PubMed · 7127930
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D M Horstmann. 1982. Rubella.. https://doi.org/10.1097/00003081-198209000-00016
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To investigate the association between anthropometric indices and morphometrically determined vertebral deformity, the authors carried out a cross-sectional study using data from the European Vertebral Osteoporosis Study (EVOS), a population-based study of vertebral osteoporosis in 36 European centers from 19 countries. A total of 16,047 EVOS subjects were included in this analysis, of whom 1,973 subjects (915 males, 1,058 females) (12.3%) aged 50 years or over had one or more vertebral deformities ("cases"). The cases were compared with the 14,074 subjects (6,539 males, 7,535 females) with morphometrically normal spines ("controls"). Data were collected on self-reported height at age 25 years and minimum weight after age 25 years, as well as on current measured height and weight. Body mass index (BMI) and height and weight change were calculated from these data. The relations between these variables and vertebral deformity were examined separately by sex with logistic regression adjusting for age, smoking, and physical activity. In females, there was a significant trend of decreasing risk with increasing quintile of current weight, current BMI, and weight gain since age 25 years. In males, subjects in the lightest quintile for these measures were at increased risk but there was no evidence of a trend. An ecologic analysis by country revealed a negative correlation between mean BMI and the prevalence of deformity in females but not in males. The authors conclude that low body weight is associated with presence of vertebral deformity.
Hematopoiesis occurs in different organs during fetal development. Several studies suggest that the growth of hematopoietic progenitors at one stage of ontogenic maturation may not be supported by a microenvironment from a different ontogenic stage. To determine if human fetal liver (FL) clonogenic progenitors can develop in an adult bone marrow (ABM) microenvironment, we compared growth of BFU-E and CFU-GM from 7-14-wk-old FL, 11-20-wk-old fetal bone marrow (FBM), umbilical cord blood (UCB), or ABM in clonogenic medium with or without ABM stroma. In contrast to BFU-E from FBM, UCB, or ABM, soluble factor(s) produced by ABM stroma severely suppressed growth of 98% of FL BFU-E by inducing apoptosis of cells beyond early erythroblast stage. The nature of the soluble factor remains unknown, although we have evidence that it is heat labile with molecular mass < 10 kD. Antibody neutralization studies indicate that TGF-beta1, IL-1, TNF-alpha, macrophage inflammatory protein (MIP)-1alpha, or IFN-gamma are not responsible. The observation that FL progenitors may not be capable of differentiating when transferred to an ABM microenvironment may have important implications for FL transplantation into postnatal recipients. Further, this demonstrates that ontogenic stage-specific interactions between hematopoietic progenitors and their microenvironment are important for the normal development of hematopoiesis.
Schwann cells (SCs) that cap neuromuscular junctions (nmjs) play roles in guiding nerve terminal growth in paralyzed and partially denervated muscles; however, the role of these cells in the day-to-day maintenance of this synapse is obscure. Neuregulins, alternatively spliced ligands for several erbB receptor tyrosine kinases, are thought to play important roles in cell-cell communication at the nmj, affecting synapse-specific gene expression in muscle fibers and the survival of terminal SCs during development. Here we show that application of a soluble neuregulin isoform, glial growth factor II (GGF2), to developing rat muscles alters terminal SCs, nerve terminals, and muscle fibers. SCs extend processes and migrate from the synapse. Nerve terminals retract from acetylcholine receptor-rich synaptic sites, and their axons grow, in association with SCs, to the ends of the muscle. These axons make effective synapses only after withdrawal of GGF2. These synaptic alterations appear to be induced by the actions of neuregulin on SCs, because SC transplants growing into contact with synaptic sites also caused withdrawal of nerve terminal branches. These results show that SCs can alter synaptic structure at the nmj and implicate these cells in the maintenance of this synapse.