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Author |
Crosby, M.B.; Svenson, J.L.; Zhang, J.; Nicol, C.J.; Gonzalez, F.J.; Gilkeson, G.S. |
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Title |
Peroxisome proliferation-activated receptor (PPAR)gamma is not necessary for synthetic PPARgamma agonist inhibition of inducible nitric-oxide synthase and nitric oxide |
Type |
Journal Article |
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Year |
2005 |
Publication |
The Journal of pharmacology and experimental therapeutics |
Abbreviated Journal |
J Pharmacol Exp Ther |
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Volume |
312 |
Issue |
1 |
Pages |
69-76 |
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Keywords |
Animals; Cell Line; Gene Expression/drug effects; Macrophages/drug effects/metabolism; Mice; Mice, Inbred C57BL; Nitric Oxide/*metabolism; Nitric Oxide Synthase/*metabolism; Nitric Oxide Synthase Type II; PPAR delta/metabolism; PPAR gamma/*agonists/deficiency; Thiazolidinediones/pharmacology |
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Abstract |
Peroxisome proliferation-activated receptor (PPAR)gamma agonists inhibit inducible nitric-oxide synthase (iNOS), tumor necrosis factor-alpha, and interleukin-6. Because of these effects, synthetic PPARgamma agonists, including thiazolidinediones, are being studied for their impact on inflammatory disease. The anti-inflammatory concentrations of synthetic PPARgamma agonists range from 10 to 50 microM, whereas their binding affinity for PPARgamma is in the nanomolar range. The specificity of synthetic PPARgamma agonists for PPARgamma at the concentrations necessary for anti-inflammatory effects is thus in question. We report that PPARgamma is not necessary for the inhibition of iNOS by synthetic PPARgamma agonists. RAW 264.7 macrophages possess little PPARgamma, yet lipopolysaccharide (LPS)/interferon (IFN)gamma-induced iNOS was inhibited by synthetic PPARgamma agonists at 20 microM. Endogenous PPARgamma was inhibited by the transfection of a dominant-negative PPARgamma construct into murine mesangial cells. In the transfected cells, synthetic PPARgamma agonists inhibited iNOS production at 10 microM, similar to nontransfected cells. Using cells from PPARgamma Cre/lox conditional knockout mice, baseline and LPS/IFNgamma-induced nitric oxide levels were higher in macrophages lacking PPARgamma versus controls. However, synthetic PPARgamma agonists inhibited iNOS at 10 microM in the PPARgamma-deficient cells, similar to macrophages from wild-type mice. These results indicate that PPARgamma is not necessary for inhibition of iNOS expression by synthetic PPARgamma agonists at concentrations over 10 microM. Intrinsic PPARgamma function, in the absence of synthetic agonists, however, may play a role in inflammatory modulation. |
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Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA |
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0022-3565 |
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PMID:15356214 |
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no |
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Call Number |
refbase @ user @ |
Serial |
73 |
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Author |
Cheung, C.; Akiyama, T.E.; Ward, J.M.; Nicol, C.J.; Feigenbaum, L.; Vinson, C.; Gonzalez, F.J. |
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Title |
Diminished hepatocellular proliferation in mice humanized for the nuclear receptor peroxisome proliferator-activated receptor alpha |
Type |
Journal Article |
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Year |
2004 |
Publication |
Cancer research |
Abbreviated Journal |
Cancer Res |
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Volume |
64 |
Issue |
11 |
Pages |
3849-3854 |
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Keywords |
Animals; Anticholesteremic Agents/pharmacology; Carcinogens/pharmacology; Cell Division; DNA Replication/drug effects; Fatty Acids/metabolism; Hepatocytes/cytology/drug effects/metabolism/*physiology; Humans; Mice; Mice, Transgenic; Oxidation-Reduction; Peroxisome Proliferators/pharmacology; Pyrimidines/pharmacology; Receptors, Cytoplasmic and Nuclear/genetics/*physiology; Species Specificity; Transcription Factors/genetics/*physiology |
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Abstract |
Lipid-lowering fibrate drugs function as agonists for the nuclear receptor peroxisome proliferator-activated receptor alpha (PPARalpha). Sustained activation of PPARalpha leads to the development of liver tumors in rats and mice. However, humans appear to be resistant to the induction of peroxisome proliferation and the development of liver cancer by fibrate drugs. The molecular basis of this species difference is not known. To examine the mechanism determining species differences in peroxisome proliferator response between mice and humans, a PPARalpha-humanized mouse line was generated in which the human PPARalpha was expressed in liver under control of the tetracycline responsive regulatory system. The PPARalpha-humanized and wild-type mice responded to treatment with the potent PPARalpha ligand Wy-14643 as revealed by induction of genes encoding peroxisomal and mitochondrial fatty acid metabolizing enzymes and resultant decrease of serum triglycerides. However, surprisingly, only the wild-type mice and not the PPARalpha-humanized mice exhibited hepatocellular proliferation as revealed by elevation of cell cycle control genes, increased incorporation of 5-bromo-2'-deoxyuridine into hepatocyte nuclei, and hepatomegaly. These studies establish that following ligand activation, the PPARalpha-mediated pathways controlling lipid metabolism are independent from those controlling the cell proliferation pathways. These findings also suggest that structural differences between human and mouse PPARalpha are responsible for the differential susceptibility to the development of hepatocarcinomas observed after treatment with fibrates. The PPARalpha-humanized mice should serve as models for use in drug development and human risk assessment and to determine the mechanism of hepatocarcinogenesis of peroxisome proliferators. |
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Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA |
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0008-5472 |
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Notes |
PMID:15172993 |
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no |
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Call Number |
refbase @ user @ |
Serial |
74 |
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Author |
Nicol, C.J.; Yoon, M.; Ward, J.M.; Yamashita, M.; Fukamachi, K.; Peters, J.M.; Gonzalez, F.J. |
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Title |
PPARgamma influences susceptibility to DMBA-induced mammary, ovarian and skin carcinogenesis |
Type |
Journal Article |
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Year |
2004 |
Publication |
Carcinogenesis |
Abbreviated Journal |
Carcinogenesis |
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Volume |
25 |
Issue |
9 |
Pages |
1747-1755 |
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Keywords |
9,10-Dimethyl-1,2-benzanthracene/*toxicity; Animals; DNA Primers/chemistry; Disease Susceptibility; Female; Heterozygote; Humans; Mammary Neoplasms, Experimental/chemically induced/*pathology; Mice; Ovarian Neoplasms/chemically induced/*pathology; RNA, Messenger/genetics/metabolism; Receptors, Cytoplasmic and Nuclear/genetics/*physiology; Reverse Transcriptase Polymerase Chain Reaction; Skin Neoplasms/chemically induced/*pathology; Survival Rate; Transcription Factors/genetics/*physiology; Zinc Fingers |
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Abstract |
Peroxisome proliferator-activated receptor gamma (PPARgamma), a member of the nuclear receptor superfamily, plays a role in adipocyte differentiation, type II diabetes, macrophage response to inflammation and is suggested to influence carcinogen-induced colon cancer. Studies done in vitro and in vivo also revealed that PPARgamma ligands might promote differentiation and/or regression of mammary tumors. To directly evaluate the role of PPARgamma in mammary carcinogenesis, PPARgamma wild-type (+/+) or heterozygous (+/-) mice were administered 1 mg 7,12-dimethylbenz[a]anthracene (DMBA) by gavage once a week for 6 weeks and followed for a total of 25 weeks. Compared with congenic PPARgamma(+/+) littermate controls, PPARgamma(+/-) mice had early evidence for increased susceptibility to DMBA-mediated carcinogenesis based on a 1.6-fold increase in the percentage of mice with skin papillomas, as well as a 1.7-fold increase in the numbers of skin papillomas per mouse (P < 0.05). Similarly, PPARgamma(+/-) mice also had a 1.5-fold decreased survival rate (P = 0.059), and a 1.7-fold increased incidence of total tumors per mouse (P < 0.01). Moreover, PPARgamma(+/-) mice had an almost 3-fold increase in mammary adenocarcinomas (P < 0.05), an over 3-fold increase in ovarian granulosa cell carcinomas (P < 0.05), an over 3-fold increase in malignant tumors (P < 0.02) and a 4.6-fold increase in metastatic incidence. These results are the first to demonstrate an increased susceptibility in vivo of PPARgamma haploinsufficiency to DMBA-mediated carcinogenesis and suggest that PPARgamma may act as a tumor modifier of skin, ovarian and breast cancers. The data also support evidence suggesting a beneficial role for PPARgamma-specific ligands in the chemoprevention of mammary, ovarian and skin carcinogenesis. |
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Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA |
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ISSN |
0143-3334 |
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Notes |
PMID:15073042 |
Approved |
no |
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Call Number |
refbase @ user @ |
Serial |
76 |
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Author |
Harman, F.S.; Nicol, C.J.; Marin, H.E.; Ward, J.M.; Gonzalez, F.J.; Peters, J.M. |
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Title |
Peroxisome proliferator-activated receptor-delta attenuates colon carcinogenesis |
Type |
Journal Article |
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Year |
2004 |
Publication |
Nature medicine |
Abbreviated Journal |
Nat Med |
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Volume |
10 |
Issue |
5 |
Pages |
481-483 |
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Keywords |
Animals; Azoxymethane/toxicity; Colonic Neoplasms/etiology/genetics/*prevention & control; Colonic Polyps/etiology/genetics/pathology/prevention & control; Disease Models, Animal; Mice; Mice, Knockout; Mice, Mutant Strains; Phenotype; Receptors, Cytoplasmic and Nuclear/deficiency/genetics/*physiology; Transcription Factors/deficiency/genetics/*physiology |
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Abstract |
Peroxisome proliferator-activated receptor-delta (PPAR-delta; also known as PPAR-beta) is expressed at high levels in colon tumors, but its contribution to colon cancer is unclear. We examined the role of PPAR-delta in colon carcinogenesis using PPAR-delta-deficient (Ppard(-/-)) mice. In both the Min mutant and chemically induced mouse models, colon polyp formation was significantly greater in mice nullizygous for PPAR-delta. In contrast to previous reports suggesting that activation of PPAR-delta potentiates colon polyp formation, here we show that PPAR-delta attenuates colon carcinogenesis. |
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Address |
Department of Veterinary Science and The Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802, USA. jmp21@psu.edu |
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1078-8956 |
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PMID:15048110 |
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no |
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Call Number |
refbase @ user @ |
Serial |
77 |
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Author |
Gavrilova, O.; Haluzik, M.; Matsusue, K.; Cutson, J.J.; Johnson, L.; Dietz, K.R.; Nicol, C.J.; Vinson, C.; Gonzalez, F.J.; Reitman, M.L. |
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Title |
Liver peroxisome proliferator-activated receptor gamma contributes to hepatic steatosis, triglyceride clearance, and regulation of body fat mass |
Type |
Journal Article |
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Year |
2003 |
Publication |
The Journal of biological chemistry |
Abbreviated Journal |
J Biol Chem |
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Volume |
278 |
Issue |
36 |
Pages |
34268-34276 |
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Keywords |
Adipose Tissue/*metabolism; Animals; Blotting, Southern; Blotting, Western; Female; Hypoglycemia/genetics; Insulin Resistance/genetics; Lipid Metabolism; Liver/*metabolism; Liver Diseases/genetics/*metabolism; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; RNA/metabolism; Receptors, Cytoplasmic and Nuclear/*genetics/*physiology; Recombination, Genetic; Thiazoles/pharmacology; *Thiazolidinediones; Time Factors; Transcription Factors/*genetics/*physiology; Triglycerides/*metabolism |
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Abstract |
Peroxisome proliferator-activated receptor gamma (PPAR gamma) is a nuclear receptor that mediates the antidiabetic effects of thiazolidinediones. PPAR gamma is present in adipose tissue and becomes elevated in fatty livers, but the roles of specific tissues in thiazolidinedione actions are unclear. We studied the function of liver PPAR gamma in both lipoatrophic A-ZIP/F-1 (AZIP) and wild type mice. In AZIP mice, ablation of liver PPAR gamma reduced the hepatic steatosis but worsened the hyperlipidemia, triglyceride clearance, and muscle insulin resistance. Inactivation of AZIP liver PPAR gamma also abolished the hypoglycemic and hypolipidemic effects of rosiglitazone, demonstrating that, in the absence of adipose tissue, the liver is a primary and major site of thiazolidinedione action. In contrast, rosiglitazone remained effective in non-lipoatrophic mice lacking liver PPAR gamma, suggesting that adipose tissue is the major site of thiazolidinedione action in typical mice with adipose tissue. Interestingly, mice without liver PPAR gamma, but with adipose tissue, developed relative fat intolerance, increased adiposity, hyperlipidemia, and insulin resistance. Thus, liver PPAR gamma regulates triglyceride homeostasis, contributing to hepatic steatosis, but protecting other tissues from triglyceride accumulation and insulin resistance. |
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Address |
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. oksanag@bdg10.niddk.nih.gov |
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ISSN |
0021-9258 |
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Notes |
PMID:12805374 |
Approved |
no |
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Call Number |
refbase @ user @ |
Serial |
81 |
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Author |
Reynhout, I.C.; Cornelissen, J.J.L.M.; Nolte, R.J.M. |
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Title |
Self-assembled architectures from biohybrid triblock copolymers |
Type |
Journal Article |
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Year |
2007 |
Publication |
Journal of the American Chemical Society |
Abbreviated Journal |
J Am Chem Soc |
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Volume |
129 |
Issue |
8 |
Pages |
2327-2332 |
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Keywords |
Horseradish Peroxidase/*chemistry; Micelles; Molecular Structure; Myoglobin/*chemistry; Particle Size; Polyethylene Glycols/*chemistry; Polymers/*chemical synthesis/chemistry; Polystyrenes/*chemistry; Surface-Active Agents/chemical synthesis/chemistry |
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Abstract |
The synthesis and self-assembly behavior of biohybrid ABC triblock copolymers consisting of a synthetic diblock, polystyrene-b-polyethylene glycol (PSm-b-PEG113), where m is varied, and a hemeprotein, myoglobin (Mb) or horse radish peroxidase (HRP), is described. The synthetic diblock copolymer is first functionalized with the heme cofactor and subsequently reconstituted with the apoprotein or the apoenzyme to yield the protein-containing ABC triblock copolymer. The obtained amphiphilic block copolymers self-assemble in aqueous solution into a large variety of aggregate structures. Depending on the protein and the polystyrene block length, micellar rods, vesicles, toroids, figure eight structures, octopus structures, and spheres with a lamellar surface are formed. |
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Address |
Institute for Molecules and Materials, Radboud University Nijmegen, Toernooiveld 1, 6525 ED Nijmegen, The Netherlands |
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English |
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ISSN |
0002-7863 |
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Notes |
PMID:17274615 |
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no |
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Call Number |
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Serial |
1832 |
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Author |
Nelson, W.A.; Keirans, J.E.; Bell, J.F.; Clifford, C.M. |
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Title |
Host-ectoparasite relationships |
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Journal Article |
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Year |
1975 |
Publication |
Journal of Medical Entomology |
Abbreviated Journal |
J Med Entomol |
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Volume |
12 |
Issue |
2 |
Pages |
143-166 |
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Keywords |
Animal Nutrition Physiology; Animals; Anoplura/physiology; *Arthropods; Birds/parasitology; Chickens/parasitology; Dermacentor/parasitology; Diptera; Ecology; Feeding Behavior; Female; Horses/parasitology; Humans; Male; Mallophaga/physiology; Mice/parasitology; Mites/physiology; Reproduction; Sarcoptes scabiei/physiology; Sheep/parasitology; Skin/parasitology; Ticks/physiology; Toxins, Biological/toxicity; Trombiculidae/physiology |
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0022-2585 |
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Notes |
PMID:808617 |
Approved |
no |
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Call Number |
Equine Behaviour @ team @ |
Serial |
2704 |
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Author |
Rumiantsev, S.N. |
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Title |
[Biological function of Clostridium tetani toxin (ecological and evolutionary aspects)] |
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Journal Article |
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Year |
1973 |
Publication |
Zhurnal Evoliutsionnoi Biokhimii i Fiziologii |
Abbreviated Journal |
Zh Evol Biokhim Fiziol |
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Volume |
9 |
Issue |
5 |
Pages |
474-480 |
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Keywords |
Animals; Cats; Chickens; Dogs; Ecology; Evolution; Goats; Guinea Pigs; Haplorhini; Horses; Insectivora; Mice; Perissodactyla; Rabbits; Rats; Sheep; *Tetanus Toxin |
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Russian |
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Original Title |
K voprosu biologicheskoi funktsii toksina Clostridium tetani (ekologicheskie i evolutsionnye aspekty |
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0044-4529 |
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Notes |
PMID:4203684 |
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no |
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Call Number |
Equine Behaviour @ team @ |
Serial |
2713 |
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Author |
Valova, G.P.; Mefod'ev, V.V. |
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Title |
[Specific features of an epidemic process in leptospiroses in northern conditions in Western Siberia] |
Type |
Journal Article |
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Year |
1972 |
Publication |
Zhurnal Mikrobiologii, Epidemiologii, i Immunobiologii |
Abbreviated Journal |
Zh Mikrobiol Epidemiol Immunobiol |
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Volume |
49 |
Issue |
11 |
Pages |
138-145 |
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Keywords |
Animals; Bird Diseases/epidemiology; Birds; Carnivora; Cattle; Cattle Diseases/epidemiology; Dog Diseases/epidemiology; Dogs; Ecology; Foxes; Horse Diseases/epidemiology; Horses; Humans; Insectivora; Leptospirosis/*epidemiology/veterinary; Mice; Rats; Reindeer; Rodent Diseases/epidemiology; Rodentia; Sheep; Sheep Diseases/epidemiology; Siberia |
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Russian |
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Original Title |
Nekotorye spetsificheskie cherty epidemicheskogo protsessa pri leptospirozakh v usloviiakh Severa v Zapadnoi Sibiri |
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ISSN |
0372-9311 |
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Notes |
PMID:4645851 |
Approved |
no |
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Call Number |
Equine Behaviour @ team @ |
Serial |
2718 |
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Author |
Nosek, J. |
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Title |
The ecology and public health importance of Dermacentor marginatus and D. reticulatus ticks in Central Europe |
Type |
Journal Article |
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Year |
1972 |
Publication |
Folia Parasitologica |
Abbreviated Journal |
Folia Parasitol (Praha) |
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Volume |
19 |
Issue |
1 |
Pages |
93-102 |
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Keywords |
Animals; Arthropod Vectors; Birds; Cattle; Czechoslovakia; Deer; Dermacentor/physiology; Dogs; Ecology; Encephalitis, Tick-Borne; Europe; Female; Goats; Horses; Insectivora; Male; Mice; Rodentia; Sheep; Swine; *Ticks |
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Place of Publication |
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English |
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Abbreviated Series Title |
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ISSN |
0015-5683 |
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Notes |
PMID:4670812 |
Approved |
no |
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Call Number |
Equine Behaviour @ team @ |
Serial |
2720 |
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