Magnesium enhances the beneficial effects of NK1 antagonist administration on blood-brain barrier permeability and motor outcome after traumatic brain injury.

The current study investigated whether adding magnesium to an NK1 tachykinin receptor antagonist after traumatic brain injury would enhance efficacy to further reduce blood-brain barrier permeability and improve functional recovery compared to either treatment alone. Sprague-Dawley rats were injured using the impact acceleration model of diffuse brain injury, and received either no treatment, MgSO (30 mg/kg IV), the NK1 antagonist n-acetyl L tryptophan (2.5 mg/kg IP), or both agents combined.

Treatment with the NK1 antagonist emend reduces blood brain barrier dysfunction and edema formation in an experimental model of brain tumors.

The neuropeptide substance P (SP) has been implicated in the disruption of the blood-brain barrier (BBB) and development of cerebral edema in acute brain injury. Cerebral edema accumulates rapidly around brain tumors and has been linked to several tumor-associated deficits. Currently, the standard treatment for peritumoral edema is the corticosteroid dexamethasone, prolonged use of which is associated with a number of deleterious side effects.

Applied anatomy of the lingual nerve: relevance to dental anaesthesia.

Objectives: (1) to classify the external morphology of the lingual nerve and investigate any relationship between its external and internal morphology, (2) to explore the fascicular structure, nerve tissue density and capillary density of the lingual nerve, and (3) to provide an anatomical explanation as to why adverse clinical outcomes more commonly affect the lingual nerve following local dental anaesthesia. Where possible, comparisons were made between the lingual and inferior alveolar nerves.

Materials And Methods: The lingual and inferior alveolar nerves were examined in 23 hemi-sectioned heads macroscopically and microscopically 2mm above the lingula.

NK1 receptor antagonists and dexamethasone as anticancer agents in vitro and in a model of brain tumours secondary to breast cancer.

Emend, an NK1 antagonist, and dexamethasone are used to treat complications associated with metastatic brain tumours and their treatment. It has been suggested that these agents exert anticancer effects apart from their current use. The effects of the NK1 antagonists, Emend and N-acetyl-L-tryptophan, and dexamethasone on tumour growth were investigated in vitro and in vivo at clinically relevant doses.

Characterisation of Walker 256 breast carcinoma cells from two tumour cell banks as assessed using two models of secondary brain tumours.

Background: Metastatic brain tumours are a common end stage of breast cancer progression, with significant associated morbidity and high mortality. Walker 256 is a rat breast carcinoma cell line syngeneic to Wistar rats and commonly used to induce secondary brain tumours. Previously there has been the assumption that the same cancer cell line from different cell banks behave in a similar manner, although recent studies have suggested that cell lines may change their characteristics over time in vitro.

Targeting classical but not neurogenic inflammation reduces peritumoral oedema in secondary brain tumours.

Dexamethasone, the standard treatment for peritumoral brain oedema, inhibits classical inflammation. Neurogenic inflammation, which acts via substance P (SP), has been implicated in vasogenic oedema in animal models of CNS injury. SP is elevated within and outside CNS tumours.

Walker 256 tumour cells increase substance P immunoreactivity locally and modify the properties of the blood-brain barrier during extravasation and brain invasion.

It is not yet known how tumour cells traverse the blood-brain barrier (BBB) to form brain metastases. Substance P (SP) release is a key component of neurogenic inflammation which has been recently shown to increase the permeability of the BBB following CNS insults, making it a possible candidate as a mediator of tumour cell extravasation into the brain. This study investigated the properties of the BBB in the early stages of tumour cell invasion into the brain, and the possible involvement of SP.

A morphometric analysis of the septal nuclei in schizophrenia and affective disorders: reduced neuronal density in the lateral septal nucleus in bipolar disorder.

The septal nuclei are assumed to play a significant role in the pathophysiology of schizophrenia and affective disorders. The aim of this study was to morphometrically characterize the septal nuclei in patients with schizophrenia, bipolar disorder, and major depressive disorder, when compared with healthy control subjects. We analyzed the septal nuclei by determining the density and size of the neurons in postmortem brains in 17 patients with schizophrenia, 8 patients with bipolar disorder, 7 patients with major depressive disorder, and 14 control subjects matched for age and gender.

Changes in the blood-CSF barrier in experimental traumatic brain injury.

Purpose: Elevation of intracranial pressure (ICP) is a major complication of traumatic brain injury (TBI), and cerebrospinal fluid (CSF) volume is a key factor in ICP regulation. Choroidal epithelial cells (CEC) form the blood-CSF barrier and their integrity is essential for controlling CSF production. In the current study, the morphology of the CEC was studied from 5 h to 28 day after TBI in the rat.

Hemoglobin crystals: a pro-inflammatory potential confounder of rat experimental intracerebral hemorrhage.

In vivo rat hemoglobin crystallization has been reported in lung, liver and kidney, but never following central nervous system injury. In the present study, we examined hemoglobin crystallization following experimental intracerebral hemorrhage (ICH) and its effects on inflammation. Ninety-one rat brains, subjected to either autologous or collagenase ICH, and vehicle controls, were retrospectively examined.

Anatomical variations in the branches of the human aortic arch: a recent study of a South Australian population.

Variations of the branches of the aortic arch are likely to occur as a result of the altered development of certain branchial arch arteries during the embryonic period of gestation. In the present investigation the pattern of branches of the aortic arch was studied in 81 cadavers from a recent South Australian population of European descent, who have migrated to (n = 38) or were born and lived in (n = 43) South Australia during the twentieth century. Two principal variations were noted in the present study.

Severity-dependent expression of pro-inflammatory cytokines in traumatic spinal cord injury in the rat.

The post-traumatic inflammatory response in acute spinal cord contusion injury was studied in the rat. Mild and severe spinal cord injury (SCI) was produced by dropping a 10 g weight from 3 and 12 cm at the T12 vertebral level. Increased immunoreactivity of TNF-alpha in mild and severe SCI was detected in neurons at 1 h post-injury, and in neurons and microglia at 6 h post-injury, with a less significant increase in mild SCI.

Early expression and cellular localization of proinflammatory cytokines interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha in human traumatic spinal cord injury.

Study Design: Post-traumatic inflammatory response was studied in 11 human cases of acute spinal cord contusion injury.

Objectives: To examine the inflammatory cellular response and the immunocytochemical expression and localization of interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha in human spinal cord after contusion injury.

Summary Of Background Data: : The post-traumatic inflammatory response plays an important role in secondary injury mechanisms after spinal cord injury, and interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha are key inflammatory mediators.

Peripheral nervous system and central nervous system pathology in rapidly progressive lower motor neuron syndrome with immunoglobulin M anti-GM1 ganglioside antibody.

Pathological studies, including novel teased peripheral nerve fiber studies, were performed in a patient who presented with a rapidly progressive, lower motor neuron syndrome and high titer of immunoglobulin M anti-GM1 ganglioside antibody. In the central nervous system, there was a severe loss of motor neurons and central chromatolysis with ubiquitin immunopositive cytoplasmic inclusions in residual motor neurons. In the peripheral nervous system, axonal degeneration of myelinated fibers in the anterior nerve roots was evident.

Electron microscope study of blood-brain barrier opening induced by immunological targeting of the endothelial barrier antigen.

Barrier vessels in the central nervous system are lined with endothelial cells which constitute the blood-brain barrier (BBB) and show selective expression of certain biochemical markers. One of these, the endothelial barrier antigen (EBA), is specific to the rat. The exact role of EBA in the BBB is not known, although several studies have shown a correlation between the reduction in EBA expression in endothelial cells and the opening of the BBB.