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  • 1
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    Association of intestinal peptide transport with a protein related to the cadherin superfamily (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-15
    Description: The first step in oral absorption of many medically important peptide-based drugs is mediated by an intestinal proton-dependent peptide transporter. This transporter facilitates the oral absorption of beta-lactam antibiotics and angiotensin-converting enzyme inhibitors from the intestine into enterocytes lining the luminal wall. A monoclonal antibody that blocked uptake of cephalexin was used to identify and clone a gene that encodes an approximately 92-kilodalton membrane protein that was associated with the acquisition of peptide transport activity by transport-deficient cells. The amino acid sequence deduced from the complementary DNA sequence of the cloned gene indicated that this transport-associated protein shares several conserved structural elements with the cadherin superfamily of calcium-dependent, cell-cell adhesion proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dantzig, A H -- Hoskins, J A -- Tabas, L B -- Bright, S -- Shepard, R L -- Jenkins, I L -- Duckworth, D C -- Sportsman, J R -- Mackensen, D -- Rosteck, P R Jr -- New York, N.Y. -- Science. 1994 Apr 15;264(5157):430-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN 46285.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8153632" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Transport ; CHO Cells ; Cadherins/*chemistry ; Carrier Proteins/*chemistry/genetics/isolation & purification/metabolism ; Cephalexin/*metabolism ; Cloning, Molecular ; Cricetinae ; Glycosylation ; Humans ; Hydrogen-Ion Concentration ; Intestinal Mucosa/*metabolism ; Leucine/analogs & derivatives/metabolism ; *Membrane Transport Proteins ; Mice ; Mice, Inbred A ; Molecular Sequence Data ; Open Reading Frames ; Sequence Homology, Amino Acid ; Transfection ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Lack of acidification in Mycobacterium phagosomes produced by exclusion of the vesicular proton-ATPase (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-04
    Description: The success of Mycobacterium species as pathogens depends on their ability to maintain an infection inside the phagocytic vacuole of the macrophage. Although the bacteria are reported to modulate maturation of their intracellular vacuoles, the nature of such modifications is unknown. In this study, vacuoles formed around Mycobacterium avium failed to acidify below pH 6.3 to 6.5. Immunoelectron microscopy of infected macrophages and immunoblotting of isolated phagosomes showed that Mycobacterium vacuoles acquire the lysosomal membrane protein LAMP-1, but not the vesicular proton-adenosine triphosphatase (ATPase) responsible for phagosomal acidification. This suggests either a selective inhibition of fusion with proton-ATPase-containing vesicles or a rapid removal of the complex from Mycobacterium phagosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sturgill-Koszycki, S -- Schlesinger, P H -- Chakraborty, P -- Haddix, P L -- Collins, H L -- Fok, A K -- Allen, R D -- Gluck, S L -- Heuser, J -- Russell, D G -- AI26889/AI/NIAID NIH HHS/ -- AI34207/AI/NIAID NIH HHS/ -- AR42370/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):678-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University Medical Center, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303277" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, CD ; Hydrogen-Ion Concentration ; Leishmania mexicana/physiology ; Lysosome-Associated Membrane Glycoproteins ; Macrophages/metabolism/*microbiology/parasitology/ultrastructure ; Membrane Fusion ; Membrane Glycoproteins/metabolism ; Mice ; Microscopy, Immunoelectron ; Mycobacterium avium/*physiology ; Mycobacterium tuberculosis/physiology ; Phagosomes/metabolism/*microbiology/parasitology/ultrastructure ; Proton-Translocating ATPases/*metabolism ; Vacuoles/metabolism/microbiology/parasitology/ultrastructure
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Mutagenesis and mapping of a mouse gene, Clock, essential for circadian behavior (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-29
    Description: In a search for genes that regulate circadian rhythms in mammals, the progeny of mice treated with N-ethyl-N-nitrosourea (ENU) were screened for circadian clock mutations. A semidominant mutation, Clock, that lengthens circadian period and abolishes persistence of rhythmicity was identified. Clock segregated as a single gene that mapped to the midportion of mouse chromosome 5, a region syntenic to human chromosome 4. The power of ENU mutagenesis combined with the ability to clone murine genes by map position provides a generally applicable approach to study complex behavior in mammals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3839659/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3839659/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vitaterna, M H -- King, D P -- Chang, A M -- Kornhauser, J M -- Lowrey, P L -- McDonald, J D -- Dove, W F -- Pinto, L H -- Turek, F W -- Takahashi, J S -- P30-CA07175/CA/NCI NIH HHS/ -- R01-DK40493/DK/NIDDK NIH HHS/ -- T32 NS071040/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- etc. -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):719-25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Physiology, Northwestern University, Evanston, IL 60208.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171325" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Chromosomes, Human, Pair 4 ; Circadian Rhythm/*genetics ; Ethylnitrosourea ; Female ; *Genes ; Genotype ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; *Mutagenesis ; Phenotype
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Replacement of diseased mouse liver by hepatic cell transplantation (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-25
    Description: Adult liver has the unusual ability to fully regenerate after injury. Although regeneration is accomplished by the division of mature hepatocytes, the replicative potential of these cells is unknown. Here, the replicative capacity of adult liver cells and their medical usefulness as donor cells for transplantation were investigated by transfer of adult mouse liver cells into transgenic mice that display an endogenous defect in hepatic growth potential and function. The transplanted liver cell populations replaced up to 80 percent of the diseased recipient liver. These findings demonstrate the enormous growth potential of adult hepatocytes, indicating the feasibility of liver cell transplantation as a method to replace lost or diseased hepatic parenchyma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rhim, J A -- Sandgren, E P -- Degen, J L -- Palmiter, R D -- Brinster, R L -- HD-23657/HD/NICHD NIH HHS/ -- HD09172/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 25;263(5150):1149-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8108734" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Genetic Markers ; Hepatectomy ; Liver/*cytology/physiology ; Liver Diseases/*surgery ; Liver Regeneration ; *Liver Transplantation ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitotic Index ; Stem Cells/cytology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Remodeling schemes of intracellular pathogens (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Small, P L -- Ramakrishnan, L -- Falkow, S -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):637-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rocky Mountain Laboratories, National Institutes of Health, National Institute of Allergy and Infectious Diseases, Hamilton, MT 59840.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303269" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigens, CD ; Endocytosis ; Humans ; Hydrogen-Ion Concentration ; Lysosome-Associated Membrane Glycoproteins ; Macrophages/enzymology/*microbiology ; Membrane Glycoproteins/metabolism ; Mice ; Mycobacterium/*physiology ; Mycobacterium tuberculosis/*physiology ; Phagosomes/*microbiology ; Proton-Translocating ATPases/*metabolism ; Vacuoles/enzymology/*microbiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    T cell receptor-MHC class I peptide interactions: affinity, kinetics, and specificity (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-08-12
    Description: The critical discriminatory event in the activation of T lymphocytes bearing alpha beta T cell receptors (TCRs) is their interaction with a molecular complex consisting of a peptide bound to a major histocompatibility complex (MHC)-encoded class I or class II molecule on the surface of an antigen-presenting cell. The kinetics of binding were measured of a purified TCR to molecular complexes of a purified soluble analog of the murine MHC class I molecule H-2Ld (sH-2Ld) and a synthetic octamer peptide p2CL in a direct, real-time assay based on surface plasmon resonance. The kinetic dissociation rate of the MHC-peptide complex from the TCR was rapid (2.6 x 10(-2) second-1, corresponding to a half-time for dissociation of approximately 27 seconds), and the kinetic association rate was 2.1 x 10(5) M-1 second-1. The equilibrium constant for dissociation was approximately 10(-7) M. These values indicate that TCRs must interact with a multivalent array of MHC-peptide complexes to trigger T cell signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corr, M -- Slanetz, A E -- Boyd, L F -- Jelonek, M T -- Khilko, S -- al-Ramadi, B K -- Kim, Y S -- Maher, S E -- Bothwell, A L -- Margulies, D H -- New York, N.Y. -- Science. 1994 Aug 12;265(5174):946-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology Section, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8052850" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biosensing Techniques ; H-2 Antigens/*metabolism ; Histocompatibility Antigen H-2D ; Kinetics ; *Major Histocompatibility Complex ; Mice ; Molecular Sequence Data ; Oligopeptides/*metabolism ; Receptors, Antigen, T-Cell, alpha-beta/*metabolism ; Solubility
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Candidate gene associated with a mutation causing recessive polycystic kidney disease in mice (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-05-27
    Description: A line of transgenic mice was generated that contains an insertional mutation causing a phenotype similar to human autosomal recessive polycystic kidney disease. Homozygotes displayed a complex phenotype that included bilateral polycystic kidneys and an unusual liver lesion. The mutant locus was cloned and characterized through use of the transgene as a molecular marker. Additionally, a candidate polycystic kidney disease (PKD) gene was identified whose structure and expression are directly associated with the mutant locus. A complementary DNA derived from this gene predicted a peptide containing a motif that was originally identified in several genes involved in cell cycle control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moyer, J H -- Lee-Tischler, M J -- Kwon, H Y -- Schrick, J J -- Avner, E D -- Sweeney, W E -- Godfrey, V L -- Cacheiro, N L -- Wilkinson, J E -- Woychik, R P -- IAG 222Y01-ES-10067/ES/NIEHS NIH HHS/ -- R01 DK45633-01/DK/NIDDK NIH HHS/ -- R01 HD25323/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 May 27;264(5163):1329-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Tennessee Graduate School of Biomedical Sciences, Biology Division, Oak Ridge National Laboratory, TN 37831-8077.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8191288" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Caenorhabditis elegans Proteins ; Crosses, Genetic ; Female ; Homozygote ; Kidney Tubules/pathology ; Liver/pathology ; Male ; Mice ; Mice, Inbred C3H ; Mice, Transgenic ; Molecular Sequence Data ; Mutagenesis, Insertional ; *Nerve Tissue Proteins ; Phenotype ; Polycystic Kidney, Autosomal Recessive/*genetics/pathology ; Proteins/chemistry/*genetics ; *Tumor Suppressor Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    The adjuvant effect of interleukin-12 in a vaccine against Leishmania major (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-01-14
    Description: Protection induced by vaccination depends on the capacity of the vaccine to elicit an appropriate immune response. In leishmaniasis, protection requires leishmanial-specific CD4+ T helper (TH) cells. Vaccination of BALB/c mice with leishmanial antigens and interleukin-12 (IL-12) promoted the development of leishmanial-specific CD4+ TH1 cells. These mice were resistant to subsequent infection with Leishmania major. Thus, IL-12 is an effective adjuvant for the initiation of protective cell-mediated immunity against leishmaniasis and may be an important component in other vaccines that need to induce cell-mediated immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Afonso, L C -- Scharton, T M -- Vieira, L Q -- Wysocka, M -- Trinchieri, G -- Scott, P -- AI-30073/AI/NIAID NIH HHS/ -- CA-20833/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Jan 14;263(5144):235-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7904381" target="_blank"〉PubMed〈/a〉
    Keywords: *Adjuvants, Immunologic ; Animals ; Antigens, Protozoan/immunology ; Cytotoxicity, Immunologic ; Interferon-gamma/biosynthesis ; Interleukin-12 ; Interleukin-4/biosynthesis ; Interleukins/*immunology ; Killer Cells, Natural/immunology ; Leishmania major/*immunology ; Leishmaniasis, Cutaneous/immunology/*prevention & control ; Lymph Nodes/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Protozoan Vaccines/*immunology ; Spleen/immunology ; T-Lymphocytes, Helper-Inducer/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Endothelial NOS and the blockade of LTP by NOS inhibitors in mice lacking neuronal NOS (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-07-22
    Description: Long-term potentiation (LTP) is a persistent increase in synaptic strength implicated in certain forms of learning and memory. In the CA1 region of the hippocampus, LTP is thought to involve the release of one or more retrograde messengers from the postsynaptic cell that act on the presynaptic terminal to enhance transmitter release. One candidate retrograde messenger is the membrane-permeant gas nitric oxide (NO), which in the brain is released after activation of the neuronal-specific NO synthase isoform (nNOS). To assess the importance of NO in hippocampal synaptic plasticity, LTP was examined in mice where the gene encoding nNOS was disrupted by gene targeting. In nNOS- mice, LTP induced by weak intensity tetanic stimulation was normal except for a slight reduction in comparison to that in wild-type mice and was blocked by NOS inhibitors, just as it was in wild-type mice. Immunocytochemical studies indicate that in the nNOS- mice as in wild-type mice, the endothelial form of NOS (eNOS) is expressed in CA1 neurons. These findings suggest that eNOS, rather than nNOS, generates NO within the postsynaptic cell during LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Dell, T J -- Huang, P L -- Dawson, T M -- Dinerman, J L -- Snyder, S H -- Kandel, E R -- Fishman, M C -- DA-00074/DA/NIDA NIH HHS/ -- DA-00266/DA/NIDA NIH HHS/ -- MH-45923/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Jul 22;265(5171):542-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, College of Physicians and Surgeons of Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7518615" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Oxidoreductases/antagonists & inhibitors/genetics/*metabolism ; Animals ; Arginine/*analogs & derivatives/pharmacology ; Electric Stimulation ; Endothelium/enzymology ; Hippocampus/drug effects/enzymology/*physiology ; In Vitro Techniques ; *Long-Term Potentiation/drug effects ; Mice ; Mutation ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase ; Nitroarginine ; Pyramidal Cells/drug effects/enzymology/*physiology ; Synaptic Transmission/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Electronic Resource
    Electronic Resource
    Un vivo depletion of murine CD8 positive T cells impairs survival during infection with a highly virulent strain ofCryptococcus neoformans (1994)
    Springer
    Mycopathologia 125 (1994), S. 7-17 
    Details
    ISSN: 1573-0832
    Keywords: Cryptococcus ; Host defense ; Lymphocyte subsets ; Mice ; Mixed Lymphocyte Reaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Cell-mediated immunity plays an important but incompletely understood role in host defense againstCryptococcus neoformans. Because of their multiple capacities as cytokine-secreting cells, cytotoxic cells, and antigen-specific suppressor cells, CD8 positive T lymphocytes could potentially either enhance or impair host defense againstC. neoformans. To determine whether CD8 T cells enhance or inhibit host defence during an infection with a highly virulent strain ofC. neoformans, we examined the effect of in vivo CD8 cell depletion on suNival and on the number of organisms in mice infected by either the intratracheal or intravenous routes. Adequacy of depletion was confirmed both phenotypically and functionally. Regardless of the route of infection, we found that survival of mice depleted of CD8 T cells was significantly reduced compared to undepleted mice. Surprisingly, however, CD8 depletion did not alter organism burden measured by quantitative CFU assay in mice infected by either route. These data demonstrate that CD8 positive T cells participate in the immune response to a highly virulent strain ofC. neoformans. By contrast to minimally virulent isolates that do not cause a life threatening infection, the immune response to a highly virulent isolate does not alter the burden of organisms, but does enhance host defense as it is necessary for the optimal survival of infected mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01103969
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