Biomechanical Evaluation of a Cadaveric Flatfoot Model and Lateral Column Lengthening Technique.

Patients with adult acquired flatfoot have progressive worsening of bony alignment with many being unable to perform a heel rise. Following reconstruction, pathologic skeletal alignment is corrected and the ability to perform a heel rise is often restored. The purpose of this study was to evaluate the relationship between forefoot liftoff forces and skeletal alignment in a cadaveric flatfoot model by assessing the effect of sequential lengthening of the lateral column using an Evans-type calcaneal osteotomy. Bony alignment was measured in 8 cadaveric specimens with the use of a 3-dimensional digitizing system. Transection of the spring ligament, pie-crusting of the plantar fascia, and cyclic axial loading of the foot was performed to create an anatomic and functional flatfoot model. An Evans-type calcaneal osteotomy using 6, 8, 10, and 12 mm wedges was performed. Specimens were mounted to a custom jig that applies tensile loads to the Achilles, peroneus brevis, peroneus longus, and tibialis posterior tendons. Creation of a flatfoot reduced the lateral talo-first metatarsal angle (Meary's angle) by 13° (23.6° ± 2.8° vs 10.6° ± 3.8°, p < .05) and forefoot force by 7% (199.3 N ± 7.3 N vs 185.4 N ± 9 N, p < .05). Sequential lengthening of the lateral column restored skeletal alignment and force transfer to the forefoot (12 mm wedge: Meary's angle 22.7° ± 3.9°, liftoff force 206.8 N ± 7.5 N). The cadaveric flatfoot model demonstrated decreased forefoot forces that were restored with an Evans-type calcaneal osteotomy wedge. This highlights the importance of restoring skeletal alignment when correcting advanced adult acquired flatfoot.

Biomechanical evaluation of coracoid tunnel size and location for coracoclavicular ligament reconstruction.

PURPOSE: The purpose of this study was to determine the effect of coracoid tunnel size and location on the biomechanical characteristics of cortical button fixation for coracoclavicular ligament reconstruction. METHODS: Thirteen matched pairs of cadaveric scapulae were used to determine the effects of coracoid tunnel size, and 6 matched pairs were used to determine the effects of coracoid tunnel location. For tunnel size, a 4.5-mm hole was drilled in the base of the coracoid of one scapula and a 6-mm hole was drilled in the contralateral scapula. For tunnel location, 2 holes were drilled: (1) The first group received a hole centered in the coracoid base and a hole 1.5 cm distal from the first, along the axis of the coracoid. (2) The second group received holes that were offset anteromedially from the first set of holes (base eccentric and distal eccentric). A cortical button-suture tape construct was placed through each tunnel, and constructs were then loaded to failure. RESULTS: For tunnel size specimens, load at ultimate failure was significantly greater for the 4.5-mm group compared with the 6-mm group (557.6 ± 48.5 N v 466.9 ± 42.2 N, P < .05). For tunnel location, load at ultimate failure was significantly greater for the centered-distal tunnel group compared with the eccentric-distal group (538.1 ± 70.2 N v 381.0 ± 68.6 N, P < .05). CONCLUSIONS: A 4.5-mm tunnel in the coracoid provided greater strength for cortical button fixation than a 6-mm tunnel. In the distal coracoid, centered tunnels provided greater strength than eccentric tunnels. CLINICAL RELEVANCE: When performing cortical button fixation at the coracoid process for coracoclavicular ligament reconstruction, a 4.5-mm tunnel provides greater fixation strength than a 6-mm tunnel. The base of the coracoid is more forgiving than the distal coracoid regarding location.

Effects of ginseng saponins on beta-amyloid-induced amnesia in rats.

We have previously demonstrated that ginseng saponins (GS) can reverse the inhibitory effect of beta-amyloid on acetylcholine (ACh) release in the hippocampal slices. The present study was carried out to examine whether GS has any beneficial effects against amnesia induced by beta-amyloid peptides in vivo. Intracerebroventricular injection of 50 microg, but not 10 microg, beta-amyloid fragment(25-35) markedly impaired the performance of rats in avoiding a shock prod, confirming the amnesiac effect of beta-amyloid. Chronically treating the rats with GS (orally, 5 days before icv beta-amyloid injection and 7 days afterward) resulted in a dose-related improvement against beta-amyloid-induced amnesia; a significant reversion was observed at the highest GS dose (80 mg/kg/day). Post-treatment analysis on K(+)-evoked [(3)H]-ACh release from the hippocampal slices showed that beta-amyloid-treatment significantly reduced ACh release from that of the control group. However, pre-treatment with GS completely protected the animal against beta-amyloid-induced reduction of hippocampal ACh release. In contrast, treating the animals with the same optimal dose of GS and duration but only after icv beta-amyloid injection was found to be ineffective in obliterating beta-amyloid's amnesiac effect. Taken together, these observations indicated that GS pre-treatment can functionally prevent the beta-amyloid-induced memory loss possibly by minimizing the inhibitory effect of beta-amyloid on hippocampal cholinergic transmission.

Effect of ginkgolides on beta-amyloid-suppressed acetylocholine release from rat hippocampal slices.

As Ginkgo has been shown to improve age-related memory de fi cits and beta-amyloid-related peptides have been suggested to play a signi fi cant role in memory degeneration in Alzheimer's disease, the present study was carried out to examine the effect of two major ginkgolides, A and B, on beta-amyloid peptide-modulated acetylcholine (ACh) release from hippocampal brain slices. Addition of beta-amyloid fragment(25-35) (0.01-1 micro M) in the superfusion medium suppressed the K(+)-evoked [(3)H]-ACh release from the rat hippocampal slices in a concentration-related manner; a 40% reduction in ACh out fl ow was observed with the highest amyloid concentration used (1 micro M). Inclusion of ginkgolide B (GKB, 0.01-10 micro M) caused a concentration-related reversion of the inhibitory effect elicited by the effective concentration of beta-amyloid (1 micro M). The reversal of the beta-amyloid-inhibited ACh release by GKB (1 micro M) was not blocked by tetrodotoxin (1 micro M) indicating a direct interaction of GKB on the cholinergic nerve terminals. In contrast, addition of the same concentration range of ginkgolide A (GKA, 0.01-10 micro M) had no effect on beta-amyloid-inhibited ACh release. These results suggest that GKB may elicit its anti-amnesic effect by minimizing the inhibitory effect of beta-amyloid peptides on cholinergic transmission.

Effects of desmopressin on prolonging survival in stable hypothermia in rats.

The aim of the present study was to examine whether minimizing plasma volume loss due to cold-induced diuresis can increase the survival time of rats maintained in long-term stable hypothermia (~24 h at a body temperature of 19 degrees C). Infusion of desmopressin (0.5-2.0 microg), a potent antidiuretic agent, during the cooling period enhanced survival over saline controls in a dose-related manner. The enhanced survival was accompanied by a significant delay in the expected increase of hematocrit and decrease of plasma volume as compared with those seen in saline controls. In contrast, treating the rats with the same dose range of another vasopressin analog, [beta-mercapto-beta,beta-cyclopentamethyl enepropionyl]-vasopressin, which has no antidiuretic action, failed to enhance survival over saline control. Further, treating the rats with the optimal dose of desmopressin (1 microg) at the later stage of hypothermia failed to elicit any beneficial effect. Our results indicate that by using desmopressin early during the cooling phase of the hypothermia, plasma volume and rheological parameters important for sustaining microcirculation can be better maintained than those seen in saline controls. These improvements may have contributed to the observed longer survival time in hypothermia.