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Article ; Online: Novel Homozygous Variants of SLC13A5 Expand the Functional Heterogeneity of a Homogeneous Syndrome of Early Infantile Epileptic Encephalopathy.

Alsemari, Abdulaziz / Guzmán-Vega, Francisco J / Meyer, Brian F / Arold, Stefan T

2023 Volume 151, Page(s) 68–72

Abstract: Background: Early infantile epileptic encephalopathy 25 (EIEE25) is a distinct type of neonatal epileptic encephalopathy caused by autosomal recessive mutations in the SLC13A5 gene. SLC13A5 encodes a transmembrane sodium/citrate cotransporter required ... ...

Abstract	Background: Early infantile epileptic encephalopathy 25 (EIEE25) is a distinct type of neonatal epileptic encephalopathy caused by autosomal recessive mutations in the SLC13A5 gene. SLC13A5 encodes a transmembrane sodium/citrate cotransporter required for regulating citrate entry into cells. Methods: Four families with recessively inherited epileptic encephalopathy were sequenced by clinically accredited laboratories using commercially available epilepsy gene panels. Patients were examined by a neurologist and were clinically diagnosed with infantile epileptic encephalopathy. Results: We present four families with global developmental delay, intellectual disability, and defective tooth development with four novel homozygous mutations in SLC13A5. The neurological examination showed spastic quadriplegia with increased deep tendon reflexes. Brain magnetic resonance imaging showed nonspecific signal abnormality of the bilateral hemispheric white matter. Despite similar clinical features, the conditions were based on different molecular mechanisms acting on SLC13A5 (abnormal splicing, large-scale deletions, and tandem-residue insertion). Conclusions: Our results extend the landscape of autosomal recessive inherited homozygous mutations in SLC13A5 that cause a distinctive syndrome of severe neonatal epileptic encephalopathy. Our observations confirm the homogeneity of epileptic encephalopathy and dental abnormalities as a distinct clinical marker for EIEE25 despite the heterogeneous functional and mutational background.
MeSH term(s)	Infant, Newborn ; Humans ; Spasms, Infantile/diagnostic imaging ; Spasms, Infantile/genetics ; Spasms, Infantile/pathology ; Epilepsy/genetics ; Brain Diseases/diagnostic imaging ; Brain Diseases/genetics ; Mutation/genetics ; Syndrome ; Citric Acid ; Symporters/genetics
Chemical Substances	Citric Acid (2968PHW8QP) ; SLC13A5 protein, human ; Symporters
Language	English
Publishing date	2023-10-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	639164-3
ISSN	1873-5150 ; 0887-8994
ISSN (online)	1873-5150
ISSN	0887-8994
DOI	10.1016/j.pediatrneurol.2023.10.005
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Article ; Online: Circulating Tumour DNA Detection By The Urine-Informed Analysis Of Archival Serum Samples From Muscle-Invasive Bladder Cancer Patients.

BinHumaid, Faisal S / Goel, Anshita / Gordon, Naheema S / Abbotts, Ben / Cheng, K K / Zeegers, Maurice P / James, Nicholas D / Altaweel, Waleed M / Seyam, Raouf M / Meyer, Brian F / Arnold, Roland / Ward, Douglas G / Bryan, Richard T

European urology

2024 Volume 85, Issue 5, Page(s) 508–509

MeSH term(s)	Humans ; Circulating Tumor DNA/genetics ; Urinary Bladder Neoplasms/pathology ; Biomarkers, Tumor/genetics ; Muscles/pathology
Chemical Substances	Circulating Tumor DNA ; Biomarkers, Tumor
Language	English
Publishing date	2024-02-01
Publishing country	Switzerland
Document type	Letter
ZDB-ID	193790-x
ISSN	1873-7560 ; 1421-993X ; 0302-2838
ISSN (online)	1873-7560 ; 1421-993X
ISSN	0302-2838
DOI	10.1016/j.eururo.2024.01.016
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Zs.A 1247: 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)
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Article ; Online: Identification of pharmacogenetic variants from large scale next generation sequencing data in the Saudi population.

Goljan, Ewa / Abouelhoda, Mohammed / ElKalioby, Mohamed M / Jabaan, Amjad / Alghithi, Nada / Meyer, Brian F / Monies, Dorota

PloS one

2022 Volume 17, Issue 1, Page(s) e0263137

Abstract: It is well documented that drug responses are related to Absorption, Distribution, Metabolism, and Excretion (ADME) characteristics of individual patients. Several studies have identified genetic variability in pharmacogenes, that are either directly ... ...

Abstract	It is well documented that drug responses are related to Absorption, Distribution, Metabolism, and Excretion (ADME) characteristics of individual patients. Several studies have identified genetic variability in pharmacogenes, that are either directly responsible for or are associated with ADME, giving rise to individualized treatments. Our objective was to provide a comprehensive overview of pharmacogenetic variation in the Saudi population. We mined next generation sequencing (NGS) data from 11,889 unrelated Saudi nationals, to determine the presence and frequencies of known functional SNP variants in 8 clinically relevant pharmacogenes (CYP2C9, CYP2C19, CYP3A5, CYP4F2, VKORC1, DPYD, TPMT and NUDT15), recommended by the Clinical Pharmacogenetics Implementation Consortium (CPIC), and collectively identified 82 such star alleles. Functionally significant pharmacogenetic variants were prevalent especially in CYP genes (excluding CYP3A5), with 10-44.4% of variants predicted to be inactive or to have decreased activity. In CYP3A5, inactive alleles (87.5%) were the most common. Only 1.8%, 0.7% and 0.7% of NUDT15, TPMT and DPYD variants respectively, were predicted to affect gene activity. In contrast, VKORC1 was found functionally, to be highly polymorphic with 53.7% of Saudi individuals harboring variants predicted to result in decreased activity and 31.3% having variants leading to increased metabolic activity. Furthermore, among the 8 pharmacogenes studied, we detected six rare variants with an aggregated frequency of 1.1%, that among several other ethnicities, were uniquely found in Saudi population. Similarly, within our cohort, the 8 pharmacogenes yielded forty-six novel variants predicted to be deleterious. Based upon our findings, 99.2% of individuals from the Saudi population carry at least one actionable pharmacogenetic variant.
MeSH term(s)	Female ; Gene Frequency ; Genotype ; High-Throughput Nucleotide Sequencing ; Humans ; Male ; Pharmacogenetics ; Pharmacogenomic Testing ; Pharmacogenomic Variants ; Polymorphism, Single Nucleotide ; Saudi Arabia
Language	English
Publishing date	2022-01-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0263137
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Article ; Online: β-catenin attenuation leads to up-regulation of activating NKG2D ligands and tumor regression in

Zou, Minjing / Al-Yahya, Suhad / Al-Alwan, Monther / BinEssa, Huda A / Khabar, Khalid S A / Almohanna, Falah / Assiri, Abdullah M / Altaweel, Abdulmohsen / Qattan, Amal / Meyer, Brian F / Alzahrani, Ali S / Shi, Yufei

Frontiers in immunology

2023 Volume 14, Page(s) 1171816

Abstract: Introduction: BRAF: Methods: In the present study, we investigated the tumorigenicity of thyroid cancer cells derived from : Results: Remarkably, the tumorigenic potential of BVE-: Conclusions: Our results indicate that active β-catenin ... ...

Abstract	Introduction: BRAF Methods: In the present study, we investigated the tumorigenicity of thyroid cancer cells derived from Results: Remarkably, the tumorigenic potential of BVE- Conclusions: Our results indicate that active β-catenin signaling inhibits NK cell-mediated immune responses against thyroid cancer cells. Targeting the β-catenin signaling pathway may have significant therapeutic benefits for
MeSH term(s)	Mice ; Animals ; Mice, Nude ; NK Cell Lectin-Like Receptor Subfamily K/genetics ; NK Cell Lectin-Like Receptor Subfamily K/metabolism ; beta Catenin/genetics ; beta Catenin/metabolism ; Carcinoma, Papillary/genetics ; Carcinoma, Papillary/metabolism ; Up-Regulation ; Proto-Oncogene Proteins B-raf ; Ligands ; Thyroid Neoplasms/pathology ; Thyroid Cancer, Papillary/genetics ; Wnt Signaling Pathway/physiology ; Membrane Proteins/metabolism
Chemical Substances	NK Cell Lectin-Like Receptor Subfamily K ; beta Catenin ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Ligands ; Raet1c protein, mouse ; Membrane Proteins
Language	English
Publishing date	2023-07-06
Publishing country	Switzerland
Document type	Journal Article ; 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.2023.1171816
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Article ; Online: Established and candidate transthyretin amyloidosis variants identified in the Saudi population by data mining.

Abouelhoda, Mohamed / Mohty, Dania / Alayary, Islam / Meyer, Brian F / Arold, Stefan T / Fadel, Bahaa M / Monies, Dorota

Human genomics

2021 Volume 15, Issue 1, Page(s) 52

Abstract: Background: Familial transthyretin (TTR) amyloidosis (ATTR) is an autosomal dominant disease with significant phenotypic heterogeneity. Its prevalence in Saudi Arabia has not previously been investigated. An existing exome variant database of Saudi ... ...

Abstract	Background: Familial transthyretin (TTR) amyloidosis (ATTR) is an autosomal dominant disease with significant phenotypic heterogeneity. Its prevalence in Saudi Arabia has not previously been investigated. An existing exome variant database of Saudi individuals, sequenced to globally investigate rare diseases in the population, was mined for TTR variants and filtered for missense mutations resulting in single amino acid changes. A total of 13,906 Saudi exomes from unrelated individuals were analyzed blindly. Results: Three TTR variants known to be associated with ATTR amyloidosis were identified. Additionally, three novel TTR mutations were identified. Structural analysis of the three novel variants suggests that at least two could be amyloidogenic. The most common variant associated with amyloidosis was p.Val142Ile (allele frequency 0.001). Further investigation of these variants and their translation to clinical practice may help to diagnose, monitor, and manage patients with ATTR amyloidosis. Conclusion: Multiple TTR variants potentially associated with systemic ATTR amyloidosis were identified in the Saudi population. Early diagnosis and intervention, facilitated by familial genetic testing of patients with ATTR amyloidosis, may benefit in the management of this disease. Early diagnosis could be enhanced through inclusion of ATTR variants in existing population-based screening programs.
MeSH term(s)	Adolescent ; Adult ; Aged ; Amyloid Neuropathies, Familial/epidemiology ; Amyloid Neuropathies, Familial/genetics ; Amyloid Neuropathies, Familial/pathology ; Child ; Data Mining ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genetic Testing ; Genetic Variation/genetics ; Humans ; Male ; Middle Aged ; Mutation, Missense/genetics ; Prealbumin/genetics ; Saudi Arabia/epidemiology ; Young Adult
Chemical Substances	Prealbumin ; TTR protein, human
Language	English
Publishing date	2021-08-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2147618-4
ISSN	1479-7364 ; 1479-7364
ISSN (online)	1479-7364
ISSN	1479-7364
DOI	10.1186/s40246-021-00351-2
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Article ; Online: Insights of Noncanonical Splice-site Variants on RNA Splicing in Patients With Congenital Hypothyroidism.

Albader, Najla / Zou, Minjing / BinEssa, Huda A / Abdi, Saba / Al-Enezi, Anwar F / Meyer, Brian F / Alzahrani, Ali S / Shi, Yufei

The Journal of clinical endocrinology and metabolism

2021 Volume 107, Issue 3, Page(s) e1263–e1276

Abstract: Context: Congenital hypothyroidism (CH) is caused by mutations in the genes for thyroid hormone synthesis. In our previous investigation of CH patients, approximately 53% of patients had mutations in either coding exons or canonical splice sites of ... ...

Abstract	Context: Congenital hypothyroidism (CH) is caused by mutations in the genes for thyroid hormone synthesis. In our previous investigation of CH patients, approximately 53% of patients had mutations in either coding exons or canonical splice sites of causative genes. Noncanonical splice-site variants in the intron were detected but their pathogenic significance was not known. Objective: This work aims to evaluate noncanonical splice-site variants on pre-messenger RNA (pre-mRNA) splicing of CH-causing genes. Methods: Next-generation sequencing data of 55 CH cases in 47 families were analyzed to identify rare intron variants. The effects of variants on pre-mRNA splicing were investigated by minigene RNA-splicing assay. Results: Four intron variants were found in 3 patients: solute carrier family 26 member 4 (SLC26A4) c.1544+9C>T and c.1707+94C>T in one patient, and solute carrier family 5 member 5 (SLC5A5) c.970-48G>C and c.1652-97A>C in 2 other patients. The c.1707+94C>T and c.970-48G>C caused exons 15 and 16 skipping, and exon 8 skipping, respectively. The remaining variants had no effect on RNA splicing. Furthermore, we analyzed 28 previously reported noncanonical splice-site variants (4 in TG and 24 in SLC26A4). Among them, 15 variants (~ 54%) resulted in aberrant splicing and 13 variants had no effect on RNA splicing. These data were compared with 3 variant-prediction programs (FATHMM-XF, FATHMM-MKL, and CADD). Among 32 variants, FATHMM-XF, FATHMM-MKL, and CADD correctly predicted 20 (63%), 17 (53%), and 26 (81%) variants, respectively. Conclusion: Two novel deep intron mutations have been identified in SLC26A4 and SLC5A5, bringing the total number of solved families with disease-causing mutations to approximately 45% in our cohort. Approximately 46% (13/28) of reported noncanonical splice-site mutations do not disrupt pre-mRNA splicing. CADD provides highest prediction accuracy of noncanonical splice-site variants.
MeSH term(s)	Congenital Hypothyroidism/genetics ; Female ; Humans ; Male ; Mutation ; RNA Splice Sites/genetics ; RNA Splicing ; Sulfate Transporters/genetics ; Symporters/genetics
Chemical Substances	RNA Splice Sites ; SLC26A4 protein, human ; Sulfate Transporters ; Symporters ; sodium-iodide symporter (4XE5NDT4K1)
Language	English
Publishing date	2021-09-29
Publishing country	United States
Document type	Journal Article ; Observational Study ; Research Support, Non-U.S. Gov't
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgab737
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Article: Wild-type S100A3 and S100A13 restore calcium homeostasis and mitigate mitochondrial dysregulation in pulmonary fibrosis patient-derived cells.

Al-Mutairy, Eid A / Al Qattan, Somaya / Khalid, Mohammed / Al-Enazi, Azizah A / Al-Saif, Maher M / Imtiaz, Faiqa / Ramzan, Khushnooda / Raveendran, Vineesh / Alaiya, Ayodele / Meyer, Brian F / Atamas, Sergei P / Collison, Kate S / Khabar, Khalid S / Hasday, Jeffrey D / Al-Mohanna, Futwan

Frontiers in cell and developmental biology

2023 Volume 11, Page(s) 1282868

Abstract: Patients with digenic S100A3 and S100A13 mutations exhibited an atypical and progressive interstitial pulmonary fibrosis, with impaired intracellular calcium homeostasis and mitochondrial dysfunction. Here we provide direct evidence of a causative effect ...

Abstract	Patients with digenic S100A3 and S100A13 mutations exhibited an atypical and progressive interstitial pulmonary fibrosis, with impaired intracellular calcium homeostasis and mitochondrial dysfunction. Here we provide direct evidence of a causative effect of the mutation on receptor mediated calcium signaling and calcium store responses in control cells transfected with mutant S100A3 and mutant S100A13. We demonstrate that the mutations lead to increased mitochondrial mass and hyperpolarization, both of which were reversed by transfecting patient-derived cells with the wild type S100A3 and S100A13, or extracellular treatment with the recombinant proteins. In addition, we demonstrate increased secretion of inflammatory mediators in patient-derived cells and in control cells transfected with the mutant-encoding constructs. These findings indicate that treatment of patients' cells with recombinant S100A3 and S100A13 proteins is sufficient to normalize most of cellular responses, and may therefore suggest the use of these recombinant proteins in the treatment of this devastating disease.
Language	English
Publishing date	2023-11-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2023.1282868
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Article ; Online: The clinical utility of rapid exome sequencing in a consanguineous population.

Monies, Dorota / Goljan, Ewa / Assoum, Mirna / Albreacan, Muna / Binhumaid, Faisal / Subhani, Shazia / Boureggah, Abdulmlik / Hashem, Mais / Abdulwahab, Firdous / Abuyousef, Omar / Temsah, Mohamad H / Alsohime, Fahad / Kelaher, James / Abouelhoda, Mohamed / Meyer, Brian F / Alkuraya, Fowzan S

Genome medicine

2023 Volume 15, Issue 1, Page(s) 44

Abstract: Background: The clinical utility of exome sequencing is now well documented. Rapid exome sequencing (RES) is more resource-intensive than regular exome sequencing and is typically employed in specialized clinical settings wherein urgent molecular ... ...

Abstract	Background: The clinical utility of exome sequencing is now well documented. Rapid exome sequencing (RES) is more resource-intensive than regular exome sequencing and is typically employed in specialized clinical settings wherein urgent molecular diagnosis is thought to influence acute management. Studies on the clinical utility of RES have been largely limited to outbred populations. Methods: Here, we describe our experience with rapid exome sequencing (RES) in a highly consanguineous population. Clinical settings included intensive care units, prenatal cases approaching the legal cutoff for termination, and urgent transplant decisions. Results: A positive molecular finding (a pathogenic or likely pathogenic variant that explains the phenotype) was observed in 80 of 189 cases (42%), while 15 (8%) and 94 (50%) received ambiguous (variant of uncertain significance (VUS)) and negative results, respectively. The consanguineous nature of the study population gave us an opportunity to observe highly unusual and severe phenotypic expressions of previously reported genes. Clinical utility was observed in nearly all (79/80) cases with positive molecular findings and included management decisions, prognostication, and reproductive counseling. Reproductive counseling is a particularly important utility in this population where the overwhelming majority (86%) of identified variants are autosomal recessive, which are more actionable in this regard than the de novo variants typically reported by RES elsewhere. Indeed, our cost-effectiveness analysis shows compelling cost savings in the study population. Conclusions: This work expands the diversity of environments in which RES has a demonstrable clinical utility.
MeSH term(s)	Pregnancy ; Female ; Humans ; Consanguinity ; Exome Sequencing ; Phenotype
Language	English
Publishing date	2023-06-21
Publishing country	England
Document type	Journal Article
ZDB-ID	2484394-5
ISSN	1756-994X ; 1756-994X
ISSN (online)	1756-994X
ISSN	1756-994X
DOI	10.1186/s13073-023-01192-5
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Article: Molecular Analysis of

Zou, Minjing / Guven, Ayla / BinEssa, Huda A / Al-Rijjal, Roua A / Meyer, Brian F / Alzahrani, Ali S / Shi, Yufei

Frontiers in genetics

2020 Volume 11, Page(s) 607517

Abstract: Context: Vitamin D-dependent rickets type 1A (VDDR1A) is a rare autosomal recessively inherited disorder due to loss-of-function mutations in the : Objective: To identify underlying genetic defects in patients with VDDR1A.: Methods: Twelve ... ...

Abstract	Context: Vitamin D-dependent rickets type 1A (VDDR1A) is a rare autosomal recessively inherited disorder due to loss-of-function mutations in the Objective: To identify underlying genetic defects in patients with VDDR1A. Methods: Twelve patients from 7 Turkish and 2 Saudi families were investigated. The coding exons and intron-exon boundaries of the Results: CYP27B1 Conclusion: Two novel frameshift
Language	English
Publishing date	2020-11-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2020.607517
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Article ; Online: Replication of Type 2 diabetes-associated variants in a Saudi Arabian population.

Li-Gao, Ruifang / Wakil, Salma M / Meyer, Brian F / Dzimiri, Nduna / Mook-Kanamori, Dennis O

Physiological genomics

2018 Volume 50, Issue 4, Page(s) 296–297

Abstract: Over 120 Type 2 diabetes (T2D) loci have been identified from genome-wide association studies (GWAS), mainly from Caucasian populations. Very limited knowledge is available on the Saudi Arabian population. In this study, 122 previously reported T2D- ... ...

Abstract	Over 120 Type 2 diabetes (T2D) loci have been identified from genome-wide association studies (GWAS), mainly from Caucasian populations. Very limited knowledge is available on the Saudi Arabian population. In this study, 122 previously reported T2D-related variants from 84 loci were examined in a Saudi Arabian cohort of 1,578 individuals (659 T2D cases and 919 controls). Eleven single nucleotide polymorphisms (SNPs) corresponding to nine independent loci had a P value <0.05. If a more stringent Bonferroni threshold of P = 4.1 × 10
MeSH term(s)	DNA-Binding Proteins/genetics ; Diabetes Mellitus, Type 2/genetics ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study ; Humans ; Odds Ratio ; Polymorphism, Single Nucleotide/genetics ; Saudi Arabia ; Transcription Factors/genetics
Chemical Substances	DNA-Binding Proteins ; Transcription Factors ; ZFAND3 protein, human
Language	English
Publishing date	2018-02-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2038823-8
ISSN	1531-2267 ; 1094-8341
ISSN (online)	1531-2267
ISSN	1094-8341
DOI	10.1152/physiolgenomics.00100.2017
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