Disease progression transit

The indications which justify such an approach are directly provided by the episode patterns. As described above, in specific parts of disease progression the disease episodes occur periodically, while they develop rather randomly before, with no exact bifurcation point in between. Accordingly, we do not expect the mechanism of episode generation to change completely when it goes from random to periodic disease episodes. We assume that this reflects disease-related alteration of the system dynamics and we expect that this also holds true for the transitions to chaotic disease patterns. 

Sarkis, A., Dalbagni, G., Cordon-Cardo, C Zhang, Z.-F., Sheinfeld, J., Fair, W., Herr, H and Reuter, V. (1993) Nuclear overexpression of p53 protein in transitional cell bladder carcinoma a marker for disease progression. J. Natl. Cancer Inst. 85, 53-59. 

At present, HIV infection or AIDS cannot be cured. One mechanism whereby the chronic phase of HIV infection may be extended and transition to AIDS delayed is via pharmacological treatment. Patients are typically prescribed a combination, or cocktail, of drags that slow down the progression of the disease. Many of these drugs produce a myriad of side effects, including sleep disturbances. 

We have emphasized the fact that the progression of mental diseases, especially major depression, is associated with significant disturbances in the circadian rhythms of autonomous functions, especially sleep-wake cycles and hormone release. These rhythms are naturally occurring but are distorted in affective disorders. The most clear distortions are often seen in the ultradian components in specific phases of the circadian cycle, e.g. in the morning peak of cortisol release or in the REM to nonREM transition during the sleep state. 

The cause of autoimmune hepatitis (AIH) is unknown. Autoimmune reactions lead to a chronic (rarely acute) inflammatory process (periportal piecemeal necrosis, infiltration of portal zones). AIH is frequently associated with autoimmune diseases of other organs. It occurs predominantly among women, particularly in younger years. Hypergammaglobulinaemia is invariably in evidence. Various autoantibodies to components of the liver parenchyma are found. The presence and specificity of these antibodies, together with the respective clinical symptoms, facilitate differentiation between the various subtypes of AIH. Diagnosis is substantiated by the response to immunosuppressive therapy. If left untreated, AIH progresses rapidly with transition to cirrhosis and/or liver failure. If treated adequately, the course taken by the disease is favourable. 

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