668 research outputs found

    A nevek szerepe a rábaszentandrásí megszólításformákban

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    A ragadványnevek nemzedéki kötöttsége egy település névrendszerében

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    A bűnözéstől a szervezett bűnözésig

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    Lectori Salutem

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    Executive Function and Attention Performance in Children with ADHD

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    The emerging literature reports that children with Attention-Deficit/Hyperactivity Disorder (ADHD) show deficits in executive functioning. To date, the combination of drug therapy with certain evidence-based non-medication interventions has been proven to be the most effective treatment for ADHD. There is a gap in the literature regarding comparing the executive functions (EF) of treatment naïve and medicated children with ADHD with both each other and typically developing children. Altogether, 50 treatment naïve and 50 medicated children with ADHD and 50 typically developing children between the ages of six and 12 were enrolled. The Mini International Neuropsychiatric Interview for Children and Adolescents (Mini Kid) and the Test of Attentional Performance for Children (KiTAP) measures were employed. Treatment naïve children with ADHD showed weaker performance on most executive function measures (12 out of 15) than either the medicated ADHD group or the controls. There were no significant differences between the medicated ADHD children and typically developing children in most KiTAP parameters (10 out of 15). Executive function impairments were observable in treatment naïve ADHD children, which draws attention to the importance of treating ADHD. Future studies should focus on the specific effects of stimulant medication on executive functions

    Cultural Autonomy in Hungary: Inward or Outward Looking?

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    Since the late 1980s, the interpretations of policy toward Hungary’s minorities—most notably the country’s 1993 minority law and the minority self-governments established as part of a system of nonterritorial autonomy (NTA)—have been the subject of debates in politics and academia in at least two critical respects. Aside from the declarative character of the law, foremost has been the question of Hungary’s kin-state activism toward Hungarians abroad and the implications this has carried for domestic minority issues. A second—and related—question has concerned the extent to which cultural autonomy and minority rights are in accordance with the needs of the Roma, by far the country’s largest ethnic minority group. A growing number of scholars have accepted the argument that the minority law was enacted because of concerns regarding Hungarian minorities living in the neighboring countries. In our view, it is more appropriate to ask instead how Hungary’s kin-state policies have influenced the opportunities for domestic groups, and, in particular, how Hungary fits into the broader context of post-Communist state- and nation-building projects. This is the approach we take in this article, which aims to unpack and reconcile the complex and seemingly contradictory findings on the Hungarian case. Our conclusions are drawn from a content analysis of parliamentary debates on the minority law—something that has never previously been undertaken. This is supplemented by semi-structured interviews with former and current politicians and minority activists

    Az érfal trombogenitása és annak szabályozása = Vessel wall thrombogenicity and its regulation

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    Fiziológiás hemosztázis ill. artériás trombózis keletkezésekor a trombociták a gyorsan áramló vérből von Willebrand faktoron keresztül tapadnak ki az érfalban lévő kollagénhez. Az érfal mátrix komponenseit vizsgálva megállapítottuk, hogy a media rétegből izolálható proteoglikánok, a perlecan és a biglycan/decorin gátolják a von Willebrand faktor kötődését a kollagénhez, és így a jelenlétükben in vitro kialakuló kollagén struktúra antitrombogén. Az adventitia proteoglikánok a kollagén trombogenitását nem befolyásolják. A media proteoglikánok antitrombotikus tulajdonsága perlecan esetében a fehérje komponenshez, míg biglycan, decorin esetében az adventitia rétegétől eltérő kondroitin szulfát/dermatán szulfát oldalláncokhoz köthető. Kimutattuk, hogy plazmin, trombin, és neutrofil granulocita metalloproteinázok fokozzák az érfal media rétegében lévő kollagén trombogenitását, ami gyulladásban ill. hemosztázisban fokozott trombózishajlamhoz vezethet. Az artériás trombusban a trombociták egymáshoz fibrinogénen, von Willebrand faktoron keresztül kapcsolódnak. Megállapítottuk, hogy fiziológiás koncentráció viszonyok esetén a von Willebrand faktor védi a fibrinogént a plazmin hasítása ellen, és bár ő is plazmin szubsztrát, a hatás nem a szubsztrátok kompetícióján alapul. Artériás trombusban a fibrinogén kb. 50 %-a fibrinné alakul, ennek degradációját a von Willebrand faktor nem befolyásolja. | In the course of hemostasis or arterial thrombosis platelets are captured from rapidly flowing blood by von Willebrand factor immobilized on vascular collagens. Collagen structures in the media layer of vessel wall, however, do not support platelet adhesion. We have found that perlecan and biglycan/decorin isolated from the media layer of the arterial wall, but none of the adventitia proteoglycans, inhibit von Willebrand factor binding to collagen and platelet adhesion to reconstituted collagen surfaces. The antithrombotic effect of perlecan is due to its core protein component, whereas the inhibitory effects of media biglycan and decorin are attributable to their chondroitin sulphate/dermatan sulphate chains, which are different from those in adventitia biglycan and decorin. We have shown that the antithrombotic properties of the media collagen structures, in situ, can be disrupted by plasmin, thrombin and matrix metalloproteases of neutrophil granulocytes, which suggests that vascular thrombogenicity may increase at sites of inflammation and when the hemostatic system is activated. In platelet-rich thrombi fibrinogen and von Willebrand factor serve as molecular bridges between platelets. Our data indicate that von Willebrand factor protects fibrinogen, but not fibrin from plasmin degradation. Although von Willebrand factor is also a substrate for plasmin, its protective effect is not due to substrate competition
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