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"Bagley, Mark"
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Networks, geography and the survival of the firm
Prior studies show that the success of firms in industrial clusters is the result of two main reasons; the transfer of knowledge and routines from parent firms to spinoffs that locate in the same locality, and the returns from co-location of firms. While previous research has largely inferred the presence of parent-spinoff networks, few studies have measured them. Furthermore, the lack of geographic precision has led to conflicting results for evidence of returns from location, as the gains from geographic proximity may not always be linear. This paper introduces network measurement and a refined geographic measure to separate these two respective channels of knowledge transfer, and analyzes their impact on firm survival (as a proxy for firm success). It is found that the gains with respect to location are nonlinear. Furthermore, a firm’s historical links formed through parent-spinoff linkages have a significant impact on survival, which differ depending on the motivations of the entrepreneur. Moreover, these channels of knowledge are complementary in nature.
Journal Article
Ultimate end
Miles Morales and the rest of the heroes of the Ultimate U face final extinction. As the end of their world becomes inevitable, will the heroes' heartbreaking sacrifices make any difference? The dramatic end of an era begins!
Book
Population genetic diversity and fitness in multiple environments
Background
When a large number of alleles are lost from a population, increases in individual homozygosity may reduce individual fitness through inbreeding depression. Modest losses of allelic diversity may also negatively impact long-term population viability by reducing the capacity of populations to adapt to altered environments. However, it is not clear how much genetic diversity within populations may be lost before populations are put at significant risk. Development of tools to evaluate this relationship would be a valuable contribution to conservation biology. To address these issues, we have created an experimental system that uses laboratory populations of an estuarine crustacean,
Americamysis bahia
with experimentally manipulated levels of genetic diversity. We created replicate cultures with five distinct levels of genetic diversity and monitored them for 16 weeks in both permissive (ambient seawater) and stressful conditions (diluted seawater). The relationship between molecular genetic diversity at presumptive neutral loci and population vulnerability was assessed by AFLP analysis.
Results
Populations with very low genetic diversity demonstrated reduced fitness relative to high diversity populations even under permissive conditions. Population performance decreased in the stressful environment for all levels of genetic diversity relative to performance in the permissive environment. Twenty percent of the lowest diversity populations went extinct before the end of the study in permissive conditions, whereas 73% of the low diversity lines went extinct in the stressful environment. All high genetic diversity populations persisted for the duration of the study, although population sizes and reproduction were reduced under stressful environmental conditions. Levels of fitness varied more among replicate low diversity populations than among replicate populations with high genetic diversity. There was a significant correlation between AFLP diversity and population fitness overall; however, AFLP markers performed poorly at detecting modest but consequential losses of genetic diversity. High diversity lines in the stressful environment showed some evidence of relative improvement as the experiment progressed while the low diversity lines did not.
Conclusions
The combined effects of reduced average fitness and increased variability contributed to increased extinction rates for very low diversity populations. More modest losses of genetic diversity resulted in measurable decreases in population fitness; AFLP markers did not always detect these losses. However when AFLP markers indicated lost genetic diversity, these losses were associated with reduced population fitness.
Journal Article
Miles Morales : the ultimate Spider-Man. Vol. 1, Revival
Miles Morales, the ultimate Spider-Man, is back in action with a new status quo and a new outlook on life! It's the anniversary of Peter Parker's death, but as the world mourns the original Spider-Man, a gathering of Spidey's friends and foes reveal some shocking truths about Peter and his world! A big, big villain from Peter's past is alive and well...and about to turn New York upside down! Now, Miles must come face to face with the worst nightmare of the Spider-Man legacy: Norman Osborn, the Green Goblin...the man who killed Peter Parker...or did he? Plus, Miles has made a huge choice about the woman he loves. Will he live to regret it?
Book
A Convenient, Rapid, Conventional Heating Route to MIDA Boronates
A cheap, conventional, sealed heating reactor proved to be a useful alternative to a microwave reactor in the synthesis of a >20-member MIDA boronate library (MIDA = N-methyliminodiacetic acid). Reaction times were 10 min and work-ups were minimal, saving on energy and solvent usage.
Journal Article
Spider-Men II
The sequel five years in the making! The first time the Amazing Peter Parker and the Ultimate Miles Morales met, things ended with a question - who is the Miles Morales of the Marvel Universe?! Now that the Miles you know and love shares a world with Peter in the mainstream MU, you're finally going to get that answer!
Book
Evaluating the Role of p38 MAPK in the Accelerated Cell Senescence of Werner Syndrome Fibroblasts
Progeroid syndromes show features of accelerated ageing and are used as models for human ageing, of which Werner syndrome (WS) is one of the most widely studied. WS fibroblasts show accelerated senescence that may result from p38 MAP kinase activation since it is prevented by the p38 inhibitor SB203580. Thus, small molecule inhibition of p38-signalling may be a therapeutic strategy for WS. To develop this approach issues such as the in vivo toxicity and kinase selectivity of existing p38 inhibitors need to be addressed, so as to strengthen the evidence that p38 itself plays a critical role in mediating the effect of SB203580, and to find an inhibitor suitable for in vivo use. In this work we used a panel of different p38 inhibitors selected for: (1) having been used successfully in vivo in either animal models or human clinical trials; (2) different modes of binding to p38; and (3) different off-target kinase specificity profiles, in order to critically address the role of p38 in the premature senescence seen in WS cells. Our findings confirmed the involvement of p38 in accelerated cell senescence and identified p38 inhibitors suitable for in vivo use in WS, with BIRB 796 the most effective.
Journal Article
Armor wars
\"Technopolis: an amazing domain of science and wonder created by the visionary genius of brothers Tony and Arno Stark. It's a real-life utopia, save for one fact: Every resident must wear armor to protect them from a deadly disease. But this near-paradise may be shattered forever when one of its few super heroes is murdered! As Baron Tony and this domain's Thor--a hammer-wielding Jim Rhodes--race to find out who killed Spyder-Man. Wilson Fisk tightens his grip on the city's underbelly. Will the Kingpin dethrone a certain genius philanthropist playboy--and plunge Technopolis into chaos? As the mystery behind the plight of Technopolis unfolds, cracks in Tony's invincible armor are exposed, and the looming crisis could pit brother against brother.\"-- Page 4 of cover.
Book
Genotoxicity and Epigenotoxicity of Carbazole-Derived Molecules on MCF-7 Breast Cancer Cells
The carbazole compounds PK9320 (1-(9-ethyl-7-(furan-2-yl)-9H-carbazol-3-yl)-N-methylmethanamine) and PK9323 (1-(9-ethyl-7-(thiazol-4-yl)-9H-carbazol-3-yl)-N-methylmethanamine), second-generation analogues of PK083 (1-(9-ethyl-9H-carbazol-3-yl)-N-methylmethanamine), restore p53 signaling in Y220C p53-mutated cancer cells by binding to a mutation-induced surface crevice and acting as molecular chaperones. In the present paper, these three molecules have been tested for mutant p53-independent genotoxic and epigenomic effects on wild-type p53 MCF-7 breast adenocarcinoma cells, employing a combination of Western blot for phospho-γH2AX histone, Comet assay and methylation-sensitive arbitrarily primed PCR to analyze their intrinsic DNA damage-inducing and DNA methylation-changing abilities. We demonstrate that small modifications in the substitution patterns of carbazoles can have profound effects on their intrinsic genotoxic and epigenetic properties, with PK9320 and PK9323 being eligible candidates as “anticancer compounds” and “anticancer epi-compounds” and PK083 a “damage-corrective” compound on human breast adenocarcinoma cells. Such different properties may be exploited for their use as anticancer agents and chemical probes.
Journal Article