Certain preconscious daytime thoughts can be resistant and these can retain a part of their cathexis as well. Unconscious impulses and day residues can come together and result in a conflict. Freud then wondered about the outcome of this wishful impulse: an unconscious instinctual demand that becomes a dream wish in the preconscious. Freud stated that this unconscious impulse could be expressed as mobility during sleep. This would be what is observed in somnambulism, though what actually makes it possible remains unknown.As of 2002, sleepwalking has not been detected in non-human primates. It is unclear whether it simply hasnt been observed yet, or whether sleepwalking is a uniquely human phenomenon. Society and culture
Opera
Vincenzo Bellinis 1831 Italian opera semiseria, La sonnambula, the plot of which is centered on the question of the innocence of the betrothed and soon-to-be married Amina, who, upon having been discovered in the bedchamber of a stranger, and despite the assurances of that stranger that Amina was entirely innocent, has been rejected by her enraged fiancé, Elvino — who, then, decides to marry another. In fact, when stressed, Amina was susceptible to somnambulism; and had come to be in the strangers bedchamber by sleep-walking along a high parapet (in full view of the operas audience). Elvino, who later observes the (exhausted by all the fuss) Amina, sleep-walking across a very high, very unstable, and very rickety bridge at the local mill, realizes his mistake, abandons his plans of marriage to the other woman, and re-unites with Amina.
Most importantly, osteoclast dysfunction mediates the pathogenesis of this disease.Osteopetrosis is caused by underlying mutations that interfere with the acidification of the osteoclast resorption pit, for example due to a deficiency of the carbonic anhydrase enzyme encoded by the CA2 gene. Carbonic anhydrase is required by osteoclasts for proton production. Without this enzyme hydrogen ion pumping is inhibited and bone resorption by osteoclasts is defective, as an acidic environment is needed to dissociate calcium hydroxyapatite from the bone matrix. As bone resorption fails while bone formation continues, excessive bone is formed.Mutations in at least nine genes cause the various types of osteopetrosis. Mutations in the CLCN7 gene are responsible for about 75 percent of cases of autosomal dominant osteopetrosis, 10 to 15 percent of cases of autosomal recessive osteopetrosis, and all known cases of intermediate autosomal osteopetrosis. TCIRG1 gene mutations cause about 50 percent of cases of autosomal recessive osteopetrosis. Mutations in other genes are less common causes of autosomal dominant and autosomal recessive forms of the disorder. The X-linked type of osteopetrosis, OL-EDA-ID, results from mutations in the IKBKG gene. In about 30 percent of all cases of osteopetrosis, the cause of the condition is unknown.The genes associated with osteopetrosis are involved in the formation, development, and function of specialized cells called osteoclasts. These cells break down bone tissue during bone remodeling, a normal process in which old bone is removed and new bone is created to replace it.