[Psychotherapy for traumatized children and adolescents--cognitive-behavioral treatments]. / Psychotherapie von traumatisierten Kindern und Jugendlichen--kognitiv-verhaltenstherapeutische Behandlungsverfahren.

According to cognitive-behavioral models, both the avoidance of trauma-associated cues, as well as cognitive distortions of the trauma and the initial symptoms thereof lead to and subsequently maintain traumatic disorders. Trauma-focused cognitive behavioral therapy often starts with stabilizing interventions such as relaxation training. The main intervention consists of exposure to external trauma-associated cues (exposure in vivo) and to mental trauma reminders (exposure in sensu). Cognitive interventions aim to modify feelings of exaggerated guilt and shame. Of the different cognitive-behavioral programmes validated, trauma-focused cognitive-behavioral therapy yields the best evidence, particularly in the treatment of sexually abused children and adolescents.

Probucol prevents early coronary heart disease and death in the high-density lipoprotein receptor SR-BI/apolipoprotein E double knockout mouse.

Mice with homozygous null mutations in the high-density lipoprotein receptor SR-BI (scavenger receptor class B, type I) and apolipoprotein E genes fed a low-fat diet exhibit a constellation of pathologies shared with human atherosclerotic coronary heart disease (CHD): hypercholesterolemia, occlusive coronary atherosclerosis, myocardial infarctions, cardiac dysfunction (heart enlargement, reduced systolic function and ejection fraction, and ECG abnormalities), and premature death (mean age 6 weeks). They also exhibit a block in RBC maturation and abnormally high plasma unesterified-to-total cholesterol ratio (0.8) with associated abnormal lipoprotein morphology (lamellar/vesicular and stacked discoidal particles reminiscent of those in lecithin/cholesterol acyltransferase deficiency and cholestasis). Treatment with the lipid-lowering, antiatherosclerosis, and antioxidation drug probucol extended life to as long as 60 weeks (mean 36 weeks), and at 5-6 weeks of age, virtually completely reversed the cardiac and most RBC pathologies and corrected the unesterified to total cholesterol ratio (0.3) and associated distinctive abnormal lipoprotein morphologies. Manipulation of the timing of administration and withdrawal of probucol could control the onset of death and suggested that critical pathological changes usually occurred in untreated double knockout mice between approximately 3 (weaning) and 5 weeks of age and that probucol delayed heart failure even after development of substantial CHD. The ability of probucol treatment to modulate pathophysiology in the double knockout mice enhances the potential of this murine system for analysis of the pathophysiology of CHD and preclinical testing of new approaches for the prevention and treatment of cardiovascular disease.