Microtubule-associated protein 1B, a growth-associated and phosphorylated scaffold protein.

Microtubule-associated protein 1B, MAP1B, is one of the major growth associated and cytoskeletal proteins in neuronal and glial cells. It is present as a full length protein or may be fragmented into a heavy chain and a light chain. It is essential to stabilize microtubules during the elongation of dendrites and neurites and is involved in the dynamics of morphological structures such as microtubules, microfilaments and growth cones. MAP1B function is modulated by phosphorylation and influences microtubule stability, microfilaments and growth cone motility. Considering its large size, several interactions with a variety of other proteins have been reported and there is increasing evidence that MAP1B plays a crucial role in the stability of the cytoskeleton and may have other cellular functions. Here we review molecular and functional aspects of this protein, evoke its role as a scaffold protein and have a look at several pathologies where the protein may be involved.

Optimal growth strategies when mortality and production rates are size-dependent

Pontryagin's maximum principle from optimal control theory is used to find the optimal allocation of energy between growth and reproduction when lifespan may be finite and the trade-off between growth and reproduction is linear. Analyses of the optimal allocation problem to date have generally yielded bang-bang solutions, i.e. determinate growth: life-histories in which growth is followed by reproduction, with no intermediate phase of simultaneous reproduction and growth. Here we show that an intermediate strategy (indeterminate growth) can be selected for if the rates of production and mortality either both increase or both decrease with increasing body size, this arises as a singular solution to the problem. Our conclusion is that indeterminate growth is optimal in more cases than was previously realized. The relevance of our results to natural situations is discussed.

Genome-wide association and longitudinal analyses reveal genetic loci linking pubertal height growth, pubertal timing and childhood adiposity.

The pubertal height growth spurt is a distinctive feature of childhood growth reflecting both the central onset of puberty and local growth factors. Although little is known about the underlying genetics, growth variability during puberty correlates with adult risks for hormone-dependent cancer and adverse cardiometabolic health. The only gene so far associated with pubertal height growth, LIN28B, pleiotropically influences childhood growth, puberty and cancer progression, pointing to shared underlying mechanisms. To discover genetic loci influencing pubertal height and growth and to place them in context of overall growth and maturation, we performed genome-wide association meta-analyses in 18 737 European samples utilizing longitudinally collected height measurements. We found significant associations (P < 1.67 × 10(-8)) at 10 loci, including LIN28B. Five loci associated with pubertal timing, all impacting multiple aspects of growth. In particular, a novel variant correlated with expression of MAPK3, and associated both with increased prepubertal growth and earlier menarche. Another variant near ADCY3-POMC associated with increased body mass index, reduced pubertal growth and earlier puberty. Whereas epidemiological correlations suggest that early puberty marks a pathway from rapid prepubertal growth to reduced final height and adult obesity, our study shows that individual loci associating with pubertal growth have variable longitudinal growth patterns that may differ from epidemiological observations. Overall, this study uncovers part of the complex genetic architecture linking pubertal height growth, the timing of puberty and childhood obesity and provides new information to pinpoint processes linking these traits.

Association between growth and blood pressure during the life course in children and adolescents

Background: Little is known on the relative importance of growth at different periods between birth and adolescence on blood pressure (BP). Objective: To assess the association between birth weight, change in body weight (growth) and BP across the entire span of childhood and adolescence. Methods: School-based surveys were conducted annually between 1998 and 2006 among all children in four school grades (kindergarten, 4th, 7th, and 10th year of compulsory school) in the Seychelles, Indian Ocean. Height and weight and BP were measured. Three cohorts of children examined twice were analyzed: 1606 children surveyed at age 5.5 and 9.1, 2557 at age 9.2 and 12.5, and 2065 at age 12.5 and 15.5, respectively. Weights at birth and at one year were extracted from medical files. Weights were expressed as Z-scores and growth was defined as a change in weight Z-scores (corresponding to weight centile crossing). The association between BP (at age 5.5, 9.2, 12.5, and 15.5) and weight at different times was assessed by linear regression. Using results of regression models of BP on all successive weights, life course plots were drawn by plotting regression coefficients against age at which weight was measured. The figure shows a life course plot of systolic BP in boys aged 15.5. Results: Without adjustment for current weight (at the time of BP measurement), birth weight was not associated with current BP, irrespective of age, excepted for girls at age 15.5 for whom a modest positive association was found. When adjusted for current weight, birth weight was negatively and modestly associated with current BP. BP was strongly associated with current weight, irrespective of age. Life course plots showed that BP was strongly associated with growth during the few preceding years but not with growth during earlier years, except for growth during the first year of life which tended to be associated with systolic BP. Conclusions: Our findings suggest that BP during childhood and adolescence is mainly determined by current body weight and recent growth.

Expanding to institutionally different countries. Reasons, Firm International Experience, and Entry Mode Choice

We examine entry mode choice and its consequences when a multinational enterprise (MNE) expands into an institutionally different country. We argue that discussions of entry mode should distinguish between informal (e.g., culture) and formal (e.g., laws) institutions, and should take into account not just the home country of the MNE and its distance to the focal host country, but the MNE's overall footprint and experience across the world in general, especially in countries with an institutional structure that is similar to that of the focal host country. Specifically, we argue that firms with experience in countries with different informal institutions will be more likely to enter via acquisitions than firms without such experience, that such experience will not matter as much in the case of formal institutions, and that such firms will exit more quickly when they enter via equity alliances than through full acquisitions. We also distinguish between balanced and unbalanced alliances and argue that balanced alliances will be more enduring, but only when the host country is culturally (not legally) different from the other countries where the MNE has experience. Our arguments suggest that entry mode should be conditioned on a firm's experience in other markets, and that intercountry differences in formal versus informal institutions have distinct influences on entry mode.