2,395 research outputs found
Kebudayaan dan pembangunan : sebuah pendekatan terhadap antroplogi terapan di Indonesia/ Colletta
xi, 333 hal.; 21 cm
Cytosolic arylamine N-acetyltransferase (NAT) deficiency in the dog and other canids due to an absence of NAT genes
The purpose of this study was to determine the molecular basis in the dog for an unusual and absolute deficiency in the activity of cytosolic N-acetyltransferase (NAT), an enzyme important for the metabolism of arylamine and hydrazine compounds. NAT activity towards two NAT substrates, p-aminobenzoic acid and sulfamethazine, was undetectable in dog liver cytosol, despite substrate concentrations ranging from 10 microM to 4 mM and a wide range of incubation times. Similarly, no protein immunoreactive to NAT antibody was evident on western blot analysis of canine liver cytosol. Southern blot analysis of genomic DNA from a total of twenty-five purebred and mixed bred dogs, and eight wild canids, probed with a full-length human NAT2 cDNA, suggested an absence of NAT sequences in all canids. Polymerase chain reaction amplification of genomic DNA using degenerate primers designed to mammalian NAT1 and NAT2 consensus sequences generated products of the expected size in human, mouse, rabbit, and cat DNA, but no NAT products in any dog or wild canids. These results support the conclusion that cytosolic NAT deficiency in the domestic dog is due to a complete absence of NAT genes, and that this defect is shared by other canids.LR: 20061115; PUBM: Print; JID: 0101032; 150-13-0 (4-Aminobenzoic Acid); 57-68-1 (Sulfamethazine); 9007-49-2 (DNA); EC 2.3.1.5 (Arylamine N-Acetyltransferase); ppublishSource type: Electronic(1
Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis
Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis
Analysis of immune-related loci identifies 48 new susceptibility variants for multiple sclerosis
Using the ImmunoChip custom genotyping array, we analyzed 14,498 subjects with multiple sclerosis and 24,091 healthy controls for 161,311 autosomal variants and identified 135 potentially associated regions (P < 1.0 × 10−4). In a replication phase, we combined these data with previous genome-wide association study (GWAS) data from an independent 14,802 subjects with multiple sclerosis and 26,703 healthy controls. In these 80,094 individuals of European ancestry, we identified 48 new susceptibility variants (P < 5.0 × 10−8), 3 of which we found after conditioning on previously identified variants. Thus, there are now 110 established multiple sclerosis risk variants at 103 discrete loci outside of the major histocompatibility complex. With high-resolution Bayesian fine mapping, we identified five regions where one variant accounted for more than 50% of the posterior probability of association. This study enhances the catalog of multiple sclerosis risk variants and illustrates the value of fine mapping in the resolution of GWAS signals
Differences in population density and energy use between birds and mammals: A microecological perspective
1. Data from 364 mammal and 564 bird species were used to compare these two taxa in the patterns of variation in population density and energy use as a function of body mass. 2. This study demonstrates previously unappreciated quantitative differences between mammals and birds. Over a wide range of sizes, population densities and rates of energy use are at least one order of magnitude higher in mammals than in birds of similar size, The highest population densities are found in species that weigh about 100 g in mammals and 30 g in birds. 3. Comparisons between mammals and birds from the same dietary category indicate that mammals maintain higher densities and use more energy than birds. Insectivorous mammals and birds maintain the lowest densities. 4. Flying mammals and birds reach lower densities and use more energy than non-flying forms. 5. These findings reveal relationships between the morphology, physiology and behaviour of individual organisms and the ecological performance of these endothermic vertebrates in populations, communities and ecosystems: relationships that have not previously been appreciated.PT: J; CR: ALLEN GT, 1987, J WILDLIFE MANAGE, V51, P739 ANDERSON S, 1977, AM MUS NOVIT, V2629, P1 ANDERSON S, 1984, AM MUS NOVIT, V2785, P1 ASHMOLE NP, 1968, SYST ZOOL, V17, P292 BARCLAY RMR, 1991, AM NAT, V137, P693 BLACKBURN TM, 1990, J ANIM ECOL, V59, P335 BLACKBURN TM, 1993, J ANIM ECOL, V62, P519 BLACKBURN TM, 1993, J ANIM ECOL, V62, P694 BLACKBURN TM, 1994, PHILOS T ROY SOC B, V343, P33 BLACKBURN TM, 1994, TRENDS ECOL EVOL, V9, P471 BLUEWEISS L, 1978, OECOLOGIA, V37, P257 BONNER JT, 1988, EVOLUTION COMPLEXITY BRADBURY JW, 1976, BEHAV ECOL SOCIOBIOL, V1, P337 BROWN JH, 1977, ECOLOGY, V54, P775 BROWN JH, 1986, NATURE, V324, P248 BROWN JH, 1987, AM NAT, V130, P1 BROWN JH, 1989, SCIENCE, V243, P1145 BROWN JH, 1993, AM NAT, V142, P573 CALDER WA, 1984, SIZE FUNCTION LIFE H CAMBEFORT Y, 1994, ACTA OECOL, V15, P165 CAMPBELL B, 1985, DICT BIRDS CARRASCAL LM, 1991, AM NAT, V138, P777 CEBALLOS G, 1995, CONSERV BIOL, V9, P559 COTGREAVE P, 1991, NATURE, V290, P699 COTGREAVE P, 1992, FUNCT ECOL, V6, P248 COTGREAVE P, 1993, TRENDS ECOL EVOL, V8, P244 COTGREAVE P, 1994, FUNCT ECOL, V8, P219 COTGREAVE P, 1994, OIKOS, V71, P89 COTGREAVE P, 1994, P ROY SOC LOND B BIO, V256, P147 COTGREAVE P, 1995, FUNCT ECOL, V9, P285 CRAIGHEAD JJ, 1973, WILDLIFE MONOGR, V33, P1 CURRIE DJ, 1993, OIKOS, V66, P353 CURRIE DJ, 1993, OIKOS, V67, P56 DAMUTH J, 1981, BIOL J LINN SOC, V15, P185 DAMUTH J, 1981, NATURE, V290, P699 DAMUTH J, 1987, BIOL J LINN SOC, V31, P193 DAMUTH J, 1991, NATURE, V351, P268 DAMUTH J, 1993, NATURE, V365, P748 DELGIUDICE GD, 1991, J WILDLIFE MANAGE, V55, P653 DUNNING JB, 1984, W BIRD BAND ASS MONO, V1 DUNNING JB, 1992, CRC HDB AVIAN BODY M EBENMAN B, 1995, OIKOS, V73, P225 GAISLER J, 1975, ACTA SCI NAT BRNO, V9, P1 GAISLER J, 1979, ECOLOGY BATS GASTON KJ, 1990, BIOL REV, V65, P105 GASTON KJ, 1991, OIKOS, V61, P434 GASTON KJ, 1993, ECOL ENTOMOL, V18, P310 GASTON KJ, 1995, PHILOS T ROY SOC B, V347, P205 GREENWOOD JJD, 1996, PHILOS T ROY SOC B, V351, P265 GREGORY RD, 1995, OIKOS, V72, P151 GRIFFITHS D, 1992, J ANIM ECOL, V61, P307 GUJARATI D, 1978, BASIC ECONOMETRICS HANCOCK JA, 1992, STORKS IBISES SPOONB HARESTAD AS, 1979, ECOLOGY, V60, P389 HARVEY PH, 1991, COMP METHOD EVOLUTIO HEMKER TP, 1984, J WILDLIFE MANAGE, V48, P1275 HOLLING CS, 1992, ECOL MONOGR, V62, P447 JUANES F, 1986, AM NAT, V128, P921 KURZEJESKI EW, 1987, J WILDLIFE MANAGE, V51, P188 LAWTON JH, 1989, OIKOS, V55, P429 LAWTON JH, 1990, PHILOS T ROY SOC B, V330, P283 MACE GM, 1983, AM NAT, V121, P120 MARQUET PA, 1990, SCIENCE, V250, P1125 MARQUET PA, 1993, THESIS U NEW MEXICO MARQUET PA, 1995, J ANIM ECOL, V64, P325 MAURER BA, 1988, ECOLOGY, V69, P1923 MCNAB BK, 1980, AM NAT, V116, P106 MCNAB BK, 1986, ECOL MONOGR, V56, P1 MCNAB BK, 1994, AM NAT, V144, P628 MEDEL RG, 1995, AM NAT, V145, P155 MILLAR JS, 1991, FUNCT ECOL, V5, P588 NAGY KA, 1987, ECOL MONOGR, V57, P111 NEE S, 1991, NATURE, V351, P312 NORBERG UM, 1986, ORNIS SCAND, V17, P253 NORBERG UM, 1987, PHIL T R SOC B, V316, P335 NOVICK A, 1971, J MAMMAL, V52, P817 NOWAK RM, 1991, WALKERS MAMMALS WORL, V1 PAGEL MD, 1988, Q REV BIOL, V63, P413 PAGEL MD, 1991, AM NAT, V138, P836 PENNYCUICK CJ, 1978, OIKOS, V30, P165 PETERS RH, 1983, ECOLOGICAL IMPLICATI PETERS RH, 1983, OECOLOGIA, V60, P89 PETERS RH, 1984, AM NAT, V128, P665 PIMM SL, 1991, BALANCE NATURE ECOLO PULLIAM HR, 1975, ECOLOGY, V56, P1158 RAYNER JMV, 1981, S ZOOL SOC LONDON, V48, P137 REDFORD KH, 1991, LATIN AM MAMMALOGY H, P227 ROBINSON JG, 1986, AM NAT, V128, P665 ROSENZWEIG ML, 1968, AM MIDL NAT, V80, P299 SCHMIDTNIELSEN K, 1983, ANIMAL PHYSL ADAPTAT SCHMIDTNIELSEN K, 1984, SCALING WHY ANIMAL S SEIDENSTICKER JC, 1973, WILDLIFE MONOGR, V35, P1 SILVA M, 1994, CONSERV BIOL, V8, P732 SILVA M, 1995, AM NAT, V145, P704 SOULE ME, 1986, BIOL CONSERV, V35, P19 STEARNS SC, 1983, OIKOS, V41, P173 STORK NE, 1987, ECOL ENTOMOL, V12, P69 STORK NE, 1993, OIKOS, V67, P483 TERBORGH J, 1990, ECOL MONOGR, V60, P213 THOMAS CD, 1990, CONSERV BIOL, V4, P324 TURNER DC, 1975, VAMPIRE BAT FIELD ST WATSON J, 1992, J ANIM ECOL, V61, P543 WELSH AH, 1988, AM NAT, V132, P277 WICKSTROM ML, 1984, J WILDLIFE MANAGE, V48, P1285 WIENS JA, 1977, GRANIVOROUS BIRDS EC, P205; NR: 105; TC: 18; J9: J ANIM ECOL; PG: 14; GA: WY474Source type: Electronic(1
Relationship between domoic acid levels in the blue mussel (Mytilus-edulis) and toxicity in mice
PT: J; CR: 1988, CAN CHEM NEWS, V10, P15 BATES SS, 1988, 57 NAT RES COUNC CAN BIRD CJ, 1988, 56 NAT RES COUNC CAN BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248 COYLE JT, 1984, EXCITOTOXINS, V39, P112 DEBONNEL G, 1989, CAN J PHYSIOL PHARM, V67, P29 FRANSON MA, 1980, STANDARD METHODS EXA IMPELLIZZERI G, 1975, PHYTOCHEMISTRY, V14, P1549 LAWRENCE JF, 1989, J CHROMATOGR, V462, P349 LITCHFIELD JT, 1949, J PHARMACOL EXP THER, V96, P99 MAEDA M, 1987, PESTIC BIOCHEM PHYS, V28, P85 QUILLIAM MA, 1988, 55 NAT RES COUNC CAN RAO DVS, 1988, CAN J FISH AQUAT SCI, V45, P2076 TAKEMOTO T, 1958, CHEM PHARM BULL, V6, P578 TAKEMOTO T, 1978, KAINIC ACID TOOL NEU, P1 WILLIAMS S, 1984, OFFICIAL METHODS ANA, P344 WRIGHT JLC, 1989, CAN J CHEM, V67, P481; NR: 17; TC: 21; J9: TOXICON; PG: 8; GA: DF893Source type: Electronic(1
Predaceous water beetles (Coleoptera: Adephaga : Dytiscidae, Gyrinidae) collected along the Horton and Thelon Rivers in the Arctic Central Barrens of Canada
Predaceous water beetles were collected during expeditions along two northern Canadian rivers during 2000 and 2002. Twelve species of Dytiscidae (including 11 named species and one additional genus identified from a larva) and one species of Gyrinidae are recorded from 20 sites along the Horton and Thelon rivers in the Central Barrens area of the Canadian Arctic. These records represent an extension of the distributions of four species to the northeast in the Northwest Territories (NWT), and two species to the northwest in Nunavut (NU). Oreodytes sanmorkii is reported for NWT and for the mainland of NU for the first time. Ilybius erichsoni, Hydroporus geniculatus, and Gyrinus opacus are reported for NU for the first time. Five species were recorded for the first time from the Southern Arctic ecozone, and one from the Taiga Shield ecozone. The majority of specimens were collected in habitats that were consistent with those previously known for each species.PT: J; CR: ALARIE Y, 1991, COLEOPTS BULL, V45, P350 ANDERSON RS, 1909, INSECTS YUKON CURRIE DC, 2000, NEWSLETTER BIOL SURV, V19, P48 CURRIE DC, 2002, NEWSLETTER BIOL SURV, V21, P59 LARSON DJ, 1991, CHECKLIST BEETLES CA, P62 LARSON DJ, 1991, COLEOPTERISTS B, V45, P280 LARSON DJ, 1997, INSECTS YUKON, P491 LARSON DJ, 2000, PREDACEOUS DIVING BE NILSSON AN, 1995, FAUNA ENTOMOLOGICA S, V32, P1 OYGUR S, 1991, B AM MUS NAT HIST, V207, P1 ROUGHLEY RE, 1991, CHECKLIST BEETLES CA, P72; NR: 11; TC: 0; J9: CAN FIELD-NATUR; PG: 9; GA: 978JVSource type: Electronic(1
Hundreds of variants clustered in genomic loci and biological pathways affect human height
Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits(1), but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait(2,3). The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P<0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways
Estimation of seed bank and seed viability of the Gulf of Saint Lawrence Aster, Symphyotrichum laurentianum, (Fernald) Nesom
The Gulf of St. Lawrence Aster, Symphyotrichum laurentianum, is a member of the family Asteraceae and is listed as "threatened" by COSEWIC (Committee on the Status of Endangered Wildlife in Canada). This rare and vulnerable halophyte grows in only a few locations in New Brunswick, Prince Edward Island, and the Magdalen Islands, Quebec. As an annual, S. laurentianum relies exclusively on its seeds to survive to the next generation. The goal of this study was to estimate the quantity of viable S. laurentianum seeds in the persistent and transient seed banks at selected sites in Prince Edward Island. Overall, the number of seeds in the transient and persistent seed banks is low. The greatest concentration of seeds was found near the surface of the soil. In addition, only a small proportion of those seeds tested positive for viability based on Tetrazolium staining. Of the seeds in the persistent and transient seed banks combined, 53% were viable whereas only 2% of the seeds in the persistent seed bank were viable. Population surveys were also completed at the five known sites (both extinct and extant) in Prince Edward Island National Park. All sites showed signs of decline based on population estimates dating back to 1993. The Covehead Pond site showed the greatest decline: from 250-300 individuals in 1993 to only 10 individuals in 2002. The population at Dune Slack also showed a dramatic decrease from approximately 65 000 in 1999, to 2 200 individuals in 2002. Monitoring of this plant and the development of a management plan for the species are critical to its survival.PT: J; CR: *COMM STAT END WIL, 2004, COSEWIC ASS UPD STAT BASKIN CC, 1998, SEEDS ECOLOGY BIOGEO FENNER M, 2000, SEEDS ECOLOGY REGENE GILBERT H, 1999, SITUATION ASTER SAIN GRABE DF, 1970, HDB SEED TESTING, V29 HOULE F, 1990, CAN FIELD NAT, V104, P455 STEWART SE, 2000, THESIS U PRINCE EDWA STEWART SE, 2001, CAN FIELD NAT, V115, P287; NR: 8; TC: 0; J9: CAN FIELD-NATUR; PG: 6; GA: 887SMSource type: Electronic(1
On the Author Correction: Magnetic field screening in hydrogen-rich high-temperature superconductors , Nat Commun 14, 5322 (2023)
I analyze the implications of the recently published Author Correction (Nat Commun 14, 5322 (2023)) to a paper by Eremets and coauthors reporting magnetization measurements on hydrides under high pressure (Nat Commun 13, 3194 (2022)) to the understanding of the validity and reproducibility of the published data. This paper is a compilation of several different papers already published or to be published in the scientific literature.The underlying measured data referred to in this article as unavailable have recently been made available at https://osf.io/7wqxb/ August 9, 202
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