Anatomy education in Ottoman-Turkish veterinary schools during 19th century and Papier-Mache models.

Veterinary medicine was recognized as a scientific discipline for the first time in 1762 in France. After a while, the first Ottoman-Turkish veterinary school was established in 1842, primarily for the improvement and welfare of army horses. There is not much detailed information about the content of the anatomy education and materials in the early days of veterinary schools apart from the anecdote that Gurlt's illustrated anatomy books were being used. The purpose of this study is to research anatomy education in the 19th century, when Ottoman-Turkish veterinary medicine was established, as well as the Papier-mâché models used in anatomy education, searching primary and secondary sources that can be accessed online. It has been determined that the normal and pathological anatomy models of humans and various domestic animals made by Dr. Auzoux were ordered to be used in the anatomy education of the newly established veterinary schools. The whereabouts of these models, which did not reference in publications until now, are unknown. However, examining these models is regarded to be crucial for understanding the veterinary anatomy perspective and educational content of the period.

[tRNA Wobble Base Modifications and Boric Acid Resistance in Yeast: Boron-Resistant Deletion Mutants Induce the General Amino Acid Control Mechanism and Activate Boron Efflux].

Boric acid is essential for plants and has many vital roles in animals and microorganisms. However, its high doses are toxic to all organisms. We previously screened yeast deletion collections to identify boric acid-resistant and susceptible mutants to identify genes that play a role in boron tolerance. Here, we analyzed boron resistant mutants (elplΔ, elp3Δ, elp6Δ, ncs2Δ, ncs6Δ and ktil2Δ) for their abilities to modulate the general amino acid control system (GAAC) and to induce boron efflux pump ATR1. The mutants analyzed in this study lack the genes that play roles in tRNA Wobble base modifications. We found that all of the boron resistant mutants activated Gcn4-dependent reporter gene activity and increased the transcript level of the ATR1 gene. Additionally, boron resistant cells accumulated less boric acid in their cytoplasm compared to the wild type cells upon boron exposure. Thus, our findings suggested that loss of wobble base modifications in tRNA leads to GAAC activation and ATR1 induction, which in turn reduced intracellular boron levels and caused boron resistance.