Sexual orientation and its impact on sexual behaviour of young people aged 15-29: a cross-sectional study.

AIMS: The aim of this study was to determine whether there was a direct relation between sexual orientation and sexual practices involving penetration; to analyse whether condom use in the first sexual relation was conditioned by sexual orientation; to verify whether consistent condom use in sexual relations was determined by sexual orientation. BACKGROUND: Recent research suggests that sexual orientation (i.e. heterosexuality, homosexuality or bisexuality) is a determining factor in high-risk sexual behaviour. DESIGN: A cross-sectional study with purposive sampling. METHODS: Data were collected between March 2013-April 2014 from 900 participants (524 males and 376 females). All participants were 15-29 years of age. Their mean age was 20·93 years. The participants were given a socio-demographic survey as well as a psychometric test on high-risk sexual behaviour, which had been used in previous studies. RESULTS: There were no statistically significant differences in relation to sexual orientation and sexual practices involving penetration either in the general model for both sexes or in the models for men and women. It was also found that sexual orientation did not significantly affect condom use in the first sexual relation. Furthermore, consistent condom use had a protector effect in the general model for homosexuals and bisexuals. In the model for men, this was also true for homosexuals and in the model for women, this was the case for bisexuals. CONCLUSION: Condom use in the first sexual relation was similar in all sexual orientations. However, the sexual orientation of the subject was found to be a determining factor in consistent condom use.

Nitration of Hsp90 on Tyrosine 33 Regulates Mitochondrial Metabolism.

Peroxynitrite production and tyrosine nitration are present in several pathological conditions, including neurodegeneration, stroke, aging, and cancer. Nitration of the pro-survival chaperone heat shock protein 90 (Hsp90) in position 33 and 56 induces motor neuron death through a toxic gain-of-function. Here we show that nitrated Hsp90 regulates mitochondrial metabolism independently of the induction of cell death. In PC12 cells, a small fraction of nitrated Hsp90 was located on the mitochondrial outer membrane and down-regulated mitochondrial membrane potential, oxygen consumption, and ATP production. Neither endogenous Hsp90 present in the homogenate nor unmodified and fully active recombinant Hsp90 was able to compete with the nitrated protein for the binding to mitochondria. Moreover, endogenous or recombinant Hsp90 did not prevent the decrease in mitochondrial activity but supported nitrated Hsp90 mitochondrial gain-of-function. Nitrotyrosine in position 33, but not in any of the other four tyrosine residues prone to nitration in Hsp90, was sufficient to down-regulate mitochondrial activity. Thus, in addition to induction of cell death, nitrated Hsp90 can also regulate mitochondrial metabolism, suggesting that depending on the cell type, distinct Hsp90 nitration states regulate different aspects of cellular metabolism. This regulation of mitochondrial homeostasis by nitrated Hsp90 could be of particular relevance in cancer cells.

Tyrosine nitration as mediator of cell death.

Nitrotyrosine is used as a marker for the production of peroxynitrite and other reactive nitrogen species. For over 20 years the presence of nitrotyrosine was associated with cell death in multiple pathologies. Filling the gap between correlation and causality has proven to be a difficult task. Here, we discuss the evidence supporting tyrosine nitration as a specific posttranslational modification participating in the induction of cell death signaling pathways.

Gender-based differences in the high-risk sexual behaviours of young people aged 15-29 in Melilla (Spain): a cross-sectional study.

BACKGROUND: Research confirms the existence of gender-based differences regarding the high-risk sexual behaviour (non-use of condoms and casual partners) of young men and women. The objectives were to provide evidence for this association; to analyse the reasons why both sexes have sexual relations with casual partners and to ascertain the motives for condom use or non-use during casual sex. METHODS: A cross-sectional study was performed on a sample of 900 participants, 524 males and 376 females. All participants were 15-29 (20.93 ± 4.071) years of age and came from four different centres (a university, two secondary schools, and a military base) in Melilla (Spain). The participants were given a socio-demographic survey as well as a psychometric text on high-risk sexual behaviour. RESULTS: The results found gender-based significant differences for sexual relations with penetration (p = 0.001), number of sexual partners (p = 0.001), and sexual relations with casual partners (p = 0.001). In all of these variables, male participants had higher percentages than female participants. Reasons for having casual sexual relations were also different for men and women, differences were found for the items, opportunity (p = 0.001), interest in knowing the other person (p = 0.015), physical excitement (p = 0.056) and drug consumption (p = 0.059). Regarding the reasons for consistent condom use with casual partners, there were differences for the item, my demand of a condom (p = 0.002). For the non-use of condoms with casual partners, differences were found for the items, I do not like to use condoms (p = 0.001) and condoms lessen sensitivity and reduce pleasure (p = 0.009). CONCLUSIONS: Men and women were found to have different high-risk sexual behaviours and practices. Of the motives for having sexual relations with casual partners, male participants considered opportunity and interest in knowing the other person to be more important than the female participants. Regarding condom use, the female participants' demand to use a condom was a significant gender-based difference. In contrast to the young women, the male participants mostly justified not using a condom because it lessened sensitivity and reduced pleasure.

Mitochondrial network dynamics in pulmonary disease: Bridging the gap between inflammation, oxidative stress, and bioenergetics.

Once thought of in terms of bioenergetics, mitochondria are now widely accepted as both the orchestrator of cellular health and the gatekeeper of cell death. The pulmonary disease field has performed extensive efforts to explore the role of mitochondria in regulating inflammation, cellular metabolism, apoptosis, and oxidative stress. However, a critical component of these processes needs to be more studied: mitochondrial network dynamics. Mitochondria morphologically change in response to their environment to regulate these processes through fusion, fission, and mitophagy. This allows mitochondria to adapt their function to respond to cellular requirements, a critical component in maintaining cellular homeostasis. For that reason, mitochondrial network dynamics can be considered a bridge that brings multiple cellular processes together, revealing a potential pathway for therapeutic intervention. In this review, we discuss the critical modulators of mitochondrial dynamics and how they are affected in pulmonary diseases, including chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), acute lung injury (ALI), and pulmonary arterial hypertension (PAH). A dysregulated mitochondrial network plays a crucial role in lung disease pathobiology, and aberrant fission/fusion/mitophagy pathways are druggable processes that warrant further exploration. Thus, we also discuss the candidates for lung disease therapeutics that regulate mitochondrial network dynamics.

Does low birth weight affect the presence of cardiometabolic risk factors in overweight and obese children?

UNLABELLED: Recent findings suggest that low-birth-weight children with current obesity are more likely to have higher systolic blood pressure levels and impaired ß-cell function than those who are obese with normal birth weight. It seems possible, however, that concurrent low birth weight with excess weight gain can exacerbate other risk factors for cardiometabolic diseases. The purpose of this study is to investigate the influence of birth weight on the lipid/apolipoprotein profile, visfatin levels, and insulin parameters in overweight/obese children. A cross-sectional study of 68 overweight/obese children was conducted. Among these children, 28 were identified with low birth weight and 40 were of normal birth weight. Blood lipid profile, apolipoproteins, visfatin, glucose, and insulin were measured. Our results show that systolic blood pressure (SBP) and diastolic blood pressure (DBP) levels, triglycerides (TG), very low-density lipoprotein cholesterol, low-density lipoprotein cholesterol (LDLc), apolipoprotein B and E, insulin, apolipoprotein B/A1 ratio, and homeostasis model assessment insulin resistance (HOMA-IR) were significantly elevated in overweight/obese low-birth-weight (LBW) children. There was a significant association of the SBP levels with TG (P=0.027), LDLc (P=0.001), HOMA-IR (P<0.001), apolipoprotein B (P=0.001), and apolipoprotein E (P=0.039). CONCLUSION: Our findings suggest that LBW children with overweight or obesity have an additional risk factor for both atherogenic and insulinogenic profile.

[Clinical and epidemiological characteristics of rotavirus infection in children of Cumaná, Venezuela]. / Características clínicas y epidemiológicas de la infección por rotavirus en niños de Cumaná, Venezuela.

The detection rate of group A human rotavirus (HRV-A), as well as its association with clinical and epidemiological parameters, was studied in children younger than 5 years old with acute diarrhea attending to the University Hospital "Antonio Patricio de Alcalá" of Cumaná, between march 2006 and september 2007. Of 241 fecal samples collected in this study, 47 (19.5%) were positive to HRV-A by immunoassay. Rotavirus were present throughout the study and the major detection rates were on march, april and may of 2006 (rates were 30,0%, 28,6% y 43,8%, respectively) and september of 2007 (37,5%). Thirty four percent of cases with HRV-A occurred in children of 7 - 12 months and males were the most affected (55.3%), as well as the worker and marginal socioeconomic classes (72,4%). Children that not received maternal feeding were the group mainly infected by HRV-A (61.7%). Most of the children (72.4%) had one to four evacuations/day, with few vomits (38.2%) and fever (10.6%). Almost all the feces (83.0%) had a liquid or semi-liquid aspect. When these results were compared with previous data of the same geographic area, we observed a two-fold decrease of the detection rate of HRV-A and the clinical symptoms were the same as reported by other authors. Of 32 children vaccinated against rotavirus, 30 (93.8%) did not have HVR-A in their feces and there was a significant association between the vaccinated children and protection.

Blood pressure levels in childhood: probing the relative importance of birth weight and current size.

Several studies have reported data supporting the idea that an impaired intrauterine environment that deprives the fetus of optimal nutrient delivery results in the predisposition of the fetus to experience cardiovascular and metabolic dysfunction in later life. However, contradictory data still exist. Our purpose was to investigate the effects of both birth weight and weight gain on the risk for high blood pressure levels in 6- to 10-year-old children. This cross-sectional study included 739 children divided into quartiles of birth weight. The mean values of both systolic and diastolic pressure were significantly different between quartiles of birth weight, with increasing blood pressure values as the birth weight decreased (P<0.001). Covariance analysis adjusting for gender, prematurity, and body mass index (BMI) showed that both systolic and diastolic pressure remained greater in the lowest than in the highest birth weight quartile. Separating those with low and normal birth weight demonstrated that the risk of childhood hypertension was significantly higher among children with low birth weight and current obesity (odds ratio [OR]: 5.0, confidence interval [CI]: 3.3 to 16.1; P=0.023). The inverse association between birth weight and blood pressure levels appears to be programmed during fetal life, while weight gain during childhood adds to this risk.

GFR estimated from cystatin C versus creatinine in children born small for gestational age.

BACKGROUND: Low birth weight caused by intrauterine growth restriction may be a risk factor for renal impairment in the adult life. STUDY DESIGN: A cross-sectional study. SETTING & PARTICIPANTS: 71 children aged 8 to 13 years living in the community of São Paulo, Brazil, were included in the study. Gestational age was within the normal range. PREDICTORS: Birth weight (range, 2,052 to 3,560 g) divided into quartiles: 2,500 g or less; 2,501 to 2,740 g; 2,741 to 3,000 g; and greater than 3,000 g. Birth weight ascertained by birth records in 43 and by recall in 28 participants. OUTCOMES & MEASUREMENTS: Cystatin C, creatinine, and glomerular filtration rate (GFR) estimated by equations using cystatin C (eGFR(cys)) or creatinine (eGFR(cr)). RESULTS: Overall, mean serum creatinine level was 0.8 +/- 0.01 (SE) mg/dL (range, 0.7 to 1.1 mg/dL); mean plasma cystatin C level was 0.9 +/- 0.02 mg/L (range, 0.5 to 1.6 mg/L), and eGFR(cr) and eGFR(cys) were 102.4 +/- 2.16 (range, 66 to 140) and 91.8 +/- 2.46 mL/min/1.73 m(2) (range, 49 to 139 mL/min/1.73 m(2)), respectively. No differences were found for serum creatinine or eGFR(cr) values among the birth-weight quartiles. There was a significant linear trend of increasing cystatin C levels (decreasing eGFR(cys)) in the lower birth-weight quartile groups (P = 0.002 and P = 0.02, respectively). Systolic blood pressure correlated with plasma cystatin C level (r = 0.31; P = 0.008) and eGFR(cys) (r = -0.26; P = 0.028). Covariance analysis adjusting for age, sex, body mass index for age compared with standards of the National Center for Health Statistics and expressed as a z score, and systolic blood pressure showed that cystatin C values remained greater in the lowest than highest birth-weight quartile (1.01 +/- 0.05 versus 0.83 +/- 0.05 mg/L; P = 0.02). LIMITATIONS: Ascertainment of birth weight by recall in some participants. Lack of measurement of microalbuminuria, absence of direct GFR measurement, and small sample size. CONCLUSIONS: Lower birth weight is associated with higher levels of cystatin C but not creatinine in 8-13 yr. old children born full-term.

Circulating renin-angiotensin system and catecholamines in childhood: is there a role for birthweight?

There have been only a few reports on the sympathoadrenal and renin-angiotensin systems in children of small gestational age. The purpose of the present study was to investigate plasma levels of ACE (angiotensin-converting enzyme) activity, angiotensin and catecholamines in 8- to 13-year-old children and to determine whether there are correlations between the components of these systems with both birthweight and BP (blood pressure) levels. This clinical study included 66 children (35 boys and 31 girls) in two groups: those born at term with an appropriate birthweight [AGA (appropriate-for-gestational age) group, n=31] and those born at term but with a small birthweight for gestational age [SGA (small-for-gestational age) group, n=35]. Concentrations of angiotensin, catecholamines and ACE activity were determined in plasma. Circulating noradrenaline levels were significantly elevated in SGA girls compared with AGA girls (P=0.036). In addition, angiotensin II and ACE activity were higher in SGA boys (P=0.024 and P=0.050 respectively). There was a significant association of the circulating levels of both angiotensin II and ACE activity with BP levels in our study population. Although the underlying mechanisms that link restricted fetal growth with later cardiovascular events are not fully understood, the findings in the present study support the link between low birthweight and overactivity of both sympathoadrenal and renin-angiotensin systems into later childhood.

The biological significance of mtNOS modulation.

In the last years, nitric oxide synthases (NOS) have been localized in mitochondria. At this site, NO yield directly regulates the activity of cytochrome oxidase, O(2) uptake and the production of reactive oxygen species. Recent studies showed that translocated neuronal nitric oxide synthase (nNOS) is posttranslationally modified including phosphorylation at Ser 1412 (in mice) and myristoylation in an internal residue. Different studies confirm that modified nNOS alpha is the main modulable isoform in mitochondria. Modulation of mtNOS was observed in different situations, like adaptation to reduced O(2) availability and hypoxia, adaptation to low environmental temperature, and processes linked to life and death by effects on kinases and transcription factors. We present here evidence about the role of mtNOS in the analyzed conditions.

Enalapril and losartan restored blood pressure and vascular reactivity in intrauterine undernourished rats.

Epidemiological studies suggest that intrauterine undernutrition plays an important role in the development of arterial hypertension and endothelial dysfunction in adulthood. We have evaluated the effect of the Renin Angiotensin System inhibition on the blood pressure and the mesenteric arteriolar reactivity of the intrauterine undernourished rats. Wistar rats were fed either normal or 50% of the normal intake diets, during the whole gestational period. In this study only the male offspring was used. At 16 weeks of age, the rats were used for the study of blood pressure, microvascular reactivity studied in vivo-in situ to Angiotensin II (Ang II), Bradykinin (Bk) and Acetylcholine (Ach) before and after either losartan (10 mg/kg/15 days) or enalapril (15 mg/kg/21 days) treatment. We also evaluated the mesenteric and plasmatic Angiotensin Converting Enzyme (ACE), renal function, lipid plasmatic content, and insulin and glucose metabolism. Intrauterine undernutrition induced hypertension and increased response of mesenteric arterioles to Ang II and decreased vasodilation to Bk and Ach. The treatments with losartan or enalapril normalized the blood pressure levels and significantly improved the arteriolar responses to Bk, Ach and reduced the response to Ang II. No differences have been detected to ACE activity, renal function, lipid content and insulin and glucose metabolism. This study shows for the first time that Renin Angiotensin System inhibitors can normalize the cardiovascular alterations induced by intrauterine undernutrition.

Long-term effects of intrauterine malnutrition on vascular function in female offspring: implications of oxidative stress.

Maternal malnutrition is known to impair fetal growth and predispose to the development of hypertension and type 2 diabetes. Recently, studies have demonstrated that intrauterine malnutrition is followed later in male offspring by oxidative stress characterized by increased superoxide generation due to activation of NADPH oxidase and reduced antioxidant defenses. However, few studies have investigated the mechanisms involved in endothelial dysfunction in female offspring. We evaluated the effects of the exogenous application of superoxide scavengers on the endothelium-dependent vasorelaxation in the mesenteric microvessels of female offspring. In addition, we examined indicative parameters of oxidative stress by measuring superoxide anion concentration and the activity of superoxide dismutase (SOD) as a marker of antioxidant defenses. Pregnant female Wistar rats were fed either a normal diet or 50% of this, throughout gestation. Intrauterine malnutrition induced hypertension and increased superoxide production without affecting SOD activity. Topical application of MnTMPyP (SOD mimetic) and apocynin (NADPH oxidase inhibitor) significantly improved the altered arteriolar responses to acetylcholine and bradykinin. In addition, incubation with apocynin reduced superoxide generation in these female offspring. The data suggest that after exposure to intrauterine malnutrition, female offspring present an increased superoxide production that is, at least in part, responsible for an endothelial dysfunction observed in these animals. These effects may be mediated via modulation of enzyme systems that generate superoxide.

Reactive nitrogen species in cellular signaling.

The transduction of cellular signals occurs through the modification of target molecules. Most of these modifications are transitory, thus the signal transduction pathways can be tightly regulated. Reactive nitrogen species are a group of compounds with different properties and reactivity. Some reactive nitrogen species are highly reactive and their interaction with macromolecules can lead to permanent modifications, which suggested they were lacking the specificity needed to participate in cell signaling events. However, the perception of reactive nitrogen species as oxidizers of macromolecules leading to general oxidative damage has recently evolved. The concept of redox signaling is now well established for a number of reactive oxygen and nitrogen species. In this context, the post-translational modifications introduced by reactive nitrogen species can be very specific and are active participants in signal transduction pathways. This review addresses the role of these oxidative modifications in the regulation of cell signaling events.

Nitric oxide, complex I, and the modulation of mitochondrial reactive species in biology and disease.

Mitochondria are the specialized organelles for energy metabolism but also participate in the production of O(2) active species, cell cycle regulation, apoptosis and thermogenesis. Classically, regulation of mitochondrial energy functions was based on the ADP/ATP ratio, which dynamically stimulates the transition between resting and maximal O(2) uptake. However, in the last years, NO was identified as a physiologic regulator of electron transfer and ATP synthesis by inhibiting cytochrome oxidase. Additionally, NO stimulates the mitochondrial production of O(2) active species, primarily O(2)(-) and H(2)O(2), and, depending on NO matrix concentration, of ONOO(-), which is responsible for the nitrosylation and nitration of mitochondrial components. By this means, alteration in mitochondrial complexes restricts energy output, further increases O(2) active species and changes cell signaling for proliferation and apoptosis through redox effects on specific pathways. These mechanisms are prototypically operating in prevalent generalized diseases like sepsis with multiorgan failure or limited neurodegenerative disorders like Parkinson's disease. Complex I appears to be highly susceptible to ONOO(-) effects and nitration, which defines an acquired group of mitochondrial disorders, in addition to the genetically induced syndromes. Increase of mitochondrial NO may follow over-expression of nNOS, induction and translocation of iNOS, and activation and/or increased content of the newly described mtNOS. Likewise, mtNOS is important in the modulation of O(2) uptake and cell signaling, and in mitochondrial pathology, including the effects of aging, dystrophin deficiency, hypoxia, inflammation and cancer.

Caracterización clínica y sociodemográfica de pacientes con psoriasis en un hospital universitario en Colombia / Clinical characterization and socio-demographic of patients with psoriasis at a university hospital in Colombia

Introducción y objetivo: La psoriasis es una enfermedad inflamatoria sistémica que afecta la piel, tiene predisposición genética y está mediada por mecanismos inmunológicos. Se presenta en 2% de la población occidental. En Colombia no hay datos epidemiológicos que permitan hacer una caracterización clínica. El objetivo de este estudio es conocer e identificar las prin-cipales variables clínicas y sociodemográficas de pacientes con diagnóstico de psoriasis en un Hospital Universitario de Colombia. Métodos: Es un estudio observacional, descriptivo, de corte transversal retrospectivo. La población estudio fueron pacientes de 13 a 90 años que ingresaron al Hospital Universitario de Santander entre 2012-2016.

Influence of birth weight on the renal development and kidney diseases in adulthood: experimental and clinical evidence.

Several clinical and experimental studies support the hypothesis that foetal programming is an important determinant of nephropathy, hypertension, coronary heart disease, and type 2 diabetes during adulthood. In this paper, the renal repercussions of foetal programming are emphasised, and the physiopathological mechanisms are discussed. The programming of renal diseases is detailed based on the findings of kidney development and functional parameters.

Association of ACE gene insertion/deletion polymorphism with birth weight, blood pressure levels, and ACE activity in healthy children.

BACKGROUND: The human angiotensin-converting enzyme (ACE) gene contains a polymorphism consisting of either an insertion (I) or a deletion (D) of a 287 bp Alu repetitive sequence in intron 16. The potential role of ACE polymorphism in the risk of developing hypertension or other cardiovascular disorders has not been determined in relation to birth weight (BW). METHODS: The ACE genotype and plasma ACE activity were determined in 167 children. Among these children, 60 were identified with low BW (LBW), and 107 were of normal BW (NBW). RESULTS: ACE activity levels were significantly elevated in LBW children compared with the NBW group (P < 0.001). There was a significant association of the ACE activity with systolic blood pressure (SBP) levels in our population (P < 0.001). Among the ACE genotypes, no significant differences were found with respect to BW (P = 0.136). However, our results revealed that LBW children had a higher D allele frequency than NBW children (P = 0.036). When analyzed by quartiles of SBP or ACE activity, we found a greater frequency of both the LBW children and those carrying the DD genotype in the highest quartiles of these parameters, whereas the NBW children tended to be in the lowest quartile (P < 0.001). Similar results were observed with the heterozygote ID children after categorization by quartiles of both SBP (P < 0.001) and ACE activity (P = 0.004). CONCLUSIONS: The ACE I/D polymorphism, especially the DD genotype, can be interpreted as a major factor in association between LBW and high BP levels.

N-domain isoform of Angiotensin I converting enzyme as a marker of hypertension: populational study.

The aim of this paper was to investigate the presence of the urinary 90 kDa N-domain ACE in a cohort of the population from Vitoria, Brazil, to verify its association with essential hypertension since this isoform could be a possible genetic marker of hypertension. Anthropometric, clinical, and laboratory parameters of the individuals were evaluated (n = 1150) and the blood pressure (BP) was measured. The study population was divided according to ACE isoforms in urine as follows: ACE 65/90/190, presence of three ACE isoforms (n = 795), ACE 90(+) (65/90) (n = 186), and ACE 90(-) (65/190) (n = 169) based on the presence (+) or absence (-) of the 90 kDa ACE isoform. The anthropometric parameters, lipid profile, serum levels of uric acid, glucose, and the systolic and diastolic BP were significantly greater in the ACE 90(+) compared with the ACE 90(-) and ACE 65/90/190 individuals. We found that 98% of individuals from the ACE 90(+) group and 38% from the ACE 65/90/190 group had hypertension, compared to only 1% hypertensive individuals in the ACE 90(-) group. There is a high presence of the 90 kDa N-domain ACE isoform (85%) in the studied population. The percentile of normotensive subjects with three isoforms was 62%. Our findings could contribute to the development of new efficient strategy to prevent and treat hypertension to avoid the development of cardiovascular disease.

Abnormalities in metalloproteinase pathways and IGF-I axis: a link between birth weight, hypertension, and vascular damage in childhood.

BACKGROUND: Although numerous studies suggest an inverse relationship between birth weight and cardiovascular disease, the mechanistic basis of this phenomenon is not fully understood. Here, we postulate that alterations in plasma concentration of matrix metalloproteinases (MMPs) and growth factors might show different associations between birth weight, blood pressure levels, and vascular function. METHODS: Concentrations of MMP-2 and its tissue inhibitor 2 (TIMP-2), MMP-9, and insulin-like growth factor-I (IGF-I) and its binding protein IGFBP-3 were measured in 64 children (34 boys, 30 girls). RESULTS: Small-for-gestational-age children exhibited elevated amounts of MMP-2, MMP-9, MMP-2/TIMP-2 ratio, MMP-9/TIMP-2 ratio, as well as lower concentration of IGF-I (P < 0.01), a known regulator of elastin synthesis. Similar findings were observed after adjustment for current age, gender, and race. The changes in the circulating levels of MMP-2, MMP-9, and IGF-I correlated significantly with birth weight, systolic blood pressure, and vascular function. Stepwise regression analysis demonstrated that MMP-2 was found to be an independent predictor of systolic blood pressure (R(2) = 0.08), whereas MMP-9 and birth weight were independent predictors of vascular dysfunction (R(2) = 0.38). CONCLUSIONS: It is possible that the association of fetal programming with elevated risk for vascular and metabolic disease in later life is, at least in part, mediated by perturbations in the MMP pathways.