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NCT02580526.

Both Mg2+ and Ca 2+ have been implicated as having roles hi the pathomechanisms of cerebral ischemia. To further study the effects of these ions on postischemic histologic outcome, fasted rats were given one of three intravenous infusions: 5.0 mmol/kg MgCl 2 , 5.0 mmol/kg MgCl 2 +0.035 units/kg regular insulin, or 1.0 mmol/kg CaCl 2 . This resulted in elevated plasma Mg 2+ or Ca 2+ concentrations in the corresponding groups. A fourth group received 0.9% NaCl (saline). Prelnfusion plasma glucose concentration was similar for all groups and was unchanged after infusion hi rats receiving either saline or MgCl 2 +insulin. In contrast, postinfusion glucose concentration was increased hi the MgCl 2 group (p<0.001) and decreased in the CaCl 2 group (p<0.001) relative to saline-treated rats. Following respective infusions, all rats underwent 10 minutes of reversible forebrain ischemia (bilateral carotid artery occlusion and systemic hypotension) followed by 7 days' recovery. Six of 12 CaCl 2 -treated rats died 2-3 days after ischemia; all other rats remained neurologically indistinguishable, without gross neurologic deficits. Histologic injury hi the neocortex and caudate was moderate in all groups. In the hippocampus, MgCl 2 +insulin resulted in 66±6% (mean±SD) dead CA1 pyramidal cells, which was similar to the amount hi saline-treated rats (68±10%). Injury was increased hi the MgCl 2 group (79±4% dead cells), while in surviving CaCl 2 -treated rats, injury was decreased (54±13%). We conclude that the increased injury hi MgCl 2 -treated rats and the decreased injury noted in surviving rats receiving CaCl 2 are due to the plasma glucose concentrations present prior to ischemia. When glucose concentration was controlled, no cerebral protective effect of MgCl 2 was evident. (Stroke 1989;20:507-512) B ecause calcium has been implicated as a mediator of ischemically induced neuronal injury, 1 investigators have attempted to ameliorate damage by using compounds known to block calcium entry. By contrast, in a small sample of cardiac arrest patients, Ruiz et al 7 failed to show cerebral protection from a treatment regimen including intravenously administered MgCl 2 .

Helping Safeguard Veterans Affairs' Hospital Buildings by Advanced Earthquake Monitoring The integrity of the Nation's hospitals is vital for the survival and functioning of the society in the aftermath of a catastrophic earthquake. I n collaboration with the U.S. Department of Veterans Affairs (VA), the National Strong Motion Project of the U.S. Geological Survey has recently installed sophisticated seismic systems that will monitor the structural integrity of hospital buildings during earthquake shaking. The new systems have been installed at more than 20 VA medical campuses across the country. These monitoring systems, which combine sensitive accelerometers and real-time computer calculations, are capable of determining the structural health of each structure rapidly after an event, helping to ensure the safety of patients and staff. Department of Veterans Affairs Department of Veterans Affairs Following the 1971 magnitude 6.6 San Fernando earthquake in Southern California, which resulted in the collapse of several hospital buildings, the U.S. Department of Veterans Affairs (VA) established its Seismic Vulnerability Assessment Program to identify and strengthen VA hospital buildings that needed to be brought up to acceptable seismic safety standards. An important component of this program is monitoring earthquake shaking in hospital buildings. Shortly after the 1971 earthquake, the U.S. Geological Survey (USGS) collaborated with the VA on installing analog accelerographs in 60 VA hospital buildings across the country. These accelerographs were mostly

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