Proceedings. Annual convention

Mode of access: Internet.

Report

Mode of access: Internet.

Savannah river and Clark Hill reservoir, Ga. and S.C. Hearings, Seventy-seventh Congress, first session. March 13, 14, and 18, 1941.

Mode of access: Internet.

Report.

Mode of access: Internet.

Biennial report

Mode of access: Internet.

Water resource projects in Louisiana : hearing before the Subcommittee on Water Resources of the Committee on Environment and Public Works, United States Senate, Ninety-eighth Congress, first session, on the Atchafalaya Basin floodway system and the Mississippi River deep draft ship channel, August 12, 1983, New Orleans, La.

Mode of access: Internet.

To establish a federal cost-sharing policy for the construction and maintenance of deep draft ports : hearing before the Subcommittee on Water Resources of the Committee on Environment and Public Works, United States Senate, Ninety-eighth Congress, first session, September 24, 1983--Portsmouth, N.H.

Mode of access: Internet.

Melbourne, Victoria. Information relative to the port.

1933 edition has title: Melbourne, Victoria. Official handbook setting forth information relative to the port.

Commercial Statistics. Water-Borne Commerce of the United States.

Title Varies: 1919-24, Commercial Statistics

Report on survey of small boat basin, Point Roberts, Washington.

Cover title.

Review of reports on Wilson Harbor, New York.

Cover title.

Port and Terminal Charges at United States Ports

Mode of access: Internet.

Ports of Miami, Port Everglades, Palm Beach, and Port Canaveral, Florida /

Includes index.

Sequence variation in the proximity of IDE may impact age at onset of both Parkinson disease and Alzheimer disease

We recently reported that a linkage disequilibrium (LD) block on chromosome 10q encompassing the gene encoding insulin-degrading enzyme (IDE) harbors sequence variants that associate with Alzheimer disease (AD). Evidence also indicated effects upon a number of quantitative indices of AD severity, including age-at-onset (AAO). Since linkage of this immediate region to AAO has been shown in both AD and Parkinson disease (PD), we have explored the possibility that polymorphism within this LD block might also influence PD. Utilizing single nucleotide polymorphisms that delineate common haplotypes from this region, we observed significant evidence of association with AAO in an Australian PD case-control sample. Analyses were complemented with AAO data from two independent Swedish AD case samples, for which previously reported findings were replicated. Results were consistent between AD and PD, suggesting the presence of equivalent detrimental and protective alleles. These data highlight a genomic region in the proximity of IDE that may contribute to AD and PD in a similar manner.

A conformationally sensitive GHR [growth hormone (GH) receptor] antibody: Impact on GH signaling and GHR proteolysis

The GH receptor (GHR) mediates metabolic and somatogenic actions of GH. Its extracellular domain (ECD; residues 1-246) has two subdomains, each with seven beta strands organized into two antiparallel beta sheets, connected by a short hinge region. Most of the ECD residues involved in GH binding reside in subdomain 1, whereas subdomain 2 harbors a dimerization interface between GHR dimers that alters conformation in response to GH. A regulated GHR metalloprotease cleavage site is in the membrane-proximal stem region of subdomain 2. We have identified a monoclonal anti-ECD antibody, anti-GHR(ext-mAb), which recognizes the rabbit and human GHRs by immunoprecipitation, but less so after GH treatment. By immunoblotting and immunoprecipitation, anti-GHR(ext-mAb) recognized a glutathione-S-transferase (GST) fusion incorporating subdomain 2, but not one including subdomain 1. In transient transfection experiments, anti-GHR(ext-mAb) failed to recognize by immunoprecipitation a previously characterized dimerization interface mutant GHR that is incompetent for signaling. In signaling experiments, brief pretreatment of GH-responsive human fibrosarcoma cells with anti-GHR(ext-mAb) dramatically inhibited GH-induced Janus kinase 2 and signal transducer and activator of transcription 5 tyrosine phosphorylation and prevented GH-induced GHR disulfide linkage (a reflection of GH-induced conformational changes). In contrast, anti-GHR(ext-mAb) only partially inhibited radiolabeled GH binding, suggesting its effects on signaling were not simply via inhibition of binding. Furthermore, anti-GHR(ext-mAb) prevented phorbol ester-stimulated GHR proteolysis, but GHR cleavage site mutants were normally recognized by the antibody, indicating that the stem region cleavage site is not a direct epitope. A Fab fragment of anti-GHR(ext-mAb) inhibited GH-induced GHR disulfide linkage and signaling, as well as phorbol ester-induced GHR proteolysis, in a fashion similar to the intact antibody. Thus, our findings suggest that anti-GHR(ext-mAb) has promise as a GH antagonist and as a tool in studies of conformational changes required for GHR activation.