Henry Tung
Position: PhD candidate
Contact: 14lwt1@queensu.ca
Program: Experimental Medicine
Bachelor’s degree: Life Sciences
Nationality: Taiwanese/Canadian
Research summary:
Multiple sclerosis (MS) is the most common neurodegenerative disease in young adults characterized by the progressive loss of motor and sensory functions. Canada, specifically, has one of the highest rates of MS worldwide with over 77,000 Canadians living with the disease. The devastating disease is caused by a flawed immune system that attacks myelin, the protective covering of our nerves. As a result, the damaged nerves cannot effectively deliver information between the brain and the rest of the body. Although current therapeutics can control symptoms and improve the quality of life, finding a cure remains an unmet need, not only for MS, but also other similar neurological disorders such Alzheimer’s disease. One of the reasons for the lack of a cure is our limited understanding of the cellular environment throughout disease progression. In particular, the role of mesenchymal stromal cells (MSCs), supportive cells that orchestrate tissue repair upon injury, is largely unknown. In my proposed research work, we aim to examine MSCs using cutting-edge technologies that provide a much higher resolution than in the past. In addition to MSCs, we will capture the behaviours of various other cell types and how they communicate with each other in response to disease. By understanding the behaviour of cells in proximity to areas which the disease is progressing or improving, we can identify the cell types and specific mechanisms responsible for causing damage and facilitating recovery. From these findings, we will initiate the development of a new therapeutic approach centering around promoting tissue regeneration rather than controlling disease progression. Overall, our work will provide a new direction for future research of MS and translate into the development of potential therapeutics.
Personal summary:
Prior to joining the Rossi Lab as a direct PhD student in 2019, I completed my BSc at Queen’s University, Kingston. Outside of work, I enjoy running, sightseeing, and trying out different types of street food. One important lesson I learnt so far in my PhD is that Mendelian genetics is a scam. You will never get the genotypes you want…
Publications:
Contact: 14lwt1@queensu.ca
ProgramPosition: PhD candidate
Contact: 14lwt1@queensu.ca
Program: Experimental Medicine
Bachelor’s degree: Life Sciences
Nationality: Taiwanese/Canadian
Research summary:
Multiple sclerosis (MS) is the most common neurodegenerative disease in young adults
characterized by the progressive loss of motor and sensory functions. Canada, specifically, has
one of the highest rates of MS worldwide with over 77,000 Canadians living with the disease.
The devastating disease is caused by a flawed immune system that attacks myelin, the protective
covering of our nerves. As a result, the damaged nerves cannot effectively deliver information
between the brain and the rest of the body. Although current therapeutics can control symptoms
and improve the quality of life, finding a cure remains an unmet need, not only for MS, but also
other similar neurological disorders such Alzheimer’s disease. One of the reasons for the lack of
a cure is our limited understanding of the cellular environment throughout disease progression.
In particular, the role of mesenchymal stromal cells (MSCs), supportive cells that orchestrate
tissue repair upon injury, is largely unknown. In my proposed research work, we aim to examine
MSCs using cutting-edge technologies that provide a much higher resolution than in the past. In
addition to MSCs, we will capture the behaviours of various other cell types and how they
communicate with each other in response to disease. By understanding the behaviour of cells in
proximity to areas which the disease is progressing or improving, we can identify the cell types
and specific mechanisms responsible for causing damage and facilitating recovery. From these
findings, we will initiate the development of a new therapeutic approach centering around
promoting tissue regeneration rather than controlling disease progression. Overall, our work will
provide a new direction for future research of MS and translate into the development of potential
therapeutics.
Personal summary:
Prior to joining the Rossi Lab as a direct PhD student in 2019, I completed my BSc at Queen’s
University, Kingston. Outside of work, I enjoy running, sightseeing, and trying out different
types of street food. One important lesson I learnt so far in my PhD is that Mendelian genetics is
a scam. You will never get the genotypes you want...
Publications:
1. Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell
diversity: Functional divergence in fibro/adipogenic progenitor and mural cell
populations. Experimental cell research, 410(1), 112947.
https://doi.org/10.1016/j.yexcr.2021.112947
2. White, Z.*, Theret, M.*, Milad, N.*, Tung, L. W., Chen, W. W., Sirois, M. G., Rossi, F.,
& Bernatchez, P. (2021). Cholesterol absorption blocker ezetimibe prevents muscle
wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia and
muscle, 10.1002/jcsm.12879. Advance online publication.
https://doi.org/10.1002/jcsm.12879
3. Theret, M., Low, M., Rempel, L., Li, F. F., Tung, L. W., Contreras, O., Chang, C. K.,
Wu, A., Soliman, H., & Rossi, F. (2021). In vitro assessment of anti-fibrotic drug activity
does not predict in vivo efficacy in murine models of Duchenne muscular dystrophy. Life
sciences, 279, 119482. https://doi.org/10.1016/j.lfs.2021.119482
4. Soliman, H., Tung, L. W., & Rossi, F. (2021). Fibroblast and Myofibroblast Subtypes:
Single Cell Sequencing. Methods in molecular biology (Clifton, N.J.), 2299, 49–84.
https://doi.org/10.1007/978-1-0716-1382-5_4
5. Eisner, C., Cummings, M., Johnston, G., Tung, L. W., Groppa, E., Chang, C., & Rossi,
F. M. (2020). Murine Tissue-Resident PDGFRα+ Fibro-Adipogenic Progenitors
Spontaneously Acquire Osteogenic Phenotype in an Altered Inflammatory Environment.
Journal of bone and mineral research: the official journal of the American Society for
Bone and Mineral Research, 35(8), 1525–1534. https://doi.org/10.1002/jbmr.4020
6. Contreras, O., Cruz-Soca, M., Theret, M., Soliman, H., Tung, L. W., Groppa, E., Rossi,
F. M., & Brandan, E. (2019). Cross-talk between TGF-β and PDGFRα signaling
pathways regulates the fate of stromal fibro-adipogenic progenitors. Journal of cell
: Experimental Medicine
Bachelor’s degree: Life Sciences
Nationality: Taiwanese/Canadian
Research summary:
Multiple sclerosis (MS) is the most common neurodegenerative disease in young adults
characterized by the progressive loss of motor and sensory functions. Canada, specifically, has
one of the highest rates of MS worldwide with over 77,000 Canadians living with the disease.
The devastating disease is caused by a flawed immune system that attacks myelin, the protective
covering of our nerves. As a result, the damaged nerves cannot effectively deliver information
between the brain and the rest of the body. Although current therapeutics can control symptoms
and improve the quality of life, finding a cure remains an unmet need, not only for MS, but also
other similar neurological disorders such Alzheimer’s disease. One of the reasons for the lack of
a cure is our limited understanding of the cellular environment throughout disease progression.
In particular, the role of mesenchymal stromal cells (MSCs), supportive cells that orchestrate
tissue repair upon injury, is largely unknown. In my proposed research work, we aim to examine
MSCs using cutting-edge technologies that provide a much higher resolution than in the past. In
addition to MSCs, we will capture the behaviours of various other cell types and how they
communicate with each other in response to disease. By understanding the behaviour of cells in
proximity to areas which the disease is progressing or improving, we can identify the cell types
and specific mechanisms responsible for causing damage and facilitating recovery. From these
findings, we will initiate the development of a new therapeutic approach centering around
promoting tissue regeneration rather than controlling disease progression. Overall, our work will
provide a new direction for future research of MS and translate into the development of potential
therapeutics.
Personal summary:
Prior to joining the Rossi Lab as a direct PhD student in 2019, I completed my BSc at Queen’s
University, Kingston. Outside of work, I enjoy running, sightseeing, and trying out different
types of street food. One important lesson I learnt so far in my PhD is that Mendelian genetics is
a scam. You will never get the genotypes you want...
Publications:
1. Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell
diversity: Functional divergence in fibro/adipogenic progenitor and mural cell
populations. Experimental cell research, 410(1), 112947.
https://doi.org/10.1016/j.yexcr.2021.112947
2. White, Z.*, Theret, M.*, Milad, N.*, Tung, L. W., Chen, W. W., Sirois, M. G., Rossi, F.,
& Bernatchez, P. (2021). Cholesterol absorption blocker ezetimibe prevents muscle
wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia andosition: PhD candidate
Contact: 14lwt1@queensu.ca
Program: Experimental Medicine
Bachelor’s degradian
Research s
Multiple sclerosis (MS) is the most common neurodegenerative disease in young adults
characterized by the progressive loss of motor and sensory functions. Canada, specifically, has
one of the highest rates of MS worldwide with over 77,000 Canadians living with the disease.
The devastating disease is caused by a flawed immune system that attacks myelin, the protective
covering of our nerves. As a result, the damaged nerves cannot effectively deliver information
between the brain and the rest of the body. Although current therapeutics can control symptoms
and improve the quality of life, finding a cure remains an unmet need, not only for MS, but also
other similar neurological disorders such Alzheimer’s disease. One of the reasons for the lack of
a cure is our limited understanding of the cellular environment throughout disease progression.
In particular, the role of mesenchymal stromal cells (MSCs), supportive cells that orchestrate
tissue repair upon injury, is largely unknown. In my proposed research work, we aim to examine
MSCs using cutting-edge technologies that provide a much higher resolution than in the past. In
addition to MSCs, we will capture the behaviours of various other cell types and how they
communicate with each other in response to disease. By understanding the behaviour of cells in
proximity to areas which the disease is progressing or improving, we can identify the cell types
and specific mechanisms responsible for causing damage and facilitating recovery. From these
findings, we will initiate the development of a new therapeutic approach centering around
promoting tissue regeneration rather than controlling disease progression. Overall, our work will
provide a new direction for future research of MS and translate into the development of potential
therapeutics.
Personal summary:
Prior to joining the Rossi Lab as a direct PhD student in 2019, I completed my BSc at Queen’s
University, Kingston. Outside of work, I enjoy running, sightseeing, and trying out different
types of street food. One important lesson I learnt so far in my PhD is that Mendelian genetics is
a scam. You will never get the genotypes you want...
Publications:
1. Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell
diversity: Functional divergence in fibro/adipogenic progenitor and mural cell
populations. Experimental cell research, 410(1), 112947.
https://doi.org/10.1016/j.yexcr.2021.112947
2. White, Z.*, Theret, M.*, Milad, N.*, Tung, L. W., Chen, W. W., Sirois, M. G., Rossi, F.,
& Bernatchez, P. (2021). Cholesterol absorption blocker ezetimibe prevents muscle
wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia and
Contact: 14lwt1@queensu.ca
Program: Experimental Medicine
Bachelor’s degree: Life Sciences
Nationality: Taiwanese/Canadian
Research summary:
Multiple sclerosis (MS) is the most common neurodegenerative disease in young adults characterized by the progressive loss of motor and sensory functions. Canada, specifically, has one of the highest rates of MS worldwide with over 77,000 Canadians living with the disease. The devastating disease is caused by a flawed immune system that attacks myelin, the protective covering of our nerves. As a result, the damaged nerves cannot effectively deliver information between the brain and the rest of the body. Although current therapeutics can control symptoms and improve the quality of life, finding a cure remains an unmet need, not only for MS, but also other similar neurological disorders such Alzheimer’s disease. One of the reasons for the lack of a cure is our limited understanding of the cellular environment throughout disease progression. In particular, the role of mesenchymal stromal cells (MSCs), supportive cells that orchestrate tissue repair upon injury, is largely unknown. In my proposed research work, we aim to examine MSCs using cutting-edge technologies that provide a much higher resolution than in the past. In addition to MSCs, we will capture the behaviours of various other cell types and how they communicate with each other in response to disease. By understanding the behaviour of cells in proximity to areas which the disease is progressing or improving, we can identify the cell types and specific mechanisms responsible for causing damage and facilitating recovery. From these findings, we will initiate the development of a new therapeutic approach centering around promoting tissue regeneration rather than controlling disease progression. Overall, our work will provide a new direction for future research of MS and translate into the development of potential therapeutics.
Personal summary:
Prior to joining the Rossi Lab as a direct PhD student in 2019, I completed my BSc at Queen’s University, Kingston. Outside of work, I enjoy running, sightseeing, and trying out different types of street food. One important lesson I learnt so far in my PhD is that Mendelian genetics is a scam. You will never get the genotypes you want…
Publications:
- Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell diversity: Functional divergence in fibro/adipogenic progenitor and mural cell populations. Experimental cell research, 410(1), 112947. https://doi.org/10.1016/j.yexcr.2021.112947
- White, Z.*, Theret, M.*, Milad, N.*, Tung, L. W., Chen, W. W., Sirois, M. G., Rossi, F., & Bernatchez, P. (2021). Cholesterol absorption blocker ezetimibe prevents muscle wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia and muscle, 10.1002/jcsm.12879. Advance online publication. https://doi.org/10.1002/jcsm.12879
- Theret, M., Low, M., Rempel, L., Li, F. F., Tung, L. W., Contreras, O., Chang, C. K., Wu, A., Soliman, H., & Rossi, F. (2021). In vitro assessment of anti-fibrotic drug activity does not predict in vivo efficacy in murine models of Duchenne muscular dystrophy. Life sciences, 279, 119482. https://doi.org/10.1016/j.lfs.2021.119482
- Soliman, H., Tung, L. W., & Rossi, F. (2021). Fibroblast and Myofibroblast Subtypes: Single Cell Sequencing. Methods in molecular biology (Clifton, N.J.), 2299, 49–84. https://doi.org/10.1007/978-1-0716-1382-5_4
- Eisner, C., Cummings, M., Johnston, G., Tung, L. W., Groppa, E., Chang, C., & Rossi, F. M. (2020). Murine Tissue-Resident PDGFRα+ Fibro-Adipogenic Progenitors Spontaneously Acquire Osteogenic Phenotype in an Altered Inflammatory Environment. Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research, 35(8), 1525–1534. https://doi.org/10.1002/jbmr.4020
- Contreras, O., Cruz-Soca, M., Theret, M., Soliman, H., Tung, L. W., Groppa, E., Rossi, F. M., & Brandan, E. (2019). Cross-talk between TGF-β and PDGFRα signaling pathways regulates the fate of stromal fibro-adipogenic progenitors. Journal of cell science, 132(19), jcs232157. https://doi.org/10.1242/jcs.232157
Contact: 14lwt1@queensu.ca
ProgramPosition: PhD candidate
Contact: 14lwt1@queensu.ca
Program: Experimental Medicine
Bachelor’s degree: Life Sciences
Nationality: Taiwanese/Canadian
Research summary:
Multiple sclerosis (MS) is the most common neurodegenerative disease in young adults
characterized by the progressive loss of motor and sensory functions. Canada, specifically, has
one of the highest rates of MS worldwide with over 77,000 Canadians living with the disease.
The devastating disease is caused by a flawed immune system that attacks myelin, the protective
covering of our nerves. As a result, the damaged nerves cannot effectively deliver information
between the brain and the rest of the body. Although current therapeutics can control symptoms
and improve the quality of life, finding a cure remains an unmet need, not only for MS, but also
other similar neurological disorders such Alzheimer’s disease. One of the reasons for the lack of
a cure is our limited understanding of the cellular environment throughout disease progression.
In particular, the role of mesenchymal stromal cells (MSCs), supportive cells that orchestrate
tissue repair upon injury, is largely unknown. In my proposed research work, we aim to examine
MSCs using cutting-edge technologies that provide a much higher resolution than in the past. In
addition to MSCs, we will capture the behaviours of various other cell types and how they
communicate with each other in response to disease. By understanding the behaviour of cells in
proximity to areas which the disease is progressing or improving, we can identify the cell types
and specific mechanisms responsible for causing damage and facilitating recovery. From these
findings, we will initiate the development of a new therapeutic approach centering around
promoting tissue regeneration rather than controlling disease progression. Overall, our work will
provide a new direction for future research of MS and translate into the development of potential
therapeutics.
Personal summary:
Prior to joining the Rossi Lab as a direct PhD student in 2019, I completed my BSc at Queen’s
University, Kingston. Outside of work, I enjoy running, sightseeing, and trying out different
types of street food. One important lesson I learnt so far in my PhD is that Mendelian genetics is
a scam. You will never get the genotypes you want...
Publications:
1. Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell
diversity: Functional divergence in fibro/adipogenic progenitor and mural cell
populations. Experimental cell research, 410(1), 112947.
https://doi.org/10.1016/j.yexcr.2021.112947
2. White, Z.*, Theret, M.*, Milad, N.*, Tung, L. W., Chen, W. W., Sirois, M. G., Rossi, F.,
& Bernatchez, P. (2021). Cholesterol absorption blocker ezetimibe prevents muscle
wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia and
muscle, 10.1002/jcsm.12879. Advance online publication.
https://doi.org/10.1002/jcsm.12879
3. Theret, M., Low, M., Rempel, L., Li, F. F., Tung, L. W., Contreras, O., Chang, C. K.,
Wu, A., Soliman, H., & Rossi, F. (2021). In vitro assessment of anti-fibrotic drug activity
does not predict in vivo efficacy in murine models of Duchenne muscular dystrophy. Life
sciences, 279, 119482. https://doi.org/10.1016/j.lfs.2021.119482
4. Soliman, H., Tung, L. W., & Rossi, F. (2021). Fibroblast and Myofibroblast Subtypes:
Single Cell Sequencing. Methods in molecular biology (Clifton, N.J.), 2299, 49–84.
https://doi.org/10.1007/978-1-0716-1382-5_4
5. Eisner, C., Cummings, M., Johnston, G., Tung, L. W., Groppa, E., Chang, C., & Rossi,
F. M. (2020). Murine Tissue-Resident PDGFRα+ Fibro-Adipogenic Progenitors
Spontaneously Acquire Osteogenic Phenotype in an Altered Inflammatory Environment.
Journal of bone and mineral research: the official journal of the American Society for
Bone and Mineral Research, 35(8), 1525–1534. https://doi.org/10.1002/jbmr.4020
6. Contreras, O., Cruz-Soca, M., Theret, M., Soliman, H., Tung, L. W., Groppa, E., Rossi,
F. M., & Brandan, E. (2019). Cross-talk between TGF-β and PDGFRα signaling
pathways regulates the fate of stromal fibro-adipogenic progenitors. Journal of cell
: Experimental Medicine
Bachelor’s degree: Life Sciences
Nationality: Taiwanese/Canadian
Research summary:
Multiple sclerosis (MS) is the most common neurodegenerative disease in young adults
characterized by the progressive loss of motor and sensory functions. Canada, specifically, has
one of the highest rates of MS worldwide with over 77,000 Canadians living with the disease.
The devastating disease is caused by a flawed immune system that attacks myelin, the protective
covering of our nerves. As a result, the damaged nerves cannot effectively deliver information
between the brain and the rest of the body. Although current therapeutics can control symptoms
and improve the quality of life, finding a cure remains an unmet need, not only for MS, but also
other similar neurological disorders such Alzheimer’s disease. One of the reasons for the lack of
a cure is our limited understanding of the cellular environment throughout disease progression.
In particular, the role of mesenchymal stromal cells (MSCs), supportive cells that orchestrate
tissue repair upon injury, is largely unknown. In my proposed research work, we aim to examine
MSCs using cutting-edge technologies that provide a much higher resolution than in the past. In
addition to MSCs, we will capture the behaviours of various other cell types and how they
communicate with each other in response to disease. By understanding the behaviour of cells in
proximity to areas which the disease is progressing or improving, we can identify the cell types
and specific mechanisms responsible for causing damage and facilitating recovery. From these
findings, we will initiate the development of a new therapeutic approach centering around
promoting tissue regeneration rather than controlling disease progression. Overall, our work will
provide a new direction for future research of MS and translate into the development of potential
therapeutics.
Personal summary:
Prior to joining the Rossi Lab as a direct PhD student in 2019, I completed my BSc at Queen’s
University, Kingston. Outside of work, I enjoy running, sightseeing, and trying out different
types of street food. One important lesson I learnt so far in my PhD is that Mendelian genetics is
a scam. You will never get the genotypes you want...
Publications:
1. Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell
diversity: Functional divergence in fibro/adipogenic progenitor and mural cell
populations. Experimental cell research, 410(1), 112947.
https://doi.org/10.1016/j.yexcr.2021.112947
2. White, Z.*, Theret, M.*, Milad, N.*, Tung, L. W., Chen, W. W., Sirois, M. G., Rossi, F.,
& Bernatchez, P. (2021). Cholesterol absorption blocker ezetimibe prevents muscle
wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia andosition: PhD candidate
Contact: 14lwt1@queensu.ca
Program: Experimental Medicine
Bachelor’s degradian
Research s
Multiple sclerosis (MS) is the most common neurodegenerative disease in young adults
characterized by the progressive loss of motor and sensory functions. Canada, specifically, has
one of the highest rates of MS worldwide with over 77,000 Canadians living with the disease.
The devastating disease is caused by a flawed immune system that attacks myelin, the protective
covering of our nerves. As a result, the damaged nerves cannot effectively deliver information
between the brain and the rest of the body. Although current therapeutics can control symptoms
and improve the quality of life, finding a cure remains an unmet need, not only for MS, but also
other similar neurological disorders such Alzheimer’s disease. One of the reasons for the lack of
a cure is our limited understanding of the cellular environment throughout disease progression.
In particular, the role of mesenchymal stromal cells (MSCs), supportive cells that orchestrate
tissue repair upon injury, is largely unknown. In my proposed research work, we aim to examine
MSCs using cutting-edge technologies that provide a much higher resolution than in the past. In
addition to MSCs, we will capture the behaviours of various other cell types and how they
communicate with each other in response to disease. By understanding the behaviour of cells in
proximity to areas which the disease is progressing or improving, we can identify the cell types
and specific mechanisms responsible for causing damage and facilitating recovery. From these
findings, we will initiate the development of a new therapeutic approach centering around
promoting tissue regeneration rather than controlling disease progression. Overall, our work will
provide a new direction for future research of MS and translate into the development of potential
therapeutics.
Personal summary:
Prior to joining the Rossi Lab as a direct PhD student in 2019, I completed my BSc at Queen’s
University, Kingston. Outside of work, I enjoy running, sightseeing, and trying out different
types of street food. One important lesson I learnt so far in my PhD is that Mendelian genetics is
a scam. You will never get the genotypes you want...
Publications:
1. Ritso, M., Tung, L. W., & Rossi, F. (2022). Emerging skeletal muscle stromal cell
diversity: Functional divergence in fibro/adipogenic progenitor and mural cell
populations. Experimental cell research, 410(1), 112947.
https://doi.org/10.1016/j.yexcr.2021.112947
2. White, Z.*, Theret, M.*, Milad, N.*, Tung, L. W., Chen, W. W., Sirois, M. G., Rossi, F.,
& Bernatchez, P. (2021). Cholesterol absorption blocker ezetimibe prevents muscle
wasting in severe dysferlin-deficient and mdx mice. Journal of cachexia, sarcopenia and
