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J Biol Chem. 2001 Mar 2;276(9):6169-76. Epub 2000 Nov 07.
The basic helix-loop-helix transcription factor HESR1 regulates endothelial cell tube formation.
Henderson AM, Wang SJ, Taylor AC, Aitkenhead M, Hughes CC.
Department of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California 92697, USA.
Human endothelial cells can be induced to form capillary-like tubular networks in collagen gels. We have used this in vitro model and representational difference analysis to identify genes involved in the formation of new blood vessels. HESR1 (HEY-1/HRT-1/CHF-2/gridlock), a basic helix-loop-helix protein related to the hairy/enhancer of split/HES family, is absent in migrating and proliferating cultures of endothelial cells but is rapidly induced during capillary-like network formation. HESR1 is detectable in all adult tissues and at high levels in well vascularized organs such as heart and brain. Its expression is also enriched in aorta and purified capillaries. Overexpression of HESR1 in endothelial cells down-regulates vascular endothelial cell growth factor receptor-2 (VEGFR2) mRNA levels and blocks proliferation, migration, and network formation. Interestingly, reduction of expression of HESR1 by antisense oligonucleotides also blocks endothelial cell network formation in vitro. Finally, HESR1 expression is altered in several breast, lung, and kidney tumors. These data are consistent with a temporal model for HESR1 action where down-regulation at the initiation of new vessel budding is required to allow VEGFR2-mediated migration and proliferation, but re-expression of HESR1 is necessary for induction of tubular network formation and continued maintenance of the mature, quiescent vessel.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11069914&dopt=Abstract
Biochim Biophys Acta. 2000 Nov 15;1502(3):330-6.
Myocardial carnitine and carnitine palmitoyltransferase deficiencies in patients with severe heart failure.
Martin MA, Gomez MA, Guillen F, Bornstein B, Campos Y, Rubio JC, de la Calzada CS, Arenas J.
Centro de Investigacion, Hospital Universitario 12 de Octubre, Madrid, Spain.
We studied myocardial tissue from 25 cardiac transplant recipients, who had end-stage congestive heart failure (CHF), and from 21 control donor hearts. Concentrations of total carnitine (TC), free carnitine (FC), short-chain acylcarnitines, long-chain acylcarnitines (LCAC) as well as carnitine palmitoyltransferase (CPT) activities were measured in myocardial tissue homogenates and referred to the concentration of non-collagen protein. Compared to controls, the concentrations of TC and FC as well as total CPT activities were significantly lower in patients. LCAC levels and the LCAC to FC ratio values were significantly greater in patients than in controls. While the malonyl-CoA sensitive fraction of CPT, which represents CPT I activity, was similar in patients and controls, the residual CPT activity after inhibition by malonyl-CoA, representing CPT II activity, was significantly reduced in patients compared to controls. Moreover, the activity of CPT in the presence of Triton X-100, which also represents the activity of CPT II, was significantly lower in patients than in controls. Malonyl-CoA concentrations required for half-maximal inhibition of CPT activity were significantly greater in patients than in controls. There was a linear relationship between ejection fraction (EF) values and concentrations of TC, FC, or total CPT activities. Values for LCAC and the LCAC to FC ratio were inversely related to EF values. We conclude that failing heart shows decreased total CPT and CPT II activities and carnitine deficiency that may be related to ventricle function.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11068176&dopt=Abstract
J Cell Sci. 2000 Dec;113 (Pt 23):4141-2.
Unconventional collagens
Knight DP.
Unconventional Collagens Types VI, VII, VIII, IX, X, XIV, XVI and XIX by S. Ricard-Blum, B. Dublet and M. van der Rest Oxford University Press (2000) pp.155. ISBN 0-19-850545-0 35.00 This thoroughly researched monograph in Oxford University Press's 'Protein Profile Series' reviews substantially all the significant literature on this interesting and highly important group of proteins. The authors use the term 'Unconventional Collagens' for the collagens of higher vertebrate connective tissues which do not, of themselves, form classical fibrils with a 68 nm banding pattern. The authors chose to omit type IV collagen as this, they claim, would have almost doubled the size of the volume. The monograph represents a very considerable achievement in three respects. Firstly it comprehensively reviews the literature on the sequence, structure, expression, post-translational modification, genetics, physiological function and pathology of each separate unconventional collagen. The thoroughness of this review is indicated by the fact that the bibliography contains no fewer than 1196 references. Secondly, the monograph identifies the modular domain structure for each collagen, clearly demonstrating that these proteins are block co-polymers mainly derived in evolution from a small number of ancestral genes. Thirdly, it starts to identify the way in which the different modules of these sticky molecules interact with each other and with other connective tissue components. This is an important start if we are to understand their vital role in the self-assembly processes which occur in embryology, tissue repair and the major degenerative and collagen gene diseases The clearly written and well set out text is supported by excellent micrographs of rotary shadowed molecules and molecular aggregates and a wealth of diagrams and tables. The book has, in my view, three minor shortcomings: a short summary chapter on type IV would enable the non-specialist reader to relate this collagen to the other non-conventional collagens. Concise summaries at the ends of each chapter would orient newcomers to the field. More significantly, apart from the brief introduction, the book lacks an overall synthesis which pulls together the findings of the separate chapters. These slight limitations aside, this book is essential reading for those engaged in connective tissue research and will do much to stimulate further activity in this area. It will also be of considerable interest to tissue engineers, pathologists and embryologists.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11069758&dopt=Abstract [PubMed - as supplied by publisher]
Rev Inst Med Trop Sao Paulo. 2002 Sep-Oct;44(5):273-8.
Quantitative analysis of cardiac lesions in chronic canine chagasic cardiomyopathy.
Caliari MV, do Pilar Machado R, de Lana M, Caja RA, Carneiro CM, Bahia MT, dos Santos CA, Magalhaes GA, Sampaio IB, Tafuri WL.
Departamento de Patologia Geral, Instituto de Ciencias Biologicas, Universidade Federal de Minas Gerais, 31270-901 Belo Horizonte, MG, Brasil. caliarcb.ufmg.br
Lesions observed in chronic chagasic cardiopathy frequently produce electrocardiographic alterations and affect cardiac function. Through a computerized morphometrical analysis we quantified the areas occupied by cardiac muscle, connective and adipose tissues in the right atrium of dogs experimentally infected with Trypanosoma cruzi. All of the infected dogs showed chronic myocarditis with variable reduction levels of cardiac muscle, fibrosis and adipose tissue replacement. In the atrial myocardium of dogs infected with Be78 and Be62 cardiac muscle represented 34 and 50%, fibrosis 28 and 32% and adipose tissue 38 and 18%, respectively. The fibrosis observed was both diffuse and focal and mostly intrafascicular, either partially or completely interrupting the path of muscle bundles. Such histological alterations probably contributed to the appearance of electrocardiographic disturbances verified in 10 out 11 dogs which are also common in human chronic chagasic cardiopathy. Fibrosis was the most important microscopic occurrence found since it produces rearrangements of collagen fibers in relation to myocardiocytes which causes changes in anatomical physiognomy and mechanical behavior of the myocardium. These abnormalities can contribute to the appearance of cardiac malfunction, arrythmias and congestive cardiac insufficiency as observed in two of the analyzed dogs. Strain Be78 caused destruction of atrial cardiac muscle higher than that induced by strain Be62.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12436168&dopt=Abstract
J Virol. 2000 Dec;74(23):11240-6.
Structural and functional analysis of the Xestia c-nigrum granulovirus matrix metalloproteinase.
Ko R, Okano K, Maeda S.
Laboratory of Molecular Entomology and Baculovirology, RIKEN, Wako, Saitama, Japan. krkail.ecc.u-tokyo.ac.jp
Sequence analysis of the Xestia c-nigrum granulovirus (XcGV) genome identified an open reading frame encoding a 469-amino-acid (54-kDa) protein with over 30% amino acid sequence identity to a region of about 150 amino acids that includes the catalytic domains of human stromelysin 1 (Str1)/matrix metalloproteinase 3 (MMP-3) (EC 3.4.24.17) and sea urchin hatching enzyme (HE). Stromelysin homologs have not been reported from baculoviruses or other viruses. Unlike human Str1 and sea urchin HE, the putative XcGV-MMP does not have a signal peptide and lacks the peptide motif involved in the cysteine switch that maintains other MMPs in an inactive form. The putative XcGV-MMP, however, possesses a conserved zinc-binding motif in its putative catalytic domain. The XcGV-MMP homolog was cloned, and a recombinant Bombyx mori nucleopolyhedrovirus (BmNPV) that expresses XcGV-MMP under the polyhedrin promoter was constructed. A distinct pattern of melanization was observed in B. mori larvae infected with MMP-expressing BmNPV. Fat body extracts from larvae overexpressing the 54-kDa recombinant MMP digested dye-impregnated collagen (Azocoll). The enzymatic activity was inhibited by two metalloproteinase inhibitors, EDTA and 1,10-phenanthroline. These results suggest that the XcGV MMP-3 gene homolog encodes a functional metalloproteinase.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11070022&dopt=Abstract
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