Project acronym TERAMIX
Project Study of Novel Low Noise Superconducting Mixers for Terahertz Radio Astronomy
Researcher (PI) Sergey Cherednichenko
Host Institution (HI) CHALMERS TEKNISKA HOEGSKOLA AB
Call Details Starting Grant (StG), PE9, ERC-2012-StG_20111012
Summary "Terahertz heterodyne receivers are valuable tools for molecular gas spectroscopy both for space (radioastronomy, planetary science) and terrestrial applications. They provide both high resolution spectral data, as well as broad bandwidth line survey data. Due to the progress in device physics, such receivers can now reach several THz. At such high radio frequencies, neither electronic nor photonic approaches for THz detectors work, but rather a combination of both is required. Superconducting devices have proven to provide sensitivity levels close to the quantum limit, hf/k. Superconducting Hot- Electron Bolometers (HEB) based on ultrathin NbN and NbTiN films are currently the only devices which are used as mixers for frequencies above 1.2THz (SIS mixer limit). However, their speed (i.e. the instantaneous bandwidth) is limited by the finite electron energy relaxation rate, of 40-100 ps. It corresponds to the bandwidth of maximum 4-5GHz. Such applications in radio astronomy as extragalactic spectroscopy, molecular line survey require this bandwidth to be doubled to say at least. In this project we will investigate response rate in ultra thin MgB2 superconducting films. Preliminary investigation measured the electron-phonon interaction time as short as 1ps. Our recent data, point out on the response rate being limited by the phonon dynamic in the thick films. We will develop technology for ultrathin MgB2 film deposition, and processing THz nanobolometers. The response rate will be investigated with regards to the film parameters. In particularly, the phonon diffusion in superconducting nanobolometers will be studied in order to enhance the instantaneous bandwidth of MgB2 mixers. We estimate that the bandwidth of the novel THz detectors will be at least doubled compared to the existing once, providing completely new functionalities for THz radio astronomical receivers."
Summary
"Terahertz heterodyne receivers are valuable tools for molecular gas spectroscopy both for space (radioastronomy, planetary science) and terrestrial applications. They provide both high resolution spectral data, as well as broad bandwidth line survey data. Due to the progress in device physics, such receivers can now reach several THz. At such high radio frequencies, neither electronic nor photonic approaches for THz detectors work, but rather a combination of both is required. Superconducting devices have proven to provide sensitivity levels close to the quantum limit, hf/k. Superconducting Hot- Electron Bolometers (HEB) based on ultrathin NbN and NbTiN films are currently the only devices which are used as mixers for frequencies above 1.2THz (SIS mixer limit). However, their speed (i.e. the instantaneous bandwidth) is limited by the finite electron energy relaxation rate, of 40-100 ps. It corresponds to the bandwidth of maximum 4-5GHz. Such applications in radio astronomy as extragalactic spectroscopy, molecular line survey require this bandwidth to be doubled to say at least. In this project we will investigate response rate in ultra thin MgB2 superconducting films. Preliminary investigation measured the electron-phonon interaction time as short as 1ps. Our recent data, point out on the response rate being limited by the phonon dynamic in the thick films. We will develop technology for ultrathin MgB2 film deposition, and processing THz nanobolometers. The response rate will be investigated with regards to the film parameters. In particularly, the phonon diffusion in superconducting nanobolometers will be studied in order to enhance the instantaneous bandwidth of MgB2 mixers. We estimate that the bandwidth of the novel THz detectors will be at least doubled compared to the existing once, providing completely new functionalities for THz radio astronomical receivers."
Max ERC Funding
1 497 775 €
Duration
Start date: 2012-10-01, End date: 2017-09-30
Project acronym ToMeTuM
Project Towards the Understanding a Metal-Tumour-Metabolism
Researcher (PI) Vojtech Adam
Host Institution (HI) VYSOKE UCENI TECHNICKE V BRNE
Call Details Starting Grant (StG), LS7, ERC-2017-STG
Summary A tumour cell uses both genetic and protein weapons in its development. Gaining a greater understanding of these lethal mechanisms is a key step towards developing novel and more effective treatments. Because the metal ion metabolism of a tumour cell is not fully understood, we will address the challenge of explaining the mechanisms of how a tumour cell copes both with essential metal ions and platinum based drugs. The metal-based mechanisms help a tumour to grow on one side and to protect itself against commonly used metal-based drugs. On the other side, the exact description of these mechanisms, which are being associated with multi-drug resistance occurrence and failure of a treatment, still remains unclear. We will reveal the mechanism of the as yet not understood biochemical and molecularly-biological relationships and correlations between metal ions and proteins in a tumour development revealing the way how to suppress the growth and development of a tumour and to markedly enhance the effectiveness of a treatment.
To achieve this goal, we will focus on metallothionein and its interactions with essential metals and metal-containing anticancer drugs (cisplatin, carboplatin, and oxaliplatin). Their actions will be monitored both in vitro and in vivo. For this purpose, we will optimize electrochemical, mass spectrometric and immune-based methods. Based on processing of data obtained, new carcinogenetic pathways will be sought on cell level and proved by genetic modifications of target genes. The discovered processes and the pathways found will then be tested on two animal experimental models mice bearing breast tumours (MCF-7 and 4T1) and MeLiM minipigs bearing melanomas.
The precise description of the tumour related pathways coping with metal ions based on metallothioneins will direct new highly effective treatment strategies. Moreover, the discovery of new carcinogenetic pathways will open a window for understanding of cancer formation and development.
Summary
A tumour cell uses both genetic and protein weapons in its development. Gaining a greater understanding of these lethal mechanisms is a key step towards developing novel and more effective treatments. Because the metal ion metabolism of a tumour cell is not fully understood, we will address the challenge of explaining the mechanisms of how a tumour cell copes both with essential metal ions and platinum based drugs. The metal-based mechanisms help a tumour to grow on one side and to protect itself against commonly used metal-based drugs. On the other side, the exact description of these mechanisms, which are being associated with multi-drug resistance occurrence and failure of a treatment, still remains unclear. We will reveal the mechanism of the as yet not understood biochemical and molecularly-biological relationships and correlations between metal ions and proteins in a tumour development revealing the way how to suppress the growth and development of a tumour and to markedly enhance the effectiveness of a treatment.
To achieve this goal, we will focus on metallothionein and its interactions with essential metals and metal-containing anticancer drugs (cisplatin, carboplatin, and oxaliplatin). Their actions will be monitored both in vitro and in vivo. For this purpose, we will optimize electrochemical, mass spectrometric and immune-based methods. Based on processing of data obtained, new carcinogenetic pathways will be sought on cell level and proved by genetic modifications of target genes. The discovered processes and the pathways found will then be tested on two animal experimental models mice bearing breast tumours (MCF-7 and 4T1) and MeLiM minipigs bearing melanomas.
The precise description of the tumour related pathways coping with metal ions based on metallothioneins will direct new highly effective treatment strategies. Moreover, the discovery of new carcinogenetic pathways will open a window for understanding of cancer formation and development.
Max ERC Funding
1 377 495 €
Duration
Start date: 2018-01-01, End date: 2022-12-31
Project acronym TRIBAL
Project A TRranslational approach to Identify Biomarkers for Asthma and Lung function impairment
Researcher (PI) Per Erik MELEN
Host Institution (HI) KAROLINSKA INSTITUTET
Call Details Starting Grant (StG), LS7, ERC-2017-STG
Summary Asthma is a chronic inflammatory disease of the airways that cause symptoms like wheezing and breathlessness. In children, asthma is the most common chronic disease and according to the WHO, more than 300 million people are affected globally. There is no curative treatment available. Persistence of childhood asthma into adult life is associated with lung function impairment and increased risk of chronic obstructive pulmonary disease, COPD. Evidence is now emerging that adult diseases, like COPD, may have their origin early in life. However, there are no established biomarkers that can accurately monitor asthma progression or predict development of COPD in adults. In this TRIBAL project, I will capitalize on rich longitudinal data and repeated bio-sampling from the Swedish BAMSE study, a world-leading population-based birth cohort of 4,089 participants with a new 24-year follow-up starting in 2017. A key aim with the new follow-up is to identify young adults in their 20s with persistent asthma and pre-stage COPD by advanced lung function assessment that includes bronchodilator and nitrogen washout tests. In TRIBAL, the unique setup is deep phenotyping of these patients describing different aspects of the respiratory system, as well as molecular characteristics of relevant bio-samples and cells. Disease-related biomarkers and involved mechanisms, from gene to protein, will be identified from early childhood to adulthood. Both the innate and the adapted immune system with detailed cell characterization will be explored in relation to exposure and disease development. Specifically, with this novel approach I will address the time point during childhood when disease processes related to persistent asthma and pre-stage COPD were initiated. The ultimate goal in TRIBAL is to provide new knowledge for targeted preventive efforts in children at risk of adult chronic lung disease, and to identify potential targets for new asthma and COPD drugs.
Summary
Asthma is a chronic inflammatory disease of the airways that cause symptoms like wheezing and breathlessness. In children, asthma is the most common chronic disease and according to the WHO, more than 300 million people are affected globally. There is no curative treatment available. Persistence of childhood asthma into adult life is associated with lung function impairment and increased risk of chronic obstructive pulmonary disease, COPD. Evidence is now emerging that adult diseases, like COPD, may have their origin early in life. However, there are no established biomarkers that can accurately monitor asthma progression or predict development of COPD in adults. In this TRIBAL project, I will capitalize on rich longitudinal data and repeated bio-sampling from the Swedish BAMSE study, a world-leading population-based birth cohort of 4,089 participants with a new 24-year follow-up starting in 2017. A key aim with the new follow-up is to identify young adults in their 20s with persistent asthma and pre-stage COPD by advanced lung function assessment that includes bronchodilator and nitrogen washout tests. In TRIBAL, the unique setup is deep phenotyping of these patients describing different aspects of the respiratory system, as well as molecular characteristics of relevant bio-samples and cells. Disease-related biomarkers and involved mechanisms, from gene to protein, will be identified from early childhood to adulthood. Both the innate and the adapted immune system with detailed cell characterization will be explored in relation to exposure and disease development. Specifically, with this novel approach I will address the time point during childhood when disease processes related to persistent asthma and pre-stage COPD were initiated. The ultimate goal in TRIBAL is to provide new knowledge for targeted preventive efforts in children at risk of adult chronic lung disease, and to identify potential targets for new asthma and COPD drugs.
Max ERC Funding
1 500 000 €
Duration
Start date: 2017-12-01, End date: 2022-11-30
Project acronym UBIQCANCER
Project THE ROLE OF UBIQUITYLATION AND DEUBIQUITINATION ENZYMES IN CANCER
Researcher (PI) Ramin Masoumi
Host Institution (HI) LUNDS UNIVERSITET
Call Details Starting Grant (StG), LS7, ERC-2010-StG_20091118
Summary The overall goal of my research is to identify and characterize genetic factors leading to tumor development in human by establishing mouse models for development of anticancer drugs. The objective of the present study is to understand the function of ubiquitin ligation enzymes and deubiquitin enzymes during progression of different human skin cancers. This is analysed by generating transgenic animals and applying tumour-promoting protocol to specifically dissect the role of these enzymes during progression of cancer on mouse skin. During the proposed studies, mice deficient in various ubiquitin mediated signaling molecules such as CYLD and Bcl-3 will be used to test their contribution to cancer development. In addition we will identify novel E3 ligation and deubiquitination enzymes involved in progression of skin cancer using a multidisciplinary approach that combines mouse genetic, masspectrometry in vivo and gene expression profiling. To correlate information obtained from animal model to the development of treatments of human cancer, we are generating human tissue platforms from skin cancer patients regenerated on immune deficient mice. This model enables to study human epithelial neoplasms under in situ conditions. The results obtained in the transgenic animals as well as human tissue platform are correlated and compared to the samples from melanoma and non-melanoma human cancer patients. Furthermore, transgenic animals and transplanted human tissues are treated with proposed drug before tumor induction to test their specificity. Using state-of-the-art approaches and techniques, this project will identify novel markers for improved diagnosis and validation of candidate drug target for skin cancer therapies.
Summary
The overall goal of my research is to identify and characterize genetic factors leading to tumor development in human by establishing mouse models for development of anticancer drugs. The objective of the present study is to understand the function of ubiquitin ligation enzymes and deubiquitin enzymes during progression of different human skin cancers. This is analysed by generating transgenic animals and applying tumour-promoting protocol to specifically dissect the role of these enzymes during progression of cancer on mouse skin. During the proposed studies, mice deficient in various ubiquitin mediated signaling molecules such as CYLD and Bcl-3 will be used to test their contribution to cancer development. In addition we will identify novel E3 ligation and deubiquitination enzymes involved in progression of skin cancer using a multidisciplinary approach that combines mouse genetic, masspectrometry in vivo and gene expression profiling. To correlate information obtained from animal model to the development of treatments of human cancer, we are generating human tissue platforms from skin cancer patients regenerated on immune deficient mice. This model enables to study human epithelial neoplasms under in situ conditions. The results obtained in the transgenic animals as well as human tissue platform are correlated and compared to the samples from melanoma and non-melanoma human cancer patients. Furthermore, transgenic animals and transplanted human tissues are treated with proposed drug before tumor induction to test their specificity. Using state-of-the-art approaches and techniques, this project will identify novel markers for improved diagnosis and validation of candidate drug target for skin cancer therapies.
Max ERC Funding
1 067 280 €
Duration
Start date: 2011-04-01, End date: 2016-03-31
