Four Chinese nationals have been charged with visa fraud after revelations that they sent information on the layout of US labs and research carried out by colleagues back to China.
The French government this week unveiled a draft science bill that promises to increase public research spending with an extra €25 billion over the next ten years.
Scientists found that M2 compared to M1 macrophage-conditioned media upregulated neonatal cardiomyocyte proliferation, suppressed myofibroblast-induced differentiation and stimulated endothelial cell tube formation.
For the hundreds of thousands of people enrolling in clinical trials every year—and for whom experimental therapies can offer a last hope—a new report provides some welcome news: Enrollment in clinical studies in the United States is on the rebound after disruptions caused by the COVID-19 pandemic.
The authors demonstrated interfacing of cardiomyocytes derived from human induced pluripotent stem cells, which were engineered to express Channelrhodopsin-2.
[npj Flexible Electronics]
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Athanasiadis, M., Afanasenkau, D., Derks, W., Tondera, C., Murganti, F., Busskamp, V., Bergmann, O., & Minev, I. R. (2020). Printed elastic membranes for multimodal pacing and recording of human stem-cell-derived cardiomyocytes. Npj Flexible Electronics, 4(1), 1–8. https://doi.org/10.1038/s41528-020-0075-z Cite
A historic €1.8-trillion (US$2.1-trillion) budget deal reached by European Union (EU) leaders to fund its next seven years — and its recovery from the coronavirus pandemic — has left scientists and research advocates disappointed.
Researchers report successful protection from doxorubicin in two independent human pluripotent stem cell-derived cardiomyocyte lines, using two potent, highly selective MAP4K4 inhibitors.
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Golforoush, P. A., Narasimhan, P., Chaves-Guerrero, P. P., Lawrence, E., Newton, G., Yan, R., Harding, S. E., Perrior, T., Chapman, K. L., & Schneider, M. D. (2020). Selective protection of human cardiomyocytes from anthracycline cardiotoxicity by small molecule inhibitors of MAP4K4. Scientific Reports, 10(1), 12060. https://doi.org/10.1038/s41598-020-68907-1 Cite
Scientists describe maturation media designed to provide oxidative substrates adapted to the metabolic needs of human induced pluripotent stem cell-derived cardiomyocytes.
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Feyen, D. A. M., McKeithan, W. L., Bruyneel, A. A. N., Spiering, S., Hörmann, L., Ulmer, B., Zhang, H., Briganti, F., Schweizer, M., Hegyi, B., Liao, Z., Pölönen, R.-P., Ginsburg, K. S., Lam, C. K., Serrano, R., Wahlquist, C., Kreymerman, A., Vu, M., Amatya, P. L., … Mercola, M. (2020). Metabolic Maturation Media Improve Physiological Function of Human iPSC-Derived Cardiomyocytes. Cell Reports, 32(3). https://doi.org/10.1016/j.celrep.2020.107925 Cite
Investigators showed that knockdown of Drosophila cofilin, an actin depolymerizing factor, disrupted both sarcomere structure and muscle function.
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Balakrishnan, M., Yu, S. F., Chin, S. M., Soffar, D. B., Windner, S. E., Goode, B. L., & Baylies, M. K. (2020). Cofilin Loss in Drosophila Muscles Contributes to Muscle Weakness through Defective Sarcomerogenesis during Muscle Growth. Cell Reports, 32(3). https://doi.org/10.1016/j.celrep.2020.107893 Cite
The authors revealed significant response differences between airway smooth muscle cells from asthma cases and controls, including genes implicated in asthma susceptibility.
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Thompson, E. E., Dang, Q., Mitchell-Handley, B., Rajendran, K., Ram-Mohan, S., Solway, J., Ober, C., & Krishnan, R. (2020). Cytokine-induced molecular responses in airway smooth muscle cells inform genome-wide association studies of asthma. Genome Medicine, 12(1), 64. https://doi.org/10.1186/s13073-020-00759-w Cite
Investigators determined the role of lysosomal-associated transmembrane protein 4B (LAPTM4B) in the regulation of autophagic flux and myocardial ischemia/reperfusion injury.
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Gu Shanshan, Tan Jiliang, Li Qiang, Liu Shenyan, Ma Jian, Zheng Yanjun, Liu Jinlong, Bi Wei, Sha Ping, Li Xuxia, Wei Meng, Cao Nan, & Yang Huang-Tian. (n.d.). Downregulation of LAPTM4B Contributes to the Impairment of the Autophagic Flux via Unopposed Activation of mTORC1 Signaling During Myocardial Ischemia/Reperfusion Injury. Circulation Research, 0(0). https://doi.org/10.1161/CIRCRESAHA.119.316388 Cite
In vitro, TWIST1 inhibition or silencing prevented pulmonary artery smooth muscle cell proliferation and migration.
[American Journal of Respiratory and Critical Care Medicine]
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TWIST1 Drives Smooth Muscle Cell Proliferation in Pulmonary Hypertension via Loss of GATA-6 and BMPR2 | American Journal of Respiratory and Critical Care Medicine | Articles in Press. (n.d.). Retrieved July 22, 2020, from https://www.atsjournals.org/doi/10.1164/rccm.201909-1884OC Cite