In human anatomy, the thigh is the area between the hip (pelvis) and the knee. Anatomically, it is part of the lower limb.The single bone in the thigh is called the femur. This bone is very thick and strong (due to the high proportion of bone tissue), and forms a ball and socket joint at the hip, and a modified hinge joint at the knee. Structure
Bones
The femur is the only bone in the thigh and serves as an attachment site for all muscles in the thigh. The head of the femur articulates with the acetabulum in the pelvic bone forming the hip joint, while the distal part of the femur articulates with the tibia and patella forming the knee. By most measures, the femur is the strongest bone in the body. The femur is also the longest bone in the body.The femur is categorised as a long bone and comprises a diaphysis, the shaft (or body) and two epiphysis or extremities that articulate with adjacent bones in the hip and knee. Muscular compartments
In cross-section, the thigh is divided up into three separate compartments, divided by fascia, each containing muscles. These compartments use the femur as an axis and are separated by tough connective tissue membranes (or septa). Each of these compartments has its own blood and nerve supply, and contains a different group of muscles.
In theory it should be easiest to deduce the origin of recently gained introns due to the lack of host-induced mutations, yet even introns gained recently did not arise from any of the aforementioned mechanisms. These findings thus raise the question of whether or not the proposed mechanisms of intron gain fail to describe the mechanistic origin of many novel introns because they are not accurate mechanisms of intron gain, or if there are other, yet to be discovered, processes generating novel introns.In intron transposition, the most commonly purported intron gain mechanism, a spliced intron is thought to reverse splice into either its own mRNA or another mRNA at a previously intron-less position. This intron-containing mRNA is then reverse transcribed and the resulting intron-containing cDNA may then cause intron gain via complete or partial recombination with its original genomic locus. Transposon insertions can also result in intron creation. Such an insertion could intronize the transposon without disrupting the coding sequence when a transposon inserts into the sequence AGGT, resulting in the duplication of this sequence on each side of the transposon. It is not yet understood why these elements are spliced, whether by chance, or by some preferential action by the transposon. In tandem genomic duplication, due to the similarity between consensus donor and acceptor splice sites, which both closely resemble AGGT, the tandem genomic duplication of an exonic segment harboring an AGGT sequence generates two potential splice sites.