Discutindo a educação ambiental no cotidiano escolar: desenvolvimento de projetos na escola formação inicial e continuada de professores

A presente pesquisa buscou discutir como a Educação Ambiental (EA) vem sendo trabalhada, no Ensino Fundamental e como os docentes desta escola compreendem e vem inserindo a EA no cotidiano escolar., em uma escola estadual do município de Tangará da Serra/MT, Brasil. Para tanto, realizou-se entrevistas com os professores que fazem parte de um projeto interdisciplinar de EA na escola pesquisada. Verificou-se que o projeto da escola não vem conseguindo alcançar os objetivos propostos por: desconhecimento do mesmo, pelos professores; formação deficiente dos professores, não entendimento da EA como processo de ensino-aprendizagem, falta de recursos didáticos, planejamento inadequado das atividades. A partir dessa constatação, procurou-se debater a impossibilidade de tratar do tema fora do trabalho interdisciplinar, bem como, e principalmente, a importância de um estudo mais aprofundado de EA, vinculando teoria e prática, tanto na formação docente, como em projetos escolares, a fim de fugir do tradicional vínculo “EA e ecologia, lixo e horta”.Facultad de Humanidades y Ciencias de la Educació

Size Matters: How to Characterize ADPKD Severity by Measuring Total Kidney Volume

Following patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD) has been challenging because serum biomarkers such as creatinine often remain normal until relatively late in the disease [...

Bladder diverticuli following injection of onabotulinum toxin A in a patient with multiple sclerosis and autosomal dominant polycystic kidney disease

Urinary incontinence due to neurogenic detrusor overactivity is common in patients with disorders of lower motor neurons controlling the bladder. Multiple sclerosis is a major cause of neurogenic detrusor overactivity, which negatively impacts quality of life. Bladder wall injection of onabotulinum toxin A can diminish spontaneous bladder contraction, urinary urgency, and urge incontinence. Herein we report a 61-year-old woman with multiple sclerosis and autosomal dominant polycystic kidney disease with bladder trabeculation developing after repeated injections of onabotulinum toxin A. Keywords: Bladder diverticuli, Onabotulinum toxin A, Botox, ADPKD, multiple sclerosis, MR

Pleural Effusions on MRI in Autosomal Dominant Polycystic Kidney Disease

Autosomal dominant polycystic kidney disease (ADPKD) has cystic fluid accumulations in the kidneys, liver, pancreas, arachnoid spaces as well as non-cystic fluid accumulations including pericardial effusions, dural ectasia and free fluid in the male pelvis. Here, we investigate the possible association of ADPKD with pleural effusion. ADPKD subjects (n = 268) and age-gender matched controls without ADPKD (n = 268) undergoing body magnetic resonance imaging from mid-thorax down into the pelvis were independently evaluated for pleural effusion by 3 blinded expert observers. Subjects with conditions associated with pleural effusion were excluded from both populations. Clinical and laboratory data as well as kidney, liver and spleen volume, pleural fluid volume, free pelvic fluid and polycystic kidney disease genotype were evaluated. Pleural effusions were observed in 56 of 268 (21%) ADPKD subjects compared with 21 of 268 (8%) in controls (p p p = 0.02) and in males were weakly correlated with the presence of free pelvic fluid (r = 0.24, p = 0.02). ADPKD subjects with pleural effusions were younger (48 ± 14 years old vs. 43 ± 14 years old) and weighed less (77 vs. 70 kg; p ≤ 0.02) than those without pleural effusions. For ADPKD subjects with pleural effusions, the mean volume of fluid layering dependently in the posterior–inferior thorax was 19 mL and was not considered to be clinically significant. Pleural effusion is associated with ADPKD, but its role in the pathogenesis of ADPKD requires further evaluation

Urine MicroRNA as Potential Biomarkers of Autosomal Dominant Polycystic Kidney Disease Progression: Description of miRNA Profiles at Baseline

<div><p>Background</p><p>Autosomal dominant polycystic kidney disease (ADPKD) is clinically heterogenic. Biomarkers are needed to predict prognosis and guide management. We aimed to profile microRNA (miRNA) in ADPKD to gain molecular insight and evaluate biomarker potential.</p><p>Methods</p><p>Small-RNA libraries were generated from urine specimens of ADPKD patients (N = 20) and patients with chronic kidney disease of other etiologies (CKD, N = 20). In this report, we describe the miRNA profiles and baseline characteristics. For reference, we also examined the miRNA transcriptome in primary cultures of ADPKD cyst epithelia (N = 10), normal adult tubule (N = 8) and fetal tubule (N = 7) epithelia.</p><p>Results</p><p>In primary cultures of ADPKD kidney cells, miRNA cistrons mir-143(2) (9.2-fold), let-7i(1) (2.3-fold) and mir-3619(1) (12.1-fold) were significantly elevated compared to normal tubule epithelia, whereas mir-1(4) members (19.7-fold), mir-133b(2) (21.1-fold) and mir-205(1) (3.0-fold) were downregulated (P<0.01). Expression of the dysregulated miRNA in fetal tubule epithelia resembled ADPKD better than normal adult cells, except let-7i, which was lower in fetal cells. In patient biofluid specimens, mir-143(2) members were 2.9-fold higher in urine cells from ADPKD compared to other CKD patients, while expression levels of mir-133b(2) (4.9-fold) and mir-1(4) (4.4-fold) were lower in ADPKD. We also noted increased abundance mir-223(1) (5.6-fold), mir-199a(3) (1.4-fold) and mir-199b(1) (1.8-fold) (P<0.01) in ADPKD urine cells. In ADPKD urine microvesicles, miR-1(2) (7.2-fold) and miR-133a(2) (11.8-fold) were less abundant compared to other CKD patients (P<0.01).</p><p>Conclusions</p><p>We found that in ADPKD urine specimens, miRNA previously implicated as kidney tumor suppressors (miR-1 and miR-133), as well as miRNA of presumed inflammatory and fibroblast cell origin (miR-223/miR-199), are dysregulated when compared to other CKD patients. Concordant with findings in the primary tubule epithelial cell model, this suggests roles for dysregulated miRNA in ADPKD pathogenesis and potential use as biomarkers. We intend to assess prognostic potential of miRNA in a followup analysis.</p></div

miRNA cistron clusters differentially expressed between ADPKD-derived and normal kidney-derived primary tubular epithelial cultures^*.

*<p>, Cutoff for presentation in this table is p-value<0.05 and FDR<0.2 in the ADPKD vs. normal comparison.</p

miRNA sequence variants that were found to be differentially expressed between ADPKD and non-ADPKD specimens.

<p>(<b>A</b>) miRNA sequence variants that were found to be differentially expressed between ADPKD cyst-derived primary cultures and normal adult kidney derived cultures (see complete list in Table S15 in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0086856#pone.0086856.s005" target="_blank">File S1</a>). (<b>B</b>) Box plot showing a composite score derived from the information in (A). The median frequency of each miRNA variant across the samples was used to generate the score; 1 point was added (or reduced) for each miRNA variant with frequency above (or below) the median frequency. (<b>C</b>) Bar plot showing a composite score derived in a manner similar to (B) from patient' urine sediment cell sequence data (contributing miRNA variants are depicted in Table S16 in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0086856#pone.0086856.s005" target="_blank">File S1</a>).</p

Hierarchically clustered study samples grouped by type and clinical characteristics.

<p>including additional non-study specimens for reference (columns) and miRNA cistrons (rows). High relative read frequency (log₂-transformed) is indicated by bright yellow shades; low frequencies in dark blue. Corresponding numerical data is presented in the supplementary tables. Abbreviations: ADPKD, autosomal dominant polycystic kidney disease; CKD, chronic kidney disease; immort, immortalized; CPM, counts per million; F, female; M, male.</p