The literature reveals a number of rare, potentially catastrophic neurologic sequelae including brain and spinal cord infarction. Most of these are thought to be due to intravascular uptake of particulate steroids. The true overall incidence remains obscure due to the lack of blinded controlled studies. Injectionists, referring physicians, and patients should be aware of the nature and potential consequences of these complications. Additionally, it is imperative for injectionists to standardize techniques to minimize complications, especially by using a test dose of local anesthetic before injection of preferably nonparticulate corticosteroid.

: SAH, subarachnoid hemorrhageUIAs, unruptured intracranial aneurysms.

Patients treated with glucocorticoids have elevated skeletal muscle ouabain binding sites. The major Na(+)-K(+)-ATPase (NKA) isoform proteins found in muscle, alpha2 and beta1, are increased by 50% in rats treated for 14 days with the synthetic glucocorticoid dexamethasone (DEX). This study addressed whether the DEX-induced increase in the muscle NKA pool leads to increased insulin-stimulated cellular K+ uptake that could precipitate hypokalemia. Rats were treated with DEX or vehicle via osmotic minipumps at one of two doses: 0.02 mg.kg(-1).day(-1) for 14 days (low DEX; n = 5 pairs) or 0.1 mg.kg(-1).day(-1) for 7 days (high DEX; n = 6 pairs). Insulin was infused at a rate of 5 mU.kg(-1).min(-1) over 2.5 h in conscious rats. Insulin-stimulated cellular K+ and glucose uptake rates were assessed in vivo by measuring the exogenous K+ infusion (K+(inf)) and glucose infusion (Ginf) rates needed to maintain constant plasma K+ and glucose concentrations during insulin infusion. DEX at both doses decreased insulin-stimulated glucose uptake as previously reported. Ginf (in mmol.kg(-1).h(-1)) was 10.2 +/- 0.6 in vehicle-treated rats, 5.8 +/- 0.8 in low-DEX-treated rats, and 5.2 +/- 0.6 in high-DEX-treated rats. High DEX treatment also reduced insulin-stimulated K+) uptake. K+(inf) (in mmol.kg(-1).h(-1)) was 0.53 +/- 0.08 in vehicle-treated rats, 0.49 +/- 0.14 in low-DEX-treated rats, and 0.27 +/- 0.08 in high-DEX-treated rats. DEX treatment did not alter urinary K+ excretion. NKA alpha2-isoform levels in the low-DEX-treated group, measured by immunoblotting, were unchanged, but they increased by 38 +/- 15% (soleus) and by 67 +/- 3% (gastrocnemius) in the high-DEX treatment group. The NKA alpha1-isoform level was unchanged. These results provide novel evidence for the insulin resistance of K+ clearance during chronic DEX treatment. Insulin-stimulated cellular K+ uptake was significantly depressed despite increased muscle sodium pump pool size.

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The Global Precipitation Measurement (GPM) Mission is a collaboration between the National Aeronautics and Space Administration (NASA) and the Japanese Aerospace Exploration Agency (JAXA), and other US and international partners, with the goal of monitoring the diurnal and seasonal variations in precipitation over the surface of the earth. These measurements will be used to improve current climate models and weather forecasting, and enable improved storm and flood warnings. This paper gives an overview of the mission architecture and addresses the status of some key trade studies, including the geolocation budgeting, design considerations for spacecraft charging, and design issues related to the mitigation of orbital debris.