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https://colab.research.google.com/drive/1gfoIqCWqSkIDQLl9ttYV9Aynm6A8T8Hc
https://colab.research.google.com/drive/1tI2rZppufK6fuivrbICde7M5pLckII3F
https://colab.research.google.com/drive/1f5STLO2ePIw6vI0cB9fPlHJEVeuwKXeb
https://colab.research.google.com/drive/1_9766vfbdi7HsqG8AAxkOHca23Vao7ZP
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Movies | Download | Watch Online | Download HD | On Widescreen | Free on Mp4 Torrent | iPhone Screener (iPhone 6, iPhone 5, iPhone 4S, iPhone 4, iPhone 3GS .Kidney tubule dysfunction resulting in a chronic reduction in the urine concentrating ability of the kidney occurs in a large number of patients suffering from a variety of diseases. The most common symptom of the syndrome is the occurrence of excessive thirst which is especially significant when accompanied by a poor diuresis. The symptoms are aggravated by a high ambient temperature because, in such conditions, the person can drink the maximum amount of water that will be excreted in the urine. The excessive thirst is largely compensated for by reducing food intake. This syndrome, which can be a major complication of diabetes, is designated as Diabetes insipidus (DI) by i. a. the International Society for Bipolar Disorders (ISBD). The DI is divided into central and peripheral DI. Both types can be subdivided into Osmotic (e.g. due to an increase in the content of the urine) and non-osmotic (e.g. due to an inability to secrete an osmotically active substance). Many cases of non-osmotic DI are ADH-dependent, e.g. as a consequence of damage to the organ of Corti in which the paraventricular organ (PVO) in humans and the paraventricular nuclei (PVN) in rats produces neuropeptide ADH. In patients suffering from DI, the secretion of ADH is not only defective, but also increased. The mechanism causing this disorder is unknown. There are data suggesting that in addition to neuropeptide ADH, ADH represents a substance that is synthesized in the epithelium of the kidney proximal tubules, and that its secretion is regulated by the nervous system.
The basic problems that must be solved are: Is ADH not only derived from the neuropeptide ADH, but also from a kidney tubule product? Does the secretion of ADH by the kidney occur in the tubules at the level of the PVO or the PVN? Is the reduction of kidney ADH-secretion the cause of the disorder of kidney ADH-secretion, which manifests itself in
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