Resistance to anticoagulant activity of heparin was observed in a patient for cardiac surgery. The activated coagulation time (ACT) was maintained over 300 seconds with additional doses of heparin which mounted to the total of 29 ml in 3 hours during cardiopulmonary bypass. Although antithrombin-III activity was not measured in this case, the heparin resistance might have been caused by the decrease in the activity of antithrombin-III which might have resulted from the preoperative malnutrition, infection of urinary tract and/or institution of intraaortic balloon pumping (IABP).
Abstract Although many methods for automated fluorescent-labeled cell detection have been proposed, not all of them assume a highly inhomogeneous background arising from complex biological structures. Here, we propose an automated cell detection algorithm that accounts for and subtracts the inhomogeneous background by avoiding high-intensity pixels in the blur filtering calculation. Cells were detected by intensity thresholding in the background-subtracted image, and the algorithm’s performance was tested on NeuN- and c-Fos-stained images in the mouse prefrontal cortex and hippocampal dentate gyrus. In addition, applications in c-Fos positive cell counting and the quantification for the expression level in double-labeled cells were demonstrated. Our method of automated detection after background assumption (ADABA) offers the advantage of high-throughput and unbiased analysis in regions with complex biological structures that produce inhomogeneous background. Highlights - We proposed a method to assume and subtract inhomogeneous background pattern. (79/85) - Cells were automatically detected in the background-subtracted image. (71/85) - The automated detection results corresponded with the manual detection. (73/85) - Detection of IEG positive cells and overlapping with neural marker were demonstrated. (85/85)
The neurotoxicity of lidocaine is not fully understood, and the primary lesion of lidocaine-induced spinal neurotoxicity has not been defined. Here we examine the effects of various concentrations of intrathecally administered lidocaine.
Methods
Forty-seven Wistar rats received 20%, 10%, 7.5%, 5%, 3%, or 0% lidocaine dissolved in distilled water, or 25% glucose solution via a chronically implanted intrathecal catheter. The spinal cord at L1, posterior and anterior roots, and cauda equina were dissected out 5 days later, sectioned, and prepared for light and electron microscopy. The effect of the agent on function was evaluated by movement of the hind limb (behavior test) and by sensory threshold (paw stimulation test). Another 7 rats were used to establish the precise locus of lesion within the posterior root after intrathecal 20% lidocaine injection.
Results
Rats treated with 10% or 20% lidocaine developed lesions both in the posterior roots and posterior columns, characterized by axonal degeneration. Rats injected with 7.5% lidocaine developed degenerative lesions limited to the posterior roots. Lesions in the posterior roots were localized to the proximal portion of the roots. Injections of 5% or less lidocaine did not cause any pathological changes. One of 5 rats receiving 20% lidocaine showed hind-limb paralysis for 4 days, but the remaining 4 rats recovered within 4 days after drug injection. Rats injected with ≤10% lidocaine were completely recovered within 4 hours. The threshold for paw stimulation was significantly decreased in rats injected with 20% lidocaine.
Conclusion
Our results suggest that spinal lidocaine neurotoxicity after supra-clinical concentrations of lidocaine is limited initially to the posterior roots at their entry to the spinal cord, and the extent and severity of the lesions are closely associated with lidocaine concentration. Unlike severe lesions in rats injected with 20% lidocaine, mild lesions caused by lower concentrations may not manifest neurofunctional deficits.
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