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Jia V. Li

Bio: Jia V. Li is an academic researcher from Imperial College London. The author has contributed to research in topics: Microbiome & Gut flora. The author has an hindex of 33, co-authored 101 publications receiving 5501 citations. Previous affiliations of Jia V. Li include Office of Population Research & University of Basel.


Papers
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Journal ArticleDOI
01 Feb 2013-Science
TL;DR: The authors investigated the role of the gut microbiome in kwashiorkor, an enigmatic form of severe acute malnutrition that is the consequence of inadequate nutrient intake plus additional environmental insults, and found that RUTF produced a transient maturation of metabolic functions that regressed when administration of RUTF was stopped.
Abstract: Kwashiorkor, an enigmatic form of severe acute malnutrition, is the consequence of inadequate nutrient intake plus additional environmental insults. To investigate the role of the gut microbiome, we studied 317 Malawian twin pairs during the first 3 years of life. During this time, half of the twin pairs remained well nourished, whereas 43% became discordant, and 7% manifested concordance for acute malnutrition. Both children in twin pairs discordant for kwashiorkor were treated with a peanut-based, ready-to-use therapeutic food (RUTF). Time-series metagenomic studies revealed that RUTF produced a transient maturation of metabolic functions in kwashiorkor gut microbiomes that regressed when administration of RUTF was stopped. Previously frozen fecal communities from several discordant pairs were each transplanted into gnotobiotic mice. The combination of Malawian diet and kwashiorkor microbiome produced marked weight loss in recipient mice, accompanied by perturbations in amino acid, carbohydrate, and intermediary metabolism that were only transiently ameliorated with RUTF. These findings implicate the gut microbiome as a causal factor in kwashiorkor.

970 citations

Journal ArticleDOI
TL;DR: The food changes performed in subjects from the same populations resulted in remarkable reciprocal changes in mucosal biomarkers of cancer risk and in aspects of the microbiota and metabolome known to affect cancer risk, best illustrated by increased saccharolytic fermentation and butyrogenesis and suppressed secondary bile acid synthesis in the African Americans.
Abstract: Rates of colon cancer are much higher in African Americans (65:100,000) than in rural South Africans (<5:100,000). The higher rates are associated with higher animal protein and fat, and lower fibre consumption, higher colonic secondary bile acids, lower colonic short-chain fatty acid quantities and higher mucosal proliferative biomarkers of cancer risk in otherwise healthy middle-aged volunteers. Here we investigate further the role of fat and fibre in this association. We performed 2-week food exchanges in subjects from the same populations, where African Americans were fed a high-fibre, low-fat African-style diet and rural Africans a high-fat, low-fibre western-style diet, under close supervision. In comparison with their usual diets, the food changes resulted in remarkable reciprocal changes in mucosal biomarkers of cancer risk and in aspects of the microbiota and metabolome known to affect cancer risk, best illustrated by increased saccharolytic fermentation and butyrogenesis, and suppressed secondary bile acid synthesis in the African Americans.

724 citations

Journal ArticleDOI
TL;DR: Advances in both sequencing technologies and metabolic profiling platforms, coupled with mathematical integration approaches, herald a new era in characterizing the role of the microbiome in metabolic signalling within the host and have far reaching implications in promoting health in both the developed and developing world.

469 citations

Journal ArticleDOI
01 Sep 2011-Gut
TL;DR: The effect of RYGB surgery on the host metabolic–microbial cross-talk augments the understanding of the metabolic phenotype of bariatric procedures and can facilitate enhanced treatments for obesity-related diseases.
Abstract: Background and aims: Bariatric surgery is increasingly performed worldwide to treat morbid obesity and is also known as metabolic surgery to reflect its beneficial metabolic effects especially with respect to improvement in type 2 diabetes. Understanding surgical weight loss mechanisms and metabolic modulation is required to enhance patient benefits and operative outcomes. Methods: The authors applied a parallel and statistically integrated bacterial profiling and metabonomic approach to characterise Roux-en-Y gastric bypass (RYGB) effects in a non-obese rat model. Results: Substantial shifts of the main gut phyla towards higher concentrations of Proteobacteria (52-fold), specifically Enterobacter hormaechei, are shown. Low concentrations of Firmicutes (4.5-fold) and Bacteroidetes (twofold) in comparison with sham-operated rats were also found. Faecal extraction studies revealed a decrease in faecal bile acids and a shift from protein degradation to putrefaction through decreased faecal tyrosine with concomitant increases in faecal putrescine and diaminoethane. Decreased urinary amines and cresols were found and indices of modulated energy metabolism were demonstrated after RYGB, including decreased urinary succinate, 2-oxoglutarate, citrate and fumarate. These changes could also indicate renal tubular acidosis, which is associated with increased flux of mitochondrial tricarboxylic acid cycle intermediates. A surgically induced effect on the gut–brain–liver metabolic axis is inferred from modulated faecal γ-aminobutyric acid and glutamate. Conclusion: This profound co-dependence of mammalian and microbial metabolism, which is systematically altered after RYGB surgery, suggests that RYGB exerts local and global metabolic effects. The effect of RYGB surgery on the host metabolic–microbial cross-talk augments our understanding of the metabolic phenotype of bariatric procedures and can facilitate enhanced treatments for obesity-related diseases.

421 citations

Journal ArticleDOI
TL;DR: The symbiotic gut microbiota modulate health and disease of the host through a series of transgenomic metabolic and immune regulatory axes and are considered possible targets for developing new personalized therapies and clinical management strategies.

408 citations


Cited by
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28 Jul 2005
TL;DR: PfPMP1)与感染红细胞、树突状组胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作�ly.
Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1(PfPMP1)与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员,通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

18,940 citations

01 Jun 2012
TL;DR: SPAdes as mentioned in this paper is a new assembler for both single-cell and standard (multicell) assembly, and demonstrate that it improves on the recently released E+V-SC assembler and on popular assemblers Velvet and SoapDeNovo (for multicell data).
Abstract: The lion's share of bacteria in various environments cannot be cloned in the laboratory and thus cannot be sequenced using existing technologies. A major goal of single-cell genomics is to complement gene-centric metagenomic data with whole-genome assemblies of uncultivated organisms. Assembly of single-cell data is challenging because of highly non-uniform read coverage as well as elevated levels of sequencing errors and chimeric reads. We describe SPAdes, a new assembler for both single-cell and standard (multicell) assembly, and demonstrate that it improves on the recently released E+V-SC assembler (specialized for single-cell data) and on popular assemblers Velvet and SoapDeNovo (for multicell data). SPAdes generates single-cell assemblies, providing information about genomes of uncultivatable bacteria that vastly exceeds what may be obtained via traditional metagenomics studies. SPAdes is available online ( http://bioinf.spbau.ru/spades ). It is distributed as open source software.

10,124 citations

01 Jan 2014
TL;DR: These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care.
Abstract: XI. STRATEGIES FOR IMPROVING DIABETES CARE D iabetes is a chronic illness that requires continuing medical care and patient self-management education to prevent acute complications and to reduce the risk of long-term complications. Diabetes care is complex and requires that many issues, beyond glycemic control, be addressed. A large body of evidence exists that supports a range of interventions to improve diabetes outcomes. These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care. While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided. These standards are not intended to preclude more extensive evaluation and management of the patient by other specialists as needed. For more detailed information, refer to Bode (Ed.): Medical Management of Type 1 Diabetes (1), Burant (Ed): Medical Management of Type 2 Diabetes (2), and Klingensmith (Ed): Intensive Diabetes Management (3). The recommendations included are diagnostic and therapeutic actions that are known or believed to favorably affect health outcomes of patients with diabetes. A grading system (Table 1), developed by the American Diabetes Association (ADA) and modeled after existing methods, was utilized to clarify and codify the evidence that forms the basis for the recommendations. The level of evidence that supports each recommendation is listed after each recommendation using the letters A, B, C, or E.

9,618 citations

Journal ArticleDOI
Evan Bolyen1, Jai Ram Rideout1, Matthew R. Dillon1, Nicholas A. Bokulich1, Christian C. Abnet2, Gabriel A. Al-Ghalith3, Harriet Alexander4, Harriet Alexander5, Eric J. Alm6, Manimozhiyan Arumugam7, Francesco Asnicar8, Yang Bai9, Jordan E. Bisanz10, Kyle Bittinger11, Asker Daniel Brejnrod7, Colin J. Brislawn12, C. Titus Brown4, Benjamin J. Callahan13, Andrés Mauricio Caraballo-Rodríguez14, John Chase1, Emily K. Cope1, Ricardo Silva14, Christian Diener15, Pieter C. Dorrestein14, Gavin M. Douglas16, Daniel M. Durall17, Claire Duvallet6, Christian F. Edwardson, Madeleine Ernst18, Madeleine Ernst14, Mehrbod Estaki17, Jennifer Fouquier19, Julia M. Gauglitz14, Sean M. Gibbons20, Sean M. Gibbons15, Deanna L. Gibson17, Antonio Gonzalez14, Kestrel Gorlick1, Jiarong Guo21, Benjamin Hillmann3, Susan Holmes22, Hannes Holste14, Curtis Huttenhower23, Curtis Huttenhower24, Gavin A. Huttley25, Stefan Janssen26, Alan K. Jarmusch14, Lingjing Jiang14, Benjamin D. Kaehler25, Benjamin D. Kaehler27, Kyo Bin Kang14, Kyo Bin Kang28, Christopher R. Keefe1, Paul Keim1, Scott T. Kelley29, Dan Knights3, Irina Koester14, Tomasz Kosciolek14, Jorden Kreps1, Morgan G. I. Langille16, Joslynn S. Lee30, Ruth E. Ley31, Ruth E. Ley32, Yong-Xin Liu, Erikka Loftfield2, Catherine A. Lozupone19, Massoud Maher14, Clarisse Marotz14, Bryan D Martin20, Daniel McDonald14, Lauren J. McIver23, Lauren J. McIver24, Alexey V. Melnik14, Jessica L. Metcalf33, Sydney C. Morgan17, Jamie Morton14, Ahmad Turan Naimey1, Jose A. Navas-Molina34, Jose A. Navas-Molina14, Louis-Félix Nothias14, Stephanie B. Orchanian, Talima Pearson1, Samuel L. Peoples35, Samuel L. Peoples20, Daniel Petras14, Mary L. Preuss36, Elmar Pruesse19, Lasse Buur Rasmussen7, Adam R. Rivers37, Michael S. Robeson38, Patrick Rosenthal36, Nicola Segata8, Michael Shaffer19, Arron Shiffer1, Rashmi Sinha2, Se Jin Song14, John R. Spear39, Austin D. Swafford, Luke R. Thompson40, Luke R. Thompson41, Pedro J. Torres29, Pauline Trinh20, Anupriya Tripathi14, Peter J. Turnbaugh10, Sabah Ul-Hasan42, Justin J. J. van der Hooft43, Fernando Vargas, Yoshiki Vázquez-Baeza14, Emily Vogtmann2, Max von Hippel44, William A. Walters31, Yunhu Wan2, Mingxun Wang14, Jonathan Warren45, Kyle C. Weber37, Kyle C. Weber46, Charles H. D. Williamson1, Amy D. Willis20, Zhenjiang Zech Xu14, Jesse R. Zaneveld20, Yilong Zhang47, Qiyun Zhu14, Rob Knight14, J. Gregory Caporaso1 
TL;DR: QIIME 2 development was primarily funded by NSF Awards 1565100 to J.G.C. and R.K.P. and partial support was also provided by the following: grants NIH U54CA143925 and U54MD012388.
Abstract: QIIME 2 development was primarily funded by NSF Awards 1565100 to J.G.C. and 1565057 to R.K. Partial support was also provided by the following: grants NIH U54CA143925 (J.G.C. and T.P.) and U54MD012388 (J.G.C. and T.P.); grants from the Alfred P. Sloan Foundation (J.G.C. and R.K.); ERCSTG project MetaPG (N.S.); the Strategic Priority Research Program of the Chinese Academy of Sciences QYZDB-SSW-SMC021 (Y.B.); the Australian National Health and Medical Research Council APP1085372 (G.A.H., J.G.C., Von Bing Yap and R.K.); the Natural Sciences and Engineering Research Council (NSERC) to D.L.G.; and the State of Arizona Technology and Research Initiative Fund (TRIF), administered by the Arizona Board of Regents, through Northern Arizona University. All NCI coauthors were supported by the Intramural Research Program of the National Cancer Institute. S.M.G. and C. Diener were supported by the Washington Research Foundation Distinguished Investigator Award.

8,821 citations

Journal ArticleDOI
08 Jun 2012-Science
TL;DR: A deeper understanding of the axes that physiologically connect the gut, liver, muscle, and brain are a prerequisite for optimizing therapeutic strategies to manipulate the gut microbiota to combat disease and improve health.
Abstract: The composition and activity of the gut microbiota codevelop with the host from birth and is subject to a complex interplay that depends on the host genome, nutrition, and life-style. The gut microbiota is involved in the regulation of multiple host metabolic pathways, giving rise to interactive host-microbiota metabolic, signaling, and immune-inflammatory axes that physiologically connect the gut, liver, muscle, and brain. A deeper understanding of these axes is a prerequisite for optimizing therapeutic strategies to manipulate the gut microbiota to combat disease and improve health.

3,509 citations