17beta-Nortestosterone (17betaN) is illegally used in livestock as a growth promoter and its endogenous production has been described in some animals, such as adult boars. In this paper, the metabolism of 17betaN in boars has been studied by gas chromatography/mass spectrometry (GC/MS) in order to identify markers of the exogenous administration. Administration studies of intramuscular 17betaN laurate to male pigs were performed. Free, sulphate and glucuronide fractions of the urine samples were separated and the steroids present were quantified by GC/MS. 17betaN was detected in some pre-administration samples. After administration, 17betaN, norandrosterone, noretiocholanolone (NorE), norepiandrosterone, 5beta-estrane-3alpha,17beta-diol and 5alpha-estrane-3beta,17beta-diol were detected in different fractions, being the most important metabolites, 17betaN excreted as a sulphate and free NorE. Samples collected in routine controls were also analyzed by GC/MS to identify endogenous compounds. 17betaN, norandrostenedione and estrone were detected in almost all the samples. No other 17betaN metabolites were detected. According to these results, the detection by GC/MS of some of the 17betaN metabolites described above, different from 17betaN, could be indicative of the exogenous administration of 17betaN to boars.
Recent reports have disagreed on whether the bioavailability of S(+)-ketoprofen is affected by the presence of R(-)-ketoprofen. To examine this directly, we designed a randomized crossover study in beagle dogs. [ C]- S(+)-ketoprofen trometamol and R(-)-ketoprofen trometamol were administered in the following percentage ratios: A, 99:1; B, 95:5; C, 90:10; D, 70:30; E, 50:50. Treatments were administered as a single oral dose of 1 mg/kg trometamol salt. Each of eight dogs received all five combinations in random order with a 1-week washout period between doses. Blood samples were taken before drug administration and at regular intervals for 240 min after dosing. A progressive increase in the plasma concentration of [ C]-S(+)-ketoprofen was observed on going from treatment E (lowest dose of S-enantiomer) to treatments containing the highest doses of ( C]-S(+)-ketoprofen. When the pharmacokinetic calculations were normalized to the dose of ( C]-S(+)-ketoprofen, we found no statistically significant differences among the normalized AUC and C values of the five treatments. Therefore, S(+)-ketoprofen absorption was linear and was not influenced by the presence of R(-)-ketoprofen. Furthermore, there were no significant differences in t values among treatments, indicating that the rate of S(+)-ketoprofen absorption was also unaffected by the presence of R(-)-ketoprofen.
Traffic calming and pedestrianization schemes are increasingly considered a solution for cities to improve air quality and foster wellbeing of the local population. Given that public opposition is considered one of the main obstacles to the introduction of this type of interventions, this paper investigates public acceptance and attitudes towards a specific urban intervention to reduce air pollution: the superblocks. Based on a survey (N=581) and focus groups (N=16) with residents in Barcelona, Spain, we analyse on the beliefs and emotions, as well as the socio-demographic characteristics of supporters and opponents to the superblocks. The results showed a significant polarization in the acceptance of the superblocks. Relative to opponents to the superblocks, supporters were younger, more likely to be female, more likely to live near a superblock, not own a car and position themselves on the left side of the ideological scale. Policy-specific beliefs, emotions, perceived process legitimacy and institutional trust were strongly associated to acceptance of the superblocks. These findings constitute a first step to the study of the social dynamics that underlie acceptance and opposition to the superblocks.
Introduction Diabetic patients may develop diabetic cardiomyopathy (DCM) and are at increased risk of myocardial infarction (MI). Yet, cardioprotection remains a challenge in the presence of comorbidities. Objectives We examined whether intravenous administration of atorvastatin during ongoing myocardial ischemia prevents against the deleterious effects of MI in DCM rats. Methods DCM was induced by streptozotocin (65 mg/kg) in Sprague Dawley rats (n = 14). 5 weeks thereafter animals exhibited a DCM phenotype associated with a significant diastolic (IVRT + 15.64 ± 5.49ms P < 0.05 vs. baseline) and systolic (LVEF, −8.63 ± 6.71% P < 0.05 vs. baseline) ventricular dysfunction. AMI was then induced by coronary ligation of the LAD for 45minutes. Early after ischemia (15minutes) DCM-rats received either i.v atorvastatin or vehicle. Animals were reperfused and sacrificed at 24h for infarct size assessment and molecular analysis. Cardiac function was monitored by echocardiography. Results No differences were detected as per the area-at-risk between both animal groups. Atorvastatin significantly reduced infarct size expansion (35% relative reduction) as compared to vehicle (15.3 ± 1.03% vs. 23.7 ± 4.3% IS/AAR; P < 0.05). LVEF, shortening fraction, and stroke volume were better preserved in atorvastatin-treated DCM rats as compared to vehicle (4.62 ± 2.55% vs. 12.4 ± 3.16%; 5.77 ± 3.74% vs. 15.9 ± 4.9%; and 58.93 ± 28.79μl vs. 101.73 ± 31.58 μl, respectively; P < 0.05). At a molecular level, atorvastatin administration was associated with a lower expression of Phosphorylated-p53 (apoptosis) and higher P-AMPK/AMP ratio (cardiac metabolism); P < 0.05 vs. vehicle). Conclusion Intravenous administration of atorvastatin during MI limits infarct size and preserves cardiac function post-MI in rats with manifest DCM supporting the cardioprotective potential of this therapeutic approach despite comorbid conditions.
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