The ISCIP Analyst, Volume VI, Issue 20

This repository item contains a single issue of The ISCIP Analyst, an analytical review journal published from 1996 to 2010 by the Boston University Institute for the Study of Conflict, Ideology, and Policy

The ISCIP Analyst, Volume VII, Issue 4

This repository item contains a single issue of The ISCIP Analyst, an analytical review journal published from 1996 to 2010 by the Boston University Institute for the Study of Conflict, Ideology, and Policy

The ISCIP Analyst, Volume VII, Issue 20

This repository item contains a single issue of The ISCIP Analyst, an analytical review journal published from 1996 to 2010 by the Boston University Institute for the Study of Conflict, Ideology, and Policy

The ISCIP Analyst, Volume VII, Issue 8

This repository item contains a single issue of The ISCIP Analyst, an analytical review journal published from 1996 to 2010 by the Boston University Institute for the Study of Conflict, Ideology, and Policy

Case-control design identifies ecological drivers of endemic coral diseases

Endemic disease transmission is an important ecological process that is challenging to study because of low occurrence rates. Here, we investigate the ecological drivers of two coral diseases-growth anomalies and tissue loss-affecting five coral species. We first show that a statistical framework called the case-control study design, commonly used in epidemiology but rarely applied to ecology, provided high predictive accuracy (67-82%) and disease detection rates (60-83%) compared with a traditional statistical approach that yielded high accuracy (98-100%) but low disease detection rates (0-17%). Using this framework, we found evidence that 1) larger corals have higher disease risk; 2) shallow reefs with low herbivorous fish abundance, limited water motion, and located adjacent to watersheds with high fertilizer and pesticide runoff promote low levels of growth anomalies, a chronic coral disease; and 3) wave exposure, stream exposure, depth, and low thermal stress are associated with tissue loss disease risk during interepidemic periods. Variation in risk factors across host-disease pairs suggests that either different pathogens cause the same gross lesions in different species or that the same disease may arise in different species under different ecological conditions

Biochemical and Genetic Characterization of PspE and GlpE, Two Single-domain Sulfurtransferases of Escherichia coli

The pspE and glpE genes of Escherichia coli encode periplasmic and cytoplasmic single-domain rhodaneses, respectively, that catalyzes sulfur transfer from thiosulfate to thiophilic acceptors. Strains deficient in either or both genes were constructed. Comparison of rhodanese activity in these strains revealed that PspE provides 85% of total rhodanese activity, with GlpE contributing most of the remainder. PspE activity was four times higher during growth on glycerol versus glucose, and was not induced by conditions that induce expression of the psp regulon. The glpE/pspE mutants displayed no apparent growth phenotypes, indicating that neither gene is required for biosynthesis of essential sulfur-containing molecules. PspE was purified by using cation exchange chromatography. Two distinct active peaks were eluted and differed in the degree of stable covalent modification, as assessed by mass spectrometry. The peak eluting earliest contained the equivalent mass of two additional sulfur atoms, whereas the second peak contained mainly one additional sulfur. Kinetic properties of purified PspE were consistent with catalysis occurring via a double-displacement mechanism via an enzyme-sulfur intermediate involving the active site cysteine. Kms for SSO32- and CN- were 2.7 mM and 32 mM, respectively, and kcat was 64s-1. The enzyme also catalyzed transfer of sulfur from thiosulfate to dithiothreitol, ultimately releasing sulfide

Coral disease time series highlight size-dependent risk and other drivers of white syndrome in a multi-species model

Coral diseases contribute to the decline of reef communities, but factors that lead to disease are difficult to detect. In the present study, we develop a multi-species model of colony-scale risk for the class of coral diseases referred to as White Syndromes, investigating the role of current or past conditions, including both environmental stressors and biological drivers at the colony and community scales. Investigating 7 years of coral survey data at five sites in Guam we identify multiple environmental and ecological associations with White Syndrome, including a negative relationship between short-term heat stress and White Syndrome occurrence, and strong evidence of increasing size-dependent White Syndrome risk across coral species. Our findings result in a generalized model used to predict colony-scale White Syndrome risk for multiple species, highlighting the value of long-term monitoring efforts to detect drivers of coral disease