Upper Alpha Based Neurofeedback Training in Chronic Stroke: Brain Plasticity Processes and Cognitive Effects.

In the present study, we investigated the effects of upper alpha based neurofeedback (NF) training on electrical brain activity and cognitive functions in stroke survivors. Therefore, two single chronic stroke patients with memory deficits (subject A with a bilateral subarachnoid hemorrhage; subject B with an ischemic stroke in the left arteria cerebri media) and a healthy elderly control group (N = 24) received up to ten NF training sessions. To evaluate NF training effects, all participants performed multichannel electroencephalogram (EEG) resting measurements and a neuropsychological test battery assessing different cognitive functions before and after NF training.

Shutting Down Sensorimotor Interferences after Stroke: A Proof-of-Principle SMR Neurofeedback Study.

Introduction: Neurofeedback training aims at learning self-regulation of brain activity underlying cognitive, emotional or physiological functions. Despite of promising investigations on neurofeedback as a tool for cognitive rehabilitation in neurological diseases, such as after stroke, there is still a lack of research on feasibility and efficiency of neurofeedback in this field.

Methods: The present study aimed at investigating behavioral and electrophysiological effects of 10 sessions of sensorimotor rhythm (SMR) neurofeedback in a 74-years-old stroke patient (UG20).

Specific effects of EEG based neurofeedback training on memory functions in post-stroke victims.

Background: Using EEG based neurofeedback (NF), the activity of the brain is modulated directly and, therefore, the cortical substrates of cognitive functions themselves. In the present study, we investigated the ability of stroke patients to control their own brain activity via NF and evaluated specific effects of different NF protocols on cognition, in particular recovery of memory.

Methods: N = 17 stroke patients received up to ten sessions of either SMR (N = 11, 12-15 Hz) or Upper Alpha (N = 6, e.

Bacterial expression and functional reconstitution of human heparanase.

Human heparanase is a heparan sulfate degrading enzyme located in the extracellular matrix playing a decisive role in angiogenesis and tumor metastasis. Translated as a 65 kDa inactive prae-form, the protein is processed into an 8 kDa and a 50 kDa subunit which form a non-covalently associated active heterodimer. We have expressed the two subunits separately in Escherichia coli which yielded active human heparanase upon reconstitution.

New targets for glycosaminoglycans and glycosaminoglycans as novel targets.

Biological functions of a variety of proteins are mediated via their interaction with glycosaminoglycans (GAGs). The structural diversity within the wide GAG landscape provides individual interaction sites for a multitude of proteins involved in several pathophysiological processes. This 'GAG angle' of such proteins as well as their specific GAG ligands give rise to novel therapeutic concepts for drug development.

Chemokine degradation by the Group A streptococcal serine proteinase ScpC can be reconstituted in vitro and requires two separate domains.

Streptococcus pyogenes is one of the most common human pathogens and possesses diverse mechanisms to evade the human immune defence. One example of its immune evasion is the degradation of the chemokine IL (interleukin)-8 by ScpC, a serine proteinase that prevents the recruitment of neutrophils to an infection site. By applying the ANTIGENome technology and using human serum antibodies, we identified Spy0416, annotated as ScpC, as a prominent antigen that induces protective immune responses in animals.