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Artículos de revistas sobre el tema "Memory Methylene blue. Brain"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 11 de febrero de 2022

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1

Callaway, Narriman Lee, Penny D. Riha, Aleksandra K. Bruchey, Zeenat Munshi y F. Gonzalez-Lima. "Methylene blue improves brain oxidative metabolism and memory retention in rats". Pharmacology Biochemistry and Behavior 77, n.º 1 (enero de 2004): 175–81. http://dx.doi.org/10.1016/j.pbb.2003.10.007.

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2

Riha, Penny D., Aleksandra K. Bruchey, David J. Echevarria y F. Gonzalez-Lima. "Memory facilitation by methylene blue: Dose-dependent effect on behavior and brain oxygen consumption". European Journal of Pharmacology 511, n.º 2-3 (marzo de 2005): 151–58. http://dx.doi.org/10.1016/j.ejphar.2005.02.001.

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3

Mori, Takashi, Naoki Koyama, Tatsuya Segawa, Masahiro Maeda, Nobuhiro Maruyama, Noriaki Kinoshita, Huayan Hou, Jun Tan y Terrence Town. "Methylene Blue Modulates β-Secretase, Reverses Cerebral Amyloidosis, and Improves Cognition in Transgenic Mice". Journal of Biological Chemistry 289, n.º 44 (25 de agosto de 2014): 30303–17. http://dx.doi.org/10.1074/jbc.m114.568212.

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Amyloid precursor protein (APP) proteolysis is required for production of amyloid-β (Aβ) peptides that comprise β-amyloid plaques in the brains of patients with Alzheimer disease (AD). Here, we tested whether the experimental agent methylene blue (MB), used for treatment of methemoglobinemia, might improve AD-like pathology and behavioral deficits. We orally administered MB to the aged transgenic PSAPP mouse model of cerebral amyloidosis and evaluated cognitive function and cerebral amyloid pathology. Beginning at 15 months of age, animals were gavaged with MB (3 mg/kg) or vehicle once daily for 3 months. MB treatment significantly prevented transgene-associated behavioral impairment, including hyperactivity, decreased object recognition, and defective spatial working and reference memory, but it did not alter nontransgenic mouse behavior. Moreover, brain parenchymal and cerebral vascular β-amyloid deposits as well as levels of various Aβ species, including oligomers, were mitigated in MB-treated PSAPP mice. These effects occurred with inhibition of amyloidogenic APP proteolysis. Specifically, β-carboxyl-terminal APP fragment and β-site APP cleaving enzyme 1 protein expression and activity were attenuated. Additionally, treatment of Chinese hamster ovary cells overexpressing human wild-type APP with MB significantly decreased Aβ production and amyloidogenic APP proteolysis. These results underscore the potential for oral MB treatment against AD-related cerebral amyloidosis by modulating the amyloidogenic pathway.
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4

Sadovnikova, Irina S., Artem P. Gureev, Daria A. Ignatyeva, Maria V. Gryaznova, Ekaterina V. Chernyshova, Ekaterina P. Krutskikh, Anastasia G. Novikova y Vasily N. Popov. "Nrf2/ARE Activators Improve Memory in Aged Mice via Maintaining of Mitochondrial Quality Control of Brain and the Modulation of Gut Microbiome". Pharmaceuticals 14, n.º 7 (23 de junio de 2021): 607. http://dx.doi.org/10.3390/ph14070607.

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Aging is one of the most serious factors for central nervous dysfunctions, which lead to cognitive impairment. New highly effective drugs are required to slow the development of cognitive dysfunction. This research studied the effect of dimethyl fumarate (DMF), methylene blue (MB), and resveratrol (RSV) on the cognitive functions of 15-month-old mice and their relationship to the maintenance of mitochondrial quality control in the brain and the bacterial composition of the gut microbiome. We have shown that studied compounds enhance mitochondrial biogenesis, mitophagy, and antioxidant defense in the hippocampus of 15-month-old mice via Nrf2/ARE pathway activation, which reduces the degree of oxidative damage to mtDNA. It is manifested in the improvement of short-term and long-term memory. We have also shown that memory improvement correlates with levels of Roseburia, Oscillibacter, ChristensenellaceaeR-7, Negativibacillus, and Faecalibaculum genera of bacteria. At the same time, long-term treatment by MB induced a decrease in gut microbiome diversity, but the other markers of dysbiosis were not observed. Thus, Nrf2/ARE activators have an impact on mitochondrial quality control and are associated with a positive change in the composition of the gut microbiome, which together lead to an improvement in memory in aged mice.
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5

Lummus, Seth y Bette Kay Kleinschmidt-DeMasters. "Methylene Blue “Avatar” Brain". Journal of Neuropathology & Experimental Neurology 72, n.º 3 (marzo de 2013): 263–65. http://dx.doi.org/10.1097/nen.0b013e318283d41a.

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Gonzalez-Lima, F. "Extinction Memory Improvement by the Metabolic Enhancer Methylene Blue". Learning & Memory 11, n.º 5 (1 de septiembre de 2004): 633–40. http://dx.doi.org/10.1101/lm.82404.

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7

R. Suryawanshi, Chandani y Vinod Nayyar. "BLUE BRAIN". INTERNATIONAL JOURNAL OF MANAGEMENT & INFORMATION TECHNOLOGY 7, n.º 2 (30 de noviembre de 2013): 1009–17. http://dx.doi.org/10.24297/ijmit.v7i2.3294.

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Today scientists are in research to create an artificial brain that can think, respond, take decision, and keep anything in memory. The main aim is to upload human brain into machine. So that man can think, take decision without any effort. After the death of the body, the virtual brain will act as the man. So, even after the death of a person we will not loose the knowledge, intelligence, personalities, feelings and memories of that man, that can be used for the development of the human society. Technology is growing faster than every thing. IBM is now in research to create a virtual brain, called Blue brain. If possible, this would be the first virtual brain of the world. IBM, in partnership with scientists at Switzerlands Ecole Polytech- nique Federale de Lausannes (EPFL) Brain and Mind Institute will begin simulating the brains biological systems and output the data as a working 3-dimensional model that will recreate the high-speed electrochemical interactions that take place within the brains interior. These include cognitive functions such as language, learning, perception and memory in addition to brain malfunction such as psychiatric disorders like depression and autism. From there, the modeling will expand to other regions of the brain and, if successful, shed light on the relationships between genetic, molecular and cognitive functions of the brain.
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8

Talley Watts, Lora, Justin Alexander Long, Jonathan Chemello, Samantha Van Koughnet, Angelica Fernandez, Shiliang Huang, Qiang Shen y Timothy Q. Duong. "Methylene Blue Is Neuroprotective against Mild Traumatic Brain Injury". Journal of Neurotrauma 31, n.º 11 (junio de 2014): 1063–71. http://dx.doi.org/10.1089/neu.2013.3193.

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9

Haouzi, Philippe, Takashi Sonobe y Annick Judenherc-Haouzi. "Hydrogen sulfide intoxication induced brain injury and methylene blue". Neurobiology of Disease 133 (enero de 2020): 104474. http://dx.doi.org/10.1016/j.nbd.2019.05.013.

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10

Lee, Yong Soo y Robert D. Wurster. "Methylene blue induces cytotoxicity in human brain tumor cells". Cancer Letters 88, n.º 2 (enero de 1995): 141–45. http://dx.doi.org/10.1016/0304-3835(94)03629-w.

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11

Rodriguez, Pavel, Amar P. Singh, Kristen E. Malloy, Wei Zhou, Douglas W. Barrett, Crystal G. Franklin, Wilson B. Altmeyer et al. "Methylene blue modulates functional connectivity in the human brain". Brain Imaging and Behavior 11, n.º 3 (10 de marzo de 2016): 640–48. http://dx.doi.org/10.1007/s11682-016-9541-6.

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12

Rojas, Julio C., Aleksandra K. Bruchey y F. Gonzalez-Lima. "Neurometabolic mechanisms for memory enhancement and neuroprotection of methylene blue". Progress in Neurobiology 96, n.º 1 (enero de 2012): 32–45. http://dx.doi.org/10.1016/j.pneurobio.2011.10.007.

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13

Eiferman, D. S., A. Fenn, J. Skendelas, Y. Huang, P. G. Popovih y J. P. Godbout. "Methylene Blue Infusion for Treatment of Traumatic Brain Injury-associated Neuroinflammation". Journal of Surgical Research 186, n.º 2 (febrero de 2014): 590. http://dx.doi.org/10.1016/j.jss.2013.11.542.

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14

Wrubel, Kathryn M., Penny D. Riha, Monica A. Maldonado, David McCollum y F. Gonzalez-Lima. "The brain metabolic enhancer methylene blue improves discrimination learning in rats". Pharmacology Biochemistry and Behavior 86, n.º 4 (abril de 2007): 712–17. http://dx.doi.org/10.1016/j.pbb.2007.02.018.

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15

Donati, Abele, Erica Adrario, Paolo Pelaia y Jean-Charles Preiser. "Methylene blue as the future protecting agent for ischemic brain injury?*". Critical Care Medicine 38, n.º 11 (noviembre de 2010): 2265–66. http://dx.doi.org/10.1097/ccm.0b013e3181f7d8f7.

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16

Echevarria, David J., Erika M. Caramillo y Francisco Gonzalez-Lima. "Methylene Blue Facilitates Memory Retention in Zebrafish in a Dose-Dependent Manner". Zebrafish 13, n.º 6 (diciembre de 2016): 489–94. http://dx.doi.org/10.1089/zeb.2016.1282.

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17

Duicu, Oana M., Andreea Privistirescu, Adrian Wolf, Alexandra Petruş, Maria D. Dănilă, Corina D. Raţiu, Danina M. Muntean y Adrian Sturza. "Methylene blue improves mitochondrial respiration and decreases oxidative stress in a substrate-dependent manner in diabetic rat hearts". Canadian Journal of Physiology and Pharmacology 95, n.º 11 (noviembre de 2017): 1376–82. http://dx.doi.org/10.1139/cjpp-2017-0074.

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Diabetic cardiomyopathy has been systematically associated with compromised mitochondrial energetics and increased generation of reactive oxygen species (ROS) that underlie its progression to heart failure. Methylene blue is a redox drug with reported protective effects mainly on brain mitochondria. The purpose of the present study was to characterize the effects of acute administration of methylene blue on mitochondrial respiration, H2O2 production, and calcium sensitivity in rat heart mitochondria isolated from healthy and 2 months (streptozotocin-induced) diabetic rats. Mitochondrial respiratory function was assessed by high-resolution respirometry. H2O2 production and calcium retention capacity were measured spectrofluorimetrically. The addition of methylene blue (0.1 μmol·L−1) elicited an increase in oxygen consumption of mitochondria energized with complex I and II substrates in both normal and diseased mitochondria. Interestingly, methylene blue elicited a significant increase in H2O2 release in the presence of complex I substrates (glutamate and malate), but had an opposite effect in mitochondria energized with complex II substrate (succinate). No changes in the calcium retention capacity of healthy or diabetic mitochondria were found in the presence of methylene blue. In conclusion, in cardiac mitochondria isolated from diabetic and nondiabetic rat hearts, methylene blue improved respiratory function and elicited a dichotomic, substrate-dependent effect on ROS production.
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18

Genrikhs, Elizaveta E., Elena V. Stelmashook, Dmitriy N. Voronkov, Svetlana V. Novikova, Olga P. Alexandrova, Mikhail V. Gulyaev y Nickolay K. Isaev. "The Delayed Neuroprotective Effect of Methylene Blue in Experimental Rat Brain Trauma". Antioxidants 9, n.º 5 (2 de mayo de 2020): 377. http://dx.doi.org/10.3390/antiox9050377.

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After traumatic brain injury (TBI), an increase in dysfunction of the limbs contralateral to injury focus was observed. Using different behavioral tests, we found that a single intravenous injection of methylene blue (MB, 1 mg/kg) 30 min after the injury reduced the impairment of the motor functions of the limbs from 7 to 120 days after TBI. Administration of methylene blue 30 min after the injury and then monthly (six injections in total) was the most effective both in terms of preservation of limb function and duration of therapeutic action. This therapeutic effect was clearly manifested from the seventh day and continued until the end of the experiment—by the 180th day after TBI. MB is known to possess antioxidant properties; it has a protective effect against TBI by promoting autophagy and minimizing lesion volume in the first two weeks after TBI. Studies of the brains on the 180th day after TBI demonstrated that the monthly treatment of animals with MB statistically significantly prevented an increase in the density of microglial cells in the ipsilateral hemisphere and a decrease in the thickness of the corpus callosum in the contralateral hemisphere in comparison with untreated animals. However, on the 180th day after TBI, the magnetic resonance imaging scan of the animal brains did not show a significant reduction in the volume of the lesion in MB-treated animals. These findings are important for understanding the development of the long-term effects of TBI and expand the required therapeutic window for targeted neuroprotective interventions.
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19

Prayson, Richard A. y Elizabeth A. Douglas. "Pistachio green brain discolouration associated with methylene blue use: an autopsy series". Pathology 42, n.º 7 (diciembre de 2010): 681–83. http://dx.doi.org/10.3109/00313025.2010.523685.

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20

Li, Lei, Li Qin, Hai-long Lu, Ping-Jing Li, Yuan-Jian Song y Rong-Li Yang. "Methylene blue improves streptozotocin-induced memory deficit by restoring mitochondrial function in rats". Brain Research 1657 (febrero de 2017): 208–14. http://dx.doi.org/10.1016/j.brainres.2016.12.024.

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21

Stern, Evan, Elsie Lee y Maria Almira. "12 “Blue Brain”: Unexpected Brain Discoloration at Autopsy Secondary to Use of Methylene Blue. Case Presentation and Review of the Literature". American Journal of Clinical Pathology 149, suppl_1 (enero de 2018): S5. http://dx.doi.org/10.1093/ajcp/aqx114.011.

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22

Rubashkin, V. Y. "About the influence of some gases on the absorption of methylene blue by the nerves and about the structure of nerve plexus". Neurology Bulletin VII, n.º 1 (25 de noviembre de 2020): 20–48. http://dx.doi.org/10.17816/nb49891.

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Who of the educated doctors and naturalists today does not know how abundant in the results and fruitful in the conclusions of the observations made in the course of these ten years with methylene blue. Injecting this wonderful reagent into the circulatory or lymphatic system of living, or just dead animals, or irrigating methylene blue tissue, which has not yet lost its vital properties, Ehrlich (1), Arnstein (2), Smirnov (3), Dogel (4) , M.D. Lavdovskiy (5), Retzius (6) and other authors found that methylene blue should be recognized as the best, one might say, the most sensitive reagent for detecting nerves and nerve plexus in various organs and tissues, not excluding the most nervous tissues such as the spinal cord and brain with their nodes and roots.
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23

Howland, Robert H. "Methylene Blue: The Long and Winding Road from Stain to Brain: Part 1". Journal of Psychosocial Nursing and Mental Health Services 54, n.º 9 (1 de septiembre de 2016): 21–24. http://dx.doi.org/10.3928/02793695-20160818-01.

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Howland, Robert H. "Methylene Blue: The Long and Winding Road From Stain to Brain: Part 2". Journal of Psychosocial Nursing and Mental Health Services 54, n.º 10 (1 de octubre de 2016): 21–26. http://dx.doi.org/10.3928/02793695-20160920-04.

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25

Gureev, Artem P., Ekaterina A. Shaforostova, Vasily N. Popov y Anatoly A. Starkov. "Methylene blue does not bypass Complex III antimycin block in mouse brain mitochondria". FEBS Letters 593, n.º 5 (20 de febrero de 2019): 499–503. http://dx.doi.org/10.1002/1873-3468.13332.

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26

Miclescu, Adriana, Hari Shanker Sharma, Cécile Martijn y Lars Wiklund. "Methylene blue protects the cortical blood–brain barrier against ischemia/reperfusion-induced disruptions*". Critical Care Medicine 38, n.º 11 (noviembre de 2010): 2199–206. http://dx.doi.org/10.1097/ccm.0b013e3181f26b0c.

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27

Iwamoto, J., M. Yoshinaga, S. P. Yang, E. Krasney y J. Krasney. "Methylene blue inhibits hypoxic cerebral vasodilation in awake sheep". Journal of Applied Physiology 73, n.º 6 (1 de diciembre de 1992): 2226–32. http://dx.doi.org/10.1152/jappl.1992.73.6.2226.

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Cerebral vasodilation in hypoxia may involve endothelium-derived relaxing factor-nitric oxide. Methylene blue (MB), an in vitro inhibitor of soluble guanylate cyclase, was injected intravenously into six adult ewes instrumented chronically with left ventricular, aortic, and sagittal sinus catheters. In normoxia, MB (0.5 mg/kg) did not alter cerebral blood flow (CBF, measured with 15-microns radiolabeled microspheres), cerebral O2 uptake, mean arterial pressure (MAP), heart rate, cerebral lactate release, or cerebral O2 extraction fraction (OEF). After 1 h of normobaric poikilocapnic hypoxia (arterial PO2 40 Torr, arterial O2 saturation 50%), CBF increased from 51 +/- 5.8 to 142 +/- 18.8 ml.min-1 x 100 g-1, cerebral O2 uptake from 3.5 +/- 0.25 to 4.7 +/- 0.41 ml.min-1 x 100 g-1, cerebral lactate release from 2 +/- 10 to 100 +/- 50 mumol.min- x 100 g-1, and heart rate from 107 +/- 5 to 155 +/- 9 beats/min (P < 0.01). MAP and OEF were unchanged from 91 +/- 3 mmHg and 48 +/- 4%, respectively. In hypoxia, 30 min after MB (0.5 mg/kg), CBF declined to 79.3 +/- 11.7 ml.min-1 x 100 g-1 (P < 0.01), brain O2 uptake (4.3 +/- 0.9 ml.min-1 x 100 g-1) and heart rate (133 +/- 9 beats/min) remained elevated, cerebral lactate release became negative (-155 +/- 60 mumol.min-1 x 100 g-1, P < 0.01), OEF increased to 57 +/- 3% (P < 0.01), and MAP (93 +/- 5 mmHg) was unchanged. The sheep became behaviorally depressed, probably because of global cerebral ischemia. These results may be related to interference with a guanylate cyclase-dependent mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
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28

Callaway, Narriman Lee, Penny D. Riha, Kathryn M. Wrubel, David McCollum y F. Gonzalez-Lima. "Methylene blue restores spatial memory retention impaired by an inhibitor of cytochrome oxidase in rats". Neuroscience Letters 332, n.º 2 (octubre de 2002): 83–86. http://dx.doi.org/10.1016/s0304-3940(02)00827-3.

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Müller, T. "Light-Microscopic Demonstration of Methylene Blue Accumulation Sites in Mouse Brain after Supravital Staining". Cells Tissues Organs 144, n.º 1 (1992): 39–44. http://dx.doi.org/10.1159/000147283.

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Katzoff, Ayelet, Tziona Ben-Gedalya, Itay Hurwitz, Nimrod Miller, Yehoshua Z. Susswein y Abraham J. Susswein. "Nitric Oxide Signals That Aplysia Have Attempted to Eat, a Necessary Component of Memory Formation After Learning That Food Is Inedible". Journal of Neurophysiology 96, n.º 3 (septiembre de 2006): 1247–57. http://dx.doi.org/10.1152/jn.00056.2006.

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Inhibiting nitric oxide (NO) synthesis during learning that food is inedible in Aplysia blocks subsequent memory formation. To gain insight into the function of NO transmission during learning we tested whether blocking NO synthesis affects aspects of feeding that are expressed both in a nonlearning context and during learning. Inhibiting NO synthesis with L-NAME and blocking guanylyl cyclase with methylene blue decreased the efficacy of ad libitum feeding. D-NAME had no effect. L-NAME also decreased rejection responses frequency, but did not affect rejection amplitude. The effect of L-NAME was explained by a decreased signaling that efforts to swallow are not successful, leading to a decreased rejection rate, and a decreased ability to reposition and subsequently consume food in ad libitum feeding. Signaling that animals have made an effort to swallow is a critical component of learning that food is inedible. Stimulation of the lips with food alone did not produce memory, but stimulation combined with the NO donor SNAP did produce memory. Exogenous NO at a concentration causing memory also excited a key neuron responding to NO, the MCC. Block of the cGMP second-messenger cascade during training by methylene blue also blocked memory formation after learning. Our data indicate that memory arises from the contingency of three events during learning that food is inedible. One of the events is efforts to swallow, which are signaled by NO by cGMP.
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Cheng, Quancheng, Xuhao Chen, Jiayi Ma, Xingyuan Jiang, Jiahui Chen, Mengqin Zhang, Yejun Wu, Weiguang Zhang y Chunhua Chen. "Effect of Methylene Blue on White Matter Injury after Ischemic Stroke". Oxidative Medicine and Cellular Longevity 2021 (2 de febrero de 2021): 1–10. http://dx.doi.org/10.1155/2021/6632411.

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Methylene blue, the FDA-grandfathered drug was proved to be neuroprotective in ischemic stroke in rat. However, the mechanism of the protective effect was unknown. In this study, we used different animal models to investigate the effect of MB administration given within and beyond the therapeutic time window on behavioral deficits and infarct volume and related mechanism about the white matter protection. Middle cerebral artery occlusion and reperfusion (MCAO) and photothrombotic middle cerebral artery occlusion (PT-MCAO) models were used. Behavioral deficits and infarct volume were measured by foot fault test, Garcia neurological score, and TTC staining. Black gold staining and western blot were used to evaluate the brain white matter injury. We found that intraperitoneal administration of MB immediately or 24 h after the MCAO or PT-MCAO surgery reduced infarct volume, improved the neurological deficits, and reduced the white matter injury via myelin basic protein (BMP) protection. These findings suggested that MB relieved the white matter injury besides neuronal protection and has potential therapeutic effects on ischemic stroke.
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32

Sharma, H. S., R. Patnaik, A. Sharma y L. Wiklund. "Cardiac arrest alters regional ubiquitin levels in the porcine brain. Neuroprotective effects of methylene blue". Journal of the Neurological Sciences 333 (octubre de 2013): e164-e165. http://dx.doi.org/10.1016/j.jns.2013.07.686.

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Fenn, Ashley M., John P. Skendelas, Daniel N. Moussa, Megan M. Muccigrosso, Phillip G. Popovich, Jonathan Lifshitz, Daniel S. Eiferman y Jonathan P. Godbout. "Methylene Blue Attenuates Traumatic Brain Injury-Associated Neuroinflammation and Acute Depressive-Like Behavior in Mice". Journal of Neurotrauma 32, n.º 2 (15 de enero de 2015): 127–38. http://dx.doi.org/10.1089/neu.2014.3514.

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Rodriguez, Pavel, Wei Zhou, Douglas W. Barrett, Wilson Altmeyer, Juan E. Gutierrez, Jinqi Li, Jack L. Lancaster, Francisco Gonzalez-Lima y Timothy Q. Duong. "Multimodal Randomized Functional MR Imaging of the Effects of Methylene Blue in the Human Brain". Radiology 281, n.º 2 (noviembre de 2016): 516–26. http://dx.doi.org/10.1148/radiol.2016152893.

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Bhurtel, Sunil, Nikita Katila, Sabita Neupane, Sunil Srivastav, Pil-Hoon Park y Dong-Young Choi. "Methylene blue protects dopaminergic neurons against MPTP-induced neurotoxicity by upregulating brain-derived neurotrophic factor". Annals of the New York Academy of Sciences 1431, n.º 1 (7 de junio de 2018): 58–71. http://dx.doi.org/10.1111/nyas.13870.

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Wiklund, Lars, Aruna Sharma y Hari Shanker Sharma. "Neuroprotection by Methylene Blue in Cerebral Global Ischemic Injury Induced Blood-Brain Barrier Disruption and Brain Pathology: A Review". CNS & Neurological Disorders - Drug Targets 15, n.º 9 (7 de octubre de 2016): 1181–87. http://dx.doi.org/10.2174/1871527315666160915114516.

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37

Weigand, Anne, Lisa Edelkraut, Markus Conrad, Simone Grimm y Malek Bajbouj. "Light-Dependent Effects of Prefrontal rTMS on Emotional Working Memory". Brain Sciences 11, n.º 4 (31 de marzo de 2021): 446. http://dx.doi.org/10.3390/brainsci11040446.

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Growing evidence suggests that colored light exposure can affect several brain functions in addition to conscious visual perception. Blue as compared to green light has especially been shown to enhance alertness and vigilance, as well as cognitive functions. However, the role of light exposure in studies using non-invasive brain stimulation remains unclear. Here, we examined the impact of light on cognitive-emotional effects of prefrontal repetitive transcranial magnetic stimulation (rTMS). In a randomized within-subjects design, twenty participants (12 males, 26 ± 4 years) were exposed to blue or green light prior and concomitant to active or sham rTMS (1Hz, 15min, 110% of the resting motor threshold), applied over the right dorsolateral prefrontal cortex (DLPFC). In each condition, an emotional working memory task (EMOBACK) was presented pre- and post-intervention. Stimuli of the EMOBACK task were positive, negative and neutral words. Our results revealed valence-specific stimulation effects in dependence of colored light exposure. More specifically, task accuracy was significantly increased for positive stimuli under blue light and for negative stimuli under green light exposure. Our findings highlight the importance of state-dependency in studies using non-invasive brain stimulation and show blue light exposure to be a potential adjunctive technique to rTMS for enhancing cognitive-emotional modulation.
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38

Khan, Muhammad Umair, Gul Hassan y Jinho Bae. "Flexible Resistive Switching Memory with a Schottky Diode Function Based on a Zinc Oxide/Methylene Blue Heterojunction". Journal of Electronic Materials 49, n.º 8 (16 de mayo de 2020): 4764–72. http://dx.doi.org/10.1007/s11664-020-08200-z.

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Bunge, Frank, Sander van den Driesche y Michael J. Vellekoop. "Gas Supply through Agarose Walls in Cell Culturing Microchips". Advances in Science and Technology 100 (octubre de 2016): 115–19. http://dx.doi.org/10.4028/www.scientific.net/ast.100.115.

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We present a novel structure to supply gases to microchambers in microfluidic chips. An exemplary application is the continuous feeding of oxygen and CO2 for on-chip cell cultivation of mammalian cells. In our device, the surrounding air diffuses into the culture medium inside the chip through a porous wall of agarose hydrogel resulting in an easy and robust design. One common method is the usage of gas permeable PDMS chips. However, liquid medium in which the cells grow is absorbed by PDMS causing unknown concentrations and memory effects. Another possibility is a complex setup where medium with already dissolved gas is pumped constantly through the chip. We designed and realized a silicon and borosilicate glass chip containing a gas permeable wall of agarose preventing leakage of medium. In order to precisely position the walls in the chip, we made use of surficial phaseguides (50nm high). The blue-bottle-experiment makes the effective dissipation of oxygen visible when the colorless leucomethylen-blue reacts to methylene-blue. Successful results were achieved when applying 0.5 g/l methylene blue, 10 g/l glucose and a pH of 12.6 set by a buffer solution. As a result a continuous color gradient through the chip was obtained, which reflects the oxygen gradient and confirms the oxygen diffusion.
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40

Al-Tahan, Farid J. "The effect of L-arginine and its antagonist L-NAME and Methylene blue on sensory and cognitive function in mice". Iraqi Journal of Veterinary Medicine 36, n.º 1 (30 de junio de 2012): 99–106. http://dx.doi.org/10.30539/iraqijvm.v36i1.553.

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The present study was done to focus light on possible enhancement of the functional performance of male mice and female in neuronal behaviors by using L-arginine as a precursor of nitric oxide (NO). The results showed increase of latency period to reach the novel object in L-arginine treated groups and decrease in both L-NAME and methylene blue treated groups in both periods of treatment (15 and 30) days and were more prominent in male than in female mice as compared with control groups. Similar results were observed in passive avoidance latency period to enter the dark compartment. There was a reduction in latency period to reach the alternative arm of T-maze test in L-arginine treated groups and increase in both L-NAME and methylene blue treated groups in both periods of treatment (15 and 30) days in both genders. It could be concluded that L-arginine-NO pathway plays an important role in improving memory in male more than female mice.
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41

Kämpfer, I., A. Seese, C. Dannenberg, R. Kluge, W. Burchert, W. H. Knapp y H. Barthel. "Improvement of Brain SPECT by Stabilization of Tc-99m-HMPAO with Methylene Blue or Cobalt Chloride". Nuklearmedizin 38, n.º 03 (1999): 80–84. http://dx.doi.org/10.1055/s-0038-1632196.

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Summary Aim: This present study was carried out to investigate whether stabilization of Tc-99m-HMPAO with methylene blue (MB) or cobalt chloride (CC) causes a sensible improvement in image quality and how cerebral to noncerebral activity ratios compare with those of Tc-99m-ECD. Methods: 30 minutes after preparation 400-600 MBq unstabilized Tc-99m-HMPAO (N = 35 patients), Tc-99m-HMPAO added with MB (N = 24 patients), added with CC (N = 30 patients) or Tc-99m-ECD (N = 28 patients) were injected. Radiochemical stability was measured in vitro with three chromatographical methods. Image quality was assessed quantitatively using two ratios, one of them determined by count densities of brain/scalp (QS), the other one by count densities of brain/ nose (QN). In addition, image quality (0 = bad, 3 = excellent) and background activity (0 = high, 3 = no) were visually assessed by three independent observers. Results: In contrast to unstabilized Tc-99m-HMPAO the integrity of the complexes of MB-Tc-99m-HMPAO, CC-Tc-99m-HMPAO and Tc-99m-ECD decreased only by a few percent during a period of 2 hours after reconstitution (66.8 ± 9.9 vs. 93.0 ± 2.5, 91.8 ± 1.9 and 96.9 ± 1.4%, p <0.001). Qs and Qn (m.v. ± SD) differed significantly between studies using unstabilized Tc-99m-HMPAO (3.0 ± 0.4 and 2.1 ± 0.3), MB-Tc-99m-HMPAO (3.4 ± 0.4 and 2.3 ± 0.3), CC-Tc-99m-H M PAO (3.6 ± 0.6 and 2.6 ± 0.4) and those using Tc-99m-ECD (4.3 ± 0.7 and 4.8 ± 1.4; p <0.05 and <0.001). Stabilization with CC or MB resulted in significant higher scoring of image quality and lower scoring of background activity in comparison to that of unstabilized Tc-99m-HMPAO, without reaching the scores obtained with Tc-99m-ECD. Conclusions: It is concluded that stabilization of Tc-99m-HMPAO with MB or CC definitely improves image quality in rCBF-SPECT, without reaching that of Tc-99m-ECD. Improvement of image quality results from the reduction of the amount of decomposition products that contribute to considerable extracerebral activity.
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42

Tretter, L., G. Horvath, A. Hölgyesi, F. Essek y V. Adam-Vizi. "Enhanced hydrogen peroxide generation accompanies the beneficial bioenergetic effects of methylene blue in isolated brain mitochondria". Free Radical Biology and Medicine 77 (diciembre de 2014): 317–30. http://dx.doi.org/10.1016/j.freeradbiomed.2014.09.024.

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43

Lee, Yong Soo, Suk Kyu Han y Robert D. Wurster. "Enhancement of methylene blue-induced cytotoxicity in human brain tumor cells by an iron chelator, deferoxamine". Archives of Pharmacal Research 18, n.º 3 (junio de 1995): 159–63. http://dx.doi.org/10.1007/bf02979188.

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44

Fenn, A. M., J. Skendelas, D. Moussa, M. M. Muccigrosso, P. G. Popovich, J. Lifshitz, D. S. Eiferman y J. P. Godbout. "16. Methylene blue infusion for treatment of traumatic brain injury-associated neuroinflammation and depressive-like behavior". Brain, Behavior, and Immunity 40 (septiembre de 2014): e5. http://dx.doi.org/10.1016/j.bbi.2014.06.036.

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45

Chertok, V. M., A. E. Kotsyuba y E. P. Kotsyuba. "HEME OXYGENASE-2 NEURONS BRAIN AND SPINAL CORD OF HUMAN". Annals of the Russian academy of medical sciences 67, n.º 6 (23 de junio de 2012): 36–41. http://dx.doi.org/10.15690/vramn.v67i6.282.

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Immune localization of heme oxygenase-2 in neurons of some nuclei of the spinal cord and brain stem in 6 men 18–44 years old who died from causes unrelated to injury of central nervous system was studied. Neurons with positive reaction are determined for all studied regions of the brain where their contents in various nuclei ranging from 0,5 to 16% of the total number of cells detected by methylene blue. In all the sensory nuclei there is a high proportion of small neurons with a high or moderate density of reaction produc deposits. Large cells of motor nuclei often exhibit negative or low intensive enzyme reaction.
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46

Telch, Michael J., Aleksandra K. Bruchey, David Rosenfield, Adam R. Cobb, Jasper Smits, Sandra Pahl y F. Gonzalez-Lima. "Effects of Post-Session Administration of Methylene Blue on Fear Extinction and Contextual Memory in Adults With Claustrophobia". American Journal of Psychiatry 171, n.º 10 (octubre de 2014): 1091–98. http://dx.doi.org/10.1176/appi.ajp.2014.13101407.

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47

ZHAO, MINGFEI, FENG LIANG, HANGDI XU, WEI YAN y JIANMIN ZHANG. "Methylene blue exerts a neuroprotective effect against traumatic brain injury by promoting autophagy and inhibiting microglial activation". Molecular Medicine Reports 13, n.º 1 (11 de noviembre de 2015): 13–20. http://dx.doi.org/10.3892/mmr.2015.4551.

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48

Zakaria, Aya, Nabila Hamdi y Reham Mahmoud Abdel-Kader. "Methylene Blue Improves Brain Mitochondrial ABAD Functions and Decreases Aβ in a Neuroinflammatory Alzheimer’s Disease Mouse Model". Molecular Neurobiology 53, n.º 2 (20 de enero de 2015): 1220–28. http://dx.doi.org/10.1007/s12035-014-9088-8.

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49

Huntington, GR y JM Pennington. "Fatal Methaemoglobinaemia Due To Intentional Sodium Nitrite Poisoning". Acute Medicine Journal 20, n.º 2 (1 de abril de 2021): 148–50. http://dx.doi.org/10.52964/amja.0856.

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We report a case of fatal methaemoglobinaema resulting from sodium nitrite poisoning. A 28 year old woman arrested in the emergency department following collapse. During resuscitation a venous blood gas revealed a methaemoglobin percentage of 81%. Following treatment with methylene blue, sodium bicarbonate and adrenaline, the methaemoglobin decreased. Prior to transfer to intensive care, a CT head revealed extensive hypoxic brain injury. Two days later brain death was confirmed on brainstem testing. Severe methaemoglobinaemia is rapidly fatal, with fast diagnosis and treatment associated with improved outcomes.
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50

Tasker, Robert C., Sati K. Sahota y Stephen R. Williams. "Bioenergetic Recovery following Ischemia in Brain Slices Studied by 31P-NMR Spectroscopy: Differential Age Effect of Depolarization Mediated by Endogenous Nitric Oxide". Journal of Cerebral Blood Flow & Metabolism 16, n.º 1 (enero de 1996): 125–33. http://dx.doi.org/10.1097/00004647-199601000-00015.

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Proximate neurotoxic mechanisms during postischemic recovery may be influenced by stage of development and complicating factors such as cortical spreading depression or secondary brain insult. Using 31P nuclear magnetic resonance spectroscopy, we have monitored pH and cellular energy metabolites phosphocreatine (PCr) and ATP in the ex vivo rat cerebral cortex before, during, and after substrate and oxygen deprivation, which represents “in vitro ischemia.” There were important developmental differences in resistance and response to an ischemic insult. Twenty-one-day-old (P21) rat cortical slices had no detectable β-ATP or PCr at the end of a 20-min insult, while γ-day-old (P7) slices had 50 ± 13.7% (mean ± SD, n = 12) and 17 ± 14.8% relative to preischemia levels, respectively. Postischemic depolarization resulted in age-dependent effects on PCr (p < 0.05): In the older tissue, depolarization significantly worsened the recovery of PCr, whereas in young tissue it ameliorated recovery. This amelioration could be prevented by inhibiting nitric oxide production with methylene blue (depolarization-methylene blue interaction, p < 0.05) and enhanced by administration of the nitric oxide donor glyceryl trinitrate (GTN; p < 0.01). However, in P21 tissue, GTN further exacerbated injury (age-GTN interaction, p < 0.01). Therefore, in this vascular-independent preparation, a neuronal or glial nitric oxide-dependent mechanism appears to confer improved postischemic bioenergetic recovery in the developing brain compared with the mature brain.
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