Search

Your search keyword '"Chen, Titi"' showing total 34 results
Start Over Author "Chen, Titi"
34 results on '"Chen, Titi"'

3. WCN24-758 RECOGNITION OF LOCAL INVESTIGATORS IN AUTHORSHIP OF COLLABORATIVE KIDNEY RESEARCH CONDUCTED IN LOW- AND LOWERMIDDLE INCOME COUNTRIES

Author

Wijewickrama, Eranga, primary, Chanchlani, Rahul, additional, Wong, Michelle, additional, Kumar, Vivek, additional, Karam, Sabine, additional, Chen, Titi, additional, Erikpo, Udeme, additional, Tannor, Elliot, additional, Calice-Silva, Viviane, additional, Anandh, Urmila, additional, Bajpai, Divya, additional, Abdul Hafidz, Muhamed Iqbal, additional, Tian, Amanda, additional, Opare-Addo, Priscilla, additional, Edeki, Imuetinyan, additional, and Kalyesubula, Robert, additional

Published
2024
Full Text
View/download PDF

9. Nurturing Global Leadership, Advocacy, Research, and Collegiality: The Unique Experience of The International Society of Nephrology Emerging Leaders Program

Author

Karam, Sabine, primary, Abdul Hafidz, Muhammad Iqbal, additional, Calice-Silva, Viviane, additional, Chen, Titi, additional, Dupuis, Sophie, additional, Ekrikpo, Udeme E., additional, Francis, Anna, additional, Jha, Vivekanand, additional, Kalyesubula, Robert, additional, Kumar, Vivek, additional, Nakhoul, Georges, additional, Pereira-Kamath, Nikhil, additional, Tannor, Elliot K., additional, Tran, Anh, additional, Wijewickrama, Eranga, additional, Wong, Michelle M.Y., additional, and Chanchlani, Rahul, additional

Published
2023
Full Text
View/download PDF

11. Capacity for the management of kidney failure in the International Society of Nephrology Oceania and South East Asia (OSEA) region: report from the 2023 ISN Global Kidney Health Atlas (ISN-GKHA)

Author

Francis, Anna, Wainstein, Marina, Irish, Georgina, Abdul Hafidz, Muhammad Iqbal, Chen, Titi, Cho, Yeoungjee, Htay, Htay, Kanjanabuch, Talerngsak, Lalji, Rowena, Neuen, Brendon L., See, Emily, Shah, Anim, Smyth, Brendan, Tungsanga, Somkanya, Viecelli, Andrea, Yeung, Emily K., Arruebo, Silvia, Bello, Aminu K., Caskey, Fergus J., Damster, Sandrine, Donner, Jo-Ann, Jha, Vivekanand, Johnson, David W., Levin, Adeera, Malik, Charu, Nangaku, Masaomi, Okpechi, Ikechi G., Tonelli, Marcello, Ye, Feng, Wong, Muh Geot, Bavanandan, Sunita, Abdul Gafor, Abdul Halim, Amouzegar, Atefeh, Bennett, Paul, Chicano, Sonia L., Davids, M. Razeen, Davison, Sara N., Diongole, Hassane M., Divyaveer, Smita, Ekrikpo, Udeme E., Ethier, Isabelle, Fong, Voon Ken, Fung, Winston Wing-Shing, Ghimire, Anukul, Gopal, Basu, Phan, Hai An Ha, Harris, David C.H., Houston, Ghenette, Ibrahim, Kwaifa Salihu, Jardine, Meg J., Jindal, Kailash, Kantachuvesiri, Surasak, Kelly, Dearbhla M., Kerr, Peter, Kim, Siah, Krishnasamy, Rathika, Kwek, Jia Liang, Lee, Vincent, Liew, Adrian, Lim, Chiao Yuen, Lydia, Aida, Nalado, Aisha M., Olanrewaju, Timothy O., Osman, Mohamed A., Petrova, Anna, Pyar, Khin Phyu, Riaz, Parnian, Saad, Syed, Sakajiki, Aminu Muhammad, Sengthavisouk, Noot, Sozio, Stephen M., Srisawat, Nattachai, Tan, Eddie, Tiv, Sophanny, Tomacruz Amante, Isabelle Dominique, Villanueva, Anthony Russell, Walker, Rachael, Walker, Robert, and Zaidi, Deenaz

Abstract

The International Society of Nephrology (ISN) region of Oceania and South East Asia (OSEA) is a mix of high- and low-income countries, with diversity in population demographics and densities. Three iterations of the ISN-Global Kidney Health Atlas (GKHA) have been conducted, aiming to deliver in-depth assessments of global kidney care across the spectrum from early detection of CKD to treatment of kidney failure. This paper reports the findings of the latest ISN-GKHA in relation to kidney-care capacity in the OSEA region. Among the 30 countries and territories in OSEA, 19 (63%) participated in the ISN-GKHA, representing over 97% of the region’s population. The overall prevalence of treated kidney failure in the OSEA region was 1203 per million population (pmp), 45% higher than the global median of 823 pmp. In contrast, kidney replacement therapy (KRT) in the OSEA region was less available than the global median (chronic hemodialysis, 89% OSEA region vs. 98% globally; peritoneal dialysis, 72% vs. 79%; kidney transplantation, 61% vs. 70%). Only 56% of countries could provide access to dialysis to at least half of people with incident kidney failure, lower than the global median of 74% of countries with available dialysis services. Inequalities in access to KRT were present across the OSEA region, with widespread availability and low out-of-pocket costs in high-income countries and limited availability, often coupled with large out-of-pocket costs, in middle- and low-income countries. Workforce limitations were observed across the OSEA region, especially in lower-middle–income countries. Extensive collaborative work within the OSEA region and globally will help close the noted gaps in kidney-care provision.

Published
2024
Full Text
View/download PDF

13. Access to and barriers to access for essential medicines in nephrology and related non-communicable diseases: a scoping review protocol

Author

Wong, Michelle, Calice-Silva, Viviane, Tannor, Elliot, Nakhoul, Georges, Kumar, Vivek, Hafidz, Muhammad, Chanchlani, Rahul, Chen, Titi, Ekrikpo, Udeme, Francis, Anna, Kalyesubula, Robert, Karam, Sabine, Pereira-Kamath, Nikhil, Wijewickrama, Eranga, Sanger, Stephanie, Vanhonsebrouck, Pauline, and Jha, Vivekanand

Subjects
access, Medicine and Health Sciences, nephrology, essential medicines
Abstract

Access to essential medicines for treatment of non-communicable diseases (NCDs) is lacking in low- and low-middle income countries. In nephrology, access to essential medicines is especially important to reduce risk of chronic kidney disease (CKD) progression, as kidney replacement therapy is unavailable or cost-prohibitive in many regions of the world. As part of the International Society of Nephrology (ISN) Emerging Leaders Program’s mandate to improve health promotion and access to prevention and management of kidney diseases globally, this scoping review aims to understand the extent of evidence regarding: 1) access to essential medicines for CKD and related NCDs, 2) barriers to access, and 3) interventions to improve access.

Published
2022
Full Text
View/download PDF

16. Access to and Barriers to Access for Essential Medicines in Nephrology and Related Non-Communicable Diseases: A Scoping Review Protocol

Author

Wong, Michelle Mon Yee, primary, Calice-Silva, Viviane, additional, Tannor, Elliot K., additional, Nakoul, Georges, additional, Kumar, Vivek, additional, Hafidz, Muhammad Iqbal Abdul, additional, Chanchlani, Rahul, additional, Chen, Titi, additional, Ekrikpo, Udeme E., additional, Francis, Anna, additional, Kalyesubula, Robert, additional, Karam, Sabine, additional, Pereira-Kamath, Nikhil, additional, Wijewickrama, Eranga, additional, Sanger, Stephanie, additional, and Jha, Vivekanand, additional

Published
2021
Full Text
View/download PDF

17. Type 1 conventional dendritic cells in kidney disease

Author

Chen, Titi

Subjects
Flt3 inhibitor, kidney disease, hemic and immune systems, dendritic cells, type 1 conventional dendritic cells, anti-GBM disease
Abstract

Dendritic cells (DCs) are central orchestrators of the immune system, which regulate both innate and adaptive immune responses. They can be broadly categorized into plasmacytoid DCs (pDCs) and conventional DCs (cDCs). cDC1s are a major subset of conventional DCs and play an important role in kidney disease. In this study, I firstly examined cDC1s in human kidney disease through analysing frozen human kidney biopsy samples. Secondly, I investigated the mechanisms of effects of cDC1s in experimental kidney disease, namely Adriamycin nephropathy and anti-GBM disease. Lastly, I explored the therapeutic potential of targeting cDC1s by repurposing Flt3 inhibitor for treatment of kidney disease. In the human study, I found that the number of cDC1s correlated with disease severity in acute tubular necrosis, number of crescents in pauci-immune glomerular nephritis, interstitial fibrosis in IgA nephropathy and lupus nephritis, as well as prognosis in IgA nephropathy. The number of CD8+ T cells also increased significantly in these conditions and cDC1 number correlated with CD8+ T cell number. These findings reflected a possible role of cDC1s in these conditions and their association with CD8+ T cells suggested a combined mechanism in keeping with the results in animal models. In the animal experiments, I studied cDC1s in vitro and in vivo using wild type as well as transgenic XCR1-DTR mice. In both Adriamycin nephropathy and anti-GBM disease, I found the number of cDC1s increased significantly. Depletion of cDC1s attenuated kidney injury, suggesting their pathogenic role. The mechanisms underlying cDC1 mediated kidney injury was demonstrated to relate to their superior ability to activate CD8+ T cells. Flt3 is a receptor tyrosine kinase which regulates the differentiation of DCs and a Flt3 inhibitor is currently being used in cancer treatment. I demonstrated that a Flt3 inhibitor can deplete cDC1s with relative specificity. The Flt3 inhibitor attenuated kidney injury in both Adriamycin nephropathy and anti-GBM disease. Therefore, repurposing Flt3 inhibitor could be a novel therapeutic strategy to treat kidney disease.

Published
2021

18. Conventional Type 1 Dendritic Cells (cDC1) in Human Kidney Diseases: Clinico-Pathological Correlations

Author

Chen, Titi, primary, Cao, Qi, additional, Wang, Ruifeng, additional, Zheng, Guoping, additional, Azmi, Farhana, additional, Wang, Jeffery, additional, Lee, Vincent W., additional, Wang, Yuan Min, additional, Yu, Hong, additional, Patel, Manish, additional, P’ng, Chow Heok, additional, Alexander, Stephen I., additional, Rogers, Natasha M., additional, Wang, Yiping, additional, and Harris, David C. H., additional

Published
2021
Full Text
View/download PDF

19. The Case | A hidden deposit

Author

Chen, Titi, primary, Wong, Nikki, additional, Visvanathan, Seethalakshmi, additional, Kwok, Fiona, additional, Radhakrishnan, Jai, additional, Harris, David, additional, and Vucak-Dzumhur, Mirna, additional

Published
2020
Full Text
View/download PDF

20. Regulatory innate lymphoid cells suppress innate immunity and reduce renal ischemia/reperfusion injury

Author

Cao, Qi, primary, Wang, Ruifeng, additional, Wang, Yiping, additional, Niu, Zhiguo, additional, Chen, Titi, additional, Wang, Chengshi, additional, Jin, Li, additional, Huang, Qingsong, additional, Li, Qing, additional, Wang, Xin Maggie, additional, Azmi, Farhana, additional, Lee, Vincent W.S., additional, Wang, Yuan Min, additional, Zheng, Guoping, additional, Alexander, Stephen I., additional, and Harris, David C.H., additional

Published
2020
Full Text
View/download PDF

21. High-Sensitivity Troponin T and C-Reactive Protein Have Different Prognostic Values in Hemo- and Peritoneal Dialysis Populations: A Cohort Study

Author

Chen, Titi, Hassan, Hicham, Qian, Pierre, Vu, Monica, and Makris, Angela

Abstract

Background-—Dialysis patients have an exceedingly high mortality rate. Biomarkers may be useful tools in risk stratification of this population. We evaluated the prognostic value of high-sensitivity cardiac troponin T (hs-cTnT) and CRP (C-reactive protein) in predicting adverse outcomes in stable hemodialysis and peritoneal dialysis (PD) patients. Variability in hs-cTnT was also examined. Methods and Results-—A retrospective cohort study included 574 dialysis patients (hemodialysis 347, PD 227). Outcomes examined included mortality and major adverse cardiovascular events, with median follow-up of 3.5 years. hs-cTnT was an independent predictor of both outcomes in hemodialysis and PD patients. Increased risk only became significant when hs-cTnT reached quintile 3 (>49 ng/L). Area under the receiver operating curve analysis showed that the addition of hs-cTnT to clinical parameters significantly improved its prognostic performance for mortality in PD patients (P=0.002). CRP was an independent predictor of both outcomes in PD patients only. Only CRP in the highest quintile (>16.8 mg/L) was associated with increased risk. hs-cTnT remained relatively stable for the whole follow-up period for hemodialysis patients, whereas for PD patients, hs-cTnT increased by 23.63% in year 2 and 29.13% in year 3 compared with baseline (P

Published
2018

23. Flt3 inhibition alleviates chronic kidney disease by suppressing CD103+ dendritic cell-mediated T cell activation

Author

Wang, Ruifeng, primary, Chen, Titi, additional, Wang, Chengshi, additional, Zhang, Zhiqiang, additional, Wang, Xin Maggie, additional, Li, Qing, additional, Lee, Vincent W S, additional, Wang, Yuan Min, additional, Zheng, Guoping, additional, Alexander, Stephen I, additional, Wang, Yiping, additional, Harris, David C H, additional, and Cao, Qi, additional

Published
2018
Full Text
View/download PDF

25. Flt3 inhibition alleviates chronic kidney disease by suppressing CD103+ dendritic cell-mediated T cell activation.

Author

Wang, Ruifeng, Chen, Titi, Wang, Chengshi, Zhang, Zhiqiang, Wang, Xin Maggie, Li, Qing, Lee, Vincent W S, Wang, Yuan Min, Zheng, Guoping, Alexander, Stephen I, Wang, Yiping, Harris, David C H, and Cao, Qi

Subjects
*CHRONIC kidney failure, *T cells, *FOCAL segmental glomerulosclerosis, *RENAL fibrosis, *PROTEIN-tyrosine kinases
Abstract

Background Chronic kidney disease (CKD) is a global public health problem, which lacks effective treatment. Previously, we have shown that CD103+ dendritic cells (DCs) are pathogenic in adriamycin nephropathy (AN), a model of human focal segmental glomerulosclerosis (FSGS). Fms-like tyrosine kinase 3 (Flt3) is a receptor that is expressed with high specificity on tissue resident CD103+ DCs. Methods To test the effect on CD103+ DCs and kidney injury of inhibition of Flt3, we used a selective Flt3 inhibitor (AC220) to treat mice with AN. Results Human CD141+ DCs, homologous to murine CD103+ DCs, were significantly increased in patients with FSGS. The number of kidney CD103+ DCs, but not CD103− DCs or plasmacytoid DCs, was significantly decreased in AN mice after AC220 administration. Treatment with AC220 significantly improved kidney function and reduced kidney injury and fibrosis in AN mice. AC220-treated AN mice had decreased levels of inflammatory cytokines and chemokines, tumor necrosis factor-α, interleukin (IL)-1β, IL-6, CCL2 and CCL5 and reduced kidney infiltration of CD4 T cells and CD8 T cells. The protective effect of AC220 was associated with its suppression of CD103+ DCs-mediated CD8 T cell proliferation and activation in AN mice. Conclusion Flt3 inhibitor AC220 effectively reduced kidney injury in AN mice, suggesting that this inhibitor might be a useful pharmaceutical agent to treat CKD. [ABSTRACT FROM AUTHOR]

Published
2019
Full Text
View/download PDF

34. Flt3 inhibition alleviates chronic kidney disease by suppressing CD103+ dendritic cell-mediated T cell activation.

Author

Wang R, Chen T, Wang C, Zhang Z, Wang XM, Li Q, Lee VWS, Wang YM, Zheng G, Alexander SI, Wang Y, Harris DCH, and Cao Q

Subjects
Animals, Cytokines metabolism, Dendritic Cells drug effects, Humans, Kidney immunology, Kidney metabolism, Lymphocyte Activation drug effects, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Renal Insufficiency, Chronic immunology, Renal Insufficiency, Chronic metabolism, Renal Insufficiency, Chronic pathology, Antigens, CD metabolism, Benzothiazoles pharmacology, Dendritic Cells immunology, Integrin alpha Chains metabolism, Kidney drug effects, Lymphocyte Activation immunology, Phenylurea Compounds pharmacology, Renal Insufficiency, Chronic prevention & control, fms-Like Tyrosine Kinase 3 antagonists & inhibitors
Abstract

Background: Chronic kidney disease (CKD) is a global public health problem, which lacks effective treatment. Previously, we have shown that CD103+ dendritic cells (DCs) are pathogenic in adriamycin nephropathy (AN), a model of human focal segmental glomerulosclerosis (FSGS). Fms-like tyrosine kinase 3 (Flt3) is a receptor that is expressed with high specificity on tissue resident CD103+ DCs., Methods: To test the effect on CD103+ DCs and kidney injury of inhibition of Flt3, we used a selective Flt3 inhibitor (AC220) to treat mice with AN., Results: Human CD141+ DCs, homologous to murine CD103+ DCs, were significantly increased in patients with FSGS. The number of kidney CD103+ DCs, but not CD103- DCs or plasmacytoid DCs, was significantly decreased in AN mice after AC220 administration. Treatment with AC220 significantly improved kidney function and reduced kidney injury and fibrosis in AN mice. AC220-treated AN mice had decreased levels of inflammatory cytokines and chemokines, tumor necrosis factor-α, interleukin (IL)-1β, IL-6, CCL2 and CCL5 and reduced kidney infiltration of CD4 T cells and CD8 T cells. The protective effect of AC220 was associated with its suppression of CD103+ DCs-mediated CD8 T cell proliferation and activation in AN mice., Conclusion: Flt3 inhibitor AC220 effectively reduced kidney injury in AN mice, suggesting that this inhibitor might be a useful pharmaceutical agent to treat CKD., (© The Author(s) 2018. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.)

Published
2019
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results