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缪菊连 《大理学院学报:综合版》2011,(2):13-15
目的:探求残数法计算药物动力学参数的简单方法。方法:采用Excel对数据进行线性回归,得出曲线方程,根据截距和斜率计算K及Ka。结果:利用Excel能正确、快速计算出K及Ka值。结论:将Excel应用残数法计算K及Ka值能减少工作量,提高准确率及工作效率。 相似文献
3.
Although all nucleated cells within a multicellular organism contain a complete copy of the genome, cell identity relies on
the expression of a specific subset of genes. Therefore, when cells divide they must not only copy their genome to their daughters,
but also ensure that the pattern of gene expression present before division is restored. While the carrier of this epigenetic
memory has been a topic of much research and debate, post-translational modifications of histone proteins have emerged in
the vanguard of candidates. In this paper we examine the mechanisms by which histone post-translational modifications are
propagated through DNA replication and cell division, and we critically examine the evidence that they can also act as vectors
of epigenetic memory. Finally, we consider ways in which epigenetic memory might be disrupted by interfering with the mechanisms
of DNA replication. 相似文献
4.
Arboleda VA Lee H Parnaik R Fleming A Banerjee A Ferraz-de-Souza B Délot EC Rodriguez-Fernandez IA Braslavsky D Bergadá I Dell'Angelica EC Nelson SF Martinez-Agosto JA Achermann JC Vilain E 《Nature genetics》2012,44(7):788-792
IMAGe syndrome (intrauterine growth restriction, metaphyseal dysplasia, adrenal hypoplasia congenita and genital anomalies) is an undergrowth developmental disorder with life-threatening consequences. An identity-by-descent analysis in a family with IMAGe syndrome identified a 17.2-Mb locus on chromosome 11p15 that segregated in the affected family members. Targeted exon array capture of the disease locus, followed by high-throughput genomic sequencing and validation by dideoxy sequencing, identified missense mutations in the imprinted gene CDKN1C (also known as P57KIP2) in two familial and four unrelated patients. A familial analysis showed an imprinted mode of inheritance in which only maternal transmission of the mutation resulted in IMAGe syndrome. CDKN1C inhibits cell-cycle progression, and we found that targeted expression of IMAGe-associated CDKN1C mutations in Drosophila caused severe eye growth defects compared to wild-type CDKN1C, suggesting a gain-of-function mechanism. All IMAGe-associated mutations clustered in the PCNA-binding domain of CDKN1C and resulted in loss of PCNA binding, distinguishing them from the mutations of CDKN1C that cause Beckwith-Wiedemann syndrome, an overgrowth syndrome. 相似文献
5.
Christine A. Howell Julian K. Wood Mark D. Dettling Kenneth Griggs Codie C. Otte Linette Lina Thomas Gardali 《西北部美国博物学家》2011,70(1)
The Least Bell’s Vireo ( Vireo bellii pusillus ) was listed as state endangered in 1980 and federally endangered in 1986 in response to a sharp population decline and range reduction. This vireo commonly bred in riparian forests throughout the Central Valley of California, but prior to 2005, no nesting pairs had been confirmed in the region in over 50 years. On 29 June 2005, a Least Bell’s Vireo nest was located in a 3-year-old riparian restoration site at the San Joaquin River National Wildlife Refuge in Stanislaus County, California. In 2006, a Least Bell’s Vireo pair returned to the refuge to successfully breed, followed by an unsuccessful attempt in 2007 by an unpaired female. These records are approximately 350 km from the nearest known breeding population and appear to be part of a growing number of sightings outside of the species’ current southern California breeding range. These nesting attempts lend credence to the idea that extirpated species can recolonize restored habitat by long-distance dispersal. 相似文献
6.
Maller JB Fagerness JA Reynolds RC Neale BM Daly MJ Seddon JM 《Nature genetics》2007,39(10):1200-1201
The association of variants in complement factors H and B with age-related macular degeneration has led to more intense genetic and functional analysis of the complement pathway. We identify a nonsynonymous coding change in complement factor 3 that is strongly associated with risk of age-related macular degeneration in a large case-control sample. 相似文献
7.
A genome-wide association study for celiac disease identifies risk variants in the region harboring IL2 and IL21 总被引:14,自引:0,他引:14
van Heel DA Franke L Hunt KA Gwilliam R Zhernakova A Inouye M Wapenaar MC Barnardo MC Bethel G Holmes GK Feighery C Jewell D Kelleher D Kumar P Travis S Walters JR Sanders DS Howdle P Swift J Playford RJ McLaren WM Mearin ML Mulder CJ McManus R McGinnis R Cardon LR Deloukas P Wijmenga C 《Nature genetics》2007,39(7):827-829
We tested 310,605 SNPs for association in 778 individuals with celiac disease and 1,422 controls. Outside the HLA region, the most significant finding (rs13119723; P = 2.0 x 10(-7)) was in the KIAA1109-TENR-IL2-IL21 linkage disequilibrium block. We independently confirmed association in two further collections (strongest association at rs6822844, 24 kb 5' of IL21; meta-analysis P = 1.3 x 10(-14), odds ratio = 0.63), suggesting that genetic variation in this region predisposes to celiac disease. 相似文献
8.
Manipulation of host-cell pathways by bacterial pathogens 总被引:3,自引:0,他引:3
Bacterial pathogens operate by attacking crucial intracellular pathways in their hosts. These pathogens usually target more than one intracellular pathway and often interact at several points in each of these pathways to commandeer them fully. Although different bacterial pathogens tend to exploit similar pathway components in the host, the way in which they 'hijack' host cells usually differs. Knowledge of how pathogens target distinct cytoskeletal components and immune-cell signalling pathways is rapidly advancing, together with the understanding of bacterial virulence at a molecular level. Studying how these bacterial pathogens subvert host-cell pathways is central to understanding infectious disease. 相似文献
9.
Wright FA Strug LJ Doshi VK Commander CW Blackman SM Sun L Berthiaume Y Cutler D Cojocaru A Collaco JM Corey M Dorfman R Goddard K Green D Kent JW Lange EM Lee S Li W Luo J Mayhew GM Naughton KM Pace RG Paré P Rommens JM Sandford A Stonebraker JR Sun W Taylor C Vanscoy LL Zou F Blangero J Zielenski J O'Neal WK Drumm ML Durie PR Knowles MR Cutting GR 《Nature genetics》2011,43(6):539-546
A combined genome-wide association and linkage study was used to identify loci causing variation in cystic fibrosis lung disease severity. We identified a significant association (P = 3.34 × 10(-8)) near EHF and APIP (chr11p13) in p.Phe508del homozygotes (n = 1,978). The association replicated in p.Phe508del homozygotes (P = 0.006) from a separate family based study (n = 557), with P = 1.49 × 10(-9) for the three-study joint meta-analysis. Linkage analysis of 486 sibling pairs from the family based study identified a significant quantitative trait locus on chromosome 20q13.2 (log(10) odds = 5.03). Our findings provide insight into the causes of variation in lung disease severity in cystic fibrosis and suggest new therapeutic targets for this life-limiting disorder. 相似文献