Die Postulate und Konstruktionen in der frühgriechischen Geometrie

Ohne Zusammenfassung     

Measurements on the electrical resistivity of thin nickel films

Résumé Dans une publication antérieure, nous avions signalé que le coefficient de température de la résistance électrique des films en nickel était négatif en dessous d'une certaine épaisseur critique (40 mµ). Au-dessus de 40 mµ, la courbe «Résistance en fonction de la température» présentait un minimum aux basses températures. A la suite de nouvelles expériences, nous avons constaté que ce phénomène est accompagné d'une déviation de la loi d'Ohm: la résistance diminue quand le courant de mesure augmente. Nous avons pu conclure que ces deux particularités ne sont qu'indirectement provoquées par la minceur des films. La cause principale est leur état de cristallisation imparfaite. En effet, après avoir subi un échauffement à 150° C pendant plusieurs heures, le coefficient de température négatif change de signe (le minimum disparaît) et la loi d'Ohm est respectée.

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Research-fellow of the Belgian «Fonds National de la Recherche Scientifique»     

NATREX AND DETERMINATION OF REAL EXCHANGE RATE OF RMB

1 IntroductionIn the past decades, a lot of 1iteratures appeared in the determination of excfiange rate, boththeoretic and empirical. One preValing paradigm is that the puxchasing power parity (PPP)holds in the long run either in weak--fOrm or in strongform. Under this hyPothesis, fluctuationsin real exchange rates are often regaJrded as temporary deviations from the long--run equllibriumexchange rate. However, these ekisting models fail to eXPlain the 1arge fluctuations in the realexchang…     

Promises of Presence

My review of Ike Kamphof’s “Webcams to Save Nature: Online Space as Affective and Ethical Space” focuses on the question how the engagement of the spectator of the described websites is temporally structured and how the discrepancy between the instantaneity of affective response and the duration of moral engagement is solved. I propose to draw on Alexander Nehamas’ philosophy of beauty as an in-between, bringing affect and ethics closer together.     

Enhancement of LFA-1-mediated cell adhesion by triggering through CD2 or CD3 on T lymphocytes

The lymphocyte function-associated molecule LFA-1 (CD11a/CD18) plays a key part in lymphocyte adhesion. Lymphocytes do not adhere spontaneously; activation of protein kinase C (PKC) by phorbol esters, however, gives rise to strong LFA-1-dependent adhesion, indicating that activation of LFA-1 is required to induce cell adhesion. We have now investigated whether the functionally important CD2 and CD3 surface structures on T lymphocytes are involved in the activation of LFA-1. The stimulation of these molecules, which causes activation of PKC, strongly promoted LFA-1-dependent adhesion. Furthermore, we demonstrate by using cells from an LFA-1-deficient patient that this enhanced lymphocyte adhesion is caused by activation of the LFA-1 molecule and not by activation of its ligands. LFA-1 was persistently activated by triggering through CD2 but only transiently by triggering through CD3. We postulate that CD2 and CD3 can differentially regulate the affinity of LFA-1 for its ligands by modulating its molecular conformation through PKC-dependent mechanisms.     

Isolation and characterization of a cDNA clone encoding the murine homologue of the human 20K T3/T-cell receptor glycoprotein

The antigen receptor on the surface of human T lymphocytes, which consists of a heterodimer of relative molecular mass (Mr) 90,000 (90K) (alpha- and beta-chains), is associated with the T3 antigen (gamma = 25K, delta = 20K and epsilon = 20K). A working model for the mode of action of the T3/T-cell receptor complex is that the clonotypic alpha- and beta-chains are involved in the recognition and binding of antigen in the context of polymorphic major histocompatibility complex (MHC) gene products on the surface of target cells. Antigen binding by the clonotypic receptor probably results in conformational changes in this structure which are recognized by and subsequently trigger the associated T3 complex to transmit signals into the cell, resulting in a proliferative response. The similarity in structure between murine and human clonotypic antigen receptors suggests that such a mechanism of recognition and activation also exists in mouse T lymphocytes, but so far there has been no evidence for the existence of a murine T3 complex. Here we demonstrate the existence of a T3 delta-chain mRNA in murine T lymphocytes. Our sequence data strongly suggest that this mouse mRNA codes for a complete T3 delta polypeptide chain and reveal some interesting properties of the protein.     

HNPCC-like cancer predisposition in mice through simultaneous loss of Msh3 and Msh6 mismatch-repair protein functions.

Cancer predisposition in hereditary non-polyposis colon cancer (HNPCC) is caused by defects in DNA mismatch repair (MMR). Mismatch recognition is attributed to two heterodimeric protein complexes: MutSalpha (refs 2, 3, 4, 5), a dimer of MutS homologues MSH2 and MSH6; and MutSbeta (refs 2,7), a dimer of MSH2 and MSH3. These complexes have specific and redundant mismatch recognition capacity. Whereas MSH2 deficiency ablates the activity of both dimers, causing strong cancer predisposition in mice and men, loss of MSH3 or MSH6 (also known as GTBP) function causes a partial MMR defect. This may explain the rarity of MSH6 and absence of MSH3 germline mutations in HNPCC families. To test this, we have inactivated the mouse genes Msh3 (formerly Rep3 ) and Msh6 (formerly Gtmbp). Msh6-deficient mice were prone to cancer; most animals developed lymphomas or epithelial tumours originating from the skin and uterus but only rarely from the intestine. Msh3 deficiency did not cause cancer predisposition, but in an Msh6 -deficient background, loss of Msh3 accelerated intestinal tumorigenesis. Lymphomagenesis was not affected. Furthermore, mismatch-directed anti-recombination and sensitivity to methylating agents required Msh2 and Msh6, but not Msh3. Thus, loss of MMR functions specific to Msh2/Msh6 is sufficient for lymphoma development in mice, whereas predisposition to intestinal cancer requires loss of function of both Msh2/Msh6 and Msh2/Msh3.