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The authors describe two patients with congenital myasthenic syndrome (CMS) with end plate acetylcholinesterase (AChE) deficiency caused by mutations in the collagenic tail (ColQ) of AChE: a homozygous C-terminal Y230S mutation in Patient 1 and Y430S and a C-terminal splice-site mutation in Patient 2. In Patient 1, a Prostigmin (neostigmine bromide) test failed to distinguish between AChE deficiency and a slow-channel CMS. Both patients responded dramatically to ephedrine therapy.

With further scaling of nanometer CMOS technologies, yield and reliability become an increasing challenge. This paper reviews the most important phenomena affecting yield and reliability. For each effect, the basic physical mechanisms causing the effect and its impact on transistor parameters are described. Possible solutions to cope/handle with these effects on the design level are discussed as well.

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