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  • 1
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    Protection against cutaneous leishmaniasis resulting from bites of uninfected sand flies (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    A novel vasodilatory peptide from the salivary glands of the sand fly Lutzomyia longipalpis (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    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
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    Genetic restriction of AIDS pathogenesis by an SDF-1 chemokine gene variant. ALIVE Study, Hemophilia Growth and Development Study (HGDS), Multicenter AIDS Cohort Study (MACS), Multicenter Hemophilia Cohort Study (MHCS), San Francisco City Cohort (SFCC) (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-07
    Description: Stromal-derived factor (SDF-1) is the principal ligand for CXCR4, a coreceptor with CD4 for T lymphocyte cell line-tropic human immunodeficiency virus-type 1 (HIV-1). A common polymorphism, SDF1-3'A, was identified in an evolutionarily conserved segment of the 3' untranslated region of the SDF-1 structural gene transcript. In the homozygous state, SDF1-3'A/3'A delays the onset of acquired immunodeficiency syndrome (AIDS), according to a genetic association analysis of 2857 patients enrolled in five AIDS cohort studies. The recessive protective effect of SDF1-3'A was increasingly pronounced in individuals infected with HIV-1 for longer periods, was twice as strong as the dominant genetic restriction of AIDS conferred by CCR5 and CCR2 chemokine receptor variants in these populations, and was complementary with these mutations in delaying the onset of AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Winkler, C -- Modi, W -- Smith, M W -- Nelson, G W -- Wu, X -- Carrington, M -- Dean, M -- Honjo, T -- Tashiro, K -- Yabe, D -- Buchbinder, S -- Vittinghoff, E -- Goedert, J J -- O'Brien, T R -- Jacobson, L P -- Detels, R -- Donfield, S -- Willoughby, A -- Gomperts, E -- Vlahov, D -- Phair, J -- O'Brien, S J -- New York, N.Y. -- Science. 1998 Jan 16;279(5349):389-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Science Applications International Corporation (SAIC), National Cancer Institute, Frederick, MD 21702, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9430590" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/genetics/*immunology/virology ; Adult ; Chemokine CXCL12 ; Chemokines/chemistry/*genetics/physiology ; *Chemokines, CXC ; Cohort Studies ; Continental Population Groups ; Disease Progression ; Genes ; Genetic Variation ; Genotype ; HIV Infections/genetics/*immunology/virology ; HIV-1/*physiology ; Heterozygote ; Humans ; Male ; Molecular Sequence Data ; Odds Ratio ; Polymorphism, Genetic ; Receptors, CCR2 ; Receptors, CCR5/genetics/physiology ; Receptors, CXCR4/metabolism ; Receptors, Chemokine/genetics/physiology ; Survival Analysis ; T-Lymphocytes/virology
    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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  • 4
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    Identification of the von Hippel-Lindau disease tumor suppressor gene (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-28
    Description: A gene discovered by positional cloning has been identified as the von Hippel-Lindau (VHL) disease tumor suppressor gene. A restriction fragment encompassing the gene showed rearrangements in 28 of 221 VHL kindreds. Eighteen of these rearrangements were due to deletions in the candidate gene, including three large nonoverlapping deletions. Intragenic mutations were detected in cell lines derived from VHL patients and from sporadic renal cell carcinomas. The VHL gene is evolutionarily conserved and encodes two widely expressed transcripts of approximately 6 and 6.5 kilobases. The partial sequence of the inferred gene product shows no homology to other proteins, except for an acidic repeat domain found in the procyclic surface membrane glycoprotein of Trypanosoma brucei.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Latif, F -- Tory, K -- Gnarra, J -- Yao, M -- Duh, F M -- Orcutt, M L -- Stackhouse, T -- Kuzmin, I -- Modi, W -- Geil, L -- New York, N.Y. -- Science. 1993 May 28;260(5112):1317-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunobiology, National Cancer Institute-Frederick Cancer Research and Development Center (NCI-FCRDC), Frederick, MD 21702-1201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8493574" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Carcinoma, Renal Cell/genetics ; Chromosomes, Human, Pair 3 ; Cloning, Molecular ; Gene Deletion ; *Genes, Tumor Suppressor ; Humans ; Kidney Neoplasms/genetics ; Membrane Glycoproteins/chemistry/*genetics ; Molecular Sequence Data ; Mutation ; Open Reading Frames ; Pedigree ; Polymorphism, Genetic ; Tumor Cells, Cultured ; von Hippel-Lindau Disease/*genetics
    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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    Langerhans cells facilitate epithelial DNA damage and squamous cell carcinoma (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 6
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    Human endothelial cell growth factor: cloning, nucleotide sequence, and chromosome localization (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-08-01
    Description: Several of the endothelial cell polypeptide mitogens that have been described probably play a role in blood vessel homeostasis. Two overlapping complementary DNA clones encoding human endothelial cell growth factor (ECGF) were isolated from a human brain stem complementary DNA library. Southern blot analysis suggested that there is a single copy of the ECGF gene and that it maps to human chromosome 5 at bands 5q31.3 to 33.2 A 4.8-kilobase messenger RNA was present in human brain stem messenger RNA. The complete amino acid sequence of human ECGF was deduced from the nucleic acid sequence of these clones; it encompasses all the well-characterized acidic endothelial cell polypeptide mitogens described by several laboratories. The ECGF-encoding open reading frame is flanked by translation stop codons and provides no signal peptide or internal hydrophobic domain for the secretion of ECGF. This property is shared by human interleukin-1, which is approximately 30 percent homologous to ECGF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaye, M -- Howk, R -- Burgess, W -- Ricca, G A -- Chiu, I M -- Ravera, M W -- O'Brien, S J -- Modi, W S -- Maciag, T -- Drohan, W N -- AG04807/AG/NIA NIH HHS/ -- HL23348/HL/NHLBI NIH HHS/ -- HL35627/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 1;233(4763):541-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3523756" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Brain Stem/metabolism ; *Chromosome Mapping ; Cloning, Molecular ; DNA/genetics ; Endothelial Growth Factors ; Growth Substances/*genetics ; Humans ; Interleukin-1/genetics ; Liver/metabolism ; Nucleic Acid Hybridization ; RNA, Messenger/genetics
    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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