou J Attanasio M Fausett BV Utsch B Khanna H Liu Y Drummond I Kawakami I Kusakabe T Tsuda M Ma L Lee H Larson RG Allen SJ Wilkinson CJ Nigg EA Shou C Lillo C Williams DS Hoppe B Kemper MJ Neuhaus T Parisi MA Glass IA Petry M Kispert A Gloy J Ganner A Walz G Zhu X Goldman D Nurnberg P Swaroop A Leroux MR Hildebrandt F 《Nature genetics》2006,38(6):674-681
908.
Truncating mutations in the Fanconi anemia J gene BRIP1 are low-penetrance breast cancer susceptibility alleles 总被引:21,自引:0,他引:21
Seal S Thompson D Renwick A Elliott A Kelly P Barfoot R Chagtai T Jayatilake H Ahmed M Spanova K North B McGuffog L Evans DG Eccles D;Breast Cancer Susceptibility Collaboration 《Nature genetics》2006,38(11):1239-1241
We identified constitutional truncating mutations of the BRCA1-interacting helicase BRIP1 in 9/1,212 individuals with breast cancer from BRCA1/BRCA2 mutation-negative families but in only 2/2,081 controls (P = 0.0030), and we estimate that BRIP1 mutations confer a relative risk of breast cancer of 2.0 (95% confidence interval = 1.2-3.2, P = 0.012). Biallelic BRIP1 mutations were recently shown to cause Fanconi anemia complementation group J. Thus, inactivating truncating mutations of BRIP1, similar to those in BRCA2, cause Fanconi anemia in biallelic carriers and confer susceptibility to breast cancer in monoallelic carriers. 相似文献
909.
910.
Recent experience with several high-profile drugs demonstrates the great challenges in developing effective and safe therapeutics. A complementary approach to the popular paradigm of disease genetics is based on inherited factors that reduce the incidence and severity of disease among individuals who are genetically predisposed to disease. We propose testing specifically for modifier genes and protective alleles among at-risk individuals and studying the efficacy of therapeutics based on the genetics of health. 相似文献