Organization of the U.S. Naval Forces on Shore at Vera Cruz, Mexico

Pamphlet outlining the command structure of the U.S. Naval forces involved in the 1914 Tampico Affair during the Mexican Revolution. The pamphlet contains the autographs of 25 naval participants, including Congressional Medal of Honor recipients Read-Admiral, later Admiral, Frank Friday Fletcher (1855-1928) and Lieutenant (j.g.), later Admiral, Jonas H. Ingram (1886-1952). Battalions include: Arkansas Battalion, Florida Battaloion, Utah Battalion, Utah Special Artillery Detachments, Chester Battalion, San Francisco Battalion, Second Naval Regiment, New Hampshire Battalion, Vermont Battalion, South Carolina Battalion, New Jersey Battalion, Third Naval Regiment, Michigan Battalion, Louisiana Battalion, Minnesota Battalion, North Dakota Battalion, and Marine Brigade.https://scholarworks.utrgv.edu/tampicoaffair/1000/thumbnail.jp

Guidebook for field trips in southern and west-central Maine, October 13, 14 and 15, 1989: New England Intercollegiate Geological Conference 81st annual meeting

Geologic fieldtrips in Main

Guidebook for field trips in southern and west-central Maine, October 13, 14 and 15, 1989: New England Intercollegiate Geological Conference 81st annual meeting: title pages, table of contents

front matte

Conversations with Veterinary Students: Attitudes, Ethics, and Animals

Interviews were conducted with 24 graduating veterinary students to examine (a) changes in their attitudes toward animals; (b) the types of experiences and procedures that they found personally distressing; (c) their perceptions of the most important ethical issues that they will face in private practice; and (d) their responses to euthanizing animals. Students’ responses differed considerably. For example, about half of the students claimed that they were not affected by euthanasia, but another 25% still were struggling with this aspect of their professional role. Rationalization was a common mechanism by which the students attempted to deal with stressful experiences. It is argued that the moral dilemmas faced by veterinary students mirror the ethical ambiguities inherent in human-animal relationships

Till The Sands of the Desert Grow Cold / music by Ernest R. Ball; words by Geo Graff Jr.

Cover: n. illus.; Publisher: M. Witmark and Sons (New York)https://egrove.olemiss.edu/sharris_c/1037/thumbnail.jp

Anti-polyQ antibodies recognize a short polyQ stretch in both normal and mutant huntingtin exon 1

Huntington's disease is caused by expansion of a polyglutamine (polyQ) repeat in the huntingtin protein. A structural basis for the apparent transition between normal and disease-causing expanded polyQ repeats of huntingtin is unknown. The “linear lattice” model proposed random-coil structures for both normal and expanded polyQ in the preaggregation state. Consistent with this model, the affinity and stoichiometry of the anti-polyQ antibody MW1 increased with the number of glutamines. An opposing “structural toxic threshold” model proposed a conformational change above the pathogenic polyQ threshold resulting in a specific toxic conformation for expanded polyQ. Support for this model was provided by the anti-polyQ antibody 3B5H10, which was reported to specifically recognize a distinct pathologic conformation of soluble expanded polyQ. To distinguish between these models, we directly compared binding of MW1 and 3B5H10 to normal and expanded polyQ repeats within huntingtin exon 1 fusion proteins. We found similar binding characteristics for both antibodies. First, both antibodies bound to normal, as well as expanded, polyQ in huntingtin exon 1 fusion proteins. Second, an expanded polyQ tract contained multiple epitopes for fragments antigen-binding (Fabs) of both antibodies, demonstrating that 3B5H10 does not recognize a single epitope specific to expanded polyQ. Finally, small-angle X-ray scattering and dynamic light scattering revealed similar binding modes for MW1 and 3B5H10 Fab–huntingtin exon 1 complexes. Together, these results support the linear lattice model for polyQ binding proteins, suggesting that the hypothesized pathologic conformation of soluble expanded polyQ is not a valid target for drug design