Out of Place. Art and Stories from the World’s Refugee Camps

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(Photo: Adoku Zambé, Il passaggio, 2023)

The exhibition Out of Place. Art and Stories from Refugee Camps Around the World, organized by the Imago Mundi Foundation in collaboration with the University of Padua and the Department of Culture of the Municipality of Padua, has been extended until August 31 in the Ancient Courtyard of Palazzo del Bo.

Open to the public daily with free admission from 8 AM to 8 PM, the exhibition is held under the patronage of the United Nations High Commissioner for Refugees (UNHCR).

Based on research conducted within 18 of the largest existing refugee camps today, the exhibition showcases the testimonies—artworks and stories—of 264 artists who currently live in these settlements or have experienced similar conditions in the past. Alongside the 284 works they created in the 10x12 cm format, the exhibition also features a video installation and an art installation, offering a broader reflection on the current global refugee crisis.

photo

After Kutupalong, in Bangladesh, the exhibition presents different testimonies from Africa with the largest refugee camps in Kenya – Dadaab and Kakuma –, another two representative settlements in Uganda – Nakivale and Bidibidi, the camp of Dzaleka in Malawi, the one in Nyabiheke, Rwanda, and the settlement of Smara with the adjacent El Aaiun, Awserd, Boujdour, and Dakhla, in Algeria. The inquiry then turns to the Middle East, to open the doors of Za’atari, the biggest camp for Syrians, and to five Palestinian camps: Baq’a, Hittin, Irbid, Madaba and Souf, all in Jordan. Added to this map are artists who, from the 1980s until the current day, have lived in similar conditions in other geographical areas, including Kurdish and Yazidi artists who tell the complicated story of their people. A section on Afghanistan features the works and stories of 40 artists who have left their country or continue to live within its borders since the Taliban takeover in 2021. Completing the exhibition are accounts of migration to Europe from Ukraine and via the Mediterranean routes, along with a section devoted to migration corridors in South and Central America, with a focus on the Mexico-U.S. border.

“Exiles, émigrés, refugees, and expatriates uprooted from their lands”, wrote Edward Said in Reflections on Exile, “must make do in new surroundings, and the creativity as well as the sadness that can be seen in what they do is one of the experiences that has still to find its chroniclers…” Borrowing the definition of refugees proposed by Said – Out of Place – the objective of the exhibition is to offer a space of artistic and narrative expression to the artists living in refugee camps, and to present them first and foremost as artists, considering their current and past refugee status as accidental in their biographies. In the light of the stories and testimonies collected here, the camps appear not only as fragile and temporary living realities, but as evolving entities, “accidental cities”, urban conglomerates destined to last over time. To give just one example as proof of an approach that, rather than causing isolation, as has happened in the past, instead tends towards the integration of long-term camps into their host countries: in 2023 Kenya announced that the two largest camps in the country – Dadaab and Kakuma – would become integrated settlements where refugees would have to coexist with local communities.

The story of reaching the camps was itself an initiatory journey and a breaking of barriers: geographical, linguistic and administrative. Carried out with the help of artists contacted directly within the camps and with the support of external collaborators, the project is a testimony to the functionality and open and dynamic communication that characterises the refugee camps reached. Despite the vicissitudes, the fact that artistic expression is still possible in the camps and that artists continue to be artists remains an extraordinary discovery. Painters, sculptors, photographers and directors born and trained in the camps, and often grouped in small communities, thanks to the support of humanitarian organisations, their stories teach powerful lessons of determination and confidence in the force of art.

To highlight the creativity that is born in the “cities of thorns”, to recall the title of Ben Rawlence’s book on life in the Dadaab complex, is the purpose of the exhibition. In short, it seeks to find that creative energy capable of transfiguring an unsustainable reality and conveying a message like Aminah Rwimo’s, an award-winning director from the Kakuma camp: “I wanted to set an example and tell my fellow survivors that whatever happened to us is now part of our lives. But this is not the end.”

 

On the occasion of World Refugee Day, the University of Padua and the Imago Mundi Foundation are hosted a talk, on June 19 at the Aula Magna of Palazzo del Bo at 5 P.M., with photojournalist and activist Giles Duley, founder of the NGO Legacy of War Foundation


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(Photo: Adoku Zambé, Il passaggio, 2023)

The exhibition Out of Place. Art and Stories from Refugee Camps Around the World, organized by the Imago Mundi Foundation in collaboration with the University of Padua and the Department of Culture of the Municipality of Padua, has been extended until August 31 in the Ancient Courtyard of Palazzo del Bo.

Open to the public daily with free admission from 8 AM to 8 PM, the exhibition is held under the patronage of the United Nations High Commissioner for Refugees (UNHCR).

Based on research conducted within 18 of the largest existing refugee camps today, the exhibition showcases the testimonies—artworks and stories—of 264 artists who currently live in these settlements or have experienced similar conditions in the past. Alongside the 284 works they created in the 10x12 cm format, the exhibition also features a video installation and an art installation, offering a broader reflection on the current global refugee crisis.

photo

After Kutupalong, in Bangladesh, the exhibition presents different testimonies from Africa with the largest refugee camps in Kenya – Dadaab and Kakuma –, another two representative settlements in Uganda – Nakivale and Bidibidi, the camp of Dzaleka in Malawi, the one in Nyabiheke, Rwanda, and the settlement of Smara with the adjacent El Aaiun, Awserd, Boujdour, and Dakhla, in Algeria. The inquiry then turns to the Middle East, to open the doors of Za’atari, the biggest camp for Syrians, and to five Palestinian camps: Baq’a, Hittin, Irbid, Madaba and Souf, all in Jordan. Added to this map are artists who, from the 1980s until the current day, have lived in similar conditions in other geographical areas, including Kurdish and Yazidi artists who tell the complicated story of their people. A section on Afghanistan features the works and stories of 40 artists who have left their country or continue to live within its borders since the Taliban takeover in 2021. Completing the exhibition are accounts of migration to Europe from Ukraine and via the Mediterranean routes, along with a section devoted to migration corridors in South and Central America, with a focus on the Mexico-U.S. border.

“Exiles, émigrés, refugees, and expatriates uprooted from their lands”, wrote Edward Said in Reflections on Exile, “must make do in new surroundings, and the creativity as well as the sadness that can be seen in what they do is one of the experiences that has still to find its chroniclers…” Borrowing the definition of refugees proposed by Said – Out of Place – the objective of the exhibition is to offer a space of artistic and narrative expression to the artists living in refugee camps, and to present them first and foremost as artists, considering their current and past refugee status as accidental in their biographies. In the light of the stories and testimonies collected here, the camps appear not only as fragile and temporary living realities, but as evolving entities, “accidental cities”, urban conglomerates destined to last over time. To give just one example as proof of an approach that, rather than causing isolation, as has happened in the past, instead tends towards the integration of long-term camps into their host countries: in 2023 Kenya announced that the two largest camps in the country – Dadaab and Kakuma – would become integrated settlements where refugees would have to coexist with local communities.

The story of reaching the camps was itself an initiatory journey and a breaking of barriers: geographical, linguistic and administrative. Carried out with the help of artists contacted directly within the camps and with the support of external collaborators, the project is a testimony to the functionality and open and dynamic communication that characterises the refugee camps reached. Despite the vicissitudes, the fact that artistic expression is still possible in the camps and that artists continue to be artists remains an extraordinary discovery. Painters, sculptors, photographers and directors born and trained in the camps, and often grouped in small communities, thanks to the support of humanitarian organisations, their stories teach powerful lessons of determination and confidence in the force of art.

To highlight the creativity that is born in the “cities of thorns”, to recall the title of Ben Rawlence’s book on life in the Dadaab complex, is the purpose of the exhibition. In short, it seeks to find that creative energy capable of transfiguring an unsustainable reality and conveying a message like Aminah Rwimo’s, an award-winning director from the Kakuma camp: “I wanted to set an example and tell my fellow survivors that whatever happened to us is now part of our lives. But this is not the end.”

 

On the occasion of World Refugee Day, the University of Padua and the Imago Mundi Foundation are hosted a talk, on June 19 at the Aula Magna of Palazzo del Bo at 5 P.M., with photojournalist and activist Giles Duley, founder of the NGO Legacy of War Foundation


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(Photo: Adoku Zambé, Il passaggio, 2023)

The exhibition Out of Place. Art and Stories from Refugee Camps Around the World, organized by the Imago Mundi Foundation in collaboration with the University of Padua and the Department of Culture of the Municipality of Padua, has been extended until August 31 in the Ancient Courtyard of Palazzo del Bo.

Open to the public daily with free admission from 8 AM to 8 PM, the exhibition is held under the patronage of the United Nations High Commissioner for Refugees (UNHCR).

Based on research conducted within 18 of the largest existing refugee camps today, the exhibition showcases the testimonies—artworks and stories—of 264 artists who currently live in these settlements or have experienced similar conditions in the past. Alongside the 284 works they created in the 10x12 cm format, the exhibition also features a video installation and an art installation, offering a broader reflection on the current global refugee crisis.

photo

After Kutupalong, in Bangladesh, the exhibition presents different testimonies from Africa with the largest refugee camps in Kenya – Dadaab and Kakuma –, another two representative settlements in Uganda – Nakivale and Bidibidi, the camp of Dzaleka in Malawi, the one in Nyabiheke, Rwanda, and the settlement of Smara with the adjacent El Aaiun, Awserd, Boujdour, and Dakhla, in Algeria. The inquiry then turns to the Middle East, to open the doors of Za’atari, the biggest camp for Syrians, and to five Palestinian camps: Baq’a, Hittin, Irbid, Madaba and Souf, all in Jordan. Added to this map are artists who, from the 1980s until the current day, have lived in similar conditions in other geographical areas, including Kurdish and Yazidi artists who tell the complicated story of their people. A section on Afghanistan features the works and stories of 40 artists who have left their country or continue to live within its borders since the Taliban takeover in 2021. Completing the exhibition are accounts of migration to Europe from Ukraine and via the Mediterranean routes, along with a section devoted to migration corridors in South and Central America, with a focus on the Mexico-U.S. border.

“Exiles, émigrés, refugees, and expatriates uprooted from their lands”, wrote Edward Said in Reflections on Exile, “must make do in new surroundings, and the creativity as well as the sadness that can be seen in what they do is one of the experiences that has still to find its chroniclers…” Borrowing the definition of refugees proposed by Said – Out of Place – the objective of the exhibition is to offer a space of artistic and narrative expression to the artists living in refugee camps, and to present them first and foremost as artists, considering their current and past refugee status as accidental in their biographies. In the light of the stories and testimonies collected here, the camps appear not only as fragile and temporary living realities, but as evolving entities, “accidental cities”, urban conglomerates destined to last over time. To give just one example as proof of an approach that, rather than causing isolation, as has happened in the past, instead tends towards the integration of long-term camps into their host countries: in 2023 Kenya announced that the two largest camps in the country – Dadaab and Kakuma – would become integrated settlements where refugees would have to coexist with local communities.

The story of reaching the camps was itself an initiatory journey and a breaking of barriers: geographical, linguistic and administrative. Carried out with the help of artists contacted directly within the camps and with the support of external collaborators, the project is a testimony to the functionality and open and dynamic communication that characterises the refugee camps reached. Despite the vicissitudes, the fact that artistic expression is still possible in the camps and that artists continue to be artists remains an extraordinary discovery. Painters, sculptors, photographers and directors born and trained in the camps, and often grouped in small communities, thanks to the support of humanitarian organisations, their stories teach powerful lessons of determination and confidence in the force of art.

To highlight the creativity that is born in the “cities of thorns”, to recall the title of Ben Rawlence’s book on life in the Dadaab complex, is the purpose of the exhibition. In short, it seeks to find that creative energy capable of transfiguring an unsustainable reality and conveying a message like Aminah Rwimo’s, an award-winning director from the Kakuma camp: “I wanted to set an example and tell my fellow survivors that whatever happened to us is now part of our lives. But this is not the end.”

 

On the occasion of World Refugee Day, the University of Padua and the Imago Mundi Foundation are hosted a talk, on June 19 at the Aula Magna of Palazzo del Bo at 5 P.M., with photojournalist and activist Giles Duley, founder of the NGO Legacy of War Foundation


[summary] => [format] => 2 [safe_value] =>

(Photo: Adoku Zambé, Il passaggio, 2023)

The exhibition Out of Place. Art and Stories from Refugee Camps Around the World, organized by the Imago Mundi Foundation in collaboration with the University of Padua and the Department of Culture of the Municipality of Padua, has been extended until August 31 in the Ancient Courtyard of Palazzo del Bo.

Open to the public daily with free admission from 8 AM to 8 PM, the exhibition is held under the patronage of the United Nations High Commissioner for Refugees (UNHCR).

Based on research conducted within 18 of the largest existing refugee camps today, the exhibition showcases the testimonies—artworks and stories—of 264 artists who currently live in these settlements or have experienced similar conditions in the past. Alongside the 284 works they created in the 10x12 cm format, the exhibition also features a video installation and an art installation, offering a broader reflection on the current global refugee crisis.

photo

After Kutupalong, in Bangladesh, the exhibition presents different testimonies from Africa with the largest refugee camps in Kenya – Dadaab and Kakuma –, another two representative settlements in Uganda – Nakivale and Bidibidi, the camp of Dzaleka in Malawi, the one in Nyabiheke, Rwanda, and the settlement of Smara with the adjacent El Aaiun, Awserd, Boujdour, and Dakhla, in Algeria. The inquiry then turns to the Middle East, to open the doors of Za’atari, the biggest camp for Syrians, and to five Palestinian camps: Baq’a, Hittin, Irbid, Madaba and Souf, all in Jordan. Added to this map are artists who, from the 1980s until the current day, have lived in similar conditions in other geographical areas, including Kurdish and Yazidi artists who tell the complicated story of their people. A section on Afghanistan features the works and stories of 40 artists who have left their country or continue to live within its borders since the Taliban takeover in 2021. Completing the exhibition are accounts of migration to Europe from Ukraine and via the Mediterranean routes, along with a section devoted to migration corridors in South and Central America, with a focus on the Mexico-U.S. border.

“Exiles, émigrés, refugees, and expatriates uprooted from their lands”, wrote Edward Said in Reflections on Exile, “must make do in new surroundings, and the creativity as well as the sadness that can be seen in what they do is one of the experiences that has still to find its chroniclers…” Borrowing the definition of refugees proposed by Said – Out of Place – the objective of the exhibition is to offer a space of artistic and narrative expression to the artists living in refugee camps, and to present them first and foremost as artists, considering their current and past refugee status as accidental in their biographies. In the light of the stories and testimonies collected here, the camps appear not only as fragile and temporary living realities, but as evolving entities, “accidental cities”, urban conglomerates destined to last over time. To give just one example as proof of an approach that, rather than causing isolation, as has happened in the past, instead tends towards the integration of long-term camps into their host countries: in 2023 Kenya announced that the two largest camps in the country – Dadaab and Kakuma – would become integrated settlements where refugees would have to coexist with local communities.

The story of reaching the camps was itself an initiatory journey and a breaking of barriers: geographical, linguistic and administrative. Carried out with the help of artists contacted directly within the camps and with the support of external collaborators, the project is a testimony to the functionality and open and dynamic communication that characterises the refugee camps reached. Despite the vicissitudes, the fact that artistic expression is still possible in the camps and that artists continue to be artists remains an extraordinary discovery. Painters, sculptors, photographers and directors born and trained in the camps, and often grouped in small communities, thanks to the support of humanitarian organisations, their stories teach powerful lessons of determination and confidence in the force of art.

To highlight the creativity that is born in the “cities of thorns”, to recall the title of Ben Rawlence’s book on life in the Dadaab complex, is the purpose of the exhibition. In short, it seeks to find that creative energy capable of transfiguring an unsustainable reality and conveying a message like Aminah Rwimo’s, an award-winning director from the Kakuma camp: “I wanted to set an example and tell my fellow survivors that whatever happened to us is now part of our lives. But this is not the end.”

 

On the occasion of World Refugee Day, the University of Padua and the Imago Mundi Foundation are hosted a talk, on June 19 at the Aula Magna of Palazzo del Bo at 5 P.M., with photojournalist and activist Giles Duley, founder of the NGO Legacy of War Foundation


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(Photo: Adoku Zambé, Il passaggio, 2023)

The exhibition Out of Place. Art and Stories from Refugee Camps Around the World, organized by the Imago Mundi Foundation in collaboration with the University of Padua and the Department of Culture of the Municipality of Padua, has been extended until August 31 in the Ancient Courtyard of Palazzo del Bo.

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(Photo: Adoku Zambé, Il passaggio, 2023)

The exhibition Out of Place. Art and Stories from Refugee Camps Around the World, organized by the Imago Mundi Foundation in collaboration with the University of Padua and the Department of Culture of the Municipality of Padua, has been extended until August 31 in the Ancient Courtyard of Palazzo del Bo.

Open to the public daily with free admission from 8 AM to 8 PM, the exhibition is held under the patronage of the United Nations High Commissioner for Refugees (UNHCR).

Based on research conducted within 18 of the largest existing refugee camps today, the exhibition showcases the testimonies—artworks and stories—of 264 artists who currently live in these settlements or have experienced similar conditions in the past. Alongside the 284 works they created in the 10x12 cm format, the exhibition also features a video installation and an art installation, offering a broader reflection on the current global refugee crisis.

photo

After Kutupalong, in Bangladesh, the exhibition presents different testimonies from Africa with the largest refugee camps in Kenya – Dadaab and Kakuma –, another two representative settlements in Uganda – Nakivale and Bidibidi, the camp of Dzaleka in Malawi, the one in Nyabiheke, Rwanda, and the settlement of Smara with the adjacent El Aaiun, Awserd, Boujdour, and Dakhla, in Algeria. The inquiry then turns to the Middle East, to open the doors of Za’atari, the biggest camp for Syrians, and to five Palestinian camps: Baq’a, Hittin, Irbid, Madaba and Souf, all in Jordan. Added to this map are artists who, from the 1980s until the current day, have lived in similar conditions in other geographical areas, including Kurdish and Yazidi artists who tell the complicated story of their people. A section on Afghanistan features the works and stories of 40 artists who have left their country or continue to live within its borders since the Taliban takeover in 2021. Completing the exhibition are accounts of migration to Europe from Ukraine and via the Mediterranean routes, along with a section devoted to migration corridors in South and Central America, with a focus on the Mexico-U.S. border.

“Exiles, émigrés, refugees, and expatriates uprooted from their lands”, wrote Edward Said in Reflections on Exile, “must make do in new surroundings, and the creativity as well as the sadness that can be seen in what they do is one of the experiences that has still to find its chroniclers…” Borrowing the definition of refugees proposed by Said – Out of Place – the objective of the exhibition is to offer a space of artistic and narrative expression to the artists living in refugee camps, and to present them first and foremost as artists, considering their current and past refugee status as accidental in their biographies. In the light of the stories and testimonies collected here, the camps appear not only as fragile and temporary living realities, but as evolving entities, “accidental cities”, urban conglomerates destined to last over time. To give just one example as proof of an approach that, rather than causing isolation, as has happened in the past, instead tends towards the integration of long-term camps into their host countries: in 2023 Kenya announced that the two largest camps in the country – Dadaab and Kakuma – would become integrated settlements where refugees would have to coexist with local communities.

The story of reaching the camps was itself an initiatory journey and a breaking of barriers: geographical, linguistic and administrative. Carried out with the help of artists contacted directly within the camps and with the support of external collaborators, the project is a testimony to the functionality and open and dynamic communication that characterises the refugee camps reached. Despite the vicissitudes, the fact that artistic expression is still possible in the camps and that artists continue to be artists remains an extraordinary discovery. Painters, sculptors, photographers and directors born and trained in the camps, and often grouped in small communities, thanks to the support of humanitarian organisations, their stories teach powerful lessons of determination and confidence in the force of art.

To highlight the creativity that is born in the “cities of thorns”, to recall the title of Ben Rawlence’s book on life in the Dadaab complex, is the purpose of the exhibition. In short, it seeks to find that creative energy capable of transfiguring an unsustainable reality and conveying a message like Aminah Rwimo’s, an award-winning director from the Kakuma camp: “I wanted to set an example and tell my fellow survivors that whatever happened to us is now part of our lives. But this is not the end.”

 

On the occasion of World Refugee Day, the University of Padua and the Imago Mundi Foundation are hosted a talk, on June 19 at the Aula Magna of Palazzo del Bo at 5 P.M., with photojournalist and activist Giles Duley, founder of the NGO Legacy of War Foundation


[summary] => [format] => 2 [safe_value] =>

(Photo: Adoku Zambé, Il passaggio, 2023)

The exhibition Out of Place. Art and Stories from Refugee Camps Around the World, organized by the Imago Mundi Foundation in collaboration with the University of Padua and the Department of Culture of the Municipality of Padua, has been extended until August 31 in the Ancient Courtyard of Palazzo del Bo.

Open to the public daily with free admission from 8 AM to 8 PM, the exhibition is held under the patronage of the United Nations High Commissioner for Refugees (UNHCR).

Based on research conducted within 18 of the largest existing refugee camps today, the exhibition showcases the testimonies—artworks and stories—of 264 artists who currently live in these settlements or have experienced similar conditions in the past. Alongside the 284 works they created in the 10x12 cm format, the exhibition also features a video installation and an art installation, offering a broader reflection on the current global refugee crisis.

photo

After Kutupalong, in Bangladesh, the exhibition presents different testimonies from Africa with the largest refugee camps in Kenya – Dadaab and Kakuma –, another two representative settlements in Uganda – Nakivale and Bidibidi, the camp of Dzaleka in Malawi, the one in Nyabiheke, Rwanda, and the settlement of Smara with the adjacent El Aaiun, Awserd, Boujdour, and Dakhla, in Algeria. The inquiry then turns to the Middle East, to open the doors of Za’atari, the biggest camp for Syrians, and to five Palestinian camps: Baq’a, Hittin, Irbid, Madaba and Souf, all in Jordan. Added to this map are artists who, from the 1980s until the current day, have lived in similar conditions in other geographical areas, including Kurdish and Yazidi artists who tell the complicated story of their people. A section on Afghanistan features the works and stories of 40 artists who have left their country or continue to live within its borders since the Taliban takeover in 2021. Completing the exhibition are accounts of migration to Europe from Ukraine and via the Mediterranean routes, along with a section devoted to migration corridors in South and Central America, with a focus on the Mexico-U.S. border.

“Exiles, émigrés, refugees, and expatriates uprooted from their lands”, wrote Edward Said in Reflections on Exile, “must make do in new surroundings, and the creativity as well as the sadness that can be seen in what they do is one of the experiences that has still to find its chroniclers…” Borrowing the definition of refugees proposed by Said – Out of Place – the objective of the exhibition is to offer a space of artistic and narrative expression to the artists living in refugee camps, and to present them first and foremost as artists, considering their current and past refugee status as accidental in their biographies. In the light of the stories and testimonies collected here, the camps appear not only as fragile and temporary living realities, but as evolving entities, “accidental cities”, urban conglomerates destined to last over time. To give just one example as proof of an approach that, rather than causing isolation, as has happened in the past, instead tends towards the integration of long-term camps into their host countries: in 2023 Kenya announced that the two largest camps in the country – Dadaab and Kakuma – would become integrated settlements where refugees would have to coexist with local communities.

The story of reaching the camps was itself an initiatory journey and a breaking of barriers: geographical, linguistic and administrative. Carried out with the help of artists contacted directly within the camps and with the support of external collaborators, the project is a testimony to the functionality and open and dynamic communication that characterises the refugee camps reached. Despite the vicissitudes, the fact that artistic expression is still possible in the camps and that artists continue to be artists remains an extraordinary discovery. Painters, sculptors, photographers and directors born and trained in the camps, and often grouped in small communities, thanks to the support of humanitarian organisations, their stories teach powerful lessons of determination and confidence in the force of art.

To highlight the creativity that is born in the “cities of thorns”, to recall the title of Ben Rawlence’s book on life in the Dadaab complex, is the purpose of the exhibition. In short, it seeks to find that creative energy capable of transfiguring an unsustainable reality and conveying a message like Aminah Rwimo’s, an award-winning director from the Kakuma camp: “I wanted to set an example and tell my fellow survivors that whatever happened to us is now part of our lives. But this is not the end.”

 

On the occasion of World Refugee Day, the University of Padua and the Imago Mundi Foundation are hosted a talk, on June 19 at the Aula Magna of Palazzo del Bo at 5 P.M., with photojournalist and activist Giles Duley, founder of the NGO Legacy of War Foundation


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(Photo: Adoku Zambé, Il passaggio, 2023)

The exhibition Out of Place. Art and Stories from Refugee Camps Around the World, organized by the Imago Mundi Foundation in collaboration with the University of Padua and the Department of Culture of the Municipality of Padua, has been extended until August 31 in the Ancient Courtyard of Palazzo del Bo.

Open to the public daily with free admission from 8 AM to 8 PM, the exhibition is held under the patronage of the United Nations High Commissioner for Refugees (UNHCR).

Based on research conducted within 18 of the largest existing refugee camps today, the exhibition showcases the testimonies—artworks and stories—of 264 artists who currently live in these settlements or have experienced similar conditions in the past. Alongside the 284 works they created in the 10x12 cm format, the exhibition also features a video installation and an art installation, offering a broader reflection on the current global refugee crisis.

photo

After Kutupalong, in Bangladesh, the exhibition presents different testimonies from Africa with the largest refugee camps in Kenya – Dadaab and Kakuma –, another two representative settlements in Uganda – Nakivale and Bidibidi, the camp of Dzaleka in Malawi, the one in Nyabiheke, Rwanda, and the settlement of Smara with the adjacent El Aaiun, Awserd, Boujdour, and Dakhla, in Algeria. The inquiry then turns to the Middle East, to open the doors of Za’atari, the biggest camp for Syrians, and to five Palestinian camps: Baq’a, Hittin, Irbid, Madaba and Souf, all in Jordan. Added to this map are artists who, from the 1980s until the current day, have lived in similar conditions in other geographical areas, including Kurdish and Yazidi artists who tell the complicated story of their people. A section on Afghanistan features the works and stories of 40 artists who have left their country or continue to live within its borders since the Taliban takeover in 2021. Completing the exhibition are accounts of migration to Europe from Ukraine and via the Mediterranean routes, along with a section devoted to migration corridors in South and Central America, with a focus on the Mexico-U.S. border.

“Exiles, émigrés, refugees, and expatriates uprooted from their lands”, wrote Edward Said in Reflections on Exile, “must make do in new surroundings, and the creativity as well as the sadness that can be seen in what they do is one of the experiences that has still to find its chroniclers…” Borrowing the definition of refugees proposed by Said – Out of Place – the objective of the exhibition is to offer a space of artistic and narrative expression to the artists living in refugee camps, and to present them first and foremost as artists, considering their current and past refugee status as accidental in their biographies. In the light of the stories and testimonies collected here, the camps appear not only as fragile and temporary living realities, but as evolving entities, “accidental cities”, urban conglomerates destined to last over time. To give just one example as proof of an approach that, rather than causing isolation, as has happened in the past, instead tends towards the integration of long-term camps into their host countries: in 2023 Kenya announced that the two largest camps in the country – Dadaab and Kakuma – would become integrated settlements where refugees would have to coexist with local communities.

The story of reaching the camps was itself an initiatory journey and a breaking of barriers: geographical, linguistic and administrative. Carried out with the help of artists contacted directly within the camps and with the support of external collaborators, the project is a testimony to the functionality and open and dynamic communication that characterises the refugee camps reached. Despite the vicissitudes, the fact that artistic expression is still possible in the camps and that artists continue to be artists remains an extraordinary discovery. Painters, sculptors, photographers and directors born and trained in the camps, and often grouped in small communities, thanks to the support of humanitarian organisations, their stories teach powerful lessons of determination and confidence in the force of art.

To highlight the creativity that is born in the “cities of thorns”, to recall the title of Ben Rawlence’s book on life in the Dadaab complex, is the purpose of the exhibition. In short, it seeks to find that creative energy capable of transfiguring an unsustainable reality and conveying a message like Aminah Rwimo’s, an award-winning director from the Kakuma camp: “I wanted to set an example and tell my fellow survivors that whatever happened to us is now part of our lives. But this is not the end.”

 

On the occasion of World Refugee Day, the University of Padua and the Imago Mundi Foundation are hosted a talk, on June 19 at the Aula Magna of Palazzo del Bo at 5 P.M., with photojournalist and activist Giles Duley, founder of the NGO Legacy of War Foundation


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(Photo: Adoku Zambé, Il passaggio, 2023)

The exhibition Out of Place. Art and Stories from Refugee Camps Around the World, organized by the Imago Mundi Foundation in collaboration with the University of Padua and the Department of Culture of the Municipality of Padua, has been extended until August 31 in the Ancient Courtyard of Palazzo del Bo.

Open to the public daily with free admission from 8 AM to 8 PM, the exhibition is held under the patronage of the United Nations High Commissioner for Refugees (UNHCR).

Based on research conducted within 18 of the largest existing refugee camps today, the exhibition showcases the testimonies—artworks and stories—of 264 artists who currently live in these settlements or have experienced similar conditions in the past. Alongside the 284 works they created in the 10x12 cm format, the exhibition also features a video installation and an art installation, offering a broader reflection on the current global refugee crisis.

photo

After Kutupalong, in Bangladesh, the exhibition presents different testimonies from Africa with the largest refugee camps in Kenya – Dadaab and Kakuma –, another two representative settlements in Uganda – Nakivale and Bidibidi, the camp of Dzaleka in Malawi, the one in Nyabiheke, Rwanda, and the settlement of Smara with the adjacent El Aaiun, Awserd, Boujdour, and Dakhla, in Algeria. The inquiry then turns to the Middle East, to open the doors of Za’atari, the biggest camp for Syrians, and to five Palestinian camps: Baq’a, Hittin, Irbid, Madaba and Souf, all in Jordan. Added to this map are artists who, from the 1980s until the current day, have lived in similar conditions in other geographical areas, including Kurdish and Yazidi artists who tell the complicated story of their people. A section on Afghanistan features the works and stories of 40 artists who have left their country or continue to live within its borders since the Taliban takeover in 2021. Completing the exhibition are accounts of migration to Europe from Ukraine and via the Mediterranean routes, along with a section devoted to migration corridors in South and Central America, with a focus on the Mexico-U.S. border.

“Exiles, émigrés, refugees, and expatriates uprooted from their lands”, wrote Edward Said in Reflections on Exile, “must make do in new surroundings, and the creativity as well as the sadness that can be seen in what they do is one of the experiences that has still to find its chroniclers…” Borrowing the definition of refugees proposed by Said – Out of Place – the objective of the exhibition is to offer a space of artistic and narrative expression to the artists living in refugee camps, and to present them first and foremost as artists, considering their current and past refugee status as accidental in their biographies. In the light of the stories and testimonies collected here, the camps appear not only as fragile and temporary living realities, but as evolving entities, “accidental cities”, urban conglomerates destined to last over time. To give just one example as proof of an approach that, rather than causing isolation, as has happened in the past, instead tends towards the integration of long-term camps into their host countries: in 2023 Kenya announced that the two largest camps in the country – Dadaab and Kakuma – would become integrated settlements where refugees would have to coexist with local communities.

The story of reaching the camps was itself an initiatory journey and a breaking of barriers: geographical, linguistic and administrative. Carried out with the help of artists contacted directly within the camps and with the support of external collaborators, the project is a testimony to the functionality and open and dynamic communication that characterises the refugee camps reached. Despite the vicissitudes, the fact that artistic expression is still possible in the camps and that artists continue to be artists remains an extraordinary discovery. Painters, sculptors, photographers and directors born and trained in the camps, and often grouped in small communities, thanks to the support of humanitarian organisations, their stories teach powerful lessons of determination and confidence in the force of art.

To highlight the creativity that is born in the “cities of thorns”, to recall the title of Ben Rawlence’s book on life in the Dadaab complex, is the purpose of the exhibition. In short, it seeks to find that creative energy capable of transfiguring an unsustainable reality and conveying a message like Aminah Rwimo’s, an award-winning director from the Kakuma camp: “I wanted to set an example and tell my fellow survivors that whatever happened to us is now part of our lives. But this is not the end.”

 

On the occasion of World Refugee Day, the University of Padua and the Imago Mundi Foundation are hosted a talk, on June 19 at the Aula Magna of Palazzo del Bo at 5 P.M., with photojournalist and activist Giles Duley, founder of the NGO Legacy of War Foundation


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(Photo: Adoku Zambé, Il passaggio, 2023)

The exhibition Out of Place. Art and Stories from Refugee Camps Around the World, organized by the Imago Mundi Foundation in collaboration with the University of Padua and the Department of Culture of the Municipality of Padua, has been extended until August 31 in the Ancient Courtyard of Palazzo del Bo.

Open to the public daily with free admission from 8 AM to 8 PM, the exhibition is held under the patronage of the United Nations High Commissioner for Refugees (UNHCR).

Based on research conducted within 18 of the largest existing refugee camps today, the exhibition showcases the testimonies—artworks and stories—of 264 artists who currently live in these settlements or have experienced similar conditions in the past. Alongside the 284 works they created in the 10x12 cm format, the exhibition also features a video installation and an art installation, offering a broader reflection on the current global refugee crisis.

photo

After Kutupalong, in Bangladesh, the exhibition presents different testimonies from Africa with the largest refugee camps in Kenya – Dadaab and Kakuma –, another two representative settlements in Uganda – Nakivale and Bidibidi, the camp of Dzaleka in Malawi, the one in Nyabiheke, Rwanda, and the settlement of Smara with the adjacent El Aaiun, Awserd, Boujdour, and Dakhla, in Algeria. The inquiry then turns to the Middle East, to open the doors of Za’atari, the biggest camp for Syrians, and to five Palestinian camps: Baq’a, Hittin, Irbid, Madaba and Souf, all in Jordan. Added to this map are artists who, from the 1980s until the current day, have lived in similar conditions in other geographical areas, including Kurdish and Yazidi artists who tell the complicated story of their people. A section on Afghanistan features the works and stories of 40 artists who have left their country or continue to live within its borders since the Taliban takeover in 2021. Completing the exhibition are accounts of migration to Europe from Ukraine and via the Mediterranean routes, along with a section devoted to migration corridors in South and Central America, with a focus on the Mexico-U.S. border.

“Exiles, émigrés, refugees, and expatriates uprooted from their lands”, wrote Edward Said in Reflections on Exile, “must make do in new surroundings, and the creativity as well as the sadness that can be seen in what they do is one of the experiences that has still to find its chroniclers…” Borrowing the definition of refugees proposed by Said – Out of Place – the objective of the exhibition is to offer a space of artistic and narrative expression to the artists living in refugee camps, and to present them first and foremost as artists, considering their current and past refugee status as accidental in their biographies. In the light of the stories and testimonies collected here, the camps appear not only as fragile and temporary living realities, but as evolving entities, “accidental cities”, urban conglomerates destined to last over time. To give just one example as proof of an approach that, rather than causing isolation, as has happened in the past, instead tends towards the integration of long-term camps into their host countries: in 2023 Kenya announced that the two largest camps in the country – Dadaab and Kakuma – would become integrated settlements where refugees would have to coexist with local communities.

The story of reaching the camps was itself an initiatory journey and a breaking of barriers: geographical, linguistic and administrative. Carried out with the help of artists contacted directly within the camps and with the support of external collaborators, the project is a testimony to the functionality and open and dynamic communication that characterises the refugee camps reached. Despite the vicissitudes, the fact that artistic expression is still possible in the camps and that artists continue to be artists remains an extraordinary discovery. Painters, sculptors, photographers and directors born and trained in the camps, and often grouped in small communities, thanks to the support of humanitarian organisations, their stories teach powerful lessons of determination and confidence in the force of art.

To highlight the creativity that is born in the “cities of thorns”, to recall the title of Ben Rawlence’s book on life in the Dadaab complex, is the purpose of the exhibition. In short, it seeks to find that creative energy capable of transfiguring an unsustainable reality and conveying a message like Aminah Rwimo’s, an award-winning director from the Kakuma camp: “I wanted to set an example and tell my fellow survivors that whatever happened to us is now part of our lives. But this is not the end.”

 

On the occasion of World Refugee Day, the University of Padua and the Imago Mundi Foundation are hosted a talk, on June 19 at the Aula Magna of Palazzo del Bo at 5 P.M., with photojournalist and activist Giles Duley, founder of the NGO Legacy of War Foundation


[summary] => [format] => 2 [safe_value] =>

(Photo: Adoku Zambé, Il passaggio, 2023)

The exhibition Out of Place. Art and Stories from Refugee Camps Around the World, organized by the Imago Mundi Foundation in collaboration with the University of Padua and the Department of Culture of the Municipality of Padua, has been extended until August 31 in the Ancient Courtyard of Palazzo del Bo.

Open to the public daily with free admission from 8 AM to 8 PM, the exhibition is held under the patronage of the United Nations High Commissioner for Refugees (UNHCR).

Based on research conducted within 18 of the largest existing refugee camps today, the exhibition showcases the testimonies—artworks and stories—of 264 artists who currently live in these settlements or have experienced similar conditions in the past. Alongside the 284 works they created in the 10x12 cm format, the exhibition also features a video installation and an art installation, offering a broader reflection on the current global refugee crisis.

photo

After Kutupalong, in Bangladesh, the exhibition presents different testimonies from Africa with the largest refugee camps in Kenya – Dadaab and Kakuma –, another two representative settlements in Uganda – Nakivale and Bidibidi, the camp of Dzaleka in Malawi, the one in Nyabiheke, Rwanda, and the settlement of Smara with the adjacent El Aaiun, Awserd, Boujdour, and Dakhla, in Algeria. The inquiry then turns to the Middle East, to open the doors of Za’atari, the biggest camp for Syrians, and to five Palestinian camps: Baq’a, Hittin, Irbid, Madaba and Souf, all in Jordan. Added to this map are artists who, from the 1980s until the current day, have lived in similar conditions in other geographical areas, including Kurdish and Yazidi artists who tell the complicated story of their people. A section on Afghanistan features the works and stories of 40 artists who have left their country or continue to live within its borders since the Taliban takeover in 2021. Completing the exhibition are accounts of migration to Europe from Ukraine and via the Mediterranean routes, along with a section devoted to migration corridors in South and Central America, with a focus on the Mexico-U.S. border.

“Exiles, émigrés, refugees, and expatriates uprooted from their lands”, wrote Edward Said in Reflections on Exile, “must make do in new surroundings, and the creativity as well as the sadness that can be seen in what they do is one of the experiences that has still to find its chroniclers…” Borrowing the definition of refugees proposed by Said – Out of Place – the objective of the exhibition is to offer a space of artistic and narrative expression to the artists living in refugee camps, and to present them first and foremost as artists, considering their current and past refugee status as accidental in their biographies. In the light of the stories and testimonies collected here, the camps appear not only as fragile and temporary living realities, but as evolving entities, “accidental cities”, urban conglomerates destined to last over time. To give just one example as proof of an approach that, rather than causing isolation, as has happened in the past, instead tends towards the integration of long-term camps into their host countries: in 2023 Kenya announced that the two largest camps in the country – Dadaab and Kakuma – would become integrated settlements where refugees would have to coexist with local communities.

The story of reaching the camps was itself an initiatory journey and a breaking of barriers: geographical, linguistic and administrative. Carried out with the help of artists contacted directly within the camps and with the support of external collaborators, the project is a testimony to the functionality and open and dynamic communication that characterises the refugee camps reached. Despite the vicissitudes, the fact that artistic expression is still possible in the camps and that artists continue to be artists remains an extraordinary discovery. Painters, sculptors, photographers and directors born and trained in the camps, and often grouped in small communities, thanks to the support of humanitarian organisations, their stories teach powerful lessons of determination and confidence in the force of art.

To highlight the creativity that is born in the “cities of thorns”, to recall the title of Ben Rawlence’s book on life in the Dadaab complex, is the purpose of the exhibition. In short, it seeks to find that creative energy capable of transfiguring an unsustainable reality and conveying a message like Aminah Rwimo’s, an award-winning director from the Kakuma camp: “I wanted to set an example and tell my fellow survivors that whatever happened to us is now part of our lives. But this is not the end.”

 

On the occasion of World Refugee Day, the University of Padua and the Imago Mundi Foundation are hosted a talk, on June 19 at the Aula Magna of Palazzo del Bo at 5 P.M., with photojournalist and activist Giles Duley, founder of the NGO Legacy of War Foundation


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“OUT OF PLACE. ARTE E STORIE DAI CAMPI RIFUGIATI NEL MONDO”

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NUOVE SFIDE PER GRANDI MAESTRI - Primo convegno nazionale dell'Unione dei Professori Emeriti delle Università italiane

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Seal of Excellence @UniPD 2025 Integrazione elenco progetti ammissibili

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Trasparenza - Daniela Mapelli Missioni 2024

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New therapeutic perspectives from the study of mechanisms underlying certain mitochondrial diseases

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“Modelling POLG mutations in mice unravels a critical role of POLγB in regulating phenotypic severity” is the title of the study published in the prestigious international journal Nature Communications by a research team led by Carlo Viscomi, Associate Professor in the Department of Biomedical Sciences at the University of Padua and Principal Investigator at the Veneto Institute of Molecular Medicine (VIMM).

The study sheds light on how mutations in a key enzyme essential to human health—DNA polymerase gamma (POLγ)—can lead to serious mitochondrial diseases. This enzyme is responsible for replicating DNA within mitochondria, the "powerhouses" of our cells. When POLγ malfunctions, mitochondrial DNA becomes unstable, with potentially severe consequences for the organism.

Diseases caused by mutations in the POLG gene are highly heterogeneous and often difficult to diagnose due to the complexity of symptoms: the same mutation can cause different symptoms in different patients. Moreover, there are currently no cures, and patients can only receive treatments aimed at relieving symptoms.

To better understand the mechanisms underlying this variability, the researchers created mutated versions of the protein to analyze their structure and function, and they replicated these mutations in mouse models to observe their effects on the entire organism.

All analyzed mutations significantly reduce POLγ activity. Using cryo-electron microscopy, the team identified structural differences between the human and mouse versions of the protein—particularly in the accessory subunit known as POLγB, which functions to stabilize the enzyme. These differences make the murine enzyme more resistant to mutations compared to the human one, helping explain why the same mutations cause milder defects in mice than in humans. Nevertheless, the mouse models retain the essential features of human diseases, such as mitochondrial DNA instability and reduced enzyme activity and stability.

“This study is important for two reasons. On one hand, it helps us better understand the molecular mechanisms behind diseases caused by POLG mutations. On the other, it opens up new perspectives for developing drugs or gene therapies capable of correcting or compensating for the defects caused by POLG mutations,” says Carlo Viscomi. “The study also highlights the value of animal models in investigating the mechanisms underlying these rare diseases, while accounting for interspecies differences. Understanding these differences is crucial for advancing research toward increasingly effective and personalized therapies.”

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“Modelling POLG mutations in mice unravels a critical role of POLγB in regulating phenotypic severity” is the title of the study published in the prestigious international journal Nature Communications by a research team led by Carlo Viscomi, Associate Professor in the Department of Biomedical Sciences at the University of Padua and Principal Investigator at the Veneto Institute of Molecular Medicine (VIMM).

The study sheds light on how mutations in a key enzyme essential to human health—DNA polymerase gamma (POLγ)—can lead to serious mitochondrial diseases. This enzyme is responsible for replicating DNA within mitochondria, the "powerhouses" of our cells. When POLγ malfunctions, mitochondrial DNA becomes unstable, with potentially severe consequences for the organism.

Diseases caused by mutations in the POLG gene are highly heterogeneous and often difficult to diagnose due to the complexity of symptoms: the same mutation can cause different symptoms in different patients. Moreover, there are currently no cures, and patients can only receive treatments aimed at relieving symptoms.

To better understand the mechanisms underlying this variability, the researchers created mutated versions of the protein to analyze their structure and function, and they replicated these mutations in mouse models to observe their effects on the entire organism.

All analyzed mutations significantly reduce POLγ activity. Using cryo-electron microscopy, the team identified structural differences between the human and mouse versions of the protein—particularly in the accessory subunit known as POLγB, which functions to stabilize the enzyme. These differences make the murine enzyme more resistant to mutations compared to the human one, helping explain why the same mutations cause milder defects in mice than in humans. Nevertheless, the mouse models retain the essential features of human diseases, such as mitochondrial DNA instability and reduced enzyme activity and stability.

“This study is important for two reasons. On one hand, it helps us better understand the molecular mechanisms behind diseases caused by POLG mutations. On the other, it opens up new perspectives for developing drugs or gene therapies capable of correcting or compensating for the defects caused by POLG mutations,” says Carlo Viscomi. “The study also highlights the value of animal models in investigating the mechanisms underlying these rare diseases, while accounting for interspecies differences. Understanding these differences is crucial for advancing research toward increasingly effective and personalized therapies.”

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“Modelling POLG mutations in mice unravels a critical role of POLγB in regulating phenotypic severity” is the title of the study published in the prestigious international journal Nature Communications by a research team led by Carlo Viscomi, Associate Professor in the Department of Biomedical Sciences at the University of Padua and Principal Investigator at the Veneto Institute of Molecular Medicine (VIMM).

The study sheds light on how mutations in a key enzyme essential to human health—DNA polymerase gamma (POLγ)—can lead to serious mitochondrial diseases. This enzyme is responsible for replicating DNA within mitochondria, the "powerhouses" of our cells. When POLγ malfunctions, mitochondrial DNA becomes unstable, with potentially severe consequences for the organism.

Diseases caused by mutations in the POLG gene are highly heterogeneous and often difficult to diagnose due to the complexity of symptoms: the same mutation can cause different symptoms in different patients. Moreover, there are currently no cures, and patients can only receive treatments aimed at relieving symptoms.

To better understand the mechanisms underlying this variability, the researchers created mutated versions of the protein to analyze their structure and function, and they replicated these mutations in mouse models to observe their effects on the entire organism.

All analyzed mutations significantly reduce POLγ activity. Using cryo-electron microscopy, the team identified structural differences between the human and mouse versions of the protein—particularly in the accessory subunit known as POLγB, which functions to stabilize the enzyme. These differences make the murine enzyme more resistant to mutations compared to the human one, helping explain why the same mutations cause milder defects in mice than in humans. Nevertheless, the mouse models retain the essential features of human diseases, such as mitochondrial DNA instability and reduced enzyme activity and stability.

“This study is important for two reasons. On one hand, it helps us better understand the molecular mechanisms behind diseases caused by POLG mutations. On the other, it opens up new perspectives for developing drugs or gene therapies capable of correcting or compensating for the defects caused by POLG mutations,” says Carlo Viscomi. “The study also highlights the value of animal models in investigating the mechanisms underlying these rare diseases, while accounting for interspecies differences. Understanding these differences is crucial for advancing research toward increasingly effective and personalized therapies.”

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“Modelling POLG mutations in mice unravels a critical role of POLγB in regulating phenotypic severity” is the title of the study published in the prestigious international journal Nature Communications by a research team led by Carlo Viscomi, Associate Professor in the Department of Biomedical Sciences at the University of Padua and Principal Investigator at the Veneto Institute of Molecular Medicine (VIMM).

The study sheds light on how mutations in a key enzyme essential to human health—DNA polymerase gamma (POLγ)—can lead to serious mitochondrial diseases. This enzyme is responsible for replicating DNA within mitochondria, the "powerhouses" of our cells. When POLγ malfunctions, mitochondrial DNA becomes unstable, with potentially severe consequences for the organism.

Diseases caused by mutations in the POLG gene are highly heterogeneous and often difficult to diagnose due to the complexity of symptoms: the same mutation can cause different symptoms in different patients. Moreover, there are currently no cures, and patients can only receive treatments aimed at relieving symptoms.

To better understand the mechanisms underlying this variability, the researchers created mutated versions of the protein to analyze their structure and function, and they replicated these mutations in mouse models to observe their effects on the entire organism.

All analyzed mutations significantly reduce POLγ activity. Using cryo-electron microscopy, the team identified structural differences between the human and mouse versions of the protein—particularly in the accessory subunit known as POLγB, which functions to stabilize the enzyme. These differences make the murine enzyme more resistant to mutations compared to the human one, helping explain why the same mutations cause milder defects in mice than in humans. Nevertheless, the mouse models retain the essential features of human diseases, such as mitochondrial DNA instability and reduced enzyme activity and stability.

“This study is important for two reasons. On one hand, it helps us better understand the molecular mechanisms behind diseases caused by POLG mutations. On the other, it opens up new perspectives for developing drugs or gene therapies capable of correcting or compensating for the defects caused by POLG mutations,” says Carlo Viscomi. “The study also highlights the value of animal models in investigating the mechanisms underlying these rare diseases, while accounting for interspecies differences. Understanding these differences is crucial for advancing research toward increasingly effective and personalized therapies.”

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“Modelling POLG mutations in mice unravels a critical role of POLγB in regulating phenotypic severity” is the title of the study published in the prestigious international journal Nature Communications by a research team led by Carlo Viscomi, Associate Professor in the Department of Biomedical Sciences at the University of Padua and Principal Investigator at the Veneto Institute of Molecular Medicine (VIMM).

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“Modelling POLG mutations in mice unravels a critical role of POLγB in regulating phenotypic severity” is the title of the study published in the prestigious international journal Nature Communications by a research team led by Carlo Viscomi, Associate Professor in the Department of Biomedical Sciences at the University of Padua and Principal Investigator at the Veneto Institute of Molecular Medicine (VIMM).

The study sheds light on how mutations in a key enzyme essential to human health—DNA polymerase gamma (POLγ)—can lead to serious mitochondrial diseases. This enzyme is responsible for replicating DNA within mitochondria, the "powerhouses" of our cells. When POLγ malfunctions, mitochondrial DNA becomes unstable, with potentially severe consequences for the organism.

Diseases caused by mutations in the POLG gene are highly heterogeneous and often difficult to diagnose due to the complexity of symptoms: the same mutation can cause different symptoms in different patients. Moreover, there are currently no cures, and patients can only receive treatments aimed at relieving symptoms.

To better understand the mechanisms underlying this variability, the researchers created mutated versions of the protein to analyze their structure and function, and they replicated these mutations in mouse models to observe their effects on the entire organism.

All analyzed mutations significantly reduce POLγ activity. Using cryo-electron microscopy, the team identified structural differences between the human and mouse versions of the protein—particularly in the accessory subunit known as POLγB, which functions to stabilize the enzyme. These differences make the murine enzyme more resistant to mutations compared to the human one, helping explain why the same mutations cause milder defects in mice than in humans. Nevertheless, the mouse models retain the essential features of human diseases, such as mitochondrial DNA instability and reduced enzyme activity and stability.

“This study is important for two reasons. On one hand, it helps us better understand the molecular mechanisms behind diseases caused by POLG mutations. On the other, it opens up new perspectives for developing drugs or gene therapies capable of correcting or compensating for the defects caused by POLG mutations,” says Carlo Viscomi. “The study also highlights the value of animal models in investigating the mechanisms underlying these rare diseases, while accounting for interspecies differences. Understanding these differences is crucial for advancing research toward increasingly effective and personalized therapies.”

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“Modelling POLG mutations in mice unravels a critical role of POLγB in regulating phenotypic severity” is the title of the study published in the prestigious international journal Nature Communications by a research team led by Carlo Viscomi, Associate Professor in the Department of Biomedical Sciences at the University of Padua and Principal Investigator at the Veneto Institute of Molecular Medicine (VIMM).

The study sheds light on how mutations in a key enzyme essential to human health—DNA polymerase gamma (POLγ)—can lead to serious mitochondrial diseases. This enzyme is responsible for replicating DNA within mitochondria, the "powerhouses" of our cells. When POLγ malfunctions, mitochondrial DNA becomes unstable, with potentially severe consequences for the organism.

Diseases caused by mutations in the POLG gene are highly heterogeneous and often difficult to diagnose due to the complexity of symptoms: the same mutation can cause different symptoms in different patients. Moreover, there are currently no cures, and patients can only receive treatments aimed at relieving symptoms.

To better understand the mechanisms underlying this variability, the researchers created mutated versions of the protein to analyze their structure and function, and they replicated these mutations in mouse models to observe their effects on the entire organism.

All analyzed mutations significantly reduce POLγ activity. Using cryo-electron microscopy, the team identified structural differences between the human and mouse versions of the protein—particularly in the accessory subunit known as POLγB, which functions to stabilize the enzyme. These differences make the murine enzyme more resistant to mutations compared to the human one, helping explain why the same mutations cause milder defects in mice than in humans. Nevertheless, the mouse models retain the essential features of human diseases, such as mitochondrial DNA instability and reduced enzyme activity and stability.

“This study is important for two reasons. On one hand, it helps us better understand the molecular mechanisms behind diseases caused by POLG mutations. On the other, it opens up new perspectives for developing drugs or gene therapies capable of correcting or compensating for the defects caused by POLG mutations,” says Carlo Viscomi. “The study also highlights the value of animal models in investigating the mechanisms underlying these rare diseases, while accounting for interspecies differences. Understanding these differences is crucial for advancing research toward increasingly effective and personalized therapies.”

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“Modelling POLG mutations in mice unravels a critical role of POLγB in regulating phenotypic severity” is the title of the study published in the prestigious international journal Nature Communications by a research team led by Carlo Viscomi, Associate Professor in the Department of Biomedical Sciences at the University of Padua and Principal Investigator at the Veneto Institute of Molecular Medicine (VIMM).

The study sheds light on how mutations in a key enzyme essential to human health—DNA polymerase gamma (POLγ)—can lead to serious mitochondrial diseases. This enzyme is responsible for replicating DNA within mitochondria, the "powerhouses" of our cells. When POLγ malfunctions, mitochondrial DNA becomes unstable, with potentially severe consequences for the organism.

Diseases caused by mutations in the POLG gene are highly heterogeneous and often difficult to diagnose due to the complexity of symptoms: the same mutation can cause different symptoms in different patients. Moreover, there are currently no cures, and patients can only receive treatments aimed at relieving symptoms.

To better understand the mechanisms underlying this variability, the researchers created mutated versions of the protein to analyze their structure and function, and they replicated these mutations in mouse models to observe their effects on the entire organism.

All analyzed mutations significantly reduce POLγ activity. Using cryo-electron microscopy, the team identified structural differences between the human and mouse versions of the protein—particularly in the accessory subunit known as POLγB, which functions to stabilize the enzyme. These differences make the murine enzyme more resistant to mutations compared to the human one, helping explain why the same mutations cause milder defects in mice than in humans. Nevertheless, the mouse models retain the essential features of human diseases, such as mitochondrial DNA instability and reduced enzyme activity and stability.

“This study is important for two reasons. On one hand, it helps us better understand the molecular mechanisms behind diseases caused by POLG mutations. On the other, it opens up new perspectives for developing drugs or gene therapies capable of correcting or compensating for the defects caused by POLG mutations,” says Carlo Viscomi. “The study also highlights the value of animal models in investigating the mechanisms underlying these rare diseases, while accounting for interspecies differences. Understanding these differences is crucial for advancing research toward increasingly effective and personalized therapies.”

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“Modelling POLG mutations in mice unravels a critical role of POLγB in regulating phenotypic severity” is the title of the study published in the prestigious international journal Nature Communications by a research team led by Carlo Viscomi, Associate Professor in the Department of Biomedical Sciences at the University of Padua and Principal Investigator at the Veneto Institute of Molecular Medicine (VIMM).

The study sheds light on how mutations in a key enzyme essential to human health—DNA polymerase gamma (POLγ)—can lead to serious mitochondrial diseases. This enzyme is responsible for replicating DNA within mitochondria, the "powerhouses" of our cells. When POLγ malfunctions, mitochondrial DNA becomes unstable, with potentially severe consequences for the organism.

Diseases caused by mutations in the POLG gene are highly heterogeneous and often difficult to diagnose due to the complexity of symptoms: the same mutation can cause different symptoms in different patients. Moreover, there are currently no cures, and patients can only receive treatments aimed at relieving symptoms.

To better understand the mechanisms underlying this variability, the researchers created mutated versions of the protein to analyze their structure and function, and they replicated these mutations in mouse models to observe their effects on the entire organism.

All analyzed mutations significantly reduce POLγ activity. Using cryo-electron microscopy, the team identified structural differences between the human and mouse versions of the protein—particularly in the accessory subunit known as POLγB, which functions to stabilize the enzyme. These differences make the murine enzyme more resistant to mutations compared to the human one, helping explain why the same mutations cause milder defects in mice than in humans. Nevertheless, the mouse models retain the essential features of human diseases, such as mitochondrial DNA instability and reduced enzyme activity and stability.

“This study is important for two reasons. On one hand, it helps us better understand the molecular mechanisms behind diseases caused by POLG mutations. On the other, it opens up new perspectives for developing drugs or gene therapies capable of correcting or compensating for the defects caused by POLG mutations,” says Carlo Viscomi. “The study also highlights the value of animal models in investigating the mechanisms underlying these rare diseases, while accounting for interspecies differences. Understanding these differences is crucial for advancing research toward increasingly effective and personalized therapies.”

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“Modelling POLG mutations in mice unravels a critical role of POLγB in regulating phenotypic severity” is the title of the study published in the prestigious international journal Nature Communications by a research team led by Carlo Viscomi, Associate Professor in the Department of Biomedical Sciences at the University of Padua and Principal Investigator at the Veneto Institute of Molecular Medicine (VIMM).

The study sheds light on how mutations in a key enzyme essential to human health—DNA polymerase gamma (POLγ)—can lead to serious mitochondrial diseases. This enzyme is responsible for replicating DNA within mitochondria, the "powerhouses" of our cells. When POLγ malfunctions, mitochondrial DNA becomes unstable, with potentially severe consequences for the organism.

Diseases caused by mutations in the POLG gene are highly heterogeneous and often difficult to diagnose due to the complexity of symptoms: the same mutation can cause different symptoms in different patients. Moreover, there are currently no cures, and patients can only receive treatments aimed at relieving symptoms.

To better understand the mechanisms underlying this variability, the researchers created mutated versions of the protein to analyze their structure and function, and they replicated these mutations in mouse models to observe their effects on the entire organism.

All analyzed mutations significantly reduce POLγ activity. Using cryo-electron microscopy, the team identified structural differences between the human and mouse versions of the protein—particularly in the accessory subunit known as POLγB, which functions to stabilize the enzyme. These differences make the murine enzyme more resistant to mutations compared to the human one, helping explain why the same mutations cause milder defects in mice than in humans. Nevertheless, the mouse models retain the essential features of human diseases, such as mitochondrial DNA instability and reduced enzyme activity and stability.

“This study is important for two reasons. On one hand, it helps us better understand the molecular mechanisms behind diseases caused by POLG mutations. On the other, it opens up new perspectives for developing drugs or gene therapies capable of correcting or compensating for the defects caused by POLG mutations,” says Carlo Viscomi. “The study also highlights the value of animal models in investigating the mechanisms underlying these rare diseases, while accounting for interspecies differences. Understanding these differences is crucial for advancing research toward increasingly effective and personalized therapies.”

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“Modelling POLG mutations in mice unravels a critical role of POLγB in regulating phenotypic severity” is the title of the study published in the prestigious international journal Nature Communications by a research team led by Carlo Viscomi, Associate Professor in the Department of Biomedical Sciences at the University of Padua and Principal Investigator at the Veneto Institute of Molecular Medicine (VIMM).

The study sheds light on how mutations in a key enzyme essential to human health—DNA polymerase gamma (POLγ)—can lead to serious mitochondrial diseases. This enzyme is responsible for replicating DNA within mitochondria, the "powerhouses" of our cells. When POLγ malfunctions, mitochondrial DNA becomes unstable, with potentially severe consequences for the organism.

Diseases caused by mutations in the POLG gene are highly heterogeneous and often difficult to diagnose due to the complexity of symptoms: the same mutation can cause different symptoms in different patients. Moreover, there are currently no cures, and patients can only receive treatments aimed at relieving symptoms.

To better understand the mechanisms underlying this variability, the researchers created mutated versions of the protein to analyze their structure and function, and they replicated these mutations in mouse models to observe their effects on the entire organism.

All analyzed mutations significantly reduce POLγ activity. Using cryo-electron microscopy, the team identified structural differences between the human and mouse versions of the protein—particularly in the accessory subunit known as POLγB, which functions to stabilize the enzyme. These differences make the murine enzyme more resistant to mutations compared to the human one, helping explain why the same mutations cause milder defects in mice than in humans. Nevertheless, the mouse models retain the essential features of human diseases, such as mitochondrial DNA instability and reduced enzyme activity and stability.

“This study is important for two reasons. On one hand, it helps us better understand the molecular mechanisms behind diseases caused by POLG mutations. On the other, it opens up new perspectives for developing drugs or gene therapies capable of correcting or compensating for the defects caused by POLG mutations,” says Carlo Viscomi. “The study also highlights the value of animal models in investigating the mechanisms underlying these rare diseases, while accounting for interspecies differences. Understanding these differences is crucial for advancing research toward increasingly effective and personalized therapies.”

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Nuove prospettive terapeutiche dallo studio dei meccanismi di alcune malattie mitocondriali

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“Modelling POLG mutations in mice unravels a critical role of POLγΒ in regulating phenotypic severity” è il titolo dello studio pubblicato sulla prestigiosa rivista internazionale «Nature Communications» dal team di ricercatori guidato da Carlo Viscomi, professore associato al Dipartimento di Scienze biomediche dell’Università di Padova e Principal investigator dell’Istituto Veneto di Medicina Molecolare (VIMM).

Lo studio ha fatto luce su come mutazioni in un enzima fondamentale per la nostra salute, la DNA Polimerasi gamma (POLγ), possano causare gravi malattie mitocondriali. Questo enzima è responsabile della replicazione del DNA nei mitocondri, le "centrali energetiche" delle nostre cellule. Quando POLγ non funziona correttamente, il DNA mitocondriale diventa instabile, con conseguenze potenzialmente molto gravi per l’organismo.

Le malattie causate da mutazioni nel gene POLG sono molto eterogenee, e spesso difficili da diagnosticare a causa della complessità dei sintomi: la stessa mutazione può infatti provocare sintomi diversi in pazienti diversi. Inoltre non esistono cure, per cui i pazienti sono sottoposti solo a trattamenti per alleviare i sintomi.

Per cercare di capire meglio i meccanismi alla base di tale variabilità, i ricercatori hanno prodotto versioni mutate della proteina per analizzarne la struttura e la funzione, e hanno riprodotto le stesse mutazioni in modelli murini per osservare gli effetti sull’intero organismo.

Tutte le mutazioni analizzate riducono in modo significativo l’attività della POLγ. Utilizzando la microscopia crioelettronica, il team ha identificato differenze strutturali tra la proteina umana e quella murina, in particolare nella subunità accessoria chiamata POLγB. che ha la funzione di stabilizzare l’enzima. Queste differenze rendono l’enzima murino più resistente alle mutazioni rispetto a quella umana e spiegano perché nei topi le stesse mutazioni causano difetti meno gravi rispetto all’uomo. Nonostante questo, i modelli murini mantengono le caratteristiche essenziali delle malattie umane, quali instabilità del DNA mitocondriale e ridotta attività e stabilità dell’enzima.

“Questo studio è importante per due motivi. Da un lato, ci aiuta a capire meglio i meccanismi molecolari delle malattie dovute a mutazioni in POLG. Dall’altro, apre nuove prospettive per lo sviluppo di farmaci o terapie geniche in grado di correggere o compensare i difetti causati dalle mutazioni di POLG - sottolinea Carlo Viscomi -. Lo studio dimostra anche quanto siano utili i modelli animali per indagare i meccanismi alla base di queste malattie rare, pur tenendo conto delle differenze tra specie. Comprendere queste differenze è fondamentale per portare avanti la ricerca verso terapie sempre più efficaci e personalizzate.”

[summary] => [format] => 2 [safe_value] =>

“Modelling POLG mutations in mice unravels a critical role of POLγΒ in regulating phenotypic severity” è il titolo dello studio pubblicato sulla prestigiosa rivista internazionale «Nature Communications» dal team di ricercatori guidato da Carlo Viscomi, professore associato al Dipartimento di Scienze biomediche dell’Università di Padova e Principal investigator dell’Istituto Veneto di Medicina Molecolare (VIMM).

Lo studio ha fatto luce su come mutazioni in un enzima fondamentale per la nostra salute, la DNA Polimerasi gamma (POLγ), possano causare gravi malattie mitocondriali. Questo enzima è responsabile della replicazione del DNA nei mitocondri, le "centrali energetiche" delle nostre cellule. Quando POLγ non funziona correttamente, il DNA mitocondriale diventa instabile, con conseguenze potenzialmente molto gravi per l’organismo.

Le malattie causate da mutazioni nel gene POLG sono molto eterogenee, e spesso difficili da diagnosticare a causa della complessità dei sintomi: la stessa mutazione può infatti provocare sintomi diversi in pazienti diversi. Inoltre non esistono cure, per cui i pazienti sono sottoposti solo a trattamenti per alleviare i sintomi.

Per cercare di capire meglio i meccanismi alla base di tale variabilità, i ricercatori hanno prodotto versioni mutate della proteina per analizzarne la struttura e la funzione, e hanno riprodotto le stesse mutazioni in modelli murini per osservare gli effetti sull’intero organismo.

Tutte le mutazioni analizzate riducono in modo significativo l’attività della POLγ. Utilizzando la microscopia crioelettronica, il team ha identificato differenze strutturali tra la proteina umana e quella murina, in particolare nella subunità accessoria chiamata POLγB. che ha la funzione di stabilizzare l’enzima. Queste differenze rendono l’enzima murino più resistente alle mutazioni rispetto a quella umana e spiegano perché nei topi le stesse mutazioni causano difetti meno gravi rispetto all’uomo. Nonostante questo, i modelli murini mantengono le caratteristiche essenziali delle malattie umane, quali instabilità del DNA mitocondriale e ridotta attività e stabilità dell’enzima.

“Questo studio è importante per due motivi. Da un lato, ci aiuta a capire meglio i meccanismi molecolari delle malattie dovute a mutazioni in POLG. Dall’altro, apre nuove prospettive per lo sviluppo di farmaci o terapie geniche in grado di correggere o compensare i difetti causati dalle mutazioni di POLG - sottolinea Carlo Viscomi -. Lo studio dimostra anche quanto siano utili i modelli animali per indagare i meccanismi alla base di queste malattie rare, pur tenendo conto delle differenze tra specie. Comprendere queste differenze è fondamentale per portare avanti la ricerca verso terapie sempre più efficaci e personalizzate.”

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“Modelling POLG mutations in mice unravels a critical role of POLγΒ in regulating phenotypic severity” è il titolo dello studio pubblicato sulla prestigiosa rivista internazionale «Nature Communications» dal team di ricercatori guidato da Carlo Viscomi, professore associato al Dipartimento di Scienze biomediche dell’Università di Padova e Principal investigator dell’Istituto Veneto di Medicina Molecolare (VIMM).

Lo studio ha fatto luce su come mutazioni in un enzima fondamentale per la nostra salute, la DNA Polimerasi gamma (POLγ), possano causare gravi malattie mitocondriali. Questo enzima è responsabile della replicazione del DNA nei mitocondri, le "centrali energetiche" delle nostre cellule. Quando POLγ non funziona correttamente, il DNA mitocondriale diventa instabile, con conseguenze potenzialmente molto gravi per l’organismo.

Le malattie causate da mutazioni nel gene POLG sono molto eterogenee, e spesso difficili da diagnosticare a causa della complessità dei sintomi: la stessa mutazione può infatti provocare sintomi diversi in pazienti diversi. Inoltre non esistono cure, per cui i pazienti sono sottoposti solo a trattamenti per alleviare i sintomi.

Per cercare di capire meglio i meccanismi alla base di tale variabilità, i ricercatori hanno prodotto versioni mutate della proteina per analizzarne la struttura e la funzione, e hanno riprodotto le stesse mutazioni in modelli murini per osservare gli effetti sull’intero organismo.

Tutte le mutazioni analizzate riducono in modo significativo l’attività della POLγ. Utilizzando la microscopia crioelettronica, il team ha identificato differenze strutturali tra la proteina umana e quella murina, in particolare nella subunità accessoria chiamata POLγB. che ha la funzione di stabilizzare l’enzima. Queste differenze rendono l’enzima murino più resistente alle mutazioni rispetto a quella umana e spiegano perché nei topi le stesse mutazioni causano difetti meno gravi rispetto all’uomo. Nonostante questo, i modelli murini mantengono le caratteristiche essenziali delle malattie umane, quali instabilità del DNA mitocondriale e ridotta attività e stabilità dell’enzima.

“Questo studio è importante per due motivi. Da un lato, ci aiuta a capire meglio i meccanismi molecolari delle malattie dovute a mutazioni in POLG. Dall’altro, apre nuove prospettive per lo sviluppo di farmaci o terapie geniche in grado di correggere o compensare i difetti causati dalle mutazioni di POLG - sottolinea Carlo Viscomi -. Lo studio dimostra anche quanto siano utili i modelli animali per indagare i meccanismi alla base di queste malattie rare, pur tenendo conto delle differenze tra specie. Comprendere queste differenze è fondamentale per portare avanti la ricerca verso terapie sempre più efficaci e personalizzate.”

[summary] => [format] => 2 [safe_value] =>

“Modelling POLG mutations in mice unravels a critical role of POLγΒ in regulating phenotypic severity” è il titolo dello studio pubblicato sulla prestigiosa rivista internazionale «Nature Communications» dal team di ricercatori guidato da Carlo Viscomi, professore associato al Dipartimento di Scienze biomediche dell’Università di Padova e Principal investigator dell’Istituto Veneto di Medicina Molecolare (VIMM).

Lo studio ha fatto luce su come mutazioni in un enzima fondamentale per la nostra salute, la DNA Polimerasi gamma (POLγ), possano causare gravi malattie mitocondriali. Questo enzima è responsabile della replicazione del DNA nei mitocondri, le "centrali energetiche" delle nostre cellule. Quando POLγ non funziona correttamente, il DNA mitocondriale diventa instabile, con conseguenze potenzialmente molto gravi per l’organismo.

Le malattie causate da mutazioni nel gene POLG sono molto eterogenee, e spesso difficili da diagnosticare a causa della complessità dei sintomi: la stessa mutazione può infatti provocare sintomi diversi in pazienti diversi. Inoltre non esistono cure, per cui i pazienti sono sottoposti solo a trattamenti per alleviare i sintomi.

Per cercare di capire meglio i meccanismi alla base di tale variabilità, i ricercatori hanno prodotto versioni mutate della proteina per analizzarne la struttura e la funzione, e hanno riprodotto le stesse mutazioni in modelli murini per osservare gli effetti sull’intero organismo.

Tutte le mutazioni analizzate riducono in modo significativo l’attività della POLγ. Utilizzando la microscopia crioelettronica, il team ha identificato differenze strutturali tra la proteina umana e quella murina, in particolare nella subunità accessoria chiamata POLγB. che ha la funzione di stabilizzare l’enzima. Queste differenze rendono l’enzima murino più resistente alle mutazioni rispetto a quella umana e spiegano perché nei topi le stesse mutazioni causano difetti meno gravi rispetto all’uomo. Nonostante questo, i modelli murini mantengono le caratteristiche essenziali delle malattie umane, quali instabilità del DNA mitocondriale e ridotta attività e stabilità dell’enzima.

“Questo studio è importante per due motivi. Da un lato, ci aiuta a capire meglio i meccanismi molecolari delle malattie dovute a mutazioni in POLG. Dall’altro, apre nuove prospettive per lo sviluppo di farmaci o terapie geniche in grado di correggere o compensare i difetti causati dalle mutazioni di POLG - sottolinea Carlo Viscomi -. Lo studio dimostra anche quanto siano utili i modelli animali per indagare i meccanismi alla base di queste malattie rare, pur tenendo conto delle differenze tra specie. Comprendere queste differenze è fondamentale per portare avanti la ricerca verso terapie sempre più efficaci e personalizzate.”

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“Modelling POLG mutations in mice unravels a critical role of POLγΒ in regulating phenotypic severity” è il titolo dello studio pubblicato sulla prestigiosa rivista internazionale «Nature Communications» dal team di ricercatori guidato da Carlo Viscomi, professore associato al Dipartimento di Scienze biomediche dell’Università di Padova e Principal investigator dell’Istituto Veneto di Medicina Molecolare (VIMM).

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“Modelling POLG mutations in mice unravels a critical role of POLγΒ in regulating phenotypic severity” è il titolo dello studio pubblicato sulla prestigiosa rivista internazionale «Nature Communications» dal team di ricercatori guidato da Carlo Viscomi, professore associato al Dipartimento di Scienze biomediche dell’Università di Padova e Principal investigator dell’Istituto Veneto di Medicina Molecolare (VIMM).

Lo studio ha fatto luce su come mutazioni in un enzima fondamentale per la nostra salute, la DNA Polimerasi gamma (POLγ), possano causare gravi malattie mitocondriali. Questo enzima è responsabile della replicazione del DNA nei mitocondri, le "centrali energetiche" delle nostre cellule. Quando POLγ non funziona correttamente, il DNA mitocondriale diventa instabile, con conseguenze potenzialmente molto gravi per l’organismo.

Le malattie causate da mutazioni nel gene POLG sono molto eterogenee, e spesso difficili da diagnosticare a causa della complessità dei sintomi: la stessa mutazione può infatti provocare sintomi diversi in pazienti diversi. Inoltre non esistono cure, per cui i pazienti sono sottoposti solo a trattamenti per alleviare i sintomi.

Per cercare di capire meglio i meccanismi alla base di tale variabilità, i ricercatori hanno prodotto versioni mutate della proteina per analizzarne la struttura e la funzione, e hanno riprodotto le stesse mutazioni in modelli murini per osservare gli effetti sull’intero organismo.

Tutte le mutazioni analizzate riducono in modo significativo l’attività della POLγ. Utilizzando la microscopia crioelettronica, il team ha identificato differenze strutturali tra la proteina umana e quella murina, in particolare nella subunità accessoria chiamata POLγB. che ha la funzione di stabilizzare l’enzima. Queste differenze rendono l’enzima murino più resistente alle mutazioni rispetto a quella umana e spiegano perché nei topi le stesse mutazioni causano difetti meno gravi rispetto all’uomo. Nonostante questo, i modelli murini mantengono le caratteristiche essenziali delle malattie umane, quali instabilità del DNA mitocondriale e ridotta attività e stabilità dell’enzima.

“Questo studio è importante per due motivi. Da un lato, ci aiuta a capire meglio i meccanismi molecolari delle malattie dovute a mutazioni in POLG. Dall’altro, apre nuove prospettive per lo sviluppo di farmaci o terapie geniche in grado di correggere o compensare i difetti causati dalle mutazioni di POLG - sottolinea Carlo Viscomi -. Lo studio dimostra anche quanto siano utili i modelli animali per indagare i meccanismi alla base di queste malattie rare, pur tenendo conto delle differenze tra specie. Comprendere queste differenze è fondamentale per portare avanti la ricerca verso terapie sempre più efficaci e personalizzate.”

[summary] => [format] => 2 [safe_value] =>

“Modelling POLG mutations in mice unravels a critical role of POLγΒ in regulating phenotypic severity” è il titolo dello studio pubblicato sulla prestigiosa rivista internazionale «Nature Communications» dal team di ricercatori guidato da Carlo Viscomi, professore associato al Dipartimento di Scienze biomediche dell’Università di Padova e Principal investigator dell’Istituto Veneto di Medicina Molecolare (VIMM).

Lo studio ha fatto luce su come mutazioni in un enzima fondamentale per la nostra salute, la DNA Polimerasi gamma (POLγ), possano causare gravi malattie mitocondriali. Questo enzima è responsabile della replicazione del DNA nei mitocondri, le "centrali energetiche" delle nostre cellule. Quando POLγ non funziona correttamente, il DNA mitocondriale diventa instabile, con conseguenze potenzialmente molto gravi per l’organismo.

Le malattie causate da mutazioni nel gene POLG sono molto eterogenee, e spesso difficili da diagnosticare a causa della complessità dei sintomi: la stessa mutazione può infatti provocare sintomi diversi in pazienti diversi. Inoltre non esistono cure, per cui i pazienti sono sottoposti solo a trattamenti per alleviare i sintomi.

Per cercare di capire meglio i meccanismi alla base di tale variabilità, i ricercatori hanno prodotto versioni mutate della proteina per analizzarne la struttura e la funzione, e hanno riprodotto le stesse mutazioni in modelli murini per osservare gli effetti sull’intero organismo.

Tutte le mutazioni analizzate riducono in modo significativo l’attività della POLγ. Utilizzando la microscopia crioelettronica, il team ha identificato differenze strutturali tra la proteina umana e quella murina, in particolare nella subunità accessoria chiamata POLγB. che ha la funzione di stabilizzare l’enzima. Queste differenze rendono l’enzima murino più resistente alle mutazioni rispetto a quella umana e spiegano perché nei topi le stesse mutazioni causano difetti meno gravi rispetto all’uomo. Nonostante questo, i modelli murini mantengono le caratteristiche essenziali delle malattie umane, quali instabilità del DNA mitocondriale e ridotta attività e stabilità dell’enzima.

“Questo studio è importante per due motivi. Da un lato, ci aiuta a capire meglio i meccanismi molecolari delle malattie dovute a mutazioni in POLG. Dall’altro, apre nuove prospettive per lo sviluppo di farmaci o terapie geniche in grado di correggere o compensare i difetti causati dalle mutazioni di POLG - sottolinea Carlo Viscomi -. Lo studio dimostra anche quanto siano utili i modelli animali per indagare i meccanismi alla base di queste malattie rare, pur tenendo conto delle differenze tra specie. Comprendere queste differenze è fondamentale per portare avanti la ricerca verso terapie sempre più efficaci e personalizzate.”

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“Modelling POLG mutations in mice unravels a critical role of POLγΒ in regulating phenotypic severity” è il titolo dello studio pubblicato sulla prestigiosa rivista internazionale «Nature Communications» dal team di ricercatori guidato da Carlo Viscomi, professore associato al Dipartimento di Scienze biomediche dell’Università di Padova e Principal investigator dell’Istituto Veneto di Medicina Molecolare (VIMM).

Lo studio ha fatto luce su come mutazioni in un enzima fondamentale per la nostra salute, la DNA Polimerasi gamma (POLγ), possano causare gravi malattie mitocondriali. Questo enzima è responsabile della replicazione del DNA nei mitocondri, le "centrali energetiche" delle nostre cellule. Quando POLγ non funziona correttamente, il DNA mitocondriale diventa instabile, con conseguenze potenzialmente molto gravi per l’organismo.

Le malattie causate da mutazioni nel gene POLG sono molto eterogenee, e spesso difficili da diagnosticare a causa della complessità dei sintomi: la stessa mutazione può infatti provocare sintomi diversi in pazienti diversi. Inoltre non esistono cure, per cui i pazienti sono sottoposti solo a trattamenti per alleviare i sintomi.

Per cercare di capire meglio i meccanismi alla base di tale variabilità, i ricercatori hanno prodotto versioni mutate della proteina per analizzarne la struttura e la funzione, e hanno riprodotto le stesse mutazioni in modelli murini per osservare gli effetti sull’intero organismo.

Tutte le mutazioni analizzate riducono in modo significativo l’attività della POLγ. Utilizzando la microscopia crioelettronica, il team ha identificato differenze strutturali tra la proteina umana e quella murina, in particolare nella subunità accessoria chiamata POLγB. che ha la funzione di stabilizzare l’enzima. Queste differenze rendono l’enzima murino più resistente alle mutazioni rispetto a quella umana e spiegano perché nei topi le stesse mutazioni causano difetti meno gravi rispetto all’uomo. Nonostante questo, i modelli murini mantengono le caratteristiche essenziali delle malattie umane, quali instabilità del DNA mitocondriale e ridotta attività e stabilità dell’enzima.

“Questo studio è importante per due motivi. Da un lato, ci aiuta a capire meglio i meccanismi molecolari delle malattie dovute a mutazioni in POLG. Dall’altro, apre nuove prospettive per lo sviluppo di farmaci o terapie geniche in grado di correggere o compensare i difetti causati dalle mutazioni di POLG - sottolinea Carlo Viscomi -. Lo studio dimostra anche quanto siano utili i modelli animali per indagare i meccanismi alla base di queste malattie rare, pur tenendo conto delle differenze tra specie. Comprendere queste differenze è fondamentale per portare avanti la ricerca verso terapie sempre più efficaci e personalizzate.”

[summary] => [format] => 2 [safe_value] =>

“Modelling POLG mutations in mice unravels a critical role of POLγΒ in regulating phenotypic severity” è il titolo dello studio pubblicato sulla prestigiosa rivista internazionale «Nature Communications» dal team di ricercatori guidato da Carlo Viscomi, professore associato al Dipartimento di Scienze biomediche dell’Università di Padova e Principal investigator dell’Istituto Veneto di Medicina Molecolare (VIMM).

Lo studio ha fatto luce su come mutazioni in un enzima fondamentale per la nostra salute, la DNA Polimerasi gamma (POLγ), possano causare gravi malattie mitocondriali. Questo enzima è responsabile della replicazione del DNA nei mitocondri, le "centrali energetiche" delle nostre cellule. Quando POLγ non funziona correttamente, il DNA mitocondriale diventa instabile, con conseguenze potenzialmente molto gravi per l’organismo.

Le malattie causate da mutazioni nel gene POLG sono molto eterogenee, e spesso difficili da diagnosticare a causa della complessità dei sintomi: la stessa mutazione può infatti provocare sintomi diversi in pazienti diversi. Inoltre non esistono cure, per cui i pazienti sono sottoposti solo a trattamenti per alleviare i sintomi.

Per cercare di capire meglio i meccanismi alla base di tale variabilità, i ricercatori hanno prodotto versioni mutate della proteina per analizzarne la struttura e la funzione, e hanno riprodotto le stesse mutazioni in modelli murini per osservare gli effetti sull’intero organismo.

Tutte le mutazioni analizzate riducono in modo significativo l’attività della POLγ. Utilizzando la microscopia crioelettronica, il team ha identificato differenze strutturali tra la proteina umana e quella murina, in particolare nella subunità accessoria chiamata POLγB. che ha la funzione di stabilizzare l’enzima. Queste differenze rendono l’enzima murino più resistente alle mutazioni rispetto a quella umana e spiegano perché nei topi le stesse mutazioni causano difetti meno gravi rispetto all’uomo. Nonostante questo, i modelli murini mantengono le caratteristiche essenziali delle malattie umane, quali instabilità del DNA mitocondriale e ridotta attività e stabilità dell’enzima.

“Questo studio è importante per due motivi. Da un lato, ci aiuta a capire meglio i meccanismi molecolari delle malattie dovute a mutazioni in POLG. Dall’altro, apre nuove prospettive per lo sviluppo di farmaci o terapie geniche in grado di correggere o compensare i difetti causati dalle mutazioni di POLG - sottolinea Carlo Viscomi -. Lo studio dimostra anche quanto siano utili i modelli animali per indagare i meccanismi alla base di queste malattie rare, pur tenendo conto delle differenze tra specie. Comprendere queste differenze è fondamentale per portare avanti la ricerca verso terapie sempre più efficaci e personalizzate.”

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“Modelling POLG mutations in mice unravels a critical role of POLγΒ in regulating phenotypic severity” è il titolo dello studio pubblicato sulla prestigiosa rivista internazionale «Nature Communications» dal team di ricercatori guidato da Carlo Viscomi, professore associato al Dipartimento di Scienze biomediche dell’Università di Padova e Principal investigator dell’Istituto Veneto di Medicina Molecolare (VIMM).

Lo studio ha fatto luce su come mutazioni in un enzima fondamentale per la nostra salute, la DNA Polimerasi gamma (POLγ), possano causare gravi malattie mitocondriali. Questo enzima è responsabile della replicazione del DNA nei mitocondri, le "centrali energetiche" delle nostre cellule. Quando POLγ non funziona correttamente, il DNA mitocondriale diventa instabile, con conseguenze potenzialmente molto gravi per l’organismo.

Le malattie causate da mutazioni nel gene POLG sono molto eterogenee, e spesso difficili da diagnosticare a causa della complessità dei sintomi: la stessa mutazione può infatti provocare sintomi diversi in pazienti diversi. Inoltre non esistono cure, per cui i pazienti sono sottoposti solo a trattamenti per alleviare i sintomi.

Per cercare di capire meglio i meccanismi alla base di tale variabilità, i ricercatori hanno prodotto versioni mutate della proteina per analizzarne la struttura e la funzione, e hanno riprodotto le stesse mutazioni in modelli murini per osservare gli effetti sull’intero organismo.

Tutte le mutazioni analizzate riducono in modo significativo l’attività della POLγ. Utilizzando la microscopia crioelettronica, il team ha identificato differenze strutturali tra la proteina umana e quella murina, in particolare nella subunità accessoria chiamata POLγB. che ha la funzione di stabilizzare l’enzima. Queste differenze rendono l’enzima murino più resistente alle mutazioni rispetto a quella umana e spiegano perché nei topi le stesse mutazioni causano difetti meno gravi rispetto all’uomo. Nonostante questo, i modelli murini mantengono le caratteristiche essenziali delle malattie umane, quali instabilità del DNA mitocondriale e ridotta attività e stabilità dell’enzima.

“Questo studio è importante per due motivi. Da un lato, ci aiuta a capire meglio i meccanismi molecolari delle malattie dovute a mutazioni in POLG. Dall’altro, apre nuove prospettive per lo sviluppo di farmaci o terapie geniche in grado di correggere o compensare i difetti causati dalle mutazioni di POLG - sottolinea Carlo Viscomi -. Lo studio dimostra anche quanto siano utili i modelli animali per indagare i meccanismi alla base di queste malattie rare, pur tenendo conto delle differenze tra specie. Comprendere queste differenze è fondamentale per portare avanti la ricerca verso terapie sempre più efficaci e personalizzate.”

[summary] => [format] => 2 [safe_value] =>

“Modelling POLG mutations in mice unravels a critical role of POLγΒ in regulating phenotypic severity” è il titolo dello studio pubblicato sulla prestigiosa rivista internazionale «Nature Communications» dal team di ricercatori guidato da Carlo Viscomi, professore associato al Dipartimento di Scienze biomediche dell’Università di Padova e Principal investigator dell’Istituto Veneto di Medicina Molecolare (VIMM).

Lo studio ha fatto luce su come mutazioni in un enzima fondamentale per la nostra salute, la DNA Polimerasi gamma (POLγ), possano causare gravi malattie mitocondriali. Questo enzima è responsabile della replicazione del DNA nei mitocondri, le "centrali energetiche" delle nostre cellule. Quando POLγ non funziona correttamente, il DNA mitocondriale diventa instabile, con conseguenze potenzialmente molto gravi per l’organismo.

Le malattie causate da mutazioni nel gene POLG sono molto eterogenee, e spesso difficili da diagnosticare a causa della complessità dei sintomi: la stessa mutazione può infatti provocare sintomi diversi in pazienti diversi. Inoltre non esistono cure, per cui i pazienti sono sottoposti solo a trattamenti per alleviare i sintomi.

Per cercare di capire meglio i meccanismi alla base di tale variabilità, i ricercatori hanno prodotto versioni mutate della proteina per analizzarne la struttura e la funzione, e hanno riprodotto le stesse mutazioni in modelli murini per osservare gli effetti sull’intero organismo.

Tutte le mutazioni analizzate riducono in modo significativo l’attività della POLγ. Utilizzando la microscopia crioelettronica, il team ha identificato differenze strutturali tra la proteina umana e quella murina, in particolare nella subunità accessoria chiamata POLγB. che ha la funzione di stabilizzare l’enzima. Queste differenze rendono l’enzima murino più resistente alle mutazioni rispetto a quella umana e spiegano perché nei topi le stesse mutazioni causano difetti meno gravi rispetto all’uomo. Nonostante questo, i modelli murini mantengono le caratteristiche essenziali delle malattie umane, quali instabilità del DNA mitocondriale e ridotta attività e stabilità dell’enzima.

“Questo studio è importante per due motivi. Da un lato, ci aiuta a capire meglio i meccanismi molecolari delle malattie dovute a mutazioni in POLG. Dall’altro, apre nuove prospettive per lo sviluppo di farmaci o terapie geniche in grado di correggere o compensare i difetti causati dalle mutazioni di POLG - sottolinea Carlo Viscomi -. Lo studio dimostra anche quanto siano utili i modelli animali per indagare i meccanismi alla base di queste malattie rare, pur tenendo conto delle differenze tra specie. Comprendere queste differenze è fondamentale per portare avanti la ricerca verso terapie sempre più efficaci e personalizzate.”

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Selezione n. 2025S25

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Selezione pubblica n. 2025S25, per esami, per la stipula di n. 1 contratto di lavoro a termine nell'Area dei Funzionari, Settore Scientifico-tecnologico, a tempo parziale (18 ore), per n. 12 mesi, ai sensi del D.Lgs. 30.03.2001, n. 165 e s.m.i., del D.Lgs. 15.06.2015, n. 81, in quanto compatibile, e del C.C.N.L. del 18.01.2024, presso il Dipartimento di Ingegneria Civile, Edile e Ambientale – ICEA.

Tecnico a supporto dello sviluppo di scenari virtuali per lo studio dei comportamenti degli utenti del sistema dei trasporti

Scadenza: 30 giugno 2025, ore 14

[summary] => [format] => 2 [safe_value] =>

Selezione pubblica n. 2025S25, per esami, per la stipula di n. 1 contratto di lavoro a termine nell'Area dei Funzionari, Settore Scientifico-tecnologico, a tempo parziale (18 ore), per n. 12 mesi, ai sensi del D.Lgs. 30.03.2001, n. 165 e s.m.i., del D.Lgs. 15.06.2015, n. 81, in quanto compatibile, e del C.C.N.L. del 18.01.2024, presso il Dipartimento di Ingegneria Civile, Edile e Ambientale – ICEA.

Tecnico a supporto dello sviluppo di scenari virtuali per lo studio dei comportamenti degli utenti del sistema dei trasporti

Scadenza: 30 giugno 2025, ore 14

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Selezione pubblica n. 2025S25, per esami, per la stipula di n. 1 contratto di lavoro a termine nell'Area dei Funzionari, Settore Scientifico-tecnologico, a tempo parziale (18 ore), per n. 12 mesi, ai sensi del D.Lgs. 30.03.2001, n. 165 e s.m.i., del D.Lgs. 15.06.2015, n. 81, in quanto compatibile, e del C.C.N.L. del 18.01.2024, presso il Dipartimento di Ingegneria Civile, Edile e Ambientale – ICEA.

Tecnico a supporto dello sviluppo di scenari virtuali per lo studio dei comportamenti degli utenti del sistema dei trasporti

Scadenza: 30 giugno 2025, ore 14

[summary] => [format] => 2 [safe_value] =>

Selezione pubblica n. 2025S25, per esami, per la stipula di n. 1 contratto di lavoro a termine nell'Area dei Funzionari, Settore Scientifico-tecnologico, a tempo parziale (18 ore), per n. 12 mesi, ai sensi del D.Lgs. 30.03.2001, n. 165 e s.m.i., del D.Lgs. 15.06.2015, n. 81, in quanto compatibile, e del C.C.N.L. del 18.01.2024, presso il Dipartimento di Ingegneria Civile, Edile e Ambientale – ICEA.

Tecnico a supporto dello sviluppo di scenari virtuali per lo studio dei comportamenti degli utenti del sistema dei trasporti

Scadenza: 30 giugno 2025, ore 14

[safe_summary] => ) ) [#formatter] => text_summary_or_trimmed [0] => Array ( [#markup] =>

Selezione pubblica n. 2025S25, per esami, per la stipula di n. 1 contratto di lavoro a termine nell'Area dei Funzionari, Settore Scientifico-tecnologico, a tempo parziale (18 ore), per n. 12 mesi, ai sensi del D.Lgs. 30.03.2001, n. 165 e s.m.i., del D.Lgs. 15.06.2015, n. 81, in quanto compatibile, e del C.C.N.L. del 18.01.2024, presso il Dipartimento di Ingegneria Civile, Edile e Ambientale – ICEA.

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2025S25-Documenti

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Per partecipare alla selezione è necessario compilare e presentare la domanda attraverso la procedura online.

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[summary] => [format] => 2 [safe_value] =>

Per partecipare alla selezione è necessario compilare e presentare la domanda attraverso la procedura online.

Leggere attentamente le istruzioni.

Procedura telematica di compilazione e presentazione della domanda

La procedura di compilazione e l'invio telematico della domanda dovranno essere completati entro la data di scadenza del Bando.

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Per partecipare alla selezione è necessario compilare e presentare la domanda attraverso la procedura online.

Leggere attentamente le istruzioni.

Procedura telematica di compilazione e presentazione della domanda

La procedura di compilazione e l'invio telematico della domanda dovranno essere completati entro la data di scadenza del Bando.

[summary] => [format] => 2 [safe_value] =>

Per partecipare alla selezione è necessario compilare e presentare la domanda attraverso la procedura online.

Leggere attentamente le istruzioni.

Procedura telematica di compilazione e presentazione della domanda

La procedura di compilazione e l'invio telematico della domanda dovranno essere completati entro la data di scadenza del Bando.

[safe_summary] => ) ) [#formatter] => text_summary_or_trimmed [0] => Array ( [#markup] =>

Per partecipare alla selezione è necessario compilare e presentare la domanda attraverso la procedura online.

Leggere attentamente le istruzioni.

Procedura telematica di compilazione e presentazione della domanda

La procedura di compilazione e l'invio telematico della domanda dovranno essere completati entro la data di scadenza del Bando.

) ) [links] => Array ( [#theme] => links__node [#pre_render] => Array ( [0] => drupal_pre_render_links ) [#attributes] => Array ( [class] => Array ( [0] => links [1] => inline ) ) [node] => Array ( [#theme] => links__node__node [#links] => Array ( [node-readmore] => Array ( [title] => Read more about 2025S25-Documenti [href] => node/119160 [html] => 1 [attributes] => Array ( [rel] => tag [title] => 2025S25-Documenti ) ) ) [#attributes] => Array ( [class] => Array ( [0] => links [1] => inline ) ) ) ) )

2025S25-Prove

Array ( [body] => Array ( [#theme] => field [#weight] => 0 [#title] => Body [#access] => 1 [#label_display] => hidden [#view_mode] => teaser [#language] => und [#field_name] => body [#field_type] => text_with_summary [#field_translatable] => 0 [#entity_type] => node [#bundle] => tab [#object] => stdClass Object ( [vid] => 493685 [uid] => 26499 [title] => 2025S25-Prove [log] => [status] => 1 [comment] => 0 [promote] => 1 [sticky] => 0 [nid] => 119159 [type] => tab [language] => it [created] => 1749464840 [changed] => 1751458568 [tnid] => 0 [translate] => 0 [revision_timestamp] => 1751458568 [revision_uid] => 26499 [body] => Array ( [und] => Array ( [0] => Array ( [value] =>

La selezione è per prova scritta e colloquio.
Le prove d'esame consistono in:

  • prova scritta con quesiti a risposta aperta, che potranno vertere sui seguenti argomenti:

- teoria e tecnica della circolazione stradale;
- progettazione e implementazione di esperimenti di laboratorio con riferimento ai comportamenti degli utenti dei sistemi di trasporto;
- strumenti per lo sviluppo di ambienti in realtà virtuale;
- elementi di statistica descrittiva e inferenziale.

  • colloquio, che potrà vertere sui seguenti argomenti:

- progettazione e implementazione di esperimenti di laboratorio con riferimento ai comportamenti degli utenti dei sistemi di trasporto;
- modellistica dei sistemi di trasporto;
- sistemi di basi di dati (linguaggio SQL);
- sistemi informativi geografici;
- normativa nazionale in tema di sicurezza degli ambienti di lavoro (in particolare: D.Lgs. n. 81/2008 e s.m.i.).
Verrà accertata la conoscenza della lingua inglese (livello di riferimento B2).

Calendario prove d'esame

- prova scritta: 22 luglio 2025, ore 15:00, presso Pineca – stanza P44, Dipartimento di Ingegneria Civile Edile e Ambientale – ICEA, Via Marzolo n. 9 Padova
- colloquio: 24 luglio 2025, ore 15:00 (e, se necessario, potrà proseguire nei giorni successivi), presso Sala Polivalente, Dipartimento di Ingegneria Civile Edile e Ambientale – ICEA, Via Marzolo n. 9 Padova

[summary] => [format] => 2 [safe_value] =>

La selezione è per prova scritta e colloquio.
Le prove d'esame consistono in:

  • prova scritta con quesiti a risposta aperta, che potranno vertere sui seguenti argomenti:

- teoria e tecnica della circolazione stradale;
- progettazione e implementazione di esperimenti di laboratorio con riferimento ai comportamenti degli utenti dei sistemi di trasporto;
- strumenti per lo sviluppo di ambienti in realtà virtuale;
- elementi di statistica descrittiva e inferenziale.

  • colloquio, che potrà vertere sui seguenti argomenti:

- progettazione e implementazione di esperimenti di laboratorio con riferimento ai comportamenti degli utenti dei sistemi di trasporto;
- modellistica dei sistemi di trasporto;
- sistemi di basi di dati (linguaggio SQL);
- sistemi informativi geografici;
- normativa nazionale in tema di sicurezza degli ambienti di lavoro (in particolare: D.Lgs. n. 81/2008 e s.m.i.).
Verrà accertata la conoscenza della lingua inglese (livello di riferimento B2).

Calendario prove d'esame

- prova scritta: 22 luglio 2025, ore 15:00, presso Pineca – stanza P44, Dipartimento di Ingegneria Civile Edile e Ambientale – ICEA, Via Marzolo n. 9 Padova
- colloquio: 24 luglio 2025, ore 15:00 (e, se necessario, potrà proseguire nei giorni successivi), presso Sala Polivalente, Dipartimento di Ingegneria Civile Edile e Ambientale – ICEA, Via Marzolo n. 9 Padova

[safe_summary] => ) ) ) [field_foglia_complessa_allegato] => Array ( ) [field_tabella] => Array ( ) [field_titolo_frontend] => Array ( [und] => Array ( [0] => Array ( [value] => Prove [format] => [safe_value] => Prove ) ) ) [name] => rossella.vezzosi [picture] => 0 [data] => b:0; [num_revisions] => 1 [current_revision_id] => 493685 [is_current] => 1 [is_pending] => [revision_moderation] => [entity_view_prepared] => 1 ) [#items] => Array ( [0] => Array ( [value] =>

La selezione è per prova scritta e colloquio.
Le prove d'esame consistono in:

  • prova scritta con quesiti a risposta aperta, che potranno vertere sui seguenti argomenti:

- teoria e tecnica della circolazione stradale;
- progettazione e implementazione di esperimenti di laboratorio con riferimento ai comportamenti degli utenti dei sistemi di trasporto;
- strumenti per lo sviluppo di ambienti in realtà virtuale;
- elementi di statistica descrittiva e inferenziale.

  • colloquio, che potrà vertere sui seguenti argomenti:

- progettazione e implementazione di esperimenti di laboratorio con riferimento ai comportamenti degli utenti dei sistemi di trasporto;
- modellistica dei sistemi di trasporto;
- sistemi di basi di dati (linguaggio SQL);
- sistemi informativi geografici;
- normativa nazionale in tema di sicurezza degli ambienti di lavoro (in particolare: D.Lgs. n. 81/2008 e s.m.i.).
Verrà accertata la conoscenza della lingua inglese (livello di riferimento B2).

Calendario prove d'esame

- prova scritta: 22 luglio 2025, ore 15:00, presso Pineca – stanza P44, Dipartimento di Ingegneria Civile Edile e Ambientale – ICEA, Via Marzolo n. 9 Padova
- colloquio: 24 luglio 2025, ore 15:00 (e, se necessario, potrà proseguire nei giorni successivi), presso Sala Polivalente, Dipartimento di Ingegneria Civile Edile e Ambientale – ICEA, Via Marzolo n. 9 Padova

[summary] => [format] => 2 [safe_value] =>

La selezione è per prova scritta e colloquio.
Le prove d'esame consistono in:

  • prova scritta con quesiti a risposta aperta, che potranno vertere sui seguenti argomenti:

- teoria e tecnica della circolazione stradale;
- progettazione e implementazione di esperimenti di laboratorio con riferimento ai comportamenti degli utenti dei sistemi di trasporto;
- strumenti per lo sviluppo di ambienti in realtà virtuale;
- elementi di statistica descrittiva e inferenziale.

  • colloquio, che potrà vertere sui seguenti argomenti:

- progettazione e implementazione di esperimenti di laboratorio con riferimento ai comportamenti degli utenti dei sistemi di trasporto;
- modellistica dei sistemi di trasporto;
- sistemi di basi di dati (linguaggio SQL);
- sistemi informativi geografici;
- normativa nazionale in tema di sicurezza degli ambienti di lavoro (in particolare: D.Lgs. n. 81/2008 e s.m.i.).
Verrà accertata la conoscenza della lingua inglese (livello di riferimento B2).

Calendario prove d'esame

- prova scritta: 22 luglio 2025, ore 15:00, presso Pineca – stanza P44, Dipartimento di Ingegneria Civile Edile e Ambientale – ICEA, Via Marzolo n. 9 Padova
- colloquio: 24 luglio 2025, ore 15:00 (e, se necessario, potrà proseguire nei giorni successivi), presso Sala Polivalente, Dipartimento di Ingegneria Civile Edile e Ambientale – ICEA, Via Marzolo n. 9 Padova

[safe_summary] => ) ) [#formatter] => text_summary_or_trimmed [0] => Array ( [#markup] =>

La selezione è per prova scritta e colloquio.
Le prove d'esame consistono in:

  • prova scritta con quesiti a risposta aperta, che potranno vertere sui seguenti argomenti:

- teoria e tecnica della circolazione stradale;
- progettazione e implementazione di esperimenti di laboratorio con riferimento ai comportamenti degli utenti dei sistemi di trasporto;
- strumenti per lo sviluppo di ambienti in realtà virtuale;
- elementi di statistica descrittiva e inferenziale.

) ) [links] => Array ( [#theme] => links__node [#pre_render] => Array ( [0] => drupal_pre_render_links ) [#attributes] => Array ( [class] => Array ( [0] => links [1] => inline ) ) [node] => Array ( [#theme] => links__node__node [#links] => Array ( [node-readmore] => Array ( [title] => Read more about 2025S25-Prove [href] => node/119159 [html] => 1 [attributes] => Array ( [rel] => tag [title] => 2025S25-Prove ) ) ) [#attributes] => Array ( [class] => Array ( [0] => links [1] => inline ) ) ) ) )

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