Salvador, Brazil

Federal University of Bahia

www.portal.ufba.br
Salvador, Brazil

The Federal University of Bahia is a public university located mainly in the city of Salvador. It is the largest university of the state of Bahia.Students can study there without paying tuition fees, as it is a public university. To join the university they must pass an annual examination, known as the "vestibular". Wikipedia.

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SAN DIEGO, May 11, 2017 (GLOBE NEWSWIRE) -- TRACON Pharmaceuticals (NASDAQ:TCON), a clinical stage biopharmaceutical company focused on the development and commercialization of novel targeted therapeutics for cancer, wet age-related macular degeneration (AMD) and fibrotic diseases, announced today that preclinical data indicating the potential clinical utility of targeting endoglin in acute myeloid leukemia (AML) and B-cell acute lymphoblastic leukemia (B-cell ALL), was published in the May 4, 2017 issue of Blood (Volume 129, Number 19, pages 2526-2536), a weekly medical journal of the American Society of Hematology. Dr. Rita Perlingeiro, Professor of Medicine, and colleagues of the University of Minnesota, along with collaborators at the Federal University of Bahia (Salvador, Brazil) and the Laboratory for the Diagnosis of Onco-Hematological Disorders (Curitiba, Brazil), identified endoglin expression on the majority of blasts from patients with AML and B-cell ALL. These endoglin expressing blasts were shown to have superior leukemogenic activity. Furthermore, the researchers demonstrated that TRACON’s endoglin antibody, TRC105, prevented the engraftment of primary AML blasts, and inhibited leukemic progression following disease establishment in mice. In both AML and B-cell ALL, TRC105 synergized with reduced intensity myeloablation to inhibit leukemogenesis in the mouse model. “We have been studying the function of endoglin in hematopoiesis for more than a decade, and the consistent expression of this receptor in the majority of acute leukemias was intriguing. Our hypothesis that endoglin expression was linked to leukemia-forming activity was proven to be true, and it was even more rewarding to witness the robust anti-leukemogenic effect of blocking endoglin signalling with TRC105, even when leukemia had already been established in the mouse,” said Dr. Perlingeiro. “We are thrilled with the potential of our basic research to contribute to the development of a new line of therapy for patients with AML and B-cell ALL.” “We are pleased to see that this promising research, conducted by Dr. Perlingeiro and her collaborators, has been published in Blood,” said Charles Theuer, M.D., Ph.D., President and CEO of TRACON. “AML and B-cell ALL represent hematologic malignancies with high unmet need and, as this data indicate, the potential utility of directly targeting endoglin may represent an additional development opportunity for TRC105.” TRC105 is a novel, clinical stage antibody to endoglin, a protein overexpressed on proliferating endothelial cells that is essential for angiogenesis, the process of new blood vessel formation. TRC105 is currently being studied in one Phase 3 and multiple Phase 2 clinical trials sponsored by TRACON or the National Cancer Institute for the treatment of solid tumors in combination with VEGF inhibitors. TRC105 has received orphan designation for the treatment of soft tissue sarcoma in both the U.S. and EU. The ophthalmic formulation of TRC105, DE-122, is currently in a Phase 1/2 trial for patients with wet AMD. TRC205, a second generation antibody to endoglin, is undergoing preclinical testing in models of fibrosis. For more information about the clinical trials, please visit TRACON’s website at www.traconpharma.com/clinical_trials.php. TRACON develops targeted therapies for cancer, ophthalmic and fibrotic diseases. The Company’s clinical-stage pipeline includes: TRC105, an endoglin antibody that is being developed for the treatment of multiple cancers; DE-122, the ophthalmic formulation of TRC105 that is being developed in wet AMD through a collaboration with Santen Pharmaceutical Company Ltd.; TRC102, a small molecule that is being developed for the treatment of lung cancer and glioblastoma; and TRC253, a small molecule that is being developed for the treatment of prostate cancer. To learn more about TRACON and its product candidates, visit TRACON's website at www.traconpharma.com. Statements made in this press release regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward‐looking statements. Such statements include, but are not limited to, statements regarding the potential benefits of TRC105 (including its potential to be developed as a treatment for AML and B-cell ALL), TRACON's plans to further develop its product candidates and expectations regarding the initiation, design and timing of future clinical trials by TRACON or third parties. Risks that could cause actual results to differ from those expressed in these forward‐looking statements include: risks associated with clinical development; whether TRACON or others will initiate or complete additional preclinical studies or clinical trials; the fact that future preclinical studies and clinical trials may not be successful or otherwise consistent with results from prior studies; potential changes in regulatory requirements in the United States and foreign countries; TRACON’s reliance on third parties for the development of its product candidates, including the conduct of its clinical trials and manufacture of its product candidates; whether TRACON will be able to obtain additional financing; and other risks described in TRACON’s filings with the Securities and Exchange Commission under the heading “Risk Factors.” All forward‐looking statements contained in this press release speak only as of the date on which they were made and are based on management’s assumptions and estimates as of such date. TRACON undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made.


SAN DIEGO, May 11, 2017 (GLOBE NEWSWIRE) -- TRACON Pharmaceuticals (NASDAQ:TCON), a clinical stage biopharmaceutical company focused on the development and commercialization of novel targeted therapeutics for cancer, wet age-related macular degeneration (AMD) and fibrotic diseases, announced today that preclinical data indicating the potential clinical utility of targeting endoglin in acute myeloid leukemia (AML) and B-cell acute lymphoblastic leukemia (B-cell ALL), was published in the May 4, 2017 issue of Blood (Volume 129, Number 19, pages 2526-2536), a weekly medical journal of the American Society of Hematology. Dr. Rita Perlingeiro, Professor of Medicine, and colleagues of the University of Minnesota, along with collaborators at the Federal University of Bahia (Salvador, Brazil) and the Laboratory for the Diagnosis of Onco-Hematological Disorders (Curitiba, Brazil), identified endoglin expression on the majority of blasts from patients with AML and B-cell ALL. These endoglin expressing blasts were shown to have superior leukemogenic activity. Furthermore, the researchers demonstrated that TRACON’s endoglin antibody, TRC105, prevented the engraftment of primary AML blasts, and inhibited leukemic progression following disease establishment in mice. In both AML and B-cell ALL, TRC105 synergized with reduced intensity myeloablation to inhibit leukemogenesis in the mouse model. “We have been studying the function of endoglin in hematopoiesis for more than a decade, and the consistent expression of this receptor in the majority of acute leukemias was intriguing. Our hypothesis that endoglin expression was linked to leukemia-forming activity was proven to be true, and it was even more rewarding to witness the robust anti-leukemogenic effect of blocking endoglin signalling with TRC105, even when leukemia had already been established in the mouse,” said Dr. Perlingeiro. “We are thrilled with the potential of our basic research to contribute to the development of a new line of therapy for patients with AML and B-cell ALL.” “We are pleased to see that this promising research, conducted by Dr. Perlingeiro and her collaborators, has been published in Blood,” said Charles Theuer, M.D., Ph.D., President and CEO of TRACON. “AML and B-cell ALL represent hematologic malignancies with high unmet need and, as this data indicate, the potential utility of directly targeting endoglin may represent an additional development opportunity for TRC105.” TRC105 is a novel, clinical stage antibody to endoglin, a protein overexpressed on proliferating endothelial cells that is essential for angiogenesis, the process of new blood vessel formation. TRC105 is currently being studied in one Phase 3 and multiple Phase 2 clinical trials sponsored by TRACON or the National Cancer Institute for the treatment of solid tumors in combination with VEGF inhibitors. TRC105 has received orphan designation for the treatment of soft tissue sarcoma in both the U.S. and EU. The ophthalmic formulation of TRC105, DE-122, is currently in a Phase 1/2 trial for patients with wet AMD. TRC205, a second generation antibody to endoglin, is undergoing preclinical testing in models of fibrosis. For more information about the clinical trials, please visit TRACON’s website at www.traconpharma.com/clinical_trials.php. TRACON develops targeted therapies for cancer, ophthalmic and fibrotic diseases. The Company’s clinical-stage pipeline includes: TRC105, an endoglin antibody that is being developed for the treatment of multiple cancers; DE-122, the ophthalmic formulation of TRC105 that is being developed in wet AMD through a collaboration with Santen Pharmaceutical Company Ltd.; TRC102, a small molecule that is being developed for the treatment of lung cancer and glioblastoma; and TRC253, a small molecule that is being developed for the treatment of prostate cancer. To learn more about TRACON and its product candidates, visit TRACON's website at www.traconpharma.com. Statements made in this press release regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward‐looking statements. Such statements include, but are not limited to, statements regarding the potential benefits of TRC105 (including its potential to be developed as a treatment for AML and B-cell ALL), TRACON's plans to further develop its product candidates and expectations regarding the initiation, design and timing of future clinical trials by TRACON or third parties. Risks that could cause actual results to differ from those expressed in these forward‐looking statements include: risks associated with clinical development; whether TRACON or others will initiate or complete additional preclinical studies or clinical trials; the fact that future preclinical studies and clinical trials may not be successful or otherwise consistent with results from prior studies; potential changes in regulatory requirements in the United States and foreign countries; TRACON’s reliance on third parties for the development of its product candidates, including the conduct of its clinical trials and manufacture of its product candidates; whether TRACON will be able to obtain additional financing; and other risks described in TRACON’s filings with the Securities and Exchange Commission under the heading “Risk Factors.” All forward‐looking statements contained in this press release speak only as of the date on which they were made and are based on management’s assumptions and estimates as of such date. TRACON undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made.


SAN DIEGO, May 11, 2017 (GLOBE NEWSWIRE) -- TRACON Pharmaceuticals (NASDAQ:TCON), a clinical stage biopharmaceutical company focused on the development and commercialization of novel targeted therapeutics for cancer, wet age-related macular degeneration (AMD) and fibrotic diseases, announced today that preclinical data indicating the potential clinical utility of targeting endoglin in acute myeloid leukemia (AML) and B-cell acute lymphoblastic leukemia (B-cell ALL), was published in the May 4, 2017 issue of Blood (Volume 129, Number 19, pages 2526-2536), a weekly medical journal of the American Society of Hematology. Dr. Rita Perlingeiro, Professor of Medicine, and colleagues of the University of Minnesota, along with collaborators at the Federal University of Bahia (Salvador, Brazil) and the Laboratory for the Diagnosis of Onco-Hematological Disorders (Curitiba, Brazil), identified endoglin expression on the majority of blasts from patients with AML and B-cell ALL. These endoglin expressing blasts were shown to have superior leukemogenic activity. Furthermore, the researchers demonstrated that TRACON’s endoglin antibody, TRC105, prevented the engraftment of primary AML blasts, and inhibited leukemic progression following disease establishment in mice. In both AML and B-cell ALL, TRC105 synergized with reduced intensity myeloablation to inhibit leukemogenesis in the mouse model. “We have been studying the function of endoglin in hematopoiesis for more than a decade, and the consistent expression of this receptor in the majority of acute leukemias was intriguing. Our hypothesis that endoglin expression was linked to leukemia-forming activity was proven to be true, and it was even more rewarding to witness the robust anti-leukemogenic effect of blocking endoglin signalling with TRC105, even when leukemia had already been established in the mouse,” said Dr. Perlingeiro. “We are thrilled with the potential of our basic research to contribute to the development of a new line of therapy for patients with AML and B-cell ALL.” “We are pleased to see that this promising research, conducted by Dr. Perlingeiro and her collaborators, has been published in Blood,” said Charles Theuer, M.D., Ph.D., President and CEO of TRACON. “AML and B-cell ALL represent hematologic malignancies with high unmet need and, as this data indicate, the potential utility of directly targeting endoglin may represent an additional development opportunity for TRC105.” TRC105 is a novel, clinical stage antibody to endoglin, a protein overexpressed on proliferating endothelial cells that is essential for angiogenesis, the process of new blood vessel formation. TRC105 is currently being studied in one Phase 3 and multiple Phase 2 clinical trials sponsored by TRACON or the National Cancer Institute for the treatment of solid tumors in combination with VEGF inhibitors. TRC105 has received orphan designation for the treatment of soft tissue sarcoma in both the U.S. and EU. The ophthalmic formulation of TRC105, DE-122, is currently in a Phase 1/2 trial for patients with wet AMD. TRC205, a second generation antibody to endoglin, is undergoing preclinical testing in models of fibrosis. For more information about the clinical trials, please visit TRACON’s website at www.traconpharma.com/clinical_trials.php. TRACON develops targeted therapies for cancer, ophthalmic and fibrotic diseases. The Company’s clinical-stage pipeline includes: TRC105, an endoglin antibody that is being developed for the treatment of multiple cancers; DE-122, the ophthalmic formulation of TRC105 that is being developed in wet AMD through a collaboration with Santen Pharmaceutical Company Ltd.; TRC102, a small molecule that is being developed for the treatment of lung cancer and glioblastoma; and TRC253, a small molecule that is being developed for the treatment of prostate cancer. To learn more about TRACON and its product candidates, visit TRACON's website at www.traconpharma.com. Statements made in this press release regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward‐looking statements. Such statements include, but are not limited to, statements regarding the potential benefits of TRC105 (including its potential to be developed as a treatment for AML and B-cell ALL), TRACON's plans to further develop its product candidates and expectations regarding the initiation, design and timing of future clinical trials by TRACON or third parties. Risks that could cause actual results to differ from those expressed in these forward‐looking statements include: risks associated with clinical development; whether TRACON or others will initiate or complete additional preclinical studies or clinical trials; the fact that future preclinical studies and clinical trials may not be successful or otherwise consistent with results from prior studies; potential changes in regulatory requirements in the United States and foreign countries; TRACON’s reliance on third parties for the development of its product candidates, including the conduct of its clinical trials and manufacture of its product candidates; whether TRACON will be able to obtain additional financing; and other risks described in TRACON’s filings with the Securities and Exchange Commission under the heading “Risk Factors.” All forward‐looking statements contained in this press release speak only as of the date on which they were made and are based on management’s assumptions and estimates as of such date. TRACON undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made.


SAN DIEGO, May 11, 2017 (GLOBE NEWSWIRE) -- TRACON Pharmaceuticals (NASDAQ:TCON), a clinical stage biopharmaceutical company focused on the development and commercialization of novel targeted therapeutics for cancer, wet age-related macular degeneration (AMD) and fibrotic diseases, announced today that preclinical data indicating the potential clinical utility of targeting endoglin in acute myeloid leukemia (AML) and B-cell acute lymphoblastic leukemia (B-cell ALL), was published in the May 4, 2017 issue of Blood (Volume 129, Number 19, pages 2526-2536), a weekly medical journal of the American Society of Hematology. Dr. Rita Perlingeiro, Professor of Medicine, and colleagues of the University of Minnesota, along with collaborators at the Federal University of Bahia (Salvador, Brazil) and the Laboratory for the Diagnosis of Onco-Hematological Disorders (Curitiba, Brazil), identified endoglin expression on the majority of blasts from patients with AML and B-cell ALL. These endoglin expressing blasts were shown to have superior leukemogenic activity. Furthermore, the researchers demonstrated that TRACON’s endoglin antibody, TRC105, prevented the engraftment of primary AML blasts, and inhibited leukemic progression following disease establishment in mice. In both AML and B-cell ALL, TRC105 synergized with reduced intensity myeloablation to inhibit leukemogenesis in the mouse model. “We have been studying the function of endoglin in hematopoiesis for more than a decade, and the consistent expression of this receptor in the majority of acute leukemias was intriguing. Our hypothesis that endoglin expression was linked to leukemia-forming activity was proven to be true, and it was even more rewarding to witness the robust anti-leukemogenic effect of blocking endoglin signalling with TRC105, even when leukemia had already been established in the mouse,” said Dr. Perlingeiro. “We are thrilled with the potential of our basic research to contribute to the development of a new line of therapy for patients with AML and B-cell ALL.” “We are pleased to see that this promising research, conducted by Dr. Perlingeiro and her collaborators, has been published in Blood,” said Charles Theuer, M.D., Ph.D., President and CEO of TRACON. “AML and B-cell ALL represent hematologic malignancies with high unmet need and, as this data indicate, the potential utility of directly targeting endoglin may represent an additional development opportunity for TRC105.” TRC105 is a novel, clinical stage antibody to endoglin, a protein overexpressed on proliferating endothelial cells that is essential for angiogenesis, the process of new blood vessel formation. TRC105 is currently being studied in one Phase 3 and multiple Phase 2 clinical trials sponsored by TRACON or the National Cancer Institute for the treatment of solid tumors in combination with VEGF inhibitors. TRC105 has received orphan designation for the treatment of soft tissue sarcoma in both the U.S. and EU. The ophthalmic formulation of TRC105, DE-122, is currently in a Phase 1/2 trial for patients with wet AMD. TRC205, a second generation antibody to endoglin, is undergoing preclinical testing in models of fibrosis. For more information about the clinical trials, please visit TRACON’s website at www.traconpharma.com/clinical_trials.php. TRACON develops targeted therapies for cancer, ophthalmic and fibrotic diseases. The Company’s clinical-stage pipeline includes: TRC105, an endoglin antibody that is being developed for the treatment of multiple cancers; DE-122, the ophthalmic formulation of TRC105 that is being developed in wet AMD through a collaboration with Santen Pharmaceutical Company Ltd.; TRC102, a small molecule that is being developed for the treatment of lung cancer and glioblastoma; and TRC253, a small molecule that is being developed for the treatment of prostate cancer. To learn more about TRACON and its product candidates, visit TRACON's website at www.traconpharma.com. Statements made in this press release regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward‐looking statements. Such statements include, but are not limited to, statements regarding the potential benefits of TRC105 (including its potential to be developed as a treatment for AML and B-cell ALL), TRACON's plans to further develop its product candidates and expectations regarding the initiation, design and timing of future clinical trials by TRACON or third parties. Risks that could cause actual results to differ from those expressed in these forward‐looking statements include: risks associated with clinical development; whether TRACON or others will initiate or complete additional preclinical studies or clinical trials; the fact that future preclinical studies and clinical trials may not be successful or otherwise consistent with results from prior studies; potential changes in regulatory requirements in the United States and foreign countries; TRACON’s reliance on third parties for the development of its product candidates, including the conduct of its clinical trials and manufacture of its product candidates; whether TRACON will be able to obtain additional financing; and other risks described in TRACON’s filings with the Securities and Exchange Commission under the heading “Risk Factors.” All forward‐looking statements contained in this press release speak only as of the date on which they were made and are based on management’s assumptions and estimates as of such date. TRACON undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made.


SAN DIEGO, May 11, 2017 (GLOBE NEWSWIRE) -- TRACON Pharmaceuticals (NASDAQ:TCON), a clinical stage biopharmaceutical company focused on the development and commercialization of novel targeted therapeutics for cancer, wet age-related macular degeneration (AMD) and fibrotic diseases, announced today that preclinical data indicating the potential clinical utility of targeting endoglin in acute myeloid leukemia (AML) and B-cell acute lymphoblastic leukemia (B-cell ALL), was published in the May 4, 2017 issue of Blood (Volume 129, Number 19, pages 2526-2536), a weekly medical journal of the American Society of Hematology. Dr. Rita Perlingeiro, Professor of Medicine, and colleagues of the University of Minnesota, along with collaborators at the Federal University of Bahia (Salvador, Brazil) and the Laboratory for the Diagnosis of Onco-Hematological Disorders (Curitiba, Brazil), identified endoglin expression on the majority of blasts from patients with AML and B-cell ALL. These endoglin expressing blasts were shown to have superior leukemogenic activity. Furthermore, the researchers demonstrated that TRACON’s endoglin antibody, TRC105, prevented the engraftment of primary AML blasts, and inhibited leukemic progression following disease establishment in mice. In both AML and B-cell ALL, TRC105 synergized with reduced intensity myeloablation to inhibit leukemogenesis in the mouse model. “We have been studying the function of endoglin in hematopoiesis for more than a decade, and the consistent expression of this receptor in the majority of acute leukemias was intriguing. Our hypothesis that endoglin expression was linked to leukemia-forming activity was proven to be true, and it was even more rewarding to witness the robust anti-leukemogenic effect of blocking endoglin signalling with TRC105, even when leukemia had already been established in the mouse,” said Dr. Perlingeiro. “We are thrilled with the potential of our basic research to contribute to the development of a new line of therapy for patients with AML and B-cell ALL.” “We are pleased to see that this promising research, conducted by Dr. Perlingeiro and her collaborators, has been published in Blood,” said Charles Theuer, M.D., Ph.D., President and CEO of TRACON. “AML and B-cell ALL represent hematologic malignancies with high unmet need and, as this data indicate, the potential utility of directly targeting endoglin may represent an additional development opportunity for TRC105.” TRC105 is a novel, clinical stage antibody to endoglin, a protein overexpressed on proliferating endothelial cells that is essential for angiogenesis, the process of new blood vessel formation. TRC105 is currently being studied in one Phase 3 and multiple Phase 2 clinical trials sponsored by TRACON or the National Cancer Institute for the treatment of solid tumors in combination with VEGF inhibitors. TRC105 has received orphan designation for the treatment of soft tissue sarcoma in both the U.S. and EU. The ophthalmic formulation of TRC105, DE-122, is currently in a Phase 1/2 trial for patients with wet AMD. TRC205, a second generation antibody to endoglin, is undergoing preclinical testing in models of fibrosis. For more information about the clinical trials, please visit TRACON’s website at www.traconpharma.com/clinical_trials.php. TRACON develops targeted therapies for cancer, ophthalmic and fibrotic diseases. The Company’s clinical-stage pipeline includes: TRC105, an endoglin antibody that is being developed for the treatment of multiple cancers; DE-122, the ophthalmic formulation of TRC105 that is being developed in wet AMD through a collaboration with Santen Pharmaceutical Company Ltd.; TRC102, a small molecule that is being developed for the treatment of lung cancer and glioblastoma; and TRC253, a small molecule that is being developed for the treatment of prostate cancer. To learn more about TRACON and its product candidates, visit TRACON's website at www.traconpharma.com. Statements made in this press release regarding matters that are not historical facts are “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. Because such statements are subject to risks and uncertainties, actual results may differ materially from those expressed or implied by such forward‐looking statements. Such statements include, but are not limited to, statements regarding the potential benefits of TRC105 (including its potential to be developed as a treatment for AML and B-cell ALL), TRACON's plans to further develop its product candidates and expectations regarding the initiation, design and timing of future clinical trials by TRACON or third parties. Risks that could cause actual results to differ from those expressed in these forward‐looking statements include: risks associated with clinical development; whether TRACON or others will initiate or complete additional preclinical studies or clinical trials; the fact that future preclinical studies and clinical trials may not be successful or otherwise consistent with results from prior studies; potential changes in regulatory requirements in the United States and foreign countries; TRACON’s reliance on third parties for the development of its product candidates, including the conduct of its clinical trials and manufacture of its product candidates; whether TRACON will be able to obtain additional financing; and other risks described in TRACON’s filings with the Securities and Exchange Commission under the heading “Risk Factors.” All forward‐looking statements contained in this press release speak only as of the date on which they were made and are based on management’s assumptions and estimates as of such date. TRACON undertakes no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made.


Chan F.K.-M.,University of Massachusetts Medical School | Luz N.F.,University of Massachusetts Medical School | Luz N.F.,Federal University of Bahia | Moriwaki K.,University of Massachusetts Medical School
Annual Review of Immunology | Year: 2015

Cell proliferation and cell death are integral elements in maintaining homeostatic balance in metazoans. Disease pathologies ensue when these processes are disturbed. A plethora of evidence indicates that malfunction of cell death can lead to inflammation, autoimmunity, or immunodeficiency. Programmed necrosis or necroptosis is a form of nonapoptotic cell death driven by the receptor interacting protein kinase 3 (RIPK3) and its substrate, mixed lineage kinase domain-like (MLKL). RIPK3 partners with its upstream adaptors RIPK1, TRIF, or DAI to signal for necroptosis in response to death receptor or Toll-like receptor stimulation, pathogen infection, or sterile cell injury. Necroptosis promotes inflammation through leakage of cellular contents from damaged plasma membranes. Intriguingly, many of the signal adaptors of necroptosis have dual functions in innate immune signaling. This unique signature illustrates the cooperative nature of necroptosis and innate inflammatory signaling pathways in managing cell and organismal stresses from pathogen infection and sterile tissue injury. © 2015 by Annual Reviews. All rights reserved.


Abreu L.M.,Federal University of Bahia
Journal of Physics: Conference Series | Year: 2016

In this work we investigate deuteron-like molecules with both open charm and bottom, within the framework of the Heavy Meson Effective Theory. Using the available information of some exotic hadronic states as inputs to fix the coupling constants of the theory, we analyze the formation of loosely-bound D (∗) B (∗)-states and estimate their relevant properties. © Published under licence by IOP Publishing Ltd.


Grant
Agency: European Commission | Branch: H2020 | Program: ERC-ADG | Phase: ERC-ADG-2014 | Award Amount: 2.35M | Year: 2016

Fifteen years ago it was widely believed that asthma was an allergic/atopic disease caused by allergen exposure in infancy; this produced atopic sensitization and continued exposure resulted in eosinophilic airways inflammation, bronchial hyper-responsiveness and reversible airflow obstruction. It is now clear that this model is at best incomplete. Less than one-half of asthma cases involve allergic (atopic) mechanisms, and most asthma in low-and-middle income countries is non-atopic. Westernization may be contributing to the global increases in asthma prevalence, but this process appears to involve changes in asthma susceptibility rather than increased exposure to established asthma risk factors. Understanding why these changes are occurring is essential in order to halt the growing global asthma epidemic.This will require a combination of epidemiological, clinical and basic science studies in a variety of environments. A key task is to reclassify asthma phenotypes. These are important to: (i) better understand the aetiological mechanisms of asthma; (ii) identify new causes; and (iii) identify new therapeutic measures. There are major opportunities to address these issues using new techniques for sample collection from the airways (sputum induction, nasal lavage), new methods of analysis (microbiome, epigenetics), and new bioinformatics methods for integrating data from multiple sources and levels. There is an unprecedented potential to go beyond the old atopic/non-atopic categorization of phenotypes. I will therefore conduct analyses to re-examine and reclassify asthma phenotypes. The key features are the inclusion of: (i) both high and low prevalence centres from both high income countries and low-and-middle income countries; (ii) much more detailed biomarker information than has been used for previous studies of asthma phenotypes; and (iii) new bioinformatics methods for integrating data from multiple sources and levels.


Perelo L.W.,Federal University of Bahia
Journal of Hazardous Materials | Year: 2010

Organic pollutants in sediments are a worldwide problem because sediments act as sinks for hydrophobic, recalcitrant and hazardous compounds. Depending on biogeochemical processes these hydrocarbons are involved in adsorption, desorption and transformation processes and can be made available to benthic organisms as well as organisms in the water column through the sediment-water interface. Most of these recalcitrant hydrocarbons are toxic and carcinogenic, they may enter the food-chain and accumulate in biological tissue. Several approaches are being investigated or have been already used to remove organic hydrocarbons from sediments. This paper provides a review on types and sources of organic pollutants as well as their behavior in sediments. It presents the advantages and disadvantages of traditional sediment remediation techniques in use, such as dredging, capping and monitored natural attenuation. Furthermore, it describes new approaches with emphasis on bioremediation, like biostimulation, bioaugmentation and phytoremediation applied to sediments. These new techniques promise to be of lower impact and more cost efficient than traditional management strategies. © 2009.


Oliveira B.G.D.,Federal University of Bahia
Physical Chemistry Chemical Physics | Year: 2013

In this paper, the intermolecular structural study asserted by the vibrational analysis in the stretch frequencies of hydrogen bonds (π⋯H) and dihydrogen bonds (H-δ⋯H +δ) have definitively been revisited by means of calculations carried out by Density Functional Theory (DFT) and topological parameters derived from the classic treatise of the Quantum Theory of Atoms in Molecules (QTAIM). As a matter of fact the π⋯H hydrogen bond is formed between the hydrofluoric acid and the CC bond of the acetylene, but the QTAIM calculations revealed a distortion in this interaction due to the formation of the ternary complex C2H2⋯2(HF). Although the π bonds of ethylene (C2H4), propylene (C2H 3(CH3)), and t-butylene (C2H 2(CH3)2) are considered proton acceptors, two hydrogen-bond types - π⋯H and C⋯H - can be observed. Over and above the analysis of the π hydrogen bonds, theoretical arguments also were used to discuss the red-shifts in the stretch frequencies of the binary dihydrogen complexes formed by BeH2⋯HX with X = F, Cl, CN, and CCH. Although a vibrational blue-shift in the stretch frequency of the H-C bond of HCF3 due to the formation of the BeH2⋯HCF 3 dihydrogen complex was obtained, unmistakable red-shifts were detected in LiH⋯HCF3, MgH2⋯HCF3, and NaH⋯HCF3. Moreover, the alkali-halogen bonds were identified in relation to the formation of the trimolecular systems NaH⋯2(HCF3) and NaH⋯2(HCCl3). At last, theoretical calculations and QTAIM molecular integrations were used to study a novel class of dihydrogen-bonded complexes (mC2H5 + ⋯nMgH2 with m = 1 or 2 and n = 1 or 2) based in the insight that MgH2 can bind with the non-localized hydrogen H +δ of the ethyl cation (C2H5 +). In an overview, QTAIM calculations were applied to evaluate the molecular topography, charge density, as well as to interpret the shifted frequencies either to red or blue caused by the formation of the hydrogen bonds and dihydrogen bonds. © the Owner Societies 2013.

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