10 results on '"Mak, Shi Ya"'
Search Results
2. Antibody glycan quality predicted from CHO cell culture media markers and machine learning
- Author
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Lakshmanan, Meiyappan, Chia, Sean, Pang, Kuin Tian, Sim, Lyn Chiin, Teo, Gavin, Mak, Shi Ya, Chen, Shuwen, Lim, Hsueh Lee, Lee, Alison P., Bin Mahfut, Farouq, Ng, Say Kong, Yang, Yuansheng, Soh, Annie, Tan, Andy Hee-Meng, Choo, Andre, Ho, Ying Swan, Nguyen-Khuong, Terry, and Walsh, Ian
- Published
- 2024
- Full Text
- View/download PDF
3. p53-dependent crosstalk between DNA replication integrity and redox metabolism mediated through a NRF2-PARP1 axis.
- Author
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Elfar, Gamal Ahmed, Aning, Obed, Ngai, Tsz Wai, Yeo, Pearlyn, Chan, Joel Wai Kit, Sim, Shang Hong, Goh, Leonard, Yuan, Ju, Phua, Cheryl Zi Jin, Yeo, Joanna Zhen Zhen, Mak, Shi Ya, Goh, Brian Kim Poh, Chow, Pierce Kah-Hoe, Tam, Wai Leong, Ho, Ying Swan, and Cheok, Chit Fang
- Published
- 2024
- Full Text
- View/download PDF
4. Excessive fatty acid oxidation induces muscle atrophy in cancer cachexia
- Author
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Fukawa, Tomoya, Yan-Jiang, Benjamin Chua, Min-Wen, Jason Chua, Jun-Hao, Elwin Tan, Huang, Dan, Qian, Chao-Nan, Ong, Pauline, Li, Zhimei, Chen, Shuwen, Mak, Shi Ya, Lim, Wan Jun, Kanayama, Hiro-omi, Mohan, Rosmin Elsa, Wang, Ruiqi Rachel, Lai, Jiunn Herng, Chua, Clarinda, Ong, Hock Soo, Tan, Ker-Kan, Ho, Ying Swan, Tan, Iain Beehuat, Teh, Bin Tean, and Shyh-Chang, Ng
- Subjects
Fatty acids -- Health aspects ,Cachexia -- Development and progression -- Risk factors -- Diagnosis -- Care and treatment -- Research ,Muscular atrophy -- Diagnosis -- Care and treatment ,Biological sciences ,Health - Abstract
Author(s): Tomoya Fukawa [1, 2, 3]; Benjamin Chua Yan-Jiang [4]; Jason Chua Min-Wen [4]; Elwin Tan Jun-Hao [4]; Dan Huang [2]; Chao-Nan Qian [5]; Pauline Ong [1, 2]; Zhimei Li [...]
- Published
- 2016
- Full Text
- View/download PDF
5. A synbiotic intervention modulates meta-omics signatures of gut redox potential and acidity in elective caesarean born infants
- Author
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Lay, Christophe, Chu, Collins Wenhan, Purbojati, Rikky Wenang, Acerbi, Enzo, Drautz-Moses, Daniela I, de Sessions, Paola Florez, Jie, Song, Ho, Eliza, Kok, Yee Jiun, Bi, Xuezhi, Chen, Shuwen, Mak, Shi Ya, Chua, Mei Chien, Goh, Anne EN, Chiang, Wen Chin, Rao, Rajeshwar, Chaithongwongwatthana, Surasith, Khemapech, Nipon, Chongsrisawat, Voranush, Martin, Rocio, JULIUS Study Group, Roeselers, Guus, Ho, Ying Swan, Hibberd, Martin L, Schuster, Stephan C, and Knol, Jan
- Abstract
BACKGROUND: The compromised gut microbiome that results from C-section birth has been hypothesized as a risk factor for the development of non-communicable diseases (NCD). In a double-blind randomized controlled study, 153 infants born by elective C-section received an infant formula supplemented with either synbiotic, prebiotics, or unsupplemented from birth until 4 months old. Vaginally born infants were included as a reference group. Stool samples were collected from day 3 till week 22. Multi-omics were deployed to investigate the impact of mode of delivery and nutrition on the development of the infant gut microbiome, and uncover putative biological mechanisms underlying the role of a compromised microbiome as a risk factor for NCD. RESULTS: As early as day 3, infants born vaginally presented a hypoxic and acidic gut environment characterized by an enrichment of strict anaerobes (Bifidobacteriaceae). Infants born by C-section presented the hallmark of a compromised microbiome driven by an enrichment of Enterobacteriaceae. This was associated with meta-omics signatures characteristic of a microbiome adapted to a more oxygen-rich gut environment, enriched with genes associated with reactive oxygen species metabolism and lipopolysaccharide biosynthesis, and depleted in genes involved in the metabolism of milk carbohydrates. The synbiotic formula modulated expression of microbial genes involved in (oligo)saccharide metabolism, which emulates the eco-physiological gut environment observed in vaginally born infants. The resulting hypoxic and acidic milieu prevented the establishment of a compromised microbiome. CONCLUSIONS: This study deciphers the putative functional hallmarks of a compromised microbiome acquired during C-section birth, and the impact of nutrition that may counteract disturbed microbiome development. TRIAL REGISTRATION: The study was registered in the Dutch Trial Register (Number: 2838 ) on 4th April 2011.
- Published
- 2021
6. Multi‐omics profiling of a CHO cell culture system unravels the effect of culture pH on cell growth, antibody titer, and product quality.
- Author
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Lee, Alison P., Kok, Yee Jiun, Lakshmanan, Meiyappan, Leong, Dawn, Zheng, Lu, Lim, Hsueh Lee, Chen, Shuwen, Mak, Shi Ya, Ang, Kok Siong, Templeton, Neil, Salim, Taha, Wei, Xiaona, Gifford, Eric, Tan, Andy Hee‐Meng, Bi, Xuezhi, Ng, Say Kong, Lee, Dong‐Yup, Ling, Wai Lam W., and Ho, Ying Swan
- Abstract
A robust monoclonal antibody (mAb) bioprocess requires physiological parameters such as temperature, pH, or dissolved oxygen to be well‐controlled as even small variations in them could potentially impact the final product quality. For instance, pH substantially affects N‐glycosylation, protein aggregation, and charge variant profiles, as well as mAb productivity. However, relatively less is known about how pH jointly influences product quality and titer. In this study, we investigated the effect of pH on culture performance, product titer, and quality profiles by applying longitudinal multi‐omics profiling, including transcriptomics, proteomics, metabolomics, and glycomics, at three different culture pH set points. The subsequent systematic analysis of multi‐omics data showed that pH set points differentially regulated various intracellular pathways including intracellular vesicular trafficking, cell cycle, and apoptosis, thereby resulting in differences in specific productivity, product titer, and quality profiles. In addition, a time‐dependent variation in mAb N‐glycosylation profiles, independent of pH, was identified to be mainly due to the accumulation of mAb proteins in the endoplasmic reticulum disrupting cellular homeostasis over culture time. Overall, this multi‐omics‐based study provides an in‐depth understanding of the intracellular processes in mAb‐producing CHO cell line under varied pH conditions, and could serve as a baseline for enabling the quality optimization and control of mAb production. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
7. Evaluation and use of disaccharides as energy source in protein-free mammalian cell cultures.
- Author
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Leong, Dawn Sow Zong, Tan, Janice Gek Ling, Chin, Christine Lin, Mak, Shi Ya, Ho, Ying Swan, and Ng, Say Kong
- Abstract
Mammalian cells are generally considered to be unable to utilize polysaccharides for cell growth because the phospholipid bilayer in the cell membrane has very low permeability to sugars. With the recent discovery of the only known animal disaccharide transporter, a sucrose transporter, we considered the potential use of polysaccharides as energy source, because that can impact biopharmaceutical manufacturing by potentially increasing carbohydrate loading in the culture medium and decreasing lactate accumulation. In this study, we found that mammalian cells can utilize maltose for growth in the absence of glucose and successfully adapted CHO-K1, CHO-DG44 and HEK293 cells to grow in glucose-free, maltose-containing serum-free protein-free media. We then cultivated a non-adapted CHO-K1 producer cell line in media containing both glucose and maltose to show that the cells can utilize maltose in a biphasic manner, that maltose enters the cells, and that maltose utilization only took place in the presence of the cells. This is the first report of a protein-free mammalian cell culture using a disaccharide as energy source. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF
8. Warburg metabolism in tumor-conditioned macrophages promotes metastasis in human pancreatic ductal adenocarcinoma.
- Author
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Penny, Hweixian Leong, Sieow, Je Lin, Adriani, Giulia, Yeap, Wei Hseun, See Chi Ee, Peter, San Luis, Boris, Lee, Bernett, Lee, Terence, Mak, Shi Ya, Ho, Ying Swan, Lam, Kong Peng, Ong, Choon Kiat, Huang, Ruby Y. J., Ginhoux, Florent, Rotzschke, Olaf, Kamm, Roger D., and Wong, Siew Cheng
- Subjects
DUCTAL carcinoma ,ADENOCARCINOMA ,METASTASIS ,TUMORS ,GLYCOLYSIS - Abstract
Patients with pancreatic ductal adenocarcinoma (PDAC) face a clinically intractable disease with poor survival rates, attributed to exceptionally high levels of metastasis. Epithelial-to-mesenchymal transition (EMT) is pronounced at inflammatory foci within the tumor; however, the immunological mechanisms promoting tumor dissemination remain unclear. It is well established that tumors exhibit the Warburg effect, a preferential use of glycolysis for energy production, even in the presence of oxygen, to support rapid growth. We hypothesized that the metabolic pathways utilized by tumor-infiltrating macrophages are altered in PDAC, conferring a pro-metastatic phenotype. We generated tumor-conditioned macrophagesin vitro, in which human peripheral blood monocytes were cultured with conditioned media generated from normal pancreatic or PDAC cell lines to obtain steady-state and tumor-associated macrophages (TAMs), respectively. Compared with steady-state macrophages, TAMs promoted vascular network formation, augmented extravasation of tumor cells out of blood vessels, and induced higher levels of EMT. TAMs exhibited a pronounced glycolytic signature in a metabolic flux assay, corresponding with elevated glycolytic gene transcript levels. Inhibiting glycolysis in TAMs with a competitive inhibitor to Hexokinase II (HK2), 2-deoxyglucose (2DG), was sufficient to disrupt this pro-metastatic phenotype, reversing the observed increases in TAM-supported angiogenesis, extravasation, and EMT. Our results indicate a key role for metabolic reprogramming of tumor-infiltrating macrophages in PDAC metastasis, and highlight the therapeutic potential of using pharmacologics to modulate these metabolic pathways. [ABSTRACT FROM PUBLISHER]
- Published
- 2016
- Full Text
- View/download PDF
9. High Extracellular K + Skews T-Cell Differentiation Towards Tumour Promoting Th2 and T reg Subsets.
- Author
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Wong BHS, Poh ZS, Wei JTC, Amuthavalli K, Ho YS, Chen S, Mak SY, Bi X, Webster RD, Shelat VG, Chandy KG, and Verma NK
- Abstract
Potassium ions (K
+ ) released from dying necrotic tumour cells accumulate in the tumour microenvironment (TME) and increase the local K+ concentration to 50 mM (high-[K+ ]e ). Here, we demonstrate that high-[K+ ]e decreases expression of the T-cell receptor subunits CD3ε and CD3ζ and co-stimulatory receptor CD28 and thereby dysregulates intracellular signal transduction cascades. High-[K+ ]e also alters the metabolic profiles of T-cells, limiting the metabolism of glucose and glutamine, consistent with functional exhaustion. These changes skew T-cell differentiation, favouring Th2 and iTreg subsets that promote tumour growth while restricting antitumour Th1 and Th17 subsets. Similar phenotypes were noted in T-cells present within the necrosis-prone core versus the outer zones of hepatocellular carcinoma (HCC)/colorectal carcinoma (CRC) tumours as analysed by GeoMx digital spatial profiling and flow-cytometry. Our results thus expand the understanding of the contribution of high-[K+ ]e to the immunosuppressive milieu in the TME., (© 2024 The Author(s). European Journal of Immunology published by Wiley‐VCH GmbH.)- Published
- 2024
- Full Text
- View/download PDF
10. A synbiotic intervention modulates meta-omics signatures of gut redox potential and acidity in elective caesarean born infants.
- Author
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Lay C, Chu CW, Purbojati RW, Acerbi E, Drautz-Moses DI, de Sessions PF, Jie S, Ho E, Kok YJ, Bi X, Chen S, Mak SY, Chua MC, Goh AEN, Chiang WC, Rao R, Chaithongwongwatthana S, Khemapech N, Chongsrisawat V, Martin R, Roeselers G, Ho YS, Hibberd ML, Schuster SC, and Knol J
- Subjects
- Biodiversity, Double-Blind Method, Humans, Infant, Infant, Newborn, Bacteria genetics, Cesarean Section adverse effects, Feces microbiology, Gastrointestinal Microbiome genetics, Metagenome genetics
- Abstract
Background: The compromised gut microbiome that results from C-section birth has been hypothesized as a risk factor for the development of non-communicable diseases (NCD). In a double-blind randomized controlled study, 153 infants born by elective C-section received an infant formula supplemented with either synbiotic, prebiotics, or unsupplemented from birth until 4 months old. Vaginally born infants were included as a reference group. Stool samples were collected from day 3 till week 22. Multi-omics were deployed to investigate the impact of mode of delivery and nutrition on the development of the infant gut microbiome, and uncover putative biological mechanisms underlying the role of a compromised microbiome as a risk factor for NCD., Results: As early as day 3, infants born vaginally presented a hypoxic and acidic gut environment characterized by an enrichment of strict anaerobes (Bifidobacteriaceae). Infants born by C-section presented the hallmark of a compromised microbiome driven by an enrichment of Enterobacteriaceae. This was associated with meta-omics signatures characteristic of a microbiome adapted to a more oxygen-rich gut environment, enriched with genes associated with reactive oxygen species metabolism and lipopolysaccharide biosynthesis, and depleted in genes involved in the metabolism of milk carbohydrates. The synbiotic formula modulated expression of microbial genes involved in (oligo)saccharide metabolism, which emulates the eco-physiological gut environment observed in vaginally born infants. The resulting hypoxic and acidic milieu prevented the establishment of a compromised microbiome., Conclusions: This study deciphers the putative functional hallmarks of a compromised microbiome acquired during C-section birth, and the impact of nutrition that may counteract disturbed microbiome development., Trial Registration: The study was registered in the Dutch Trial Register (Number: 2838 ) on 4th April 2011.
- Published
- 2021
- Full Text
- View/download PDF
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