LIVIVO - Search results -

Search results

Result 1 - 10 of total 180

Search options

Article ; Online: Revisiting the Effects of Blood Pressure on Kidney Function: New Insights From a Mendelian Randomization Analysis.

Gill, Dipender / Pan, Yang / Lash, James P / Kelly, Tanika N

Hypertension (Dallas, Tex. : 1979)

2022 Volume 79, Issue 12, Page(s) 2682–2684

MeSH term(s)	Mendelian Randomization Analysis ; Blood Pressure/genetics ; Polymorphism, Single Nucleotide ; Kidney ; Genome-Wide Association Study
Language	English
Publishing date	2022-11-09
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.122.19445
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1488: 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

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.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Clonal haematopoiesis, ageing and kidney disease.

Vlasschaert, Caitlyn / Lanktree, Matthew B / Rauh, Michael J / Kelly, Tanika N / Natarajan, Pradeep

Nature reviews. Nephrology

2023 Volume 20, Issue 3, Page(s) 161–174

Abstract: Clonal haematopoiesis of indeterminate potential (CHIP) is a preclinical condition wherein a sizeable proportion of an individual's circulating blood cells are derived from a single mutated haematopoietic stem cell. CHIP occurs frequently with ageing - ... ...

Abstract	Clonal haematopoiesis of indeterminate potential (CHIP) is a preclinical condition wherein a sizeable proportion of an individual's circulating blood cells are derived from a single mutated haematopoietic stem cell. CHIP occurs frequently with ageing - more than 10% of individuals over 65 years of age are affected - and is associated with an increased risk of disease across several organ systems and premature death. Emerging evidence suggests that CHIP has a role in kidney health, including associations with predisposition to acute kidney injury, impaired recovery from acute kidney injury and kidney function decline, both in the general population and among those with chronic kidney disease. Beyond its direct effect on the kidney, CHIP elevates the susceptibility of individuals to various conditions that can detrimentally affect the kidneys, including cardiovascular disease, obesity and insulin resistance, liver disease, gout, osteoporosis and certain autoimmune diseases. Aberrant pro-inflammatory signalling, telomere attrition and epigenetic ageing are potential causal pathophysiological pathways and mediators that underlie CHIP-related disease risk. Experimental animal models have shown that inhibition of inflammatory cytokine signalling can ameliorate many of the pathological effects of CHIP, and assessment of the efficacy and safety of this class of medications for human CHIP-associated pathology is ongoing.
MeSH term(s)	Animals ; Humans ; Clonal Hematopoiesis ; Hematopoiesis/physiology ; Aging ; Hematopoietic Stem Cells/metabolism ; Acute Kidney Injury/metabolism ; Mutation
Language	English
Publishing date	2023-10-26
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/s41581-023-00778-x
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6334: 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.MG 107: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Examination of Serum Metabolome Altered by Dietary Carbohydrate, Milk Protein, and Soy Protein Interventions Identified Novel Metabolites Associated with Blood Pressure: The ProBP Trial.

Changwei, Li / Bundy, Joshua D / Tian, Ling / Zhang, Ruiyuan / Chen, Jing / Kelly, Tanika N / He, Jiang

Molecular nutrition & food research

2023 Volume 67, Issue 20, Page(s) e2300044

Abstract: Scope: This study aims to discover metabolites of dietary carbohydrate, soy and milk protein supplements and evaluate their roles in blood pressure (BP) regulation in the protein and blood pressure (ProBP), a cross-over trial.: Methods and results: ... ...

Abstract	Scope: This study aims to discover metabolites of dietary carbohydrate, soy and milk protein supplements and evaluate their roles in blood pressure (BP) regulation in the protein and blood pressure (ProBP), a cross-over trial. Methods and results: Plasma metabolites are profiled at pre-trial baseline and after 8 weeks of supplementation with carbohydrate, soy protein, and milk protein, respectively, among 80 ProBP participants. After Bonferroni correction (α = 6.49 × 10 Conclusions: The study identifies molecular signatures of dietary interventions. Erucate (22:1n9) increases systolic BP. Acylcholine enhances and cheese intake reduces the BP lowering effect of soy protein supplement.
MeSH term(s)	Humans ; Blood Pressure ; Dietary Carbohydrates/pharmacology ; Metabolome ; Milk Proteins ; Soybean Proteins/pharmacology ; Cross-Over Studies
Chemical Substances	Dietary Carbohydrates ; Milk Proteins ; Soybean Proteins
Language	English
Publishing date	2023-08-31
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2160372-8
ISSN	1613-4133 ; 1613-4125
ISSN (online)	1613-4133
ISSN	1613-4125
DOI	10.1002/mnfr.202300044
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Effects of epigenetic age acceleration on kidney function

Yang Pan / Xiao Sun / Zhijie Huang / Ruiyuan Zhang / Changwei Li / Amanda H. Anderson / James P. Lash / Tanika N. Kelly

Clinical Epigenetics, Vol 15, Iss 1, Pp 1-

a Mendelian randomization study

2023 Volume 14

Abstract: ... of log-transformed estimated glomerular filtration rate (log-eGFR; n = 5,67,460) and GWAS meta-analyses ... of EAA (n = 34,710). An allele score-based Mendelian randomization leveraging individual-level data ... from UK Biobank participants (n = 4,33,462) further examined the effects of EAA on kidney function ...

Abstract	Abstract Background Previous studies have reported cross-sectional associations between measures of epigenetic age acceleration (EAA) and kidney function phenotypes. However, the temporal and potentially causal relationships between these variables remain unclear. We conducted a bidirectional two-sample Mendelian randomization study of EAA and kidney function. Genetic instruments for EAA and estimate glomerular filtration rate (eGFR) were identified from previous genome-wide association study (GWAS) meta-analyses of European-ancestry participants. Causal effects of EAA on kidney function and kidney function on EAA were assessed through summary-based Mendelian randomization utilizing data from the CKDGen GWAS meta-analysis of log-transformed estimated glomerular filtration rate (log-eGFR; n = 5,67,460) and GWAS meta-analyses of EAA (n = 34,710). An allele score-based Mendelian randomization leveraging individual-level data from UK Biobank participants (n = 4,33,462) further examined the effects of EAA on kidney function. Results Using summary-based Mendelian randomization, we found that each 5 year increase in intrinsic EAA (IEAA) and GrimAge acceleration (GrimAA) was associated with − 0.01 and − 0.02 unit decreases in log-eGFR, respectively (P = 0.02 and P = 0.09, respectively), findings which were strongly supported by allele-based Mendelian randomization study (both P < 0.001). Summary-based Mendelian randomization identified 24% increased odds of CKD with each 5-unit increase in IEAA (P = 0.05), with consistent findings observed in allele score-based analysis (P = 0.07). Reverse-direction Mendelian randomization identified potentially causal effects of decreased kidney function on HannumAge acceleration (HannumAA), GrimAA, and PhenoAge acceleration (PhenoAA), conferring 3.14, 1.99, and 2.88 year decreases in HanumAA, GrimAA, and PhenoAA, respectively (P = 0.003, 0.05, and 0.002, respectively) with each 1-unit increase in log-eGFR. Conclusion This study supports bidirectional causal relationships between ...
Keywords	Epigenetic age acceleration ; Kidney function ; Mendelian randomization ; eGFR ; CKD ; Medicine ; R ; Genetics ; QH426-470
Subject code	616
Language	English
Publishing date	2023-04-01T00:00:00Z
Publisher	BMC
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 ; Online: Effects of epigenetic age acceleration on kidney function: a Mendelian randomization study.

Pan, Yang / Sun, Xiao / Huang, Zhijie / Zhang, Ruiyuan / Li, Changwei / Anderson, Amanda H / Lash, James P / Kelly, Tanika N

Clinical epigenetics

2023 Volume 15, Issue 1, Page(s) 61

Abstract	Background: Previous studies have reported cross-sectional associations between measures of epigenetic age acceleration (EAA) and kidney function phenotypes. However, the temporal and potentially causal relationships between these variables remain unclear. We conducted a bidirectional two-sample Mendelian randomization study of EAA and kidney function. Genetic instruments for EAA and estimate glomerular filtration rate (eGFR) were identified from previous genome-wide association study (GWAS) meta-analyses of European-ancestry participants. Causal effects of EAA on kidney function and kidney function on EAA were assessed through summary-based Mendelian randomization utilizing data from the CKDGen GWAS meta-analysis of log-transformed estimated glomerular filtration rate (log-eGFR; n = 5,67,460) and GWAS meta-analyses of EAA (n = 34,710). An allele score-based Mendelian randomization leveraging individual-level data from UK Biobank participants (n = 4,33,462) further examined the effects of EAA on kidney function. Results: Using summary-based Mendelian randomization, we found that each 5 year increase in intrinsic EAA (IEAA) and GrimAge acceleration (GrimAA) was associated with - 0.01 and - 0.02 unit decreases in log-eGFR, respectively (P = 0.02 and P = 0.09, respectively), findings which were strongly supported by allele-based Mendelian randomization study (both P < 0.001). Summary-based Mendelian randomization identified 24% increased odds of CKD with each 5-unit increase in IEAA (P = 0.05), with consistent findings observed in allele score-based analysis (P = 0.07). Reverse-direction Mendelian randomization identified potentially causal effects of decreased kidney function on HannumAge acceleration (HannumAA), GrimAA, and PhenoAge acceleration (PhenoAA), conferring 3.14, 1.99, and 2.88 year decreases in HanumAA, GrimAA, and PhenoAA, respectively (P = 0.003, 0.05, and 0.002, respectively) with each 1-unit increase in log-eGFR. Conclusion: This study supports bidirectional causal relationships between EAA and kidney function, pointing to potential prevention and therapeutic strategies.
MeSH term(s)	Genome-Wide Association Study ; Mendelian Randomization Analysis ; Cross-Sectional Studies ; DNA Methylation ; Kidney ; Epigenesis, Genetic
Language	English
Publishing date	2023-04-08
Publishing country	Germany
Document type	Meta-Analysis ; Journal Article
ZDB-ID	2553921-8
ISSN	1868-7083 ; 1868-7075
ISSN (online)	1868-7083
ISSN	1868-7075
DOI	10.1186/s13148-023-01476-y
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Hypertension in India.

Li, Changwei / Kelly, Tanika N

Journal of hypertension

2014 Volume 32, Issue 6, Page(s) 1189–1191

MeSH term(s)	Humans ; Hypertension/diagnosis ; Hypertension/epidemiology ; Hypertension/therapy
Language	English
Publishing date	2014-06
Publishing country	England
Document type	Comment ; Editorial
ZDB-ID	605532-1
ISSN	1473-5598 ; 0263-6352 ; 0952-1178
ISSN (online)	1473-5598
ISSN	0263-6352 ; 0952-1178
DOI	10.1097/HJH.0000000000000158
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1885: 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)
Zs.MO 614: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Emerging evidence on the role of clonal hematopoiesis of indeterminate potential in chronic kidney disease.

Huang, Zhijie / Vlasschaert, Caitlyn / Robinson-Cohen, Cassianne / Pan, Yang / Sun, Xiao / Lash, James P / Kestenbaum, Bryan / Kelly, Tanika N

Translational research : the journal of laboratory and clinical medicine

2022 Volume 256, Page(s) 87–94

Abstract: Chronic kidney disease (CKD) was responsible for 1.2 million deaths globally in 2016. Despite the large and growing burden of CKD, treatment options are limited and generally only preserve kidney function. Characterizing molecular precursors to incident ... ...

Abstract	Chronic kidney disease (CKD) was responsible for 1.2 million deaths globally in 2016. Despite the large and growing burden of CKD, treatment options are limited and generally only preserve kidney function. Characterizing molecular precursors to incident and progressive CKD could point to critically needed prevention and treatment strategies. Clonal hematopoiesis of indeterminate potential (CHIP) is typically characterized by the clonal expansion of blood cells carrying somatic mutations in specific driver genes. An age-related disorder, CHIP is rare in the young but common in older adults. Recent studies have identified causal associations between CHIP and atherosclerotic cardiovascular disease which are most likely mediated by inflammation, a hallmark of CKD. Animal evidence has supported causal effects of CHIP on kidney injury, inflammation, and fibrosis, providing impetus for human research. Although prospective epidemiologic studies investigating associations of CHIP with development and progression of CKD are few, intriguing findings have been reported. CHIP was significantly associated with kidney function decline and end stage kidney disease in the general population, although effect sizes were modest. Recent work suggests larger associations of CHIP with kidney disease progression in CKD patients, but further investigations in this area are needed. In addition, the accumulating literature has identified some heterogeneity in associations between CHIP and kidney endpoints across study populations, but reasons for these differences remain unclear. The current review provides an in-depth exploration into this nascent area of research, develops a conceptual framework linking CHIP to CKD, and discusses the clinical and public health implications of this work.
MeSH term(s)	Animals ; Humans ; Aged ; Clonal Hematopoiesis ; Prospective Studies ; Hematopoiesis/genetics ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/complications ; Inflammation/complications ; Mutation ; Cardiovascular Diseases/etiology
Language	English
Publishing date	2022-12-28
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2246684-8
ISSN	1878-1810 ; 1532-6543 ; 1931-5244
ISSN (online)	1878-1810 ; 1532-6543
ISSN	1931-5244
DOI	10.1016/j.trsl.2022.12.009
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ud II Zs 42: 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 ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Sex, gut microbiome, and cardiovascular disease risk.

Razavi, Alexander C / Potts, Kaitlin S / Kelly, Tanika N / Bazzano, Lydia A

Biology of sex differences

2019 Volume 10, Issue 1, Page(s) 29

Abstract: Key differences exist between men and women in the determinants and manifestations of cardiovascular and cardiometabolic diseases. Recently, gut microbiome-host relations have been implicated in cardiovascular disease and associated metabolic conditions; ...

Abstract	Key differences exist between men and women in the determinants and manifestations of cardiovascular and cardiometabolic diseases. Recently, gut microbiome-host relations have been implicated in cardiovascular disease and associated metabolic conditions; therefore, gut microbiota may be key mediators or modulators driving the observed sexual dimorphism in disease onset and progression. While current evidence regarding pure physiological sex differences in gut microbiome composition is modest, robust research suggests that gut microbiome-dependent metabolites may interact with important biological pathways under sex hormone control, including toll-like receptor and flavin monooxygenase signaling. Here, we review key sex differences in gut microbiome interactions with four primary determinants of cardiovascular disease, impaired glucose regulation, dyslipidemia, hypertension, and obesity. Through this process, we propose important sex differences in downstream metabolic pathways that may be at the interface of the gut microbiome and cardiovascular disease.
MeSH term(s)	Animals ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/microbiology ; Diet ; Female ; Gastrointestinal Microbiome ; Humans ; Male ; Risk Factors ; Sex Characteristics
Language	English
Publishing date	2019-06-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2587352-0
ISSN	2042-6410 ; 2042-6410
ISSN (online)	2042-6410
ISSN	2042-6410
DOI	10.1186/s13293-019-0240-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Genomic Innovation in Early Life Cardiovascular Disease Prevention and Treatment.

Li, Changwei / Pan, Yang / Zhang, Ruiyuan / Huang, Zhijie / Li, Davey / Han, Yunan / Larkin, Claire / Rao, Varun / Sun, Xiao / Kelly, Tanika N

Circulation research

2023 Volume 132, Issue 12, Page(s) 1628–1647

Abstract: Cardiovascular disease (CVD) is a leading cause of morbidity and mortality globally. Although CVD events do not typically manifest until older adulthood, CVD develops gradually across the life-course, beginning with the elevation of risk factors observed ...

Abstract	Cardiovascular disease (CVD) is a leading cause of morbidity and mortality globally. Although CVD events do not typically manifest until older adulthood, CVD develops gradually across the life-course, beginning with the elevation of risk factors observed as early as childhood or adolescence and the emergence of subclinical disease that can occur in young adulthood or midlife. Genomic background, which is determined at zygote formation, is among the earliest risk factors for CVD. With major advances in molecular technology, including the emergence of gene-editing techniques, along with deep whole-genome sequencing and high-throughput array-based genotyping, scientists now have the opportunity to not only discover genomic mechanisms underlying CVD but use this knowledge for the life-course prevention and treatment of these conditions. The current review focuses on innovations in the field of genomics and their applications to monogenic and polygenic CVD prevention and treatment. With respect to monogenic CVD, we discuss how the emergence of whole-genome sequencing technology has accelerated the discovery of disease-causing variants, allowing comprehensive screening and early, aggressive CVD mitigation strategies in patients and their families. We further describe advances in gene editing technology, which might soon make possible cures for CVD conditions once thought untreatable. In relation to polygenic CVD, we focus on recent innovations that leverage findings of genome-wide association studies to identify druggable gene targets and develop predictive genomic models of disease, which are already facilitating breakthroughs in the life-course treatment and prevention of CVD. Gaps in current research and future directions of genomics studies are also discussed. In aggregate, we hope to underline the value of leveraging genomics and broader multiomics information for characterizing CVD conditions, work which promises to expand precision approaches for the life-course prevention and treatment of CVD.
MeSH term(s)	Humans ; Aged ; Young Adult ; Adult ; Child ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/prevention & control ; Genome-Wide Association Study ; Genomics ; Risk Factors
Language	English
Publishing date	2023-06-08
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.123.321999
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ui IV Zs.70: 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)
Ui IV Zs.60: 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 ▾
- See ZB MED holdings
- Order with fees

Article ; Online: A longitudinal study of polygenic score and cognitive function decline considering baseline cognitive function, lifestyle behaviors, and diabetes among middle-aged and older US adults.

Liu, Tingting / Li, Changwei / Zhang, Ruiyuan / Millender, Eugenia Flores / Miao, Hongyu / Ormsbee, Michael / Guo, Jinzhen / Westbrook, Adrianna / Pan, Yang / Wang, Jing / Kelly, Tanika N

Alzheimer's research & therapy

2023 Volume 15, Issue 1, Page(s) 196

Abstract: Background: Genomic study of cognition decline while considering baseline cognition and lifestyle behaviors is scarce. We aimed to evaluate the impact of a polygenic score for general cognition on cognition decline rate, while considering baseline ... ...

Abstract	Background: Genomic study of cognition decline while considering baseline cognition and lifestyle behaviors is scarce. We aimed to evaluate the impact of a polygenic score for general cognition on cognition decline rate, while considering baseline cognition and lifestyle behaviors, among the general population and people with diabetes, a patient group commonly affected by cognition impairment. Methods: We tested associations of the polygenic score for general cognition with annual changing rates of cognition measures in 8 years of follow-up among 12,090 White and 3100 Black participants of the Health and Retirement Study (HRS), a nationally representative sample of adults aged 50 years and older in the USA. Cognition measures including word recall, mental status, and total cognitive score were measured biannually. To maximize sample size and length of follow-up, we treated the 2010 wave of survey as baseline, and follow-up data until 2018 were analyzed. Baseline lifestyle behaviors, APOE status, and measured cognition were sequentially adjusted. Given racial differences in polygenic score, all analyses were conducted by race. Results: The polygenic score was significantly associated with annual changing rates of all cognition measures independent of lifestyle behaviors and APOE status. Together with age and sex, the polygenic score explained 29.9%, 15.9%, and 26.5% variances of annual changing rates of word recall, mental status, and total cognitive scores among Whites and explained 17.2%, 13.9%, and 18.7% variance of the three traits among Blacks. Among both White and Black participants, those in the top quartile of polygenic score had the three cognition measures increased annually, while those in the bottom quartile had the three cognition measures decreased annually. After further adjusting for the average cognition assessed in 3 visits around baseline, the polygenic score was still positively associated with annual changing rates of all cognition measures for White (P ≤ 2.89E - 19) but not for Black (P ≥ 0.07) participants. In addition, among participants with diabetes, physical activity offset the genetic susceptibility to decline of mental status (interaction P ≤ 0.01) and total cognitive scores (interaction P = 0.03). Conclusions: Polygenic score predicted cognition changes in addition to measured cognition. Physical activity offset genetic risk for cognition decline among diabetes patients.
MeSH term(s)	Middle Aged ; Humans ; Adult ; Aged ; Longitudinal Studies ; Cognitive Dysfunction/epidemiology ; Cognition ; Diabetes Mellitus/epidemiology ; Life Style ; Apolipoproteins E/genetics
Chemical Substances	Apolipoproteins E
Language	English
Publishing date	2023-11-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/s13195-023-01343-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

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

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

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