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排序方式: 共有226条查询结果,搜索用时 15 毫秒
171.
The contribution of product and industry knowledge to the accuracy of sales forecasting was investigated by examining the company forecasts of a leading manufacturer and marketer of consumable products. The company forecasts of 18 products produced by a meeting of marketing, sales, and production personnel were compared with those generated by the same company personnel when denied specific product knowledge and with the forecasts of selected judgemental and statistical time series methods. Results indicated that product knowledge contributed significantly to forecast accuracy and that the forecast accuracy of company personnel who possessed industry forecasting knowledge (but not product knowledge) was not significantly different from the time series based methods. Furthermore, the company forecasts were more accurate than averages of the judgemental and statistical time series forecasts. These results point to the importance of specific product information to forecast accuracy and accordingly call into question the continuing strong emphasis on improving extrapolation techniques without consideration of the inclusion of non-time series knowledge. 相似文献
172.
David B. Lawrence 《Journal of forecasting》1991,10(4):425-443
This paper reviews, extends and applies alternative normative decision models for the assessment of the value of forecast information, concentrating primarily on the factors influencing the tractability of assessment and interpretation in specific decision problems. As an empirical illustration of t lhe models, the paper presents a valuation analysis of the published judgmental price forecasts of a veteran analyst of the hog market to a perfectly competitive farm enterprise. 相似文献
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175.
通过对水稻RAPD反应条件比较研究,建立了对除草剂敏感致死水稻RAPD的最适反应体系和反应扩增程序,即在25μl反应体系中,含10 mM Tris-HCl(pH8.0),10 mM KCl,8 mM(NH4)2SO4,0.05%NP-40,2.0 mM MgCl2,0.1 mM(each)dTNPs,20 ng引物,20ng基因组DNA,1.5 U的Taq酶.反应扩增程序为:94℃变性2 min;扩增40个循环,每循环包括:94℃变性10 s,40℃退火30 s,72℃延伸1.5 min;最终延伸5 min. 相似文献
176.
177.
Ding L Getz G Wheeler DA Mardis ER McLellan MD Cibulskis K Sougnez C Greulich H Muzny DM Morgan MB Fulton L Fulton RS Zhang Q Wendl MC Lawrence MS Larson DE Chen K Dooling DJ Sabo A Hawes AC Shen H Jhangiani SN Lewis LR Hall O Zhu Y Mathew T Ren Y Yao J Scherer SE Clerc K Metcalf GA Ng B Milosavljevic A Gonzalez-Garay ML Osborne JR Meyer R Shi X Tang Y Koboldt DC Lin L Abbott R Miner TL Pohl C Fewell G Haipek C Schmidt H Dunford-Shore BH Kraja A Crosby SD Sawyer CS Vickery T Sander S Robinson J 《Nature》2008,455(7216):1069-1075
Determining the genetic basis of cancer requires comprehensive analyses of large collections of histopathologically well-classified primary tumours. Here we report the results of a collaborative study to discover somatic mutations in 188 human lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are probably involved in carcinogenesis. The frequently mutated genes include tyrosine kinases, among them the EGFR homologue ERBB4; multiple ephrin receptor genes, notably EPHA3; vascular endothelial growth factor receptor KDR; and NTRK genes. These data provide evidence of somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers--including NF1, APC, RB1 and ATM--and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B. The observed mutational profiles correlate with clinical features, smoking status and DNA repair defects. These results are reinforced by data integration including single nucleotide polymorphism array and gene expression array. Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment. 相似文献
178.
Repairing research integrity 总被引:1,自引:0,他引:1
179.
Kishimoto M Antonucci R Blaes O Lawrence A Boisson C Albrecht M Leipski C 《Nature》2008,454(7203):492-494
Quasars are thought to be powered by supermassive black holes accreting surrounding gas. Central to this picture is a putative accretion disk which is believed to be the source of the majority of the radiative output. It is well known, however, that the most extensively studied disk model-an optically thick disk which is heated locally by the dissipation of gravitational binding energy-is apparently contradicted by observations in a few major respects. In particular, the model predicts a specific blue spectral shape asymptotically from the visible to the near-infrared, but this is not generally seen in the visible wavelength region where the disk spectrum is observable. A crucial difficulty has been that, towards the infrared, the disk spectrum starts to be hidden under strong, hot dust emission from much larger but hitherto unresolved scales, and thus has essentially been impossible to observe. Here we report observations of polarized light interior to the dust-emitting region that enable us to uncover this near-infrared disk spectrum in several quasars. The revealed spectra show that the near-infrared disk spectrum is indeed as blue as predicted. This indicates that, at least for the outer near-infrared-emitting radii, the standard picture of the locally heated disk is approximately correct. 相似文献
180.
Chen Y Zhu J Lum PY Yang X Pinto S MacNeil DJ Zhang C Lamb J Edwards S Sieberts SK Leonardson A Castellini LW Wang S Champy MF Zhang B Emilsson V Doss S Ghazalpour A Horvath S Drake TA Lusis AJ Schadt EE 《Nature》2008,452(7186):429-435
Identifying variations in DNA that increase susceptibility to disease is one of the primary aims of genetic studies using a forward genetics approach. However, identification of disease-susceptibility genes by means of such studies provides limited functional information on how genes lead to disease. In fact, in most cases there is an absence of functional information altogether, preventing a definitive identification of the susceptibility gene or genes. Here we develop an alternative to the classic forward genetics approach for dissecting complex disease traits where, instead of identifying susceptibility genes directly affected by variations in DNA, we identify gene networks that are perturbed by susceptibility loci and that in turn lead to disease. Application of this method to liver and adipose gene expression data generated from a segregating mouse population results in the identification of a macrophage-enriched network supported as having a causal relationship with disease traits associated with metabolic syndrome. Three genes in this network, lipoprotein lipase (Lpl), lactamase beta (Lactb) and protein phosphatase 1-like (Ppm1l), are validated as previously unknown obesity genes, strengthening the association between this network and metabolic disease traits. Our analysis provides direct experimental support that complex traits such as obesity are emergent properties of molecular networks that are modulated by complex genetic loci and environmental factors. 相似文献