Open field locomotion by zinc deficient adult male mice

Summary Adult male mice maintained on a zinc-free diet display a statistically significant increase in open field locomotion compared to controls. However, excess zinc (100 times the established recommended daily allowance) does not produce a change compared to controls.     

Phagocytosis of14C clnitrophenyl poly L-lysine by peritoneal exudate cells from guinea-pigs

Résumé Respectivement, les cochons d'Inde des races II et XIII immunisés répondent et ne répondent pas au poly-l-lysine conjugués. Par contre, nous savons qu'ils sont également capables de phagocyter le¹⁴C-DNP-PLL dans la mesure où le sont les cellules des exudats du péritoine.     

Further applications of pentachlorophenyl active esters in the synthesis of peptides

Zusammenfassung Pentachlorophenylaktivierte Ester von N-Carbobenzoxy-aminosäuren verbinden sich in guten Ausbeuten mit Dicyclohexylaminsalzen von Aminosäuren. Um die Hydrolyse zu vermeiden, wurde eine Kombination der Methoden der gemischten Anhydriden und pentachlorophenylaktivierten Estern zur Verlängerung der Peptidenketten benützt.     

Karyotypes of the panamint kangaroo rat (Dipodomys panamintinus (Merriam))

Résumé Le rat KangourouDipodomys panamintinus a 4 sous-espèces. Le représentatif karyotype de 4 des sousespèces a 17 métacentriques et 14 chromosomes acrocentriques.Dipodomys panamintinus caudatus, géographiquement isolé des autres, a 16 métacentriques et 15 chromosomes acrocentriques. Le nombre fondamental est 96 pour les espèces.

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We wish to acknowledge the kind assistance of the following people in preparation of this paper: Mr.Dave Dunaway, Resident Naturalist, U.S. Forest Service; Mrs.Tilly Chamness, Coordinator, Natural Resource Management, Naval Weapon Center, China Lake.     

The turbidimetric evaluation of platelet aggregation caused by bacterial lipopolysaccharide

Zusammenfassung Die Aggregation von Blutplättchen durchEscherichia coli Endotoxin wurde untersucht: Die Blutplättchenanhäufung erweist sich anfänglich als langsam, dann aber als sehr schnelle Abnahme der optischen Dichte eines blutplättchenreichen Plasmas. Die schnelle Abnahme der optischen Dichte konnte durch Heparin, und zwar nur in grösserer Menge, unterdrückt werden. Der Beginn der schnellen Ansammlung wurde durch Adenosin verzögert, wobei aber Adenosin keine Wirkung auf den Grad der Anhäufung durch das Endotoxin hatte. Die Ergebnisse weisen darauf hin, dass in vitro Thrombin und Adenosindiphosphat die Thrombozytenaggregation durch Endotoxin unterstützen.

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Supported by U.S.P.H.S. grant No. H-7150.

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U.S.P.H.S. Research Career Development Award Recipient.     

A syndrome of altered cardiovascular, craniofacial, neurocognitive and skeletal development caused by mutations in TGFBR1 or TGFBR2

We report heterozygous mutations in the genes encoding either type I or type II transforming growth factor beta receptor in ten families with a newly described human phenotype that includes widespread perturbations in cardiovascular, craniofacial, neurocognitive and skeletal development. Despite evidence that receptors derived from selected mutated alleles cannot support TGFbeta signal propagation, cells derived from individuals heterozygous with respect to these mutations did not show altered kinetics of the acute phase response to administered ligand. Furthermore, tissues derived from affected individuals showed increased expression of both collagen and connective tissue growth factor, as well as nuclear enrichment of phosphorylated Smad2, indicative of increased TGFbeta signaling. These data definitively implicate perturbation of TGFbeta signaling in many common human phenotypes, including craniosynostosis, cleft palate, arterial aneurysms, congenital heart disease and mental retardation, and suggest that comprehensive mechanistic insight will require consideration of both primary and compensatory events.     

Quantitative trait loci mapped to single-nucleotide resolution in yeast

Identifying the genetic variation underlying quantitative trait loci remains problematic. Consequently, our molecular understanding of genetically complex, quantitative traits is limited. To address this issue directly, we mapped three quantitative trait loci that control yeast sporulation efficiency to single-nucleotide resolution in a noncoding regulatory region (RME1) and to two missense mutations (TAO3 and MKT1). For each quantitative trait locus, the responsible polymorphism is rare among a diverse set of 13 yeast strains, suggestive of genetic heterogeneity in the control of yeast sporulation. Additionally, under optimal conditions, we reconstituted approximately 92% of the sporulation efficiency difference between the two genetically distinct parents by engineering three nucleotide changes in the appropriate yeast genome. Our results provide the highest resolution to date of the molecular basis of a quantitative trait, showing that the interaction of a few genetic variants can have a profound phenotypic effect.     

Agonist/endogenous peptide-MHC heterodimers drive T cell activation and sensitivity

Alphabeta T lymphocytes are able to detect even a single peptide-major histocompatibility complex (MHC) on the surface of an antigen-presenting cell. This is despite clear evidence, at least with CD4+ T cells, that monomeric ligands are not stimulatory. In an effort to understand how this remarkable sensitivity is achieved, we constructed soluble peptide-MHC heterodimers in which one peptide is an agonist and the other is one of the large number of endogenous peptide-MHCs displayed by presenting cells. We found that some specific combinations of these heterodimers can stimulate specific T cells in a CD4-dependent manner. This activation is severely impaired if the CD4-binding site on the agonist ligand is ablated, but the same mutation on an endogenous ligand has no effect. These data correlate well with analyses of lipid bilayers and cells presenting these ligands, and indicate that the basic unit of helper T cell activation is a heterodimer of agonist peptide- and endogenous peptide-MHC complexes, stabilized by CD4.