LIVIVO - Search results -

Search results

Result 1 - 10 of total 17

Article ; Online: In situ

Lopes, Filipa M / Kimber, Susan J / Bantounas, Ioannis

2021 Volume 11, Issue 17, Page(s) e4150

Abstract: MicroRNAs are small RNAs that negatively regulate gene expression and play an important role in fine-tuning molecular pathways during development. There is increasing interest in studying their function in the kidney, but the majority of studies to date ... ...

Abstract	MicroRNAs are small RNAs that negatively regulate gene expression and play an important role in fine-tuning molecular pathways during development. There is increasing interest in studying their function in the kidney, but the majority of studies to date use kidney cell lines and assess the total amounts of miRNAs of interest either by qPCR or by high-throughput methods such as next generation sequencing. However, this provides little information as to the distribution of the miRNAs in the developing kidney, which is crucial in deciphering their role, especially as there are multiple kidney cell types, each with its own specific transcriptome. Thus, we present a protocol for obtaining spatial information for miRNA expression during kidney development by
Language	English
Publishing date	2021-09-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.4150
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article ; Online: Envisioning treating genetically-defined urinary tract malformations with viral vector-mediated gene therapy.

Lopes, Filipa M / Woolf, Adrian S / Roberts, Neil A

Journal of pediatric urology

2021 Volume 17, Issue 5, Page(s) 610–620

Abstract: Human urinary tract malformations can cause dysfunctional voiding, urosepsis and kidney failure. Other affected individuals, with severe phenotypes on fetal ultrasound screening, undergo elective termination. Currently, there exist no specific treatments ...

Abstract	Human urinary tract malformations can cause dysfunctional voiding, urosepsis and kidney failure. Other affected individuals, with severe phenotypes on fetal ultrasound screening, undergo elective termination. Currently, there exist no specific treatments that target the primary biological disease mechanisms that generate these urinary tract malformations. Historically, the pathogenesis of human urinary tract malformations has been obscure. It is now established that some such individuals have defined monogenic causes for their disease. In health, the implicated genes are expressed in either differentiating urinary tract smooth muscle cells, urothelial cells or peripheral nerve cells supplying the bladder. The phenotypes arising from mutations of these genes include megabladder, congenital functional bladder outflow obstruction, and vesicoureteric reflux. We contend that these genetic and molecular insights can now inform the design of novel therapies involving viral vector-mediated gene transfer. Indeed, this technology is being used to treat individuals with early onset monogenic disease outside the urinary tract, such as spinal muscular atrophy. Moreover, it has been contended that human fetal gene therapy, which may be necessary to ameliorate developmental defects, could become a reality in the coming decades. We suggest that viral vector-mediated gene therapies should first be tested in existing mouse models with similar monogenic and anatomical aberrations as found in people with urinary tract malformations. Indeed, gene transfer protocols have been successfully pioneered in newborn and fetal mice to treat non-urinary tract diseases. If similar strategies were successful in animals with urinary tract malformations, this would pave the way for personalized and potentially curative treatments for people with urinary tract malformations.
MeSH term(s)	Animals ; Genetic Therapy ; Mice ; Urinary Tract/diagnostic imaging ; Urogenital Abnormalities ; Vesico-Ureteral Reflux
Language	English
Publishing date	2021-07-07
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2237683-5
ISSN	1873-4898 ; 1477-5131
ISSN (online)	1873-4898
ISSN	1477-5131
DOI	10.1016/j.jpurol.2021.07.002
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 6387: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Serum-Free Organ Culture of the Embryonic Mouse Ureter.

Lopes, Filipa M / Woolf, Adrian S

Methods in molecular biology (Clifton, N.J.)

2019 Volume 1926, Page(s) 31–38

Abstract: The ability to explant and then maintain embryonic tissues in organ culture makes it feasible to study the growth and differentiation of whole organs, or parts or combinations of them, in three dimensions. Moreover, the possible effects of biochemical ... ...

Abstract	The ability to explant and then maintain embryonic tissues in organ culture makes it feasible to study the growth and differentiation of whole organs, or parts or combinations of them, in three dimensions. Moreover, the possible effects of biochemical manipulations or mutations can be explored by visualizing a growing organ. The mammalian renal tract comprises the kidney, ureter, and urinary bladder, and the focus of this chapter is organ culture of the embryonic mouse ureter in serum-free defined medium. Over the culture period, rudiments grow in length, smooth muscle differentiates, and the ureters then undergo peristalsis in a proximal to distal direction.
MeSH term(s)	Animals ; Gene Expression Regulation, Developmental ; Kidney/embryology ; Mice ; Mutation/genetics ; Organ Culture Techniques/methods ; Peristalsis/physiology ; Ureter/embryology ; Urinary Bladder/embryology
Language	English
Publishing date	2019-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-9021-4_3
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Predicting congenital renal tract malformation genes using machine learning.

Kabir, Mitra / Stuart, Helen M / Lopes, Filipa M / Fotiou, Elisavet / Keavney, Bernard / Doig, Andrew J / Woolf, Adrian S / Hentges, Kathryn E

Scientific reports

2023 Volume 13, Issue 1, Page(s) 13204

Abstract: Congenital renal tract malformations (RTMs) are the major cause of severe kidney failure in children. Studies to date have identified defined genetic causes for only a minority of human RTMs. While some RTMs may be caused by poorly defined environmental ... ...

Abstract	Congenital renal tract malformations (RTMs) are the major cause of severe kidney failure in children. Studies to date have identified defined genetic causes for only a minority of human RTMs. While some RTMs may be caused by poorly defined environmental perturbations affecting organogenesis, it is likely that numerous causative genetic variants have yet to be identified. Unfortunately, the speed of discovering further genetic causes for RTMs is limited by challenges in prioritising candidate genes harbouring sequence variants. Here, we exploited the computer-based artificial intelligence methodology of supervised machine learning to identify genes with a high probability of being involved in renal development. These genes, when mutated, are promising candidates for causing RTMs. With this methodology, the machine learning classifier determines which attributes are common to renal development genes and identifies genes possessing these attributes. Here we report the validation of an RTM gene classifier and provide predictions of the RTM association status for all protein-coding genes in the mouse genome. Overall, our predictions, whilst not definitive, can inform the prioritisation of genes when evaluating patient sequence data for genetic diagnosis. This knowledge of renal developmental genes will accelerate the processes of reaching a genetic diagnosis for patients born with RTMs.
MeSH term(s)	Child ; Humans ; Mice ; Animals ; Artificial Intelligence ; Kidney/abnormalities ; Urinary Tract/abnormalities ; Machine Learning
Language	English
Publishing date	2023-08-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-38110-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Congenital Disorders of the Human Urinary Tract: Recent Insights From Genetic and Molecular Studies.

Woolf, Adrian S / Lopes, Filipa M / Ranjzad, Parisa / Roberts, Neil A

Frontiers in pediatrics

2019 Volume 7, Page(s) 136

Abstract: The urinary tract comprises the renal pelvis, the ureter, the urinary bladder, and the urethra. The tract acts as a functional unit, first propelling urine from the kidney to the bladder, then storing it at low pressure inside the bladder which ... ...

Abstract	The urinary tract comprises the renal pelvis, the ureter, the urinary bladder, and the urethra. The tract acts as a functional unit, first propelling urine from the kidney to the bladder, then storing it at low pressure inside the bladder which intermittently and completely voids urine through the urethra. Congenital diseases of these structures can lead to a range of diseases sometimes associated with fetal losses or kidney failure in childhood and later in life. In some of these disorders, parts of the urinary tract are severely malformed. In other cases, the organs appear grossly intact yet they have functional deficits that compromise health. Human studies are beginning to indicate monogenic causes for some of these diseases. Here, the implicated genes can encode smooth muscle, neural or urothelial molecules, or transcription factors that regulate their expression. Furthermore, certain animal models are informative about how such molecules control the development and functional differentiation of the urinary tract. In future, novel therapies, including those based on gene transfer and stem cell technologies, may be used to treat these diseases to complement conventional pharmacological and surgical clinical therapies.
Language	English
Publishing date	2019-04-11
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2711999-3
ISSN	2296-2360
ISSN	2296-2360
DOI	10.3389/fped.2019.00136
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: The miR-199a/214 Cluster Controls Nephrogenesis and Vascularization in a Human Embryonic Stem Cell Model.

Bantounas, Ioannis / Lopes, Filipa M / Rooney, Kirsty M / Woolf, Adrian S / Kimber, Susan J

Stem cell reports

2020 Volume 16, Issue 1, Page(s) 134–148

Abstract: MicroRNAs (miRNAs) are gene expression regulators and they have been implicated in acquired kidney diseases and in renal development, mostly through animal studies. We hypothesized that the miR-199a/214 cluster regulates human kidney development. We ... ...

Abstract	MicroRNAs (miRNAs) are gene expression regulators and they have been implicated in acquired kidney diseases and in renal development, mostly through animal studies. We hypothesized that the miR-199a/214 cluster regulates human kidney development. We detected its expression in human embryonic kidneys by in situ hybridization. To mechanistically study the cluster, we used 2D and 3D human embryonic stem cell (hESC) models of kidney development. After confirming expression in each model, we inhibited the miRNAs using lentivirally transduced miRNA sponges. This reduced the WT1
MeSH term(s)	Antagomirs/metabolism ; Capillaries/pathology ; Cell Culture Techniques ; Cell Differentiation ; Down-Regulation ; Human Embryonic Stem Cells/cytology ; Human Embryonic Stem Cells/metabolism ; Humans ; Kidney Tubules, Proximal/blood supply ; Kidney Tubules, Proximal/cytology ; Kidney Tubules, Proximal/metabolism ; MicroRNAs/metabolism ; Models, Biological ; Neovascularization, Physiologic ; Sialoglycoproteins/genetics ; Sialoglycoproteins/metabolism ; WT1 Proteins/genetics ; WT1 Proteins/metabolism
Chemical Substances	Antagomirs ; MIRN214 microRNA, human ; MicroRNAs ; Sialoglycoproteins ; WT1 Proteins ; WT1 protein, human ; mirn199 microRNA, human ; podocalyxin
Language	English
Publishing date	2020-12-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2720528-9
ISSN	2213-6711 ; 2213-6711
ISSN (online)	2213-6711
ISSN	2213-6711
DOI	10.1016/j.stemcr.2020.11.007
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Neurogenic Defects Occur in

Grenier, Celine / Lopes, Filipa M / Cueto-González, Anna M / Rovira-Moreno, Eulàlia / Gander, Romy / Jarvis, Benjamin W / McCloskey, Karen D / Gurney, Alison M / Beaman, Glenda M / Newman, William G / Woolf, Adrian S / Roberts, Neil A

Kidney international reports

2023 Volume 8, Issue 7, Page(s) 1417–1429

Abstract: Introduction: Urofacial, or Ochoa, syndrome (UFS) is an autosomal recessive disease featuring a dyssynergic bladder with detrusor smooth muscle contracting against an undilated outflow tract. It also features an abnormal grimace. Half of individuals ... ...

Abstract	Introduction: Urofacial, or Ochoa, syndrome (UFS) is an autosomal recessive disease featuring a dyssynergic bladder with detrusor smooth muscle contracting against an undilated outflow tract. It also features an abnormal grimace. Half of individuals with UFS carry biallelic variants in Methods: We describe a new family with Results: The index case presented antenatally with urinary tract (UT) dilatation, and postnatally had urosepsis and functional bladder outlet obstruction. He had the grimace that, together with UT disease, characterizes UFS. Although Conclusion: Putting this family in the context of all reported UT disease-associated
Language	English
Publishing date	2023-04-30
Publishing country	United States
Document type	Journal Article
ISSN	2468-0249
ISSN (online)	2468-0249
DOI	10.1016/j.ekir.2023.04.017
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Overactivity or blockade of transforming growth factor-β each generate a specific ureter malformation.

Lopes, Filipa M / Roberts, Neil A / Zeef, Leo Ah / Gardiner, Natalie J / Woolf, Adrian S

The Journal of pathology

2019 Volume 249, Issue 4, Page(s) 472–484

Abstract: Transforming growth factor-β (TGFβ) has been reported to be dysregulated in malformed ureters. There exists, however, little information on whether altered TGFβ levels actually perturb ureter development. We therefore hypothesised that TGFβ has ... ...

Abstract	Transforming growth factor-β (TGFβ) has been reported to be dysregulated in malformed ureters. There exists, however, little information on whether altered TGFβ levels actually perturb ureter development. We therefore hypothesised that TGFβ has functional effects on ureter morphogenesis. Tgfb1, Tgfb2 and Tgfb3 transcripts coding for TGFβ ligands, as well as Tgfbr1 and Tgfbr2 coding for TGFβ receptors, were detected by quantitative polymerase chain reaction in embryonic mouse ureters collected over a wide range of stages. As assessed by in situ hybridisation and immunohistochemistry, the two receptors were detected in embryonic urothelia. Next, TGFβ1 was added to serum-free cultures of embryonic day 15 mouse ureters. These organs contain immature smooth muscle and urothelial layers and their in vivo potential to grow and acquire peristaltic function can be replicated in serum-free organ culture. Such organs therefore constitute a suitable developmental stage with which to define roles of factors that affect ureter growth and functional differentiation. Exogenous TGFβ1 inhibited growth of the ureter tube and generated cocoon-like dysmorphogenesis. RNA sequencing suggested that altered levels of transcripts encoding certain fibroblast growth factors (FGFs) followed exposure to TGFβ. In serum-free organ culture exogenous FGF10 but not FGF18 abrogated certain dysmorphic effects mediated by exogenous TGFβ1. To assess whether an endogenous TGFβ axis functions in developing ureters, embryonic day 15 explants were exposed to TGFβ receptor chemical blockade; growth of the ureter was enhanced, and aberrant bud-like structures arose from the urothelial tube. The muscle layer was attenuated around these buds, and peristalsis was compromised. To determine whether TGFβ effects were limited to one stage, explants of mouse embryonic day 13 ureters, more primitive organs, were exposed to exogenous TGFβ1, again generating cocoon-like structures, and to TGFβ receptor blockade, again generating ectopic buds. As for the mouse studies, immunostaining of normal embryonic human ureters detected TGFβRI and TGFβRII in urothelia. Collectively, these observations reveal unsuspected regulatory roles for endogenous TGFβ in embryonic ureters, fine-tuning morphogenesis and functional differentiation. Our results also support the hypothesis that the TGFβ up-regulation reported in ureter malformations impacts on pathobiology. Further experiments are needed to unravel the intracellular signalling mechanisms involved in these dysmorphic responses. © 2019 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
MeSH term(s)	Animals ; Cell Differentiation ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Gene Expression Regulation, Developmental ; Gestational Age ; Humans ; Mice ; Morphogenesis ; Organ Culture Techniques ; Receptors, Transforming Growth Factor beta/genetics ; Receptors, Transforming Growth Factor beta/metabolism ; Signal Transduction ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta/pharmacology ; Ureter/abnormalities ; Ureter/drug effects ; Ureter/metabolism ; Urogenital Abnormalities/genetics ; Urogenital Abnormalities/metabolism ; Urothelium/abnormalities ; Urothelium/drug effects ; Urothelium/metabolism
Chemical Substances	Receptors, Transforming Growth Factor beta ; Transforming Growth Factor beta ; Fibroblast Growth Factors (62031-54-3)
Language	English
Publishing date	2019-10-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3119-7
ISSN	1096-9896 ; 0022-3417
ISSN (online)	1096-9896
ISSN	0022-3417
DOI	10.1002/path.5335
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Ud II Zs.12: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Narrowing the chromosome 22q11.2 locus duplicated in bladder exstrophy-epispadias complex.

Beaman, Glenda M / Woolf, Adrian S / Lopes, Filipa M / Guo, Shuang Andrew / Harkness, J Robert / Cervellione, Raimondo M / Keene, David / Mushtaq, Imran / Clatworthy, Menna R / Newman, William G

Journal of pediatric urology

2022 Volume 18, Issue 3, Page(s) 362.e1–362.e8

Abstract: Introduction: Bladder exstrophy-epispadias complex (BEEC) comprises a spectrum of anterior midline congenital malformations, involving the lower urinary tract. BEEC is usually sporadic, but families with more than one affected member have been reported, ...

Abstract	Introduction: Bladder exstrophy-epispadias complex (BEEC) comprises a spectrum of anterior midline congenital malformations, involving the lower urinary tract. BEEC is usually sporadic, but families with more than one affected member have been reported, and a twin concordance study supported a genetic contribution to pathogenesis. Moreover, diverse chromosomal aberrations have been reported in a small subset of individuals with BEEC. The commonest are 22q11.2 microduplications, identified in approximately 3% of BEEC index cases. Objectives: We aimed to refine the chromosome 22q11.2 locus, and to determine whether the encompassed genes are expressed in normal developing and mature human urinary bladders. Results: Using DNA from an individual with CBE, the 22q11.2 duplicated locus was refined by identification of a maternally inherited 314 kb duplication (chr22:21,147,293-21,461,017), as depicted in this image. Moreover, the eight protein coding genes within the locus were found to be expressed during normal developing and mature bladders. To determine whether duplications in any of these individual genes were associated with CBE, we undertook copy number analyses in 115 individuals with CBE without duplications of the whole locus. No duplications of individual genes were found. Discussion: The current study has refined the 22q11.2 locus associated with BEEC and has shown that the eight protein coding genes are expressed in human bladders both during antenatal development and postnatally. Nevertheless, the precise biological explanation as to why duplication of the phenocritical region of 22q11 confers increased susceptibility to BEEC remains to be determined. The fact that individuals with CBE without duplications of the whole locus also lacked duplication of any of the individual genes suggests that in individuals with BEEC and duplication of the 22q11.2 locus altered dosage of more than one gene may be important in BEEC etiology. Conclusions: The study has refined the 22q11.2 locus associated with BEEC and has shown that the eight protein coding genes within this locus are expressed in human bladders.
MeSH term(s)	Bladder Exstrophy/genetics ; Bladder Exstrophy/pathology ; Chromosomes/metabolism ; Epispadias/genetics ; Epispadias/pathology ; Female ; Humans ; Pregnancy ; Urinary Bladder/abnormalities
Language	English
Publishing date	2022-04-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2237683-5
ISSN	1873-4898 ; 1477-5131
ISSN (online)	1873-4898
ISSN	1477-5131
DOI	10.1016/j.jpurol.2022.04.006
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 6387: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Experimental long-term diabetes mellitus alters the transcriptome and biomechanical properties of the rat urinary bladder.

Hindi, Emad A / Williams, Craig J / Zeef, Leo A H / Lopes, Filipa M / Newman, Katie / Davey, Martha M M / Hodson, Nigel W / Hilton, Emma N / Huang, Jennifer L / Price, Karen L / Roberts, Neil A / Long, David A / Woolf, Adrian S / Gardiner, Natalie J

Scientific reports

2021 Volume 11, Issue 1, Page(s) 15529

Abstract: Diabetes mellitus (DM) is the leading cause of chronic kidney disease and diabetic nephropathy is widely studied. In contrast, the pathobiology of diabetic urinary bladder disease is less understood despite dysfunctional voiding being common in DM. We ... ...

Abstract	Diabetes mellitus (DM) is the leading cause of chronic kidney disease and diabetic nephropathy is widely studied. In contrast, the pathobiology of diabetic urinary bladder disease is less understood despite dysfunctional voiding being common in DM. We hypothesised that diabetic cystopathy has a characteristic molecular signature. We therefore studied bladders of hyperglycaemic and polyuric rats with streptozotocin (STZ)-induced DM. Sixteen weeks after induction of DM, as assessed by RNA arrays, wide-ranging changes of gene expression occurred in DM bladders over and above those induced in bladders of non-hyperglycaemic rats with sucrose-induced polyuria. The altered transcripts included those coding for extracellular matrix regulators and neural molecules. Changes in key genes deregulated in DM rat bladders were also detected in db/db mouse bladders. In DM rat bladders there was reduced birefringent collagen between detrusor muscle bundles, and atomic force microscopy showed a significant reduction in tissue stiffness; neither change was found in bladders of sucrose-treated rats. Thus, altered extracellular matrix with reduced tissue rigidity may contribute to voiding dysfunction in people with long-term DM. These results serve as an informative stepping stone towards understanding the complex pathobiology of diabetic cystopathy.
MeSH term(s)	Animals ; Diabetes Mellitus, Experimental/metabolism ; Enzyme-Linked Immunosorbent Assay ; Male ; Microscopy, Atomic Force ; Oligonucleotide Array Sequence Analysis ; Rats ; Rats, Wistar ; Transcriptome/genetics ; Transcriptome/physiology ; Urinary Bladder/metabolism
Language	English
Publishing date	2021-07-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-94532-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito