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81.
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Nils Bomer Niels Grote Beverborg Martijn F. Hoes Koen W. Streng Mathilde Vermeer Martin M. Dokter Jan IJmker Stefan D. Anker John G.F. Cleland Hans L. Hillege Chim C. Lang Leong L. Ng Nilesh J. Samani Jasper Tromp Dirk J. van Veldhuisen Daan J. Touw Adriaan A. Voors Peter van der Meer 《European journal of heart failure》2020,22(8):1415-1423
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Renhai Cao Hong Ji Ninghan Feng Yin Zhang Xiaojuan Yang Patrik Andersson Yuping Sun Katerina Tritsaris Anker Jon Hansen Steen Dissing Yihai Cao 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(39):15894-15899
Interplay between various lymphangiogenic factors in promoting lymphangiogenesis and lymphatic metastasis remains poorly understood. Here we show that FGF-2 and VEGF-C, two lymphangiogenic factors, collaboratively promote angiogenesis and lymphangiogenesis in the tumor microenvironment, leading to widespread pulmonary and lymph-node metastases. Coimplantation of dual factors in the mouse cornea resulted in additive angiogenesis and lymphangiogenesis. At the molecular level, we showed that FGFR-1 expressed in lymphatic endothelial cells is a crucial receptor that mediates the FGF-2–induced lymphangiogenesis. Intriguingly, the VEGFR-3–mediated signaling was required for the lymphatic tip cell formation in both FGF-2– and VEGF-C–induced lymphangiogenesis. Consequently, a VEGFR-3–specific neutralizing antibody markedly inhibited FGF-2–induced lymphangiogenesis. Thus, the VEGFR-3–induced lymphatic endothelial cell tip cell formation is a prerequisite for FGF-2–stimulated lymphangiogenesis. In the tumor microenvironment, the reciprocal interplay between FGF-2 and VEGF-C collaboratively stimulated tumor growth, angiogenesis, intratumoral lymphangiogenesis, and metastasis. Thus, intervention and targeting of the FGF-2– and VEGF-C–induced angiogenic and lymphangiogenic synergism could be potentially important approaches for cancer therapy and prevention of metastasis. 相似文献
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Stephan von Haehling Joerg C. Schefold Ewa A. Jankowska Jochen Springer Ali Vazir Paul R. Kalra Anja Sandek Günter Fauler Tatjana Stojakovic Michael Trauner Piotr Ponikowski Hans-Dieter Volk Wolfram Doehner Andrew J.S. Coats Philip A. Poole-Wilson Stefan D. Anker 《Journal of the American College of Cardiology》2012
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PS Spencer K Vandemaele M Richer VS Palmer S Chungong M Anker Y Ayana ML Opoka BN Klaucke A Quarello JK Tumwine 《African health sciences》2013,13(2):183-204
Background
Nodding Syndrome is a seizure disorder of children in Mundri County, Western Equatoria, South Sudan. The disorder is reported to be spreading in South Sudan and northern Uganda.Objective
To describe environmental, nutritional, infectious, and other factors that existed before and during the de novo 1991 appearance and subsequent increase in cases through 2001.Methods
Household surveys, informant interviews, and case-control studies conducted in Lui town and Amadi village in 2001–2002 were supplemented in 2012 by informant interviews in Lui and Juba, South Sudan.Results
Nodding Syndrome was associated with Onchocerca volvulus and Mansonella perstans infections, with food use of a variety of sorghum (serena) introduced as part of an emergency relief program, and was inversely associated with a history of measles infection. There was no evidence to suggest exposure to a manmade neurotoxic pollutant or chemical agent, other than chemically dressed seed intended for planting but used for food. Food use of cyanogenic plants was documented, and exposure to fungal contaminants could not be excluded.Conclusion
Nodding Syndrome in South Sudan has an unknown etiology. Further research is recommended on the association of Nodding Syndrome with onchocerciasis/mansonelliasis and neurotoxins in plant materials used for food. 相似文献89.
90.
Macdougall IC Canaud B de Francisco AL Filippatos G Ponikowski P Silverberg D van Veldhuisen DJ Anker SD 《European journal of heart failure》2012,14(8):882-886
Growing awareness that heart failure, renal impairment, and anaemia are frequent co‐morbidities which can exacerbate one another in a vicious circle of clinical deterioration has led to the concept of the cardiorenal anaemia syndrome (CRAS). The role of iron deficiency within this complex interplay has been less well examined. Scrutiny of data from the recent FAIR‐HF trial raises a new hypothesis: is it time for ‘CRAS’ to be supplemented with new acronyms such as CRIDS (cardiorenal–iron deficiency syndrome) or even CRAIDS (cardiorenal–anaemia–iron deficiency syndrome)? Iron deficiency occurs frequently in heart failure patients with or without anaemia. It not only impairs oxygen transport through reduced erythropoiesis, but adversely affects oxidative metabolism, cellular energetics, and immune mechanisms, and the synthesis and degradation of complex molecules such as DNA. One large observational study in patients with heart failure found iron deficiency to be an independent predictor of death or urgent heart transplantation (hazard ratio 1.58, 95% confidence interval 1.14–2.17, P = 0.005). In the FAIR‐HF trial, i.v. iron therapy was associated with significant improvements in physical functioning in iron‐deficient patients with heart failure, even in non‐anaemic patients in whom haemoglobin levels did not change following i.v. iron administration. Key questions regarding the use of i.v. iron supplementation in the setting of heart failure merit exploration and could readily be answered by appropriately designed clinical trials. It is to be hoped that these important clinical trials are conducted, to permit a more subtle characterization of the patient's pathological condition and interventional requirements. 相似文献