Spontaneous disease formation

This profile of changes was comparable to that seen in patients with conventional cholesterol gallstone disease, the only difference being that, as a result of OT, the chemistry probably developed in days or weeks, as opposed to months or years in the case of spontaneous gallstone formation. ... 

A number of disorders have been identified that are primarily caused by the presence of abnormal platelet levels in the blood. Thrombocythaemia is a disease characterized by abnormal megakaryocyte proliferation, leading to elevated blood platelet levels. In many instances, this results in an elevated risk of spontaneous clot formation within blood vessels. In other instances, the platelets produced are defective, which can increase the risk of spontaneous or prolonged bleeding events. 

Asthma is an extremely complex condition characterized by variable and reversible airways obstmction combiaed with nonspecific bronchial hypersensitivity (1 3). The cause of asthma, which is not always readily diagnosed (4), remains unknown. Days, if not weeks, ate needed to document the spontaneous reversal of the airways obstmction ia some patients. Asthmatics experience both an immediate hypersensitivity response and a delayed late-phase reaction, each mediated by a different pathway. Chronic asthma has come to be viewed as an inflammatory disease (5). The late-phase reaction plays a key role ia iaduciag and maintaining the inflammatory state which ia turn is thought to iaduce the bronchial hyperresponsiveness (6). The airways obstmction results from both contraction of airways smooth muscle and excessive bronchial edema. Edema, a characteristic of inflammatory states, is accompanied, ia this case, by the formation of a viscous mucus which can completely block the small airways. 

The earliest uses of microorganisms to treat human disease can be traced to the belief that formation of pus in some way drained off noxious humours responsible for systemic conditions. Although the spontaneous appearance of pus in their patients wounds satisfied most physicians, deliberate contamination of wounds was also practised. Bizarre concoctions of bacteria such as ointment of pigs dung and herb sclerata were favoured during the Middle Ages. Both early central European and South... 

Association of Pain, neuropathic pain is defined as pain initiated or caused by a primary lesion, dysfunction in the nervous system". Neuropathy can be divided broadly into peripheral and central neuropathic pain, depending on whether the primary lesion or dysfunction is situated in the peripheral or central nervous system. In the periphery, neuropathic pain can result from disease or inflammatory states that affect peripheral nerves (e.g. diabetes mellitus, herpes zoster, HIV) or alternatively due to neuroma formation (amputation, nerve transection), nerve compression (e.g. tumours, entrapment) or other injuries (e.g. nerve crush, trauma). Central pain syndromes, on the other hand, result from alterations in different regions of the brain or the spinal cord. Examples include tumour or trauma affecting particular CNS structures (e.g. brainstem and thalamus) or spinal cord injury. Both the symptoms and origins of neuropathic pain are extremely diverse. Due to this variability, neuropathic pain syndromes are often difficult to treat. Some of the clinical symptoms associated with this condition include spontaneous pain, tactile allodynia (touch-evoked pain), hyperalgesia (enhanced responses to a painful stimulus) and sensory deficits. 

How pathogenic mutations in PRNP cause prion disease has yet to be resolved. However, in most cases the mutation is thought to lead to an increased tendency of PrPc to form PrPSc, although there is evidence to suggest that this may not be solely attributable to decreased thermodynamic stability of mutated PrPc. Experimentally manipulated mutations of the prion gene can lead to spontaneous neurodegeneration without the formation... 

Prions also have the ability to trigger conformational change in their normal counterpart proteins in the brain, causing these to also adopt the improper configuration. In this fashion, the prion can essentially replicate itself. Because the conformational structure assumed during prion formation is thermodynamically stable, prions are exceedingly resistant to inactivation (128, 129). In addition, they can be transmitted orally. The effect of these traits is that the disease is not solely dependent on spontaneous generation to infect an individual or population, but it also can be acquired by consumption of infected tissue. 

Spontaneous ectopic germinal-center formation has long been recognized to occur in human autoimmune diseases and is a source of somatically mutated high-affinity autoandbodies. 

Mutations that interfere with collagen fiber formation mostly cause lethal or nonlethal osteogenesis imperfecta, also known as brittle bone disease. The bones break easily and apparently spontaneously. The disorder occurs in about one in 50,000 live births in the US. Osteogenesis imperfecta is clinically divided by whether the teeth are also affected. They may appear opalescent blue-gray or yellow-brown because of abnormal dentin calcification. 

Ketone body formation, which occurs within the matrix of liver mitochondria, begins with the condensation of two acetyl-CoAs to form acetoacetyl-CoA. Then acetoacetyl-CoA condenses with another acetyl-CoA to form /3-hydroxy-/3-methylglutaryl-CoA (HMG-CoA). In the next reaction, HMG-CoA is cleaved to form acetoacetate and acetyl-CoA. Acetoacetate is then reduced to form /3-hydroxybutyrate. Acetone is formed by the spontaneous decarboxylation of acetoacetate when the latter molecule s concentration is high. (This condition, referred to as ketosis, occurs in uncontrolled diabetes, a metabolic disease discussed in Special Interest Box 16.3, and during starvation. In both of these conditions there is a heavy reliance on fat stores and /3-oxidation of fatty acids to supply energy.)... 

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