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Article ; Online: A critical analysis: combination therapy with simultaneous delivery of spinal cord stimulation modalities: COMBO randomized controlled trial.

Socci, John A / Patel, Yogen

2023 Volume 13, Issue 8, Page(s) 423–424

Language	English
Publishing date	2023-09-13
Publishing country	England
Document type	Letter
ZDB-ID	2617136-3
ISSN	1758-1877 ; 1758-1869
ISSN (online)	1758-1877
ISSN	1758-1869
DOI	10.2217/pmt-2023-0064
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Article ; Online: Leukoencephalopathy caused by a 17p13.3 microdeletion.

Wade, Charles / Williams, Thomas / Labrum, Robyn / Patel, Yogen / Cali, Elisa / Davagnanam, Indran / Adams, Matthew E / Barkhof, Frederik / Murphy, Elaine / Chataway, Jeremy / Houlden, Henry / Lynch, David S

Journal of neurology, neurosurgery, and psychiatry

2024 Volume 95, Issue 3, Page(s) 290–292

MeSH term(s)	Humans ; Leukoencephalopathies/diagnostic imaging ; Leukoencephalopathies/genetics ; Intellectual Disability ; Chromosome Deletion
Language	English
Publishing date	2024-02-14
Publishing country	England
Document type	Letter
ZDB-ID	3087-9
ISSN	1468-330X ; 0022-3050
ISSN (online)	1468-330X
ISSN	0022-3050
DOI	10.1136/jnnp-2023-331986
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Article ; Online: Genetic testing for mitochondrial disease: the United Kingdom best practice guidelines.

Mavraki, Eleni / Labrum, Robyn / Sergeant, Kate / Alston, Charlotte L / Woodward, Cathy / Smith, Conrad / Knowles, Charlotte V Y / Patel, Yogen / Hodsdon, Philip / Baines, Jack P / Blakely, Emma L / Polke, James / Taylor, Robert W / Fratter, Carl

European journal of human genetics : EJHG

2022 Volume 31, Issue 2, Page(s) 148–163

Abstract: Primary mitochondrial disease describes a diverse group of neuro-metabolic disorders characterised by impaired oxidative phosphorylation. Diagnosis is challenging; >350 genes, both nuclear and mitochondrial DNA (mtDNA) encoded, are known to cause ... ...

Abstract	Primary mitochondrial disease describes a diverse group of neuro-metabolic disorders characterised by impaired oxidative phosphorylation. Diagnosis is challenging; >350 genes, both nuclear and mitochondrial DNA (mtDNA) encoded, are known to cause mitochondrial disease, leading to all possible inheritance patterns and further complicated by heteroplasmy of the multicopy mitochondrial genome. Technological advances, particularly next-generation sequencing, have driven a shift in diagnostic practice from 'biopsy first' to genome-wide analyses of blood and/or urine DNA. This has led to the need for a reference framework for laboratories involved in mitochondrial genetic testing to facilitate a consistent high-quality service. In the United Kingdom, consensus guidelines have been prepared by a working group of Clinical Scientists from the NHS Highly Specialised Service followed by national laboratory consultation. These guidelines summarise current recommended technologies and methodologies for the analysis of mtDNA and nuclear-encoded genes in patients with suspected mitochondrial disease. Genetic testing strategies for diagnosis, family testing and reproductive options including prenatal diagnosis are outlined. Importantly, recommendations for the minimum levels of mtDNA testing for the most common referral reasons are included, as well as guidance on appropriate referrals and information on the minimal appropriate gene content of panels when analysing nuclear mitochondrial genes. Finally, variant interpretation and recommendations for reporting of results are discussed, focussing particularly on the challenges of interpreting and reporting mtDNA variants.
MeSH term(s)	Pregnancy ; Female ; Humans ; Genome-Wide Association Study ; Mitochondrial Diseases/genetics ; DNA, Mitochondrial/genetics ; Genetic Testing/methods ; Mitochondria/genetics ; Genome, Mitochondrial
Chemical Substances	DNA, Mitochondrial
Language	English
Publishing date	2022-12-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1141470-4
ISSN	1476-5438 ; 1018-4813
ISSN (online)	1476-5438
ISSN	1018-4813
DOI	10.1038/s41431-022-01249-w
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Article ; Online: Poster 244 An Unusual Cause of Coma from Consumption of Red Yeast Rice: A Case Report.

Patel, Yogen / Behar, Alex B / Shah, Chirag D / Kasi, Ravi E

PM & R : the journal of injury, function, and rehabilitation

2016 Volume 8, Issue 9S, Page(s) S239–S240

Language	English
Publishing date	2016-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2608988-9
ISSN	1934-1563 ; 1934-1482
ISSN (online)	1934-1563
ISSN	1934-1482
DOI	10.1016/j.pmrj.2016.07.277
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Article ; Online: Diagnostic yield of rare skeletal dysplasia conditions in the radiogenomics era.

Sabir, Ataf H / Morley, Elizabeth / Sheikh, Jameela / Calder, Alistair D / Beleza-Meireles, Ana / Cheung, Moira S / Cocca, Alessandra / Jansson, Mattias / Lillis, Suzanne / Patel, Yogen / Yau, Shu / Hall, Christine M / Offiah, Amaka C / Irving, Melita

BMC medical genomics

2021 Volume 14, Issue 1, Page(s) 148

Abstract: Background: Skeletal dysplasia (SD) conditions are rare genetic diseases of the skeleton, encompassing a heterogeneous group of over 400 disorders, and represent approximately 5% of all congenital anomalies. Developments in genetic and treatment ... ...

Abstract	Background: Skeletal dysplasia (SD) conditions are rare genetic diseases of the skeleton, encompassing a heterogeneous group of over 400 disorders, and represent approximately 5% of all congenital anomalies. Developments in genetic and treatment technologies are leading to unparalleled therapeutic advances; thus, it is more important than ever to molecularly confirm SD conditions. Data on 'rates-of-molecular yields' in SD conditions, through exome sequencing approaches, is limited. Figures of 39% and 52.5% have been reported in the USA (n = 54) and South Korea (n = 185) respectively. Methods: We discuss a single-centre (in the UK) experience of whole-exome sequencing (WES) in a cohort of 15 paediatric patients (aged 5 months to 12 years) with SD disorders previously molecularly unconfirmed. Our cohort included patients with known clinical diagnoses and undiagnosed skeletal syndromes. Extensive phenotyping and expert radiological review by a panel of international SD radiology experts, coupled with a complex bioinformatics pipeline, allowed for both gene-targeted and gene-agnostic approaches. Results: Significant variants leading to a likely or confirmed diagnosis were identified in 53.3% (n = 8/15) of patients; 46.7% (n = 7/15) having a definite molecular diagnosis and 6.7% (n = 1/15) having a likely molecular diagnosis. We discuss this in the context of a rare disease in general and specifically SD presentations. Of patients with known diagnoses pre-WES (n = 10), molecular confirmation occurred in 7/10 cases, as opposed to 1/5 where a diagnosis was unknown pre-test. Thus, diagnostic return is greatest where the diagnosis is known pre-test. For WGS (whole genome sequencing, the next iteration of WES), careful case selection (ideally of known diagnoses pre-test) will yield highest returns. Conclusions: Our results highlight the cost-effective use of WES-targeted bioinformatic analysis as a diagnostic tool for SD, particularly patients with presumed SD, where detailed phenotyping is essential. Thorough co-ordinated clinical evaluation between clinical, radiological, and molecular teams is essential for improved yield and clinical care. WES (and WGS) yields will increase with time, allowing faster diagnoses, avoiding needless investigations, ensuring individualised patient care and patient reassurance. Further diagnoses will lead to increased information on natural history/mechanistic details, and likely increased therapies and clinical trials.
MeSH term(s)	Whole Exome Sequencing
Language	English
Publishing date	2021-06-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1755-8794
ISSN (online)	1755-8794
DOI	10.1186/s12920-021-00993-0
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Article ; Online: Specialist multidisciplinary input maximises rare disease diagnoses from whole genome sequencing.

Nature communications

2022 Volume 13, Issue 1, Page(s) 6324

Abstract: Diagnostic whole genome sequencing (WGS) is increasingly used in rare diseases. However, standard, semi-automated WGS analysis may overlook diagnoses in complex disorders. Here, we show that specialist multidisciplinary analysis of WGS, following an ... ...

Abstract	Diagnostic whole genome sequencing (WGS) is increasingly used in rare diseases. However, standard, semi-automated WGS analysis may overlook diagnoses in complex disorders. Here, we show that specialist multidisciplinary analysis of WGS, following an initial 'no primary findings' (NPF) report, improves diagnostic rates and alters management. We undertook WGS in 102 adults with diagnostically challenging primary mitochondrial disease phenotypes. NPF cases were reviewed by a genomic medicine team, thus enabling bespoke informatic approaches, co-ordinated phenotypic validation, and functional work. We enhanced the diagnostic rate from 16.7% to 31.4%, with management implications for all new diagnoses, and detected strong candidate disease-causing variants in a further 3.9% of patients. This approach presents a standardised model of care that supports mainstream clinicians and enhances diagnostic equity for complex disorders, thereby facilitating access to the potential benefits of genomic healthcare. This research was made possible through access to the data and findings generated by the 100,000 Genomes Project: http://www.genomicsengland.co.uk .
MeSH term(s)	Humans ; Rare Diseases/diagnosis ; Rare Diseases/genetics ; Whole Genome Sequencing ; Phenotype ; Genome
Language	English
Publishing date	2022-11-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-32908-7
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Article ; Online: Cross-region reduction in 5-hydroxymethylcytosine in Alzheimer's disease brain.

Condliffe, Daniel / Wong, Andrew / Troakes, Claire / Proitsi, Petroula / Patel, Yogen / Chouliaras, Leonidas / Fernandes, Cathy / Cooper, Jonathan / Lovestone, Simon / Schalkwyk, Leonard / Mill, Jonathan / Lunnon, Katie

Neurobiology of aging

2014 Volume 35, Issue 8, Page(s) 1850–1854

Abstract: Epigenetic processes play a key role in the central nervous system and altered levels of 5-methylcytosine have been associated with a number of neurologic phenotypes, including Alzheimer's disease (AD). Recently, 3 additional cytosine modifications have ... ...

Abstract	Epigenetic processes play a key role in the central nervous system and altered levels of 5-methylcytosine have been associated with a number of neurologic phenotypes, including Alzheimer's disease (AD). Recently, 3 additional cytosine modifications have been identified (5-hydroxymethylcytosine, 5-formylcytosine, and 5-carboxylcytosine), which are thought to be intermediate steps in the demethylation of 5-methylcytosine to unmodified cytosine. Little is known about the frequency of these modifications in the human brain during health or disease. In this study, we used immunofluorescence to confirm the presence of each modification in human brain and investigate their cross-tissue abundance in AD patients and elderly control samples. We identify a significant AD-associated decrease in global 5-hydroxymethylcytosine in entorhinal cortex and cerebellum, and differences in 5-formylcytosine levels between brain regions. Our study further implicates a role for epigenetic alterations in AD.
MeSH term(s)	5-Methylcytosine/analogs & derivatives ; Aged ; Aged, 80 and over ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Brain/metabolism ; Cytosine/analogs & derivatives ; Cytosine/metabolism ; Epigenesis, Genetic/genetics ; Female ; Fluorescent Antibody Technique ; Humans ; Ivermectin/analogs & derivatives ; Male ; Methylation
Chemical Substances	5-formylcytosine ; demethylavermectins ; 5-hydroxymethylcytosine (1123-95-1) ; 5-Methylcytosine (6R795CQT4H) ; Ivermectin (70288-86-7) ; Cytosine (8J337D1HZY)
Language	English
Publishing date	2014-02-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2014.02.002
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Article: Low prevalence of BRCA1 exon rearrangements in familial and young sporadic breast cancer patients.

Ellis, David / Patel, Yogen / Yau, Shu C / Hodgson, Shirley V / Abbs, Stephen J

Familial cancer

2006 Volume 5, Issue 4, Page(s) 323–326

Abstract: BRCA1 exon deletions and duplications have been reported in a number of studies, and in order to design an effective mutation screening strategy in a diagnostic setting it is import to determine the frequency of this type of mutation in breast and ... ...

Abstract	BRCA1 exon deletions and duplications have been reported in a number of studies, and in order to design an effective mutation screening strategy in a diagnostic setting it is import to determine the frequency of this type of mutation in breast and ovarian cancer patients. We have designed and applied quantitative fluorescent PCR (QF-PCR) assays to screen for BRCA1 exon rearrangements in breast cancer patients both with and without a family history. A panel of 182 familial patients was screened, and an exon 3-7 deletion mutation was detected in a patient with a family history of breast and ovarian cancer. Additionally, we detected a duplication of exons 18-19 in an early onset sporadic breast cancer patient from a panel of 100 patients tested. These data indicate that in the absence of any founder mutations, screening for BRCA1 exon rearrangements does not significantly increase the overall BRCA1 mutation detection rate in patients referred to a genetics clinic because of either a family history and/or an early onset of disease.
MeSH term(s)	Adult ; Breast Neoplasms/genetics ; Exons ; Female ; Gene Rearrangement ; Genes, BRCA1 ; Humans ; Polymerase Chain Reaction
Language	English
Publishing date	2006
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1502496-9
ISSN	1389-9600
ISSN	1389-9600
DOI	10.1007/s10689-006-0001-0
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Article: Role of Environmental Confounding in the Association between FKBP5 and First-Episode Psychosis.

Frontiers in psychiatry

2014 Volume 5, Page(s) 84

Abstract: Background: Failure to account for the etiological diversity that typically occurs in psychiatric cohorts may increase the potential for confounding as a proportion of genetic variance will be specific to exposures that have varying distributions in ... ...

Abstract	Background: Failure to account for the etiological diversity that typically occurs in psychiatric cohorts may increase the potential for confounding as a proportion of genetic variance will be specific to exposures that have varying distributions in cases. This study investigated whether minimizing the potential for such confounding strengthened the evidence for a genetic candidate currently unsupported at the genome-wide level. Methods: Two hundred and ninety-one first-episode psychosis cases from South London, UK and 218 unaffected controls were evaluated for a functional polymorphism at the rs1360780 locus in FKBP5. The relationship between FKBP5 and psychosis was modeled using logistic regression. Cannabis use (Cannabis Experiences Questionnaire) and parental separation (Childhood Experience of Care and Abuse Questionnaire) were included as confounders in the analysis. Results: Association at rs1360780 was not detected until the effects of the two environmental factors had been adjusted for in the model (OR = 2.81, 95% CI 1.23-6.43, p = 0.02). A statistical interaction between rs1360780 and parental separation was confirmed by stratified tests (OR = 2.8, p = 0.02 vs. OR = 0.89, p = 0.80). The genetic main effect was directionally consistent with findings in other (stress-related) clinical phenotypes. Moreover, the variation in effect magnitude was explained by the level of power associated with different cannabis constructs used in the model (r = 0.95). Conclusion: Our results suggest that the extent to which genetic variants in FKBP5 can influence susceptibility to psychosis may depend on other etiological factors. This finding requires further validation in large independent cohorts. Potentially this work could have translational implications; the ability to discriminate between genetic etiologies based on a case-by-case understanding of previous environmental exposures would confer an important clinical advantage that would benefit the delivery of personalizable treatment strategies.
Language	English
Publishing date	2014-07-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564218-2
ISSN	1664-0640
ISSN	1664-0640
DOI	10.3389/fpsyt.2014.00084
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Article ; Online: Pandemic peak SARS-CoV-2 infection and seroconversion rates in London frontline health-care workers

Houlihan, Catherine F / Vora, Nina / Byrne, Thomas / Lewer, Dan / Kelly, Gavin / Heaney, Judith / Gandhi, Sonia / Spyer, Moira J / Beale, Rupert / Cherepanov, Peter / Moore, David / Gilson, Richard / Gamblin, Steve / Kassiotis, George / McCoy, Laura E / Swanton, Charles / Hayward, Andrew / Nastouli, Eleni / Aitken, Jim /

Allen, Zoe / Ambler, Rachel / Ambrose, Karen / Ashton, Emma / Avola, Alida / Balakrishnan, Samutheswari / Barns-Jenkins, Caitlin / Barr, Genevieve / Barrell, Sam / Basu, Souradeep / Beesley, Clare / Bhardwaj, Nisha / Bibi, Shahnaz / Bineva-Todd, Ganka / Biswas, Dhruva / Blackman, Michael J / Bonnet, Dominique / Bowker, Faye / Broncel, Malgorzata / Brooks, Claire / Buck, Michael D / Buckton, Andrew / Budd, Timothy / Burrell, Alana / Busby, Louise / Bussi, Claudio / Butterworth, Simon / Byrne, Fiona / Byrne, Richard / Caidan, Simon / Campbell, Joanna / Canton, Johnathan / Cardoso, Ana / Carter, Nick / Carvalho, Luiz / Carzaniga, Raffaella / Chandler, Natalie / Chen, Qu / Churchward, Laura / Clark, Graham / Clayton, Bobbi / Cobolli Gigli, Clementina / Collins, Zena / Cottrell, Sally / Crawford, Margaret / Cubitt, Laura / Cullup, Tom / Davies, Heledd / Davis, Patrick / Davison, Dara / D'Avola, Annalisa / Dearing, Vicky / Debaisieux, Solene / Diaz-Romero, Monica / Dibbs, Alison / Diring, Jessica / Driscoll, Paul C / Earl, Christopher / Edwards, Amelia / Ekin, Chris / Evangelopoulos, Dimitrios / Faraway, Rupert / Fearns, Antony / Ferron, Aaron / Fidanis, Efthymios / Fitz, Dan / Fleming, James / Frederico, Bruno / Gaiba, Alessandra / Gait, Anthony / Gaul, Liam / Golding, Helen M / Goldman, Jacki / Goldstone, Robert / Gomez Dominguez, Belen / Gong, Hui / Grant, Paul R / Greco, Maria / Grobler, Mariana / Guedan, Anabel / Gutierrez, Maximiliano G / Hackett, Fiona / Hall, Ross / Halldorsson, Steinar / Harris, Suzanne / Hashim, Sugera / Healy, Lyn / Herbst, Susanne / Hewitt, Graeme / Higgins, Theresa / Hindmarsh, Steve / Hirani, Rajnika / Hope, Joshua / Horton, Elizabeth / Hoskins, Beth / Howell, Michael / Howitt, Louise / Hoyle, Jacqueline / Htun, Mint R / Hubank, Michael / Huerga Encabo, Hector / Hughes, Deborah / Hughes, Jane / Huseynova, Almaz / Hwang, Ming-Shih / Instrell, Rachael / Jackson, Deborah / Jamal-Hanjani, Mariam / Jenkins, Lucy / Jiang, Ming / Johnson, Mark / Jones, Leigh / Kanu, Nnennaya / Kiely, Louise / King Spert Teixeira, Anastacio / Kirk, Stuart / Kjaer, Svend / Knuepfer, Ellen / Komarov, Nikita / Kotzampaltiris, Paul / Kousis, Konstantinos / Krylova, Tammy / Kucharska, Ania / Labrum, Robyn / Lambe, Catherine / Lappin, Michelle / Lee, Stacey-Ann / Levett, Andrew / Levett, Lisa / Levi, Marcel / Liu, Hon-Wing / Loughlin, Sam / Lu, Wei-Ting / MacRae, James I / Madoo, Akshay / Marczak, Julie A / Martensson, Mimmi / Martinez, Thomas / Marzook, Bishara / Matthews, John / Matz, Joachim M / McCall, Samuel / McKay, Fiona / McNamara, Edel C / Minutti, Carlos M / Mistry, Gita / Molina-Arcas, Miriam / Montaner, Beatriz / Montgomery, Kylie / Moore, Catherine / Moraiti, Anastasia / Moreira-Teixeira, Lucia / Mukherjee, Joyita / Naceur-Lombardelli, Cristina / Nelson, Aileen / Nicod, Jerome / Nightingale, Luke / Nofal, Stephanie / Nurse, Paul / Nutan, Savita / Oedekoven, Caroline / O'Garra, Anne / O'Leary, Jean D / Olsen, Jessica / O'Neill, Olga / Ordonez Suarez, Paula / O'Reilly, Nicola / Osborne, Neil / Pabari, Amar / Pajak, Aleksandra / Papayannopoulos, Venizelos / Patel, Namita / Patel, Yogen / Paun, Oana / Peat, Nigel / Peces-Barba Castano, Laura / Perez Caballero, Ana / Perez-Lloret, Jimena / Perrault, Magali S / Perrin, Abigail / Poh, Roy / Poirier, Enzo Z / Polke, James M / Pollitt, Marc / Prieto-Godino, Lucia / Proust, Alize / Shah Punatar, Rajvee / Puvirajasinghe, Clinda / Queval, Christophe / Ramachandran, Vijaya / Ramaprasad, Abhinay / Ratcliffe, Peter / Reed, Laura / Reis e Sousa, Caetano / Richardson, Kayleigh / Ridewood, Sophie / Roberts, Rowenna / Rodgers, Angela / Romero Clavijo, Pablo / Rosa, Annachiara / Rossi, Alice / Roustan, Chloe / Rowan, Andrew / Sahai, Erik / Sait, Aaron / Sala, Katarzyna / Sanderson, Theo / Santucci, Pierre / Sardar, Fatima / Sateriale, Adam / Saunders, Jill A / Sawyer, Chelsea / Schlott, Anja / Schweighoffer, Edina / Segura-Bayona, Sandra / Shaw, Joe / Shin, Gee Yen / Silva Dos Santos, Mariana / Silvestre, Margaux / Singer, Matthew / Snell, Daniel M / Song, Ok-Ryul / Steel, Louisa / Strange, Amy / Sullivan, Adrienne E / Tan, Michele SY / Tautz-Davis, Zoe H / Taylor, Effie / Taylor, Gunes / Taylor, Harriet B / Taylor-Beadling, Alison / Teixeira Subtil, Fernanda / Terré Torras, Berta / Toolan-Kerr, Patrick / Torelli, Francesca / Toteva, Tea / Treeck, Moritz / Trojer, Hadija / Tsai, Ming-Han C / Turner, James MA / Turner, Melanie / Ule, Jernej / Ulferts, Rachel / Vanloo, Sharon P / Veeriah, Selvaraju / Venkatesan, Subramanian / Vousden, Karen / Wack, Andreas / Walder, Claire / Walker, Philip A / Wang, Yiran / Ward, Sophia / Wenman, Catharina / Wiliams, Luke / Williams, Matthew J / Wong, Wai Keong / Wright, Joshua / Wu, Mary / Wynne, Lauren / Xiang, Zheng / Yap, Melvyn / Zagalak, Julian A / Zecchin, Davide / Zillwood, Rachel / Matthews, Rebecca / Severn, Abigail / Adam, Sajida / Enfield, Louise / McBride, Angela / Gärtner, Kathleen / Edwards, Sarah / Lorencatto, Fabiana / Michie, Susan / Manley, Ed / Shahmanesh, Maryam / Lukha, Hinal / Prymas, Paulina / McBain, Hazel / Shortman, Robert / Wood, Leigh / Davies, Claudia / Williams, Bethany / Ng, Kevin W / Cornish, Georgina H / Faulkner, Nikhil / Riddell, Andrew / Hobson, Philip / Agua-Doce, Ana / Bartolovic, Kerol / Russell, Emma / Carr, Lotte / Sanchez, Emilie / Frampton, Daniel / Byott, Matthew / Paraskevopoulou, Stavroula M / Crayton, Elise / Meyer, Carly / Gkouleli, Triantafylia / Stoltenberg, Andrea / Ranieri, Veronica / Byrne, Tom / Roberts, Fiona / Hatipoglu, Emine

The Lancet

2020 Volume 396, Issue 10246, Page(s) e6–e7

Keywords	General Medicine ; covid19
Language	English
Publisher	Elsevier BV
Publishing country	us
Document type	Article ; Online
ZDB-ID	3306-6
ISSN	1474-547X ; 0023-7507 ; 0140-6736
ISSN (online)	1474-547X
ISSN	0023-7507 ; 0140-6736
DOI	10.1016/s0140-6736(20)31484-7
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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