PubMed · 5347243
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N R Niles. 1969. Structure and function: why did the heart stop?. https://doi.org/10.1378/chest.56.5.370
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STUDY DESIGN: A biomechanical study was conducted during a 3.5-day period to test for changes occurring in pullout strengths of cancellous screws inserted into human cadaveric vertebral bodies. OBJECTIVES: To quantify, within the testing time of 3.5 days, the possible changes to the mechanical properties of cadaveric vertebral bodies, resulting from structural degradation caused by postmortem, time-dependent, autolytic processes during mechanical testing of implant-bone biomechanics. SUMMARY OF BACKGROUND DATA: Biomechanical testing of whole spinal implants and analysis of the screw-bone interface of spinal implants is an area of clinical interest that frequently requires the use of cadaveric spine specimens. Changes in vertebral bone properties during the testing period may invalidate experimental results, but no data are available on degradation of bone during the testing period. METHODS: Anterior oblique cancellous screws were inserted into human vertebral bodies from which the ventral cortex had been removed. The pullout strength was measured at 0, 24, 60, and 84 hours after insertion. The tests were performed on 48 human vertebral bodies, which were stored by freezing to -23 C, thawed for testing, and kept at room temperature during the testing time for as long as 84 hours. RESULTS: The axial pullout strength showed no statistically significant change during 84 hours (P = 0.15). There were no significant differences attributable to vertebral level from T4 to L4, probably because the ventral cortices had been removed (P = 0.7). CONCLUSIONS: During 3.5 days, there were no changes in pullout strength of vertebral cancellous bone. In biomechanical studies during a maximum period of 3 days with a small number of cadaveric spines (e.g., four spine specimen) the time-dependent changes in pullout strength play a less significant role than do the interspine differences. Interspine differences should be regarded as an important factor to be considered in the design of biomechanical tests.
The autolysis loop of thrombin comprises nine residues, from Glu146 to Lys149e, five of which (Ala149a-Lys149e) are inserted relative to trypsin and chymotrypsin. Deletion of the insertion Ala149a-Lys149e causes no significant change in the properties of the enzyme, except for a slight enhancement of protein C activation. Deletion of the entire Glu146-Lys149e loop, however, reduces fibrinogen clotting 240-fold, but decreases protein C activation only 2-fold. This loop-less mutant is de facto an exclusive activator of protein C, having lost the primary procoagulant function of thrombin. Because the autolysis loop affects fibrinogen binding, but not protein C activation, it provides a target for new drugs designed to suppress exclusively the procoagulant activity of thrombin.
Genetic prodrug activation therapy shows promise as a therapeutic option for the treatment of cancer as well as a variety of other diseases. It involves the insertion of a gene encoding a drug-metabolizing enzyme into cells and the systemic administration of a prodrug. The prodrug is converted to a cytotoxic agent by the action of the expressed enzyme. To ensure that the enzyme is only expressed in the targeted subset of cells, the transcriptional apparatus of a gene that is unique to this subset is used to regulate the gene encoding the drug-metabolizing enzyme. As with all types of gene therapy, one of the major obstacles to successful clinical treatment is the development of safe and effective gene delivery systems.