Robust estimation of bacterial cell count from optical density

Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals <1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data

Constant of heat conduction and stabilization of bus bar conductor

Background: Although commonly used in adults to detect early atherosclerosis, the value of the carotid intima-media thickness (CIMT) in children and adolescents is not clear. This marker has an inheritable component that supports the notion of a genetic influence. Among the genes studied as candidates for atherosclerosis development are those for chemokines, cytokines, and adhesion molecules because of their participation in atheroma formation through monocyte recruitment and migration. Methods: We analyzed the relationship between CIMT and functional polymorphic variants in the genes for chemokines and proinflammatory cytokines associated with cardiovascular events in adults in lean and obese but otherwise healthy 6- to 19-year-old subjects. Results: In the obese group, systolic blood pressure correlated negatively (r =-0.332; p = 0.008) and the TNF-308A allele correlated positively (r = 0.262; p = 0.040) with CIMT. The mean CIMT was higher in obese individuals with the TNF-308A allele than in those with TNF-308G allele (p = 0.041). In a multiple regression model for the total population, an increase in CIMT was explained by body mass index, systolic and diastolic blood pressure, and the TNF-308A and CCL2-2518A alleles (r2 = 0.321; p = 0.022). Conclusions: This study contributes to the understanding of the pathophysiology of atherosclerosis and suggests that genetic markers of an increased inflammatory response and its deleterious effects are already present in obese children and adolescents. " 2008 IMSS.",,,,,,"10.1016/j.arcmed.2008.07.007",,,"http://hdl.handle.net/20.500.12104/40345","http://www.scopus.com/inward/record.url?eid=2-s2.0-55249084641&partnerID=40&md5=2167552431211ce90f6e1ae18a933d60",,,,,,"8",,"Archives of Medical Research",,"75

Contribution of TNF-308A and CCL2-2518A to Carotid Intima-Media Thickness in Obese Mexican Children and Adolescents

Background: Although commonly used in adults to detect early atherosclerosis, the value of the carotid intima-media thickness (CIMT) in children and adolescents is not clear. This marker has an inheritable component that supports the notion of a genetic influence. Among the genes studied as candidates for atherosclerosis development are those for chemokines, cytokines, and adhesion molecules because of their participation in atheroma formation through monocyte recruitment and migration. Methods: We analyzed the relationship between CIMT and functional polymorphic variants in the genes for chemokines and proinflammatory cytokines associated with cardiovascular events in adults in lean and obese but otherwise healthy 6- to 19-year-old subjects. Results: In the obese group, systolic blood pressure correlated negatively (r =-0.332; p\ua0= 0.008) and the TNF-308A allele correlated positively (r = 0.262; p = 0.040) with CIMT. The mean CIMT was higher in obese individuals with the TNF-308A allele than in those with TNF-308G allele (p = 0.041). In a multiple regression model for the total population, an increase in CIMT was explained by body mass index, systolic and diastolic blood pressure, and the TNF-308A and CCL2-2518A alleles (r2 = 0.321; p = 0.022). Conclusions: This study contributes to the understanding of the pathophysiology of atherosclerosis and suggests that genetic markers of an increased inflammatory response and its deleterious effects are already present in obese children and adolescents. © 2008 IMSS