The objectives of this study were to learn how hip fracture patients fall, and to compare the mechanics of their falls with those falls that did not result in hip fracture. In this way we sought to obtain reliable insight into the etiology and pathogenesis of hip fracture and fracture prevention. A total of 206 consecutive patients with fresh hip fracture and 100 controls were interviewed and examined between October 1994 and May 1996. The only inclusion criterion was that the fracture had occurred within 24 hours of hospital admittance. The control subjects were admitted from the same community after an accidental fall that did not result in hip fracture. The characteristics of the accident were determined by personal interview and examination of the patients within 24 hours of the event. In 98% of the hip fracture patients, the fracture was a result of a fall. The majority of the patients (76%) reported that they had fallen directly to the side. Forty-eight fracture cases had one or more eyewitnesses and their reports supported this observation. In 56% of the hip fracture patients, a fresh subcutaneous hematoma was seen on the greater trochanter of the proximal femur; such a hematoma was rare in the controls (6%) (P < 0. 001), and this gave evidence for the direct impact of the greater trochanter during the fall of the hip fracture subjects. Most of the elderly fallers who fractured a hip did not manage to break the fall, e.g., with an outstretched arm. In conclusion, our results suggest that a typical hip fracture is the result of a fall and a subsequent impact on the greater trochanter of the proximal femur. The clinical implication of this finding is that effective prevention of hip fractures could be achieved by the diminution of the number and severity of falls of the elderly. We suggest that the severity of the falls (impacts on the greater trochanter) could be decreased by an external hip protector.

This study demonstrates the presence of tight junction antigens in adult and developing human epidermis. Indirect immunofluorescence labeling and immunoelectron microscopy with antibodies to ZO-1 and occludin localized tight junction components ZO-1 and occludin to a narrow zone of the granular cells of adult epidermis. Double immunolabeling for tight junction components with adherens junction or desmosome proteins suggested that occludin is more specific for tight junctions than ZO-1, which may also be associated with adherens junctions. In developing skin, tight junctions interconnected the peridermal cells, and after the fetal stratification localized to the granular cell layer. Immunolabeling of psoriasis, lichen planus, and ichthyosis vulgaris, representing aberrant differentiation of the epidermis, showed that these conditions were associated with relocation of ZO-1 and occludin to the spinous cells. Cultures of epidermal keratinocytes, which offer a useful model for the formation of cellular contacts, revealed that tight junction components, ZO-1 and occludin, displayed a marked degree of colocalization relatively late during the process when the fusion zone had assumed a linear appearance. This suggests that the formation of adherens junctions and desmosomes precedes that of tight junctions. We speculate that the epidermal barrier, isolating the human body from the external environment, is in part formed by tight junctions of stratum granulosum.

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Aspiration of meconium produces an inflammatory reaction resulting in necrotic changes in lung tissue. To further investigate the mechanisms of the meconium-induced early pulmonary injury, twenty 10-12-d-old piglets were studied for lung tissue ultrastructural and apoptotic changes and phospholipase A2 activity. Twelve piglets received an intratracheal bolus (3 mL/kg) of a 20-mg/mL (thin, n = 6) or 65-mg/mL (thick, n = 6) mixture of human meconium, and control piglets (n = 5) received the same amount of intratracheal saline. Three ventilated piglets with no aspiration were also studied. Pulmonary hemodynamics and systemic oxygenation were followed for 6 h after meconium or saline insufflation. In the control groups, the pulmonary tissue showed open alveolar spaces and intact vascular walls, whereas meconium administration resulted in severe pneumonitis, with alveolar spaces filled with inflammatory exudate. Meconium instillation additionally resulted in edematous changes in the vascular walls and alveolar epithelium, whereas type II pneumocytes were intact. The amount of apoptotic cells was increased, especially in the respiratory epithelium, and the catalytic activity of phospholipase A2 in lung tissue samples was significantly elevated after thick meconium instillation. This activity rise proved to be mainly because of human group I phospholipase A2, introduced by meconium. Our data thus show that aspiration of meconium leads to severe lung tissue inflammation with early ultrastructural changes in the pulmonary alveolar walls and is associated with apoptotic cell death in the epithelium, already during the first hours after the insult. These results further suggest that high phospholipase A2 activity, mainly introduced into the lungs within the meconium, may have an important role in the initiation of these alterations in neonatal lungs.

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