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  • 1
    Publication Date: 2000-11-18
    Description: Despite the fact that Leishmania are transmitted exclusively by sand flies, none of the experimental models of leishmaniasis have established infection via sand fly bites. Here we describe a reproducible murine model of Leishmania major infection transmitted by Phlebotomus papatasi. Prior exposure of mice to bites of uninfected sand flies conferred powerful protection against Leishmania major that was associated with a strong delayed-type hypersensitivity response and with interferon-gamma production at the site of parasite delivery. These results have important implications for the epidemiology of cutaneous leishmaniasis and suggest a vaccination strategy against this and possibly other vector-borne diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kamhawi, S -- Belkaid, Y -- Modi, G -- Rowton, E -- Sacks, D -- New York, N.Y. -- Science. 2000 Nov 17;290(5495):1351-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11082061" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dermis/immunology/parasitology ; Disease Models, Animal ; Ear ; Epidermis/immunology/parasitology ; Female ; Humans ; Hypersensitivity, Delayed ; *Insect Bites and Stings ; *Insect Vectors/parasitology ; Interferon-gamma/biosynthesis ; Interleukins/biosynthesis ; *Leishmania major/physiology ; Leishmaniasis, Cutaneous/*immunology/parasitology/*transmission ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; *Phlebotomus/parasitology ; Saliva/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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  • 2
    Publication Date: 1989-01-13
    Description: Salivary gland lysates of the sand fly Lutzomyia longipalpis contain a potent vasodilator that aids the fly to feed on the blood of its vertebrate hosts. Chromatographic analysis, antibody reactivity, and data obtained from bioassays of the salivary erythema-inducing factor indicate striking similarity with human calcitonin gene-related peptide. The erythema-inducing factor is, however, at least one order of magnitude more potent than calcitonin gene-related peptide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ribeiro, J M -- Vachereau, A -- Modi, G B -- Tesh, R B -- AI18694-0481/AI/NIAID NIH HHS/ -- AI21049/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Jan 13;243(4888):212-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Tropical Public Health, Harvard School of Public Health, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2783496" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/drug effects/physiology ; Calcitonin/pharmacology ; Calcitonin Gene-Related Peptide ; Chromatography, High Pressure Liquid ; Diptera ; Erythema ; Humans ; In Vitro Techniques ; Muscle, Smooth, Vascular/drug effects/*physiology ; Neuropeptides/pharmacology ; Rabbits ; Salivary Proteins and Peptides/*isolation & purification/pharmacology ; Vasodilation ; *Vasodilator Agents
    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
    Publication Date: 2013-06-12
    Description: The mammalian gut ecosystem has considerable influence on host physiology, but the mechanisms that sustain this complex environment in the face of different stresses remain obscure. Perturbations to the gut ecosystem, such as through antibiotic treatment or diet, are at present interpreted at the level of bacterial phylogeny. Less is known about the contributions of the abundant population of phages to this ecological network. Here we explore the phageome as a potential genetic reservoir for bacterial adaptation by sequencing murine faecal phage populations following antibiotic perturbation. We show that antibiotic treatment leads to the enrichment of phage-encoded genes that confer resistance via disparate mechanisms to the administered drug, as well as genes that confer resistance to antibiotics unrelated to the administered drug, and we demonstrate experimentally that phages from treated mice provide aerobically cultured naive microbiota with increased resistance. Systems-wide analyses uncovered post-treatment phage-encoded processes related to host colonization and growth adaptation, indicating that the phageome becomes broadly enriched for functionally beneficial genes under stress-related conditions. We also show that antibiotic treatment expands the interactions between phage and bacterial species, leading to a more highly connected phage-bacterial network for gene exchange. Our work implicates the phageome in the emergence of multidrug resistance, and indicates that the adaptive capacity of the phageome may represent a community-based mechanism for protecting the gut microflora, preserving its functional robustness during antibiotic stress.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3710538/" 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/PMC3710538/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Modi, Sheetal R -- Lee, Henry H -- Spina, Catherine S -- Collins, James J -- DP1 OD003644/OD/NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jul 11;499(7457):219-22. doi: 10.1038/nature12212. Epub 2013 Jun 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biomedical Engineering, Boston University, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23748443" target="_blank"〉PubMed〈/a〉
    Keywords: Aerobiosis ; Ampicillin/pharmacology ; Animals ; Anti-Bacterial Agents/*pharmacology ; Bacteriophages/*drug effects/genetics/isolation & purification ; Ciprofloxacin/pharmacology ; Drug Resistance, Microbial/*drug effects/genetics ; Feces/*microbiology/*virology ; Female ; Gene Transfer, Horizontal/drug effects/genetics ; Genes, Viral/drug effects/genetics ; Genome, Viral/*genetics ; Host Specificity/drug effects ; Metagenome/drug effects/*genetics ; Mice ; Symbiosis/drug effects/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2012-01-10
    Description: Polyaromatic hydrocarbons (PAHs) are prevalent, potent carcinogens, and 7,12-dimethylbenz[a]anthracene (DMBA) is a model PAH widely used to study tumorigenesis. Mice lacking Langerhans cells (LCs), a signatory epidermal dendritic cell (DC), are protected from cutaneous chemical carcinogenesis, independent of T cell immunity. Investigation of the underlying mechanism revealed that LC-deficient skin was relatively resistant to DMBA-induced DNA damage. LCs efficiently metabolized DMBA to DMBA-trans-3,4-diol, an intermediate proximal to oncogenic Hras mutation, and DMBA-treated LC-deficient skin contained significantly fewer Hras mutations. Moreover, DMBA-trans-3,4-diol application bypassed tumor resistance in LC-deficient mice. Additionally, the genotoxic impact of DMBA on human keratinocytes was significantly increased by prior incubation with human-derived LC. Thus, tissue-associated DC can enhance chemical carcinogenesis via PAH metabolism, highlighting the complex relation between immune cells and carcinogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3753811/" 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/PMC3753811/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Modi, Badri G -- Neustadter, Jason -- Binda, Elisa -- Lewis, Julia -- Filler, Renata B -- Roberts, Scott J -- Kwong, Bernice Y -- Reddy, Swapna -- Overton, John D -- Galan, Anjela -- Tigelaar, Robert -- Cai, Lining -- Fu, Peter -- Shlomchik, Mark -- Kaplan, Daniel H -- Hayday, Adrian -- Girardi, Michael -- 085780/Wellcome Trust/United Kingdom -- K08 AR002072/AR/NIAMS NIH HHS/ -- P30 CA016359/CA/NCI NIH HHS/ -- R01 AR056632/AR/NIAMS NIH HHS/ -- R01 CA102703/CA/NCI NIH HHS/ -- R01-AR044077/AR/NIAMS NIH HHS/ -- R01-AR056632/AR/NIAMS NIH HHS/ -- R01CA102703/CA/NCI NIH HHS/ -- T32 AR007016/AR/NIAMS NIH HHS/ -- Cancer Research UK/United Kingdom -- Department of Health/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):104-8. doi: 10.1126/science.1211600.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22223807" target="_blank"〉PubMed〈/a〉
    Keywords: 9,10-Dimethyl-1,2-benzanthracene/*analogs & derivatives/metabolism/toxicity ; Animals ; Aryl Hydrocarbon Hydroxylases/metabolism ; Carcinogens/*metabolism/*toxicity ; Carcinoma, Squamous Cell/*chemically induced/metabolism ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cytochrome P-450 CYP1A1/metabolism ; Cytochrome P-450 CYP1B1 ; *DNA Damage ; Genes, ras ; Humans ; Keratinocytes/metabolism/pathology ; Langerhans Cells/immunology/*metabolism ; Mice ; Mice, Transgenic ; Skin Neoplasms/*chemically induced/metabolism ; T-Lymphocytes/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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