Faculty Bibliography

The purpose of this study was to determine the solidification rates for BoneSource (hydroxyapatite cement) mixed with sterile water versus BoneSource mixed with 0.25 ml of sodium phosphate. The average time for cure for BoneSource mixed with sterile water was 99 minutes, with a SD of 5.3 minutes. The average time for cure for BoneSource and sodium phosphate was 43 minutes, with a SD of 3.6 minutes (P < 0.0003). The average temperature for BoneSource in sterile water was 19.1 degrees C with a SD of 0.082, and the average temperature of BoneSource in sodium phosphate was 20.1 degrees C, with a SD of 0.1. Therefore, sodium phosphate shows that there is a significantly decreased amount of time required to solidify BoneSource and it remains isothermic throughout this reaction

The ability of immature animals and newborns to orchestrate successful calvarial reossification is well described. This capacity is markedly attenuated in mature animals and in humans greater than 2 years of age. Previous studies have implicated the dura mater as critical to successful calvarial reossification. The authors have previously reported that immature, but not mature, dural tissues are capable of elaborating a high expression of osteogenic growth factors and extracellular matrix molecules. These findings led to the hypothesis that a differential expression of osteogenic growth factors and extracellular matrix molecules by immature and mature dural tissues may be responsible for the clinically observed phenotypes (i.e., immature animals reossify calvarial defects; mature animals do not). This study continues to explore the hypothesis through an analysis of transforming growth factor (TGF)-beta3, collagen type III, and alkaline phosphatase mRNA expression. Northern blot analysis of total RNA isolated from freshly harvested immature (n = 60) and mature (n = 10) dural tissues demonstrated a greater than three-fold, 18-fold, and nine-fold increase in TGF-beta3, collagen type III, and alkaline phosphatase mRNA expression, respectively, in immature dural tissues as compared with mature dural tissues. Additionally, dural cell cultures derived from immature (n = 60) and mature dura mater (n = 10) were stained for alkaline phosphatase activity to identify the presence of osteoblast-like cells. Alkaline phosphatase staining of immature dural cells revealed a significant increase in the number of alkaline phosphatase-positive cells as compared with mature dural tissues (p < 0.001). In addition to providing osteogenic humoral factors (i.e., growth factors and extracellular matrix molecules), this finding suggests that immature, but not mature, dura mater may provide cellular elements (i.e., osteoblasts) that augment successful calvarial reossification. These studies support the hypothesis that elaboration of osteogenic growth factors (i.e., TGF-beta33) and extracellular matrix molecules (i.e., collagen type III and alkaline phosphatase) by immature, but not mature, dural tissues may be critical for successful calvarial reossification. In addition, these studies suggest for the first time that immature dural tissues may provide cellular elements (i.e., osteoblasts) to augment this process

Groin lymphorrhea is an uncommon but serious complication of vascular and cardiac surgery as well as interventional procedures that cannulate the femoral vessels. Treatment options are somewhat controversial. For lymphocutaneous fistulas, a commonly used current modality is early surgical ligation with the assistance of blue-dye staining of the lymphatic anatomy. The purpose of this case series is to give the first description of a new, less invasive, approach using subatmospheric pressure dressing therapy for the treatment of the challenging problem of lymphocutaneous fistulas of the groin.

Although it is one of the most commonly occurring craniofacial congenital disabilities, craniosynostosis (the premature fusion of cranial sutures) is nearly impossible to prevent because the molecular mechanisms that regulate the process of cranial suture fusion remain largely unknown. Recent studies have implicated the dura mater in determining the fate of the overlying cranial suture; however, the molecular biology within the suture itself has not been sufficiently investigated. In the murine model of cranial suture fusion, the posterior frontal suture is programmed to begin fusing by postnatal day 12 in rats (day 25 in mice), reliably completing bony union by postnatal day 22 (day 45 in mice). In contrast, the sagittal suture remains patent throughout the life of the animal. Using this model, this study sought to examine for the first time what differences in gene expression--if any--exist between the two sutures with opposite fates. For each series of experiments, 35 to 40 posterior frontal and sagittal suture complexes were isolated from 6-day-old Sprague-Dawley rat pups. Suture-derived cell cultures were established, and ribonuicleic acid was derived from snap-frozen, isolated suture tissue. Results demonstrated that molecular differences between the posterior frontal and sagittal suture complexes were readily identified in vivo, although these distinctions were lost once the cells comprising the suture complex were cultured in vitro. Hypothetically, this change in gene expression resulted from the loss of the influence of the underlying dura mater. Significant differences in the expression of genes encoding extracellular matrix proteins existed in vivo between the posterior frontal and sagittal sutures. However, the production of the critical, regulatory cytokine transforming growth factor beta-1 was equal between the two suture complexes, lending further support to the hypothesis that dura mater regulates the fate of the overlying cranial suture

Contracture is a major detriment to functional recovery from large wounds. To determine the relative value of dermal replacement and epidermal coverage in inhibiting wound contraction, five full-thickness wounds (all 5 x 5 cm2) were placed on the back of 8 swine and treated in the following manner: (1) open wound, (2) porcine acellular dermis (analogous to AlloDerm for human use), (3) porcine acellular dermis with epidermal autograft placed 7 days postwounding, (4) porcine acellular dermis with immediate epidermal autograft, and (5) conventional-thickness autograft. Scar dimensions and punch biopsies were taken at days 14 and 30 postwounding. The planimetry results demonstrated that wound contraction was significantly greater with the open wounds (group 1) than all other wounds with a dermal substitute. Furthermore, wounds with initial epidermal coverage had significantly less contraction than unepithelialized wounds (14.8 +/- 1.1 cm2 at day 14 in wound group 2 vs. 20.4 +/- 0.6 cm2 in wound group 4; p < 0.05). Biopsy results revealed that wounds with initial epithelial coverage had the least amount of inflammation. These findings suggest that both dermal matrix and epidermal coverage contribute to an inhibition of wound contraction and that prompt epithelial coverage appears to impede contraction by reducing inflammation

A cross-facial nerve graft (CFNG) can be used to restore the blink reflex following facial paralysis. However, the efficacy of a CFNG depends on the ability of regenerating axons to breach two nerve coaptations and reinnervate endplates in denervated muscle. The neurons involved, facial motor neurons, are androgen-dependent. Testosterone enhances facial-nerve regeneration and accelerates blink-reflex recovery following nerve crush. The current study tested the hypothesis that testosterone administered to castrated or normal adult male rats would enhance axonal regeneration through a CFNG, and thereby enhance recovery of the blink reflex. To test this hypothesis, 20 adult male rats were randomly assigned to four groups, (1) normal, intact; (2) castrated; (3) castrated with testosterone proprionate (TP) administration; and (4) normal, intact with TP Each rat underwent transection of the left facial nerve, and a CFNG using the saphenous nerve as an interpositional graft, with coaptations to the ipsilateral and contralateral zygomatic branches, was carried out. Assessments included return of blink reflex, electrophysiology, quantification of motor endplates, and axonal numbers. The data from the blink reflex evaluation, the electrophysiologic assessment, and the endplate quantification suggested that TP may have an effect on regeneration through a CFNG, but that the differences between groups were not statistically significant. In contrast, exogenously administered TP significantly enhanced the number of axons that entered the nerve graft. These data suggest that pharmacologic doses of testosterone may enhance recovery following a CFNG

A 43-year-old man sustained severe injuries to his lower limbs with extensive soft-tissue damage and bilateral tibial-fibular fractures. Acutely, the patient underwent external fixation and a free latissimus dorsi flap for soft-tissue coverage of the left leg. However, the tibia had a nonviable butterfly fragment that left a 7-cm defect after debridement. Subsequently, the contralateral fractured fibula was used as a bridging vascularized graft for this tibial defect. The transfer of a fibula containing the zone of injury from a previous high-energy fracture has not been reported. This case demonstrates the successful microvascular transfer of a previously fractured fibula for the repair of a contralateral tibial bony defect

An acquired chromosomal translocation, t(8;13)(p11;q11-12), observed in a distinctive type of stem cell leukemia/lymphoma syndrome, leads to the fusion of the 5' portion of ZNF198 and the 3' portion of FGFR1. ZNF198-FGFR1 fusion transcripts encode 4 to 10 zinc fingers, a proline-rich region, and the intracellular portion of the FGFR1 (fibroblast growth factor receptor 1) receptor tyrosine kinase. We demonstrate that the ZNF198 proline-rich region constitutes a novel self-association domain. When fused to the intracellular domain of FGFR1, the ZNF198 proline-rich region is sufficient to cause oligomerization, FGFR1 tyrosine kinase activation, and transformation of Ba/F3 cells to IL-3 independent growth. (Blood. 2000;96:699-704)