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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Gene Review

BDM  -  behavior disorder modifier

Homo sapiens

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Disease relevance of BDM

  • In the second group of eight patients followed for 13.9 +/- 2.1 months, the mean body weight decreased by 27 percent or 38.8 Kg., due to a 26.6 Kg. reduction in BF and a 13.0 Kg. decrease in the BDM [1].
  • During reperfusion following ischemia, shortening in early systole was markedly reduced to 16.5 +/- 2.9; BDM caused a similar reduction to 16.5 +/- 8 [2].
  • The Birth Defects Monitoring Programme (BDMP) is a nationwide surveillance system that monitors 1 million births per year, about a third of all births in the U.S. It relies on diagnoses from newborn discharge summaries to ascertain affected infants [3].
  • In both the state-based surveillance systems and BDMP, the annual rate of spina bifida for the total population declined during the period 1983-1990 [4].
  • BDMP data allowed analysis of rate trends for the four census regions of the United States. RESULTS: Data from both surveillance systems showed an approximate doubling of hypospadias rates in the 1970s and 1980s [5].
 

High impact information on BDM

  • In studies on the calcium current in the myocytes, addition of BDM was associated with reduced calcium current at any potential [6].
  • Maximal shortening velocity of ferret papillary muscles was increased in the presence of BDM from 1.55 +/- 0.24 to 2.04 +/- 0.33 mm/sec [6].
  • Our results indicate that BDM affects both calcium availability and responsiveness of the myofilaments to Ca2+ [6].
  • We selected a concentration of BDM that was not expected to affect sarcolemmal calcium flux and action potential duration in cardiac tissue [6].
  • In both cases, addition of BDM resulted in a reduction of peak intracellular calcium released from the sarcoplasmic reticulum and a reduction of peak twitch force [6].
 

Chemical compound and disease context of BDM

 

Biological context of BDM

  • In this manuscript, we present a novel protein acetylation prediction program named PAIL, prediction of acetylation on internal lysines, implemented in a BDM (Bayesian Discriminant Method) algorithm [7].
  • BDM (2,3 butanedione, 2 monoxime) treatment that inhibits chromosome movement and cytokinesis also altered myosin distributions in anaphase spindles and contractile rings, consistent with the physiological effects, suggesting also that myosin needs to be active in order to be properly distributed [8].
  • 1. Most of the shortening occurred during early diastole (53.0 +/- 6.8 for reperfusion, and 54.0 +/- 10.3 for BDM) [2].
  • This resulted in an increased bone turnover and decreased BDM after prolonged hemodialysis even though efforts were made to maintain the homeostasis of Ca and P metabolism in hemodialysis patients by using various therapeutic approaches [9].
  • Thus, our results showed that the BDMP cell was more fungicidal than a macrophage and up-regulated major histocompatibility complex type II and the CD86 costimulatory molecule with the production of proinflammatory cytokines [10].
 

Anatomical context of BDM

  • We investigated the effects of 1 and 3 mM 2,3-butanedione monoxime (BDM, diacetyl monoxime) on excitation and contraction of cardiac muscle in several types of preparations at various levels of organization [6].
  • In addition, the antagonists of actin-myosin contractility BDM and ML-7 provoked the dispersion of focal adhesions and the decrease of alpha-smooth muscle actin content in stress fibers of pulmonary fibroblasts, which constitutively show large focal adhesions and numerous stress fibers that contain alpha-smooth muscle actin [11].
  • BDM distorted dynamic I(M3) responses to sinusoidal length oscillations in a manner consistent with an increased cross-bridge contribution to total sarcomere compliance, rather than a changed S1 lever orientation in BDM [12].
  • It was previously demonstrated that an inhibitor of actin-myosin interaction, BDM (2,3-butanedione monoxime), suppresses myofibril formation in muscle cells in culture [13].
  • Based on these data, we decided to investigate the interaction of B-1-derived mononuclear phagocytes (BDMP) with C. neoformans to elucidate the possible influence of this cell in the progression of the disease [10].
 

Associations of BDM with chemical compounds

  • Inhibitors of ROK (dominant-negative ROK and Y-27632) and of the downstream target of ROK, myosin-II (ML7, BDM, and dominant-negative myosin-II), were used to test this idea [14].
  • The muscle relaxant, BDM, reduced tetanic M3 meridional x-ray reflection intensity (I(M3)), M3 spacing (d(M3)), and the equatorial I(11)/I(10) ratio in a manner consistent with a reduction in the fraction of S1 bound to actin rather than by generation of low-force S1-actin isomers [12].
  • 5. Addition of 5 mm BDM (2,3-butandione-2-monoxime), an inhibitor of actomyosin ATPase partially reverses this shift, suggesting that the mutation impairs the normal function of cTnI to fully inhibit formation of force-generating crossbridges in the absence of Ca(2)(+) [15].
  • Kinetic studies of the benzylamine additions to benzylidenediethylmalonates (BDM: YC(6)H(4)CH[double bond]C(COOEt)(2)) in acetonitrile at 20.0 degrees C are reported [16].
  • METHODS: Five isolated pig hearts (CTRL) were perfused for 90 min at constant flow (1 ml g(-1) min(-1)) with non-recirculating blood containing 30 mM BDM and 26 MBq/l of fluorine-18 2-fluoro-2-deoxyglucose (IFDG) [17].
 

Other interactions of BDM

  • Hence, other factor(s) might be responsible for the muscle pathology in DMD and BDM [18].
 

Analytical, diagnostic and therapeutic context of BDM

  • The physician can gather statistics on the parameters and qualifiers of the extracted ECG records using statistical program packages (BDMP, SCSS) and a decision support system (AS) [19].

References

  1. Alterations in body composition following intestinal bypass for morbid obesity. Spanier, A.H., Kurtz, R.S., Shibata, H.R., MacLean, L.D., Shizgal, H.M. Surgery (1976) [Pubmed]
  2. Experimental Evaluation of the Elastic Determinants of Myocardial Function in vivo. Kedem, J., Guan, X., Norgard, S., Trivedi, M., Drzewiecki, G., Li, J.K. Cardiovascular engineering (Dordrecht, Netherlands) (2006) [Pubmed]
  3. Congenital malformations surveillance: two American systems. Edmonds, L.D., Layde, P.M., James, L.M., Flynt, J.W., Erickson, J.D., Oakley, G.P. International journal of epidemiology. (1981) [Pubmed]
  4. Prevalence of spina bifida at birth--United States, 1983-1990: a comparison of two surveillance systems. Lary, J.M., Edmonds, L.D. MMWR. CDC surveillance summaries : Morbidity and mortality weekly report. CDC surveillance summaries / Centers for Disease Control. (1996) [Pubmed]
  5. Hypospadias trends in two US surveillance systems. Paulozzi, L.J., Erickson, J.D., Jackson, R.J. Pediatrics (1997) [Pubmed]
  6. Contractile deactivation and uncoupling of crossbridges. Effects of 2,3-butanedione monoxime on mammalian myocardium. Gwathmey, J.K., Hajjar, R.J., Solaro, R.J. Circ. Res. (1991) [Pubmed]
  7. Prediction of N(epsilon)-acetylation on internal lysines implemented in Bayesian Discriminant Method. Li, A., Xue, Y., Jin, C., Wang, M., Yao, X. Biochem. Biophys. Res. Commun. (2006) [Pubmed]
  8. Myosin localization during meiosis I of crane-fly spermatocytes gives indications about its role in division. Silverman-Gavrila, R.V., Forer, A. Cell Motil. Cytoskeleton (2003) [Pubmed]
  9. Conjunctival and corneal calcification and bone metabolism in hemodialysis patients. Tokuyama, T., Ikeda, T., Sato, K., Mimura, O., Morita, A., Tabata, T. Am. J. Kidney Dis. (2002) [Pubmed]
  10. Nitric oxide-dependent killing of Cryptococcus neoformans by B-1-derived mononuclear phagocyte. Ghosn, E.E., Russo, M., Almeida, S.R. J. Leukoc. Biol. (2006) [Pubmed]
  11. Focal adhesion features during myofibroblastic differentiation are controlled by intracellular and extracellular factors. Dugina, V., Fontao, L., Chaponnier, C., Vasiliev, J., Gabbiani, G. J. Cell. Sci. (2001) [Pubmed]
  12. Effects of the number of actin-bound S1 and axial force on X-ray patterns of intact skeletal muscle. Griffiths, P.J., Bagni, M.A., Colombini, B., Amenitsch, H., Bernstorff, S., Funari, S., Ashley, C.C., Cecchi, G. Biophys. J. (2006) [Pubmed]
  13. Effects of BTS (N-benzyl-p-toluene sulphonamide), an Inhibitor for Myosin-Actin Interaction, on Myofibrillogenesis in Skeletal Muscle Cells in Culture. Kagawa, M., Sato, N., Obinata, T. Zool. Sci. (2006) [Pubmed]
  14. Rho-kinase and myosin-II control phagocytic cup formation during CR, but not FcgammaR, phagocytosis. Olazabal, I.M., Caron, E., May, R.C., Schilling, K., Knecht, D.A., Machesky, L.M. Curr. Biol. (2002) [Pubmed]
  15. Effects of the mutation R145G in human cardiac troponin I on the kinetics of the contraction-relaxation cycle in isolated cardiac myofibrils. Kruger, M., Zittrich, S., Redwood, C., Blaudeck, N., James, J., Robbins, J., Pfitzer, G., Stehle, R. J. Physiol. (Lond.) (2005) [Pubmed]
  16. Kinetics and mechanism of the addition of benzylamines to benzylidenediethylmalonates in acetonitrile. Oh, H.K., Kim, I.K., Lee, H.W., Lee, I. J. Org. Chem. (2004) [Pubmed]
  17. Role of glycolysis in the energy production for the non-mechanical myocardial work in isolated pig hearts. Bendjelid, K., Canet, E., Rayan, E., Casali, C., Revel, D., Janier, M. Current medical research and opinion. (2003) [Pubmed]
  18. Is the normal content of sulfhydryl groups attributable to sparing from dystrophic pathology in dystrophin-deficient muscles? Niebrój-Dobosz, I., Fidziańska, A., Glinka, Z., Hausmanowa-Petrusewicz, I. Folia neuropathologica / Association of Polish Neuropathologists and Medical Research Centre, Polish Academy of Sciences. (2002) [Pubmed]
  19. An electrocardiogram database incorporated into the hospital information system. Nose, Y., Akazawa, K., Yokota, M., Watanabe, Y., Nakamura, M. Medical informatics = Médecine et informatique. (1987) [Pubmed]
 
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