Effects of residential greenness on attention in a longitudinal study at 8 and 11-13 years.

In an urbanizing world, with 55% of the population living in cities, it is essential to design friendly and healthy ones. An emerging body of evidence has associated greenspace exposure with improved cognitive development, including attentional function; however, the longitudinal studies looking at the association with attentional function are still scarce. Therefore, the objective of this study was to analyze the association of the exposure to greenspace and attention in school children. This study was based on 751 participants at 8 years and 598 at 11-13 years of two sub-cohorts of the INMA cohort study in Gipuzkoa and Asturias, Spain. Greenspace exposure at home was characterized using four indicators: (i) average of Normalized Difference Vegetation Index (NDVI) and (ii) Vegetation Continuous Field (VCF) in buffers of 100 m, 300 m, and 500 m around the residential address, (ii) availability of a green space within 300 m from the residential address, and (iv) residential distance to green spaces. Participants' attention was characterized twice at ages of 8 and 11 years, using the computerized Attentional Network Test (ANT). General linear models were used for the cross-sectional analyses and linear mixed effects model for the longitudinal analyses. Our cross-sectional analyses showed a statistical significant protective association between average NDVI at 300 m and inattentiveness (-7.20, CI 95%: 13.74; -0.67). In our longitudinal analyses, although we generally observed beneficial associations between greenspace exposure and attention, none attained statistical significance. No statistically significant indirect effect were seen for NO2. Our findings add to the emerging body of evidence on the role of green spaces in neurodevelopment, which can provide the evidence base for implementing intervention aimed at promoting neurodevelopment in urban children.

[Molecular diagnosis of adult dominant polycystic kidney disease in the Canary Islands]. / Diagnóstico molecular de la Poliquistosis Renal Autosómica Dominante en la Comunidad Autónoma de Canarias.

Adult dominant polycystic kidney disease is an hereditary condition responsible for 6% of end-stage renal failure in Spain. Two genes were located in chromosomes 16 and 4 as related to this age-dependent disease in the 90s (PKD1 and PKD2). The diagnosis can be easily achieved by sonographic study, but molecular analysis by means of linkage analysis has the advantage of an early diagnosis in asymptomatic genetic carriers, with a view to the preventive follow-up of these subjects and genetic counselling. In this paper we present the results of molecular analysis of 30 families with Adult Dominant Polycystic Kidney Disease (from the province of Las Palmas Spain), carried out linkage analysis with two series of microsatellite markers located within or in the vicinity ofPKD1 (D16S521, KG8, AC2.5, CW2, SM7) and PKD2 (D4S1538, D4S1534, D4S423,D4S414) genes. The objectives of the study were: first, to verify the informativeness, and therefore, the usefulness of these markers for family studies in our population; and second,to assess the sensitivity and specificity of the genetic analysis in our population. Most of the markers showed a high heterozygosity, comparable to data in other studies. Considering the alleles of the different markers together in a chromosome as an haplotype increased the informativeness of the markers, and allowed the unequivocal identification of genetic data in 97.7% of patients and 88.7% of healthy subjects. The sensitivity and specificity of the genetic analysis were 90.7% (CI 95%: 85.7-95.7) and 86.8% (CI 95%: 80.6-93.0), respectively.

Association of angiotensinogen M235T and A(-6)G gene polymorphisms with coronary heart disease with independence of essential hypertension: the PROCAGENE study. Prospective Cardiac Gene.

OBJECTIVES: We examined the relationship between the angiotensinogen (AGT) gene M235T polymorphism, the variant promoter of the AGT gene A(-6)G and the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and coronary heart disease (CHD) in native Gran Canaria Island habitants, who have the highest rates of CHD in Spain. BACKGROUND: Some studies subject that the ACE (I/D) polymorphism could be associated with CHD, while AGT (M235T) has been related to essential hypertension. METHODS: We studied 304 subjects with angiographic evidence of coronary artery disease and a clinical diagnosis of myocardial infarction or unstable angina and 315 age- and gender-matched controls. Blood was drawn and DNA extracted. Angiotensin-converting enzyme (I/D) gene polymorphism was analyzed by polymerase chain reaction (PCR) and AGT gene polymorphisms by restriction fragment length polymorphism-PCR and mutagenically-separated PCR. RESULTS: The ACE (I/D) polymorphism showed no association with CHD, whereas the frequency distribution of AGT (M235T) genotypes among patients and controls (235T: 29.1% and 19.0%; M235T: 48.5% and 50.2%; M235: 22.4% and 30.8%, respectively) was statistically different (p = 0.005) and not related to the presence of essential hypertension. Similar results were observed with the AGT A(-6)G polymorphism. In multiple logistic regression analysis, CHD odds ratio associated with 235T and M235 homozygotes were 1.7 (1.1 to 2.6) and 0.54 (0.36 to 0.82), respectively. CONCLUSIONS: This study shows that genetic variation of the AGT (M235T), but not the ACE (I/D), genotypes contributes to the presence of CHD independently of blood pressure profile in a subset of the Spanish population with a high prevalence of cardiovascular disease.

[Valsartan in patients with arterial hypertension and type 2 diabetes mellitus. The lapaval study]. / Efecto del valsartin sobre la presión arterial y función renal en pacientes con hipertensión arterial y diabetes mellitus tipo 2. Estudio Lapaval.

UNLABELLED: Arterial hypertension and diabetes mellitus give rise to a situation of high cardiovascular risk. The potential renoprotection from inhibition of the renin-angiotensin system is a valid option in this type of patient. OBJECTIVE: Evaluate the effect of valsartan on blood pressure (BP) and renal function in albuminuric patients with type 2 diabetes and arterial hypertension. PATIENTS AND METHODS: This was a prospective, observational study. Seventy-four diabetic patients with a blood pressure of > or = 140/90 mmHg, with micro or macroalbuminuria and a) blood creatinine levels lower 1.5 mg/dl (group 1) or b) blood creatinine levels between 1.5 and 2 mg/dl (group 2), were studied and followed up for a 12-week period. Treatment was started with valsartan 80 mg/d, increasing to 160 mg/d, adding torasemide at a dose of 5 mg/d if the target blood pressure of 130/85 mmHg has not been achieved. The degree of BP reduction was analyzed comparatively using a mercury sphygmomanometer and a semi-automatic monitor, the Omron HEM 705 CP. RESULTS: All patients showed a significant reduction of the systolic (SBP) and diastolic (DBP) blood pressures (p< 0.001) over the study period, decreasing from 150.7 +/- 12.8 to 130.8 +/- 9.6 and from 94.7 +/- 7.7 to 76.8 +/- 6.3 mmHg, respectively. A significant reduction was observed only for diastolic blood pressure (101.4 +/- 8.8 to 79.4 +/- 5.6; p < 0.001) in the group 2 of patients. Lowest BP values were always obtained with the semiautomatic device. At the end of the study, 9.5% maintained valsartan 80 mg/d and 36.5% reqcuired the addition of a second or third drug to valsartan 160 mg in order to achieve the therapeutic target BP A significant reduction was observed in the microalbuminuria (75.5 +/- 9.5 to 54.7 +/- 7.3 microg/min; p < 0.001) and macroalbuminuria (n = 20; 0.93 +/- 0.4 to 0.68 +/- 0.4 g/day; p < 0.001). CONCLUSION: Valsartan significantly reduced SBP and DBP Valsartan at 160 mg/d had a significantly greater effect in reducing micro and macroalbuminuria. No changes were observed in renal function, HbA1c or serum potassium. The rate of adverse events was very low.

Low turnover bone disease is the more common form of bone disease in CAPD patients.

CAPD is considered a risk factor for low turnover bone disease. This was previously attributed to aluminum accumulation. We evaluated by biochemical and histomorphometric parameters (including double tetracycline labelling), 26 patients maintained on CAPD for 12-14 months. Three (11.5%) showed mild hyperparathyroidism, 5 (19.2%) osteitis fibrosa, 3 (11.5%) mixed forms, 4 (15%) osteomalacia and 11 (42.3%) adynamic bone disease. Only one patient with diabetes mellitus showed an aluminum stained bone surface > 10%. Intact PTH serum levels were lower in LTBD (133.2 +/- 128 vs 468.2 +/- 451 pg/ml; p < 0.05). We also evaluated prospectively 11 patients who underwent a bone biopsy at start of dialysis and after 12 months of CAPD treatment. Bone biopsies pre CAPD demonstrated normal-high bone turnover disease in 8/11 (72.7%) and low turnover bone disease in 3/11 (27%). In the follow-up biopsies, 2 patients showed osteitis fibrosa and other two mild forms. Low turnover bone disease was found in 7 patients (3 osteomalacia and 4 adynamic bone disease). We conclude that the predominant bone lesion in our CAPD patients is low turnover bone disease, predominantly adynamic forms, and aluminum does not seem to play a role on its genesis. Low intact PTH serum levels may be a predictor of low turnover bone disease.

[Effects of carvedilol in rats with induced chronic kidney failure]. / Efectos del carvedilol en ratas con insuficiencia renal crónica inducida.

Hypertensive mechanisms are postulated to play a major role in the progressive glomerulosclerosis (GS) after renal mass reduction. Previous studies have demonstrated differences in the progression to glomerulosclerosis with the use of different antihypertensive drugs. We analyzed whether the use of carvedilol (CVD), a new beta-adrenoceptor antagonist and vasodilator slows the progression of glomerulosclerosis in 5/6 nephrectomised (Nx) rats. Fifty-four adult Sprague-Dawley rats were distributed among five groups, four with 5/6 Nx, vehicle treated and CVD at 5, 10 and 20 mg/kg/day and sham (no renal ablation or drug treatment). Tailcuff blood pressure, serum creatinine and urine protein concentration were measured. At the end of the experiment remnant kidney was removed for morphometric studies. Rats treated with 10 and 20 mg/kg/day of CVD showed controlled systemic blood pressure. Serum creatinine was similar in all treated groups with CVD, and half the levels observed in the vehicle-treated rats. The prevalence of glomerular lesions was closely associated with the degree of proteinuria. Eleven weeks after 5/6 Nx, vehicle-treated rats exhibited marked GS with 76% of affected glomeruli and creatinine retention. By contrast, renal injury was largely prevent in those rats treated with 10 and 20 mg/kg/day of CVD. Tuft enlargement occurred in all groups but was more prominent in vehicle-treated group, 1.5 times higher than the group treated with 20 mg/kg/day of CVD. Although, these data demonstrate the importance of systemic blood pressure control in the renal protective efficacy of carvedilol, other less-known mechanisms of this drug must be investigated.

Effects of the novel multiple-action agent carvedilol on severe nephrosclerosis in renal ablated rats.

Antihypertensive drugs have differing effects on renal hemodynamics and morphology. We analyzed whether the use of a new beta adrenoceptor antagonist and vasodilator, carvedilol (CVD), slows the progression of nephrosclerosis and whether the renoprotective effect as well as reduction in cardiac hypertrophy is dependent on the degree of blood pressure reduction. Fifty-four adult male Sprague-Dawley rats were distributed among five groups: group I served as untreated controls with 5/6 nephrectomy (Nx); group II, sham (no renal ablation or drug treatment); group III, CVD 5 (5/6 Nx and treatment with oral CVD at 5 mg/kg/day); group IV, CVD 10 (5/6 Nx and treatment with oral CVD at 10 mg/kg/day); and group V, CVD 20 (5/6 Nx and treatment with oral CVD at 20 mg/kg/day). Tail-cuff blood pressure and 24-hr urine samples were obtained before and at 3, 5 and 11 weeks of treatment with CVD. At the end of the study period, blood was taken to measure serum creatinine, plasma renin activity and CVD levels, as well as the remnant kidney and heart for morphological studies. There was a significant reduction in 24-hr U(ProtV) in all the CVD-treated groups, and it was increasingly evident with the highest dose used. However, only rats receiving doses of 10 and 20 mg/kg/day of CVD exhibited significant decreases in blood pressure. Elevated serum creatinine levels seen in untreated controls were significantly decreased by CVD in treated rats (P < .01), indicating that glomerular filtration rate was improved by this drug. This was associated with a significant increase in U(NaV). Concomitant and significant (P < .01) decreases in plasma renin activity were observed in sham and CVD-treated rats. CVD-treated animals had considerably reduced renal damage (P < .01) and cardiac hypertrophy (P < .01) compared with untreated controls. These data indicate that CVD is effective in delaying progression of renal damage and provides beneficial effects in the remnant kidney and cardiac hypertrophy, even at nonhypotensive doses.