The lower lateral limit is the anterior crest of the ilium and Pouparts ligament, which runs from the anterior superior spine of the ilium to the spine of the pubis. These lower limits are marked by visible grooves. Just above the pubic spines on either side are the external abdominal rings, which are openings in the muscular wall of the abdomen through which the spermatic cord emerges in the male, and through which an inguinal hernia may rupture. One method by which the location of the abdominal contents can be appreciated is to draw three horizontal and two vertical lines. Horizontal lines
The highest of the former is the transpyloric line of C. Addison, which is situated halfway between the suprasternal notch and the top of the pubic symphysis, and often cuts the pyloric opening of the stomach an inch to the right of the mid-line. The hilum of each kidney is a little below it, while its left end approximately touches the lower limit of the spleen. It corresponds to the first lumbar vertebra behind. The second line is the subcostal line, drawn from the lowest point of the subcostal arch (tenth rib). It corresponds to the upper part of the third lumbar vertebra, and it is an inch or so above the umbilicus. It indicates roughly the transverse colon, the lower ends of the kidneys, and the upper limit of the transverse (3rd) part of the duodenum.
The extra copies of key chromosome 21 genes underlie their increased susceptibility to AMKL by promoting the development of a certain type of inactivating mutation in the GATA1 gene. The GATA1 gene resides on the X chromosome and codes for two transcription factors, GATA1 and a shorter version, GATA1-S. GATA1 and GATA1-S contribute to regulating the expression of genes that control the maturation of megakaryoblasts to promegakaryocytes, megakaryocytes, and platelets as well as the maturation of erythroblasts to red blood cells. GATA1-S appears less active than GATA1 in controlling some of the genes that promote megakaryoblast maturation but more active than GATA1 in stimulating megakaryoblast proliferation. Various GATA1 mutations that cause this gene to make GATA1-S but unable to make GATA1 result in the excessive proliferation of platelet precursor cells, reductions in the levels of circulating blood platelets, mild reductions in the levels of circulating red blood cells, and the development of transient myeloproliferative disease (TMD). TMD is a disorder involving the excessive proliferation of non-malignant megakaryoblasts and descendent cells due to the cited truncating mutations in the GATA1 gene. TMD is a necessary predecessor to DS-AMKL.Down syndrome fetuses and neonates with one of the cited types of GATA1 truncating mutations are in rare cases asymptomatic (i.e. silent TMD) but more commonly exhibit in utero or during the first months of live accumulations of immature megakaryoblasts in, and sometimes life-threatening injury to, the fetal blood-forming organ, the liver, and other tissues.