Citations

Abstract Between 1935 and 1974, 3598 episodes of head trauma among Olmsted County, Minnesota, residents resulted in 1097 skull fractures. Of these, 53% were simple, 16% were depressed, 12% were compound, and 19% were basilar. The age- and sex-adjusted incidence of skull fractures was 44.3 per 100,000 person-years overall, was somewhat greater in the urban than in the rural areas of Olmsted County, and was relatively stable for the final 30 years of the study. Age-specific incidence rates were highest for the very young, and simple linear fractures were the predominant type of skull fracture in this age group and among the elderly. The male:female ratio of incidence rates varied from 2.1:1 to 4.5:1 depending on fracture type. Motor vehicle accidents accounted for 38% of the skull fractures and were a particularly important cause among young males. Falls accounted for 37% of the skull fractures and were the major cause of fractures in the elderly and pediatric age groups. The results of this population-based study may be helpful in formulating recommendations for the evaluation and management of head-injured patients.

Abstract The pathogenesis of postlaminectomy spinal deformity and instability in children was evaluated by reviewing appropriate roentgenographic findings. First, we reviewed spine roentgenograms of patients below 40 years of age who underwent spinal fusion for deformity and instability of the spine developing after a multiple level laminectomy. Two types of deformity were recognized on the roentgenograms: increased mobility between the vertebral bodies and wedging deformity of the ventral aspect of the vertebral bodies. Second, we did a follow-up study of another group of patients who had undergone laminectomy. We found the same two types of deformity in children, but not in adult patients. The incidence of deformity was higher after laminectomies of the cervical or cervicothoracic region than after lumbar laminectomies. Our data suggest that postlaminectomy spinal deformity can develop in children without irradiation or facet injury. The deformity is due to a wedging change in the cartilaginous portion of the vertebral body and to the viscoelasticity of ligaments in children. When treatment of this complication becomes necessary, anterior fusion may be effective in arresting progression. Prophylactic measures against the development of deformity are discussed. Our hypothesis concerning the mechanism of development of this complication supports the rationale of osteoplastic laminar resection and reconstruction instead of laminectomy, particularly in the management of children.

Chronic lymphocytic leukemia (CLL) patients with p53 pathway dysfunction have poor responses to conventional chemoimmunotherapy and short survival. This small but important cohort of CLL patients would benefit from early identification and appropriate management. The challenge is to develop clinically useful tests of p53 pathway function.

Identified in an RNA interference screen, proteins that prevent spindle multipolarity in human cancer cells may prove to be promising drug targets.

Osteoporosis is an important clinical problem, affecting more than 50% of people over age 50 yr. Estrogen signaling is critical for maintaining proper bone density, and the identification of an endogenous selective estrogen receptor (ER) modulator, 27-hydroxycholesterol (27HC), suggests a mechanism by which nutritional/metabolic status can influence bone biology. With its levels directly correlated with cholesterol, a new possibility emerges wherein 27HC links estrogen and cholesterol signaling to bone homeostasis. In these studies, we found that increasing concentrations of 27HC, both by genetic and pharmacological means, led to decreased bone mineral density that was associated with decreased bone formation and increased bone resorption. Upon manipulation of endogenous estrogen levels, many of the responses to elevated 27HC were altered in such a way as to implicate ER as a likely mediator. In a model of postmenopausal bone loss, some pathologies associated with elevated 27HC were exacerbated by the absence of endogenous estrogens, suggesting that 27HC may act both in concert with and independently from classic ER signaling. These data provide evidence for interactions between estrogen signaling, cholesterol and metabolic disease, and osteoporosis. Patients with high cholesterol likely also have higher than average 27HC, perhaps putting them at a higher risk for bone loss and fracture. More studies are warranted to fully elucidate the mechanism of action of 27HC in bone and to identify ways to modulate this pathway therapeutically.