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39 results on '"Lemmink, H.H."'

3. Deciduous Teeth as an Alternative DNA Source for Postmortem Genetic Testing

Author

Rijdt, W.P. Te, Mieremet, R.H.P., Kraaijenbrink, T., Regieli, J.J., Lemmink, H.H., Jan, S.Z., Knijff, P. de, Hoedemaekers, Y.M., Rijdt, W.P. Te, Mieremet, R.H.P., Kraaijenbrink, T., Regieli, J.J., Lemmink, H.H., Jan, S.Z., Knijff, P. de, and Hoedemaekers, Y.M.

Abstract

Contains fulltext : 220426.pdf (Publisher’s version ) (Closed access)

Published
2020

4. Germline AGO2 mutations impair RNA interference and human neurological development

Author

Lessel, D., Zeitler, D.M., Reijnders, M.R.F., Kazantsev, A., Nia, F. Hassani, Bartholomäus, A., Martens, V., Bruckmann, A., Graus, V., McConkie-Rosell, A., McDonald, M., Lozic, B., Tan, E.S., Gerkes, E., Johannsen, J., Denecke, J., Telegrafi, A., Zonneveld-Huijssoon, E., Lemmink, H.H., Cham, B.W.M., Kovacevic, T., Ramsdell, L., Foss, K., Duc, D. Le, Mitter, D., Syrbe, S., Merkenschlager, A., Sinnema, M., Panis, B., Lazier, J., Osmond, M., Hartley, T., Mortreux, J., Busa, T., Missirian, C., Prasun, P., Lüttgen, S., Mannucci, I., Lessel, I., Schob, C., Kindler, S., Pappas, J., Rabin, R., Willemsen, M.H., Gardeitchik, T., Löhner, K., Rump, P., Dias, K.R., Evans, C.A., Andrews, P.I., Roscioli, T., Brunner, H.G., Chijiwa, C., Lewis, M.E.S., Jamra, R.A., Dyment, D.A., Boycott, K.M., Stegmann, A.P.A., Kubisch, C., Tan, Ene-Choo, Mirzaa, G.M., McWalter, K., Kleefstra, T., Pfundt, R.P., Ignatova, Z., Meister, G., Kreienkamp, H.J., Lessel, D., Zeitler, D.M., Reijnders, M.R.F., Kazantsev, A., Nia, F. Hassani, Bartholomäus, A., Martens, V., Bruckmann, A., Graus, V., McConkie-Rosell, A., McDonald, M., Lozic, B., Tan, E.S., Gerkes, E., Johannsen, J., Denecke, J., Telegrafi, A., Zonneveld-Huijssoon, E., Lemmink, H.H., Cham, B.W.M., Kovacevic, T., Ramsdell, L., Foss, K., Duc, D. Le, Mitter, D., Syrbe, S., Merkenschlager, A., Sinnema, M., Panis, B., Lazier, J., Osmond, M., Hartley, T., Mortreux, J., Busa, T., Missirian, C., Prasun, P., Lüttgen, S., Mannucci, I., Lessel, I., Schob, C., Kindler, S., Pappas, J., Rabin, R., Willemsen, M.H., Gardeitchik, T., Löhner, K., Rump, P., Dias, K.R., Evans, C.A., Andrews, P.I., Roscioli, T., Brunner, H.G., Chijiwa, C., Lewis, M.E.S., Jamra, R.A., Dyment, D.A., Boycott, K.M., Stegmann, A.P.A., Kubisch, C., Tan, Ene-Choo, Mirzaa, G.M., McWalter, K., Kleefstra, T., Pfundt, R.P., Ignatova, Z., Meister, G., and Kreienkamp, H.J.

Abstract

Contains fulltext : 229431.pdf (publisher's version ) (Open Access), ARGONAUTE-2 and associated miRNAs form the RNA-induced silencing complex (RISC), which targets mRNAs for translational silencing and degradation as part of the RNA interference pathway. Despite the essential nature of this process for cellular function, there is little information on the role of RISC components in human development and organ function. We identify 13 heterozygous mutations in AGO2 in 21 patients affected by disturbances in neurological development. Each of the identified single amino acid mutations result in impaired shRNA-mediated silencing. We observe either impaired RISC formation or increased binding of AGO2 to mRNA targets as mutation specific functional consequences. The latter is supported by decreased phosphorylation of a C-terminal serine cluster involved in mRNA target release, increased formation of dendritic P-bodies in neurons and global transcriptome alterations in patient-derived primary fibroblasts. Our data emphasize the importance of gene expression regulation through the dynamic AGO2-RNA association for human neuronal development.

Published
2020

6. Identification of Co14A5 defects in Alport's syndrome by immunohistochemistry of skin

Author

Loop, F. van de, Monnens, L.A.H., Schröder, C.H., Lemmink, H.H., Timmer, E., and Smeets, H.J.M.

Subjects
Study of the mutation of the human type IV collagen gene which is affected in the Alports" syndrome, Karakterisering van mutaties die leiden tot het syndroom van Alport
Abstract

Item does not contain fulltext 8 p.

Published
1999

7. A novel KCNA1 mutation causing episodic ataxia type I

Author

Lassche, S., Lainez, S., Bloem, B.R., Warrenburg, B.P.C. van de, Hofmeijer, J., Lemmink, H.H., Hoenderop, J.G., Bindels, R.J.M., and Drost, G.

Subjects
Renal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11], Disorders of movement Donders Center for Medical Neuroscience [Radboudumc 3]
Abstract

Contains fulltext : 137863.pdf (Publisher’s version ) (Closed access) We describe the clinical phenotype of a novel de novo KNCA1 mutation, and functional characterization of the effects of the mutation on Kv1.1 channel function. HEK293 cells were transfected transiently with either wild-type or mutant channels. Representative currents were evoked after application of a series of square voltage steps from -80 mV to +50 mV in 200-ms intervals from Vh = -80 mV. Extracellular K(+) was added to evoke tail currents. Equal amounts of wild-type and Kv1.1(I262M) mutant DNA were transfected transiently in HEK293 cells to evaluate the influence of the mutation. We found that Kv1.1(I262M) leads to a defective voltage-gated potassium channel. Coexpression studies revealed a dominant-negative effect. We describe the phenotype of a novel KCNA1 mutation causing episodic ataxia. Patch-clamp studies confirm the pathogenicity of the mutation in vitro and suggest that it is dominant with respect to wild-type.

Published
2014

8. Mutations in the gene encoding the inwardly-rectifying renal potassium channel, ROMK, cause the antenatal variant of Barrter syndrome : evidence for genetic heterogeneity

Author

Károlyi, L., Konrad, M., Köckerling, A., Ziegler, A., Zimmermann, D.K., Roth, B., Wieg, C., Grzeschik, K.H., Koch, M.C., Seyberth, H.W., Vargas, R., Forestier, C., Jean, G., Deschaux, M., Rizzoni, G.F., Niaudet, P., Antignac, C., Feldmann, D., Lorridon, F., Cougoureux, E., Laroze, F., Alessandri, J.-L., David, L., Saunier, P., Deschenes, G., Hildebrandt, F., Vollmer, M., Proesmans, W., Brandis, M., Heuvel, L.P.W.J. van den, Lemmink, H.H., Nillesen, W., Monnens, L.A.H., Knoers, N.V.A.M., Guay-Woodford, L.M., Wright, C.J., Madrigal, G., and Hebert, S.C.

Subjects
Cultured, Ion Transport, Cells, Molecular, Molecular Probe Techniques, Hospitalized, Kidney, Kidney Function Tests, Urogenital Abnormalities (Non MeSH), Basement Membrane, Urethra, Urethral Diseases, Cell Adhesion, Kidney Diseases, Endothelium, Cloning, Molecular, Child, Gram-Negative Bacterial Infections, GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries), Child, Hospitalized, Peritoneal Dialysis, Cells, Cultured, Cloning
Abstract

Contains fulltext : 24466___.PDF (Publisher’s version ) (Open Access)

Published
1997

9. The clinical spectrum of type IV collagen mutations

Author

Lemmink, H.H., Schröder, C.H., Monnens, L.A.H., and Smeets, H.J.M.

Subjects
Study of the mutation of the human type IV collagen gene which is affected in the Alports" syndrome, Karakterisering van mutaties die leiden tot het syndroom van Alport, Characterization of mutations causing Alport's syndrome, GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries)
Abstract

Contains fulltext : 25010___.PDF (Publisher’s version ) (Open Access)

Published
1997

11. Mutations in BICD2, which encodes a Golgin and Important Motor Adaptor, Cause Congenital Autosomal-Dominant Spinal Muscular Atrophy

Author

Neveling, K., Martinez-Carrera, L., Hölker, I., Heister, A., Verrips, A., Hosseini-Barkooie, S.M., Gilissen, C.F.H.A., Vermeer, S., Pennings, M.C.P., Meijer, R., Riele, M.G.E. te, Frijns, C.J., Suchowersky, O., MacLaren, L., Rudnik-Schöneborn, S., Sinke, R.J., Zerres, K., Lowry, R.B., Lemmink, H.H., Garbes, L., Veltman, J.A., Schelhaas, H.J., Scheffer, H., Wirth, B., Neveling, K., Martinez-Carrera, L., Hölker, I., Heister, A., Verrips, A., Hosseini-Barkooie, S.M., Gilissen, C.F.H.A., Vermeer, S., Pennings, M.C.P., Meijer, R., Riele, M.G.E. te, Frijns, C.J., Suchowersky, O., MacLaren, L., Rudnik-Schöneborn, S., Sinke, R.J., Zerres, K., Lowry, R.B., Lemmink, H.H., Garbes, L., Veltman, J.A., Schelhaas, H.J., Scheffer, H., and Wirth, B.

Abstract

Contains fulltext : 116576.pdf (publisher's version ) (Closed access)

Published
2013

12. Mutation in mitochondrial tRNA gene associated with progressive kidney disease

Author

Janssen, J.J.M., Maassen, J.A., Woude, F. van der, Lemmink, H.H., Ouweland, J.M.W. van den, Hart, L.M. 't, Smeets, H.J.M., Bruyn, J.A., and Lemkes, H.H.D.J.

Subjects
Study of the mutation of the human type IV collagen gene which is affected in the Alports" syndrome, Karakterisering van mutaties die leiden tot het syndroom van Alport, Onderzoek van mitochondrieel DNA in het kader van diagnostiek van mitochondriële myopathieen, Analysis of mitochondrial DNA as part of the diagnosis of mitochondrial myopathies
Abstract

Item does not contain fulltext 7 p.

Published
1997

13. Molecular genetics of Alport syndrome

Author

Lemmink, H.H., Monnens, L.A.H., Smeets, H.J.M., Schröder, C.H., and Radboud University Nijmegen

Subjects
Study of the mutation of the human type IV collagen gene which is affected in the Alports" syndrome, Karakterisering van mutaties die leiden tot het syndroom van Alport, GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries)
Abstract

Contains fulltext : mmubn000001_254623085.pdf (Publisher’s version ) (Open Access) Promotores : L. Monnens, H. Smeets en C. Schröder 150 p.

Published
1997

15. Autosomal dominant Alport syndrome linked to the type IV collagen alpha3 and alpha4 genes

Author

Jefferson, J.A., Lemmink, H.H., Hughes, A.E., Hill, C.M., Smeets, H.J.M., Doherty, C.C., and Maxwell, A.P.

Subjects
Study of the mutation of the human type IV collagen gene which is affected in the Alports" syndrome, Karakterisering van mutaties die leiden tot het syndroom van Alport, Characterization of mutations causing Alport's syndrome
Abstract

Item does not contain fulltext 5 p.

Published
1997

16. SMN genotypes producing less SMN protein increase susceptibility to and severity of sporadic ALS.

Author

Veldink, J.H., Kalmijn, S., Hout, A.H. van der, Lemmink, H.H., Groeneveld, G.J., Lummen, C., Scheffer, H., Wokke, J.H.J., Berg, L.H. van den, Veldink, J.H., Kalmijn, S., Hout, A.H. van der, Lemmink, H.H., Groeneveld, G.J., Lummen, C., Scheffer, H., Wokke, J.H.J., and Berg, L.H. van den

Abstract

Item does not contain fulltext, BACKGROUND: ALS is believed to be multifactorial in origin with modifying genes affecting its clinical expression. Childhood-onset spinal muscular atrophy (SMA) is an autosomal recessive disorder of motor neurons, caused by mutations of the survival motor neuron (SMN) gene. The SMN gene exists in two highly homologous variants: SMN1, the causative gene responsible for the production of the majority of functional SMN protein, and SMN2, responsible for the production of less protein but sufficient for modifying the SMA phenotype. OBJECTIVE: To test whether SMN genotypes are associated with susceptibility to and severity of sporadic ALS. METHODS: We performed competitive quantitative PCR analysis for both SMN1 and SMN2 genes in 242 clinically well-defined ALS patients and 175 controls. The combined determination of SMN1 and SMN2 copies also allowed for an estimation of the level of SMN for each patient (estimated SMN protein level = SMN1 copy number + 0.20 x SMN2 copy number). RESULTS: One copy of SMN1 was associated with an increased risk of developing ALS (odds ratio = 4.1, 95% CI = 1.2 to 14.2, p = 0.02) and ALS patients carried fewer SMN2 copy numbers (p < 0.001). Sixty-one percent of patients had an estimated protein SMN level < or = 2.2 vs only 36% of controls (p = 0.0000004). Multivariate Cox regression analyses showed that lower SMN2 copy numbers and lower levels of estimated SMN protein (hazard ratio = 1.3, 95% CI = 1.1 to 1.6, p = 0.03) were associated with an increased mortality rate. CONCLUSIONS: SMN genotypes producing less SMN protein increase susceptibility to and severity of ALS.

Published
2005

20. Dystrophic epidermolysis bullosa inversa with COL7A1 mutations and absence of GDA-J/F3 protein.

Author

Kahofer, P., Bruckner-Tuderman, L., Metze, D., Lemmink, H.H., Scheffer, H., Smolle, J., Kahofer, P., Bruckner-Tuderman, L., Metze, D., Lemmink, H.H., Scheffer, H., and Smolle, J.

Abstract

Item does not contain fulltext, Epidermolysis bullosa dystrophica inversa (DEB-I) is a very rare disease characterized by autosomal recessive inheritance that causes blistering and erosions on the trunk and extremities occurring in early infancy with a predilection for flexural and mucosal areas thereafter. Ultrastructural findings show dermolytic blistering and absent or rudimentary anchoring fibrils as in generalized forms of dystrophic epidermolysis bullosa. Immunoreactivity for type VII collagen, however, is preserved. We present two patients with DEB-I with compound heterozygosity for the two different COL7A1 mutations, one of them (Arg2069Cys in exon 74) carried by the heterozygous mother, the other one (Lys142Arg in exon 3) carried by the heterozygous father, accompanied by absence of the associated anchoring fibrils protein GDA-J/F3.

Published
2003

21. Antenatal Bartter syndrome with sensorineural deafness: refinement of the locus on chromosome 1p31

Author

Volmer, M., Jeck, N., Lemmink, H.H., Vargas-Poussou, R., Feldmann, D., Konrad, M., Beekmann, F., Heuvel, L.P.W.J. van den, Deschenes, G., Guay-Woodford, L.M., Antignac, C., Seyberth, H.W., Hildebrandt, F., Knoers, N.V.A.M., Volmer, M., Jeck, N., Lemmink, H.H., Vargas-Poussou, R., Feldmann, D., Konrad, M., Beekmann, F., Heuvel, L.P.W.J. van den, Deschenes, G., Guay-Woodford, L.M., Antignac, C., Seyberth, H.W., Hildebrandt, F., and Knoers, N.V.A.M.

Abstract

Item does not contain fulltext

Published
2000

22. Mutations in the chloride channel gene CLCNKB as a cause of classic Bartter syndrome.

Author

Konrad, M., Volmer, M., Lemmink, H.H., Heuvel, L.P.W.J. van den, Jeck, N., Vargas-Poussou, R., Lakings, A., Ruf, R., Deschenes, G., Antignac, C., Guay-Woodford, L.M., Knoers, N.V.A.M., Seyberth, H.W., Feldmann, D., Hildebrandt, F., Konrad, M., Volmer, M., Lemmink, H.H., Heuvel, L.P.W.J. van den, Jeck, N., Vargas-Poussou, R., Lakings, A., Ruf, R., Deschenes, G., Antignac, C., Guay-Woodford, L.M., Knoers, N.V.A.M., Seyberth, H.W., Feldmann, D., and Hildebrandt, F.

Abstract

Item does not contain fulltext

Published
2000

24. Identification of novel mutations in the thiazide-sensitive NaCl cotransporter gene in patients with Gitelman syndrome from different geographical origin

Author

Lemmink, H.H., Knoers, N.V.A.M., Karolyi, L., Dijk, H.A. van, Niaudet, P., Antignac, C., Guay-Woodford, L.M., Goodyer, P., Carel, J., Hermes, A., Seyberth, H.W., Monnens, L.A.H., Heuvel, L.P.W.J. van den, Lemmink, H.H., Knoers, N.V.A.M., Karolyi, L., Dijk, H.A. van, Niaudet, P., Antignac, C., Guay-Woodford, L.M., Goodyer, P., Carel, J., Hermes, A., Seyberth, H.W., Monnens, L.A.H., and Heuvel, L.P.W.J. van den

Abstract

Item does not contain fulltext

Published
1998

25. Novel mutations in the thiazide-sensitive NaCl cotransporter gene in patients with Gitelman syndrome with predominant localization to the C-terminal domain

Author

Lemmink, H.H., Knoers, N.V.A.M., Károlyi, L., Dijk, H.A. van, Niaudet, P., Antignac, C., Guay-Woodford, L.M., Goodyer, P., Carel, J., Hermus, A.R.M.M., Seyberth, H.W., Monnens, L.A.H., Heuvel, L.P.W.J. van den, Lemmink, H.H., Knoers, N.V.A.M., Károlyi, L., Dijk, H.A. van, Niaudet, P., Antignac, C., Guay-Woodford, L.M., Goodyer, P., Carel, J., Hermus, A.R.M.M., Seyberth, H.W., Monnens, L.A.H., and Heuvel, L.P.W.J. van den

Abstract

Item does not contain fulltext

Published
1998

26. Novel molecular variants of the Na-K-2Cl cotransporter gene are responsible for antenatal Bartter syndrome

Author

Vargas-Poussou, R., Feldmann, D., Volmer, M., Konrad, M., Kelly, L., Heuvel, L.P.W.J. van den, Tebourbi, L., Brandis, M., Karolyi, L., Hebert, S.C., Lemmink, H.H., Deschenes, G., Hildebrandt, F., Seyberth, H.W., Guay-Woodford, L.M., Knoers, N.V.A.M., Antignac, C., Vargas-Poussou, R., Feldmann, D., Volmer, M., Konrad, M., Kelly, L., Heuvel, L.P.W.J. van den, Tebourbi, L., Brandis, M., Karolyi, L., Hebert, S.C., Lemmink, H.H., Deschenes, G., Hildebrandt, F., Seyberth, H.W., Guay-Woodford, L.M., Knoers, N.V.A.M., and Antignac, C.

Abstract

Item does not contain fulltext

Published
1998

27. Molecular genetics of Alport syndrome

Author

Monnens, L.A.H., Smeets, H.J.M., Schröder, C.H., Lemmink, H.H., Monnens, L.A.H., Smeets, H.J.M., Schröder, C.H., and Lemmink, H.H.

Abstract

Katholieke Universiteit Nijmegen, 4 december 1997, Promotor : Monnens, L.A.H. Co-promotores : Smeets, H.J.M., Schröder, C.H., Item does not contain fulltext

Published
1997

28. Functional analysis of ROMK gene mutations in antenatal Bartter syndrome

Author

Lemmink, H.H., Heuvel, L.P.W.J. van den, Buskens, C., Kansen, M., Kemp, A. van der, Monnens, L.A.H., Os, C.H. van, Knoers, N.V.A.M., Bindels, R.J., Lemmink, H.H., Heuvel, L.P.W.J. van den, Buskens, C., Kansen, M., Kemp, A. van der, Monnens, L.A.H., Os, C.H. van, Knoers, N.V.A.M., and Bindels, R.J.

Abstract

Item does not contain fulltext

Published
1997

29. Linkage of Gitelman syndrome to the thiazide-sensitive sodium-chloride cotransporter gene and identification of mutations in Dutch families

Author

Lemmink, H.H., Heuvel, L.P.W.J. van den, Dijk, H.A. van, Merkx, G.F.M., Smilde, T.J., Taschner, P.E.M., Monnens, L.A.H., Hebert, S.C., Knoers, N.V.A.M., Lemmink, H.H., Heuvel, L.P.W.J. van den, Dijk, H.A. van, Merkx, G.F.M., Smilde, T.J., Taschner, P.E.M., Monnens, L.A.H., Hebert, S.C., and Knoers, N.V.A.M.

Abstract

Item does not contain fulltext

Published
1996

30. Benign familial hematuria due to mutation of the type IV collagen alpha-4 gene

Author

Lemmink, H.H., Nillesen, W.N., Mochizuki, T., Schröder, C.H., Brunner, H.G., Oost, B.A. van, Monnens, L.A.H., Smeets, H.J.M., Lemmink, H.H., Nillesen, W.N., Mochizuki, T., Schröder, C.H., Brunner, H.G., Oost, B.A. van, Monnens, L.A.H., and Smeets, H.J.M.

Abstract

Contains fulltext : 23426___.PDF (publisher's version ) (Open Access)

Published
1996

31. Mutational analyses in Gitelman syndrome

Author

Heuvel, L.P.W.J. van den, Lemmink, H.H., Tachner, P.E.M., Vargas, R., Niaudet, P., GuayWoodford, L.M., Goodyer, P., Monnens, L., Hebert, S.C., Knoers, N.V.A.M., Heuvel, L.P.W.J. van den, Lemmink, H.H., Tachner, P.E.M., Vargas, R., Niaudet, P., GuayWoodford, L.M., Goodyer, P., Monnens, L., Hebert, S.C., and Knoers, N.V.A.M.

Abstract

Item does not contain fulltext

Published
1996

32. Hereditary disorders of the glomerular basement membrane

Author

Smeets, H.J.M., Knoers, N.V.A.M., Heuvel, L.P.W.J. van den, Lemmink, H.H., Schröder, C.H., Monnens, L.A.H., Smeets, H.J.M., Knoers, N.V.A.M., Heuvel, L.P.W.J. van den, Lemmink, H.H., Schröder, C.H., and Monnens, L.A.H.

Abstract

Item does not contain fulltext

Published
1996

36. Constitutive NF-?B DNA-binding activity in AML is frequently mediated by a Ras/PI3-K/PKB-dependent pathway.

Author

Birkenkamp, K.U., Geugien, M., Schepers, H., Westra, J., Lemmink, H.H., and Vellenga, E.

Subjects
ACUTE myeloid leukemia, NF-kappa B, APOPTOSIS, PROTEIN kinases, GUANOSINE triphosphatase genes, GENE expression
Abstract

In the present study, we aimed to elucidate the mechanism responsible for constitutive NF-?B DNA-binding activity in AML cells. Intervening in aberrant signaling pathway provides a rational approach for in vivo targeting of AML cells. Constitutive NF-?B DNA-binding activity was observed in 16 of 22 (73%) investigated AML cases and was, in general, associated with resistance to spontaneous apoptosis. Indeed, inhibition of NF-?B activity by the NF-?B inhibitor SN-50 peptide resulted in enhanced chemotherapy-induced apoptosis. In the majority of cases, constitutive NF-?B activity was mediated by a Ras/PI3 kinase (PI3-K)/protein kinase B (PKB)-mediated pathway. The PI3-K inhibitor Ly294002 and the Ras inhibitor L-744832 both inhibited PKB phosphorylation and NF-?B DNA-binding activity. The constitutive activation of Ras GTP-ase was caused by mutations in the gene encoding for N-Ras in 29% of the cases. The constitutive NF-?B activity could so far not be ascribed to the autocrine production of growth factors or to mutations in the Flt3 receptor, since anti-GM-CSF, -IL-1, -IL6, -TNFa or the tyrosine kinase inhibitor AG1296 did not affect the NF-?B DNA-binding activity. The present study demonstrates that Ras activation is an important pathway for triggering the NF-?B pathway in AML cells.Leukemia (2004) 18, 103-112. doi:10.1038/sj.leu.2403145 [ABSTRACT FROM AUTHOR]

Published
2004
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