LIVIVO - Search results -

Search results

Result 1 - 10 of total 23

Search options

Article ; Online: Gain-of-function MARK4 variant associates with pediatric neurodevelopmental disorder and dysmorphism.

Samra, Simran / Sharma, Mehul / Vaseghi-Shanjani, Maryam / Del Bel, Kate L / Byres, Loryn / Lin, Susan / Dalmann, Joshua / Salman, Areesha / Mwenifumbo, Jill / Modi, Bhavi P / Biggs, Catherine M / Boelman, Cyrus / Clarke, Lorne A / Lehman, Anna / Turvey, Stuart E

HGG advances

2023 Volume 5, Issue 1, Page(s) 100259

Abstract: Microtubule affinity-regulating kinase 4 (MARK4) is a serine/threonine kinase that plays a key role in tau phosphorylation and regulation of the mammalian target of rapamycin (mTOR) pathway. Abnormal tau phosphorylation and dysregulation of the mTOR ... ...

Abstract	Microtubule affinity-regulating kinase 4 (MARK4) is a serine/threonine kinase that plays a key role in tau phosphorylation and regulation of the mammalian target of rapamycin (mTOR) pathway. Abnormal tau phosphorylation and dysregulation of the mTOR pathway are implicated in neurodegenerative and neurodevelopmental disorders. Here, we report a gain-of-function variant in
MeSH term(s)	Humans ; Child ; Gain of Function Mutation ; Protein Serine-Threonine Kinases/genetics ; Microtubules/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Neurodevelopmental Disorders/genetics
Chemical Substances	Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; MARK4 protein, human (EC 2.7.1.-)
Language	English
Publishing date	2023-12-01
Publishing country	United States
Document type	Journal Article
ISSN	2666-2477
ISSN (online)	2666-2477
DOI	10.1016/j.xhgg.2023.100259
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.

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: Inborn Errors of Immunity Associated With Type 2 Inflammation in the USIDNET Registry.

Smith, Kelsey L / Dai, Darlene / Modi, Bhavi P / Sara, Rahnuma / Garabedian, Elizabeth / Marsh, Rebecca A / Puck, Jennifer / Secord, Elizabeth / Sullivan, Kathleen E / Turvey, Stuart E / Biggs, Catherine M

Frontiers in immunology

2022 Volume 13, Page(s) 831279

Abstract: Background: Monogenic conditions that disrupt proper development and/or function of the immune system are termed inborn errors of immunity (IEIs), also known as primary immunodeficiencies. Patients with IEIs often suffer from other manifestations in ... ...

Abstract	Background: Monogenic conditions that disrupt proper development and/or function of the immune system are termed inborn errors of immunity (IEIs), also known as primary immunodeficiencies. Patients with IEIs often suffer from other manifestations in addition to infection, and allergic inflammation is an increasingly recognized feature of these conditions. Methods: We performed a retrospective analysis of IEIs presenting with allergic inflammation as reported in the USIDNET registry. Our inclusion criteria comprised of patients with a reported monogenic cause for IEI where reported lab eosinophil and/or IgE values were available for the patient prior to them receiving potentially curative therapy. Patients were excluded if we were unable to determine the defective gene underlying their IEI. Patients were classified as having eosinophilia or elevated IgE when their record included at least 1 eosinophil count or IgE value that was greater than the age stratified upper limit of normal. We compared the proportion of patients with eosinophilia or elevated IgE with the proportion of samples in a reference population that fall above the upper limit of normal (2.5%). Results: The query submitted to the USIDNET registry identified 1409 patients meeting inclusion criteria with a monogenic cause for their IEI diagnosis, of which 975 had eosinophil counts and 645 had IgE levels obtained prior to transplantation or gene therapy that were available for analysis. Overall, 18.8% (183/975) of the patients evaluated from the USIDNET registry had eosinophilia and 20.9% (135/645) had an elevated IgE. IEIs caused by defects in 32 genes were found to be significantly associated with eosinophilia and/or an elevated IgE level, spanning 7 of the 10 IEI categories according to the International Union of Immunological Societies classification. Conclusion: Type 2 inflammation manifesting as eosinophilia or elevated IgE is found in a broad range of IEIs in the USIDNET registry. Our findings suggest that allergic immune dysregulation may be more widespread in IEIs than previously reported.
MeSH term(s)	Eosinophilia ; Humans ; Immunoglobulin E ; Inflammation/genetics ; Registries ; Retrospective Studies
Chemical Substances	Immunoglobulin E (37341-29-0)
Language	English
Publishing date	2022-02-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.831279
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Exome sequencing enables diagnosis of X-linked hypohidrotic ectodermal dysplasia in patient with eosinophilic esophagitis and severe atopy.

Modi, Bhavi P / Del Bel, Kate L / Lin, Susan / Sharma, Mehul / Richmond, Phillip A / van Karnebeek, Clara D M / Chan, Edmond S / Avinashi, Vishal / Rehmus, Wingfield E / Biggs, Catherine M / Wasserman, Wyeth W / Turvey, Stuart E

Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology

2021 Volume 17, Issue 1, Page(s) 9

Abstract: ... a pathogenic nonsense variant in EDA (NM_001399.4: c.766 C>T; p. Gln256Ter). This study highlights how exome ...

Abstract	X-linked hypohidrotic ectodermal dysplasia (XLHED) is the most common form of ectodermal dysplasia. Clinical and genetic heterogeneity between different ectodermal dysplasia types and evidence of incomplete penetrance and variable expressivity increase the potential for misdiagnosis. We describe a family with X-linked hypohidrotic ectodermal dysplasia (XLHED) presenting with variable expressivity of symptoms between affected siblings. In addition to the classical signs of hypohidrosis, hypotrichosis and hypodontia, the index patient-a 5 year old boy, also presented with a severe atopy phenotype that was not observed in the other two affected brothers. Exome sequencing in the index and the mother identified a pathogenic nonsense variant in EDA (NM_001399.4: c.766 C>T; p. Gln256Ter). This study highlights how exome sequencing was crucial in establishing a precise molecular diagnosis of XLHED by enabling us to rule out other differential diagnoses including NEMO deficiency syndrome, that was initially presented as a clinical diagnosis to the family.
Language	English
Publishing date	2021-01-14
Publishing country	England
Document type	Letter
ZDB-ID	2434973-2
ISSN	1710-1492 ; 1710-1484
ISSN (online)	1710-1492
ISSN	1710-1484
DOI	10.1186/s13223-021-00510-z
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 6713: 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: Inborn errors of immunity manifesting as atopic disorders.

Vaseghi-Shanjani, Maryam / Smith, Kelsey L / Sara, Rahnuma J / Modi, Bhavi P / Branch, Anna / Sharma, Mehul / Lu, Henry Y / James, Elliot L / Hildebrand, Kyla J / Biggs, Catherine M / Turvey, Stuart E

The Journal of allergy and clinical immunology

2021 Volume 148, Issue 5, Page(s) 1130–1139

Abstract: Inborn errors of immunity are traditionally best known for enhancing susceptibility to infections. However, allergic inflammation, among other types of immune dysregulation, occurs frequently in patients with inborn errors of immunity. As such, the term ... ...

Abstract	Inborn errors of immunity are traditionally best known for enhancing susceptibility to infections. However, allergic inflammation, among other types of immune dysregulation, occurs frequently in patients with inborn errors of immunity. As such, the term primary atopic disorders (PADs) was recently coined to describe the group of heritable monogenic allergic disorders. It is becoming increasingly important for clinicians to recognize that allergic diseases such as food allergy, atopic dermatitis, and allergic asthma are expressions of misdirected immunity, and in patients who present with severe, early-onset, or coexisting allergic conditions, these can be indications of an underlying PAD. Identifying monogenic allergic disease through next-generation sequencing can dramatically improve outcomes by allowing the use of precision-based therapy targeting the patient's underlying molecular defect. It is therefore imperative that clinicians recognize PADs to be able to provide informed therapeutic options and improve patient outcomes. Here, we summarize the clinical features commonly seen with each of the currently known PADs, identify clinical warning signs that warrant assessment for PADs, and lastly, discuss the benefits of timely diagnosis and management of these conditions.
MeSH term(s)	Disease Management ; Disease Susceptibility ; Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; Hypersensitivity, Immediate/diagnosis ; Hypersensitivity, Immediate/epidemiology ; Hypersensitivity, Immediate/etiology ; Hypersensitivity, Immediate/therapy ; Immunity/genetics ; Phenotype
Language	English
Publishing date	2021-08-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2021.08.008
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

Uh III Zs.92: 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: Recurrent sterile abscesses in a case of X-linked neutropenia.

Biggs, Catherine M / Modi, Bhavi / Steinraths, Michelle / Del Bel, Kate / Pourshahnazari, Persia / Griffiths, Cameron / Forrest, David M / Prendiville, Julie / Dutz, Jan P / Turvey, Stuart E / Cameron, Scott B

Pediatric dermatology

2020 Volume 37, Issue 4, Page(s) 742–744

Abstract: Cutaneous manifestations are common in monogenic immune disorders, including both infectious and non-infectious etiologies. We report follow-up of a case initially published in Pediatric Dermatology in 2001 of a 13-year-old boy with a history of ... ...

Abstract	Cutaneous manifestations are common in monogenic immune disorders, including both infectious and non-infectious etiologies. We report follow-up of a case initially published in Pediatric Dermatology in 2001 of a 13-year-old boy with a history of inflammatory skin lesions and neutropenia who developed neutrophilic dermatoses precipitated by G-CSF. Whole exome sequencing performed at 36 years of age revealed a gain-of-function mutation in the WAS gene, leading to a diagnosis of X-linked neutropenia. This case report provides closure on a decades-long diagnostic odyssey and underscores the importance of genetic sequencing in patients who present with unusual dermatologic findings.
MeSH term(s)	Abscess/diagnosis ; Abscess/genetics ; Adolescent ; Child ; Humans ; Male ; Neutropenia/diagnosis ; Neutropenia/genetics ; Skin Diseases ; Whole Exome Sequencing
Language	English
Publishing date	2020-03-23
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	605539-4
ISSN	1525-1470 ; 0736-8046
ISSN (online)	1525-1470
ISSN	0736-8046
DOI	10.1111/pde.14146
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 1882: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Human DENND1A.V2 Drives

Teves, Maria E / Modi, Bhavi P / Kulkarni, Rewa / Han, Angela X / Marks, Jamaia S / Subler, Mark A / Windle, Jolene / Newall, Jordan M / McAllister, Jan M / Strauss, Jerome F

International journal of molecular sciences

2020 Volume 21, Issue 7

Abstract: ... ...

Abstract	The
MeSH term(s)	Adrenal Glands/metabolism ; Androgens/biosynthesis ; Animals ; Biomarkers ; Biopsy ; Death Domain Receptor Signaling Adaptor Proteins/metabolism ; Disease Models, Animal ; Disease Susceptibility ; Female ; Gene Expression Regulation ; Genetic Vectors/genetics ; Guanine Nucleotide Exchange Factors/metabolism ; Humans ; Immunohistochemistry ; Mice ; Ovary/metabolism ; Polycystic Ovary Syndrome/etiology ; Polycystic Ovary Syndrome/metabolism ; Polycystic Ovary Syndrome/pathology ; Steroid 17-alpha-Hydroxylase/genetics
Chemical Substances	Androgens ; Biomarkers ; DENND1A protein, human ; Death Domain Receptor Signaling Adaptor Proteins ; Guanine Nucleotide Exchange Factors ; CYP17A1 protein, human (EC 1.14.14.19) ; Steroid 17-alpha-Hydroxylase (EC 1.14.14.19)
Language	English
Publishing date	2020-04-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21072545
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Human complete NFAT1 deficiency causes a triad of joint contractures, osteochondromas, and B-cell malignancy.

Blood

2022 Volume 140, Issue 17, Page(s) 1858–1874

Abstract: ... 2023_2026delTACC; p.Tyr675Thrfs∗18) and presented with joint contractures, osteochondromas, and ...

Abstract	The discovery of humans with monogenic disorders has a rich history of generating new insights into biology. Here we report the first human identified with complete deficiency of nuclear factor of activated T cells 1 (NFAT1). NFAT1, encoded by NFATC2, mediates calcium-calcineurin signals that drive cell activation, proliferation, and survival. The patient is homozygous for a damaging germline NFATC2 variant (c.2023_2026delTACC; p.Tyr675Thrfs∗18) and presented with joint contractures, osteochondromas, and recurrent B-cell lymphoma. Absence of NFAT1 protein in chondrocytes caused enrichment in prosurvival and inflammatory genes. Systematic single-cell-omic analyses in PBMCs revealed an environment that promotes lymphomagenesis with accumulation of naïve B cells (enriched for oncogenic signatures MYC and JAK1), exhausted CD4+ T cells, impaired T follicular helper cells, and aberrant CD8+ T cells. This work highlights the pleiotropic role of human NFAT1, will empower the diagnosis of additional patients with NFAT1 deficiency, and further defines the detrimental effects associated with long-term use of calcineurin inhibitors.
MeSH term(s)	Humans ; Calcineurin/genetics ; Contracture ; Leukemia, B-Cell/genetics ; Leukemia, B-Cell/metabolism ; Neoplasm Recurrence, Local ; NFATC Transcription Factors/genetics ; NFATC Transcription Factors/metabolism ; Osteochondroma ; Lymphoma, B-Cell/genetics ; Lymphoma, B-Cell/metabolism
Chemical Substances	Calcineurin (EC 3.1.3.16) ; NFATC Transcription Factors
Language	English
Publishing date	2022-07-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2022015674
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uh III Zs.140: 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)
Zs.MO 364: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Clinical IRAK4 deficiency caused by homozygosity for the novel

Jia, Alicia / James, Elliot / Lu, Henry Y / Sharma, Mehul / Modi, Bhavi P / Biggs, Catherine M / Hildebrand, Kyla J / Chomyn, Alanna / Erdle, Stephanie / Kular, Hasandeep / Turvey, Stuart E

Cold Spring Harbor molecular case studies

2020 Volume 6, Issue 3

Abstract: The innate immune system allows for rapid recognition of pathogens. Toll-like receptor (TLR) signaling is a key aspect of the innate immune response, and interleukin-1 receptor-associated kinase 4 (IRAK4) plays a vital role in the TLR signaling cascade. ... ...

Abstract	The innate immune system allows for rapid recognition of pathogens. Toll-like receptor (TLR) signaling is a key aspect of the innate immune response, and interleukin-1 receptor-associated kinase 4 (IRAK4) plays a vital role in the TLR signaling cascade. Each TLR recognizes a distinct set of pathogen-associated molecular patterns (PAMPs) that encompass conserved microbial components such as lipopolysaccharides and flagellin. Upon binding of PAMPs and TLR activation, TLR intracellular domains initiate the oligomerization of the myeloid differentiation primary response 88 (MyD88), IRAK1, IRAK2, and IRAK4 signaling platform known as the Myddosome complex while also triggering the Toll/IL-1R domain-containing adaptor-inducing IFN-β (TRIF)-dependent pathway. The Myddosome complex initiates signal transduction pathways enabling the activation of NF-κB and mitogen-activated protein kinase (MAPK) transcription factors and the subsequent production of inflammatory cytokines. Human IRAK4 deficiency is an autosomal recessive inborn error of immunity that classically presents with blunted or delayed inflammatory response to infection and susceptibility to a narrow spectrum of pyogenic bacteria, particularly
MeSH term(s)	Alleles ; Amino Acid Substitution ; Family ; Genetic Association Studies ; Genetic Predisposition to Disease ; Homozygote ; Humans ; Infant ; Interleukin-1 Receptor-Associated Kinases/genetics ; Male ; Models, Biological ; Pedigree ; Phenotype ; Primary Immunodeficiency Diseases/diagnosis ; Primary Immunodeficiency Diseases/genetics
Chemical Substances	IRAK4 protein, human (EC 2.7.11.1) ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1)
Language	English
Publishing date	2020-06-12
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2835759-0
ISSN	2373-2873 ; 2373-2873
ISSN (online)	2373-2873
ISSN	2373-2873
DOI	10.1101/mcs.a005298
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Human DENND1A.V2 Drives Cyp17a1 Expression and Androgen Production in Mouse Ovaries and Adrenals

Maria E. Teves / Bhavi P. Modi / Rewa Kulkarni / Angela X. Han / Jamaia S. Marks / Mark A. Subler / Jolene Windle / Jordan M. Newall / Jan M. McAllister / Jerome F. Strauss

International Journal of Molecular Sciences, Vol 21, Iss 2545, p

2020 Volume 2545

Abstract: The DENND1A locus is associated with polycystic ovary syndrome (PCOS), a disorder characterized by androgen excess. Theca cells from ovaries of PCOS women have elevated levels of a DENND1A splice variant (DENND1A.V2). Forced expression of this variant in ...

Abstract	The DENND1A locus is associated with polycystic ovary syndrome (PCOS), a disorder characterized by androgen excess. Theca cells from ovaries of PCOS women have elevated levels of a DENND1A splice variant (DENND1A.V2). Forced expression of this variant in normal theca cells increases androgen biosynthesis and CYP17A1 expression, whereas knockdown of the transcript in PCOS theca cells reduced androgen production and CYP17A1 mRNA. We attempted to create a murine model of PCOS by expressing hDENND1A.V2 using standard transgenic approaches. There is no DENND1A.V2 protein equivalent in mice, and the murine Dennd1a gene is essential for viability since Dennd1a knockout mice are embryonically lethal, suggesting that Dennd1a is developmentally critical. Three different hDENND1A.V2 transgenic mice lines were created using CMV, Lhcgr , and TetOn promoters. The hDENND1A.V2 mice expressed hDENND1A.V2 transcripts. While hDENND1A.V2 protein was not detectable by Western blot analyses, appropriate hDENND1A.V2 immunohistochemical staining was observed. Corresponding Cyp17a1 mRNA levels were elevated in ovaries and adrenals of CMV transgenic mice, as were plasma steroid production by theca interstitial cells isolated from transgenic ovaries. Even though the impact of robust hDENND1A.V2 expression could not be characterized, our findings are consistent with the notion that elevated hDENND1A.V2 has a role in the hyperandrogenemia of PCOS.
Keywords	polycystic ovary syndrome ; DENND1A ; ovaries ; adrenals ; androgens ; Cyp17a1 ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	572
Language	English
Publishing date	2020-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

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: Adult GAMT deficiency: A literature review and report of two siblings.

Modi, Bhavi P / Khan, Haq Nawaz / van der Lee, Robin / Wasim, Muhammad / Haaxma, Charlotte A / Richmond, Phillip A / Drögemöller, Britt / Shah, Suleman / Salomons, Gajja / van der Kloet, Frans M / Vaz, Fred M / van der Crabben, Saskia N / Ross, Colin J / Wasserman, Wyeth W / van Karnebeek, Clara D M / Awan, Fazli Rabbi

Molecular genetics and metabolism reports

2021 Volume 27, Page(s) 100761

Abstract: Guanidinoacetate methyltransferase (GAMT) deficiency is a creatine deficiency disorder and an inborn error of metabolism presenting with progressive intellectual and neurological deterioration. As most cases are identified and treated in early childhood, ...

Abstract	Guanidinoacetate methyltransferase (GAMT) deficiency is a creatine deficiency disorder and an inborn error of metabolism presenting with progressive intellectual and neurological deterioration. As most cases are identified and treated in early childhood, adult phenotypes that can help in understanding the natural history of the disorder are rare. We describe two adult cases of GAMT deficiency from a consanguineous family in Pakistan that presented with a history of global developmental delay, cognitive impairments, excessive drooling, behavioral abnormalities, contractures and apparent bone deformities initially presumed to be the reason for abnormal gait. Exome sequencing identified a homozygous nonsense variant in
Language	English
Publishing date	2021-04-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2821908-9
ISSN	2214-4269
ISSN	2214-4269
DOI	10.1016/j.ymgmr.2021.100761
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

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

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

Order via subito