Keratin 8 expression in head and neck epithelia.

Background: The intermediate filament forming protein keratin 8 (K8) is a tumour-associated antigen, which was shown to be over-expressed in a variety of malignancies. Here, we present a study of K8 expression in squamous epithelia of the head and neck area, including normal mucosa, hyperplastic and dysplastic leukoplakia, carcinomas of different sub-localisations, and lymph node metastases.

Methods: K8 expression was assessed upon immunohistochemistry with specific antibodies in cryosections of primary tumours of the head and neck area.

Enhanced poly(ADP-ribose) polymerase-1 activation contributes to recombinant tissue plasminogen activator-induced aggravation of ischemic brain injury in vivo.

Recombinant tissue plasminogen activator (rt-PA) treatment improves functional outcome after acute ischemic stroke, inducing reperfusion by its thrombolytic activity. Conversely, there is evidence that rt-PA can mediate neuronal damage after ischemic brain injury in vivo. In addition to other mechanisms, enhancement of N-methyl-D-aspartate (NMDA) receptor signalling has been proposed to underlie rt-PA-mediated neurotoxicity.

Deletion of cellular prion protein results in reduced Akt activation, enhanced postischemic caspase-3 activation, and exacerbation of ischemic brain injury.

Background And Purpose: The physiological function of cellular prion protein (PrPc) is not yet understood. Recent findings suggest that PrPc may have neuroprotective properties, and its absence increases susceptibility to neuronal injury. The purpose of this study was to elucidate the role of PrPc in ischemic brain injury in vivo.

Expression time course and spatial distribution of activated caspase-3 after experimental status epilepticus: contribution of delayed neuronal cell death to seizure-induced neuronal injury.

Pilocarpine-induced status epilepticus (PCSE) is a widely used model to study neurodegeneration in limbic structures after prolonged epileptic seizures. However, mechanisms mediating neuronal cell death in this model require further characterization. Examining the expression time course and spatial distribution of activated caspase-3, we sought to determine the role of apoptosis in PCSE-mediated neuronal cell death.

Upregulation of cellular prion protein (PrPc) after focal cerebral ischemia and influence of lesion severity.

The pathological isoform of the prion protein (PrP(Sc)) has been identified to mediate transmissible spongiform encephalopathies like Creutzfeldt-Jakob disease (CJD). In contrast, the physiological function of the normal cellular prion protein (PrP(c)) is not yet understood. Recent findings suggest that PrP(c) may have neuroprotective properties and that its absence increases susceptibility to oxidative stress and neuronal injury.

Gender-specific risk of perioperative complications in carotid endarterectomy patients with contralateral carotid artery stenosis or occlusion.

Carotid endarterectomy (CEA) has been shown to be effective in stroke prevention in selected patients. Some studies, however, identified gender as an independent risk factor for perioperative CEA complications demonstrating an increased rate of perioperative stroke or death in women. Furthermore, contralateral internal carotid artery (ICA) occlusion has been associated with higher rates of perioperative CEA complications.

Color-coded duplex sonography for diagnosis of testicular torsion.

By color-coded duplex sonography moving structures are visualized as red or blue colors within a normal gray-scale B-mode ultrasound image. Thus, blood flow even within small vessels can be visualized clearly. Color-coded duplex sonographic examination was performed in 11 patients who presented with scrotal pain.