Novel biochar and hydrochar for the adsorption of 2-nitrophenol from aqueous solutions: An approach using the PVSDM model.

Two new adsorbents, namely avocado-based hydrochar and LDH/bone-based biochar, were developed, characterized, and applied for adsorbing 2-nitrophenol. The pore volume and surface diffusion model (PVSDM) was numerically solved for different geometries and applied to interpret the adsorption decay curves. Both adsorbents presented interesting textural and physicochemical characteristics, which achieved maximum adsorption capacities of 761 mg/g for biochar and 562 mg/g for hydrochar. The adsorption equilibrium data were well fitted by Henry isotherm. Besides, thermodynamic investigation revealed endothermic adsorption with the occurrence of electrostatic interactions. PVSDM predicted the adsorption decay curves for different adsorbent geometries at different initial concentrations of 2-nitrophenol. The surface diffusion was the main intraparticle mass transport mechanism. Furthermore, the external mass transfer and surface diffusion coefficients increased with the increase of 2-nitrophenol concentration.

Single and competitive dye adsorption onto chitosan-based hybrid hydrogels using artificial neural network modeling.

Chitosan-based hybrid hydrogels such as chitosan hydrogel (CH), chitosan hydrogel with activated carbon (CH-AC), scaffold-chitosan hydrogel (SCH), scaffold-chitosan hydrogel with activated carbon (SCH-AC) and scaffold-chitosan hydrogel with carbon nanotubes (SCH-CN) were synthesized, characterized and applied to adsorb Acid Blue 9 (AB) and Allura Red AC (AR) from single and simultaneous binary liquid systems. Experimental results revealed competitive adsorption as the adsorption capacity was reduced in binary system for each dye. In addition, SCH-CN presented the highest adsorption capacity for both dyes, indicating that the modification increased the number of active sites and the functionalization with OH groups favored the interactions with sulfonated groups of the dyes. A predictive artificial neural network (ANN) was implemented to forecast the adsorption capacity for AB and AR dyes as a function of initial molar concentration of each dye, adsorption time, porosity and mass percentage of carbonaceous material on each hydrogel. The network was trained with the Levenberg-Marquardt back-propagation optimization, and according to the high correlation coefficient (R = 0.9987) and low values of root mean square error (RMSE = 0.0119), sum of the absolute error (SAE = 0.7541) and sum of squares error (SSE = 0.0132), the best topology was found to be 5-10-10-10-2. The ANN proved to be effective in predicting dye adsorption capacity of each hydrogel, even for the competitive adsorption, as the R values were close to unity for all simulation systems.

Hyperuricemia and Risk of Cardiovascular Outcomes: The Experience of the URRAH (Uric Acid Right for Heart Health) Project.

The latest European Guidelines of Arterial Hypertension have officially introduced uric acid evaluation among the cardiovascular risk factors that should be evaluated in order to stratify patient's risk. In fact, it has been extensively evaluated and demonstrated to be an independent predictor not only of all-cause and cardiovascular mortality, but also of myocardial infraction, stroke and heart failure. Despite the large number of studies on this topic, an important open question that still need to be answered is the identification of a cardiovascular uric acid cut-off value. The actual hyperuricemia cut-off (> 6 mg/dL in women and 7 mg/dL in men) is principally based on the saturation point of uric acid but previous evidence suggests that the negative impact of cardiovascular system could occur also at lower levels. In this context, the Working Group on uric acid and CV risk of the Italian Society of Hypertension has designed the Uric acid Right for heArt Health project. The primary objective of this project is to define the level of uricemia above which the independent risk of CV disease may increase in a significantly manner. In this review we will summarize the first results obtained and describe the further planned analysis.

Vascular remodeling after carotid artery stenting.

Carotid stenting is an alternative to endarterectomy for the treatment of carotid stenosis. To determine the role of vascular remodeling after stent placement, we studied 19 high surgical risk patients undergoing carotid stenting for severe stenosis. Using high-resolution ultrasound, we evaluated the intima-media thickness (IMT), the intima-intima diameter, and the adventitia-adventitia diameter at prespecified sites of the carotid artery tree during 3 years of follow-up. The IMT of internal carotid artery, at the site of maximum stenosis, increased significantly from 0 mm after 24 hours, to 0.41 mm at 3 months, to 0.48 mm at 6 months, and to 0.51 mm at 3 years of follow-up. In the same site, diameters and residual stenosis (range 29-24%) did not change over time. Our study showed that stent is self-expanding against the atherosclerotic plaque within the 3-year follow-up period. Despite neointima formation, the intima-intima diameter does not change without worsening of the residual stenosis.

Contribution of adventitial fibroblasts to neointima formation and vascular remodeling: from innocent bystander to active participant.

The adventitial layer surrounding the blood vessels has long been exclusively considered a supporting tissue the main function of which is to provide adequate nourishment to the muscle layers of tunica media. Although functionally interconnected, the adventitial and medial layers are structurally interfaced at the external elastic lamina level, clearly distinguishable at the maturational phase of vascular morphogenesis. Over the last few years the "passive" role that the adventitia seemed to play in experimental and spontaneous vascular pathologies involving proliferation, migration, differentiation, and apoptosis of vascular smooth muscle cells (VSMCs) has been questioned. It has been demonstrated that fibroblasts from the adventitia display an important partnership with the resident medial VSMCs in terms of phenotypic conversion, proliferation, apoptotic, and migratory properties the result of which is neointima formation and vascular remodeling. This article is an attempt at reviewing the major themes and more recent findings dealing with the phenotypic conversion process that leads adventitial "passive" (static) fibroblasts to become "activated" (mobile) myofibroblasts. This event shows some facets in common with vascular morphogenesis, ie, the process of recruitment, incorporation, and phenotypic conversion of cells surrounding the primitive endothelial tube in the definitive vessel wall. We hypothesize that during the response to vascular injuries in the adult, "activation" of adventitial fibroblasts is, at least in part, reminiscent of a developmental program that also invests, although with distinct spatiotemporal features, medial VSMCs.

Specific cellular features of atheroma associated with development of neointima after carotid endarterectomy: the carotid atherosclerosis and restenosis study.

BACKGROUND: The purpose of this study was to investigate whether some cellular and molecular features of tissue retrieved at carotid endarterectomy are associated with the extent of neointima formation at ultrasound follow-up. METHODS AND RESULTS: One hundred fifty patients were studied. Endarterectomy specimens were tested by immunocytochemistry with the use of (1) monoclonal antibodies that identify smooth muscle cells (SMCs) and fetal-type SMCs on the basis of smooth muscle and nonmuscle myosin content, (2) the anti-macrophage HAM 56, and (3) the anti-lymphocyte CD45RO. The maximum intima-media thickness (M-IMT) of the revascularized vessel was assessed by the use of B-mode ultrasonography 6 months after surgery. The M-IMT values were related positively to the number of SMCs (r=0.534, P<0.0005) and negatively to that of macrophages and lymphocytes (r=-0.428, P<0.0005, and -0.538, P=0.001, respectively). Patients were classified as class 1 (M-IMT 1.3 mm). An abundance of SMCs, mostly of fetal type, was found in the plaque of class 3 patients, whereas lesions from class 1 patients were rich in macrophages and lymphocytes. In the multivariate analysis, factors related to M-IMT were the number of SMCs and the percentage of fetal-type SMCs present in the plaque. CONCLUSIONS: Although the classic risk factors did not play a role, an abundance of SMCs and a scarcity of macrophages characterized the primary lesion of patients in whom neointima developed after surgery. In patients in whom neointima did not develop, lesions were rich in macrophages and lymphocytes. This approach can be useful in defining patients at risk of restenosis.

Review article: the metabolic syndrome--a chronic cardiovascular inflammatory condition.

The atherosclerotic process is regulated by inflammatory mechanisms, which also appear to be involved in the modulation of insulin-resistance, a key player in the pathogenesis of the metabolic syndrome (MS). The interaction between components of the clinical phenotype of the MS with its biological phenotype (insulin resistance, dyslipidaemia, etc.) contributes to the development of a pro-inflammatory state characterized by an increased oxidative stress (i.e. oxidized lipoproteins) and a chronic, subclinical vascular inflammation, as also suggested by the increased C reactive protein (CRP) concentration found in patients with MS. The subclinical inflammatory state peculiar of the MS modulates the atherosclerotic process at different stages, resulting in: (i) endothelial dysfunction and increased expression of endothelial adhesion molecules; (ii) an enhanced recruitment of monocytes within the arterial wall, in the early stages of the atherosclerotic process; leading to (iii) the formation of an unstable atherosclerotic plaque, rich in inflammatory cells, which is the culprit lesion in the vast majority of both coronary and cerebrovascular events observed in with MS.

Visceral obesity, but not metabolic syndrome, is associated with the presence of post-thrombotic syndrome.

INTRODUCTION: The relationship between metabolic syndrome (MetS), and the development of post-thrombotic syndrome (PTS) is currently unknown. MATERIALS AND METHODS: We enrolled 120 patients with a previous episode of deep venous thrombosis (DVT) diagnosed more than 2years apart from the enrollment. Presence of MetS was identified according to NCEP ATP III criteria and Villalta Score (VS) was used to establish the presence of PTS (VS≥5). RESULTS: We identified 49 (40.8%) subjects with clinical diagnosed of PTS. Patients with or without PTS showed comparable age and temporal distance from DVT event. We observed higher BMI (p=0.005) and waist circumference (p=0.006) among subjects with VS≥5 as compared to patients without PTS. No differences between the two groups were found in terms of lipid profile, blood pressure, diabetes, hs-CRP level and ongoing medications. The prevalence of MetS was equally distributed among patients with or without PTS (20% vs 26% respectively, p=0.64). Among the individual components of MetS only the prevalence of visceral adiposity was significantly increased in subjects affected by PTS (OR 2.81, p=0.008). Moreover, a significant linear correlation was found between VS and waist circumference in the entire cohort (r=0,354, p<0.0001). CONCLUSION: There is no evidence of association between MetS and PTS. However, the degree of visceral adiposity is strongly correlated with the presence and severity of post-thrombotic disease.

Predictors of vascular remodelling in hypertensive subjects with well-controlled blood pressure levels.

We evaluated the structural/functional characteristics of the arterial wall in a cohort of hypertensives with well-controlled blood pressure (BP) levels. We studied 40 hypertensives with well-controlled BP. We assessed by B-mode ultrasound the mean intima-media thickness (mean-IMT) and maximum-IMT (M-MAX) of carotid artery (common, bulb, internal) bilaterally. Endothelial function was evaluated by post-occlusion flow-mediated dilation (FMD) of the brachial artery. Along with traditional risk factors, we studied the impact of serum high-sensitivity C-reactive protein (hs-CRP) and osteoprotegerin (OPG). Forty normotensive subjects served as controls. In the hypertensives, the BP levels were well controlled (office BP: 129/79 mm Hg, ambulatory BP monitoring: 121/75 mm Hg). Compared with controls, higher BP levels and body mass index were present in hypertensives, whereas age and metabolic parameters were similar. In hypertensives, the IMT (mean-IMT 0.68 mm, M-MAX 0.81 mm) was significantly higher than in controls (mean-IMT 0.60 mm, M-MAX 0.71 mm). FMD was impaired in hypertensives (5.9%) compared with controls (9.2%). In multivariate analyses, it turned out that in hypertensives IMT parameters were related to age, hs-CRP and OPG. Low-density lipoprotein (LDL) cholesterol was the only factor related to FMD. IMT and FMD had no relationship with BP levels. In conclusion, in hypertensives with well-controlled BP, the pro-atherogenic remodelling (IMT) is mainly dependent on age and the inflammatory cytokines, OPG in particular. The functional impairment of the arterial wall (FMD) was related to the levels of LDL cholesterol. Under these conditions, when the impact of BP is minimized, the role of inflammatory cytokines and lipids on structural/functional remodelling becomes predominant.

Sympathetic drive and vascular damage in hypertension and atherosclerosis.

Current knowledge of the links between the sympathetic nervous system and vascular damage in hypertension and atherosclerosis is summarized. The main mechanisms leading to the structural changes of the arterial wall as a consequence of enhanced adrenergic drive are reported. Hemodynamic mechanisms, including increase in pressure leading to changes in the arterioles and alteration of flow pattern with impact mainly in the large arteries, respectively, account for the typical target organ damage observed in hypertension and is involved in the development of atherosclerotic lesions. Regarding the direct effect of catecholamines, the atherogenic effects of epinephrine and norepinephrine in the absence of changes in blood pressure and cholesterol levels have been demonstrated in vivo in monkeys and rabbits. In rats, catecholamine administration induces polyploidization of aortic smooth muscle cells in vivo and in vitro. Regarding the effects of lipid metabolism, adrenergic stimulation may induce free fatty acid transformation into triglycerides with secondary increase in very low density lipoprotein plasma levels and decrease of very low density lipoprotein transformation into high density lipoprotein through circulating lipoprotein lipase inhibition. Catecholamines may also increase cholesterol levels of the arterial wall, probably by triggering the acyl-cholesterol-acyl-transferase activity. Finally, indirect evidence of the pathogenetic role played by the sympathetic system in the development of vascular disease derives from the results of experiments showing that sympatholytic agents are capable of reducing both medial hypertrophy and atherogenesis. beta-Blockers, alpha- and beta-blockers, and centrally acting sympatholytic agents not only ameliorate hemodynamics but also appear to inhibit the direct effects of catecholamines on the arterial wall.

Relationship of tachycardia with high blood pressure and metabolic abnormalities: a study with mixture analysis in three populations.

Faster resting heart rate has been shown to be associated with a higher risk of developing hypertension and a greater incidence of cardiovascular morbidity and mortality. The aim of this study was to investigate the distribution of heart rate and its relationship with blood pressure and other cardiovascular risk factors in three populations. One European general population (Belgian study), one North American general population (Tecumseh study), and one European hypertensive population (HARVEST trial) were studied. Within each population, mixture analysis was used to investigate whether a mixture of two normal distributions explained the variance in heart rate better than a single distribution. In the men of all populations, mixture analysis identified a larger subpopulation of subjects with normal heart rate and a smaller one with fast heart rate. The subgroups with tachycardia had higher blood pressure and lipid levels than those with normal heart rate. In the populations in which they were measured, fasting insulin and postload glucose were also higher in the men with faster heart rate. A subgroup with tachycardia could also be singled out among the women from Tecumseh, but no relation between heart rate and blood pressure could be found. These findings show that in Western societies, high heart rate pertains to a distinct subgroup of subjects, who are more frequently men and exhibit the characteristic features of the insulin resistance syndrome. Sympathetic overactivity is likely to be the mechanism underlying this clinical condition.

Changes in rat ventricular isomyosins with regression of cardiac hypertrophy.

The changes in ventricular isomyosin composition and Ca2+-activated ATPase activity occurring with regression of both hypertension and cardiac hypertrophy were investigated by using polyacrylamide gel electrophoresis under nondenaturing conditions, heavy chain peptide mapping, and an enzymatic assay. Eight control male Wistar rats and 14 two-kidney, one clip (Goldblatt II) hypertensive rats were studied from the fifth week of age. At 10 weeks of age, five Goldblatt II rats and four normotensive controls were killed. Five other Goldblatt II rats underwent nephrectomy of the ischemic kidney, which resulted in subsequent normalization of blood pressure. The remaining four control, four Goldblatt II rats, and five nephrectomized rats were killed at 15 weeks of age. Both the 10- and 15-week-old hypertensive rats had a significantly higher (p less than 0.001) biventricular weight to body weight ratio than the age-matched controls (3.84 +/- 0.76 X 10(-2) vs 2.75 +/- 0.25 X 10(-2); 5.93 +/- 2.26 X 10(-2) vs 2.65 +/- 0.17 X 10(-2]. The 15-week-old nephrectomized rats had a biventricular weight to body weight ratio (2.90 +/- 0.25 X 10(-2] close to that of age-matched controls and significantly lower (p less than 0.05) than that of age-matched hypertensive rats. In both the 10- and 15-week-old hypertensive rats left ventricular myosin Ca2+-activated ATPase activity was significantly lower (p less than 0.001) than in the age-matched controls (0.44 +/- 0.03 vs 0.59 +/- 0.06; 0.24 +/- 0.05 vs 0.48 +/- 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Ventricular myosin and creatine-kinase isoenzymes in hypertensive rats treated with captopril.

In the myocardium, myosin and creatine kinase isoforms possess different capacities for using O2 and energy-rich phosphates. We studied electrophoretically the distribution of these isoforms in 19 hypertensive rats (two-kidney, one clip model of hypertension) and in age-matched controls. After 6 weeks of hypertension, seven rats were treated with captopril (2 mg/kg daily) for 4 weeks, six were left hypertensive for another 4 weeks, and the remaining rats were killed under ether anesthesia. In the latter, ventricular mass was significantly higher than in controls; V3 isomyosin was 32.3 +/- 6.8% versus 0%, and both creatine kinase-MB and -BB were increased at the expense of creatine kinase-MM (creatine kinase-MB = 29 +/- 2.8% vs. 14.7 +/- 1.8%, p less than 0.001; creatine kinase-BB = 3.1 +/- 0.6% vs. 1.7 +/- 0.8%, p less than 0.001). After 10 weeks of hypertension, ventricular mass, V3 isomyosin, and both creatine kinase-MB and -BB isoforms were found to be persistently higher than in controls. At the same time, captopril-treated rats showed reduced but not normalized blood pressure levels, normalized ventricular mass, and prevalence of the V1 isomyosin (56.9 +/- 22% vs. 47.9 +/- 23.8% in normotensive controls, p = NS). However, higher levels of creatine kinase-MB and -BB were still found in these rats in comparison with the normotensive controls (creatine kinase-MB = 22.4 +/- 5.4% vs. 15.8 +/- 2.8%, p less than 0.025; creatine kinase-BB = 2.3 +/- 0.1% vs. 1.8 +/- 0.3%, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Correlation between the presence of an immature smooth muscle cell population in tunica media and the development of atherosclerotic lesion. A study on different-sized rabbit arteries from cholesterol-fed and Watanabe heritable hyperlipemic rabbits.

Mapping the distribution of an immature smooth muscle cell (SMC) subpopulation in large- and small-sized arterial vessels was carried out in normocholesterolemic rabbits and compared with the mapping atherosclerotic lesions in endogenously (Watanabe heritable hyperlipemic, WHHL) and exogenously derived (cholesterol-fed, CT) hypercholesterolemic rabbits. This cell subset is identified by a specific myosin isoform content and displays an intermediate degree of differentiation between fetal- and adult-type SMC. Monoclonal anti-myosin antibodies, immunofluorescence procedures, and different arterial segments of a rabbit vessel tree, i.e. from aorta to dental pulp (common carotid, external carotid, lingual, facial, maxillary, inferior alveolar arteries, and dental branches of alveolar arteries) were studied. WHHL of different ages (3 to 12 months), and two different concentrations of CT (2% and 0.2%) in the diet for 3 and 12 months, respectively, were used. The results of the present study indicate that: (1) using a diet with a higher percentage of CT (rabbits fed 2% CT-diet for 3 months) there is maximum expansion of atherosclerotic lesions from the aorta up to the maxillary artery; (2) localization of atherosclerotic lesions with a lower CT content in the diet is dependent on the duration of feeding and may involve the aorta up to the external carotid artery; (3) the development of the atherosclerotic lesion in hypercholesterolemic rabbit is strictly related to the appearance of an intermediate SMC subtype; (4) atherosclerotic lesions occur only in those arterial sites which, in corresponding normocholesterolemic rabbit, contain intermediate-type SMC; and (5) no differences can be found in the distribution of SMC subpopulations present in the lesions from WHHL, CT-fed animals, or at various arterial levels, whereas some discrepancies can be shown in aortic atherogenesis.

Hematoporphyrin binding to cultured aortic smooth muscle cells from spontaneously atherosclerotic turkey.

Porphyrins are known to be accumulated in vivo by tumors and atherosclerotic plaques. We studied the interaction of cultured aortic smooth muscle cells (SMC) from spontaneously atherosclerotic Broad Breasted White Turkeys (BBWT) with free hematoporphyrin (Hp) and low density lipoprotein (LDL)-Hp complexes. A significantly higher binding of LDL-Hp to SMC as compared to free Hp was observed. These data indicate that porphyrin binding to vascular SMC represents a possible mechanism for porphyrin accumulation by atherosclerotic plaques. This process is mediated, at least in part, by LDL.

Left ventricular hypertrophy in hypertension. Changes in isomyosins and creatine-kinase isoenzymes.

In hypertension, the heart of small mammals can express different isoenzymic forms of proteins under the influence of overload and other modulating factors. The increase in ventricular mass is generally paralleled by progressive changes in the isoforms of at least two proteins that are involved in the contraction process, namely, myosin and creatine-kinase. This review summarizes the biochemical and molecular changes occurring during progression and with regression of cardiac hypertrophy in rats, humans, and other animals, and focuses on the role played by antihypertensive drugs in modulation of ventricular isomyosins. The implications of these observations for humans remain to be fully determined.

Smooth muscle cell types at different aortic levels and in microvasculature of rabbits with renovascular hypertension.

BACKGROUND: The monoclonal antimyosin antibodies smooth muscle (SM)-E7, non-muscle (NM)-G2 and NM-F6 recognize smooth muscle myosin heavy chains, and A- and B-like non-muscle myosin heavy chains, respectively. On this basis, aortic smooth muscle cell types have been identified as adult (SM-E7-positive), postnatal (SM-E7- and NM-G2-positive) and fetal (SM-E7-, NM-G2- and NM-F6-positive). We have demonstrated previously that hypertrophy of the smooth muscle cell layer of the upper aorta in two-kidney, one clip hypertensive rabbits is achieved via a selective increase in postnatal-type smooth muscle cells. OBJECTIVE: To monitor the time-course change of postnatal-type smooth muscle cells along the entire aortic tree and to define the phenotypic characteristics of the microvasculature in the same rabbit model. MATERIALS AND METHODS: Hypertensive rabbits were killed 0.5, 1, 2.5, 4, 6 and 8 months after clipping. Normotensive age-matched rabbits served as controls. The entire aorta was frozen during perfusion at a constant pressure for morphometric and immunocytochemical studies. Transverse cryosections were taken 1 cm from the aortic valve (level A), immediately after the anonymous trunk (level B), immediately before the diaphragm (level C), and near the bifurcation (level D). Small vessels and arterioles were studied in psoas skeletal muscle and in left ventricular myocardium. RESULTS: On the whole, aortae from hypertensive rabbits displayed a striking increase in postnatal-type smooth muscle cells at all levels by 4 months of hypertension and a progressive decrease in the number of these cells to near the control value by 8 months of hypertension. A peculiar pattern of myosin heavy chain expression was found in the microvasculature. In control and in hypertensive rabbits, both at 4 and at 8 months, small vessels and arterioles were equally reactive with the three antimyosin heavy chain antibodies. This indicates a basic prevalence of fetal-type smooth muscle cells, which is little influenced by blood pressure. CONCLUSIONS: The present data elucidate some of the basic changes which the entire aortic segment and microvasculature undergo in the present experimental model.

Effects of a traditional lifestyle on the cardiovascular risk profile: the Amondava population of the Brazilian Amazon. Comparison with matched African, Italian and Polish populations.

OBJECTIVE: To determine the relationships between lifestyle and cardiovascular risk factors among the Brazilian Amondava, one of the world's most isolated populations. DESIGN: Cross-sectional, population-based study. Four age- and sex-matched samples from Brazil Africa, Italy and Poland, representing different levels of modernization, were compared. Body weight, height, blood pressure, serum cholesterol and glycaemia were measured, and a standard questionnaire administered. Data concerning dietary habits and physical activity were collected. A personal socio-economic score was calculated, on the basis of type of economy, level of formal education, type of occupation, type of habitat, availability of piped water and electricity, main source of income, housing conditions, availability of radio, television or personal computer, knowledge of a second language, and organized health facilities. SETTING: Primary epidemiological screening, at an institution. RESULTS: Among the Amondava blood pressure was always <140/90 mm Hg, it did not increase with age and was not correlated with any other variable; 46.6% of subjects had systolic blood pressure <100 mm Hg. Blood pressure among the Amondava (109.6+/-11.1/69.5+/-6.4 mm Hg) was on average lower (P<0.0001) than in all other samples. Among the Amondava, the concentration of total cholesterol was always <200 mg/dl, i.e. similar to that of Africans whose diet included large amounts of vegetable foodstuffs; 90% had glycaemia (<80 mg/dl), and their mean value was the lowest (55.1+/-14.9 mg/dl) of all the groups. CONCLUSIONS: In addition to a possible genetic predisposition not analysed in this study, a traditional lifestyle (no contact with civilization, diet based on complex carbohydrates and vegetables, high energy expenditure) may protect against the development of hypertension, hypercholesterolaemia, and diabetes.

Blood pressure, serum cholesterol and nutritional state in Tanzania and in the Amazon: comparison with an Italian population.

OBJECTIVE: To confirm that westernization of dietary habits represents a stimulus for the expression of cardiovascular risk. DESIGN: Three representative age- and sex-matched samples of general populations of three continents were compared cross-sectionally by analysis of variance. PARTICIPANTS: In total 1110 subjects aged 22-89 years, divided into three groups (370 from Tanzania and Uganda, 370 from the Amazonian region of Brazil, and 370 from northern Italy; 111 men and 259 women in each group). RESULTS: The blood pressure of Africans eating a low-salt fish and vegetable' diet was lower than those of Brazilians, whose diet was based on cereals and meat, and highly urbanized Italians. The systolic blood pressure was correlated to the body mass index for all three populations, but with age only for the Brazilians and Italians. The total cholesterol level and body mass index, both of which are low among Africans, increased progressively with increasing economic level. CONCLUSIONS: Transition from a rural to an urbanized lifestyle is accompanied by a rise in the main cardiovascular risk factors; the present data also show that environmental rather than racial factors have a crucial impact on the risk pattern of populations.

Impact of nifedipine on vascular smooth muscle cell differentiation. Implications for atherogenesis.

Although vascular smooth muscle cells (SMCs) play a key role in the development of atherosclerotic lesions, they are not a homogeneous cell type. Myosin has been used as a marker of SMC differentiation in order to identify distinct SMC populations in the adult rabbit aorta. The medial layer of the normal adult aorta contains predominantly 'adult' type SMCs, which express smooth muscle (SM) myosin isoforms exclusively, and a minority of 'immature' type SMCs, which coexpress SM and nonmuscle (NM) myosin isoforms. The size of this latter SMC subpopulation, showing the 'immature' pattern of myosin isoform expression, increases markedly in the aortic media during experimental atherogenesis, and represents a major SMC type in the atherosclerotic plaque. The dihydropyridine derivative, nifedipine, has a marked effect on NM myosin expression and SMC differentiation in vitro. In vivo, short term administration of nifedipine resulted in the disappearance of 'immature' type SMCs from the aortic media of both normocholesterolaemic and hypercholesterolaemic adult rabbits. Moreover, in a model of atherosclerosis prevention, nifedipine significantly reduced the area of aortic intimal thickening and reduced the size of the 'immature' type SMC population both in the aortic media and intima of the hypercholesterolaemic rabbit.