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- [Medicine] Molecular therapy: A possibility for treating stroke patients
- Professor Sung-Rae Cho(left) and Associate Professor Hyongbum Kim(right) Yonsei University College of Medicine ■ Medicine / Molecular therapy: A possibility for treating stroke patients Patients who have suffered from ischemic stroke may be able to restore their motor functions through transient in situ expression of pluripotency factors Patients who have suffered from ischemic stroke may be able to restore their ability to move through a method described as using “transient in situ expression of pluripotency factors”, according to research teams at Yonsei University College of Medicine led by professors Sung-Rae Cho of the Department of Rehabilitation Medicine and Hyongbum Kim of the Department of Pharmacology. They announced that transient expression of four pluripotency factors (specifically, Oct4, Sox2, Myc, and Klf4) dramatically promoted functional restoration from brain damage and improved motor function in mouse models with ischemic stroke. In a laboratory bench, mature cells can be reprogrammed to become induced pluripotent stem (iPS) cells by exogenous expression of the pluripotency-associated transcription factors. Moreover, transient expression of pluripotency factors renders cells into an activated plastic status, poising them to transform into other types of cells , depending on the environment. In this study, a total of 62 reprogrammable mice in which the four reprogramming factors were expressed in the presence of doxycycline were used. A stroke, or brain ischemia, was induced by temporarily stopping blood flow to the brain for twenty minutes, after which the lateral ventricles of mice were continuously given doxycycline into with an osmotic pump for one week. One month after treatment, the number of neural stem cells had increased in the subventricular zone of the reprogrammable mice injected with doxycycline, significantly more than the saline control group. There was also a remarkable increase in glial cells, responsible for the growth and support of neurons, in the striatum. Furthermore, in vivo pluripotency factor expression caused neuroprotective effects, such as increased numbers of mature neurons and levels of synaptic connection, or synaptic markers, in the striatum. Most importantly, motor recovery from ischemic brain injury, such as a stroke, can be promoted by cell proliferation and angiogenesis. “This study was the first experiment to investigate whether in situ transient expression of pluripotency factors can enhance functional recovery from ischemic injury.” explained Professor Cho. “Hopefully in the future, these results with provide a basis for novel therapeutic modality development not only for stroke patients, but for patients with neurodegenerative diseases as well.” Updated in Feb 2017 Reference Seo, J. H., Lee, M.-Y., Yu, J. H., Kim, M.-S., Song, M., Seo, C. H., Kim, H., Cho, S.-R., “In situ pluripotency factor expression promotes functional recovery from cerebral ischemia” Molecular Therapy, doi: 10.1038/mt.2016.124
- 통합관리자 2017.02.20
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- [Medicine] Gene mutation found causing kidney stones
- Professor Min Goo Lee(left) and Assistant Professor Heon Yung Gee(right) Yonsei University College of Medicine ■ Medicine / Gene mutation found causing kidney stones Mutations in a gene was found to be the culprit of kidney stone formation Research teams of Drs. Min Goo Lee and Heon Yung Gee in the Department of Pharmacology at the Yonsei University College of Medicine in collaboration with Dr. Hildebrandt in the Boston Children’s Hospital at Harvard University found mutations in a gene called SLC26A1 to be the culprit of kidney stone formation. The research results were released in the June 2016 issue of the American Journal of Human Genetics. Kidney stones form when minerals in urine are hardened like stones in the kidney and urinary tract. When kidney stones are present, the symptoms are severe pain in the back and sides and bloody urine (hematuria). It is also accompanied by a number of complications, such as painful urination (dysuria), difficulty in holding urine, or more frequent urination. Thus far, approximately 30 genes that trigger kidney stones have been discovered, but these genes only account for 15-20% of kidney stone patients. Causes for the remaining patients is still unclear. The Boston Children’s Hospital and Dr. Gee research team analyzed the genetic makeup of blood samples from 348 registered kidney stone patients consisting of 147 adults and 201 children. They found that kidney stones formed when autosomal recessive mutations occurred in the SLC26A1 gene. Dr. Lee explained, “Kidney stones occur in about 5-20% of the population,” and “although there can be various causes like inadequate water intake or obesity, the family history and frequent recurrence rate suggest that genetic factors can also contribute the disease.” In addition, the research teams pointed out that for individuals with SLC26A1 mutations, the use of acetaminophen, a common fever-reducing pain reliever, can cause a loss of appetite and in severe cases can lead to liver damage, such as hepatitis or even liver failure. Dr. Gee said that acetaminophen is widely used by adults as well as children who show symptoms of fever and recommended that kidney stone patients should consult a doctor and exercise caution when taking medication. Updated in Feb 2017 Reference Gee, H. Y., Jun, I., Braun, D. A., Lawson, J. A., Halbritter, J., Shril, S., Nelson, C. P., Tan, W., Stein, D., Wassner, A. J., Ferguson, M. A., Gucev, Z., Sayer, J. A., Milosevic, D., Baum, M., Tasic, V., Lee, M. G., Hildebrandt, F., “Mutations in SLC26A1 Cause Nephrolithiasis” American Journal of Human Genetics, doi: 10.1016/j.ajhg.2016.03.026
- 통합관리자 2017.02.20
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- [Medicine] Causes for irreversible lung cancer treatment drug tolerance identified
- Associate Professor Byoung Chul Cho(left) and Assistant Professor Hye Ryun Kim(right) Yonsei University College of Medicine ■ Medicine / Causes for irreversible lung cancer treatment drug tolerance identified Researchers at Yonsei bring potential for developing new targeted lung cancer treatment drug Researchers at Yonsei University have found the causes of tolerance of drugs used to treat irreversible lung cancer. Following this discovery, there is now potential to develop new targeted lung cancer treatment drugs. Research teams led by professors Byoung Chul Cho and Hye Ryun Kim at the Yonsei Cancer Center Department of Medical Oncology claim to have found the cause of patients’ tolerance to anti-cancer drugs, specifically those who are afflicted with BRAF-mutated lung cancer (BRAF V600E genetic mutation non-small-cell lung cancer). The research results were published in the July 2016 issue of Molecular Cancer Therapeutic. The anti-cancer drug dabrafenib, used to treat malignant melanoma, has also been the standard medicine for treatment of BRAF-mutated lung cancer. However, over the course of treatment, patients’ increasing tolerance to the drug causes a drop in effectiveness of the treatment. The research team focused on the relapse of activity over time related to the activity-regulating ERK enzyme, or extracellular signal-regulated kinase, of dabrafenib. In an animal model experiment on mice, it was found that a protein, the RIP2 enzyme, was the cause of ERK enzyme stimulation. The researchers explained that in order to maintain effective treatment over time, suppressor drugs targeting the reactivating ERK enzyme need to be used together with the treatment, and that the results of this experiment are especially meaningful in the potential for development of target medications to help overcome drug resistance. Updated in Feb 2017 Reference Kim, S.-M., Kim, H., Jang, K. W. Kim, M. H., Sohn, J., Yun M. R., Kang, H. N., Kang, C. W., Kim, H. R., Lim, S. M., Moon, Y. W., Kim, J. H., Paik, S., Cho, B. C., “EGFR-mediated reactivation of MAPK signaling induces acquired resistance to GSK2118436 in BRAF V600E-Mutant NSCLC cell lines” Molecular Cancer Therapeutics, doi: 10.1158/1535-7163.MCT-15-0375
- 통합관리자 2017.02.20
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- [Medicine] Happy brains have higher capacity to cope with “bad information”
- Professor Jae-Jin Kim Gangnam Severance Hospital Department of Psychiatry ■ Medicine / Happy brains have higher capacity to cope with “bad information” Yonsei research team finds those with greater life satisfaction have more brain activity for coping with negative information What is the relationship between human brain function and life satisfaction, our so-called “happiness”? Recent research shows that when presented with negative, i.e., bad, information, those who have higher levels of life satisfaction tend to exhibit more brain activity that allows one to cope with that information. Research teams, led by Professor Jae-Jin Kim of the Gangnam Severance Hospital Department of Psychiatry and Professor Eun-Joo Kim of the Yonsei University Graduate School of Education, reached the conclusion after measuring the neural activity of a random sample of 40 people, 20 male and 20 female. The experiment focused on the medial prefrontal cortex which plays an important role in the brain’s reception of external stimuli. Current research has established that the medial prefrontal cortex has an effect on “individual self-esteem,” but has yet to reveal any difference in one’s life satisfaction. Participants were first surveyed and asked to score statements such as, “I am satisfied with my life,” and, “At this point in my life I have been living as I wish.” Their responses created a scoring system for life satisfaction, and the participants were divided into a high-scoring group of 19 people, and a low-scoring group of 21 people. Researchers used functional magnetic resonance imaging, or fMRI, to observe medial prefrontal cortex activity when the participants were presented with positively or negatively associated words paired with their own or others’ faces. When the high-scoring group saw negative words, the medial prefrontal cortex became activated, and connections to other areas of the brain that regulate emotion became pronounced. On the other hand, when the lower-ranking groups were presented with positive words, they showed activated medial prefrontal cortices, but there was no observed connection activity with other areas of the brain. “The results are proof that those who are more satisfied with their life are more likely to exhibit positive responses to negative external information,” Professor Jae-Jin Kim explained. “Although the low-scoring group exhibited activity in the medial prefrontal cortex when presented with a positive word, we can see that they are not effectively processing the external stimulus because it does not extend to a real behavioral connection.” “The human brain is structured to be able to effectively handle bad information,” Kim continued, and emphasized the more that cognitive structure is utilized, the higher life satisfaction and potential for satisfaction we have. “Utilizing the medial prefrontal cortex is not a medical treatment, but a social attitude that must be realized. Social conditions need to be set to facilitate individuals to perceive their own lives in a good light.” This paper was published in the multidisciplinary open access journal, PLOS One, on Feb 22, 2016. Updated in Feb 2017 Reference Kim, E. J., Kyeong, S., Cho, S. W., Chun, J.-W., Park, H.-J., Kim, J., Kim, J., Dolan, R. J., Kim, J.-J., “Happier people show greater neural connectivity during negative self-referential processing” PLoS ONE, doi: 10.1371/journal.pone.0149554
- 통합관리자 2017.02.20
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- [Medicine] Method found to halt progression of Parkinson’s disease
- Professor Phil Hyu Lee Yonsei University College of Medicine ■ Medicine / Method found to halt progression of Parkinson’s disease A research team led by Professor Phil Hyu Lee found a new way to counter the progression of irreversible Parkinson’s disease A group of researchers at Yonsei have found a new way to counter the progression of irreversible Parkinson’s disease. As toxic α-synuclein spreads and travels from one brain area to another, neurons degenerate and die. Thus, the progression of Parkinson’s disease is dependent on how well the α-synuclein proteins are controlled within the brain. A team led by Professor Phil Hyu Lee at the Yonsei University Severance Hospital Department of Neurology transplanted human mesenchymal stem cells (MSCs) into animal models of Parkinson’s disease and observed that MSCs exert neuroprotective properties through inhibition of extracellular α-synuclein transmission between regions of the brain. The results of the study were published in the February 2016 online edition of Cell Reports. Researchers compared the progression of α-synuclein pathology in mouse models of Parkinson’s disease injected with MSCs and a control group mice without MSC injection. Unlike the control group, Parkinson’s disease pathology did not progress in the MSC-injected experimental group with functional improvement of parkinsonian motor deficits. Specifically, researchers found that the interaction between Galectin-1, a protein secreted by the MSCs, and NMDA receptors inhibited the transmission of aggregated α-synuclein in cellular and animal models. “There is still no drug that can offset the neurologically degenerative effects of Parkinson’s disease,” said Professor Phil Hyu Lee. “But additional research may show that the utilization of NMDA receptors, similar to its current role in anticonvulsants and treatment for dementia, could possibly be developed into a drug that can delay the natural progression of Parkinson’s disease.” Updated in Feb 2017 Reference Oh, S. H., Kim, H. N., Park, H. J., Shin, J. Y., Bae, E.-J., Sunwoo, M. K., Lee, S.-J., Lee, P. H., “Mesenchymal Stem Cells Inhibit Transmission of α-Synuclein by Modulating Clathrin-Mediated Endocytosis in a Parkinsonian Model” Cell Reports, doi: 10.1016/j.celrep.2015.12.075
- 통합관리자 2017.02.20
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- [Medicine] Unlocking the secret of Lorenzo’s Oil
- Professor Dong-Wook Kim Yonsei University College of Medicine Associate Professor Je-Wook Yu Yonsei University College of Medicine ■ Medicine / Unlocking the secret of Lorenzo’s Oil A team of researchers at Yonsei University revealed a novel mechanism in the pathogenesis of X-ALD The plot of a 1992 film starring Susan Sarandon and Nick Nolte, Lorenzo’s Oil, is based on the true story of a couple who searched for a treatment for their son afflicted with an incurable disease, X-linked adrenoleukodystropy (X-ALD). A team of researchers at Yonsei University revealed a novel mechanism in the pathogenesis of X-ALD. A joint research team of Drs. Dong-Wook Kim and Je-Wook Yu at Yonsei University College of Medicine analyzed induced pluripotent stem cells (iPSCs) from ALD patients and discovered key molecules that shed light on the pathological mechanism of disease. Their results were published in Nature Communications. X-ALD is a rare genetic disease caused by a loss of function mutation in the peroxisomal transporter ABCD1. This disease is strikingly associated with the accumulation of very long-chain fatty acids (VLCFA), which were considered to cause nerve damage from cerebral inflammation. It typically afflicts boys under the age of 10, and after about six months after the first symptoms appear the affected patient loses eyesight and hearing. Within two years, the patient falls into a vegetative state and succumbs to his illness. By observing iPS cells made from the somatic cells of ALD patients, the researchers found that the VLCFA themselves are not the direct cause of cerebral inflammation in X-ALD patients, but in fact revealed that X-ALD-derived iPSC shows the overproduction of 25-hydroxycholesterol (25-HC) in response to VLCFA. The researchers also found that 25-HC causes cerebral inflammation through activation of the NLRP3 inflammasome. When mice were injected with excessive amounts of 25-HC, the researchers observed signs of ALD. Alternatively, cerebral inflammation decreased when the same substance was blocked. Professor Kim explained the significance of the findings: “The results of the study confirm that cerebral inflammation, the critical symptom of ALD, is caused by 25-HC. What remains now is to find a substance that can block it, and we will have an effective treatment for ALD.” Updated in Feb 2017 Reference Jang, J., Park, S., Jin Hur, H., Cho, H.-J., Hwang, I., Pyo Kang, Y., Im, I., Lee, H., Lee, E., Yang, W., Kang, H.-C., Won Kwon, S., Yu, J.-W., Kim, D.-W., “25-hydroxycholesterol contributes to cerebral inflammation of X-linked adrenoleukodystrophy through activation of the NLRP3 inflammasome” Nature Communications, doi: 10.1038/ncomms13129
- 통합관리자 2017.02.20
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- [Medicine] Find protein to treat sepsis
- Professor Joo-Heon Yoon (left) and Ji-Hwan Ryu (right) Yonsei University College of Medicine ■ Medicine / Find protein to treat sepsis A joint research team at Yonsei found that sestrin-2 can be used to treat sepsis Researchers Find Protein to Treat Sepsis Researchers at Yonsei University have discovered a way to treat sepsis, a potentially deadly condition in which severe inflammation throughout the body is brought on when toxins produced by bacteria enter the bloodstream. A joint research team led by Yonsei University College of Medicine professors Yoon Joo-heon and Ryu Ji-hwan has found that sestrin-2, a protein found in the human body, can be used to treat sepsis. The results of the study were published in the June 2016 volume of Autophage. Researchers compared the vital reactions of control mice with naturally occurring sestrin-2 and mice which had no sestrin-2 protein after sepsis was induced. The results showed that sestrin-2 plays a role in reducing inflammatory response. The study revealed a regulatory mechanism of reducing severe inflammation in which sestrin-2 blocks the so-called “signal” that triggers inflammation. The cell organs that signal an immune response are called mitochondria. Mitochondria are the organelles responsible for creating energy within a cell and are often referred to as the “powerhouse of the cell.” If microorganisms invade, mitochondria are injured and trigger an immune response. Generally, damaged mitochondria then die and fade away. However, in the case that damaged mitochondria does not dissolve and remains behind, it results in a stronger immune response. It is then that sestrin-2 removes the damaged mitochondria to prevent further immune response. According to Professor Yoon, this study suggests a new potential treatment for sepsis, which is difficult to do with antibiotics alone. In addition to treatment of sepsis, Yoon hopes that it will provide a foundation for further research into treatment methods for geriatric diseases as well. Updated in Feb 2017 Reference Kim. M.-J., Bae, S. H., Ryu, J.-C., Kwon, Y., Oh, J.-H., Kwon, J., Moon, J.-S., Kim, K., Miyawaki, A., Lee, M. G., Shin, J., Kim, Y. S., Kim, C.-H., Ryter, S. W., Choi, A. M. K., Rhee, S. G., Ryu, J.-H., Yoon, J.-H., “SESN2/sestrin2 suppresses sepsis by inducing mitophagy and inhibiting NLRP3 activation in macrophages” Autophagy, doi: 10.1080/15548627.2016.1183081
- 통합관리자 2017.02.20
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- [Medicine] Live and let dye: Probes enabling immune cells to announce their success
- Associate Professor Ji-Hwan Ryu (yjh@yuhs.ac) Yonsei University College of Medicine ■ Medicine / Live and let dye: Probes enabling immune cells to announce their success Yonsei biochemists develop a fluorescent probe capable of signaling immune-cell destruction of invading pathogens Among the many roles played by the human immune system, capturing and destroying invading bacterial pathogens is among the most important. However, the destruction of these pathogens results in production of molecules that can be harmful to cells and tissues. Moreover, the accumulation of these molecules can potentially result in the initiation of cardiovascular and inflammatory diseases. Researchers are continually engaged in the discovery of methods that enable the detection of such molecules in order to promote their use as diagnostic indicators of disease progression. A recent paper by Ryu et al. (2016) and published in Nature Protocols described the creation and application of a novel chemical-based fluorescent probe capable of detecting one such molecule, hypochlorous acid (HOCl). Upon infection, immune cells called neutrophils capture and destroy pathogens in highly acidic compartments. This process results in the generation of large amounts of HOCl that, when not appropriately managed, can lead to cellular dysfunction. Alternatively, HOCl has also been shown to exert anti-cancer activities and promote processes that help our immune system “learn” about how to effectively fight infections. Given its contrasting roles, methods capable of detecting HOCl have become important for helping researchers determine which biological pathways are associated with its positive and negative effects. Fluorescent probes are a widely used method allowing scientists to visualize interactions between molecules. In such cases, a fluorescent signal occurs whenever one molecule interacts with its target. Using a low-cost, commercially available dye, Ryu et al. (2016) developed a fluorescent probe specific for HOCl and capable of “finding” this molecule in the highly acidic environments of immune cells. In addition, based on the importance of probes binding only to their specific molecular targets, Ryu et al. (2016) showed that their probe “found” its target at rates that exceeded current commercially available HOCl-specific probes. Testing the probe in vivo To demonstrate the use of their probe in different biological environments, Ryu et al. (2016) described experiments performed on both fruit flies and mice. The fruit fly experiment was described in a previous study published by their lab [Lee et al. (2013)] and demonstrated the in vivo ability of the probe to signal the presence of increased amounts of HOCl following bacterial infection. Success in a mammalian model In order to demonstrate the efficacy of this method in a mammalian system, immune cells were removed from mice and infected with bacteria. After the cells captured and destroyed the bacteria, resulting in production of HOCl, researchers were able to observe fluorescent signals indicating that the probe had effectively “found” the products and reported their presence. Given the importance of showing the ability of the probe to work under physiological conditions, a respiratory infection was initiated in mice, followed by isolation of immune cells from their lungs. Upon administration of the probe to these cells, the researchers observed fluorescent signals confirming the ability of probe to detect HOCl production in response to infection. Conclusion Given the involvement of this molecule in both positive and negative aspects of mammalian diseases, the development of affordable methods that allow researchers to identify the differences between these pathways is critical. The protocols described by Chen et al. (2016) offer an opportunity to investigate HOCl, specifically, as a potential anticancer therapeutic, as well as its role in the progression of diseases, including rheumatoid arthritis and atherosclerosis. Updated in Feb 2017 Reference X. Chen, K.-A. Lee, X. Ren, J.-C. Ryu, G. Kim, J.-H. Ryu, W.-J. Lee, J. Yoon, “Synthesis of a highly HOCl-selective fluorescent probe and its use for imaging HOCl in cells and organisms”, Nature Protocols, doi: 10.1038/nprot.2016.062
- 통합관리자 2017.02.20
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- [Life Sciences] Rub your hands and improve memory – fantasy or reality?
- Associate Professor Seung-Woo Cho (right) Department of Biotechnology, Yonsei University ■ Life Sciences / Rub your hands and improve memory – fantasy or reality? A team of Yonsei biotechnologists and neuroscientists suggests that triboelectricity can be used to convert somatic cells to neurons Strokes, brain tumors, and neurodegenerative diseases such as multiple sclerosis, Alzheimer’s disease, and Parkinson’s disease, irreversibly destroy neurons in the brain, condemning people to permanent incapacitation or death. Neuronal degeneration is also the primary cause of memory loss and cognitive decline in elderly people. Therefore, neuroscientists have been working on strategies to restore the neuronal population in the brain, which is decreased by aging or disease. Among them, the conversion of pluripotent stem cells to neurons shows promise, but there are ethical issues associated with the use of human embryos. Another approach is direct reprogramming of somatic cells into neurons through transfer of neuron-specific genes; however, one of the major problems is gene delivery, as viral vectors are efficient but unsafe, while non-viral methods using naked DNA, although safe, have low efficiency. These challenges were addressed by scientists from Yonsei University led by Professor Seung-Woo Cho, who have developed a novel approach to stimulate conversion of somatic cells into neurons using triboelectricity. How does it work? The technology is based on the triboelectric effect, a phenomenon that each of us encounters in everyday life when we can feel, hear, and even see sparks (electrical charges) produced by contact or friction between dissimilar materials, such as hair and comb, skin and polyester clothes, etc. The effect has been known from ancient times as “tribo” means “rub” in Greek; however, it began to be exploited only recently, when nanotechnologists created triboelectric generators – devices that can harvest the ambient mechanical energy produced by such trivial activities as, for example, walking or rubbing hands, and convert it to electricity. In their study, Professor Seung-Woo Cho, Professor Taeyoon Lee, and their colleagues transfected fibroblasts with genes encoding neuron-specific transcription factors using non-viral methods such as electroporation and biodegradable polymeric nanoparticles and subjected them to triboelectric stimulation. Triboelectricity was obtained by periodic press and release of two parallel plates made, respectively, of aluminum (Al) and polydimethylsiloxane (PDMS), materials that demonstrate the maximal degree of static charge polarity and, thus, can generate the strongest current. Surface friction between the plates produced triboelectric charges and current between the two electrodes connected to the cell culture substrate made of highly conductive material (Figure). As a result, cultured fibroblasts were exposed to biphasic triboelectric current, which substantially accelerated their differentiation to neurons and increased the number of converted neuronal cells to 14.17% – the highest efficiency of neuronal transformation achieved to date using non-viral gene delivery. The converted cells had functional characteristics of mature neurons as evidenced by the presence of neuronal markers and electrophysiological activity. Y. Jin, J. Seo, J. –S. Lee, S. Shin , H.-J. Park, S. Min , E. Cheong , T. Lee, S.-W. Cho., “Triboelectric Nanogenerator Accelerates Highly Efficient Nonviral Direct Conversion and In Vivo Reprogramming of Fibroblasts to Functional Neuronal Cells”. Advanced Materials, 2016, Vol 28, Pages 7365-7374. Copyright Wiley-VCH Verlag GmbH & Co. KGaA, Reproduced with permission. Triboelectric stimulation for direct conversion of fibroblasts into neurons. Contact between the plates induces surface friction (intensified by PDMS’s micro-pillar structure) and electron transfer from the Al layer (light blue) to the PDMS layer (dark blue) (i). In the releasing state, negative charges on the PDMS layer generate positive charges in the Cu electrode (yellow), creating difference in electric potential between the two plates (ii) and inducing current through cell culture substrate made of conductive titanium film deposited on the silicon surface (middle panel). The current continues until a sufficient distance is reached between the plates (iii); then, the top plate is pressed again and electrons flow in the opposite direction (iv). Thus, the triboelectric nanogenerator can produce biphasic electricity. Success in a mammalian model How can triboelectricity enhance the fibroblast-to-neuron transformation? To answer this question, the researchers performed confocal microscopy and protein expression analysis and found that electrical stimulation induced influx of Ca2+ ions, which activated intracellular signaling proteins triggering neuronal differentiation. However, the results obtained in cell cultures may not necessarily be representative of the situation in an organism. Therefore, the scientists tested their triboelectric nanogenerator in mice who received intradermal injections of polymeric nanoparticles carrying neuronal transcription factors. Triboelectic current generated by the nanostimulator connected to the mouse skin increased the conversion of dermal fibroblasts into neuronal cells by over 100 times, proving that it is a powerful inducer of transformation from somatic cells to neurons in vivo. Conclusions Thus, the novel strategy based on triboelectric energy harvesting represents a less invasive non-viral method for rapid and efficient reprogramming of somatic cells into mature functional neurons, laying out a new direction for addressing challenges in the treatment of neurodegenerative diseases, stroke, and age-related neuronal loss. As the next step, the team of Professor Cho plans to develop a triboelectric nanostimulator that can collect energy from such body activities as breathing and cardiac pulses. The hope is that these portable self-powered nanoelectronic devices harnessing renewable energy sources such as human motions might one day be used for individual regulation of brain activity. Updated in Feb 2017 Reference Y. Jin, J. Seo, J. –S. Lee, S. Shin , H.-J. Park, S. Min , E. Cheong , T. Lee, S.-W. Cho, “Triboelectric Nanogenerator Accelerates Highly Effi cient Nonviral Direct Conversion and In Vivo Reprogramming of Fibroblasts to Functional Neuronal Cells”, Advanced Materials, doi: 10.1002/adma.201601900
- 통합관리자 2017.02.20
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- [Engineering/Technology] Making Molecular MIMO Work
- Associate Professor Chan-Byoung Chae School of Integrated Technology, Yonsei University ■ Engineering & Technology / Making Molecular MIMO Work A group of researchers, including Prof. Chan-Byoung Chae, develops a novel MIMO design for molecular communication For communication systems operating on the microscale or nanoscale level, various technical problems occur: Is the antenna small enough? Can the wavelength of your communication signal be transmitted effectively? Are your data rates being hampered by interference? Researchers are looking at other ways to send signals from point A to B, and they have found an innovative approach: molecular communication, where data travels as chemical instead of electromagnetic signals. Koo, Lee, Yilmaz, Farsad, Eckford, and Chae (2016) present a novel approach in their paper, “Molecular MIMO: From Theory to Prototype” published in the IEEE Journal on Selected Areas in Communication. In their approach, they build on molecular communication via diffusion (MCvD), and add a multiple-input multiple-output (MIMO) technique to deal specifically with signal interference. An MCvD system consists of three main components: transmitter, receiver, and fluid environment between the transmitter and the receiver. Transmitter nodes send molecules of data (symbols) into the system, and those molecules travel through the medium; the receiver nodes capture these molecules and convert them to data. Although several molecular systems have been proposed, the capabilities of the available molecular communications are rather primitive; their data rate is too low for commercial applications. In their study, the authors added a MIMO technique to improve the efficiency of the MCvD systems. Transmitting molecules via multiple nodes may provide higher data rate communication than the single-in single-out (SISO) approach. Some of the key points of the current study are described below. Considering ISI and ILI for a molecular communication system MIMO techniques need to deal with inter-symbol interference (ISI) and inter-link interference (ILI). ISI occurs when a signal introduces a propagation delay that interferes with other symbol taps, whereas ILI occurs when a signal interferes with other communication links that are in physically proximity. The molecular communication system used in this research comprises a 3D environment with two point sources and two spherical receive antennas. The communication medium is a fluid. After the transmitter releases “messenger molecules” into the fluid, those molecules travel via diffusion, and the receive antennas count the number of molecules that reach the spherical surface. To investigate the effectiveness of their MIMO technique, the scientists first implemented a software simulation to ascertain their claim, and then constructed a macro-scale physical testbed to examine their concept in a lab . The model function and the proposed algorithms The team used a model function to fit the simulation data. This formula is analogous to the one in a molecular SISO system in a 3D environment, with variable control coefficients. A similar model function was used in previous studies to model noise effects in an SISO testbed and to model a molecular MIMO channel. Next, after deriving formulas for ISI and ILI, the researchers proposed a series of detection algorithms specific to molecular MIMO systems. The authors calculated and analyzed the performance of their MIMO system in terms of the bit error rate. In addition, the authors examined the link-level performance of the proposed detection algorithms while varying the number of emitted molecules and symbol duration. Using SIR in the performance analysis In their performance analysis, the authors considered signal-to-interference ratio (SIR). The SIR is the ratio of the expected number of molecules transmitted from the intended transmitter in the intended time slot to the mean ILI plus ISI for a one-shot signal. The authors investigated the effects of various topological conditions on the SIR. The results showed that, to reduce interference, decreasing the transmitter–receiver distance and increasing the size of the receive antennas is more effective than increasing the separation of the antennas. The world’s first molecular MIMO testbed To verify their concept physically, the authors designed the world’s first molecular MIMO testbed, which comprises a molecular MIMO transmitter and receiver. The transmitter and receiver were equipped with multiple transmit nozzles and receive sensors and they are exploited to increase the data rate. The propagation distance between the transmitter and the receiver was approximately 1 m. This low-cost platform is modifiable and programmable. Experimental results show that the MIMO system could achieve transmission rates that were 1.7 times higher than those obtained from SISO systems. Conclusion The current study sheds light on achieving higher data rate communication using MIMO. Since data rates in molecular communications are affected by interference, the authors suggested using a MIMO system for MCvD that considers ISI and ILI. Four symbol detection algorithms were proposed, and the effect of varying topological conditions on the SIR was investigated. The results showed that decreasing the transmitter–receiver distance and increasing the size of the receive antennas are more effective at reducing interference than increasing the separation of the antennas. The world’s first molecular MIMO testbed to verify the proposed concept was developed, and it achieved transmission rates 1.7 times higher than those obtained from the molecular SISO system. For this testbed, the authors received the prestigious IEEE INFOCOM Best Demo Award in 2015. Updated in Feb 2017 Reference B.H. Koo, C. Lee, H.B. Yilmaz, N. Farsad, A. Eckford, C.B. Chae, “Molecular MIMO: From Theory to Prototype”, IEEE Journal on Selected Areas in Communications, doi: 10.1109/JSAC.2016.2525538
- 통합관리자 2017.02.20