G-1 Appeal Activity in the Public Assistance Programs, November 2009

This report contains information on the Appeal Activity in the Public Assistance Programs. Programs included are FIP (Iowa’s TANF program), Title IV-D (Child Support), Food Stamps (USDA Food Assistance Program), Title XIX (Medicaid), Title XX (Social Services Block Grant), Juvenile Parole, State Supplemental Assistance, Other, Food Stamp Fraud, FIP Fraud, RCA (Refugee Cash Assistance) Fraud, and a total for all the programs. This report is issued monthly.

G-1 Appeal Activity in the Public Assistance Programs, December 2009

This report contains information on the Appeal Activity in the Public Assistance Programs. Programs included are FIP (Iowa’s TANF program), Title IV-D (Child Support), Food Stamps (USDA Food Assistance Program), Title XIX (Medicaid), Title XX (Social Services Block Grant), Juvenile Parole, State Supplemental Assistance, Other, Food Stamp Fraud, FIP Fraud, RCA (Refugee Cash Assistance) Fraud, and a total for all the programs. This report is issued monthly.

UBVRI photometry of G, K, M Hipparcos stars

UBVRI data are presented for a set of 229 late-type stars, most of them being high proper motion stars. All these data are part of the Input Catalog planned observations for the Hipparcos mission.

UBVRI photometry of G, K, M Hipparcos stars. II.

As indicated by Grenon (1989), the data of the present series of reports on the UBVRI photometry of late-type stars in the Hipparcos Input Catalog are to be employed in computations of Hipparcos observing time, as well as in evaluating the observability of faint stars by the satellite. Attention is here given to late type stars in the V = 8-12 range, including distant red giants in the Galactic plane (Hipparcos proposal 189), as well as high proper motion stars included in the G, LTT, LP, and MCC catalogs.

Mutational and computational analysis of the alpha(1b)-adrenergic receptor. Involvement of basic and hydrophobic residues in receptor activation and G protein coupling.

To investigate their role in receptor coupling to G(q), we mutated all basic amino acids and some conserved hydrophobic residues of the cytosolic surface of the alpha(1b)-adrenergic receptor (AR). The wild type and mutated receptors were expressed in COS-7 cells and characterized for their ligand binding properties and ability to increase inositol phosphate accumulation. The experimental results have been interpreted in the context of both an ab initio model of the alpha(1b)-AR and of a new homology model built on the recently solved crystal structure of rhodopsin. Among the twenty-three basic amino acids mutated only mutations of three, Arg(254) and Lys(258) in the third intracellular loop and Lys(291) at the cytosolic extension of helix 6, markedly impaired the receptor-mediated inositol phosphate production. Additionally, mutations of two conserved hydrophobic residues, Val(147) and Leu(151) in the second intracellular loop had significant effects on receptor function. The functional analysis of the receptor mutants in conjunction with the predictions of molecular modeling supports the hypothesis that Arg(254), Lys(258), as well as Leu(151) are directly involved in receptor-G protein interaction and/or receptor-mediated activation of the G protein. In contrast, the residues belonging to the cytosolic extensions of helices 3 and 6 play a predominant role in the activation process of the alpha(1b)-AR. These findings contribute to the delineation of the molecular determinants of the alpha(1b)-AR/G(q) interface.

[Lettre autographe signée de G. Dejean adressée à Escudier, Rome, 20 février 1859]

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