How Can Urban Policies Improve Air Quality and Help Mitigate Global Climate Change: a Systematic Mapping Review.

Tackling climate change at the global level is central to a growing field of scientific research on topics such as environmental health, disease burden, and its resulting economic impacts. At the local level, cities constitute an important hub of atmospheric pollution due to the large amount of pollutants that they emit. As the world population shifts to urban centers, cities will increasingly concentrate more exposed populations. Yet, there is still significant progress to be made in understanding the contribution of urban pollutants other than CO2, such as vehicle emissions, to global climate change. It is therefore particularly important to study how local governments are managing urban air pollution. This paper presents an overview of local air pollution control policies and programs that aim to reduce air pollution levels in megacities. It also presents evidence measuring their efficacy. The paper argues that local air pollution policies are not only beneficial for cities but are also important for mitigating and adapting to global climate change. The results systematize several policy approaches used around the world and suggest the need for more in-depth cross-city studies with the potential to highlight best practices both locally and globally. Finally, it calls for the inclusion of a more human rights-based approach as a mean of guaranteeing of clean air for all and reducing factors that exacerbate climate change.

Association of testosterone with estrogen abolishes the beneficial effects of estrogen treatment by increasing ROS generation in aorta endothelial cells.

Testosterone has been added to hormone replacement therapy to treat sexual dysfunction in postmenopausal women. Whereas estrogen has been associated with vascular protection, the vascular effects of testosterone are contradictory and the effects of its association with estrogen are largely unknown. In this study we determined the effects of testosterone associated with conjugated equine estrogen (CEE) on vascular function using a model of hypertensive postmenopausal female: ovariectomized spontaneously hypertensive rats. Female spontaneously hypertensive rats were divided into sham-operated, ovariectomized (OVX), and OVX treated for 15 days with either CEE alone (OVX+CEE) or associated with testosterone (OVX+CEE+T). Angiotensin II (ANG II)-induced contraction was markedly increased in aortic rings from OVX compared with sham-operated rats. CEE treatment restored ANG-II responses, a beneficial effect abrogated with CEE+T. CEE treatment also increased endothelium-dependent relaxation, which was impaired in OVX rats. This effect was lost by CEE+T. Treatment of aortas with losartan (ANG-II type-1 receptor antagonist) or apocynin (NADPH-oxidase inhibitor) restored the endothelium-dependent relaxation in OVX and CEE+T, establishing an interplay between ANG-II and endothelial dysfunction in OVX and CEE+T. The benefits by CEE were associated with downregulation of NADPH-oxidase subunits mRNA expression and decreased reactive oxygen species generation. The association of testosterone with CEE impairs the benefits of estrogen on OVX-associated endothelial dysfunction and reactive oxygen species generation in rat aorta by a mechanism that involves phosphorylation of the cytosolic NADPH-oxidase subunit p47(phox).

Factors associated with overweight in children living in the neighbourhoods of an urban area of Brazil.

OBJECTIVE: The present study aimed to investigate the individual and family determinants of being overweight among children younger than 10 years of age. DESIGN: Cross-sectional survey. Direct data on children's age, food intake, physical activity, type of transportation used and anthropometric measurements, as well as the education level of the mothers, were collected by trained interviewers. SETTING: Population-based study in the city of Santos, Brazil. SUBJECTS: A total of 531 children under 10 years of age (302 aged <6 years, 229 aged ≥6 years), living in the city of Santos. RESULTS: The overall prevalence of overweight and obesity (BMI-for-age Z-score >1) was 35·4 % for children under 6 years and 38·9 % for children aged 6-10 years. The socio-economic status of the family was associated with being overweight for both age groups. Logistic regression analysis showed that the lower the socio-economic status, the higher the likelihood of being overweight, among both younger children (OR = 7·73; P = 0·02) and older children (OR = 1·98; P = 0·04). The use of active transportation was associated with a lower likelihood of being overweight, but only among younger children (OR = 1·70; P = 0·05). CONCLUSIONS: Socio-economic status seems to be an important individual-level determinant of overweight in children. Public policies should consider promoting the use of active transportation, as the results showed it to have a positive effect on reducing overweight issues. The high prevalence of overweight in younger children suggests that this age group should be a priority in health-promoting interventions.

Metformin reduces the stimulatory effect of obesity on in vivo Walker-256 tumor development and increases the area of tumor necrosis.

AIMS: The objective of this study was to analyze the influence of obesity and insulin resistance on tumor development and, in turn, the effect of insulin sensitizing agents. MAIN METHODS: Male offspring of Wistar rats received monosodium glutamate (400mg/kg) (obese) or saline (control) from the second to sixth day after birth. Sixteen-week-old control and obese rats received 5×10(5) Walker-256 tumor cells, subcutaneously injected into the right flank. Some of the obese and control rats received concomitant treatment with metformin (300mg/kg) by gavage. At the 18th week, obesity was characterized. The percentage of rats that developed tumors, the tumor relative weight and the percentage of cachexia incidence were analyzed. The tumor tissue was evaluated histologically by means of hematoxylin and eosin staining. KEY FINDINGS: Metformin did not correct the insulin resistance in obese rats. The tumor development was significantly higher in the obese group, whereas metformin treatment reduced it. After pathological analysis, we observed that the tumor tissues were similar in all groups except for adipocytes, which were found in greater quantity in the obese and metformin-treated obese groups. The area of tumor necrosis was higher in the group treated with metformin when compared with the untreated one. SIGNIFICANCE: Metformin reduced Walker-256 tumor development but not cachexia in obese rats. The reduction occurred independently of the correction of insulin resistance. Metformin increased the area of necrosis in tumor tissues, which may have contributed to the reduced tumor development.

Amlodipine reduces the antimigratory effect of diclofenac in spontaneously hypertensive rats.

Amlodipine, an antihypertensive drug, and diclofenac, an antiinflammatory drug, may generally be combined, particularly in elderly patients; therefore, the potential for their interaction is high. We aim to determine if amlodipine interferes with the antimigratory effect of diclofenac. For this, male spontaneously hypertensive rats (SHRs) were treated with either diclofenac (1 mg.kg.d, 15 d) alone or combined with amlodipine (10 mg.kg.d, 15 d). Leukocyte rolling, adherence, and migration were studied by intravital microscopy. Diclofenac did not change (180.0 +/- 2.3), whereas amlodipine combined (163.4 +/- 5.1) or not (156.3 +/- 4.3) with diclofenac reduced the blood pressure (BP) levels in SHR (183.1 +/- 4.4). Diclofenac and amlodipine reduced leukocyte adherence, migration, and ICAM-1 expression, whereas only diclofenac reduced rolling leukocytes as well. Combined with amlodipine, the effect of the diclofenac was reduced. Neither treatment tested increased the venular shear rate or modified the venular diameters, number of circulating leukocytes, P-selectin, PECAM-1, L-selectin, or CD-18 expressions. No difference could be found in plasma concentrations of both drugs given alone or in association. In conclusion, amlodipine reduces leukocyte migration in SHR, reducing endothelial cell ICAM-1 expression. Amlodipine reduces the effect of the diclofenac, possibly by the same mechanism. A pharmacokinetic interaction as well as an effect on the other adhesion molecules tested could be discarded.

Decreased endothelium-dependent vasodilation in diabetic female rats: role of prostanoids.

Overproduction of vasoconstrictor prostanoids and reduced prostacyclin levels have been related to the male diabetic-linked vascular dysfunction. However, it is not clear yet if these changes also occur in diabetic females. The aim of this study was to verify the role of prostanoids in the vascular dysfunction of diabetic female rats. The parameters studied were the mesenteric arteriolar reactivity (intravital microscopy and isolated perfused arteriolar bed), prostanoid measurement (enzyme immunoassay), superoxide generation (intravital fluorescence microscopy), and the presence of peroxynitrite (Western blot for nitrotyrosine-containing proteins). The response to acetylcholine was decreased in arterioles of diabetic female rats and diclofenac, but not ridogrel, corrected the altered response. The unstimulated (basal) release of thromboxane B2 (TXB2), but not prostaglandin F2alpha (PGF2alpha) or 6-keto-PGF1alpha, was increased in the mesenteric perfusate from diabetic female rats. Increased production of PGF2alpha and 6-keto-PGF1alpha, but not TXB2, was induced by acetylcholine in diabetic arterioles. The superoxide generation was increased in diabetic female rats and diclofenac corrected it. Diabetes increased nitrotyrosine-containing proteins in mesenteric microvessels. In conclusion, our data show that the increase of constrictor prostanoid release, most likely PGF2alpha, could be involved in the reduced endothelium-dependent vasodilation of diabetic female rats. In addition, the enhanced activation of cyclooxygenase may be a source of superoxide anion generation in this model.

Differential effects of chloral hydrate- and ketamine/xylazine-induced anesthesia by the s.c. route.

The proper use of anesthetics in animal experimentation has been intensively studied. In this study we compared the use of chloral hydrate (500 mg kg(-1)) and ketamine (167 mg kg(-1)) combined with xylazine (33 mg kg(-1)) by the s.c. route in male Wistar rats. Chloral hydrate and ketamine/xylazine produced a depth of anesthesia and analgesia sufficient for surgical procedures. The decrease of systolic and diastolic blood pressure was of a higher magnitude in rats anesthetized with chloral hydrate than with ketamine/xylazine. The initial microvascular diameter and blood flow velocity did not differ between both agents. On the other hand, ketamine/xylazine reduced the heart rate more intensively than chloral hydrate. Both anesthetics promoted an increase in arterial pCO(2) and a decrease in pH levels compared to unanesthetized animals. The blood glucose levels were of a higher magnitude in rats after ketamine/xylazine anesthesia than after chloral hydrate. In mesenteric arterioles studied in vivo, ketamine/xylazine anesthesia reduced the constrictive effect of noradrenaline and the dilator effect of bradykinin. However, both anesthetics did not modify the vasodilator effect promoted by acetylcholine. Based on our data, we concluded that both anesthetics alter metabolic and hemodynamic parameters, however the use of chloral hydrate in studies of microvascular reactivity in vivo is more appropriate since ketamine/xylazine reduces the responses to vasoactive agents and increases blood glucose levels.