HG 186.9-187.0 D.E.

Coarse grained sediment with a few fine grained matrices. Brown sediment with small to medium sized clasts. Clasts range from sub-angular to sub-rounded. Organic material present. It contains rotation structures throughout as well as edge-to-edge grain crushing. Fine grained clay domains are present and lineations can also be seen. Minor amounts of grain stacking can also be seen.

HG 186.9-187.0 D.E. Thin Section

Coarse grained sample with grains varying from small to medium in size. They range from sub-angular to sub-rounded in shape. The sample is abundant in lineations and comet structures. Minor amounts of grain stacking are present. Inclusions of a clay rich, fine grained domain.

Diagram of Lot 142 and Lot 186 showing the line of the road in red

Diagram of Lot 142 and Lot 186 showing the line of the road in red, Dec.10, 1856.

Map of measurements of lot no.186

Map of measurements of lot no.186, Dec. 19, 1855.

Map of measurements of lots no.185 and 186 by George Strohan

Map of measurements of lots no.185 and 186 by George Strohan, Dec. 29, 1855.

Contradicción del artículo 49 con el 186 de la Ley Federal del Trabajo

Tesis (Maestría en Derecho Laboral ) U.A.N.L.

Das Israelitische Vorschuss-Institut in Hamburg 186 - 1916

von N. M. Nathan

Ms. hebr. oct. 186 - Memorbuch de-ḳehilah ḳedoshah Offenbach

Vorbesitzer: Eljāqīm Carmoly

Comparison against 186 canid whole genome sequences reveals survival strategies of an ancient clonally transmissible canine tumor.

Canine transmissible venereal tumor (CTVT) is a parasitic cancer clone that has propagated for thousands of years via sexual transfer of malignant cells. Little is understood about the mechanisms that converted an ancient tumor into the world's oldest known continuously propagating somatic cell lineage. We created the largest existing catalog of canine genome-wide variation and compared it against two CTVT genome sequences, thereby separating alleles derived from the founder's genome from somatic drivers of clonal transmissibility. We show that CTVT has undergone continuous adaptation to its transmissible allograft niche, with overlapping mutations at every step of immunosurveillance, particularly self-antigen presentation and apoptosis. We also identified chronologically early somatic mutations in oncogenesis- and immune-related genes that may represent key initiators of clonal transmissibility. Thus, we provide the first insights into the specific genomic aberrations that underlie CTVT's dogged perseverance in canids around the world.