Inflation and the E M S

Abstract

Since the European Monetary System was instituted in March 1979, there has been a dramatic reduction in the inflation rates of member countries. This development is widely attributed to the EMS itself. The purpose of this paper is to argue that the theoretical and empirical basis for such a claim is far from conclusive. On the theoretical side, the paper develops a model which highlights two issues. First, changes in the 'rules" of the exchange rate system need not coincide with changes in expectations about Central Bank behavior. In fact, expectations in France do not seem to have changed until policy makers "got tough" in 1982-83. Second, different researchers have made quite different assumptions about exactly what "rules" the EMS imposes. The paper shows that how the system works matters in terms of the effect joining will have on inflation. On the empirical side, the paper shows that effects which have been attributed to the EMS are in large part due to the global deflation since 1979 and to the fact that EMS members had relatively low inflation before 1979. However, even these estimates should be interpreted with caution. They are very sensitive to time period and to which nonEMS countries are included in the sample.

Glycine N-Methyltransferase Is an Example of Functional Diversity

“…Previously, B[e]P had been demonstrated to be a selective ligand for the 4 S PAH-binding protein (17)(18)(19)(20)(21)(22)(23). In the present study, we have shown that this PAH is also able to induce the expression of CYP1A1 in the GNMT-transfected CHO cells, whereas TCDD, a prototypic ligand for the Ah receptor, failed to do so.…”

“…In addition, heat shock protein 90 plays an important role in the intracellular localization of the Ah receptor (see review in Ref. 42).Evidence has been published suggesting that the induction of rat CYP1A1 after treatment with PAHs, such as B[a]P or B[e]P, may require an Ah receptor-independent pathway mediated by another cytosolic receptor protein, the 4 S PAHbinding protein (17)(18)(19)(20)(21)(22)(23). Both the Ah receptor and 4 S PAHbinding protein exhibit distinct ligand binding specificities, with 3-methylcholanthrene interacting with both.…”

Binding characteristics of 4‐S proteins from rat and mouse liver High affinity of ellipticines

“…Nevertheless, no relation exists between the lipophilicity of ellipticines, determined by high-performance liquid chromatography, and the binding to the 4-S protein (data not shown). Finally, we have observed, with others [l, 4,5,141, that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was totally devoid of affinity for the 4-S protein. pyrene (10 nM) and competing ligands (from 1 nM to 100 pM) were incubated with cytosol ( 5 mg protein in 1 ml) from untreated DBA/2 mouse liver for 1 h at 4°C.…”

“…From the binding theory one would expect that the ICs0 for nonradioactive competitor should be 10 nM when it is tested against 10 nM [3H]3-methylcholanthrene. This large discrepancy, which had not been observed with Ah receptors [13], well illustrates the difficulty in making reliable quantitative determinations on binding parameters for hydrophobic compounds in cytosols that contain several components: 10 nM [3H]3-methylcholanthrene is a saturating concentration for Ah receptors but not for 4-S protein (data not shown), this ligand displaying a weak affinity for the 4-S protein [5]. This feature, associated with the presence in the cytosol of the Ah receptor, a much more specific binder of 3-methylcholanthrene provides a suitable explanation of the discrepancy observed in Fig.…”

Mutator phenotype of BCR – ABL transfected Ba/F3 cell lines and its association with enhanced expression of DNA polymerase β

“…Strong evidence supported that this phenotypic evolution is associated with the induction of genetic instability at the chromosomal level, including both numerical and structural chromosomal abnormalities in p210bcr/abl transformed cells, but these events are relatively rare occurrences in culture cells unless defects in DNA metabolism like repair, recombination, or replication, suggesting that genetic alteration at the nucleotide level may be involved (Laneuville et al, 1992). Furthermore, the secondary activation of N-ras (Ahuja et al, 1991;Collins et al, 1989;LeMaistre et al, 1989) and c-myc (McCarthy et al, 1984) genes and the functional inactivation of the anti-oncogene p53 observed frequently in patients developing blast crisis support the hypothesis of an early alteration of a genè guardian' of the genome confering a mutator phenotype at the nucleotide level (Loeb, 1991). Finally, genomic instability of microsatellite repeats associated with a late genetic event during the evolution of CML has been demonstrated (Wada et al, 1994).…”