排序方式: 共有33条查询结果,搜索用时 15 毫秒
1.
在iOS开发过程中,因为系统自带方法对应的功能不足,使部分业务需求不能有效地实现.为此,首先对Runtime库的主要API接口用途进行了研究,找到可利用的接口;然后对Runtime消息转发机制进行研究,证明函数调用的实质就是消息的传递;最后通过实际案例,证明了应用Runtime可以解决系统方法不足的问题.结果 表明,通... 相似文献
2.
Lanigan F O'Connor D Martin F Gallagher WM 《Cellular and molecular life sciences : CMLS》2007,64(24):3159-3184
During its lifetime, the mammary gland undergoes many phases of development and differentiation. Much of this occurs during
puberty, when the ductal epithelium expands by branching morphogenesis, invading the surrounding fat pad to form an organised
mammary tree. Throughout its existence, the epithelium will go through several cycles of proliferation and cell death during
pregnancy, lactation and involution. Many of the signalling mechanisms which control the initial invasion of the fat pad by
the epithelium, and regulate its continuing plasticity, can be harnessed or corrupted by tumour cells in order to support
their aberrant growth and progression towards invasion. This is true not just for the epithelial cells themselves but also
for cells in the surrounding microenvironment, including fibroblasts, macrophages and adipocytes. This review examines the
complex web of signalling and adhesion interactions controlling branching morphogenesis, and how their alteration can promote
malignancy. Current in vivo and in vitro mammary gland models are also discussed. (Part of a Multi-author Review) 相似文献
3.
Fedeles SV Tian X Gallagher AR Mitobe M Nishio S Lee SH Cai Y Geng L Crews CM Somlo S 《Nature genetics》2011,43(7):639-647
Autosomal dominant polycystic liver disease results from mutations in PRKCSH or SEC63. The respective gene products, glucosidase IIβ and SEC63p, function in protein translocation and quality control pathways in the endoplasmic reticulum. Here we show that glucosidase IIβ and Sec63p are required in mice for adequate expression of a functional complex of the polycystic kidney disease gene products, polycystin-1 and polycystin-2. We find that polycystin-1 is the rate-limiting component of this complex and that there is a dose-response relationship between cystic dilation and levels of functional polycystin-1 following mutation of Prkcsh or Sec63. Reduced expression of polycystin-1 also serves to sensitize the kidney to cyst formation resulting from mutations in Pkhd1, the recessive polycystic kidney disease gene. Finally, we show that proteasome inhibition increases steady-state levels of polycystin-1 in cells lacking glucosidase IIβ and that treatment with a proteasome inhibitor reduces cystic disease in orthologous gene models of human autosomal dominant polycystic liver disease. 相似文献
4.
Crossan GP van der Weyden L Rosado IV Langevin F Gaillard PH McIntyre RE;Sanger Mouse Genetics Project Gallagher F Kettunen MI Lewis DY Brindle K Arends MJ Adams DJ Patel KJ 《Nature genetics》2011,43(2):147-152
The evolutionarily conserved SLX4 protein, a key regulator of nucleases, is critical for DNA damage response. SLX4 nuclease complexes mediate repair during replication and can also resolve Holliday junctions formed during homologous recombination. Here we describe the phenotype of the Btbd12 knockout mouse, the mouse ortholog of SLX4, which recapitulates many key features of the human genetic illness Fanconi anemia. Btbd12-deficient animals are born at sub-Mendelian ratios, have greatly reduced fertility, are developmentally compromised and are prone to blood cytopenias. Btbd12(-/-) cells prematurely senesce, spontaneously accumulate damaged chromosomes and are particularly sensitive to DNA crosslinking agents. Genetic complementation reveals a crucial requirement for Btbd12 (also known as Slx4) to interact with the structure-specific endonuclease Xpf-Ercc1 to promote crosslink repair. The Btbd12 knockout mouse therefore establishes a disease model for Fanconi anemia and genetically links a regulator of nuclease incision complexes to the Fanconi anemia DNA crosslink repair pathway. 相似文献
5.
6.
7.
8.
9.
Acetylcholine activates both nicotinic and muscarinic receptors in the central nervous system. Although the action of acetylcholine at muscarinic receptor has been well characterized, relatively little is known at the cellular level concerning nicotinic receptor stimulation in brain. Central nicotinic receptors have been implicated in Alzheimer's disease, seizure activity, the generation of slow-wave theta rhythm in the hippocampus and the potential abuse liability of nicotine. At the neuronal level, nicotinic agonists have been most often associated with postsynaptically mediated excitation and membrane depolarization at various sites, including Renshaw spinal motoneurons, locus coeruleus and the medial habenular nucleus. Nicotine acting presynaptically can produce either excitation or inhibition indirectly through the release of endogeneous transmitters or modulators. Whereas a direct inhibitory effect of nicotine has been suggested by one in vivo extracellular recording study in rat cerebellar Purkinje neurons, the mechanism(s) underlying this action is not yet known. We now report our findings obtained using in vitro intracellular methods in a submerged brain slice preparation in which application of nicotinic agonists to rat dorsolateral septal neurons reveal a direct membrane hyperpolarization mediated by an increase in potassium conductance. 相似文献
10.
R. M. Donati M. A. Warnecke N. I. Gallagher 《Cellular and molecular life sciences : CMLS》1966,22(4):270-272
Résumé Après 96 h de jeûne, le rat consomme moins d'oxygène et ses erythrocytes moins de radiotriiodothyronine. La thyroïde de l'animal en état de jeûne absorbe davantage d'iode radioactif administré pendant 24 h et la concentration thyroïdienne en thyroxine est augmentée. Le jeûne ne modifie pas la perte intestinale de la radiothyroxine. L'administration de TSH ne rétablit pas complètement la fonction thyroïdienne, bien que la courbe de la clearance plasmatique de la radiothyroxine des rats affamés se rapproche alors de celle observée après l'administration de TSH chez les animaux nourris normalement. 相似文献