Mpo notes

In the Hepburn romanization system, Godzilla's name is rendered as "Gojira", whereas in the Kunrei romanization system it is rendered as "Gozira". In the original film, the fins were added for purely aesthetic purposes, in order to further differentiate Godzilla from any other living or extinct creature.

Mpo notes

It works at several levels. It has a basic recognition function for many bacteria, can alert and recruit phagocytes, enhance visibility of bacteria to phagocytes and sometimes even lyse bacteria. The complement system can be activated by at least three separate pathways.

The two evolutionary older pathways are the so-called "alternative" and the lectin pathways. Both are activated on many bacterial surfaces, contributing to innate immunity. The third pathway, which is mainly antibody-activated and hence part of the adaptive immune system, developed much later, but was identified first.

Somewhat unfairly, it is therefore called the "classical pathway". The alternative Mpo notes of complement activation starts with the spontaneous hydroysis of an internal thioester bond in the plasma complement component C3 to result in C3 H2O.

The changed conformation of C3 H2O enables binding of the plasma protein factor B which is in turn cleaved into fragments Ba and Bb by the plasma protease factor D. While BY diffuses away, the C3 H2O Bb complex is a soluble C3 convertase which proceeds to cleave a number of C3 molecules, resulting in small, soluble C3a and a larger fragment, C3b, which normally is rapidly inactivated.

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In case C3b is generated near a bacterial or cellular surface, it binds covalently to this surface. The process just described now repeats on the membrane: The further development depends on the nature of the surface in question.

Mpo notes

If C3b binds to the membrane of one of our own cells, the process of activation is inhibited by one of several different protective proteins, Mpo notes damage to the cell. A bacterial surface lacks these inhibitors, allowing the complement cascade to proceed.

Facilitated by the bacterial surface, factor P properdine stabilizes the membrane-bound C3bBb complex. This complex, the C3 convertase of the alternative pathway, subsequently works as an amplifying tool, rapidly cleaving hundreds of additional C3 molecules.

Soluble C3a diffuses into the surroundings, recruiting phagocytes to the site of infection by chemotaxis. C3b fragments and their cleavage products C3d, C3dg and C3bi are deposited on the bacterial surface in increasing numbers and are recognized by specific complement receptors CR1-CR4 present on the membrane of phagocytes.

This function, making the bacterium a "delicacy" for phagocytes, is called opsonization, from the Greek word for goody.

The complement cascade does not stop at this point: The smaller cleavage products C3a, C4a, C5a, sometimes called "anaphylatoxins", have additional functions in their own right: The lectin pathway of complement activation exploits the fact that many bacterial surfaces contain mannose sugar molecules in a characteristic spacing.

These, by cleaving C4 and C2, generate a second type of C3 convertase consisting of C4b and C2b, with ensuing events identical to those of the alternative pathway. The classical pathway usually starts with antigen-bound antibodies recruiting the C1q component, followed by binding and sequential activation of C1r and C1s serine proteases.

Yet, this pathway can also be activated in the absence of antibodies by the plasma protein CRP C-reactive proteinwhich binds to bacterial surfaces and is able to activate C1q.

Lecture Notes in Immunology: Function of the Human Immune System

This is desirable when unwanted complement activation causes hemolysis, as in paroxysmal nocturnal hemoglobinuria or in some forms of hemolytic uremic syndrome.

For the lytic pathway's importance in fighting meningococcal infections, Eculizumab treatment increases the risk of these infections, which may be prevented by previous vaccination.

Mpo notes

As its name implies, this process is initiated when a complex of three plasma proteins is formed by contact with certain negatively charged surfaces. Such surfaces may be collagen, basal membranes, or aggregated platelets in case of a laceration, or bacterial surfaces in case of an infection. Factor XII is activated by contact with the negatively charged surface, starting the entire coagulation cascade.

In addition, factor XII cleaves prekallikrein, releasing the active protease kallikrein that in turn releases the nonapeptide bradykinin from HMWK.

Bradykinin enhances small vessel permeability, dilates small vessels indirectly via the endothelium but otherwise favors contraction of smooth muscle and is the strongest mediator of pain known. Bradykinin and other kinins have a short half life, being inactivated by peptidases including angiotensin converting enzyme ACE.

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ACE inhibitors, frequently used to lower blood pressure, have the common side effect of inducing cough. This is believed to be due to an increase in bradykinin activity. Driven by blood pressure, plasma is filtrated out of the vessels showing enhanced permeability, forming tissue lymph.

This is diverted to the regional lymph nodes, where phagocytes and other leukocytes are waiting to initiate further defense measures. Activation of the plasma protein cascades is in many regards a precondition for the next step, the activation of cellular systems at the infection site.CORPUS CHRISTI METROPOLITAN PLANNING ORGANIZATION (MPO) TECHNICAL ADVISORY COMMITTEE (TAC) MEETING NOTES.

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