Viral Shunt

DOM Release The Viral Shunt, Algal Exudates, and Sloppy Feeding... 

The inefficiency of microbial heterotrophy does have a side benefit as it enhances nutrient remineralization rates. This serves to increase the availability of inorganic nitrogen and phosphorus for the photoautotrophs. The multiple roles of bacteria in the marine food web were shown in Figure 23.2, with the component of the food web controlled by the algal herbivores depicted on the left side and the microbial loop on the right. The viral shunt acts on both pathways. 

Acquired hyperammonemia Liver disease is a common cause of hyperammonemia in adults. It may be a result of an acute po cess, for example, viral hepatitis, ischemia, or hepatotoxins. Cirrhosis of the liver caused by alcoholism, hepatitis, or biiary obstruction may result in formation of collateral circulation around the liver. As a result, portal blood is shunted directly rto the systemic circulation and does not have access to the ter. The detoxification of ammonia (that is, its conversion to urea) is, therefore, severely impaired, leading to elevated levels of cicu lating ammonia. 

Liver cirrhosis is among the top 10 causes of death in the Western world. The disease occurs after chronic damage to hepatic cells, mainly hepatocytes, which can be caused by viral hepatitis, chronic alcohol abuse or toxic injury, biliary disease, and metabolic liver disorders [64], Liver cirrhosis is characterized by an abnormal deposition of connective tissue in the liver, which hampers the normal functions of the liver. Other features of the disease are general tissue damage, chronic inflammation, and the conversion of normal liver architecture into structurally abnormal nodules. Secondary to these anatomical changes are disturbances in the liver function and in the hemodynamics leading to portal hypertension and intrahepatic shunting [39, 64, 103],... 

In theory, there are three causes for the occurrence of HPS (since hypoventilation is not deemed a possible cause) (1.) arteriovenous shunts, (2.) disturbed alveolo-capillary oxygen diffusion in terms of impaired diffusion-perfusion, and (3.) mismatches between ventilation and perfusion. Consequently, there are numerous liver diseases which are associated with HPS. Transient HPS in acute viral hepatitis A and B has recently been reported. (17, 38) (s. tab. 18.1)... 

PGE2 inhibition in macrophages may also unleash bronchial cytotoxic lymphocytes, generated by chronic viral infection, leading to destruction of virus-infected cells in the respiratory tract (80). When urticaria occurs, it may result from increased release of leukotrienes LTC4, D4, and E4, which also induces bronchoconstriction, with a shunt of arachidonic acid toward lipoxygenation in aspirin-sensitive asthmatics (SEDA-18, 93). Aspirin-... 

Seawater DOM has numerous sources and sinks and a range of potential reactions. Sources of the sub-micron components include exudation from phytoplankton, microbial degradation of bioparticles, animal wastes (excretion), viral infection of bacteria, sloppy feeding by zooplankton and other animals, and input of dissolved molecules from rivers and surface sediments. Removal mechanisms include photodegradation, sorption to sinking particles, and microbial utilization. Tritiated thymidine and leucine uptake experiments indicate that up to half of the carbon formed by photosynthesis is shunted via dissolved organic molecule intermediates into bacteria. 

Primary peritonitis in adults occurs most commonly in association with alcoholic cirrhosis, especially in its end stage, or with ascites caused by postnecrotic cirrhosis, chronic active hepatitis, acute viral hepatitis, congestive heart failure, malignancy, systemic lupus erythematosus, or nephritic syndrome. It also may result from the use of a peritoneal catheter for dialysis or central nervous system ventriculoperitoneal shunting for hydrocephalus. Rarely, primary peritonitis occurs without apparent underlying disease. 

The precise pathogenesis of the central nervous system (CNS) signs and symptoms that accompany liver failure (hepatic encephalopathy) in patients such as Percy Veere is not completely understood. These changes are, however, attributable in part to toxic materials that are derived from the metabolism of nitrogenous substrates by bacteria in the gut that circulate to the liver in the portal vein. These materials "bypass" their normal metabolism by the liver cells, however, because the acute inflammatory process of viral hepatitis severely limits the ability of liver cells to degrade these compounds to harmless metabolites. As a result, these toxins are "shunted" into the hepatic veins unaltered and eventually reach the brain through the systemic circulation ("portal-systemic encephalopathy"). 

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