Cholinesterases. Structure, function, mechanism, genetics and cell biology.

International audienc

Electrical Modeling of Long-Wavelength VCSELs for Intrinsic Parameters Extraction

We present an efficient method to model the small-signal modulation response of a long-wavelength VCSEL chip using an equivalent electrical circuit. This circuit serves two distinct purposes. Based on T-Matrix formalism, it is used to remove the parasitics contribution originating from the electrical access of the chip in order to obtain the optical cavity intrinsic frequency response as defined by the rate equations. The same circuit is also used to extract the intrinsic cavity parameters since every circuit element represents a physical optical cavity entity. The extraction of reliable intrinsic parameters requires that the circuit element values be representative of the device under test. To achieve this, we have developed a new methodology based on static and dynamic measurements such as the S-parameters and the turn-on delay time. In accordance with this procedure, each element of the cavity is fixed without numerical optimization. The good agreement between measured and simulated curves confirm the validity of the technique used

Genetic inactivation of acetylcholinesterase causes functional and structural impairment of mouse soleus muscles

International audienceAcetylcholinesterase (AChE) plays an essential role in neuromuscular transmission. Not surprisingly, neuromuscular transmission during repetitive nerve stimulation is severely depressed in the AChE knockout mouse (KO). However, whether this deficit in AChE leads to skeletal muscle changes is not known. We have studied the in vitro contractile properties of the postural and locomotor soleus muscles of adult KO and normal (wildtype, WT) mice, and this was completed by histological and biochemical analyses. Our results show that muscle weight, crosssectional area of muscle fibres and absolute maximal isometric force are all reduced in KO mice compared with WT mice. Of interest, the relative amount of slow myosin heavy chain (MHC-1) in muscle homogenates and the percentage of muscle fibres expressing MHC-1 are decreased in the KO mice. Surprisingly, AChE ablation does not modify twitch kinetics, absolute maximal power, fatigue resistance or citrate synthase activity, despite the reduced number of slow muscle fibres. Thus, a deficit in AChE leads to alterations in the structure and function of muscles but these changes are not simply related to the reduced body weight of KO mice. Our results also suggest that this murine model of congenital myasthenic syndrome with endplate AChE deficiency combines alterations in both neurotransmission and intrinsic muscle properties

Single-wall carbon nanotubes for optical limiting

International audienc