14 下列何者不是休克治療失敗（refractory shock或irreversible shock）的可能原因？

大腦嚴重缺血（severe cerebral ischemia）

血液容積持續不足（persistent reduction of blood volume）

心肌受到抑制而衰竭（myocardial depression / failure）

急性呼吸窘迫症候群（acute respiratory distress syndrome, ARDS）

B:

B IS HYPOVOLEMIC SHOCK

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15 正常時，下列何種immunoglobulin（Ig）在血中濃度最高？何種最低？

IgM最高，IgA最低 IgA最高，IgG最低 IgE最高，IgM最低 IgG最高，IgE最低

D

GE

THINK GE: THAT IS A BRIGHT IDEA!!!!

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17 下列有關nitric oxide synthase（NOS）的敘述，何者正確？

NOS 1（nNOS）存在於神經系統，可被交感神經刺激而活化

NOS 2（iNOS）存在於免疫細胞及巨噬細胞（macrophage），可被bradykinin活化

NOS 3（eNOS）存在於血管內皮細胞（endothelial cell），可被cytokine活化

NOS 1、NOS 2及NOS 3所產生之NO會被血紅素（hemoglobin）去活化

D

nNOS

Neuronal NOS (nNOS) produces NO in nervous tissue in both the central and peripheral nervous system. Neuronal NOS also performs a role in cell communication and is associated with plasma membranes. nNOS action can be inhibited by NPA (N-propyl-L-arginine). This form of the enzyme is specifically inhibited by 7-nitroindazole.^[8]

The subcellular localisation of nNOS in skeletal muscle is mediated by anchoring of nNOS to dystrophin. nNOS contains an additional N-terminal domain, thePDZ domain^[9].

[edit]iNOS

As opposed to the critical calcium-dependent regulation of constitutive NOS enzymes (nNOS and eNOS), iNOS has been described as calcium-insensitive, likely due to its tight non-covalent interaction with calmodulin (CaM) and Ca²⁺. While evidence for ‘baseline’ iNOS expression has been elusive, IRF1 and NF-κB-dependent activation of the inducible NOS promoter supports an inflammation mediated stimulation of this transcript.

From a functional perspective, it is important to recognize that induction of the high-output iNOS usually occurs in an oxidative environment, and thus high levels of NO have the opportunity to react with superoxide leading to peroxynitrite formation and cell toxicity.

These properties may define the roles of iNOS in host immunity, enabling its participation in anti-microbial and anti-tumor activities as part of the oxidative burst of macrophages.^[10]

It has been suggested that pathologic generation of nitric oxide through increased iNOS production may decrease tubal ciliary beats and smooth muscle contractions and thus affect embryo transport, which may consequently result in ectopic pregnancy.^[11]

[edit]eNOS

Main article: Endothelial NOS

Endothelial NOS (eNOS), also known as nitric oxide synthase 3 (NOS3), generates NO in blood vessels and is involved with regulating vascular function. A constitutive Ca²⁺ dependent NOS provides a basal release of NO. eNOS is associated with plasma membranes surrounding cells and the membranes of Golgi bodies within cells. eNOS localisation to endothelial membranes is mediated by cotranslational N-terminal myristoylation and post-translationalpalmitoylation^[