Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0002736 (amyotrophic lateral sclerosis)
 19,048 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It's 2000 HRS on a Friday evening. You're assigned to an ALS engine company, and you're just settling down after a busy day when you're dispatched along with a BLS ambulance to a report of a sick person outside a local club where they're holding a concert. During your response, dispatch advises that they're receiving multiple calls on the incident and are dispatching a second BLS ambulance to the call. * As you turn the corner and approach the scene, you notice a haze in the air coming from an industrial site on the same side of the street and see approximately 200 people exiting the club in haste. Several dozen patrons line the street between the club and the subway station. They're coughing and crying, and several are vomiting. * The driver stops the engine in front of the subway entrance, which is located approximately 500 feet from the club and uphill and upwind from the haze. The scene is overwhelming, even to the captain, who turns to you-as the paramedic on the crew-and asks what you want done first. Your first thought is, Triage. But you know that triaging these patients is more complicated than your everyday two-car collision.
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PMID:Medical triage for WMD incidents incidents: an adaptation of daily triage. 1848 52

Amyotrophic lateral sclerosis (ALS) is the most frequent adult-onset motor neuron disease, and accumulating evidence indicates that oxidative mechanisms contribute to ALS pathology, but classical antioxidants have not performed well in clinical trials. The aim of this work was to investigate the effect of treatment with hydrogen molecule on the development of disease in mutant SOD1 G93A transgenic mouse model of ALS. Treatment of mutant SOD1 G93A mice with hydrogen-rich saline (HRS, i.p.) significantly delayed disease onset and prolonged survival, and attenuated loss of motor neurons and suppressed microglial and glial activation. Treatment of mutant SOD1 G93A mice with HRS inhibited the release of mitochondrial apoptogenic factors and the subsequent activation of downstream caspase-3. Furthermore, treatment of mutant SOD1 G93A mice with HRS reduced levels of protein carbonyl and 3-nitrotyrosine, and suppressed formation of reactive oxygen species (ROS), peroxynitrite, and malondialdehyde. Treatment of mutant SOD1 G93A mice with HRS preserved mitochondrial function, marked by restored activities of Complex I and IV, reduced mitochondrial ROS formation and enhanced mitochondrial adenosine triphosphate synthesis. In conclusion, hydrogen molecule may be neuroprotective against ALS, possibly through abating oxidative and nitrosative stress and preserving mitochondrial function.
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PMID:Treatment with Hydrogen-Rich Saline Delays Disease Progression in a Mouse Model of Amyotrophic Lateral Sclerosis. 2653 17