Surgical treatment of cerebral abscess with the use of a mobile ultralow-field MRI.

Surgical intervention in cerebral abscess is indicated to confirm diagnosis, to identify pathogens for specific antibiotic therapy, or to reduce mass effect. Regarding long-term outcome, freehand or stereotactic aspiration are equally efficient compared to surgical resection. However, direct observation of relief of mass effect is not possible by either method.

BH3 mimetics reactivate autophagic cell death in anoxia-resistant malignant glioma cells.

Here, we investigated the specific roles of Bcl-2 family members in anoxia tolerance of malignant glioma. Flow cytometry analysis of cell death in 17 glioma cell lines revealed drastic differences in their sensitivity to oxygen withdrawal (<0.1% O(2)).

Upregulation of DR5 by proteasome inhibitors potently sensitizes glioma cells to TRAIL-induced apoptosis.

This study was undertaken to explore the potential of new therapeutic approaches designed to reactivate cell death pathways in apoptosis-refractory gliomas and to characterize the underlying molecular mechanisms of this reactivation. Here we investigated the sensitivity of a panel of glioma cell lines (U87, U251, U343, U373, MZ-54, and MZ-18) to apoptosis induced by the death receptor ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), TRAIL in combination with gamma irradiation, and TRAIL in combination with proteasome inhibitors (MG132 and epoxomicin). Analysis of these six glioma cell lines revealed drastic differences in their sensitivity to these treatments, with two of the six cell lines revealing no significant induction of cell death in response to TRAIL alone.

Apoptosis meets autophagy-like cell death in the ischemic penumbra: Two sides of the same coin?

Autophagy is a homeostatic cellular process required for the recycling of proteins and damaged organelles, and in most scenarios is believed to promote cell survival. However, there is accumulating evidence that under certain pathological situations, autophagy can also trigger and mediate programmed cell death (type II death). Despite the well-established pathophysiological role of apoptosis (type I cell death) in post-ischemic neuron death, there is now increasing interest whether alternative types of programmed cell death might be involved in regulation of neuronal death after both global and focal cerebral ischemia.

Pineal parenchymal tumor of intermediate differentiation: diagnostic pitfalls and discussion of treatment options of a rare tumor entity.

Tumors of the pineal region are uncommon, comprising approximately 0.4-1% of all intracranial tumors in adults in European and American series. Histopathologically, they are a very heterogeneous group of tumors.

Pharmacological inhibition of Bcl-2 family members reactivates TRAIL-induced apoptosis in malignant glioma.

The major aim of this study was to develop novel therapeutic approaches to potentiate and reactivate apoptosis induced by TNF-Related Apoptosis Inducing Ligand (TRAIL) in malignant glioma. Analysis of five glioma cell lines (U87, U251, U373, MZ-54 and MZ-18) indicated that only two of the cell lines were sensitive to apoptosis induced by TRAIL alone. TRAIL resistance was not correlated to expression levels of the death receptors DR4 and DR5 or the decoy receptors DcR1 and DcR2, suggesting that it was mediated by inactivation of TRAIL-induced downstream signalling.

Recombinant expression of coagulation factor VIII in hepatic and non-hepatic cell lines stably transduced with third generation lentiviral vectors comprising the minimal factor VIII promoter.

Background: Lentiviral vectors have the capacity to transduce stably non-dividing, differentiated and undifferentiated cells of various tissues, including liver. To obtain high-level expression of transgenes, vectors often rely on viral promoters. However, recent data suggest that the supraphysiologic expression from ubiquitous viral promoters may not be beneficial and harbor the risk of oncogene activation.

The amyloid precursor protein potentiates CHOP induction and cell death in response to ER Ca2+ depletion.

Here we investigated the role of the amyloid precursor protein (APP) in regulation of Ca(2+) store depletion-induced neural cell death. Ca(2+) store depletion from the endoplasmic reticulum (ER) was induced by the SERCA (Sarco/Endoplasmic Reticulum Calcium ATPase) inhibitor thapsigargin which led to a rapid induction of the unfolded protein response (UPR) and a delayed activation of executioner caspases in the cultures. Overexpression of APP potently enhanced cytosolic Ca(2+) levels and cell death after ER Ca(2+) store depletion in comparison to vector-transfected controls.

Induction of transcription factor CEBP homology protein mediates hypoglycaemia-induced necrotic cell death in human neuroblastoma cells.

Oxygen and glucose deprivation are direct consequences of tissue ischaemia. We explored the interaction of hypoxia and hypoglycaemia on cell survival and gene expression in the absence of glutamatergic signalling using human SH-SY5Y neuroblastoma cells as a model. In agreement with previous investigations in non-neural cells, prolonged hypoxia (0.

TGF-{beta}1 activates two distinct type I receptors in neurons: implications for neuronal NF-{kappa}B signaling.

Transforming growth factor-betas (TGF-betas) are pleiotropic cytokines involved in development and maintenance of the nervous system. In several neural lesion paradigms, TGF-beta1 exerts potent neuroprotective effects. Neurons treated with TGF-beta1 activated the canonical TGF-beta receptor I/activin-like kinase receptor 5 (ALK5) pathway.

Regulation of gene expression by the amyloid precursor protein: inhibition of the JNK/c-Jun pathway.

The amyloid precursor protein (APP) has been suggested to regulate gene expression. GeneChip analysis and in vitro kinase assays revealed potent APP-dependent repression of c-Jun, its target gene SPARC and reduced basal c-Jun N-terminal kinase (JNK) activity in PC12 cells overexpressing APP. UV-induced activation of the JNK signalling pathway and subsequent apoptosis were likewise reduced by APP and this effect could be mimicked by the indirect JNK inhibitor CEP-11004.

S100B potently activates p65/c-Rel transcriptional complexes in hippocampal neurons: Clinical implications for the role of S100B in excitotoxic brain injury.

Increased serum levels of S100B are positively correlated with multiple forms of CNS damage, such as stroke, CNS trauma and neurodegenerative diseases, but also in psychiatric disorders. However, it is currently not known whether increased serum levels of S100B reflect a neuroregenerative or neurodegenerative response. Since glutamate receptor overactivation (excitotoxicity) may contribute to neuronal pathology in psychiatric disorders, we investigated the effect of S100B on N-methyl-d-aspartate (NMDA)-induced neuronal cell death.

The Influence of Hyperbaric Oxygenation (HBO) on Proliferation and Differentiation of Human Keratinocyte Cultures In Vitro.

A drop in tissue oxygen partial pressure below 30 mm Hg as a result of reduced perfusion in an extensive area of acute skin damage, or where a large number of chronic skin defects occur, inhibits collagen synthesis and neoangiogenesis in the various phases of wound healing. Subsequent granulation and epithelialisation are correspondingly impaired.Hyperbaric oxygenation is now recognised as a valuable supplementary method of treatment for problematic wounds.

Gene expression during ER stress-induced apoptosis in neurons: induction of the BH3-only protein Bbc3/PUMA and activation of the mitochondrial apoptosis pathway.

Endoplasmic reticulum (ER) stress has been implicated in the pathogenesis of ischemic and neurodegenerative disorders. Treatment of human SH-SY5Y neuroblastoma cells with tunicamycin, an inhibitor of protein glycosylation, rapidly induced the expression of target genes of the unfolded protein response. However, prolonged treatment also triggered a delayed, caspase-dependent cell death.

Droperidol causes a dose-dependent prolongation of the QT interval.

To further investigate possible prolongation of the frequency-corrected QT interval (QTc interval) after administration of droperidol (DRO), we studied 40 surgical patients who were randomly assigned to one of three groups, receiving an intravenous (IV) injection of either 0.1 mg/kg (Group 1, n = 10), 0.175 mg/kg (Group 2, n = 10), or 0.

Midazolam does not antagonize fentanyl-mediated analgesia in surgical patients.

Study Objective: To determine whether midazolam possesses a clinically significant antianalgesic action in surgical patients.

Design: Randomized, controlled study.

Setting: Inpatient anesthesia at a university department of neurosurgery.