Sustained attention, visual processing speed, and IQ in children and adolescents with Schizophrenia Spectrum disorder and Psychosis Not Otherwise Specified.

To investigate the cognitive functioning of children and adolescents with Schizophrenia Spectrum disorders and Psychosis Not Otherwise Specified, 22 child and adolescent psychiatric inpatients and day-hospital patients at a state psychiatric hospital with Schizophrenia Spectrum disorders, 30 with Psychosis Not Otherwise Specified, and 130 with other psychiatric disorders, ages 8 to 17 years, were administered the Wechsler Intelligence Scale for Children-III for psychological assessment at admission. The Performance IQs of the ADHD and the Conduct Disorder and Oppositional Defiant Disorder groups were significantly higher than those of the Schizophrenia Spectrum and the Psychosis Not Otherwise Specified groups, and the Full Scale IQs of the Conduct Disorder and Oppositional Defiant Disorder group were significantly higher than those of the Schizophrenia Spectrum group and the Psychosis Not Otherwise Specified group. The Coding scores of the ADHD group were significantly higher than those of the Schizophrenia Spectrum, the Psychosis Not Otherwise Specified, and the Bipolar Disorder groups.

Secretion of pigment epithelium-derived factor. Mutagenic study.

Pigment epithelium-derived factor (PEDF), a neurotrophic and antiangiogenic protein, is an extracellular component of the retinal interphotoreceptor matrix which has been shown to be secreted by human fetal retinal pigment epithelial cells. It belongs to the serpin superfamily and contains the typical exposed reactive center loop. The function of this loop is still unknown.

The PKA phosphorylation of vitronectin: effect on conformation and function.

Vitronectin (Vn) stabilizes the inhibitory form of plasminogen activator inhibitor-1 (PAI-1), an important modulator of fibrinolysis. We have previously reported that Vn is specifically phosphorylated by PKA (at Ser378), a kinase we have shown to be released from platelets upon their physiological activation. Here we describe the molecular consequences of this phosphorylation and show (by circular dichroism, and by phosphorylation with casein kinase II) that it acts by modulating the conformation of Vn.

Truncated vitronectins: binding to immobilized fibrin and to fibrin clots, and their subsequent interaction with cells.

The plasminogen activator inhibitor-1 (PAI-1) is stabilized in its inhibitory conformation by binding to Vitronectin (Vn). The anchorage of PAI-1 to the fibrin fibers was recently shown to be mediated by Vn, and as such to modulate fibrinolysis. Here we report the mapping of the fibrin binding sites in Vn using truncated recombinant Vns, and show that two segments of Vn are involved: one at its carboxyl terminus (within residues 348-459) and one at its amino terminus (within residues 1-44).

Localization of protein kinase A and vitronectin in resting platelets and their translocation onto fibrin fibers during clot formation.

Physiological stimulation of platelets with thrombin brings about the release of protein kinase A (PKA) into the plasma. In human blood, this kinase singles out and phosphorylates vitronectin (Vn), a multifunctional regulatory protein, which was proposed to play an important role in the control of fibrinolysis. Here we present immuno-cytochemical evidence to show: (i) that intact platelets possess on their surface an ecto-PKA which can preferentially phosphorylate Vn; (ii) that in the resting platelet, both the catalytic and the regulatory subunits of PKA are present on the platelet surface, in the surface-connected canalicular system, and within the alpha-granules of the platelets; (iii) that the process initiated upon platelet activation, which leads to the formation of fibrin fibers and consequently forms the fibrin net, is accompanied by a translocation of PKA, of Vn, and of PAI-1 onto the fibrin fibers.