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Author Al-Nouri, Z.L.; Reese, J.A.; Terrell, D.R.; Vesely, S.K.; George, J.N. url  openurl
  Title Drug-induced thrombotic microangiopathy: a systematic review of published reports Type Journal Article
  Year 2015 Publication Abbreviated Journal Blood  
  Volume 125 Issue 4 Pages 616-618  
  Keywords  
  Abstract Many patients with syndromes of thrombotic microangiopathy (TMA), including thrombotic thrombocytopenic purpura and hemolytic-uremic syndrome, have been reported to have a drug-induced etiology, and many different drugs have been suspected as a cause of TMA. We established criteria to assess the strength of evidence for a causal association of a drug with TMA and systematically searched for all published reports of drug-induced TMA. We identified 1569 articles: 604 were retrieved for review, 344 reported evaluable data for 586 individual patients, 43 reported evaluable data on 46 patient groups. Seventy-eight drugs were described; 22 had evidence supporting a definite causal association with TMA. Three drugs accounted for 61 of the 104 patient reports with definite evidence (quinine, 34; cyclosporine, 15; tacrolimus, 12). Twenty additional drugs had evidence supporting a probable association with TMA. These criteria and data can provide support for clinicians evaluating patients with suspected TMA.  
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  Series Volume Series Issue Edition  
  ISSN 0006-4971 ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number UofT @ mathieu.lemaire @ Serial (down) 45847  
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Author Andrade-Oliveira, V.; Amano, M.T.; Correa-Costa, M.; Castoldi, A.; Felizardo, R.J.; de Almeida, D.C.; Bassi, E.J.; Moraes-Vieira, P.M.; Hiyane, M.I.; Rodas, A.C.; Peron, J.P.; Aguiar, C.F.; Reis, M.A.; Ribeiro, W.R.; Valduga, C.J.; Curi, R.; Vinolo, M.A.; Ferreira, C.M.; Câmara, N.O. url  openurl
  Title Gut Bacteria Products Prevent AKI Induced by Ischemia-Reperfusion Type Journal Article
  Year 2015 Publication Abbreviated Journal J Am Soc Nephrol  
  Volume 26 Issue 8 Pages 1877-1888  
  Keywords  
  Abstract Short-chain fatty acids (SCFAs) are fermentation end products produced by the intestinal microbiota and have anti-inflammatory and histone deacetylase-inhibiting properties. Recently, a dual relationship between the intestine and kidneys has been unraveled. Therefore, we evaluated the role of SCFA in an AKI model in which the inflammatory process has a detrimental role. We observed that therapy with the three main SCFAs (acetate, propionate, and butyrate) improved renal dysfunction caused by injury. This protection was associated with low levels of local and systemic inflammation, oxidative cellular stress, cell infiltration/activation, and apoptosis. However, it was also associated with an increase in autophagy. Moreover, SCFAs inhibited histone deacetylase activity and modulated the expression levels of enzymes involved in chromatin modification. In vitro analyses showed that SCFAs modulated the inflammatory process, decreasing the maturation of dendritic cells and inhibiting the capacity of these cells to induce CD4(+) and CD8(+) T cell proliferation. Furthermore, SCFAs ameliorated the effects of hypoxia in kidney epithelial cells by improving mitochondrial biogenesis. Notably, mice treated with acetate-producing bacteria also had better outcomes after AKI. Thus, we demonstrate that SCFAs improve organ function and viability after an injury through modulation of the inflammatory process, most likely via epigenetic modification.  
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  ISSN 1046-6673 ISBN Medium  
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  Notes Approved no  
  Call Number UofT @ mathieu.lemaire @ Serial (down) 45839  
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Author Amendola, L.M.; Dorschner, M.O.; Robertson, P.D.; Salama, J.S.; Hart, R.; Shirts, B.H.; Murray, M.L.; Tokita, M.J.; Gallego, C.J.; Kim, D.S.; Bennett, J.T.; Crosslin, D.R.; Ranchalis, J.; Jones, K.L.; Rosenthal, E.A.; Jarvik, E.R.; Itsara, A.; Turner, E.H.; Herman, D.S.; Schleit, J.; Burt, A.; Jamal, S.M.; Abrudan, J.L.; Johnson, A.D.; Conlin, L.K.; Dulik, M.C.; Santani, A.; Metterville, D.R.; Kelly, M.; Foreman, A.K.; Lee, K.; Taylor, K.D.; Guo, X.; Crooks, K.; Kiedrowski, L.A.; Raffel, L.J.; Gordon, O.; Machini, K.; Desnick, R.J.; Biesecker, L.G.; Lubitz, S.A.; Mulchandani, S.; Cooper, G.M.; Joffe, S.; Richards, C.S.; Yang, Y.; Rotter, J.I.; Rich, S.S.; O’Donnell, C.J.; Berg, J.S.; Spinner, N.B.; Evans, J.P.; Fullerton, S.M.; Leppig, K.A.; Bennett, R.L.; Bird, T.; Sybert, V.P.; Grady, W.M.; Tabor, H.K.; Kim, J.H.; Bamshad, M.J.; Wilfond, B.; Motulsky, A.G.; Scott, C.R.; Pritchard, C.C.; Walsh, T.D.; Burke, W.; Raskind, W.H.; Byers, P.; Hisama, F.M.; Rehm, H.; Nickerson, D.A.; Jarvik, G.P. url  openurl
  Title Actionable exomic incidental findings in 6503 participants: challenges of variant classification Type Journal Article
  Year 2015 Publication Abbreviated Journal Genome Res  
  Volume 25 Issue 3 Pages 305-315  
  Keywords  
  Abstract Recommendations for laboratories to report incidental findings from genomic tests have stimulated interest in such results. In order to investigate the criteria and processes for assigning the pathogenicity of specific variants and to estimate the frequency of such incidental findings in patients of European and African ancestry, we classified potentially actionable pathogenic single-nucleotide variants (SNVs) in all 4300 European- and 2203 African-ancestry participants sequenced by the NHLBI Exome Sequencing Project (ESP). We considered 112 gene-disease pairs selected by an expert panel as associated with medically actionable genetic disorders that may be undiagnosed in adults. The resulting classifications were compared to classifications from other clinical and research genetic testing laboratories, as well as with in silico pathogenicity scores. Among European-ancestry participants, 30 of 4300 (0.7%) had a pathogenic SNV and six (0.1%) had a disruptive variant that was expected to be pathogenic, whereas 52 (1.2%) had likely pathogenic SNVs. For African-ancestry participants, six of 2203 (0.3%) had a pathogenic SNV and six (0.3%) had an expected pathogenic disruptive variant, whereas 13 (0.6%) had likely pathogenic SNVs. Genomic Evolutionary Rate Profiling mammalian conservation score and the Combined Annotation Dependent Depletion summary score of conservation, substitution, regulation, and other evidence were compared across pathogenicity assignments and appear to have utility in variant classification. This work provides a refined estimate of the burden of adult onset, medically actionable incidental findings expected from exome sequencing, highlights challenges in variant classification, and demonstrates the need for a better curated variant interpretation knowledge base.  
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  Series Volume Series Issue Edition  
  ISSN 1088-9051 ISBN Medium  
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  Notes Approved no  
  Call Number UofT @ mathieu.lemaire @ Serial (down) 45831  
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Author Akchurin, O.; Reidy, K.J. url  openurl
  Title Genetic causes of proteinuria and nephrotic syndrome: impact on podocyte pathobiology Type Journal Article
  Year 2015 Publication Abbreviated Journal Pediatr Nephrol  
  Volume 30 Issue 2 Pages 221-233  
  Keywords  
  Abstract In the past 20 years, multiple genetic mutations have been identified in patients with congenital nephrotic syndrome (CNS) and both familial and sporadic focal segmental glomerulosclerosis (FSGS). Characterization of the genetic basis of CNS and FSGS has led to the recognition of the importance of podocyte injury to the development of glomerulosclerosis. Genetic mutations induce injury due to effects on the podocyte’s structure, actin cytoskeleton, calcium signaling, and lysosomal and mitochondrial function. Transgenic animal studies have contributed to our understanding of podocyte pathobiology. Podocyte endoplasmic reticulum stress response, cell polarity, and autophagy play a role in maintenance of podocyte health. Further investigations related to the effects of genetic mutations on podocytes may identify new pathways for targeting therapeutics for nephrotic syndrome.  
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  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0931-041x ISBN Medium  
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  Notes Approved no  
  Call Number UofT @ mathieu.lemaire @ Serial (down) 45820  
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Author Al-Awqati, Q. url  openurl
  Title Kidney growth and hypertrophy: the role of mTOR and vesicle trafficking Type Journal Article
  Year 2015 Publication Abbreviated Journal J Clin Invest  
  Volume 125 Issue 6 Pages 2267-2270  
  Keywords  
  Abstract The kidney, like other organs, grows in constant proportion to the rest of the body. When one kidney is removed, the remaining one hypertrophies. In a comprehensive series of studies, Chen et al. show that growth during maturation is mediated by the mTORC1 signaling pathway, which is induced by EGF-like peptides, and requires PI3K, PDK, AKT, mTORC2, and activation of mTORC1 through the combined effects of TSC and RHEB as part of a multiprotein complex localized on lysosomes. However, compensatory growth is mediated by amino acids, which act on mTORC1 independently of the previous pathway, and requires a class III PI3K (VPS34) that is known to be involved in vesicle trafficking to the lysosomes.  
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  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0021-9738 ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number UofT @ mathieu.lemaire @ Serial (down) 45804  
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Author Ali, M.I.; Chen, X.; Didion, S.P. url  openurl
  Title Heterozygous eNOS deficiency is associated with oxidative stress and endothelial dysfunction in diet-induced obesity Type Journal Article
  Year 2015 Publication Abbreviated Journal Physiol Rep  
  Volume 3 Issue 12 Pages  
  Keywords  
  Abstract Heterozygous endothelial nitric oxide synthase (eNOS) deficiency is associated with normal endothelium-dependent responses, however, little is known regarding the mechanisms that maintain or impair endothelial function with heterozygous eNOS deficiency. The goals of this study were to (1) determine mechanism(s) which serve to maintain normal endothelial function in the absence of a single eNOS gene; and (2) to determine whether heterozygous eNOS deficiency predisposes blood vessels to endothelial dysfunction in response to a high-fat diet (HFD). Responses of carotid arteries were examined in wild-type (eNOS(+/+)) and heterozygous eNOS-deficient (eNOS(+/-)) treated with either vehicle (saline), N(G)-nitro-L-arginine (L-NNA, 100 μmol/L), an inhibitor of nitric oxide synthase, or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 1 μmol/L), an inhibitor of soluble guanylyl cyclase (sGC), and in eNOS(+/+) and eNOS(+/-) mice fed a control (10%) or a 45% HFD (kcal from fat). Responses to acetylcholine (ACh) were similar in vehicle-treated arteries from eNOS(+/+) and eNOS(+/-) mice, and were equally inhibited by L-NNA and ODQ. Phosphorylation of eNOS Ser1176, a site associated with increased eNOS activity, was significantly greater in eNOS(+/-) mice most likely as a compensatory response for the loss of a single eNOS gene. In contrast, responses to ACh were markedly impaired in carotid arteries from eNOS(+/-), but not eNOS(+/+), mice fed a HFD. Vascular superoxide levels as well as plasma levels of the pro-inflammatory cytokine interleukin-6 (IL-6) were selectively increased in HFD-fed eNOS(+/-) mice. In reconstitution experiments, IL-6 produced concentration-dependent impairment of endothelial responses as well as greater increases in NADPH-stimulated superoxide levels in arteries from eNOS(+/-) mice fed a control diet compared to eNOS(+/+) mice. Our findings of increased Ser1176-phosphorylation reveal a mechanism by which NOS- and sGC-dependent endothelial function can be maintained with heterozygous eNOS deficiency. In addition, heterozygous eNOS deficiency predisposes blood vessels to developing endothelial dysfunction in response to a HFD. The impairment produced by a HFD in eNOS(+/-) mice appears to be mediated by IL-6-induced increases in vascular superoxide. These findings serve as an important example of eNOS haploinsufficiency, one that may contribute to the development of carotid artery disease in obese humans.  
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  ISSN 2051-817x ISBN Medium  
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  Call Number UofT @ mathieu.lemaire @ Serial (down) 45799  
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Author Allum, F.; Shao, X.; Guénard, F.; Simon, M.M.; Busche, S.; Caron, M.; Lambourne, J.; Lessard, J.; Tandre, K.; Hedman, Å.K.; Kwan, T.; Ge, B.; Multiple, T.H.E.R.C.; Rönnblom, L.; McCarthy, M.I.; Deloukas, P.; Richmond, T.; Burgess, D.; Spector, T.D.; Tchernof, A.; Marceau, S.; Lathrop, M.; Vohl, M.C.; Pastinen, T.; Grundberg, E. url  openurl
  Title Characterization of functional methylomes by next-generation capture sequencing identifies novel disease-associated variants Type Journal Article
  Year 2015 Publication Abbreviated Journal Nat Commun  
  Volume 6 Issue Pages 7211  
  Keywords  
  Abstract Most genome-wide methylation studies (EWAS) of multifactorial disease traits use targeted arrays or enrichment methodologies preferentially covering CpG-dense regions, to characterize sufficiently large samples. To overcome this limitation, we present here a new customizable, cost-effective approach, methylC-capture sequencing (MCC-Seq), for sequencing functional methylomes, while simultaneously providing genetic variation information. To illustrate MCC-Seq, we use whole-genome bisulfite sequencing on adipose tissue (AT) samples and public databases to design AT-specific panels. We establish its efficiency for high-density interrogation of methylome variability by systematic comparisons with other approaches and demonstrate its applicability by identifying novel methylation variation within enhancers strongly correlated to plasma triglyceride and HDL-cholesterol, including at CD36. Our more comprehensive AT panel assesses tissue methylation and genotypes in parallel at ∼4 and ∼3 M sites, respectively. Our study demonstrates that MCC-Seq provides comparable accuracy to alternative approaches but enables more efficient cataloguing of functional and disease-relevant epigenetic and genetic variants for large-scale EWAS.  
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  Series Volume Series Issue Edition  
  ISSN 2041-1723 ISBN Medium  
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  Notes Approved no  
  Call Number UofT @ mathieu.lemaire @ Serial (down) 45631  
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Author Aoki-Kinoshita, K.F. isbn  openurl
  Title Glycoinformatics: Overview Type Book Chapter
  Year 2015 Publication Glycoinformatics: Overview Abbreviated Journal  
  Volume Glycoscience: Biology and Medicine Issue Pages 185-192  
  Keywords  
  Abstract Because of the many different glycan-related databases now publicly available, a number of different glycan structure representations are used to graphically and textually display glycans structures. This overview provides an easy reference to each representation format as well as links to several major databases and web resources that may be useful for glycobiologists. Many of the major databases, glycan sequence and structure representation formats, and tools that are currently available and used in the glycoscience field will be …  
  Address  
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  Publisher Springer Place of Publication Tokyo Editor Endo, T.; Seeberger, P.H.; Hart, G.W.; Wong, C.-H.; Taniguchi, N.  
  Language Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN 978-4-431-54836-2 Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number UofT @ mathieu.lemaire @ Serial (down) 45629  
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Author Andersson, R.; Sandelin, A.; Danko, C.G. url  openurl
  Title A unified architecture of transcriptional regulatory elements Type Journal Article
  Year 2015 Publication Abbreviated Journal Trends Genet  
  Volume 31 Issue 8 Pages 426-433  
  Keywords  
  Abstract Gene expression is precisely controlled in time and space through the integration of signals that act at gene promoters and gene-distal enhancers. Classically, promoters and enhancers are considered separate classes of regulatory elements, often distinguished by histone modifications. However, recent studies have revealed broad similarities between enhancers and promoters, blurring the distinction: active enhancers often initiate transcription, and some gene promoters have the potential to enhance transcriptional output of other promoters. Here, we propose a model in which promoters and enhancers are considered a single class of functional element, with a unified architecture for transcription initiation. The context of interacting regulatory elements and the surrounding sequences determine local transcriptional output as well as the enhancer and promoter activities of individual elements.  
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  ISSN 0168-9525 ISBN Medium  
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  Notes Approved no  
  Call Number UofT @ mathieu.lemaire @ Serial (down) 45626  
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Author Alsady, M.; Baumgarten, R.; Deen, P.M.; de Groot, T. url  openurl
  Title Lithium in the Kidney: Friend and Foe Type Journal Article
  Year 2015 Publication Abbreviated Journal J Am Soc Nephrol  
  Volume Issue Pages  
  Keywords Nephrology  
  Abstract Trace amounts of lithium are essential for our physical and mental health, and administration of lithium has improved the quality of life of millions of patients with bipolar disorder for >60 years. However, in a substantial number of patients with bipolar disorder, long-term lithium therapy comes at the cost of severe renal side effects, including nephrogenic diabetes insipidus and rarely, ESRD. Although the mechanisms underlying the lithium-induced renal pathologies are becoming clearer, several recent animal studies revealed that short-term administration of lower amounts of lithium prevents different forms of experimental AKI. In this review, we discuss the knowledge of the pathologic and therapeutic effects of lithium in the kidney. Furthermore, we discuss the underlying mechanisms of these seemingly paradoxical effects of lithium, in which fine-tuned regulation of glycogen synthase kinase type 3, a prime target for lithium, seems to be key. The new discoveries regarding the protective effect of lithium against AKI in rodents call for follow-up studies in humans and suggest that long-term therapy with low lithium concentrations could be beneficial in CKD.  
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  ISSN 1046-6673 ISBN Medium  
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  Notes Approved no  
  Call Number UofT @ mathieu.lemaire @ Serial (down) 45624  
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