Longitudinal analysis of 934 adults aged >= 65 years enrolled in the Invecchiare in Chianti study was conducted. Grip strength, knee extension strength, and lower extremity power were measured at baseline and 3 years postenrollment. Mobility function (gait speed and self-reported mobility disability) was measured at 3 and 6 years postenrollment. Classification and regression tree analysis was used to predict mobility decline from Years 3 to 6.

Men with knee extension strength < 19.2 kg and grip strength < 39.0 kg had clinically meaningful declines

in gait speed of .24 m/s. Furthermore, men with power < 105 W were nearly nine times more likely to develop incident mobility disability (likelihood ratio = 8.68; 95% confidence interval = 3.91, 19.44). Among women, knee extension strength < 18.0 kg was associated with a minimal gait speed decline of 0.06 m/s, and women with leg power < 64 W were three times more likely to develop incident mobility disability (likelihood ratio = 3.01; 95% confidence

interval = 1.79, 5.08). Three-year changes in strength and power did not predict mobility decline in either sex.

Findings suggest that strength and power measured at one time point are more predictive of mobility decline than 3-year changes and that low strength and power are particularly powerful risk factors in men.”
“A developmental constraint is a mechanism that limits the possibility of a phenotype to evolve. There is growing evidence for the existence of developmental constraints

in the biological literature. We hypothesize that a developmental constraint prevents the savant syndrome, despite its positive aspects, from spreading in the population. Here, the developmental constraint is the result of the high interactivity among body parts in an early stage in embryological development, namely early organogenesis or the phylotypic stage. The interactivity during this stage involves all components of the embryo, and as a result mutations that affect one part of the embryo also affect other parts. We hypothesize that a mutation, which gives rise to the development of the positive aspects of the savant syndrome (e.g., an impressive memory capacity), will virtually always have a deleterious effect on the development of other phenotypic traits (e.g., resulting in autism and/or impaired motor coordination). Thus, our hypothesis states that the savant syndrome cannot spread in the population because of this developmental constraint. The finding that children with savant syndrome often have autism and physical anomalies, which are known to be established during early organogenesis, supports our hypothesis. (c) 2007 Elsevier Ireland Ltd. All rights reserved.”
“The biosynthesis and export of bacterial cell-surface polysaccharides is known to occur through several distinct mechanisms.