Forces of various nickel titanium closed coil springs.

OBJECTIVE: To compare the forces generated by 14 different 9 mm springs supplied by five different companies. MATERIALS AND METHODS: Five replicates of 14 different 9 mm springs were evaluated, resulting in 70 total specimens. Each was extended once from its resting length to 12 mm and then was deactivated. All tests were performed in a 37 degrees C water bath. Forces were recorded at the 12 mm extension and deactivation distances of 9 mm, 6 mm, 3 mm, and 1 mm using an MTS force gauge. Data were collected with Testworks software, version 4.0, and were analyzed by analysis of variance (ANOVA) with one factor alternated. RESULTS: Mean peak load forces at 12 mm were significantly different between springs, and these forces varied from 147 to 474 grams. Mean unload forces measured at 9 mm, 6 mm, and 3 mm of deactivation values were highly variable, and only 6 of the 14 springs exhibited a "physiologic" mean unload force of 50 grams or less over the total deactivation range. CONCLUSIONS: Few springs tested exhibited physiologic peak load forces and constant deactivation forces. This study suggests that labeling of nickel titanium closed coil springs is confusing and misleading.

Dentate granule cells form hilar basal dendrites in a rat model of hypoxia-ischemia.

Hilar basal dendrites form on dentate granule cells following seizures. To determine whether other brain insults cause the formation of hilar basal dendrites, a model of global cerebral hypoxia/ischemia was used. Rats underwent a transient induction of ischemia by occlusion of both common carotid arteries followed by reperfusion. Hippocampal slices were prepared from these animals 1 month after the ischemic insult, and granule cells were labeled with a retrograde tracing technique after biocytin injections into stratum lucidum of CA3b. Ischemic rats had numerous biocytin-labeled granule cells with hilar basal dendrites located at the hilar border of the granule cell layer. Quantitative analysis of ischemic rats compared to controls showed a significant increase in the percentage of biocytin-labeled granule cells with hilar basal dendrites. These data demonstrate that other brain insults in addition to epilepsy may result in the formation of hilar basal dendrites on granule cells.

Temporal profile of hilar basal dendrite formation on dentate granule cells after status epilepticus.

Granule cells with hilar basal dendrites (HBDs) are found after status epilepticus (SE) in three rat models of temporal lobe epilepsy. These granule cells are commonly located at the hilar border and could be newly born granule cells based on their location. The aim of this study was to determine how long it takes for HBDs to form on granule cells after SE. Pilocarpine was injected to induce SE and rats were killed at different times: 3 days, 1, 2, and 3 weeks after SE. Biocytin was injected into CA3 stratum lucidum of hippocampal slices to label granule cells with HBDs. The number, morphology, and length of HBDs were analyzed at the different time points. Basal processes of granule cells from rats killed 3 days after pilocarpine injection were judged not to be HBDs because they were short in length and did not ramify in the hilus. "True" HBDs were detected as early as 7 and 8 days after pilocarpine-induced SE. Similar frequencies of granule cells with HBDs were observed at the later time points. This study shows that HBDs can form on granule cells as early as 1 week following SE. These results are consistent with the hypothesis that HBDs on granule cells may be generated from seizure-induced, de novo granule cells, however, alternative explanations that some or all HBDs arise from pre-SE generated granule cells cannot be ruled out at this time and will require further examination.