Nomenclature of eukaryotic DNA polymerases

Nomenclature of eukaryotic DNA polymerases
复制标题

真核DNA聚合酶的命名法

DOI:
10.1126/science.1179222
复制
发表时间:
1975
期刊:
影响因子:
56.9
通讯作者:
D. Korn
D. Korn
中科院分区:
综合性期刊1区
文献类型:
--
作者:
A. Weissbach;D. Baltimore;F. Bollum;R. Gallo;D. Korn

文献摘要

被引文献

相似文献

可见实验(表1)。可以认为,在去甲肾上腺素几乎完全耗尽后,去甲肾上腺素的额外微小且不可检测的减少可能超过某个临界阈值,并导致进食的释放。然而,如果这是真的,我们也可以预期,在我们实验室的150多只大鼠中,至少有一些已经超过了这个阈值,这些大鼠在以前的实验中通过6-OH-DA注射或电解损伤经历了VNAB破坏。实际上,联合病变组8只动物中有7只每天进食量超过本实验室先前研究的任何VNAB动物。我们的结果可以解释为什么Gold(5)最有效的下丘脑损伤与腹侧束的分布一致。下丘脑内侧病变破坏部分VNAB的弥漫性投射,应导致异常的摄食过多,如本研究中观察到的双重病变。因此,内侧下丘脑的摄食过多和腹侧束的摄食过多是可分离的现象;证据是:(i)去甲肾上腺素损失仅在夜间引起摄食过多,总体上较少的摄食过多,(ii)下丘脑损伤引起过度进食,而没有去甲肾上腺素耗尽,以及(iii)两种形式的破坏结合产生的摄食过多水平等于
vious experiment (Table 1). It could be argued that after a nearly complete depletion of norepinephrine an additional small and undetectable decrease in norepinephrine might surpass some critical threshold and lead to the release of eating. However, if this were true we would also expect this threshold would have been surpassed in at least some of the more than 150 rats in our laboratory which have undergone VNAB destruction via 6-OH-DA injection or electrolytic lesions in previous experiments. In actuality, seven of the eight animals in the combined lesion group ate more food per day than any of the previous VNAB animals studied in this laboratory. Our results would explain why Gold's (5) most effective hypothalamic lesions coincided with the distribution of the ventral bundle. Lesions in the medial hypothalamus that destroy portions of the diffuse projections of the VNAB should lead to exceptional hyperphagia such as that observed with dual lesions in the present study. Thus, medial hypothalamic hyperphagia and ventral bundle hyperphagia are separable phenomena; the evidence is: (i) norepinephrine loss caused hyperphagia only at night and less hyperphagia overall, (ii) hypothalamic lesions caused overeating without norepinephrine depletion, and (iii) the two forms of destruction combined produced a level of hyperphagia equal to