Hormones will be elevated in response to the conditions of the body. In other words, the body's hormones will be elevated in order to provide a negative feedback response. When blood glucose is high, insulin is released to lower these levels to the normal range. In contrast, when blood glucose is low, glucagon is released to raise these levels back to normal.

Thyroxine (T4) is released by the thyroid in order to increase the basal metabolic activity of the body, causing it to produce more ATP energy. Parathyroid hormone is released to stimulate osteoclast activity and raise blood calcium levels when they are too low.

TSH is secreted by the anterior pituitary in response to TRH (thyrotropin-releasing hormone), which is secreted by the hypothalamus. TSH then acts on the thyroid to stimulate the release of thyroid hormone into the blood. Adequate levels of thyroid hormone then cause negative feedback on the hypothalamus and pituitary to decrease the release of TRH and TSH. 

In primary hypothyroidism, the problem lies in the thyroid-- the thyroid is not releasing enough thyroid hormone and it can be due to a variety of causes. What's important here is that there is no negative feedback on the pituitary to decrease its synthesis of TSH and therefore, the TSH levels are higher. It's just not able to function to increase the level of thyroid hormone and bring it to normal. 

Thyrotropin-releasing hormone leads to the stimulation of prolactin at the same time as thyroid-stimulating hormone. Oxytocin and antidiuretic hormone are produced by the hypothalamus and stored and secreted by the posterior pituitary. Somatostatin and growth hormone are not influenced by thyrotropin-releasing hormone. 

Oxytocin and antidiuretic hormone are released from the posterior pituitary. All other choices are released from the anterior pituitary.

Sarcomeres are composed of thick and thin filaments. The thin filament is composed of polymerized actin, while the thick filament is composed of myosin. Titin is a protein that spans the full range of the sarcomere, and is involved in stability and elasticity in the muscle. Collagen is not a primary component of sarcomeres.

The sliding filament theory describes the mechanism that allows muscles to contract. According to this theory, myosin (a motor protein) binds to actin. The myosin then alters its configuration, resulting in a "stroke" that pulls on the actin filament and causes it to slide across the myosin filament. The overall process shortens the sarcomere structure, but does not change the actual length of either filament.

The correct answer is ATP and calcium ions. Myosin head activation to form a cross-bridge with actin requires ATP, and the cleavage of ATP to ADP + P_i contracts the myosin head and pulls the actin. Calcium is required to expose actin binding sites for myosin in conjunction with troponin. 

In the sliding filament theory, myosin heads attach to an actin filament, bend to pull the actin filaments closer together, then release, reattach, and pull again. Energy from ATP is required for the myosin head to release from the actin filament—otherwise the myosin heads would remain in the same place, and the muscle would not contract. Even though the filaments are moving, the filaments themselves never actually get shorter or longer.

When ATP stores are depleted, myosin becomes incapable of detaching from actin, and the muscle remains in a taut, flexed state. This is the cause of rigor mortis.

The myosin head will hydrolyze the . Being bound to ADP, this allows the myosin head to form crossbridges by binding to actin. As ADP detaches from the myosin head, the head will produce the power stroke motion, where the myosin heads will rotate toward the sarcomeres. The myosin head will be locked in this position, attached to the actin, until another ATP molecule comes and attaches to the myosin head. This will allow the head to detach from actin and reorient itself to complete the process again. 

Osteogenic cells are a type of stem cell that differentiate into osteoblasts, which allow bone to form. Eventually, osteoblasts will become enveloped into the bone matrix and differentiate into osteocytes. Osteoclasts have the opposite function of osteoblasts, and are responsible for the resorption of bone matrix. This releases calcium into the bloodstream by breaking down bone.