Der positive Promotor‐Effekt von Bund der negative Effekt von P in NiB‐ bzw. NiP‐Hydrierungskatalysatoren lassen sich durch den Einfluß von B und P auf die Elektronendichte im Ni erklären: B gibt Elektronen an das Ni ab, während P Elektronen aus dem Ni abzieht, was eine Zunahme der Aktivität mit steigendem B‐Gehalt und eine Abnahme der Aktivität mit steigendem P‐Gehalt der Katalysatoroberfläche zur Folge hat.

. In heterologous cells, PSD-95 (or chapsyn-110) can cluster NMDA receptors and Shaker's K ϩ channels (4). A disulfide-bridge formation between a pair of cysteine residues located near the NH 2 terminus of PSD-95 has been proposed to be responsible for this clustering (5). Although this bridge can form only a dimer or tetramer of PSD-95, the disulfide-bridge formation is insufficient to explain the clustering. A conflicting result shows that this pair of cysteine residues is the palmitoylation site involved in the membrane sorting and in the synaptic targeting (6, 7). Therefore, the molecular mechanism underlying receptor clustering mediated by this protein remains unknown. A further analysis of PSD-95 mutant mice has revealed that, whereas NMDA receptors are targeted into excitatory synapses, the receptor-mediated signals appear to be perturbed (8). A family of PSD-95 binding proteins has also been isolated, although their functions are as yet unclear (9-11). The COOH termini of the GluR2 and GluR3 subunits of ␣-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors interact with the PDZ domain-containing protein GRIP (12), its related protein ABP (13), and a protein known to interact with protein kinase C, PICK1 (14). Of these, PICK1 induces AMPA receptor clustering in heterologous expression system (14). In spite of these accumulating evidences, there have been no insights into particular molecular motifs of these scaffold proteins in receptor clustering.Homer 1a͞vesl-1S, an immediate-response protein for a variety of neuronal stimuli (15, 16), binds to group 1 metabotropic glutamate receptors (mGluRs) (15). Because of the presence of a GLGF motif, this protein was initially considered to be a single PDZ domain-containing protein. Recent crystal structure analysis has revealed that the NH 2 -terminal region of this protein contains an enabled͞VASP homology 1 (EVH1) domain, which binds to the COOH-terminal sequence, TPPSPFR, of mGluR1, but not to a S͞TXV motif at the COOH terminus of the NR2 subunits of NMDA receptors or of Shaker's K ϩ channels (17). We have recently isolated a member of the Homer 1a͞vesl-1S protein family, named PSD-Zip45 (18). The same protein has been independently identified as Homer 1c (19) and vesl-1L (20). In this paper, we called this protein PSD-Zip45 for short. The NH 2 terminus of this protein is identical to Homer 1a͞vesl-1S, and its COOH terminus is composed of a coiled-coil structure and two leucine-zipper motifs (18)(19)(20). We have also demonstrated the self-multimerizing ability of the COOH terminus in this protein (18). These features suggest that this protein is a potent candidate for subsynaptic scaffold proteins.Here, we demonstrated immunohistochemically that PSDZip45 and mGluR1␣ are largely colocalized to synapses of the cerebellar molecular layer. In contrast, the localizations of PSD-Zip45 and group 1 mGluRs in the hippocampus were segregated. In cultured hippocampal neurons, PSD-Zip45 and NMDA receptors were preferentially colocalized to dendritic spines. ...

To examine the prevalence of abnormalities in the insulin receptor structure gene in Japanese with non-insulin-dependent diabetes mellitus (NIDDM), a population of 51 patients with NIDDM was screened for mutations in this gene. Patient genomic DNAs of both alleles corresponding to 22 exons of the gene were amplified by polymerase chain reaction (PCR). The PCR products on pUC19 were sequenced. Three patients with heterozygous missense mutation Thr831-->Ala831 in exon 13 and one patient with heterozygous missense mutation Tyr1334-->Cys1334 in exon 22 of the beta-subunits were identified. Linkage analysis of one of the families plus statistical studies showed that the mutation Thr831-->Ala831 is possibly responsible for the onset of NIDDM. In COS cells transiently expressing both mutant receptor cDNAs and a cDNA of a M(r) 85,000 regulatory subunit of phosphatidylinositol 3-kinase (PI 3-kinase), the mutation Tyr1334-->Cys1334 impaired binding of the receptor with the M(r) 85,000 subunit of PI 3-kinase, but linkage analysis of the family showed that the mutation did not cosegregate with NIDDM in the pedigree. Therefore, one missense mutation (Thr831-->Ala831) in the insulin receptor, as found in three patients, is possibly involved in the etiology of a subset of the 51 NIDDM patients.

The qkI gene encodes an RNA binding protein which was identified as a candidate for the classical neurologic mutation, qk v . Although qkI is involved in glial cell differentiation in mice, qkI homologues in other species play important roles in various developmental processes. Here, we show a novel function of qkI in smooth muscle cell differentiation during embryonic blood vessel formation. qkI null embryos died between embryonic day 9.5 and 10.5. Embryonic day 9.5 qkI null embryos showed a lack of large vitelline vessels in the yolk sacs, kinky neural tubes, pericardial effusion, open neural tubes and incomplete embryonic turning. Using X-gal and immunohistochemical staining, qkI is first shown to be expressed in endothelial cells and smooth muscle cells. Analyses of qkI null embryos in vivo and in vitro revealed that the vitelline artery was too thin to connect properly to the yolk sac, thereby preventing remodeling of the yolk sac vasculature, and that the vitelline vessel was deficient in smooth muscle cells. Addition of QKI and platelet-endothelial cell adhesion molecule-1 positive cells to an in vitro para-aortic splanchnopleural culture of qkI null embryos rescued the vascular remodeling deficit. These data suggest that QKI protein has a critical regulatory role in smooth muscle cell development, and that smooth muscle cells play an important role in inducing vascular remodeling.

Room-temperature 129Xe NMR is a convenient means of studying heterogeneous distributions of HMB in N a y , providing the heterogeneity length scales are larger than about 10 pm. Such situations may lend themselves to NMR chemical shift imaging methods in which a linear magnetic field gradient might be used to image xenon profiles in samples possessing macroscopic adsorbate heterogeneities. The suitability of multiple-quantum NMR spectroscopy for probing adsorbate distributions quantitatively is due primarily to the sensitivity of the technique to the number of dipole-dipole coupled spins in a collection of isolated molecules. Counting the number of proton spins in clusters of chemisorbed organic species yields information on their spatial distributions and, thus, about microstructural features of the adsorption sites themselves. Because of the central importance of these sites to the reaction process, multiple-quantum NMR represents a potentially valuable means by which a catalyst's microscopic adsorbate structure can be correlated with its chemical reaction properties. Such information, used in conjunction with the macroscopic adsorbate distributions measured by '29Xe N M R spectroscopy, is key to characterizing intracrystalline mass transport and adsorption of reactant species within zeolitic catalysts. Acknowledgment. We thank D. N. Shykind and M. Trecoske for assistance with the multiple-quantum experiments and with zeolite sample preparation. M. G.Physicochemical characterization of calcined and sulfided CoO/SiO, catalysts were carried out to reveal the interaction modes between cobalt and SiOz using XPS, TPR, TEM, DRS-VIS, and XRD techniques. The CoO/Si02 catalysts were prepared by an impregnation method using cobalt acetate as well as cobalt nitrate and by an ion-exchange technique. It was found that several kinds of cobalt species are formed on CoO/SiO,. These species are assigned to Co304, Co-Si4 mixed oxide, surface Co3+ species, surface silicate, surface Co2+ species in the order of the TPR reduction temperature. Their proportions strongly depended on the starting salt, cobalt content, and preparation method. Cobalt acetate was found to provide highly dispersed CoO/Si02 catalysts with a uniform distribution of cobalt species throughout the catalyst particles as compared to conventionally employed cobalt nitrate. The proportion of Co3+ greatly decreased when cobalt acetate was used instead of cobalt nitrate. All the cobalt species interacting with SiO, were found to be sulfided at 673 K. It was demonstrated that sulfided CoO/Si02 catalysts prepared from cobalt acetate show several times higher hydrogenation activity than the catalysts from cobalt nitrate. On the basis of the XPS characterization of uncalcined precursors, the effects of starting salt on the cobalt-Si0, interaction modes and cobalt dispersion and distribution are discussed.