12 resultados para in-cylinder pressure

em DigitalCommons@The Texas Medical Center


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The Renin-Angiotensin system (RAS) regulates blood pressure through its effects on vascular tone, renal hemodynamics, and renal sodium and fluid balance. The genes encoding the four major components of the RAS, angiotensinogen, renin, angiotensin I-converting enzyme (ACE), and angiotensin II receptor type 1 (AT1), have been investigated as candidate genes in the pathogenesis of essential hypertension. However, studies have primarily focused on small samples of diseased individuals, and, therefore, have provided little information about the determinants of interindividual variation in blood pressure (BP) in the general population.^ Using data from a large population-based sample from Rochester, MN, I have evaluated the contribution of variation in the region of the RAS genes to interindividual variation in systolic, diastolic, and mean arterial pressure in the population-at-large. Marker genotype data from four polymorphisms located within or very near these genes were first collected on 3,974 individuals from 583 randomly ascertained three-generation pedigrees. Haseman-Elston regression and variance component methods of linkage analysis were then carried out to estimate the proportion of interindividual variance in BP attributable to the effects of variation at these four measured loci.^ A significant effect of the ACE locus on interindividual variation in mean arterial pressure (MAP) was detected in a sample of siblings belonging to the youngest generation. After allowing for measured covariates, this effect accounted for 15-25% of the interindividual variance in MAP, and was even greater in a subset with a positive family history of hypertension. When gender-specific analyses were carried out, this effect was significant in males but not in females. Extended pedigree analyses also provided evidence for an effect of the ACE locus on interindividual variation in MAP, but no difference between males and females was observed. Circumstantial evidence suggests that the ACE gene itself may be responsible for the observed effects on BP, although the possibility that other genes in the region may be at play cannot be excluded.^ No definitive evidence for an effect of the renin, angiotensinogen, or AT1 loci on interindividual variation in BP was obtained in this study, suggesting that the impact of these genes on BP may not be great in the Caucasian population-at-large. However, this does not preclude a larger effect of these genes in some subsets of individuals, especially among those with clinically manifest hypertension or coronary heart disease, or in other populations. ^

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Hypertension (HT) is mediated by the interaction of many genetic and environmental factors. Previous genome-wide linkage analysis studies have found many loci that show linkage to HT or blood pressure (BP) regulation, but the results were generally inconsistent. Gene by environment interaction is among the reasons that potentially explain these inconsistencies between studies. Here we investigate influences of gene by smoking (GxS) interaction on HT and BP in European American (EA), African American (AA) and Mexican American (MA) families from the GENOA study. A variance component-based method was utilized to perform genome-wide linkage analysis of systolic blood pressure (SBP), diastolic blood pressure (DBP), and HT status, as well as bivariate analysis for SBP and DBP for smokers, non-smokers, and combined groups. The most significant results were found for SBP in MA. The strongest signal was for chromosome 17q24 (LOD = 4.2), increased to (LOD = 4.7) in bivariate analysis but there was no evidence of GxS interaction at this locus (p = 0.48). Two signals were identified only in one group: on chromosome 15q26.2 (LOD = 3.37) in non-smokers and chromosome 7q21.11 (LOD = 1.4) in smokers, both of which had strong evidence for GxS interaction (p = 0.00039 and 0.009 respectively). There were also two other signals, one on chromosome 20q12 (LOD = 2.45) in smokers, which became much higher in the combined sample (LOD = 3.53), and one on chromosome 6p22.2 (LOD = 2.06) in non-smokers. Neither peak had very strong evidence for GxS interaction (p = 0.08 and 0.06 respectively). A fine mapping association study was performed using 200 SNPs in 30 genes located under the linkage signals on chromosomes 15 and 17. Under the chromosome 15 peak, the association analysis identified 6 SNPs accounting for a 7 mmHg increase in SBP in MA non-smokers. For the chromosome 17 linkage peak, the association analysis identified 3 SNPs accounting for a 6 mmHg increase in SBP in MA. However, none of these SNPs was significant after correcting for multiple testing, and accounting for them in the linkage analysis produced very small reductions in the linkage signal. ^ The linkage analysis of BP traits considering the smoking status produced very interesting signals for SBP in the MA population. The fine mapping association analysis gave some insight into the contribution of some SNPs to two of the identified signals, but since these SNPs did not remain significant after multiple testing correction and did not explain the linkage peaks, more work is needed to confirm these exploratory results and identify the culprit variations under these linkage peaks. ^

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Purpose. The central concepts in pressure ulcer risk are exposure to external pressure caused by inactivity and tissue tolerance to pressure, a factor closely related to blood flow. Inactivity measures are effective in predicting pressure ulcer risk. The purpose of the study is to evaluate whether a physiological measure of skin blood flow improves pressure ulcer risk prediction. Skin temperature regularity and self-similarity, as proxy measures of blood flow, and not previously described, may be undefined pressure ulcer risk factors. The specific aims were to determine whether a sample of nursing facility residents at high risk of pressure ulcers classified using the Braden Scale for Pressure Sore Risk© differ from a sample of low risk residents according to (1) exposure to external pressure as measured by resident activity, (2) tissue tolerance to external pressure as measured by skin temperature, and (3) skin temperature fluctuations and recovery in response to a commonly occurring stressor, bathing and additionally whether (4) scores on the Braden Scale mobility subscale score are related to entropy and the spectral exponent. ^ Methods. A two group observational time series design was used to describe activity and skin temperature regularity and self-similarity, calculating entropy and the spectral exponent using detrended fluctuation analysis respectively. Twenty nursing facility residents wore activity and skin temperature monitors for one week. One bathing episode was observed as a commonly occurring stressor for skin temperature.^ Results. Skin temperature multiscale entropy (MSE), F(1, 17) = 5.55, p = .031, the skin temperature spectral exponent, F(1, 17) = 6.19, p = .023, and the activity mean MSE, F(1, 18) = 4.52, p = .048 differentiated the risk groups. The change in skin temperature entropy during bathing was significant, t(16) = 2.55, p = .021, (95% CI, .04-.40). Multiscale entropy for skin temperature was lowest in those who developed pressure ulcers, F(1, 18) = 35.14, p < .001.^ Conclusions. This study supports the tissue tolerance component of the Braden and Bergstrom conceptual framework and shows differences in skin temperature multiscale entropy between pressure ulcer risk categories, pressure ulcer outcome, and during a commonly occurring stressor. ^

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Objective. Loud noises in neonatal intensive care units (NICUs) may impede growth and development for extremely low birthweight (ELBW, < 1000 grams) newborns. The objective of this study was to measure the association between NICU sound levels and ELBW neonates' arterial blood pressure to determine whether these newborns experience noise-induced stress. ^ Methods. Noise and arterial blood pressure recordings were collected for 9 ELBW neonates during the first week of life. Sound levels were measured inside the incubator, and each subject's arterial blood pressures were simultaneously recorded for 15 minutes (at 1 sec intervals). Time series cross-correlation functions were calculated for NICU noise and mean arterial blood pressure (MABP) recordings for each subject. The grand mean noise-MABP cross-correlation was calculated for all subjects and for lower and higher birthweight groups for comparison. ^ Results. The grand mean noise-MABP cross-correlation for all subjects was mostly negative (through 300 sec lag time) and nearly reached significance at the 95% level at 111 sec lag (mean r = -0.062). Lower birthweight newborns (454-709 g) experienced significant decreases in blood pressure with increasing NICU noise after 145 sec lag (peak r = -0.074). Higher birthweight newborns had an immediate negative correlation with NICU sound levels (at 3 sec lag, r = -0.071), but arterial blood pressures increased to a positive correlation with noise levels at 197 sec lag (r = 0.075). ^ Conclusions. ELBW newborns' arterial blood pressure was influenced by NICU noise levels during the first week of life. Lower birthweight newborns may have experienced an orienting reflex to NICU sounds. Higher birthweight newborns experienced an immediate orienting reflex to increasing sound levels, but arterial blood pressure increased approximately 3 minutes after increases in noise levels. Increases in arterial blood pressure following increased NICU sound levels may result from a stress response to noise. ^

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The relationship between degree of diastolic blood pressure (DBP) reduction and mortality was examined among hypertensives, ages 30-69, in the Hypertension Detection and Follow-up Program (HDFP). The HDFP was a multi-center community-based trial, which followed 10,940 hypertensive participants for five years. One-year survival was required for inclusion in this investigation since the one-year annual visit was the first occasion where change in blood pressure could be measured on all participants. During the subsequent four years of follow-up on 10,052 participants, 568 deaths occurred. For levels of change in DBP and for categories of variables related to mortality, the crude mortality rate was calculated. Time-dependent life tables were also calculated so as to utilize available blood pressure data over time. In addition, the Cox life table regression model, extended to take into account both time-constant and time-dependent covariates, was used to examine the relationship change in blood pressure over time and mortality.^ The results of the time-dependent life table and time-dependent Cox life table regression analyses supported the existence of a quadratic function which modeled the relationship between DBP reduction and mortality, even after adjusting for other risk factors. The minimum mortality hazard ratio, based on a particular model, occurred at a DBP reduction of 22.6 mm Hg (standard error = 10.6) in the whole population and 8.5 mm Hg (standard error = 4.6) in the baseline DBP stratum 90-104. After this reduction, there was a small increase in the risk of death. There was not evidence of the quadratic function after fitting the same model using systolic blood pressure. Methodologic issues involved in studying a particular degree of blood pressure reduction were considered. The confidence interval around the change corresponding to the minimum hazard ratio was wide and the obtained blood pressure level should not be interpreted as a goal for treatment. Blood pressure reduction was attributed, not only to pharmacologic therapy, but also to regression to the mean, and to other unknown factors unrelated to treatment. Therefore, the surprising results of this study do not provide direct implications for treatment, but strongly suggest replication in other populations. ^

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The determinants of change in blood pressure during childhood and adolescence were studied in a cohort of U.S. national probability sample of 2146 children examined on two occasions during the Health Examination Survey. Significant negative correlations between the initial level and the subsequent changes in blood pressure were observed. The multiple regression analyses showed that the major determinants of systolic blood pressure (SBP) change were change in weight, baseline SBP, and baseline upper arm girth. Race, time interval between examinations, baseline age, and height change were also significant determinants in SBP change. For the change in diastolic blood pressure (DBP), baseline DBP, baseline weight, and weight change were the major determinants. Baseline SBP, time interval and race were also significant determinants. Sexual maturation variables were also considered in the subgroup analysis for girls. Weight change was the most important predictor of the change in SBP for the group of girls who were still in the pre-menarchal or pre-breast maturation status at the time of the follow-up examination, and who had started to menstruate or to develop breast maturation at sometime between the two examinations. Baseline triceps skinfold thickness or initial SBP were more important variables than weight change for the group of girls who had already experienced menarche or breast maturation at the time of the initial survey. For the total group, pubic hair maturation was found to be a significant predictor of SBP change at the 5% significance level. The importance of weight change and baseline weight for the changes in blood pressure warrants further study. ^

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Complex molecular events underlie vertebrate eye development and disease. The eye is composed of two major tissue types: the anterior and posterior segments. During development, the retinal progenitor cells differentiate into six neuronal and one non-neuronal cell types. These cell types later organize into the distinct laminar structure of the mature retina which occupies the posterior segment. In the developed anterior segment, both the ciliary body and trabecular meshwork regulate intraocular pressure created by the aqueous humor. The disruption in intraocular pressure can lead to a blinding condition called glaucoma. To characterize molecular mechanisms governing retinal development and glaucoma, two separate mouse knockout lines carrying mutations in math5 and myocilin were subjected to a series of in vivo analyses. ^ Math5 is a murine homologue of Drosophila atonal , a bHLH proneural gene essential for the formation of photoreceptor cells. The expression of math5 coincides with the onset of retinal ganglion cell differentiation. The targeted deletion of mouse math5 revealed that a null mutation inhibits the formation of a majority of the retinal ganglion cells. The mutation also interferes with the normal development of other retinal cell types such as amacrine, bipolar and photoreceptor cells. These results suggest that math5 is a proneural gene responsible for differentiation of retinal ganglion cells and may also have a role in normal development of other neuronal cell types within the retina. ^ Myocilin has two unique protein coding regions bearing homology to non-muscle myosin of Dictyostelium discoideum and to olfactomedin, an extracellular matrix molecule first described in the olfactory epithelium of the bullfrog. Recently, autosomal dominant forms of myocilin mutations have been found in individuals with primary open-angle glaucoma. The genetic linkage to glaucoma suggests a role of myocilin in normal intraocular pressure and ocular function. However, the analysis of mice heterozygous and homozygous for a targeted null mutation in myocilin indicates that it is dispensable for normal intraocular pressure or ocular function. Additionally, the lack of a discernable phenotype in both heterozygous and null mice suggests that haploinsufficiency is not a critical mechanism for MYOC-associated glaucoma in humans. Instead, disease-causing mutations likely act by gain of function. ^ In summary, these studies provide novel insights into the embryonic development of the vertebrate retina, and also begin to uncover the molecular mechanisms responsible for the pathogenesis of glaucoma. ^

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Environmental tobacco smoke (ETS) is a well established health hazard, being causally associated to lung cancer and cardiovascular disease. ETS regulations have been developed worldwide to reduce or eliminate exposure in most public places. Restaurants and bars constitute an exception. Restaurants and bar workers experience the highest ETS exposure levels across several occupations, with correspondingly increased health risks. In Mexico, previous exposure assessment in restaurants and bars showed concentrations in bars and restaurants to be the highest across different public and workplaces. Recently, Mexico developed at the federal level the General Law for Tobacco Control restricting indoors smoking to separated areas. AT the local level Mexico City developed the Law for the Protection of Non-smokers Health, completely banning smoking in restaurants and bars. Studies to assess ETS exposure in restaurants and bars, along with potential health effects were required to evaluate the impact of these legislative changes and to set a baseline measurement for future evaluations.^ A large cross-sectional study conducted in restaurants and bars from four Mexican cities was conducted from July to October 2008, to evaluate the following aims: Aim 1) Explore the potential impact of the Mexico City ban on ETS concentrations through comparison of Mexico City with other cities. Aim 2). Explore the association between ETS exposure, respiratory function indicators and respiratory symptoms. Aim 3). Explore the association between ETS exposure and blood pressure and heart rate.^ Three cities with no smoking ban were selected: Colima (11.5% smoking prevalence), Cuernavaca (21.5% smoking prevalence) and Toluca (27.8% smoking prevalence). Mexico City (27.9% smoking prevalence), the only city with a ban at the time of the study, was also selected. Restaurants and bars were randomly selected from municipal records. A goal of 26 restaurants and 26 bars per city was set, 50% of them under 100 m2. Each establishment was visited during the highest occupancy shift, and managers and workers answered to a questionnaire. Vapor-phase nicotine was measured using passive monitors, that were activated at the beginning and deactivated at the end of the shift. Also, workers participated at the beginning and end of the shift in a short physical evaluation, comprising the measurement of Forced Expiratory Volume in the first second (FEV1) and Peak Expiratory Flow (PEF), as well as blood pressure and heart rate.^ A total of 371 establishments were invited, 219 agreed to participate for a 60.1% participation rate. In them, 828 workers were invited, 633 agreed to participate for a 76% participation rate. Mexico City had at least 4 times less nicotine compared to any of the other cities. Differences between Mexico City and other cities were not explained by establishment characteristics, such as ventilation or air extraction. However, differences between cities disappeared when ban mechanisms, such as policy towards costumer's smoking, were considered in the models. An association between ETS exposure and respiratory symptoms (cough OR=1.27, 95%CI=1.04, 1.55) and respiratory illness (asthma OR=1.97, 95%CI=1.20, 3.24; respiratory illness OR=1.79, 95%CI=1.10, 2.94) was observed. No association between ETS and phlegm, wheezing or respiratory infections was observed. No association between ETS and any of the spirometric indicators was observed. An association between ETS exposure and increased systolic and diastolic blood pressure at the end of the shift was observed among non-smokers (systolic blood pressure beta=1.51, 95%CI=0.44, 2.58; diastolic blood pressure beta=1.50, 95%CI=0.72, 2.28). The opposite effect was observed in heavy smokers, were increased ETS exposure was associated with lower blood pressure at the end of the shift (systolic blood pressure beta=1.90, 95%CI=-3.57, -0.23; diastolic blood pressure beta=-1.46, 95%CI=-2.72, -0.02). No association in light smokers was observed. No association for heart rate was observed. ^ Results from this dissertation suggest Mexico City's smoking ban has had a larger impact on ETS exposure. Ventilation or air extraction, mechanisms of ETS control suggested frequently by tobacco companies to avoid smoking bans were not associated with ETS exposure. This dissertation suggests ETS exposure could be linked to changes in blood pressure and to increased respiratory symptoms. Evidence derived from this dissertation points to the potential negative health effects of ETS exposure in restaurants and bars, and provides support for the development of total smoking bans in this economic sector. ^

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In The Woodlands, Texas, 346 students in grades 9-12, age 14-18 participated in a screening examination for cardiovascular risk factors. The relationships between blood pressure with Type-A-behavior and its components were evaluated. Type-A-behavior was measured using the Hunter-Wolf Type-A-behavior scale.^ The following results refer to the current 24-item version of the Hunter-Wolf Type-A-behavior scale and subscales derived in the Bogalusa study which thereafter were applied to The Woodlands population.^ No significant differences in blood pressure were observed among children in the highest vs. lowest quintile of the Type-A-behavior score or subscales scores. The correlation coefficients of blood pressure with the Type-A-behavior and its components were small and non-significant in both boys and girls. Multiple regression analyses conducted by sex, showed that after adjustment for age, weight and height, the addition of the total Type-A-behavior score or subscale scores did not increase significantly the amount of the variability explained for any of the blood pressure components.^ These analyses were repeated with results from the original 17-item version of the Hunter-Wolf Type-A-behavior scale and subscales derived in Bogalusa. Similarly, no relationship was observed between the 17-item Type-A-behavior score or subscales scores with blood pressure levels in The Woodlands population.^ Finally, it was important to determine whether subscales derived within The Woodlands population would differ from those described in Bogalusa and would relate differently to blood pressure among students in The Woodlands. The corresponding analyses showed that the subscales derived from the two studies were different, but in fact neither set of subscales was importantly related with blood pressure in The Woodlands population.^ The results of this study are largely consistent with those obtained by Hunter and Wolf in Bogalusa, who among the white population found only the factor "Eagerness-Energy" to be associated with fourth phase diastolic blood pressure among girls. Even this relationship which they observed was weak and inconsistent across sex-race groups and blood pressure components. This study does not support even this positive finding. In conclusion, evidence indicates that blood pressure is not associated with Type-A-behavior or its components as measured by the Hunter-Wolf Type-A-behavior scale among white adolescents. ^

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This project is based on secondary analyses of data collected in Starr County, Texas from 1981 till 1991 to determine the prevalence, incidence and risk factors for macular edema in Hispanics with non-insulin-dependent diabetes in Starr County, Texas. Two studies were conducted. The first study examined the prevalence of macular edema in this population. Of the 310 diabetics that were included in the study 22 had macular edema. Of these 22 individuals 9 had clinically significant macular edema. Fasting blood glucose was found to be significantly associated with macular edema. For each 10 mg/dl increase in fasting blood glucose there was a 1.07 probability of an increase in the risk of having macular edema. Individuals with fasting blood glucose $\ge$200 mg/dl were found to be more than three times at risk of having macular edema compared to those with fasting blood glucose $<$200 mg/dl.^ In the second study the incidence and the risk factors that could cause macular edema in this Hispanic population were examined. 240 Hispanics with non-insulin-dependent diabetes mellitus and without macular edema were followed for 1223 person-years. During the follow-up period 27 individuals developed macular edema (2.21/100 person-years). High fasting blood glucose and glycosylated hemoglobin were found to be strong and independent risk factors for macular edema. Participants taking insulin were 3.9 times more at risk of developing macular edema compared to those not taking insulin. Systolic blood pressure was significantly related to macular edema, where each 10 mmHg increase in systolic blood pressure was associated with a 1.3 increase in the risk of macular edema.^ In summary, this study suggests that hyperglycemia is the main underlying factor for retinal pathological changes in this diabetic population, and that macular edema probably is not the result of sudden change in the blood glucose level. It also determined that changes in blood pressure, particularly systolic blood pressure, could trigger the development of macular edema.^ Based on the prevalence reported in this study, it is estimated that 35,500 Hispanic diabetics in the US have macular edema. This imposes a major public health challenge particularly in areas with high concentration of Mexican Americans. It also highlights the importance of public health measures directed to Mexican Americans such as health education, improved access to medical care, and periodic and careful ophthalmologic examination by ophthalmologists knowledgeable and experienced in the management of diabetic macular edema. ^

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Cardiovascular disease (CVD) is the single greatest cause of death in the United States, accounting for nearly 2400 deaths each day. It is estimated that 79.4 million American adults have some form of the disease, and CVD mortality rates are greater than those of cancer, chronic lower respiratory diseases, accidents and diabetes mellitus combined. Psychosocial stress is a nontraditional risk factor for CVD, and can contribute to the clustering of traditional risk factors as well as to vascular manifestations of the disease. The Transcendental Meditation (TM) technique has been researched as a cost effective intervention aimed at decreasing psychosocial stress. This literature review attempts to analyze randomized controlled clinical trials of TM on cardiovascular disease outcomes. Eleven studies met inclusion criteria and are described below, with statistically significant positive outcomes observed in each study. Studies are grouped by primary outcome reported in the categories of cardiovascular function, blood pressure, and exercise tolerance. The TM intervention significantly decreased insulin resistance, heart rate variability, and carotid intima media thickness and improved exercise tolerance compared to control groups. Seven studies also reported significant decreases in blood pressure among hypertensive and normotensive subjects. Five studies focused solely on African American subjects, a population that has disproportionately higher rates of CVD and hypertension, and found significant improvements in CVD outcomes. Further research is recommended to establish the efficacy of TM on CVD outcomes. Future trials should include larger sample populations, wider ethnic distributions of subjects, and longer follow-up to ascertain the impact of this particular stress reduction technique on cardiovascular disease.^

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The pattern of change in cardiovascular risk factors, blood pressure (SBP and DBP) and plasma total cholesterol (TC), over time, their tracking and their relation to anthropometric measurements during the first year of life were investigated. Also, the effect of breast feeding on TC and the relationship of blood pressure measurements and family history of CVD risk factors were examined. One hundred five newborn term, healthy infants who were seen at a pediatric clinic in The Woodlands, Texas were followed longitudinally from 2 weeks to 1 year of age. TC, blood pressure, weight and length of the infants were measured at age 2 weeks, and again at 2, 4, 6, 9 and 12 months. In addition, family history, maternal and paternal, of CVD risk factors was obtained. Data analyses included only 40 infants who completed one year of follow up.^ At 2 weeks of age, the median value for TC was 23 mg/dl higher for females than for males. This difference disappeared as infants got older. For males, most of the increase in TC median levels, from 114 to 137 mg/dl, occurred between the ages of 2 weeks and 2 months, whereas for the female group, TC levels increased moderately, about 10 mg/dl, between 9 and 12 months of age. Tracking of TC was examined by using Spearman's correlation analysis. There were strong correlations between measurements taken as early as 2 weeks of age with later measurements. These correlations were stronger and more significant for males than for females (for males, r varied between 0.51 to 0.70, whereas for females, r varied between 0.11 to 0.70). The association of body measurements with TC is no more than modest and is closer for female infants than for male infants. Analysis, also, showed that infants who received breast milk had a TC mean value 47 mg/dl higher than that for infants who received formula milk only during the period of breast feeding and this difference disappeared by age 12 months.^ In both genders, most of the increase in blood pressure (about 10-15 mmHg in both SBP and DBP) occurred during the first 4 months of life. Most of the increase for male infants occurred during the first 2 months of life, while for females, the increase in SBP and DBP was between the age of 2 and 4 months. Neither SBP nor DBP track well during the first year of life and most of the correlations between measurements at different ages were not significant for either gender. The cross-sectional relationship of blood pressure measurements and selected body measurements was assessed. For females, only at age of 12 months did DBP have positive and significant correlations with weight, length and Quetelet index (r = 0.57, 0.60 and 0.57, respectively). There were no significant correlations between blood pressure and body measurements for males. Finally, analysis showed that maternal history of CV risk factors was significantly related to SBP in the female infant group, but not for males. For DBP, neither maternal nor paternal history was related. ^