Deficiencies in basic hydrologic data. Report of the Special Advisory Committee on Standards and Specifications for Hydrologic Data.

Thorndike Saville, chairman.

Inventory of public groundwater supply : system deficiencies of urban areas /

Bibliography: p. 4.

Inventory of public surface [water] supply : system deficiencies.

Bibliography: leaf 5.

An authentic biography of General La Fayette. In which many errors and deficiencies existing in the memoirs heretofore published, are corrected and supplied.

Mode of access: Internet.

Le vicomte de Bragelonne, ou, dix ans plus tard : complement des trois mousquetaires et de vingt ans aprés /

Sequel: Louise de La Vallière.

The diagnosis of glanders by complement fixation /

"April 7, 1911."

Past is prologue : educational deficiencies and the youth labor market problem /

Includes bibliographical references (leaves 17-21).

An examination of Commodore Porter's Exposition in which some of the errors and inaccuracies of that publication are rectified, and some of its deficiencies supplied.

Mode of access: Internet.

Digest of appropriations for the support of the government of the United States for the service of the fiscal year ending ..., and on account of deficiencies for prior years, made by the ... session of the ... Congress /

Description based on: 1901/1902.

Le vicomte de Bragelonne; ou, Dix ans plus tard; complement des Trois mousquetaires et de Vingt ans apres.

On cover: Nouvelle collection Michel Levy. Written in collaboration with Auguste Maquet. Sequel: Louis de La Valliere.

Nutritional deficiencies in livestock,

Mode of access: Internet.

Potent cyclic antagonists of the complement C5a receptor on human polymorphonulcear leukocytes. Relationships between structures and activity

Human C5a is a plasma protein with potent chemoattractant and pro-inflammatory properties, and its overexpression correlates with severity of inflammatory diseases. C5a binds to its G protein-coupled receptor (C5aR) on polymorphonuclear leukocytes (PMNLs) through a high-affinity helical bundle and a low-affinity C terminus, the latter being solely responsible for receptor activation. Potent and selective C5a antagonists are predicted to be effective anti-inflammatory drugs, but no pharmacophore for small molecule antagonists has yet been developed, and it would significantly aid drug design. We have hypothesized that a turn conformation is important for activity of the C terminus of C5a and herein report small cyclic peptides that are stable turn mimics with potent antagonism at C5aR on human PMNLs. A comparison of solution structures for the C terminus of C5a, small acyclic peptide ligands, and cyclic antagonists supports the importance of a turn for receptor binding. Competition between a cyclic antagonist and either C5a or an acyclic agonist for C5aR on PMNLs supports a common or overlapping binding site on the C5aR. Structure-activity relationships for 60 cyclic analogs were evaluated by competitive radioligand binding with C5a (affinity) and myeloperoxidase release (antagonist potency) from human PMNLs, with 20 compounds having high antagonist potencies (IC50, 20 nM(-1) muM). Computer modeling comparisons reveal that potent antagonists share a common cyclic backbone shape, with affinity-determining side chains of defined volume projecting from the cyclic scaffold. These results define a new pharmacophore for C5a antagonist development and advance our understanding of ligand recognition and receptor activation of this G protein-coupled receptor.

The role of the complement system in ischemia-reperfusion injury

Ischemia-reperfusion (I/R) injury is a common clinical event with the potential to seriously affect, and sometimes kill, the patient. Interruption of blood supply causes ischemia, which rapidly damages metabolically active tissues. Paradoxically, restoration of blood flow to the ischemic tissues initiates a cascade of pathology that leads to additional cell or tissue injury. I/R is a potent inducer of complement activation that results in the production of a number of inflammatory mediators. The use of specific inhibitors to block complement activation has been shown to prevent local tissue injury after I/R. Clinical and experimental studies in gut, kidney, limb, and liver have shown that I/R results in local activation of the complement system and leads to the production of the complement factors C3a, C5a, and the membrane attack complex. The novel inhibitors of complement products may find wide clinical application because there are no effective drug therapies currently available to treat I/R injuries.