Answer: AND Explanation.
Lisa consumed too much water in too short of a time. This led to water leaking into the brain and disrupting the cerebrospinal fluid concentrations, impairing neural tissue activity
The structures are nephrons which gets blood through the [renal artery]. The nephrons also consist of the [afférent and efferent artérioles], the latter of which is much narrower causing a high pressure to exist in the [glomerulus] (blood vessels in that ball structure) so that ultrafiltration can occur and the ultrafiltrate is passed into the [Bowman’s capsule]. The Bowman’s capsule consists of podocytes which are cells that form a microscopic pore so that small molecules can pass through (ions and such). There is the [proximal convoluted tube] that makes the contents flow downwards (and allows water to exit so the water potential inside is low) and the [distal convoluted tube] that makes the contents go upwards (and allows water to re-enter which increases the water potential inside). These are both partially permeable and set up a concentration gradient for the reabsorption of water from the urine. These tubes lead into the [collecting duct] which further reabsorb the water.
All the structures of the kidney are in [ ].
1- Answer : B (AUG AAA CGU CCU)
2- Answer : B (TAC AAA AGA GGG)
3- Answer : C (GGCGATACG)
<span>he Streptococcus pneumoniae capsule is vital for virulence and may inhibit complement activity and phagocytosis. However, there are only limited data on the mechanisms by which the capsule affects complement and the consequences for S. pneumoniae interactions with phagocytes. Using unencapsulated serotype 2 and 4 S. pneumoniae mutants, we have confirmed that the capsule has several effects on complement activity. The capsule impaired bacterial opsonization with C3b/iC3b by both the alternative and classical complement pathways and also inhibited conversion of C3b bound to the bacterial surface to iC3b. There was increased binding of the classical pathway mediators immunoglobulin G (IgG) and C-reactive protein (CRP) to unencapsulated S. pneumoniae, indicating that the capsule could inhibit classical pathway complement activity by masking antibody recognition of subcapsular antigens, as well as by inhibiting CRP binding. Cleavage of serum IgG by the enzyme IdeS reduced C3b/iC3b deposition on all of the strains, but there were still marked increases in C3b/iC3b deposition on unencapsulated TIGR4 and D39 strains compared to encapsulated strains, suggesting that the capsule inhibits both IgG-mediated and IgG-independent complement activity against S. pneumoniae. Unencapsulated strains were more susceptible to neutrophil phagocytosis after incubation in normal serum, normal serum treated with IdeS, complement-deficient serum, and complement-deficient serum treated with IdeS or in buffer alone, suggesting that the capsule inhibits phagocytosis mediated by FcÎł receptors, complement receptors, and nonopsonic receptors. Overall, these data show that the S. pneumoniae capsule affects multiple aspects of complement- and neutrophil-mediated immunity, resulting in a profound inhibition of opsonophagocytosis.</span>
<span>Mitochondriom is the awnser
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