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The sympathetic nervous system (SNS) functions as an integrative peripheral nervous system to regulate vital organ function, in part by release of norepinephrine (NE). Disease states as varied as Parkinsons disease, spinal cord injury, diabetes, heart failure, and sepsis can all lead to dysfunction of the SNS and patient morbidity. Feedback modulation of NE release occurs by activation of alpha2A and alpha2C adrenergic receptors (ARs) on sympathetic neurons. Neuropharmacological differences between these two autoreceptors are not completely known, thus limiting development of specific drugs for disease treatment.Modulation of sympathetic neuron signaling occurs by feedback inhibition of neurotransmitter release (autoreceptors), mediated in part via alpha2A and/or alpha2C adrenergic receptors. Previous research suggests that these two AR subtypes may have overlapping but unique physiological roles in neuronal signaling; however the basis for these differences is not completely known. Cellular localization is an important determinant of specialized function between homologous receptors. Preliminary data in cultured sympathetic ganglion neurons (SGN) and other cell types have found different temporal and spatial components to alpha2A&C AR localization and trafficking. These differences may relate to characteristics of SGN in culture (e.g. neurotransmitter phenotype) and thus may be important determinants of differential alpha2A&C AR modulation of neurotransmitter release. Using an array of molecular and cellular approaches and single cell amperometric analysis of neurotransmitter release, it should be possible to further delineate the interplay between protein structure, cellular localization, and physiological function of each receptor subtype. Resultant discoveries will be relevant to other similar neuromodulatory systems involved in pain and neural processing, including cannabinoid, opiate, and metabotropic glutamate receptors.
Can Nitrous Oxide (Laughing Gas) be Used as a Sedative for GI Endoscopy Procedures?
Nitrous oxide (commonly known as 'laughing gas') is often used during dental and other
outpatient procedures, because it is easy to administer, is short-acting and rapidly clears
from the body following the procedure.
The investigators hypothesize that use of Nitrous oxide during GI endoscopy may enhance
patient comfort during the procedure and speed-up post-procedure recovery, while minimizing
the fatigue and mental fogginess some patients report the day after receiving standard
sedative and narcotic drugs used routinely for the procedure.
The investigators are interested in determining if adding Nitrous Oxide to commonly used
sedation drugs will decrease fatigue, mental fogginess, and nausea/vomiting, as well as
determine when the patient felt fully recovered from the effects of all sedatives given for
Stanford is currently not accepting patients for this trial.
For more information, please contact SPECTRUM, .
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Assess Safety and Efficacy of ELAD (Extracorporeal Liver Assist System) in Subjects With Alcohol-Induced Liver Failure
The primary objective of the study is to evaluate safety and efficacy of ELAD® with respect
to overall survival (OS) of subjects with a clinical diagnosis of alcohol-induced liver
decompensation (AILD) up to at least Study Day 91, with follow-up Protocol VTI-208E providing
additional survival data up to a maximum of 5 years that will be included, as available,
through VTI-208 study termination (after the last surviving enrolled subject completes Study
Secondary objectives are to determine the proportion of survivors at Study Days 28 and 91.
Exploratory objectives are to evaluate the ability of ELAD to stabilize liver function,
measured using the Model for End Stage Liver Disease (MELD)-based time to progression (TTP)
up to Study Day 91, and the proportion of progression-free survivors (PFS) up to Study Days
28 and 91. Progression is defined as death or the first observed increase of at least 5
points from End of Study Day 1 MELD score (for both the ELAD and Control groups) until at
least 24 hours after the ELAD Treatment Period is ended (end of Day 7 for Controls) and up to
both End of Study Days 28 and 91 following Randomization.