[Disintegration of social cognitive processes in schizophrenia].

Unlabelled: Despite rapid development of research on social cognition (SC) impairments in schizophrenia, efforts are still made to generate new, broader theoretical models which include the neural network approach to those dysfunctions. The aim of this study was the evaluation of the structure of SC in patients with schizophrenia in comparison to healthy subjects.

Methods: The studied groups consisted of 55 subjects: 30 patients with paranoid schizophrenia according to DSM-IV criteria, and 25 control healthy subjects matched for age, gender and education to the clinical group.

[A creator of modern surgery--Johann von Mikulicz-Radecki and contemporary ophthalmologists at the University of Wroclaw at the turn of the 19th-20th century].

The authors present the history of the life and achievements of Jan Mikulicz-Radecki as the creator of modern surgery and his own school of surgery, especially during his work at the Wroclaw University in 1890-1905 years. The contemporary ophthalmologists as Richard Foerster, Hermann Ludwig Cohn, Wilhelm Uhthoff and theirs famous coworkers are also presented.

Ebelactone B, an inhibitor of extracellular cathepsin A-type enzyme, suppresses platelet aggregation ex vivo in renovascular hypertensive rats.

The present study was undertaken to investigate whether ebelactone B, an inhibitor of bradykinin and angiotensin I hydrolysis by serine carboxypeptidase Y-like enzymes, could influence platelet aggregation ex vivo in renovascular hypertensive rats (2-kidney, 1-clip Goldblatt model, 2K1C). We found that ebelactone B (5 mg/kg) administrated subcutaneously once a day for 5 days, 5 weeks after the development of hypertension, or a single dose of ebelactone B (0.5 mg/kg) injected intravenously into 2K1C hypertensive rats before the induction of arterial thrombosis, both markedly suppressed collagen-induced platelet aggregation in whole blood.

Lysosomal high molecular weight multienzyme complex.

Three acidic glycosidases: beta-galactosidase (beta-GAL, EC 3.2.1.