Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Effect of a matrix metalloproteinase inhibitor on host resistance against Listeria monocytogenes infection (2000)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 29 (2000), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Hydroxy acid-based matrix metalloproteinase (MMP) inhibitors have been shown to inhibit tumor infiltration and growth, endotoxin shock, and acute graft-versus-host disease. Blockade of the release of soluble tumor necrosis factor-α (TNF-α) and CD95 ligand (CD95L; FasL) from cell-associated forms is reportedly involved in the mechanism of the drug effect. We investigated the effect of a MMP inhibitor, KB-R7785, on host resistance against Listeria monocytogenes infection, in which TNF-α is essentially required for the defense, in mice. The administration of KB-R7785 exacerbated listeriosis, while the drug prevented lethal shock induced by lipopolysaccharide and d-galactosamine. KB-R7785 inhibited soluble TNF-α production in spleen cell cultures stimulated by heat-killed L. monocytogenes and the drug treatment reduced serum TNF-α levels in infected mice, whereas the compound was ineffective on the modulation of interferon-γ and interleukin-10 production. The effect of KB-R7785 was considered to be dependent on TNF-α because the drug failed to affect L. monocytogenes infection in anti-TNF-α monoclonal antibody-treated mice and TNF-α knockout mice. Anti-CD95L monoclonal antibody was also ineffective on the infection. These results suggest that induction of infectious diseases, to which TNF-α is critical in host resistance, should be considered in MMP inhibitor-treated hosts.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.2000.tb01522.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Roles of endogenous cytokines in liver apoptosis of mice in lethal Listeria monocytogenes infection (2000)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 28 (2000), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Various bacterial pathogens have been identified as mediators of apoptosis. Apoptosis reportedly shows both detrimental and beneficial effects on biological functions. We studied the role of liver apoptosis in lethal Listeria monocytogenes infection and the regulation of apoptosis by endogenous cytokines during infection. Apoptosis was observed in the spleen but not in the liver of infected mice, whereas the induction of liver necrosis was evident by rising levels of serum aminotransferases in these animals. Apoptosis was detected in the liver of L. monocytogenes-infected mice which had been treated with monoclonal antibody (mAb) against tumor necrosis factor-α (TNF-α) or interleukin-6 (IL-6), or in TNF-α−/− mice, but not in γ- interferon (IFN-γ)−/− mice or mice which had been treated with mAb against IL-4 or IL-10. Augmentation of liver apoptosis in mice treated with mAb against TNF-α or IL-6 or in TNF-α−/− mice correlated with the increase in bacterial numbers in the organ, while no augmentation of apoptosis was observed in the liver of IFN-γ−/− mice irrespective of the marked increase in bacterial numbers in the organs, indicating that augmentation of liver apoptosis may not be merely due to the increase in bacterial growth in the organs. These results suggest that TNF-α and IL-6 may play an important role in protecting the liver from apoptosis in lethal L. monocytogenes infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.2000.tb01495.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Cloning of thyroid hormone receptor genes expressed in metamorphosing flounder (1994)
    Chichester [u.a.] : Wiley-Blackwell
    Developmental Genetics 15 (1994), S. 378-382 
    Details
    ISSN: 0192-253X
    Keywords: Thyroid hormone receptor ; metamorphosis ; fish ; cDNA cloning ; Life and Medical Sciences ; Genetics
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: Two distinct cDNAs encoding thyroid hormone receptors (THRs) were cloned from a λ gtl0 library prepared from the whole bodies of metamorphosing flounder larvae (Paralichfhys olivaceus). Deduced amino acid sequences of the two isolated cDNAs shared 96% and 92% homologies in their DNA- and hormone-binding domains, respectively. These were highly conserved when compared to THRs for other vertebrates: 88-96% in the DNA-binding domain and 84-94% in the hormone-binding domain. Other receptors in the nuclear receptor family showed lower homologies than those of THRs. Both THRs for the flounder had higher homologies with the α-type THRs of other vertebrates than with the β-type. Thus, the two THRs for flounder were designated as fTHRαA and fTHRαB. © 1994 Wiiey-Liss, Inc.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/dvg.1020150409
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Genetics of obesity in KK mouse and effects of A y allele on quantitative regulation (1998)
    Springer
    Mammalian genome 9 (1998), S. 506-510 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. KK mouse is known as a polygenic model for non-insulin-dependent diabetes mellitus with moderate obesity. To identify the quantitative trait loci (QTLs) responsible for the body weight in KK, linkage analysis with 97 microsatellite markers was carried out into 192 F2 progeny, comprising 93 mice with a/a genotype at agouti locus and 99 mice with A y /a genotype, of a cross between C57BL/6J female and KK-Ay (Ay congenic) male, thereby the influence of A y allele on the quantitative regulation of body weight was also examined. In F2 a/a mice, we identified a QTL on Chromosome (Chr) 4, and two loci with suggestive linkage on Chrs 15 and 18. In F2 A y /a mice, a QTL was identified on Chr 6, and two loci with suggestive linkage were identified on Chrs 4 and 16. That the QTL on Chr 4 was held in common between F2 a/a and F2 A y /a progenies implies that this locus may be a primary component regulating body weight in KK and KK-Ay. These results suggest that the body weight in KK is controlled by multiple genes, and the different combination of loci is involved in the presence of A y allele. The QTL on Chr 6 seemed to determine the body weight by controlling fat deposition, because the linkage was identified on body weight and adiposity, and is suggested to be a component involved in the metabolic pathway in obesity caused by the A y allele.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003359900809
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Genetic analysis of neonatal death with growth retardation in F1 male Dh/+ mice (1999)
    Springer
    Mammalian genome 10 (1999), S. 777-783 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Nearly all F1 male mice with Dh/+ genotype between DDD female and DH–Dh/+ male die within a few days after birth; however, this is not observed in the reciprocal cross. The F1 Dh/+ males usually exhibit growth retardation prior to death. To identify the putative genetic locus or loci in DDD genome that cause the abnormalities in the presence of the Dh, a linkage analysis was carried out in backcross progeny of a cross of (DDD female × DH–+/+ male) F1 female × DH–Dh/+ male. Appearance of growth retardation was examined from the day of birth, and both growth-retarded and normally weaned Dh/+ males were genotyped for microsatellite marker loci spanning autosomes and the X Chromosome (Chr). Significant evidence for linkage was identified on the distal edge of the X Chr, near the microsatellite marker of DXMit135. Furthermore, among mice from DDD female × reciprocal F1 Dh/+ male produced between DH–Dh/+ and progenitor strains (C57BL/6J, C3H/HeJ and BALB/cA), only the progeny from ♀DDD ×♂(♀DH–Dh/+×♂C3H/HeJ) F1 Dh/+ male did not show any lethality and/or growth retardation. Thus, the lethality in F1 Dh/+ males accompanied by growth retardation is caused by the interactions between the Dh gene, X Chr, and Y Chr. Based on the CAG repeat sequence length polymorphism among Mus musculus musculus Sry gene, C3H/HeJ was different from C57BL/6J, BALB/cA, and DH. These data suggest that there are at least two functional types of Y Chr in Mus musculus musculus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003359901091
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Quantitative trait loci that modify the sootiness of yellow pigmentation in KK-A y /a mice (2000)
    Springer
    Mammalian genome 11 (2000), S. 639-644 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Compared with C57BL/6J-A y /a, KK-A y /a mice have yellow fur that is markedly darker. Furthermore, there is a considerable variation in the tone of color with a continuous range in F2 progeny produced from C57BL/6J females and KK-A y /a males. The aims of this study are to reveal the phenotypic differences between the two A y congenic strains and to elucidate the genetic factors responsible for the sooty yellow pigmentation in the KK background. On the basis of a chemical analysis, the sootiness in KK-A y /a was the result of increased eumelanin (PTCA) and decreased pheomelanin (AHP). A statistically significant QTL was identified on Chromosome (Chr) 15, responsible for the AHP content. No significant loci responsible for PTCA were identified. On the other hand, on the basis of an optical analysis for color difference and overall sootiness, significant evidence of linkage was identified on the proximal part of Chr 15, in the region similar to AHP QTL. The overall sootiness is thus controlled solely by the locus on Chr 15 in F2 progeny; however, the KK allele at this locus significantly increased the AHP content.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003350010136
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...