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Abstract:Marriage patterns can be well understood only if researchers employ measures of marriage rates that are appropriate for the question asked. In this paper, we provide evidence that the two classes of measures typically used in the literature, the number of new marriages per population and the share of individuals currently or ever married within an age range, generally lead to misleading inference when used to study the probability someone marries during his or her life or fertile life, how it evolves, and how it differs across populations. An alternative measure, the share of individuals ever married in a given cohort by a given age, is better suited for such studies. When researchers are interested in year-on-year changes in marriage probabilities of singles, age-specific marriage hazards are more reliable than population-based measures. We conclude by discussing implications of our findings for studies of the drivers and consequences of marriage formation.

Insulin secretion rates are greater after oral glucose than after parenteral administration of an equivalent glucose load. This augmented -cell secretory response to an oral glucose load results from the release of mainly two gut hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1, which potentiate glucose-induced insulin secretion. Because of their insulinotropic action, their abnormal secretion may be involved in the pathogenesis of the hyperinsulinemia of childhood obesity. In this study, we used the hyperglycemic clamp with a small oral glucose load to assess the effect of childhood obesity on GIP response in seven prepubertal lean and 11 prepubertal obese children and in 14 lean adolescents and 10 obese adolescents. Plasma glucose was acutely raised to 11 mM by infusing i.v. glucose and kept at this concentration for 180 min. Each subject ingested oral glucose (30 g) at 120 min, and the glucose infusion was adjusted to maintain the plasma glucose plateau. Basal insulin and C-peptide concentrations and insulin secretion rates (calculated by the deconvolution method) were significantly greater in obese children compared with lean children (p< 0.001). Similarly, during the first 120 min of the clamp, insulin secretion rates were higher in obese than lean children. After oral glucose, plasma insulin, C-peptide, and insulin secretion rates further increased in all four groups. This incretin effect was 2-fold greater in obese versuslean adolescents (p< 0.001). Circulating plasma GIP concentrations were similar at baseline in all four groups and remained unchanged during the first 120 min of the clamp. After oral glucose, plasma GIP concentrations rose sharply in all groups (p< 0.002). Of note, the rise in GIP was similar in both lean and obese children. In conclusion, under conditions of stable hyperglycemia, the ingestion of a small amount of glucose elicited equivalent GIP responses in both lean and obese children. However, despite similar GIP responses, insulin secretion was markedly augmented in obese adolescents. Thus, in juvenile obesity, excessive alimentary -cell stimulation may be independent of the increased release of GIP.

Insulin secretion rates are greater after oral glucose than after parenteral administration of an equivalent glucose load. This augmented ß-cell secretory response to an oral glucose load results from the release of mainly two gut hormones: gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1, which potentiate glucose-induced insulin secretion. Because of their insulinotropic action, their abnormal secretion may be involved in the pathogenesis of the hyperinsulinemia of childhood obesity. In this study, we used the hyperglycemic clamp with a small oral glucose load to assess the effect of childhood obesity on GIP response in seven prepubertal lean and 11 prepubertal obese children and in 14 lean adolescents and 10 obese adolescents. Plasma glucose was acutely raised to 11 mM by infusing i.v. glucose and kept at this concentration for 180 min. Each subject ingested oral glucose (30 g) at 120 min, and the glucose infusion was adjusted to maintain the plasma glucose plateau. Basal insulin and C-peptide concentrations and insulin secretion rates (calculated by the deconvolution method) were significantly greater in obese children compared with lean children (p < 0.001). Similarly, during the first 120 min of the clamp, insulin secretion rates were higher in obese than lean children. After oral glucose, plasma insulin, C-peptide, and insulin secretion rates further increased in all four groups. This incretin effect was 2-fold greater in obese versus lean adolescents (p < 0.001). Circulating plasma GIP concentrations were similar at baseline in all four groups and remained unchanged during the first 120 min of the clamp. After oral glucose, plasma GIP concentrations rose sharply in all groups (p < 0.002). Of note, the rise in GIP was similar in both lean and obese children. In conclusion, under conditions of stable hyperglycemia, the ingestion of a small amount of glucose elicited equivalent GIP responses in both lean and obese children. However, despite similar GIP responses, insulin secretion was markedly augmented in obese adolescents. Thus, in juvenile obesity, excessive alimentary ß-cell stimulation may be independent of the increased release of GIP.

Thirty-one pairs of clavicles obtained from human cadavers ranging in age from full-term stillborn to fourteen years were studied morphologically and radiographically. Specimen roentgenography using air/cartilage interfacing demonstrated the osseous and cartilaginous portions of the epiphyses. Overall longitudinal growth appeared to occur to a greater degree in the sternal end, which also developed a secondary ossification center. No comparable ossification was seen in the acromion. The curve patterns differed in the acromial and sternal ends. The sternoclavicular joint has a meniscus throughout postnatal development. This was demonstrated by air arthrography. Finally, the sternoclavicular joint was dislocated anteriorly and posteriorly to duplicate trauma to this region. Roentgenographic aspects of development are discussed and illustrated to provide a reference index.

Thirty-six manubriosternal composites from skeletally immature cadavers were examined morphologically and radiographically. Sternebral ossification followed certain patterns. The manubrium (first sternebra) usually had one primary ossification center and one or two smaller centers. These usually were caudad to the major center (longitudinally bifid). The second sternebra invariably had only one ossification center. The third and fourth sternebrae had latitudinal (right-left) bifid ossification centers, undoubtedly a result of the original formation of the sternum from two longitudinal mesenchymal anlagen. Occasionly the fourth sternebra exhibited longitudinally bifid ossification. The usual pattern was ossification of four sternebrae, although a fifth was intermittently present. The xiphisternum (not a true sternebra) was infrequently ossified.

A unique specimen of unilateral Sprengel's deformity, and contralateral normal pectoral girdle, were studied morphologically and roentgenographically. The cervical spine exhibited multiple abnormalities involving both the vertebral centra as well as the posterior elements (Klippel-Feil abnormality). A small spina bifida involving C5 and C6 was present. Abnormalities of the spinous processes included an articulation with a well-formed omovertebral bone that also articulated with the vertebral (infraspinatus) margin of the scapula. Secondary (presumed epiphyseal) ossification was present in the omovertebral bone at the distal end. The scapula was deformed, especially in the supraspinatus portion. The clavicle was shorter and had a different contour.

Avulsion of a linear portion of the tibial periosteum, without apparent injury to the underlying cortical bone, eventually led to the formation of a longitudinal segment of ectopic bone. This bone was membranous, laminar bone derived from the avulsed periosteum. No remodeling (osteon formation) was evident. Two regions of pseudarthrosis were present, with one being the source of the patient's chronic pain. This injury represents specific trauma to the membranous, appositional growth mechanism of the diaphysis comparable to a fracture disrupting the endochondral ossification mechanism of the epiphysis and physis.