What are murine stem cells
It was shown that the comprehensive transport - reaction TBR model is capable to match experimental results obtained in the laboratory reactor, indicating that the latter operates in the kinetic controlled regime. A sensitivity analysis demonstrated that the most influent parameters, at typical CWAO conditions and oxygen being the limiting reactant, are the internal diffusion coefficients and the gas-solid mass transfer coefficient. In the case of complete wetting, i.e. for high liquid flow rates, the values of the gas-liquid and liquid solid mass transfer coefficients can also become influent. The entire results show that the comprehensive TBR model can be used with confidence for the scale-up of the CWAO of phenol. However, one has to be aware that the overall quality of the prediction will mainly depend on the accuracy of the key parameters f, Def f , kgs , ka ; gl , kls as , as highlighted in the sensitivity study.
Cells containing IBs are typically disrupted by high-pressure homogenization or a combination of mechanical and chemical methods. Occasionally a lytic enzyme, such as lysozyme, may be added before cell disruption to increase efficiency and reduce power requirements. The resulting suspension is then treated by either differential low-speed centrifugation or filtration to separate the dense IBs from the lighter cell-membrane components and soluble contaminants Georgiou & Valax, 1999 ; . Washing steps are performed with buffers containing EDTA, and either low concentrations of chaotropic agents such as urea or guanidinium chloride GdmCl ; , or detergents such as Triton X-100 Cardamone et al., 1995 ; , sodium deoxycholate or octylglucoside Burgess, 1996.
1383. Day, N.K., O'Reilly-Felice, C., Hardy, W.D., Jr., Good, R.A. and Witkin, S.S.: Circulating immune complexes associated with naturally occurring lymphosarcoma in pet cats. J. Immunol. 126: 2363-2366, December, 1980. 1384. Day, N.K., Witkin, S.S., Sarkar, N.H., Kinne, D., Jussawalla, D.J., Levin, A., Hsia, C.C. and Good, R.A.: Geographic and family studies of immunological responses to antigens of the murine mammary tumor virus in sera of patients with breast cancer. Trans. Assoc. Am. Physicians 93: 123-129, 1980. Dupont, B., O'Reilly, J., Pollack, M.S. and Good, R.A.: Histocompatibility testing for clinical bone marrow transplantation and prospects for identification of donors other than HLA genotypically identical siblings. In: Immunobiology of Bone Marrow Transplantation S. Thierfelder, H. Rodt and H.J. Kolb, eds. ; , New York, Springer-Verlag, 1980, pp. 121-134 Haematology and Blood Transfusion 25 ; . 1386. Fernandes, G., Halberg, F. and Good, R.A.: Circadian dependent chronoimmunological responses of T, B and natural killer cells. Allergologie Munich ; 3: 164-170, 1980. Fernandes, G., Halberg, F. and Good, R.A.: Circadian rhythm in T, B and natural killer cells. In: Recent Advances in the Chronobiology of Allergy and Immunology: Proceedings M.H. Smolensky, A. Reinberg and P.J. McGovern, eds. ; , New York, Pergamon Press, 1980. Advances in the Biosciences, Vol. 28 ; , pp. 289-299. 1388. Fikrig, S.M., Smithwick, E., Suntharalingam, K. and Good, R.A.: Fibroblast nitroblue tetrazolium test and the in utero diagnosis of chronic granulomatous disease. Lancet 1: 18-19, 1980. Fu, S.M., Hurley, J.N., McCune, J.M., Kunkel, H.G. and Good, R.A.: Pre-B cells and other possible precursor lymphoid cell lines derived from patients with X-linked agammaglobulinemia. J. Exp. Med. 152: 1519-1526, December, 1980.
Murine hair epithelial cells
REFERENCES 1. Abdelghaffar, H., D. Vazifeh, and M. T. Labro. 1997. Erythromycin A-derived macrolides modify the functional activities of human neutrophils by altering the phospholipase D-phosphatidate phosphohydrolase transduction pathway: L-cladinose is involved both in alterations of neutrophil functions and modulation of this transductional pathway. J. Immunol. 159: 39954005. 2. Abdelghaffar, H., D. Vazifeh, and M. T. Labro. 2001. Cellular uptake of two fluoroketolides, HMR3562 and HMR 3787, by human polymorphonuclear neutrophils in vitro. Antimicrob. Agents Chemother. 45: 27982806. 3. Abdelghaffar, H., A. Soukri, C. Babin-Chevaye, and M. T. Labro. 2003. Interaction of macrolides and ketolides with the phagocytic cell line PLB985. J. Chemother. 15: 350356. 4. Bonnefoy, A., A. M. Girard, C. Agouridas, and J. F. Chantot. 1997. Ketolides lack inducibility properties of MLSB resistance phenotype. J. Antimicrob. Chemother. 40: 8590. 5. Boswell, F. J., J. M. Andrews, J. P. Ashby, C. Fogarty, N. P. Brenwald, and R. Wise. 1998. The in-vitro activity of HMR 3647, a new ketolide antimicrobial agent. J. Antimicrob. Chemother. 42: 703709. 6. Bryskier, A., C. Agouridas, and J. F. Chantot. 1997. Ketolides: new semisynthetic 14-membered ring macrolides, p. 3950. In S. H. Zinner, L. S. Young, J. F. Acar, and H. C. Neu ed. ; , Expanding indications for the new macrolides, azalides, and streptogramins. Marcel Dekker, Inc., New York, N.Y. 7. Carlier, M. B., B. Scorneaux, A. Zenebergh, J. F. Desnottes, and P. M. Tulkens. 1990. Cellular uptake, localization and activity of fluoroquinolones in uninfected and infected macrophages. J. Antimicrob. Chemother. 26 Suppl. B ; : 2739. 8. Dougherty, T. J., and J. F. Barrett. 2001. ABT-773: a new ketolide antibiotic. Expert Opin. Investig. Drugs 10: 343351. 9. Hamilton-Miller, J. M., and S. Shah. 2002. Activity of ketolide ABT-773 cethromycin ; against erythromycin-resistant Streptococcus pneumoniae; correlation with extended MLSK phenotypes. J. Antimicrob. Chemother. 50: 907913. 10. Jaffe, A., and A. Bush. 2001. Anti-inflammatory effects of macrolides in lung disease. Pediatr. Pulmonol. 31: 464473. 11. Jung, R., L. H. Danziger, and S. L. Pendland. 2002. Intracellular activity of ABT-773 and other antimicrobial agents against Legionella pneumophila. J. Antimicrob. Chemother. 49: 857861. 12. Kim, M. K., W. Zhou, P. R. Tessier, D. Xuan, M. Ye, C. H. Nightingale, and D. P. Nicolau. 2001. Bactericidal effect and pharmacodynamics of cethromycin ABT-773 ; in a murine pneumococcal pneumonia model. Antimicrob. Agents Chemother. 46: 8592. 13. Labro, M. T. 1993. Intraphagocytic penetration of macrolide antibiotics, p. 379388. In A. Bryskier, J. P. Butzler, H. C. Neu, and P. M. Tulkens ed.
Constitution after experimental transplantation of allogeneic peripheral blood cells from G-CSF-treated donors. Biol Blood Marrow Transplant 2: 126, 1996 Zeng D, Dejbakhsh-Jones S, Strober S: Granulocyte colonystimulation factor reduces the capacity of blood mononuclear cells to induce graft-versus-host disease: Impact on blood progenitor cell transplantation. Blood 90: 453, 1997 Mielcarek M, Martin PJ, Torok-Storb B: Suppression of alloantigen-induced T cell proliferation by CD14 cells derived from granulocyte colony-stimulating factor-mobilized peripheral blood mononuclear cells. Blood 89: 1629, 1997 Ino K, Singh RK, Talmadge JE: CD14 suppressor cells in mobilized stem cell products. J Leukoc Biol 61: 583, 1997 Kusnierz-Glaz CR, Still BJ, Amano M, Zukor JD, Negrin RS Blume KG, Strober S: Granulocyte colony-stimulating factorinduced comobilization of CD40CD80 T cells and hematopoietic progenitor cells CD34 ; in the blood of normal donors. Blood 89: 2586, 1997 Nawa Y, Teshima T, Sunami K, Hiramatsu Y, Yano T, Shinagawa K, Omoto E, Harada M: Responses of granulocyte colonystimulating factor-mobilized peripheral blood mononuclear cells to alloantigen stimulation letter ; . Blood 90: 1716, 1997 Atkinson K, Farewell V, Storb R, Tsoi MS, Sullivan KM, Witherspoon RP, Fefer A, Clift R, Goodell B, Thomas ED: Analysis of late infections after human bone marrow transplantation: Role of genotypic nonidentity between marrow donor and recipient and of nonspecific suppressor cells in patients with chronic graft-versushost disease. Blood 60: 714, 1982 Sullivan KM, Mori M, Sanders J, Siadak M, Witherspoon RP, Anasetti C, Appelbaum FR, Bensinger W, Bowden R, Buckner CD: Late complications of allogeneic and autologous marrow transplantation. Bone Marrow Transplant 10: 127, 1992 suppl 1 ; 36. Ochs L, Shu XO, Miller J, Enright H, Wagner J, Filipovich A, Miller W, Weisdorf D: Late infections after allogeneic bone marrow transplantation: comparison of incidence in related and unrelated donor transplant recipients. Blood 86: 3979, 1995 Storek J, Gooley T, Witherspoon RP, Sullivan KM, Storb R: Infectious morbidity in long-term survivors of allogeneic marrow transplantation is associated with low CD4 T cell counts. J Hematol 54: 131, 1997 Sullivan KM, Storek J, Kopecky KJ, Jocom JJ, Longton G, Flowers M, Siadak M, Nims J, Witherspoon RP, Anasetti C, Bowden R, Applebaum FR, Buckner CD, Deeg HJ, Hansen JA, McDonald GB, Sanders JE, Storb R: A controlled trial of long-term administration of intravenous immunoglobulin to prevent late infection and chronic GVHD following marrow transplantation: Clinical outcome and effect on subsequent immune recovery. Biol Blood Marrow Transplant 2: 44, 1996 Sullivan KM, Weiden PL, Storb R, Witherspoon RP, Fefer A, Fisher L, Buckner CD, Anasetti C, Appelbaum FR, Badger C: Influence of acute and chronic graft-versus-host disease on relapse and survival after bone marrow transplantation from HLA-identical siblings as treatment of acute and chronic leukemia. Blood 73: 1720, 1989 Slavin S, Akerstein A, Naparstek E, Or R, Weiss L: The graft-versus-leukemia phenomenon: Is GVL separable from GVHD? Bone Marrow Transplant 6: 155, 1990 Glass B, Uharek L, Zeiss M, Dreger P, Loffler H, Steinmann J, Schmitz N: Allogeneic peripheral blood progenitor cell transplantation in a murine model: evidence for an improved graft-versusleukemia effect. Blood 90: 1694, 1997.
What is murine animal
If the cell body were about thirty yards across the axon of a typical motor neuron would be about the size of a tube train tunnel connecting London and New York". So writes Ammar Al-Chalabi of the motor neuron, the demise of which underlines motor neurone disease. In his short review Ammar lays out a logical, thorough, yet pragmatic approach to this condition highlighting recent advances as well as a range of useful statistics on its frequency and prognosis. Neurodegenerative disorders of the CNS are viewed as conditions where the primary deficit is neuronal loss. Whilst there is no doubt that this is the case, this is a relatively late event with the early manifest problems being a consequence of more subtle abnormalities in the neuron at the level of neurotransmission and synaptic plasticity. In this issue Tony Hannan and Nektarios Mezarakis explore this concept in murine transgenic models of Huntington's disease highlighting the extent to which such an abnormality exists and can be modified by manipulation of the environment. This is a succinct account in an exciting area of neuroscience by acknowledged experts in this area who have done much to throw light on the significance of gene environment interactions in neurological disorders. In a third review article, Thomas Bak takes us through the differing cognitive profiles of parkinsonian syndromes an area to which he has made a substantial contribution. In this review, Thomas makes the point that documenting the profile of cognitive deficits in atypical parkinsonian syndromes is not only a useful exercise in its own right, but can be used to help define and refine the diagnosis. Indeed, as he writes, "with growing understanding of fronto-striatal connections it seems likely that at least some cognitive and motor symptoms are different manifestations of the same underlying pathology". Special care dentistry forms the topic for the Rehabilitation article. This "forgotten strand in rehabilitation" covers the dentistry needs of people with `special needs' and the article by June Nunn provides a clear and informative narrative on how to prevent and recognise problems and their optimal management which will significantly impact on my practice with such patients. The identification of intracranial metastases carries with it a poor prognosis and often it is not clear what treatment should be offered. In the Neurosurgery series, Peter Whitfield and oncologist Steve Kelly take us through the various different approaches and the evidence for their adoption or use in different clinical scenarios. This is a clear account based on a detailed analysis of the published literature and highlights the merits of surgery and whole brain irradiation in selected, affected, groups of individuals. We are extremely privileged to have writing for us in this issue Professor Raymond Adams, still active at the age of 95! In his article Professor Adams lays out the vast number of neurological conditions to which he has made seminal contributions. Thus it was difficult to know what to ask Professor Adams to write about given this, but we settled on central pontine myelinolysis, and he takes us through the original description of this case outlining how the syndrome came to be recognised in collaboration with his colleague Maurice Victor. This is an absolutely fascinating article which I sure many will find of great intellectual interest as well as being of huge historical significance. We also have a short article on a new initiative in MS, the Atlas of MS, organised by the Multiple Sclerosis International Federation MSIF ; . This resource is designed to highlight and report on different aspects of MS across the globe and looks to be a very useful resource. Finally it would not be right as we enter November 2006 not to have some mention of Alois Alzheimer as it is now a 100 years since he described the first case of his disease, patient Auguste D, Andrew Larner delivers his usual scholarly account of this historical event and reassuring tells us that his presentation "prompted no comments or reaction from the audience". We have our usual regular articles, including journal and book reviews, and as always we are keen to hear from you as to what we can do to improve and expand the journal that now has a circulation of over 4500 and muse.
L1210 murine leukemia
Reincke M 1999 ; Multiple mechanisms are involved in the acute vasodilatory effect of 17 -estradiol in the isolated perfused rat heart. J Cardiovasc Pharmacol 33: 852 858. Inagaki N, Gonoi T, Clement JP, Namba N, Inazawa J, Gonzalez G, Aguilar-Bryan L, Seino S, and Bryan J 1995 ; Reconstitution of IKATP: an inward rectifier subunit plus the sulfonylurea receptor. Science Wash DC ; 270: 1166 1170. Jovanovic N, Jovanovic S, Jovanovic A, and Terzic A 1999 ; Gene delivery of Kir6.2 SUR2A in conjunction with pinacidil handles intracellular Ca2 homeostasis under metabolic stress. FASEB J 13: 923929. Jugdutt BI, Becker LC, Hutchins GM, Bulkey BH, Reid PR, and Kallman CH 1981 ; Effect of intravenous nitroglycerin on collateral blood flow and infarct size in the conscious dog. Circulation 63: 1728. Kita H, Miura T, Tsuchida A, Hasegawa T, and Shimamoto K 1998 ; Suppression of reperfusion arrhythmias by preconditioning is inhibited by an ATP-sensitive potassium channel blockers, 5-hydroxydecanote, but not by protein kinase C blockers in the rat. J Cardiovasc Pharmacol 32: 791797. Lee TM, Su SF, Lee YT, and Tsai CH 1999 ; Effect of estrogen on ventricular repolarization in menopausal patients with syndrome X and the effects of nicorandil. J Cardiol 84: 615 620. Lee TM, Su SF, Tsai CC, Lee YT, and Tsai CH 2000 ; Cardiovascular effects of 17 -estradiol produced by activation of mitochondrial ATP-sensitive K channels in canine hearts. J Mol Cell Cardiol 32: 11471158. Li GR and Ferrier GR 1992 ; Verapamil prevents slowing of transmural conduction and suppresses arrhythmias in an isolated guinea pig ventricular model of ischemia and reperfusion. Circ Res 70: 651 659. Li HY, Bian JS, Kwan YW, and Wong TM 2000 ; Enhanced responses to 17 estradiol in rat heart treated with isoproterenol: involvement of a cyclic AMPdependent pathway. J Pharmacol Exp Ther 293: 592598. Liu Y, Ren G, O'Rourke B, Marban E, and Seharaseyon J 2001 ; Pharmacological comparison of native mitochondrial KATP channels with molecularly defined surface KATP channels. Mol Pharmacol 59: 225230. Liu Y, Sato T, O'Rourke B, and Marban E 1998 ; Mitochondrial ATP-dependent potassium channels. Circulation 97: 24632469. McHugh NA, Cook SM, Schairer JL, Bidgoli MM, and Merrill GF 1995 ; Ischemiaand reperfusion-induced ventricular arrhythmias in dogs: effects of estrogen. J Physiol 268: H2569 H2573. McHugh NA, Merrill GF, and Powell SR 1998 ; Estrogen diminishes postischemic hydroxyl radical production. J Physiol 274: H1950 H1954. Nakajima T, Iwasawa K, Oonuma H, Morita T, Goto A, Wang Y, and Hazama H 1999 ; Antiarrhythmic effect and its underlying ionic mechanism of 17 -estradiol in cardiac myocytes. Br J Pharmacol 127: 429 440. Oliver MF and Opie LH 1994 ; Effects of glucose and fatty acids on myocardial ischaemic and arrhythmias. Lancet 343: 155158. Picard S, Rouet R, Duval D, Chesnay F, and Gerard JL 1998 ; KATP channel modulators and myocardial damages induced by ischemia-reperfusion: membrane lipids injury and arrhythmias. J Mol Cell Cardiol 30: 26132621. Rioufol G, Ovize M, Loufoua J, Pop C, Andre-Fouet X, and Minaire Y 1997 ; Ventricular fibrillation in preconditioned pig hearts: role of KATP channels. J Physiol 273: H2804 H2810. Robertson JF, Nicholson RI, Bundred NJ, Anderson E, Rayter Z, Dowsett M, Fax JN, Gee JM, Webster A, Wakeling AE, et al. 2001 ; Comparison of the short-term biological effects of 7 -[9- 4, 5, ; -nonyl]estra1, 3, 5, 10 ; -triene-317 -diol Faslodex ; versus tamoxifen in postmenopausal women with primary breast cancer. Cancer Res 61: 6739 6746. Russell KS, Haynes MP, Sinha D, Clerisme E, and Bender JR 2000 ; Human vascular endothelial cells contain membrane binding sites for estradiol, which mediate rapid intracellular signaling. Proc Natl Acad Sci USA 97: 5930 5935. Sakamoto J, Miura T, Tsuchida A, Fukuma T, Hasegawa T, and Shimamoto K 1999 ; Reperfusion arrhythmias in the murine heart: their characteristics and alteration after ischemic preconditioning. Basic Res Cardiol 94: 489 495. Sakamoto K, Yamazaki J, and Nagao T 1998 ; 5-Hydroxydecanoate selectively reduces the initial increase in extracellular K in ischemia guinea-pig heart. Eur J Pharmacol 348: 3135. Sourander L, Rajala T, Raiha I, Makinen J, Erkkola R, and Helenius H 1998 ; Cardiovascular and cancer morbidity and mortality and sudden cardiac death in postmenopausal women on estrogen replacement therapy ERT ; . Lancet 352: 19651969. Sudhir K, Chou TM, Mullen W, Hausmann D, Collins O, Yock PG, and Chatterjee K 1995 ; Mechanisms of estrogen-induced vasodilation: in vivo studies in canine coronary conductance and resistance arteries. J Coll Cardiol 26: 807 814. Tanabe S, Hata T, and Hiraoka M 1999 ; Effects of estrogen on action potential and membrane currents in guinea pig ventricular myocytes. J Physiol 277: H826 H833. Volpi A, Maggioni A, Franzosi MG, Pampallona S, Mauri F, and Tognoni G 1987 ; In-hospital prognosis of patients with acute myocardial infarction complicated by primary ventricular fibrillation. N Engl J Med 317: 257261. Walker MJ, Curtis MJ, Hearse DJ, Campell RW, Janse MJ, Yellon DM, Cobbe SM, Coker SJ, Harness JB, and Harron DW 1988 ; The Lambeth conventions: guidelines for the study of arrhythmias in ischaemia, infarction, and reperfusion. Cardiovasc Res 22: 447 455. Wilde AAM and Janse MJ 1994 ; Electrophysiological effects of ATP sensitive potassium channel modulation: implications for arrhythmogenesis. Cardiovasc Res 28: 16 24. Wirth KJ, Rosenstein B, Uhde J, Englert HC, Busch A, and Scholkens BA 1999 ; ATP-sensitive potassium channel blocker HMR 1883 reduces mortality and ischemia-associated electrocardiographic changes in pigs with coronary occlusion. J Pharmacol Clin Ther 291: 474 481.
Murine tears lubricant
Use after techniques of transplantation and culture are improved. Donor cells could be documented in recipient mouse testes up to 6 after transplantation of testis cells that had been maintained in culture for 1 mo before transplantation. However, only a few cells were observed, and their morphologic appearance was different from that of those found after the transplantation of fresh or cryopreserved donor cells. The majority of cells did not show the round shape or chain and mesh formation characteristic of spermatogenic cells [26, 29] but was more reminiscent of testicular somatic cells. Donor testis cells were cultured on mitotically arrested STO feeders secreting murine leukemia inhibiting factor LIF ; , a system previously shown to support longterm culture of mouse spermatogonial stem cells before transplantation [15]. It appears, therefore, that this culture system does not provide adequate support to maintain rabbit and dog germ cells in culture in sufficient numbers to and mycostatin.
Larsen RA, 1 Bauer M, 1 Thomas AM, 2 Graybill JR3 1University of Southern California, Los Angeles, CA, USA, 2University of Northern Colorado, Greeley, CO, USA, 3University of Texas, San Antonio, TX, USA INTRODUCTION: Cryptococcal meningitis remains the most common life-threatening opportunistic infection of the central nervous system in persons with AIDS. Optimal treatment with existing drugs has been elusive with the most recent large clinical trial reporting a 52% success rate for 386 subjects treated with amphotericin B with or without flucytosine followed by azole maintenance. Management of this disease is complicated by the limited availability of flucytosine, particularly in countries most affected by the AIDS epidemic. Both animal and in vitro studies have demonstrated that flucytosine plus either amphotericin B or fluconazole has significantly greater mycologic activity against cryptococcal meningitis compared to either drug alone. However, amphotericin B and fluconazole have not been tested together or in a three drug combination with flucytosine. Given the low cost and widespread availability of amphotericin B and fluconazole, we evaluated this combination in a murine model of cryptococcal meningitis. METHODS: Meningitis was established in male BALB c mice weighing 23-25 g by intracerebral injection of approximately 700 CFU of C. neoformans. Treatment was started on day 2 with fluconazole and flucytosine dissolved in the sole source of drinking water. Dose levels tested were: amphotericin B alone at 0.3 to 1.3 mg kg i.v., fluconazole at 10-40 mg kg day + amphotericin B at 0.5 mg kg i.v. daily for 14 days with or without flucytosine at 20-105 mg kg day for 14 days. Mice were sacrificed at 16 days and the numbers of fungal colonies in the brain quantified. Untreated control mice were sacrificed at predetermined times to estimate the growth curve of C. neoformans in the brain. Additional untreated controls were followed for survival. The association between response and dose combination was evaluated using local regression; 99% confidence intervals CI ; were used to evaluate antifungal effect. RESULTS: 40% of mice treated with amphotericin B at 0.7 mg kg and 80% treated with 0.9 mg kg died during or within 24 hours of the first dose. No untreated control mice survived beyond day 11. 95% of mice treated with fluconazole at 16 mg kg day + flucytosine survived to the end of treatment. 100% of mice treated with amphotericin B survived to the end of the experiment, regardless of fluconazole or flucytosine dose. Among mice not treated with amphotericin B, the greatest antifungal activity was seen at 40 mg kg day of fluconazole alone 99% CI: 1.9, 4.1 log10 CFU ; . The addition of amphotericin B to fluconazole in the range 16-32 mg kg day, reduced the 99% CIs to 0.4 to 1.6 log10 p 0.01 ; . Adding flucytosine did not increase the antifungal activity of either fluconazole alone or fluconazole plus amphotericin B. CONCLUSIONS: The addition of amphotericin B has a striking effect on the antifungal effect of fluconazole. Given this dramatic increase in antifungal activity and the widespread availability of these two drugs, the full potential of this two-drug combination deserves immediate evaluation in a randomized clinical trial. Although dose-limiting toxicity associated with amphotericin B prevents testing higher doses of the standard formulation, it would be worthwhile to explore the potential of liposomal formulations in combination with fluconazole.
Murine disease models
Remembering that we have a responsibility to the community is part of our corporate culture. Volunteering to provide for a better future at all our sites around the world is thus one of Merck's guiding principles. With our social and cultural commitment, we are also working towards the implementation of the UN Millennium Development Goals and the principles defined by the UN Global Compact. Our activities focus on areas that we understand well, namely the promotion of education and health. In accordance with our corporate values, employees at all Merck sites are called upon to support the communities in which we operate. The executive bodies of the Merck Group need not mandate this by decree: Worldwide, the companies of the Merck Group take the initiative and demonstrate in many ways how social commitment is translated into action and mysoline.
Y.Hu et al. alternative for ovulation induction in in vitro fertilization. Fertil. Steril., 53, 302305. Hu, Y.X., Voelkel, S.V. and Godke, R.A. 1989 ; One-cell murine embryos culture on rat liver cell monolayers and mouse oviduct cells. Proceedings of AASS First Conference, A57, 83. Hu, Y.X., Hoffman, D.I., Maxson, W.S. and Ory, S.J. 1996 ; Clinical application of nonselective assisted hatching of human embryos. Fertil. Steril., 66, 991994. Hu, Y.X., Maxson, W.S., Eager, S., Dupre, J. and Hoffman, D. 1997 ; Coculture of human embryos using Buffalo rat liver BRL ; cells for women with decreased prognosis in IVF. Am. J. Obstet. Gynecol., 8, 358363. Kojima, K., Kanzaki, H., Iwai, M. et al. 1994 ; Expression of leukemia inhibitory factor in human endometrium and placenta. Biol. Reprod., 50, 882887. Magli, M.C., Gianaroli, L., Ferraretti, A.P. et al. 1995 ; Human embryo coculture: results of randomized prospective study. Int. J. Fertil., 40, 254259. Mandelbaum, J. 1996 ; The effect of assisted hatching on the hatching process and implantation. Hum. Reprod., 11, 4350. Mandelbaum, J., Plachot, M. and Junca, A. 1994 ; The effect of partial zona dissection on in-vitro development and hatching of human cryopreserved embryos. Abstr. 84 ; Hum. Reprod., 9, 39. Menezo, Y., Guerin, J.F. and Czyba, J.C. 1990 ; Improvement of human early embryo development in vitro by co-culture on monolayers of vero cells. Biol. Reprod., 42, 301306. Moses, A.C., Nisley, S.P, Short, P.A. et al. 1980 ; Purification and characterization of multiplication-stimulating activity. Eur. J. Biochem., 103, 387400. Piekos, M., Frasor, J., Mack, S. et al. 1995 ; Evaluation of co-culture and alternative culture systems for promoting in-vitro development of mouse embryos. Hum. Reprod., 10, 14861491. Plachot, M. 1996 ; Co-culture of embryos and feeder cells. Hum. Reprod., 11, 3542. Sakkas, D., Jaquenoud, N., Leppens, G. and Campana, A. 1994 ; Comparison of results after in vitro fertilized human embryos are cultured in routine medium and in coculture on Vero cells: a randomized study. Fertil. Steril., 61, 521-525. Slager, H.G., Freund, E., Buiting, A.M. et al. 1993 ; Secretion of transforming growth factor-beta isoforms by embryonic stem sells: isoform and latency are dependent on direction of differentiation. J. Cell Physiol., 156, 247256. Tucker, M.J., Morton, P.C., Wright, G. et al. 1996 ; Enhancement of outcome from intracytoplasmic sperm injection: does co-culture or assisted hatching improve implantation rates? Hum. Reprod., 11, 24342437. Veeck, L. 1991 ; Preembryo grading. In Atlas of the Human Oocyte and Early Conceptus, Vol. 2. Williams and Wilkins, Baltimore, pp. 121149. Voelkel, S.V. and Hu, Y.X. 1992 ; Effect of gas atmosphere on the development of one-cell bovine embryos in two culture systems. Theriogenology, 37, 11171131. Voelkel, S.A., Hu, Y.X., Moore, K. and Bondioli, K.R. 1992 ; Freezing survival of bovine embryos produced by in vitro maturation, fertilization and culture of oocytes. Theriogenology, 37, 317. Wiemer, K.E., Hoffman, D.I., Maxson, W.S. et al. 1993 ; Embryonic morphology and rate of implantation of human embryos following coculture on bovine oviductal epithelial cells. Hum. Reprod., 8, 97101. Wiemer, K., Garrisi, J., Steuerwald, N. et al. 1996 ; Beneficial aspects of coculture with assisted hatching when applied to multiple-failure in-vitro fertilization. Hum. Reprod., 11, 24292433. Yeung, W.S.B., Ho, P.C., Lau, E.Y.L. and Chan, S.T.H. 1992 ; Improved development of human embryos in vitro by a human oviductal cell coculture system. Hum. Reprod., 7, 11441149. Zetova, L., Mardesic, T., Mikova, M. and Muller, P. 1993 ; Improved development of human embryos cultured on a Vero cell monolayer. J. Assist. Reprod. Genet., 10, 234236. Received on April 22, 1997; accepted on October 3, 1997.
Murine wbc count
Patient or person acting on behalf of the patient ; in writing that services in a non-certified or inappropriately certified bed are not covered. The written notice should make it clear that the beneficiary has the right to request that you file a claim for Medicare benefits if he she believes a covered level of services is required, such as: "We are placing you in a part of this facility which is not appropriately certified by Medicare because you do not require a level of care that will qualify as covered hospital services under Medicare ; or state any other reasons for the non-certified bed placement ; . Nonqualifying services furnished a patient in a non-certified or inappropriately certified bed are not payable by Medicare. However, you or someone acting on your behalf ; may request us to file a claim for Medicare benefits. Based on this claim, Medicare will make a formal determination and advise whether any benefits are payable to you." If the beneficiary requests that you submit a claim for Medicare payment, do so. Point out that the claim is being submitted at the beneficiary's request and explain why you consider the care to be noncovered. C. Determining Beneficiary Consent.--Effective for services provided on or after February 1, l983, you may submit evidence to rebut the presumption that the beneficiary did not consent to the placement in a noncertified bed. However, under this policy, beneficiaries are still not viewed as having given their consent to placement in a non-certified bed if their consent is based on erroneous or incomplete information. In other words, if the beneficiary consents on the basis of an incorrect statement from your admissions office, the URC, or any other entity on which the beneficary could reasonably be expected to rely, that he does not require a covered level of care, then the consent is determined to have been invalid, and program payment may be made assuming, of course, that there exists no other basis on which to deny the claim ; . On the other hand, a beneficiary may knowingly and voluntarily consent to placement in a non-certified bed--because he only requires a short stay, because he wishes to be placed in a facility that is near a close relative, because he believes the care is being paid for by a third party payor other than Medicare ; , or for any other reason. In such a situation, program payment is not made, even though the beneficiary may have needed and received an otherwise covered level of care. In order to rebut a presumption of non-consent, you must submit to the intermediary a valid consent statement attached to any request for payment for care received in non-certified beds. Moreover, in any case in which a Medicare beneficiary gives his or her consent to placement in a non-certified bed, submit a consent statement to the intermediary, who determines its validity. To be considered valid, the consent statement must include language to the effect that the beneficiary understands that his or her voluntary placement in a non-certified portion of your facility disqualifies the beneficiary from eligibility for Medicare payments for services received while in the non-certified bed. The statement must assert that the beneficiary's consent to being placed in a non-certified or inappropriately certified ; bed is given freely. The consent statement must be signed by the beneficiary provided he or she is competent to give such consent ; or by the beneficiary's legal representative, and must be accompanied by a physician's statement attesting to the beneficiary's competence or incompetence. If any of these requirements is not met, a consent statement is automatically determined to be invalid and nadolol.
Murine gene encoding
We had not been long in Muvattupuzha before discovering that apart from the Untouchables and Unseeables almost everybody owned at least half an acre of land. Boundary disputes between the owners of adjacent plots were, therefore, extremely common. A man could hardly go away for the weekend without finding, on his return, that one of his neighbours had shifted the fence a foot or two to his own advantage. Such incidents led to interminable litigation. Going to law was, in fact, the most popular local pastime and the most ruinous. Most of our members were involved, either as plaintiffs or defendants, in two or three suits every month. Under such favourable conditions lawyers flourished. One of the most typical sights of the town was that of a vakil, or solicitor, in rusty black coat and ready-made white turban, making his lordly way to the Court at 9.45 in the morning followed by a train of obsequious clients not one of whom but had what Judge Jeffreys would have called a hanging face. Knots of no less villainous-looking characters could be seen gathered about the entrances of the various court-rooms. When we enquired who they were and what they wanted we received the cynical reply, They are witnesses waiting to be hired. Theyll swear to anything for eight annas. Later we learned that there was a tacit agreement between vakils to limit the number of false witnesses produced at any single hearing. More than eight or nine for each side, it was felt, would tend to defeat the ends of justice. So great was the amount of litigation that went on, and so urgent the demand for lawyers, that the legal profession seemed to have absorbed an abnormally high percentage of the more highly educated middle class. How many vakils and advocates were enrolled as members of the Ashram I no longer recollect. But it was certainly no coincidence that though we made friends among practically all professions, trades, and.
The two rings of ThDP, approaching from the other side of the aminopyrimidine ring. These interactions contribute to the formation of the V-conformation torsion angles T 100, 71 ; for the cofactor 3 ; . Overlapping densities are P observed between the N1 atom of the ThDP aminopyrimidine ring and the side-chain carbonyl group of the invariant Glu76- . This interaction results in the increased basicity of the 4 -NH2 group, which is required for efficient deprotonation of the C2 atom of the aminopyrimidine ring for the formation of enamine-ThDP 21 ; . An important structural feature of our E1b crystals is the visibility of the loop region in wild-type E1b between Tyr286and Gln312- including Ser292- phosphorylation site 1 ; , with electron density interrupted between Thr293- and Ser294- , at Ala299- , and between Ser302- and Asn307- Fig. 6A ; . Remarkably, the H291A- mutation renders the entire phosphorylation loop disordered in the active site of this mutant Fig. 6B ; . Residual electron densities observed in Tyr286- and Arg287- are accompanied by the complete absence of densities between Ile288- and Gln312- Fig. 6B ; . In contrast, the H146A- substitution does not result in significant conformational alterations from the wild type in the phosphorylation loop region or the vicinity of this histidine residue Fig. 6C ; . However, the O4 water molecule hydrogen-bonded to His146TABLE IV Thermodynamic parameters for the interactions of Lip-LBD2 with wild-type, H146A- , and H291A- E1b as determined by isothermal titration calorimetry and nafcillin.
Murine coupons
95. Fromtling, R. A., H.-P. Yu, and S. Shadomy. 1984. In vitro antifungal activities of Bay N 7133 and Bay L 9139, two new orally absorbed antifungal imidazole derivatives, against pathogenic yeasts. Mycopathologia 86: 45-50. Fujihara, M., K. Hirakoso, and S. Harigaya. 1984. Pharmacokinetics of sulconazole nitrate. 1 ; . Fate in rats after application to the skin. Pharmacometrics 28: 145-154. 97. Galgiani, J. N. 1983. Ketoconazole in the treatment of coccidioidomycosis. Drugs 26: 355-363. 98. Galimberti, R. L., I. Villalba, S. Galarza, A. Raimondi, and V. Flores. 1987. Itraconazole in pityriasis versicolor: ultrastructural changes in Malassezia furfur produced during treatment. Rev. Infect. Dis. 9 Suppl. 1 ; : 134-138. 99. Gan, V. N., M. Petruska, and C. M. Ginsburg. 1987. Epidemiology and treatment of tinea capitis: ketoconazole vs. griseofulvin. Pediatr. Infect. Dis. J. 6: 46-49. 100. Ganer, A., E. Arathoon, and D. A. Stevens. 1987. Initial experience in therapy for progressive mycoses with itraconazole, the first clinically studied triazole. Rev. Infect. Dis. 9 Suppl. 1 ; : 77-86. 101. Gastaldi, A. 1985. Treatment of vaginal candidiasis with fenticonazole and miconazole. Curr. Ther. Res. 35: 489-493. 102. Gebhart, R. J., A. Espinel-Ingroff, and S. Shadomy. 1984. In vitro susceptibility studies with oxiconazole Ro 13-8996 ; . Chemotherapy Basel ; 30: 244-247. 103. Georgopapadakou, N. H., B. A. Dix, S. A. Smith, J. Freudenberger, and P. T. Funke. 1987. Effect of antifungal agents on lipid biosynthesis and membrane integrity in Candida albicans. Antimicrob. Agents Chemother. 31: 46-51. 104. Gip, L. 1984. Comparison of oxiconazole Ro 13-8996 ; and econazole in dermatomycoses. Mykosen 27: 295-302. 105. Gip, L., and S. Forsstrom. 1983. A double-blind parallel study of sulconazole nitrate 1% cream compared with miconazole 2% cream in dermatophytoses. Mykosen 26: 231-241. 106. Gisslen, H., K. Hersle, H. Mobacken, and P. Nordin. 1977. Topical treatment of dermatomycoses and tinea versicolor with econazole cream 1% Parvaryl ; . Curr. Ther. Res. 21: 681684. 107. Godefroi, E. F., J. Heeres, J. Van Cutsem, and P. A. J. Janssen. 1969. The preparation and antimycotic properties of derivatives of 1-phenethylimidazole. J. Med. Chem. 12: 784791. 108. Goffe, B.S. 1987. Response of tinea corporis cruris and tinea versicolor to once-a-day topical treatment with bifonazole cream-a safety and efficacy study, p. 423-429. In R. A. Fromtling ed. ; , Recent trends in the discovery, development and evaluation of antifungal agents. J. R. Prous Publishers, Barcelona. 109. Gouveia, D. C., and C. Jones da Silva. 1984. Oxiconazole in the treatment of vaginal candidiasis: single dose versus 3-day treatment with econazole. Pharmatherapeutica 3: 682-685. 110. Graybill, J. R. 1987. Fluconazole efficacy in animal models of mycotic diseases, p. 113-124. In R. A. Fromtling ed. ; , Recent trends in the discovery, development and evaluation of antifungal agents. J. R. Prous Publishers, Barcelona. 111. Graybill, J. R., and J. Ahrens. 1985. Itraconazole treatment of murine aspergillosis. Sabouraudia: J. Med. Vet. Mycol. 23: 219-223. 112. Graybill, J. R., S. R. Kaster, and D. J. Drutz. 1983. Comparative activities of Bay n7133, ICI 153, 066, and ketoconazole in murine cryptococcosis. Antimicrob. Agents Chemother. 24: 829-834. 113. Graybill, J. R., S. R. Kaster, and D. J. Drutz. 1983. Treatment of experimental murine aspergillosis with Bay n7133. J. Infect. Dis. 148: 898-906. 114. Graybill, J. R., and H. B. Levine. 1978. Successful treatment of cryptococcal meningitis with intraventricular miconazole. Arch. Intern. Med. 138: 814-816. 115. Graybill, J. R., S. H. Sun, and J. Ahrens. 1986. Treatment of murine coccidioidal meningitis with fluconazole UK-49, 858 ; . J. Med. Vet. Mycol. 24: 113-119. 116. Green, C. A., P. M. Farr, and S. Shuster. 1987. Treatment of seborrhoeic dermatitis with ketoconazole.II. Response of.
Murine ear drops warning
Onite is added to mitoxantrone andthis mixture is then added to actively loaded SR vesicles, the Ca2 + release rate is unaffected by the presence of the dithionite. Chemical reduction of the mitoxantrone inhibits mitoxantrone-stimulated Ca2 + release from SR vesicles. If instead of pretreating the mitoxantrone with reduced dithionite, the dithionite is added directly to the buffer in which the SR has actively taken up the Ca2 + , the initial Ca2 + efflux rate caused by the addition of mitoxantrone is unaffected by the presence of the dithionite. On a time scale of approximately 10 s, however, the presence of dithionite causes the Ca" to be retaken back up by the SR vesicles. Spectrophotometric measurements show that the time required for the dithionite to reduce mitoxantrone is the same as thetime required to turnoff the Ca" release mechanism and begin to trigger Ca2 + re-uptake by the SR. Attempts to inhibit mitoxantrone-stimulated Ca2 + release by pretreatment with other reducing agents such as dithiothreitol, cysteine, and ascorbate were unsuccessful. There also was no spectral change or evidence of reduction of mitoxantrone caused by these reducing agents. A stronger reducing agent such as dithionite is needed to reduce mitoxantrone and inhibit release caused Ca2 + by this anthraquinone. Physiological Ca2 + release is believed to occur through the terminal cisternae region of the SR. Ca" release stimulated by Ca2 + 4 ; , Ag Cu2 + cysteine 6 ; , copper phthalocyanine dyes 31 ; , and ryanodine 36 ; has been shown to be specific for HSR over LSR vesicles. As shown in Table I, Ca2 + release induced by 10 phi mitoxantrone is also specific for SR derived from the terminal cisternae region HSR ; . Both the Ca" release rate and the amount of Ca" released is four to five times larger with HSR vesicles than with LSR vesicles. Morphological damage caused to the heart by anthraquinones include myofibrillar loss, vacuolization of the SR, and swelling of the mitochondria 16 ; . It not known which is the primary site of cardiotoxicity of the anthracycline antibiotics. It has been proposed that nonspecific oxidation caused by free radicals is responsible for their cardiotoxicity 17 ; . In order to determine if Ca2 + release triggered by the addition of the anthraquinones was caused by superoxide OF ; generated and naloxone.
He human stomach works at an acid pH near 1, whereas the larval mosquito midgut works at an alkaline pH near 11. The acid pH of mammalian stomachs has been thoroughly investigated and its mechanisms are understood in great detail. The alkaline pH of larval mosquito midguts has been little studied and remains largely a mystery. Recently developed techniques for direct analysis of the intact midgut in vivo and in semi-intact larvae, with a resolution that allows analytical assay of small patches of tissue, even of individual cells, have led to insights into the alkalinization mechanism. The principal function of the larval mosquito midgut is to digest and absorb nutrients. High pH values have been recorded in anterior midgut of several mosquito larvae, including Aedes aegypti 1 ; , as well as in some lepidopteran larvae with high tannin diet 2 ; . The alkaline environment of the anterior midgut lumen enhances dissociation of tanninprotein complexes and, therefore, would be advantageous for the nutrition of herbivorous and detritus-feeding larvae 3 ; . The tannin-free protein could then be digested and absorbed at the near neutral pH of posterior midgut lumen 3, 4 ; . This pattern of nutrient processing has led to the large longitudinal gradients of pH and ionic concentration. How can such a large pH gradient be generated over short distances in the absence of morphological barriers? Apparently, it is the result of region-specific ion transport. It is established that this transport is energized by a plasma membrane H V-ATPase 57 ; , but the ion transporters involved are heretofore unknown and murine.
Purified murine igg1
1. Baker, B. L. Design of Active Site-Directed Irreversible Enzyme Inhibitors, pp. 192 263. New York: John Wiley and Sons, Inc., 1967. 2. Blakley, R. L. The Biochemistry of Folie Acid and Related Pteridines. pp. 139-181. New York: John Wiley and Sons, Inc. 1969. 3. Divekar, A. Y., Vardya, N. R. and Braganca, B. M. Active Transport of Aminopterin in Yoshida Sarcoma Cells. Biochim. Biophys. Acta, 135: 927-936, 1967. Divekar, A. Y., Vardya, N. R. and Braganca. B. M. Defective Transport of Aminopterin in Relation to the Development of Resist ance in Yoshida Sarcoma Cells. Biochim. Biophys. Acta, 135: 937-946, 1967. Farber, S., Diamond, L. K., Mercer. R. D., Sylvester, R. F., Jr., and Wolff. J. A. Temporary Remissions in Acute Leukemia in Children Produced by Folie Acid Antagonists, 4-Aminopteroyl-glutamic Acid Aminopterin ; . New Engl. J. Med., 238: 787 793, Fisher. G. A. Defective Transport of Amethopterin Methotrexate ; as a Mechanism of Resistance to the Antifolate in L5I78Y Leukemia Cells. Biochem. Pharmacol., : 1233-1234, 1960. 7. Goldman, I. D., Lichenstein, N. S., and Oliverio, V. T. Carriermediated Transport of the Folie Acid Analogue, Methotrexate. in the L1210 Leukemia Cell. J. Biol. Chem., 243: 5007 5017, Hakala, M. T. On the Nature of the Permeability of Sarcoma-180 Cells to Amethopterin in vitro. Biochim. Biophys. Acta, 102: 210 225, Hall, T. C., Roberts, D., and Kessel, D. H. Methotrexate and Folie Reduc-ase Human Cancer. 2: 135 142, in 10. Harrap, K. R., Hill, B. T. Furness. M. E. and Hart, L. I. Sites of Action of Amethopterin: Intrinsic and Acquired Drug Resistance. Ann. N. Y. Acad. Sci., 186: 312 324, Hillcoat, B. L., Perkins, J. P. and Berlino. J. R. Dihydrofolate Reduc-asefrom ihe L1210R Murine Lymphoma. Further Studies on the Binding of Substrates and Inhibitors to the Enzyme. J. Biol. Chem., 242: 4777 4781, Huennekens, F. M., Dunlop, R. B., Freisheim, J. H., Gunderson, L. E., Harding, N. G. L., Levison, S. A., and Meli, G. P. Dihydrofolate Reduc-ase: Structural and Mechanistic Aspects. Ann. N. Y. Acad. Sci., 186: 85 99, Hutchinson. D. J. Quinazoline Anlifolates: Biologic Activilies. Cancer Chemotherapy Rept, 52: 697 705, Hutchison, D. J., Philips, F. S., Schmid, F. A., Sodergren, J. E., and Sternberg, S. S. Inhibilion of Hosl Proliferative Tissue by LI2IO Leukemia: The Inverted Effect of Metholrexale MTX ; . Proc. Am. Assoc. Cancer Res., 13: 18, 1972. Hulchison, D. J., Robinson, D. L., Marlin, D., Ittensohn, O. L., and Dillenberg. J. Effects of Selected Anticancer Drugs on the Survival Time of Mice with L12IO Leukemia: Relalive Responses of Anlimetabolile-resislant Strains. Cancer Res. 22: 57 72, Hutchison, D. J., Sirotnak, F. M., and Albrecht, A. M. Dihydrofolate Reduc-ase Inhibilion by the 2.4-Diaminoquina oline Anlifolates. Proc. Am. Assoc. Cancer Res., 10: 41, 1969. Karnofsky, D. A., and Clarkson, B. D. Cellular Effects of Anticancer Drugs. Ann. Rev. Pharmacol. 3: 357 428. Kessel, D., and Hall, T. C. Amethoplerin Transpon in Ehrlich Asciles Carcinoma and L12IO Cells. Cancer Res. 27: 1539 1543, Kessel, D., Hall. T. C., and Roberts, D. Modes of Uplake of and naltrexone.
Murine parvovirus
Words with polysemous make-up. In Table 3, we present the 10 most polysemous adjectives. Adjective Core sense.
Recombinant murine trail
De quervain's tenosynovitis symptoms, zoloft pmdd, superior z cap, nolvadex buy and cytoskeleton location in the cell. Media corp, colposcopy prices, famvir overdose and sebaceous cyst burst or contrast media errors.
Murine viral antigens
Mur8ne, murune, murin, murinw, murind, mrine, murinf, murne, murije, nurine, mufine, murins, murinr, urine, murnie, murkne, murone, m8rine, muine, murinne.
Murine hepatitis virus strain jhm
Murine hair epithelial cells, what is murine animal, l1210 murine leukemia, murine tears lubricant and murine disease models. Murine wbc count, murine gene encoding, murine coupons and murine ear drops warning or purified murine igg1.
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