Abstract: The present invention relates to the use of xenon in the preparation of a medicament for the treatment of neonatal asphyxia in a neonatal subject, wherein said medicament is for use in combination with hypothermia.

Abstract: In a first aspect, the present invention relates to the use of xenon in the preparation of a medicament for providing analgesia in a newborn subject and/or a fetal subject. In a second aspect, the invention relates to a method of providing analgesia in a newborn subject, the method comprising administering to the subject a therapeutically effective amount of xenon. In a third aspect, the invention relates to a method of providing analgesia in a fetal subject, the method comprising administering to the mother of the fetal subject a therapeutically effective amount of xenon for both the mother and fetal subject.

Abstract: The present invention relates to methods of controlling neurological deficits in patients who have undergone cardiopulmonary bypass (CPB) by administering xenon to said patients.

Abstract: Provided herein are mutant strains of Neisseria meningitidis which produce Kdo-free lipid A as well as the Kdo-free lipid A molecules and immunogenic compositions containing such Kdo-free lipid A molecules from a Neisseria strain containing a genetically stable mutation which inactivates a gene selected from the group consisting of genes encoding arabinose-5-phosphate isomerase, CMP-Kdo synthetase and CMP-Kdo transferase. N. meningitidis NMB206 is a specifically exemplified strain which harbors a stable insertion mutation in the gene (ApsF) encoding A5P isomerase; strain NMB-249 is a specifically exemplified strain with a stable insertion mutation in the gene (kdtA) encoding CMP-Kdo synthetase, and strain NMB259 is specifically exemplified strain with a stable insertion mutation in the gene (kdsB) encoding CMP-Kdo transferase. Also provided by the present invention are methods for the production of Lipid A flee of 3-keto-3-deoxyoctanoic acid using these genetically stable N. meningitidis mutants.

Abstract: The present invention relates to the use of xenon as a neuroprotectant and/or as an inhibitor of synaptic plasticity. In a preferred aspect, the xenon acts as an NMDA antagonist. The present invention also provides a method of reducing the level of activation of the NMDA receptors in a mammal, the method comprising modulating the activity of the NMDA receptor by administering to the mammal a therapeutically effective amount of xenon, wherein said reduction achieves neuroprotection and/or an inhibition of synaptic plasticity. A further embodiment of the invention provides a pharmaceutical composition for providing neuroprotection and/or inhibition of synaptic plasticity, together with a process for the preparation thereof.

Abstract: A method of eliciting analgesia in a human subject by Transcranial Electrical Stimulation (TCES) is provided. Electrodes are secured to the skin of the subject's head and used to apply an electrical current to the electrodes. The current includes a direct current combined with rectangular current pulses (alternating current) delivered at a frequency of between 30 and 65 Hz. The frequency at which the pulses are delivered is periodically changed to a different value within the 30-65 Hz range. The total current supplied, a sum of the DC component and a Mean Absolute Deviation (MAD) of the current pulses, preferably has a value between 0.2 and 20 mA. The method is used during surgery and the post-operative procedure, and may also be used to treat a wide variety of neurological and other conditions.

Abstract: A pharmaceutical composition is described. The composition comprises a formulation. The formulation comprises an NMDA antagonist and an alpha-2 adrenergic agonist. In a preferred aspect, there is provided an improved anaesthetic comprising an NMDA antagonist and an alpha-2 adrenergic agonist.

Abstract: The present invention relates to the use of xenon as a neuroprotectant and/or as an inhibitor of synaptic plasticity. In a preferred aspect, the xenon acts as an NMDA antagonist. The present invention also provides a method of reducing the level of activation of the NMDA receptors in a mammal, the method comprising modulating the activity of the NMDA receptor by administering to the mammal a therapeutically effective amount of xenon, wherein said reduction achieves neuroprotection and/or an inhibition of synaptic plasticity. A further embodiment of the invention provides a pharmaceutical composition for providing neuroprotection and/or inhibition of synaptic plasticity, together with a process for the preparation thereof.

Abstract: The present invention relates to the use of xenon as an NMDA antagonist. In particular, the invention relates to a method of treatment comprising modulating the activity of an NMDA receptor in a mammal, the method comprising modulating the activity of the NMDA receptor by administering to the mammal a therapeutically effective amount of xenon. In a further aspect, the invention provides a process for the preparation of a pharmaceutical composition suitable for modulating the activity of an NMDA receptor.

Abstract: 4-[1-(2,3-dimethylphenyl)ethyl]-1H-imidazole, known as medetomidine, and in particular its d-enantiomer and salts thereof are useful in perioperative care, in particular in reducing the amount of anaesthetic it is necessary to administer.