‘We are labeled as gang members, even though we are not’: belonging, aspirations and social mobility in Cartagena

This paper explores how belonging and aspirations interact to shape marginalized young Colombians’ strategies for upward social mobility. Recent literature has argued that in the context of inequality and poverty, social mobility is constrained by people’s inability to aspire to and/or achieve their aspirations. The majority of this literature is from the economics field and looks at the way poverty acts as a brake on social mobility. This paper provides an additional interdisciplinary analysis of the role of ‘belonging’ (to places and social class) in influencing aspirations of young Colombians. Findings are based on ethnographic fieldwork with young people from two marginalized neighborhoods in Cartagena. It is argued that aspirations are closely linked to belonging and the extent to which young people feel integral to or distanced from their localities. Using a Bourdieusian perspective, the paper examines how belonging is developed and how it influences behavior, orientations and future prospects. This approach generates insights into young people’s apparent low aspirations beyond the explanation of internal behavioral poverty traps. In so doing, it provides a more comprehensive understanding of how societal structures limit aspiration development and achievement

A Complete Pathway Model for Lipid A Biosynthesis in Escherichia coli.

Lipid A is a highly conserved component of lipopolysaccharide (LPS), itself a major component of the outer membrane of Gram-negative bacteria. Lipid A is essential to cells and elicits a strong immune response from humans and other animals. We developed a quantitative model of the nine enzyme-catalyzed steps of Escherichia coli lipid A biosynthesis, drawing parameters from the experimental literature. This model accounts for biosynthesis regulation, which occurs through regulated degradation of the LpxC and WaaA (also called KdtA) enzymes. The LpxC degradation signal appears to arise from the lipid A disaccharide concentration, which we deduced from prior results, model results, and new LpxK overexpression results. The model agrees reasonably well with many experimental findings, including the lipid A production rate, the behaviors of mutants with defective LpxA enzymes, correlations between LpxC half-lives and cell generation times, and the effects of LpxK overexpression on LpxC concentrations. Its predictions also differ from some experimental results, which suggest modifications to the current understanding of the lipid A pathway, such as the possibility that LpxD can replace LpxA and that there may be metabolic channeling between LpxH and LpxB. The model shows that WaaA regulation may serve to regulate the lipid A production rate when the 3-deoxy-D-manno-oct-2-ulosonic acid (KDO) concentration is low and/or to control the number of KDO residues that get attached to lipid A. Computation of flux control coefficients showed that LpxC is the rate-limiting enzyme if pathway regulation is ignored, but that LpxK is the rate-limiting enzyme if pathway regulation is present, as it is in real cells. Control also shifts to other enzymes if the pathway substrate concentrations are not in excess. Based on these results, we suggest that LpxK may be a much better drug target than LpxC, which has been pursued most often