The theory theory thrice over: the child as scientist, Superscientist or social institution?

Alison Gopnik and Andrew Meltzoff have argued for a view they call the ‘theory theory’: theory change in science and children are similar. While their version of the theory theory has been criticized for depending on a number of disputed claims, we argue that there is a fundamental problem which is much more basic: the theory theory is multiply ambiguous. We show that it might be claiming that a similarity holds between theory change in children and (i) individual scientists, (ii) a rational reconstruction of a Superscientist, or (iii) the scientific community. We argue that (i) is false, (ii) is non-empirical (which is problematic since the theory theory is supposed to be a bold empirical hypothesis), and (iii) is either false or doesn't make enough sense to have a truth-value. We conclude that the theory theory is an interesting failure. Its failure points the way to a full, empirical picture of scientific development, one that marries a concern with the social dynamics of science to a psychological theory of scientific cognition.     

Cycling or not cycling: cell cycle regulatory molecules and adult neurogenesis

The adult brain most probably reaches its highest degree of plasticity with the lifelong generation and integration of new neurons in the hippocampus and olfactory system. Neural precursor cells (NPCs) residing both in the subgranular zone of the dentate gyrus and in the subventricular zone of the lateral ventricles continuously generate neurons that populate the dentate gyrus and the olfactory bulb, respectively. The regulation of NPC proliferation in the adult brain has been widely investigated in the past few years. Yet, the intrinsic cell cycle machinery underlying NPC proliferation remains largely unexplored. In this review, we discuss the cell cycle components that are involved in the regulation of NPC proliferation in both neurogenic areas of the adult brain.     

Capping of concanavalin A- or ricin-binding sites does not influence phagocytosis in polymorphonuclear leukocytes

Summary Rabbit polymorphonuclear leukocytes (PMNs) were capped with territin-conjugated concanavalin A or ricin, and then allowed to phagocytose yeast cells. Phagocytic activity and lectin distribution were determined by ultrastructural morphometry. Capped PMNs were found to phagocytose as efficiently as control PMNs, and always to ingest the particles with a lectin-free portion of their plasma membrane. This clearly indicates that concanavalin A- and ricin-binding sites of the PMN membrane are not involved in the recognition and phagocytosis of yeast particles.     

Complex changes in the suckling rat's small intestine by the end of the third week of life

Zusammenfassung Die Zusammenhänge zwischen den histologischen Veränderungen und dem Wechsel des Enzymmusters im Darm der Ratte während des Über-ganges von Milch-zur Festnahrung werden beschrieben.     

Molecular mechanism underlying the association of Coronin-7 with Golgi membranes

Coronin-7 (Crn7) is a ubiquitous mammalian WD40-repeat protein that localizes to the Golgi complex, interacts with AP-1 adaptor complex via binding of a tyrosine-288-based sorting signal to the mu1-subunit of AP-1, and participates in the maintenance of the Golgi structure and function. Here, we define the requirements for the recruitment of Crn7 from the cytosol to the Golgi. We establish that Src activity is indispensable for the interaction of Crn7 with Golgi membranes. Crn7 binds Src in vivo and can be phosphorylated by recombinant Src in vitro. We demonstrate that tyrosine-758 is the major Src phosphorylation site. Further, to be targeted to membranes Crn7 requires the presence of cargo in the Golgi complex. Finally, downregulation of the mu1-subunit of AP-1 leads to the dispersal of Crn7 from the Golgi membranes. We propose a mechanism whereby sequential events of protein interaction and posttranslational modification result in the membrane targeting of Crn7.     

Evidence that the prostaglandin-like substances fromPropionibacterium acnes are not identical with PGE2

Summary The prostaglandin-like substances (PLS) isolated fromP. acnes were investigated by reversed phase chromatography and gas chromatography-mass spectrometry. These analyses demonstrated that PLS were not identical with PGE₂, which supports a concept of PLS as a potential mediator of the inflammatory process in acne vulgaris.     

Case study research in the social sciences

In this paper, we offer an introduction to case study research in the social sciences. We begin with a discussion of the definition of case study research. Next, we point to various purposes that case study research may serve in the social sciences and then turn to outline the main philosophical issues raised by case study research. Finally, we briefly present the papers in this special issue.     

Polymorphism in the regulatory sequence of the human hsp70-1 gene does not affect heat shock factor binding or heat shock protein synthesis

A bi-allelic polymorphism found in the regulatory region of the human heat shock (HS) protein (HSP) hsp70-1 gene, which comprises an A-->C transversion, 3 bp upstream of the HS element (HSE), has been associated with extended HLA haplotypes. In view of the chaperoning and protective functions of Hsp70, we investigated whether this hsp70-1 bi-allelic polymorphism could modulate the stress response, which may relate to enhanced resistance or susceptibility to certain diseases. We compared the basal and HS-induced HS factor (HSF)-binding activity of the two polymorphic HSEs, hsp70-1 mRNA accumulation and HSP expression in two human Epstein Barr virus (EBV)-transformed B cell lines typed for hsp70-1 promoter alleles. Our results suggest that hsp70-1 promoter polymorphism does not influence HSF-binding activity, hsp70 mRNA accumulation or synthesis in human EBV-transformed B cell lines.     

Decrease of mRNA levels and biosynthesis of sucrase-isomaltase but not dipeptidylpeptidase IV in forskolin or monensin-treated Caco-2 cells

Treatment for 48 h of differentiated, confluent Caco-2 cells with 2.5 10^?5 M forskolin or 10^?6 M monensin, which produces a significant decrease of the de novo biosynthesis of sucrase-isomaltase, does not change quantitatively the de novo biosynthesis of dipeptidylpeptidase IV. Western blot analysis and silver nitrate staining indicate that neither drug induces any modification in the steady state expression of these two brush border hydrolases. Northern blot analysis shows that the level of dipeptidylpeptidase IV mRNA does not change in treated as compared to control Caco-2 cells. In contrast, forskolin and monensin dramatically decrease the level of sucrase-isomaltase mRNA. These observations suggest a separate regulation of biosynthesis for sucrase-isomaltase and dipeptidylpeptidase IV in intestinal cells. The mechanisms responsible for such a difference are discussed. Among them, the role of glucose metabolism, which is perturbed by both drugs, appears to be of crucial importance.