|
Keith M Ellis suggested this exercise:
Go ten years back and pick an issue of Nature. Use the papers that appear in that issue as a small sample. Now see:in defense of his assertion that "Science relies upon authority; not, as a practical day-to-day matter, falsification." I thought I'd have a go at it, so I chose the issue of 11th February 1993, picked out the biology papers, deleted a couple that were too far from my expertise and then picked every second one of those that were left. First out of the blocks was: Nature 361, 536 - 538 (1993)From the abstract, here's what I'm looking to verify: Here we use in situ hybridization to show that messenger RNA for three... adenylyl cyclases is not found in the corpus striatum. We have isolated and expressed a complementary DNA encoding new adenylyl cyclase whose selective concentration in the corpus striatum indicates that it may be responsible for the synaptic actions of dopamine.So then I went to the Science Citations Index online: the paper has been cited 124 times. As I scanned the list of papers citing the Glatt and Snyder paper, this looked likely: Lee KW, Hong JH, Choi IY, et al.so I read (skimmed) that, since I could get the full text online, and found: The type 5 adenylyl cyclase (AC5) has been thought to be a component of dopamine receptor signaling, primarily because it was highly concentrated in striatum where D1 and D2 were expressed abundantly (Glatt and Snyder, 1993; Matsuoka et al., 1997)which tells me that the cyclase Glatt and Snyder found is now called AC5 (its existence having been confirmed when other groups worked with it; you could read some adenylyl cyclase reviews to confirm that stringently if you wanted to). I went and got the full text of the Matsuoka reference: Differential expression of type I, II, and V adenylyl cyclase gene in the postnatal developing rat brainwhere I found: AC5 mRNA was expressed to a limited extent in the neonatal brain, but levels dramatically increased during the second postnatal week in restricted regions, including the striatum, nucleus accumbens, and olfactory tubercle.which provides direct experimental proof of Glatt and Snyder's localisation of type V AC. Next up: Nature 361, 541 - 543 (1993)Looking to verify: We report here the lack of CD40L expression in four unrelated male children with the hyper-IgM syndrome. CD40L transcripts in these patients showed either deletions or point mutations clustered within a limited region of the CD40L extracellular domain.Citations: 444; from the list: Winkelstein JA, Marino MC, Ochs H, et al. The X-linked hyper-IgM syndrome - Clinical and immunologic features of 79 patients MEDICINE 82 (6): 373-384 NOV 2003from which: The X-linked hyper-IgM syndrome is an uncommon primary immunodeficiency disease caused by mutations in the gene for CD40 ligand, a T-lymphocyte cell surface molecule (1, 4, 11, 19, 29).DiSanto et al. is ref 11, so that looks like four papers confirming not only their observation but their prediction that the mutations caused the disease. Here are those papers: Allen RC, Armitage RJ, Conley ME, Rosenblatt H, Jenkins NA, Copeland NG, et al. CD40 ligand gene defects responsible for X-linked hyper-IgM syndrome. Science. 1993; 259:990-993.So I called that good, and now I'm getting a bit fed up. Here are the papers I picked but didn't analyse: Nature 361, 547 - 549 (1993) |