Clonidine as a Treatment of Behavioural Disturbances in Autism Spectrum Disorder: A Systematic Literature Review.

Background: Agitation and aggression are commonly cited reasons for psychiatry consultation for individuals diagnosed with autism spectrum disorder (ASD). While risperidone and aripiprazole do not carry Health Canada approval for management of ASD-associated irritability, both are used for this indication but are not universally effective and carry substantial risk of adverse effects. This necessitates use of off-label medications to assist in management of behavioral dysregulation.

The KATP channel Kir6.2 subunit content is higher in glycolytic than oxidative skeletal muscle fibers.

It has long been suggested that in skeletal muscle, the ATP-sensitive K(+) channel (K(ATP)) channel is important in protecting energy levels and that abolishing its activity causes fiber damage and severely impairs function. The responses to a lack of K(ATP) channel activity vary between muscles and fibers, with the severity of the impairment being the highest in the most glycolytic muscle fibers. Furthermore, glycolytic muscle fibers are also expected to face metabolic stress more often than oxidative ones.

KATP channel deficiency in mouse flexor digitorum brevis causes fibre damage and impairs Ca2+ release and force development during fatigue in vitro.

Activation of the K(ATP) channels results in faster fatigue rates as the channels depress action potential amplitude, whereas abolishing the channel activity has no effect in whole extensor digitorum longus (EDL) and soleus muscles. In this study, we examined the effects of abolished K(ATP) channel activity during fatigue at 37 degrees C on free intracellular Ca(2+) (Ca(2+)(i)) and tetanic force using single muscle fibres and small muscle bundles from the flexor digitorum brevis (FDB). K(ATP) channel deficient muscle fibres were obtained (i) pharmacologically by exposing wild-type fibres to glibenclamide, and (ii) genetically using null mice for the Kir6.

Determinants of inducible brain natriuretic peptide promoter activity.

Atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) are polypeptide hormones belonging to the cardiac-derived mammalian natriuretic peptide system. These hormones share the same biological properties and receptors and both play important roles in the maintenance of fluid and electrolyte balance and in cardiovascular growth. Most hemodynamic and neurohumoral stimuli can coordinately increase ANF and BNP gene expression.