A simple thermodynamic system model for the analysis and evaluation of possible SOFC system concepts with regard to reachable electric efficiency is presented. All reforming concepts, various available fuels and anode off‐gas recirculation are included in the model. Furthermore, the model allows the characterization of the reforming conditions necessary to reach the calculated and desired electric efficiencies by the use of two dimensionless energy flow ratios, which are introduced. It is presented how to quickly assess system concepts and identify system concepts that are particularly interesting due to a simple process, high electric efficiency, or preferably a combination of those. Within the experimental section, the model is used to support the system design process of a biogas‐driven SOFC system with partial oxidation as reforming concept, without anode off‐gas recirculation. Since adjustable operating parameters are input into the model, the parameters' influence on efficiency and reforming conditions can be analyzed. With the model real system effects are investigated making it possible to reach a maximum gross electric efficiency of 0.55 with the real designed system.

The automated high-volume production of lightweight and intelligent composite parts is one of the key technologies for the automotive industry. Modern concepts introduce “intelligent” parts by integrating sensor networks into the composite. These networks record different physical signals and can even work as active components. A popular application scenario is the permanent structural health monitoring. This paper presents a novel high-volume production technology that addresses the integration of large piezoceramic sensor and actor elements in glass fibre polyurethane composite parts using the Multi-Fibre-Injection (MFI) spraying technology. By directly integrating the piezo fibres, this technology combines sensor production and part production into one single step. First experiments showed that such piezoceramic sensors are functional. Other experiments demonstrated the successful integration of different electronic components and batteries into composite parts.

Objective The association between hypertension in pregnancy and future cardiovascular disease (CVD) increasingly is recognized. We aimed to assess the role of hypertension in pregnancy as an independent risk factor for hypertension, coronary heart disease (CHD), and stroke later in life. Methods Women who participated in the Phase 2 (2000–2004) Family Blood Pressure Program study (n = 4782) were categorized into women with no history of pregnancy lasting more than 6 months (n = 718), women with no history of hypertension in pregnancy (n = 3421), and women with a history of hypertension in at least one pregnancy (n = 643). We used Kaplan–Meier and Cox proportional hazard models to estimate and contrast the risks of subsequent diagnoses of hypertension, CHD, and stroke among the groups. Results Women with a history of hypertension in pregnancy, compared with those without such a history, were at increased risks for the subsequent diagnoses of hypertension (50% hypertensive at the age 53 vs. 60, P < 0.001), CHD (14% estimated event rate vs. 11%, P = 0.009), and stroke (12% estimated event rate vs. 5%, P < 0.001). The increased risk for subsequent hypertension remained significant after controlling for race, family history of CVD, smoking, dyslipidemia, and diabetes mellitus, with an adjusted hazard ratio of 1.88 [95% confidence interval (CI) 1.49–2.39, P < 0.001]. After controlling for traditional risk factors, including subsequent hypertension, the increased risk for stroke remained statistically significant (hazard ratio 2.10, 95% CI 1.19–3.71, P = 0.01), but not for CHD. Conclusion Hypertension in pregnancy may be an independent risk factor for subsequent diagnoses of hypertension and stroke.

Almost all our detailed knowledge about the endothelium is proximate knowledge about its structure, development, and functioning, and how its dysfunctions lead to disease. The other, evolutionary half of endothelial biology has been neglected. Some researchers are unfamiliar with the fundamental distinction between proximate and evolutionary questions, and methods for formulating and testing evolutionary hypotheses about the endothelium remain underappreciated. This chapter offers a brief overview of the distinction between evolutionary and proximate explanations, followed by an introduction to evolutionary medicine and its applications to the endothelium.

Pulse pressure, the difference between systolic and diastolic blood pressure, is an independent risk factor for cardiovascular disease. Increased pulse pressure reflects reduced compliance of arteries and is a marker of atherosclerosis. To locate genes that affect pulse pressure, a genome-wide linkage scan for quantitative trait loci influencing pulse pressure was performed using variance components methods as implemented in sequential oligogenic linkage analysis routines. The analysis sample included 10 798 participants in 3320 families who were recruited as part of the Family Blood Pressure Program and were phenotyped with an oscillometric blood pressure measurement device using a consistent protocol across centers. Pulse pressure was adjusted for the effects of sex, age, age2, age-by-sex interaction, age2-by-sex interaction, body mass index, and field center to remove sources of variation other than the genetic effects related to pulse pressure. Significant linkage was observed on chromosome 18 (logarithm of odds [LOD]=3.2) in a combined racial sample, chromosome 20 (LOD=4.4), and 17 (LOD=3.6) in Hispanics, chromosome 21 (LOD=4.3) in whites, chromosome 19 (LOD=3.1) in a combined sample of blacks and whites, and chromosome 7 (logarithm of odds [LOD]=3.1) in blacks from the GenNet Network. Our genome scan shows significant evidence for linkage for pulse pressure in multiple areas of the genome, supporting previous published linkage studies. The identification of these loci for pulse pressure and the apparent congruence with other blood pressure phenotypes provide increased support that these regions contain genes influencing blood pressure phenotypes.

A polymorphism (Gly460Trp) in the alpha-adducin gene coding sequence has been found in linkage disequilibrium with hypertension in two white populations, and the 460Trp variant is significantly associated with salt sensitivity. We examined the relationship of this polymorphism to blood pressure change over time. The present study is part of the NHLBI Family Blood Pressure Program, a large multicenter study of the genetic determinants of high blood pressure, and includes 88 white subjects who were studied at baseline and 6 years later. No subject received blood pressure medication at any time during the period. All subjects were genotyped by Taqman, and subjects were classified as Gly/Gly or Trp (Gly/Trp + Trp/Trp). Changes over time (Δ) was calculated as value at 6 years minus value at baseline. Urine Na was measured on an untimed spot collection and is expressed as mmol/gr creatinine. Data are expressed as mean ± SD. Significance was accepted at P < 0.05.

Hunt et al showed that a polymorphism in the angiotensinogen gene (AGT) is associated with the development of hypertension (Hunt et al. Hypertens 1998;32:393–401). The objective of this study was to analyze the relationship of the angiotensinogen M235T polymorphism on blood pressure change over time in normotensive subjects with a family history of hypertension. The present study is part of the NHLBI Family Blood Pressure Program, a large multicenter study of the genetic determinants of high blood pressure. The present analysis includes 84 white subjects that were studied at baseline and after 6 years follow-up. No subject received blood pressure medication at any time during the study. All subjects were genotyped for the angiotensinogen M235T polymorphism by Taqman, and subjects were classified as C/C, C/T and T/T. Data are expressed as mean ± SD. Differences (Δ) were calculated as value follow-up minus value baseline. Significance was accepted at P < 0.05. Gender distribution was not significantly different among the groups (Chi-Square = n.s.). Subjects with C/C had the greatest Δ DBP (see table). *P < 0.05 vs C/T, T/T *P < 0.05 vs C/T, T/T These observations were independent of changes in body mass index (BMI) or waist circumference. We are currently performing haplotype analysis of 10 additional SNPs of the AGT gene.

BACKGROUND:Dopamine receptor genes are candidates for hypertension susceptibility. Locally released dopamine increases renal sodium excretion, and defective renal dopamine receptor signaling has been shown to play a role in hypertension. Dopamine-4 receptors are expressed in juxtaglomerular and cortical collecting cells, where dopamine activation could alter sodium and water metabolism and affect blood pressure (BP). The dopamine-4 receptor (DRD4) gene has a 16 amino acid (48 base pairs [bp]) repeat polymorphism located in exon 3 where a G-protein binding area is encoded. The long allele (defined as at least one 7 to 10 repeat) has been associated with the personality trait Novelty Seeking and with substance abuse, but associations between dopamine-4 receptor polymorphisms and BP have not been reported.METHODS:We genotyped 479 female and 385 male subjects of white ethnicity at the DRD4 repeat polymorphism site and classified each subject as having either the long or short genotype.RESULTS:We found associations between the DRD4 long allele and increased systolic BP (P = .031), diastolic BP (P = .034), and a history of regular alcohol use (P = .008). Furthermore, for systolic BP (P = .009) and pulse pressure (P = .002), we found evidence for an interaction between dopamine-4 receptor alleles and age, indicating that the effects of dopamine-4 receptor variants on BP increase with age.CONCLUSION:In this white population, the long variant of the DRD4 gene is associated with a 3-mm Hg higher systolic and 2-mm Hg higher diastolic BP.

Genome-wide variance components linkage analysis was performed on 4 latent factors underlying metabolic syndrome derived from 10 risk factors. The latent factors represent obesity and insulin, blood pressure, lipids and insulin, and central obesity. The metabolic syndrome factor scores were derived in 4 ethnic groups recruited in 3 Networks of the Family Blood Pressure Program: GENOA (blacks, Hispanics, and whites), HyperGEN (blacks and whites), SAPPHIRe (Asians). Heritabilities of metabolic syndrome factors ranged from 66% for obesity and insulin to 11% for blood pressure factor. We observed higher heritabilities for obesity and insulin, and lipids and insulin, whereas those for blood pressure and central obesity were smaller. Linkage analysis detected two major quantitative trait loci. One of them linked to the obesity and insulin factor with a lod score of 3.94 ( P =0.00001, marker GATA11A06, D18S53, 41.24 cM) at marker positions linkage (lod 4.71, at 46.84 cM at 1-cM-apart distances linkage), located on chromosome 18p11.21 in GENOA black. The other linked to the blood pressure factor with a lod score of 3.22 ( P =0.000059, marker GATA49C09, D17S1290, 82 cM) at marker positions linkage (lod 3.56, at 84.63 cM for 1 cM apart distances linkage) located on chromosome 17q23.1 in Hispanics. These quantitative trait loci, together with 4 additional ones with lod scores >2.5, and 30 additional ones with lod score >1.7, offer hope for dissecting the genetic architecture of metabolic syndrome with beneficial implications for molecular diagnosis, prognosis, and in potential medical intervention.

Arterial stiffness (ArSt) differs between men and women, and we have also previously reported gender-related differences in regional ArSt that are independent of age, height and weight. The aim of this study was to examine the relationship of total body potassium (TBK), which is related to vascular function and blood pressure, to ArSt in men and women. Eighty-seven subjects (males n=31, females n=56, age 47±15 yrs) from the GenNet Study of the NHLBI Family Blood Pressure Program participated. A noninvasive transducer (DynaPulse200M) was used to determine blood pressure (SBP, DBP and MAP) and systemic (S) and brachial (B)ArSt: vascular compliance (SVC and BVC), resistance (SVR and BVR) and brachial compliance (BAC) and distensibility (BAD). TBK and fat mass (FM) were measured by bioelectrical impedance (BIA). Results are expressed as mean ± SEM with a level of significance of p < 0.05, using a two-tailed unpaired Student's t-test. Males were significantly taller (178±1.1 vs. 163±0.8 cms, p<.0001) and heavier (98±3.5 vs. 78±2.6 Kg, p<.0001) and had a higher DBP (82±1.5 vs. 76±1.2 mm Hg, p=.004) than females. There were no significant differences between males and females for age, SBP, MAP or heart rate. BIA and ArSt parameters are shown in table 1. After adjustments for height, weight and age, male-female differences in BAC, BAR and TBK remained significant. TBK was directly correlated with SVC (r=.469, p=.0001) and BAC (r=.788, p=.0001) and inversely correlated with SVR (r=−.292, p=.006) and BAR (r=−.683, p=.0001). TBK was not correlated with BAD. Similar trends were observed with FM. TBK correlates with both systemic and local ArSt measures in men and women. Male-female differences in TBK and brachial ArSt were independent of gender differences in height, weight and age. We conclude that TBK may contribute to regulation of ArSt and may help to explain gender-related differences in vascular function.

Low red blood cell K (RBCKi) is associated to higher blood pressure (BP), increased insulin resistance and is probably associated to adducin which is involved in regulation of actin cytoskeleton and ion transport across the cell membrane.The present study is part of the NHLBI Family Blood Pressure Program, a large multicenter study of the genetic determinants of high BP. The present analysis includes 221 subjects. A subgroup of 49 subjects were genotyped for the alpha-adducin gene. Venous blood was drawn in fasting and centrifuged immediately, plasma and RBC were separated and buffy coat was discarded. Urinary Na/K ratio was measured in a spot and overnight collections. All subjects were untreated and on ad lib diet. The genotyping was performed by Taqman, and subjects were classified as Gly/Gly or Trp (Gly/Trp + Trp/Trp). RBCKi and urinary Na and K were assayed by flame photometry. Subjects were classified as low or high RBCKi by mixture analysis. Data are expressed as mean ± SEM. Significance was accepted at P < 0.05.All subjects were not receiving any medication that could alter the K homeostasis. Subjects with low RBCKi had higher DBP (P = 0.002) and SBP (P = 0.004) than subjects with high RBCKi independently of age, height, weight, NA/K ratio (spot and overnight) and urinary Na and K excretion (spot and overnight) corrected by urinary creatinine. From a total of 221 subjects, there were 6 subjects with diabetes mellitus, all of them with low RBCKi (chi square = 8.42, P = 0.003). Subjects with the Gly allele (n =24) had significantly lower RBCKi than subjects with the Trp allele (n=25; 83 ± 1 vs. 86 ± 1 mmol/L cell, P <0.05), however there were no differences in SBP and DBP. This study shows that subjects with low RBCKi have higher BP and greater risk of having diabetes mellitus than subjects with high RBCKi. The measurement of RBCKi could be a marker for membrane K alteration occurring in other cells although its relationship with the Gly allele is not well understood. See Table 1.

Background. A tendency to experience negative affect, as measured by the neuroticism component of the Neuroticism, Extraversion, and Openness Personality Inventory (NEO-PI), is a trait marker for major depression. Epidemiologic studies indicate a strong genetic component, but to date few specific genetic variants have been definitively implicated. A serotonin transporter promoter polymorphism (5-HTTLPR) has been extensively studied in neuroticism and several psychiatric disorders, with inconclusive results. A GABA(A) receptor alpha6 subunit variant (Pro385Ser) has been associated with alcohol-related traits but has not been studied in neuroticism or depression.Methods. A total of 384 subjects who completed the NEO-PI were genotyped at 5-HTTLPR and Pro385Ser. Associations between polymorphisms and both alcohol use and personality domains were tested.Results: The 5-HTTLPR short allele (p = .008) and Pro385Ser Pro allele (p = .003) are associated with higher neuroticism scores. The 5-HTTLPR long allele (p = .006), but not Pro385Ser, is also associated with an increased presence of alcohol use. In addition, there is a nonsignificant suggestion of an interaction: the effect of 5-HTTLPR on neuroticism might be dependent on the Pro385Ser genotype.Conclusions: These findings support a role for the serotonin transporter and GABA(A) alpha6 subunit in depression-related traits.

Potassium (K) depletion has a pathogenetic role in hypertension and stroke and its possible association with AS has not been described. The aim of this study is to determine whether TBK is associated with AS. The present study is part of the NHLBI Family Blood Pressure Program, a large multicenter study of the genetic determinants of high BP. The present analysis includes 87 subjects. Noninvasive transducer (DynaPulse200M) was used to determine SBP, DBP and MAP; systemic vascular compliance (SVC) and resistance (SVR); and brachial compliance (BAC), distensibility (BAD) and resistance (BAR). TBK, fat mass (FM), and body cell mass (BCM) were obtained by bioelectrical impedance analysis. SAS was used for the analysis. Results are expressed as mean ± SEM, level of significance of P < 0.05. Mean values were compared using two tailed unpaired Student's t-test. Males had higher height (178 ± 1 vs 163 ± 1 cm P < 0.001), weight (98 ± 4 vs 78 ± 3 Kg, P<.0001) and DBP (82 ± 2 vs 76 ± 1 mm Hg P = 0.04 than females. Males had significantly higher SVC, BAC, TBK and BCM, and lower BAR and FM than females. After adjusting for confounding factors, BAC, BAR and TBK remains significant. TBK and BCM shown direct correlation with SVC (r = 0.5 P = 0.0001, r = 0.5 P = 0.0001) and BAC (r= 0.8 P =.0001, r = 0.8 P = 0.0001), and inverse correlation with SVR (r = − 0.3 P= 0.006, r = − 0.3 P= 0.003) and BAR (r = −0.7 P = 0.0001, r = − 0.7 P = 0.0001). A similar trend was observed with FM. No correlation was observed with BAD. There were no significant differences age, SBP (136 ± 3 vs 133 ± 2 mm Hg), MAP (100 ± 2 vs 96 ± 1 mm Hg) and heart rate. This is the first study showing a relationship between AS and TBK. Knowing the importance of K in arterial tone regulation and its protective effect against free radicals formation, vascular smooth muscle proliferation and arterial thrombosis, it is plausible to propose that K modulates AS and explains gender differences in AS. (See Table)

Am J Hypertens (2004) 17, 197A–197A; doi: 10.1016/j.amjhyper.2004.03.520

Am J Hypertens (2004) 17, 09A–09A; doi: 10.1016/j.amjhyper.2004.03.017

Chromosome 2 has been consistently identified as a genomic region with genetic linkage evidence suggesting that one or more loci contributes to blood pressure and hypertension status. As with all complex disease traits, following-up linkage evidence to identify the underlying susceptibility gene(s) is an arduous yet biologically and clinically important task. Using combined positional candidate gene methods, the Family Blood Pressure Program (FBPP) has concentrated efforts in narrowing a large region of chromosome 2, demonstrating evidence for linkage in several populations, and identifying underlying candidate hypertension susceptibility gene(s). Initial informatics efforts identified the boundaries of the region and the known genes within it. A total of 82 polymorphic sites in 8 genes were genotyped in a large hypothesis-generating sample consisting of 1640 African Americans, 1339 whites, and 1616 Mexican Americans. After resampling-based false discovery adjustment, SLC4A5 , a sodium bicarbonate transporter, was identified as a primary candidate gene for hypertension. Polymorphisms in SLC4A5 were subsequently genotyped and analyzed for validation in two other subcomponents of the FBPP, each contributing African Americans (N=461; N=778) and whites (N=550; N=967). Again, single nucleotide polymorphisms within this gene were significantly associated with blood pressure levels and hypertension status. Although not identifying a single causal gene variant that is significantly associated with blood pressure levels and hypertension status across all samples, the results further implicate SLC4A5 as a candidate hypertension susceptibility gene. Moreover, the present study validates previous evidence for one or more genes on chromosome 2 that influence hypertension-related phenotypes in the population-at-large.