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2,4-Dichlorophenoxyacetic acid (2,4-D) is an herbicide widely used in crops against broadleaf weeds. However, 2,4-D residues are considered an environmental pollutant in bodies of water. Phytoremediation with Plectranthus neochilus is a substantial strategy to remove 2,4-D from the aquatic environment. The objective of this study was to verify the efficiency of the association of the photostimulus by Light Emitting Diodes (LED) with P. neochilus to improve phytoremediation of 2,4-D in water. Phytoremediation was evaluated with the following samples: natural light, white LED, blue LED, and red LED, with and without the plant as controls. The data corresponding to the validation of the method were in accordance with the required parameters: R 2 : 0.9926; RSD: 1.74%; LOD: 0.075 mg.L -1 ; LOQ: 0.227 mg.L -1 and recovery by SPE was 76.57%. The efficiency of the association of LED with P. neochilus in the 28 days was: ambient light + plant (47.0%); white light + plant (37.10%); blue light + plant (26.80%); red light + plant (3.32%). This study demonstrated, for the first time, the efficiency of using LEDs light in association with P. neochilus for the phytoremediation of 2,4-D in water.

Environmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor alpha (ERalpha); these cell lines stably express estrogen response element (beta-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1-10 microM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ERalpha-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, gamma-hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed.

The aim of this study was to investigate the diagnostic approach to recently diagnosed hypertensive patients by primary care physicians in Italy and to find out whether general practitioners manage these patients according to 1999 WHO/ISH guideline recommendations. In total, 228 consecutive patients (117 men and 111 women, mean age 51+/-12 years) with recently diagnosed hypertension (<2 years) referred for the first time to six outpatient hypertension centres throughout Italy were included in the study. The primary care physicians' approach was evaluated during the specialist visit by a specific questionnaire containing detailed questions about diagnostic work-up and treatment made at the time of the first diagnosis of hypertension. At the study visit, 71% of the patients were on treatment with antihypertensive drugs and 18.7% of them had blood pressure (BP) values lower than 140/90 mmHg. A complete clinical and laboratory evaluation according to the minimum work-up suggested by the guidelines had been carried out in only 10% of the patients. A full physical examination had been performed in 60% of the patients, electrocardiogram in 54%, serum total cholesterol in 53%, glucose in 49%, creatinine in 49%, urine analysis in 46%, potassium in 42%, and fundus oculi in 19%. Additional investigations such as ambulatory BP monitoring, echocardiogram, carotid ultrasonogram, and microalbuminuria had been carried out in a minority of patients (21, 18, 9, and 3%, respectively). The impact on hypertension guidelines on patients' management in everyday primary care practice appears marginal. Thus, our findings indicate that the majority of general practitioners manage hypertensive patients according to a simple BP-based approach rather than a more integrated approach based on global risk stratification.

Nonsteroidal antiinflammatory drugs may affect blood pressure (BP) control in hypertensive patients receiving drug treatment, but data on the effects of low-dose aspirin are scanty. This study assessed the effects of chronic treatment with low doses of aspirin (100 mg/day) on clinic and ambulatory systolic (SBP) and diastolic (DBP) BP in hypertensives on chronic, stable antihypertensive therapy. The study was conducted in the framework of the Primary Prevention Project (PPP), a randomized, controlled factorial trial on the preventive effect of aspirin or vitamin E in people with one or more cardiovascular risk factors. Fifteen Italian hypertension units studied 142 hypertensive patients (76 men, 66 women; mean age 59 +/- 5.9 years) treated with different antihypertensive drugs: 71 patients were randomized to aspirin and 71 served as controls. All patients underwent a clinic BP evaluation with an automatic sphygmomanometer and a 24-h ambulatory BP monitoring, at baseline and after 3 months of aspirin treatment. At the end of the study the changes in clinic SBP and DBP were not statistically different in treated and untreated subjects. Ambulatory SBP and DBP after 3 months of aspirin treatment were similar to baseline: deltaSBP -0.5 mmHg (95% confidence intervals [CI] from -1.9 to +2.9 mm Hg) and deltaDBP -1.1 mm Hg (95% CI from -2.5 to +0.3 mm Hg). The pattern was similar in the control group. No interaction was found between aspirin and the most used antihypertensive drug classes (angiotensin converting enzyme inhibitors and calcium antagonists). Despite the relatively small sample size our results seem to exclude any significant influence of low-dose aspirin on BP control in hypertensives under treatment.

A randomized controlled open trial studied the effect of vitamin E supplementation (300 mg/day) on clinic and 24-h ambulatory blood pressure (BP) in 142 treated hypertensive patients. After 12 weeks, clinic BP decreased whether or not patients were randomized to vitamin E. Ambulatory BP showed no change in systolic BP and a small decrease in diastolic BP (-1.6 mm Hg, 95% confidence intervals from -2.8 to -0.4 mm Hg), approaching statistical significance in comparison to the control group (P = .06). Vitamin E supplementation thus seems to have no clinically relevant effect on BP in hypertensive patients already under controlled treatment.

The distribution of the major platelet membrane glycoproteins (GP), Ib, IX, IIb-IIIa and IV (or CD36), which play important roles as receptors for adhesive molecules in haemostasis and thrombosis, was studied in 34 patients with myeloproliferative disorders (MPD): 13 had essential thrombocythaemia (ET), 12 had polycythaemia vera (PV) and nine had chronic myelogenous leukaemia (CML). Only occasionally were modifications of the numbers of GPIb or GPIIb-IIIa measured using the binding of specific radiolabelled antibodies to platelets. In contrast, 2-3-fold increases of the total CD36 content and the surface CD36 expression were measured in almost all patients studied, using a radioimmunoassay and the direct binding of the radiolabelled antibody, FA6-152, to the platelet surface, respectively. These results indicate that the abnormality affected both the external and internal CD36 pools. Therefore platelet CD36 may be a useful tool for the diagnosis and the follow-up of MPD patients. Surface CD36 has been proposed as a platelet receptor for thrombospondin, an adhesive glycoprotein that is released from platelets upon activation and promotes aggregate formation. Despite a 2-fold increase of CD36 molecules, resting and thrombin-activated platelets from ET patients expressed the same amount of thrombospondin as normal platelets, suggesting that there is not a direct correlation between the CD36 expression and thrombospondin binding either spontaneously or after activation.

We describe a case of a 34-year-old male patient first hospitalized in February '93 for stroke (concomitant dilated-hypertrophic cardiomyopathy was noted), and then in April '93 for congestive heart failure. The presence of myopathy, encephalopathy, lactic acidosis and stroke episode allows for the diagnosis of MELAS syndrome, proven by a specific point mutation in mitochondrial DNA. In this case we were able to observe not only the electrocardiographic and echocardiographic features of hypertrophic cardiomyopathy, previously described in mitochondrial encephalomyopathies, but we were also able to monitor the rapid evolution of this cardiomyopathy towards the hypokinetic dilated form with severe impairment of systolic function; this transition was due to changes in the heart anatomy and structure with reduction in the left ventricular (LV) wall thickness and dilatation of all chambers. The remodeling of LV geometry seems to be not definite and capable of dynamic evolution, as suggested by clinical and echocardiographic findings evaluated six months after the hospitalization. In this patient, we obtained a mid-term favourable clinical outcome using inotropic drugs and Ubiquinone (coenzyme Q), an intermediate substrate of the energetic metabolism, which seems to be poorly synthetized because of the early enzymatic defects in the mitochondrial respiratory chain.

Fifty-eight male subjects admitted to an intensive coronary care unit were interviewed and underwent psychometric testing on the second--third day after a severe heart attack (infarct). Seven-ten days following admission, the clinical condition of the patients was evaluated by the attending cardiological staff and rated on a three point scale. The patients were divided, on the basis of the clinical rating, into two groups: improved (N = 25) and non-improved (N = 33). Life history characteristics, MMPI personality profiles, and State-Trait anxiety scores were then compared for the two groups. The not-improved group showed the higher scores on almost all the MMPI scales, higher anxiety scores and more work-related problems than the improved group. Such data give some empirical support to the hypothesis that the physiological and hemodynamical conditon of the cardiac patient is in some way correlated with the patient's style of coping with stress, and his history of previous life stress situations.