A new easy method for determination of surface adhesion of phototrophic biofilms.

Terrestrial cyanobacteria grow as phototrophic biofilms and offer a wide spectrum of interesting products. For cultivation of phototrophic biofilms different reactor concepts have been developed in the last years. One of the main influencing factors is the surface material and the adhesion strength of the chosen production strain. In this work a flow chamber was developed, in which, in combination with optical coherence tomography and computational fluid dynamics simulation, an easy analysis of adhesion forces between different biofilms and varied surface materials is possible. Hereby, differences between two cyanobacteria strains and two surface materials were shown. With longer cultivation time of biofilms adhesion increased in all experiments. Additionally, the content of extracellular polymeric substances was analyzed and its role in surface adhesion was evaluated. To test the comparability of obtained results from the flow chamber with other methods, analogous experiments were conducted with a rotational rheometer, which proved to be successful. Thus, with the presented flow chamber an easy to implement method for analysis of biofilm adhesion was developed, which can be used in future research for determination of suitable combinations of microorganisms with cultivation surfaces on lab scale in advance of larger processes.

Influence of wettability and surface design on the adhesion of terrestrial cyanobacteria to additive manufactured biocarriers.

Productive biofilms are gaining growing interest in research due to their potential of producing valuable compounds and bioactive substances such as antibiotics. This is supported by recent developments in biofilm photobioreactors that established the controlled phototrophic cultivation of algae and cyanobacteria. Cultivation of biofilms can be challenging due to the need of surfaces for biofilm adhesion. The total production of biomass, and thus production of e.g. bioactive substances, within the bioreactor volume highly depends on the available cultivation surface. To achieve an enlargement of surface area for biofilm photobioreactors, biocarriers can be implemented in the cultivation. Thereby, material properties and design of the biocarriers are important for initial biofilm formation and growth of cyanobacteria. In this study, special biocarriers were designed and additively manufactured to investigate different polymeric materials and surface designs regarding biofilm adhesion of the terrestrial cyanobacterium Nostoc flagelliforme (CCAP 1453/33). Properties of 3D-printed materials were characterized by determination of wettability, surface roughness, and density. To evaluate the influence of wettability on biofilm formation, material properties were specifically modified by gas-phase fluorination and biofilm formation was analyzed on biocarriers with basic and optimized geometry in shaking flask cultivation. We found that different polymeric materials revealed no significant differences in wettability and with identical surface design no significant effect on biomass adhesion was observed. However, materials treated with fluorination as well as optimized biocarrier design showed improved wettability and an increase in biomass adhesion per biocarrier surface.

Insights into the Development of Phototrophic Biofilms in a Bioreactor by a Combination of X-ray Microtomography and Optical Coherence Tomography.

As productive biofilms are increasingly gaining interest in research, the quantitative monitoring of biofilm formation on- or offline for the process remains a challenge. Optical coherence tomography (OCT) is a fast and often used method for scanning biofilms, but it has difficulty scanning through more dense optical materials. X-ray microtomography (µCT) can measure biofilms in most geometries but is very time-consuming. By combining both methods for the first time, the weaknesses of both methods could be compensated. The phototrophic cyanobacterium Tolypothrix distorta was cultured in a moving bed photobioreactor inside a biocarrier with a semi-enclosed geometry. An automated workflow was developed to process µCT scans of the biocarriers. This allowed quantification of biomass volume and biofilm-coverage on the biocarrier, both globally and spatially resolved. At the beginning of the cultivation, a growth limitation was detected in the outer region of the carrier, presumably due to shear stress. In the later phase, light limitations could be found inside the biocarrier. µCT data and biofilm thicknesses measured by OCT displayed good correlation. The latter could therefore be used to rapidly measure the biofilm formation in a process. The methods presented here can help gain a deeper understanding of biofilms inside a process and detect any limitations.

[Genetic factors in myocardial infarction--Results from a candidate gene and a genome-wide approach between beta blockers]. / Genetische Einflüsse beim Herzinfarkt Ergebnisse eines Kandidatengen- und eines genomweiten Ansatzes.

BACKGROUND: Coronary artery disease and myocardial infarction are the most frequent causes of death in the Western societies. Even nowadays, every second myocardial infarction is lethal and hits the patients unexpectedly without previous signs or symptoms. In order to install preventive measures most efficiently, it is necessary to have a detailed knowledge on the pathophysiology of the disease. The identification of patients who are at high risk for suffering from myocardial infarction can be done with epidemiological methods, such as the determination of "traditional" risk factors, like arterial hypertension, hypercholesterolemia, diabetes mellitus or smoking), or eventually in the future using molecular genetic testing. This is of great importance especially for asymptomatic siblings and children from myocardial infarction patients. POLYMORPHISMS: Although traditional risk factors occur frequently in families, they explain only in part the familial accumulation of coronary artery disease. Furthermore, stron genetic effects on the development of coronary artery disease and myocardial infarction have been demonstrated in several studies. These genetic effects can be examined by 1. a candidate gene approach, or 2. a systematic screening of the whole genome. In the first step, several polymorphisms (sequence variations) wee examined in several candidate genes in which a significant influence on a cardiovascular risk factor or intermediate phenotype (such as atherogeneic lipid profile or arterial hypertension) has been shown in the literature. We thus examined in a large population of patients with myocardial infarction and a sample of the general population the effects of the HindIII polymorphism in the lipoproteinlipase gene, of the -344T/C promoter polymorphism in the aldosterone synthase gene and of the 825C/T polymorphism in the gene of the beta3 subunit of the G protein gene (GNB3). In the general population, we could show an association with unfavorable lipid levels in men and in postmenopausal (but not premenopausal) women for the H2H2 genotype of the HindIII lipoproteinlipase polymorphism. However, the theoretical increase in risk for this genotype is not large enough to demonstrate a significant association with myocardial infarction in the population examined. With the promoter polymorphism in the aldosterone synthase gene, anthropometrical and echocardiographical data did not suggest that the polymorphism is a risk factor for myocardial infarction nor for left ventricular remodeling after myocardial infarction, which was observed in earlier studies. Furthermore, we could show an association with arterial hypertension in our general population sample with the polymorphism in the GNB3 gene. However, no association could be demonstrated for this polymorphism with myocardial infarction. AFFECTED SIB-PAIR APPROACH: In a systematic screening of the genome for genes that are relevant in the pathogenesis of coronary artery disease or myocardial infarction, an affected sib-pair approach was followed. 1,261 families were identified in which at least two brothers or sisters were affected with myocardial infarction or severe coronary artery disease, such as percutaneous coronary intervention or coronary after bypass grafting. In a subpopulation of 513 families and 1,407 individuals, we performed a total genome screening. The analyses using the variance component method and the SOLAR program revealed a susceptibility locus for myocardial infarction of chromosome 14q32 with a lod score of 3.89 (genome-wide p < 0.05). This locus comprises a region of about seven centi-Morgan and contains approximately 150 genes. Furthermore, a comprehensive analysis including the cardiovascular risk factors showed that 1. this myocardial infarction locus is unique and does not overlap with chromosomal loci for well-established risk factors, 2. cardiovascular risk factors, such as Lp(a), diabetes mellitus, serum lipids, or arterial hypertension have strong genetic components. CONCLUSION: These findings do not exclude a role of cardiovascular s do not exclude a role of cardiovascular risk factors or candidate genes in the pathogenesis of myocardial infarction, but rather demonstrate that risk factors may act as surrogates of specific underlying disease mechanisms. It is thus necessary to perform a comprehensive analysis of complex polygenic diseases, such as myocardial infarction, including both, established cardiovascular risk factors and genomic data.

Gender-specific differences of cardiac remodeling in subjects with left ventricular dysfunction: a population-based study.

BACKGROUND: Recent studies suggest that female gender is associated with a lower prevalence and a more benign prognosis of heart failure. In the current population-based study, it was our objective to evaluate the implications of gender on the association between impaired left ventricular (LV) function and mass as well as neurohumoral activation. METHODS AND RESULTS: A total of 1883 subjects (992 female, 891 male) of two MONICA surveys in Augsburg, Germany, were analyzed. Participants of one of these surveys were additionally characterized with respect to neurohormonal activation. As compared to men, women were characterized by a slightly higher LV ejection fraction (EF, Teichholz-Method, 65.4 +/- 0.3% vs. 63.4 +/- 0.3, P<0.01) and a markedly lower LV mass index (LVMI 81 +/- 1 g/m(2) vs. 96 +/- 1, P<0.01). As compared to men with normal LV function, those with LV dysfunction (EF below mean minus two standard deviations, S.D.) were characterized by significantly increased LV mass (LVMI +48%, P<0.01), plasma BNP (+373%, P<0.01) and ANP (+57%, P<0.01), while no significant changes were observed in women (LVMI +3%, BNP +48%, ANP +27%, all P=n.s). Only a small subgroup of women with severe LVD (EF below mean - 3 S.D.) was characterized by significantly increased LV mass (LVMI +23%, P<0.05 vs. control and LVD), however, this increase was less pronounced as compared to men with severe LVD (LVMI +46%, P<0.01 vs. control). Gender-specific differences between LV function and structure were also confirmed by multivariate analysis. While LVMI was independently and significantly correlated with EF in male subjects in addition to systolic blood pressure, age, and body mass index (all P<0.01), these parameters displaced EF as a predictor of LVMI in female subjects. CONCLUSIONS: Men with moderate or severe LV dysfunction are characterized by an increase in both LV mass and cardiac natriuretic peptide plasma concentrations. In contrast, LV mass and natriuretic peptide concentrations increase to a lesser extent and only with severe LV dysfunction in women. These observational data suggest gender-specific control of myocardial adaptations to hemodynamic overload and a more rapid induction of LV hypertrophy during myocardial dysfunction in male subjects.