The book on iatrogenic Creutzfeldt-Jakob disease (CJD) in humans is almost closed. This form of CJD transmission via medical misadventures was first detected in 1974. Today, only occasional CJD cases with exceptionally long incubation periods still appear. The main sources of the largest outbreaks were tissues from human cadavers with unsuspected CJD that were used for dura mater grafts and growth hormone extracts. A few additional cases resulted from neurosurgical instrument contamination, corneal grafts, gonadotrophic hormone, and secondary infections from blood transfusions. Although the final solution to the problem of iatrogenic CJD is still not available (a laboratory test to identify potential donors who harbor the infectious agent), certain other measures have worked well: applying special sterilization of penetrating surgical instruments, reducing the infectious potential of donor blood and tissue, and excluding donors known to have higher than normal risk for CJD.

Sphere drag data from throughout the twentieth century are available in tabular form. However, much of the data arose from experiments in small diameter cylindrical vessels, where the results might have been influenced by the wall effect. Wall effect corrections developed by others were applied to 178 of the 480 data points collected. This corrected data set is believed to be free of the influence of wall effects. Existing drag and settling velocity correlations were compared to this data set. In addition, new correlations of the same forms were developed using the corrected data. Two new correlations of sphere terminal velocity are proposed, one applicable for all Reynolds numbers less than 2ϫ10 5 , and the other designed to predict settling velocities with exceptional accuracy for terminal Reynolds numbers less than 4,000, a region that contains almost all applications of interest in environmental engineering. The trial and error solution for settling velocity using the Fair and Geyer equation for drag should be retired in favor of the direct calculation available from these new correlations.

OBJECTIVESWe aimed to quantify the frequency and nature of early complications after implantable cardioverter-defibrillator (ICD) implantation in general practice, and estimate the incremental costs of those complications to the health care system. BACKGROUND Cardioverter-defibrillator implantation rates are rising quickly. Little has been published regarding the outcomes and costs of these procedures in unselected populations. METHODSUsing Medicare Provider Analysis and Review (MedPAR) files, we identified 30,984 admissions containing procedure codes for new ICD or cardiac resynchronization therapy defibrillator implantation in fiscal year 2003. The frequencies of eight complicating diagnoses during these admissions were determined. Length of stay (LOS) and total hospital costs, derived using whole-hospital cost to charge ratios, were calculated for each admission. The incremental effects of any and each complication on LOS and hospital cost were estimated in multivariable models, adjusting for demographic factors and comorbid conditions. RESULTSThe mean cost for all admissions was $42,184 (median $37,902) with mean LOS of 4.7 days (median 2.0 days). One or more complications were coded in 10.8% of admissions, most commonly "mechanical complication of the ICD" and hemorrhage/hematoma. The occurrence of any complication increased adjusted LOS by 3.4 days and costs by $7,251. Each of the individual complications was associated with highly significant increases in both LOS (1 to 10 days) and hospital cost ($5,000 to $20,000). CONCLUSIONS In fiscal 2003, 10.8% of Medicare patients undergoing cardioverter-defibrillator implantation experienced one or more early complications, associated with significant increases in LOS and costs. Efforts to reduce these complications could have significant clinical and financial benefits. (J Am Coll Cardiol 2006;47:2493-7)

Fibroblasts possess several distinct mechanisms that control cellular adhesion to extracellular matrix macromolecules. Monoclonal antibodies to a 140-kilodalton (kD) cell surface glycoprotein inhibited the adhesion of fibroblastic Chinese hamster ovary cells to fibronectin-coated substrata but did not inhibit adhesion to substrata coated with vitronectin, laminin, serum, or other adhesive macromolecules. Thus the 140-kD glycoprotein appears to be involved in the fibronectin-mediated adhesion mechanism but not in other adhesion processes.

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The key polyamine catabolizing enzyme spermidine-spermine N1-acetyltransferase (SSAT) is among the few genes known to be inducible by the natural polyamines. Certain polyamine analogs markedly exaggerate this response and thus provide useful tools for studying the underlying regulatory mechanisms. As shown here, the analog which most potently induces SSAT activity, N1, N11-diethylnorspermine (DENSPM), increases SSAT mRNA in MALME-3M human melanoma cells to a maximum of > 20-fold and immunodetectable SSAT protein to > 300-fold. By comparison, the natural polyamine spermine is far less effective, increasing SSAT mRNA by approximately 3-fold and protein by approximately 7-fold. In particular, the difference in mRNA accumulation by spermine and the analog was shown to be due to differential effects on both gene transcription and mRNA stabilization. Although the analog DENSPM has been regarded as the most potent inducer of SSAT activity and mRNA, we now report that inhibitors of protein synthesis are capable of increasing SSAT mRNA to nearly comparable levels. Inhibitor-induced accumulation in SSAT mRNA was shown to involve increased gene transcription and mRNA stabilization. This suggests that, under basal conditions, SSAT gene expression is suppressed by a labile protein (or proteins). While induction of SSAT mRNA by inhibitors of protein synthesis only occurred at concentrations which blocked protein synthesis, that by DENSPM took place at concentrations which did not. The combination of either protein inhibitor with DENSPM or spermine produced an additive increase in SSAT mRNA. Taken together, these findings suggest the involvement of two separate but possibly converging pathways in the regulation of SSAT mRNA, one mediated by polyamines and their analogs and the other mediated by a labile repressor of SSAT gene transcription and/or mRNA stabilization. In addition to its apparent regulatory importance, induction of SSAT mRNA by inhibitors of protein synthesis represents a potentially useful system for studying the posttranscriptional regulation of this interesting gene.