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Journal articles on the topic 'Lithium cells'

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Author: Grafiati

Published: 4 June 2021

Last updated: 6 September 2023

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1

Ziebert, Carlos, Corneliu Barbu, and Tomas Jezdinsky. "Calorimetric studies and safety tests on lithion-ion cells and post-lithium cells." Open Access Government 37, no. 1 (January 9, 2023): 416–17. http://dx.doi.org/10.56367/oag-037-10412.

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Calorimetric studies and safety tests on lithion-ion cells and post-lithium cells Open Access Government interviews Dr Carlos Ziebert, of the Karlsruhe Institute of Technology (KIT), who explores the thermal and safety properties of batteries across calorimetric studies. The group batteries – calorimetry and safety – focus on calorimetric studies and safety tests on lithium-ion cells and post-lithium cells. Depending on the cell size and application, different types of calorimeters are used in Europe's largest Battery Calorimeter Laboratory, established in 2011. It provides seven Accelerating Rate Calorimeters (ARCs) from Thermal Hazard Technology allowing the evaluation of thermodynamic, thermal and safety data for Lithium-ion and post-Li cells on material, cell, and pack levels for both normal and abuse conditions (thermal, electrical, mechanical). The lab also includes glove boxes for cell assembly and disassembly, many temperature chambers, a thermal camera, and cyclers with several hundred channels. It contains extremely sensitive 3D Calvet calorimeters, providing thermodynamic parameters and gas chromatography-mass spectrometry systems from Perkin-Elmer for venting gas analysis.

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2

Hammond, WP, ER Rodger, and DC Dale. "Lithium augments GM-CSA generation in canine cyclic hematopoiesis." Blood 69, no. 1 (January 1, 1987): 117–23. http://dx.doi.org/10.1182/blood.v69.1.117.bloodjournal691117.

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Cyclic hematopoiesis in gray collie dogs can be cured by lithium treatment. We examined the mechanism of lithium's effect by developing an assay for the canine equivalent of GM-CSF (called GM-CSA). Phytohemagglutinin (PHA)-stimulated canine blood mononuclear cells produce GM-CSA in a dose-dependent manner; this GM-CSA stimulates more neutrophil-containing colonies than does endotoxin-treated dog serum. Production of GM-CSA by PHA-stimulated normal dog cells was not altered by lithium. However, cells from gray collies during their neutrophilic period increased their GM-CSA when lithium (2 mEq/L) was added to low doses of PHA, whereas neutropenic gray collie cells did not. These data suggest that lithium could modulate cyclic hematopoiesis by increasing intramedullary GM-CSA at the time when marrow neutrophilic progenitor cells are at their nadir.

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3

Urquidi-Macdonald, Mirna, Homero Castaneda, and Angela M. Cannon. "Lithium fuel cells:." Electrochimica Acta 47, no. 15 (June 2002): 2495–503. http://dx.doi.org/10.1016/s0013-4686(02)00109-3.

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4

Hammond, WP, ER Rodger, and DC Dale. "Lithium augments GM-CSA generation in canine cyclic hematopoiesis." Blood 69, no. 1 (January 1, 1987): 117–23. http://dx.doi.org/10.1182/blood.v69.1.117.117.

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Abstract Cyclic hematopoiesis in gray collie dogs can be cured by lithium treatment. We examined the mechanism of lithium's effect by developing an assay for the canine equivalent of GM-CSF (called GM-CSA). Phytohemagglutinin (PHA)-stimulated canine blood mononuclear cells produce GM-CSA in a dose-dependent manner; this GM-CSA stimulates more neutrophil-containing colonies than does endotoxin-treated dog serum. Production of GM-CSA by PHA-stimulated normal dog cells was not altered by lithium. However, cells from gray collies during their neutrophilic period increased their GM-CSA when lithium (2 mEq/L) was added to low doses of PHA, whereas neutropenic gray collie cells did not. These data suggest that lithium could modulate cyclic hematopoiesis by increasing intramedullary GM-CSA at the time when marrow neutrophilic progenitor cells are at their nadir.

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5

Bugga, Ratnakumar V., and Marshall C. Smart. "Lithium Plating Behavior in Lithium-Ion Cells." ECS Transactions 25, no. 36 (December 17, 2019): 241–52. http://dx.doi.org/10.1149/1.3393860.

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6

Auborn, J. J., and Y. L. Barberio. "Lithium Intercalation Cells Without Metallic Lithium: and." Journal of The Electrochemical Society 134, no. 3 (March 1, 1987): 638–41. http://dx.doi.org/10.1149/1.2100521.

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7

Gilmour, A., C. O. Giwa, J. C. Lee, and A. G. Ritchie. "Lithium rechargeable envelope cells." Journal of Power Sources 65, no. 1-2 (March 1997): 219–24. http://dx.doi.org/10.1016/s0378-7753(97)02475-0.

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8

Kilroy, W. P., C. Schlaikjer, P. Polsonetti, and M. Jones. "Optimized lithium oxyhalide cells." Journal of Power Sources 44, no. 1-3 (April 1993): 715–23. http://dx.doi.org/10.1016/0378-7753(93)80223-c.

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9

Münstedt, H., G. Köhler, H. Möhwald, D. Naegele, R. Bitthin, G. Ely, and E. Meissner. "Rechargeable polypyrrole/lithium cells." Synthetic Metals 18, no. 1-3 (February 1987): 259–64. http://dx.doi.org/10.1016/0379-6779(87)90890-3.

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10

Yoshimatsu, Isamu, Toshiro Hirai, and Jun‐ichi Yamaki. "Lithium Electrode Morphology during Cycling in Lithium Cells." Journal of The Electrochemical Society 135, no. 10 (October 1, 1988): 2422–27. http://dx.doi.org/10.1149/1.2095351.

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11

Morni, N. M., and A. K. Arof. "Chitosan–lithium triflate electrolyte in secondary lithium cells." Journal of Power Sources 77, no. 1 (January 1999): 42–48. http://dx.doi.org/10.1016/s0378-7753(98)00170-0.

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12

Bäuerlein, Peter, Rudolf Herr, Matthias Kloss, Jörg Kümpers, Matthias Maul, and Eberhard Meissner. "Advanced lithium ion cells with lithium manganese spinel." Journal of Power Sources 81-82 (September 1999): 585–88. http://dx.doi.org/10.1016/s0378-7753(99)00226-8.

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13

Manickam, M., and M. Takata. "Lithium intercalation cells LiMn2O4/LiTi2O4 without metallic lithium." Journal of Power Sources 114, no. 2 (March 2003): 298–302. http://dx.doi.org/10.1016/s0378-7753(02)00586-4.

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14

Buel, Amber, Rodrigo Naves, Tethia Mbana, Chander Raman, and Patrizia De Sarno. "Therapeutic effect of lithium in EAE: Effects on dendritic cells and encephalitogenic activity of T cells. (96.16)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 96.16. http://dx.doi.org/10.4049/jimmunol.184.supp.96.16.

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Abstract We have reported that the GSK3 inhibitor, lithium, is therapeutic in acute and relapsing remitting EAE. We have now determined that lithium treatment is effective in attenuating EAE induced by Th1 encephalitogenic T-cells but not Th17 cells. These results were obtained from passive transfer experiments in which encephalitogenic Th1 or Th17 cells were transferred into lithium-treated or untreated naïve recipients. Consistent with this observation, lithium treatment was also ineffective in inhibiting EAE in IFN-γR1-/- mice. Various experiments indicated that the primary target of lithium therapy in vivo were cells of the innate immune system such as, dendritic cells (DC) rather than T-cells. Using primary dendritic cells obtained from spleens and lymph nodes or bone marrow derived DC (BMDC), we have determined that lithium does not affect LPS or CpG-induced maturation of DC. Remarkably, lithium treated DC were as or more efficient than untreated DC in their ability to process and present ovalbumin to OTII T-cells or MOG35-55 peptide to T-cells from 2D2 TCR transgenic mice. These observations raise the possibility that lithium-treatment of DC alters the chemokine and cytokine profile involved in migration and/or Th-subset specific differentiation. Overall, our findings that pharmacological inhibition of GSK3 is effective in Th1 EAE but not Th17 EAE has crucial implications for identifying and treating MS patients.

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15

Poudel, Pragati, Zhijia Du, Boryann (Bor Yann) Liaw, Takuto Iriyama, and Guangsheng Zhang. "(Digital Presentation) Protective Effects of Lithium Plating on High Temperature Degradation of Lithium-Ion Cells." ECS Meeting Abstracts MA2022-01, no. 2 (July 7, 2022): 443. http://dx.doi.org/10.1149/ma2022-012443mtgabs.

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Lithium plating and solid electrolyte interphase (SEI) growth are two main degradation mechanisms of lithium-ion cells. While lithium plating can occur during low temperature charging and/or fast charging, SEI growth is accelerated during high temperature operation. Here we report an interesting observation that lithium plating shows protective effects on high temperature degradation of lithium-ion cells. As shown in Figure 1, two baseline commercially available lithium-ion cells were cycled only at 60 °C. They rapidly degraded which can be attributed to SEI growth. In comparison, the other two cells were pre-cycled at 5 °C and experienced rapid degradation due to lithium plating. But when these two cells with lithium plating were further cycled at 60 °C, they showed slower degradation than the baseline cells. Similar results were also observed for cells cycled at 45 °C as shown in Figure 2. These preliminary results suggest that lithium plating has protective effects for high temperature cycling of lithium-ion cells. Such effects were further observed in lab-made lithium-ion cells with low negative/positive (N/P) ratio. As shown in Figure 3, baseline cells (N/P ratio=1.25) degraded quickly during 60 °C cycling (21 mA constant current charging to 4.2 V and 21 mA constant current discharging to 2.8 V). In comparison, low N/P ratio cells (N/P ratio=0.8) that had lithium plating induced during formation showed very stable discharge capacity for more than 600 cycles before abrupt degradation. Further analysis of these results will be reported. Figure 1

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16

Fateev, Sergei Anatol'evich, Natal'ya Vladimirovna Polyakova, and Vladimir Prokop'evich Kondratov. "Prolonged testing of lithium-fluorocarbon cells." Electrochemical Energetics 12, no. 2 (2012): 82–87. http://dx.doi.org/10.18500/1608-4039-2012-12-2-82-87.

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Prolonged testing of lithium-fluorocarbon cells for pacemakers to evaluate the shape of the discharge curve are carried with the purpose of an estimation of the form at the end of operation. It is shown that flatter discharge curve of the differ-current sources with a high content of fluorocarbon. The estimation of capacity fluorocarbon-lithium cells made for various discharge conditions.

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17

Takeuchi, Esther S., and William C. Thiebolt. "Lithium Deposition in Prismatic Lithium Cells during Intermittent Discharge." Journal of The Electrochemical Society 138, no. 9 (September 1, 1991): L44—L45. http://dx.doi.org/10.1149/1.2086072.

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18

Sun, Xiao-Guang, Shun Wan, Hong Yu Guang, Youxing Fang, Kimberly Shawn Reeves, Miaofang Chi, and Sheng Dai. "New promising lithium malonatoborate salts for high voltage lithium ion batteries." Journal of Materials Chemistry A 5, no. 3 (2017): 1233–41. http://dx.doi.org/10.1039/c6ta07757a.

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Three new lithium salts, lithium difluoro-2-methyl-2-fluoromalonaoborate, lithium difluoro-2-ethyl-2-fluoromalonaoborate, and lithium difluoro-2-propyl-2-fluoro malonaoborate exhibit good cycling stability with high coulombic efficiencies in LiNi_0.5Mn_1.5O₄ and graphite based half-cells and full cells.

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19

Zhang, Zejun. "Research Progress of Cathode Materials for Graphene-based Fuel Cells." Academic Journal of Science and Technology 5, no. 2 (March 30, 2023): 179–82. http://dx.doi.org/10.54097/ajst.v5i2.6860.

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Graphite is the most widely used cathode material for commercial lithium-ion batteries at present, and the increasing market demand puts forward higher requirements for lithium storage performance of graphite cathode materials. Graphene is a kind of cathode material with great development potential, and its lithium storage performance is influenced by many factors such as structural characteristics, oxygen-containing functional groups and impurity atoms, which leads to complex lithium storage behavior and mechanism. When the polymer with lithium storage activity is compounded with graphene as cathode material, the lithium storage performance is affected by the reversibility of polymer redox and the composite structure. In this article, the working principle of Li-lon and the lithium intercalation mechanism of graphite are introduced, and the research status and progress of graphite cathode materials in surface modification and structural regulation in recent years are emphatically reviewed.

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20

Yang, Chunhao, Bo Zhu, Mingjie Zhan, and Zi-Chun Hua. "Lithium in Cancer Therapy: Friend or Foe?" Cancers 15, no. 4 (February 8, 2023): 1095. http://dx.doi.org/10.3390/cancers15041095.

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Lithium, a trace element important for fetal health and development, is considered a metal drug with a well-established clinical regime, economical production process, and a mature storage system. Several studies have shown that lithium affects tumor development by regulating inositol monophosphate (IMPase) and glycogen synthase kinase-3 (GSK-3). Lithium can also promote proliferation and programmed cell death (PCD) in tumor cells through a number of new targets, such as the nuclear receptor NR4A1 and Hedgehog-Gli. Lithium may increase cancer treatment efficacy while reducing side effects, suggesting that it can be used as an adjunctive therapy. In this review, we summarize the effects of lithium on tumor progression and discuss the underlying mechanisms. Additionally, we discuss lithium’s limitations in antitumor clinical applications, including its narrow therapeutic window and potential pro-cancer effects on the tumor immune system.

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21

Herr, Rudolf. "Organic electrolytes for lithium cells." Electrochimica Acta 35, no. 8 (August 1990): 1257–65. http://dx.doi.org/10.1016/0013-4686(90)90059-9.

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22

Basu, Samar, and Forrest A. Trumbore. "Lithium‐Niobium Triselenide Coin Cells." Journal of The Electrochemical Society 139, no. 12 (December 1, 1992): 3379–85. http://dx.doi.org/10.1149/1.2069087.

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23

Novák, P., B. Klápště, and P. Podhájecký. "CuO cathode in lithium cells." Journal of Power Sources 15, no. 2-3 (June 1985): 101–8. http://dx.doi.org/10.1016/0378-7753(85)80065-3.

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24

Levy, Samuel C., and Per Bro. "Reliability analysis of lithium cells." Journal of Power Sources 26, no. 1-2 (May 1989): 223–30. http://dx.doi.org/10.1016/0378-7753(89)80030-8.

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25

Jun, Hasegawa, and Suzuki Katsuhiko. "5498764 Negative electrode for lithium secondary cells and lithium secondary cells using the same." Journal of Power Sources 66, no. 1-2 (May 1997): 183. http://dx.doi.org/10.1016/s0378-7753(97)89717-0.

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26

Martin, Cameron, Matthew Genovese, A. J. Louli, Rochelle Weber, and J. R. Dahn. "Cycling Lithium Metal on Graphite to Form Hybrid Lithium-Ion/Lithium Metal Cells." Joule 4, no. 6 (June 2020): 1296–310. http://dx.doi.org/10.1016/j.joule.2020.04.003.

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27

Barker, J., R. K. B. Gover, P. Burns, A. Bryan, M. Y. Saidi, and J. L. Swoyer. "Performance Evaluation of Lithium Vanadium Fluorophosphate in Lithium Metal and Lithium-Ion Cells." Journal of The Electrochemical Society 152, no. 9 (2005): A1776. http://dx.doi.org/10.1149/1.1990068.

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28

Keister, P., J. M. Greenwood, C. F. Holmes, and R. T. Mead. "Performance of lithium alloy/lithium and calcium/ lithium anodes in thionyl chloride cells." Journal of Power Sources 15, no. 4 (August 1985): 239–44. http://dx.doi.org/10.1016/0378-7753(85)80076-8.

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29

Alsady, Mohammad, Theun de Groot, Marleen L. A. Kortenoeven, Claudia Carmone, Kim Neijman, Melissa Bekkenkamp-Grovenstein, Udo Engelke, et al. "Lithium induces aerobic glycolysis and glutaminolysis in collecting duct principal cells." American Journal of Physiology-Renal Physiology 314, no. 2 (February 1, 2018): F230—F239. http://dx.doi.org/10.1152/ajprenal.00297.2017.

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Lithium, given to bipolar disorder patients, causes nephrogenic diabetes insipidus (Li-NDI), a urinary-concentrating defect. Li-NDI occurs due to downregulation of principal cell AQP2 expression, which coincides with principal cell proliferation. The metabolic effect of lithium on principal cells, however, is unknown and investigated here. In earlier studies, we showed that the carbonic anhydrase (CA) inhibitor acetazolamide attenuated Li-induced downregulation in mouse-collecting duct (mpkCCD) cells. Of the eight CAs present in mpkCCD cells, siRNA and drug treatments showed that downregulation of CA9 and to some extent CA12 attenuated Li-induced AQP2 downregulation. Moreover, lithium induced cell proliferation and increased the secretion of lactate. Lithium also increased urinary lactate levels in wild-type mice that developed Li-NDI but not in lithium-treated mice lacking ENaC, the principal cell entry site for lithium. Inhibition of aerobic glycolysis with 2-deoxyglucose (2DG) attenuated lithium-induced AQP2 downregulation in mpkCCD cells but did not attenuate Li-NDI in mice. Interestingly, NMR analysis demonstrated that lithium also increased the urinary succinate, fumarate, citrate, and NH4+ levels, which were, in contrast to lactate, not decreased by 2DG. Together, our data reveal that lithium induces aerobic glycolysis and glutaminolysis in principal cells and that inhibition of aerobic glycolysis, but not the glutaminolysis, does not attenuate Li-NDI.

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30

Giordani, Vincent, Jasim Uddin, Vyacheslav S. Bryantsev, Gregory V. Chase, and Dan Addison. "High Concentration Lithium Nitrate/Dimethylacetamide Electrolytes for Lithium/Oxygen Cells." Journal of The Electrochemical Society 163, no. 13 (2016): A2673—A2678. http://dx.doi.org/10.1149/2.0951613jes.

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31

Vaughey, J. T., Andrea M. Geyer, Nathanael Fackler, Christopher S. Johnson, K. Edstrom, H. Bryngelsson, Roy Benedek, and Michael M. Thackeray. "Studies of layered lithium metal oxide anodes in lithium cells." Journal of Power Sources 174, no. 2 (December 2007): 1052–56. http://dx.doi.org/10.1016/j.jpowsour.2007.06.194.

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32

Brissot, C., M. Rosso, J. N. Chazalviel, and S. Lascaud. "Concentration measurements in lithium/polymer–electrolyte/lithium cells during cycling." Journal of Power Sources 94, no. 2 (March 2001): 212–18. http://dx.doi.org/10.1016/s0378-7753(00)00589-9.

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33

Bohinsky, Amy, Sobana Perumaram Rangarajan, Yevgen Barsukov, and Partha P. Mukherjee. "Preventing Lithium Plating during Fast Charging of Lithium-Ion Cells." ECS Meeting Abstracts MA2020-02, no. 3 (November 23, 2020): 594. http://dx.doi.org/10.1149/ma2020-023594mtgabs.

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34

Du, Yang, Yun Qian, Xiaomei Tang, Yan Guo, Shuang Chen, Mingzhu Jiang, Bingyu Yang, et al. "Chloroquine attenuates lithium-induced NDI and proliferation of renal collecting duct cells." American Journal of Physiology-Renal Physiology 318, no. 5 (May 1, 2020): F1199—F1209. http://dx.doi.org/10.1152/ajprenal.00478.2019.

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Lithium is widely used in psychiatry as the golden standard for more than 60 yr due to its effectiveness. However, its adverse effect has been limiting its long-term use in clinic. About 40% of patients taking lithium develop nephrogenic diabetes insipidus (NDI). Lithium can also induce proliferation of collecting duct cells, leading to microcyst formation in the kidney. Lithium was considered an autophagy inducer that might contribute to the therapeutic benefit of neuropsychiatric disorders. Thus, we hypothesized that autophagy may play a role in lithium-induced kidney nephrotoxicity. To address our hypothesis, we fed mice with a lithium-containing diet with chloroquine (CQ), an autophagy inhibitor, concurrently. Lithium-treated mice presented enhanced autophagy activity in the kidney cortex and medulla. CQ treatment significantly ameliorated lithium-induced polyuria, polydipsia, natriuresis, and kaliuresis accompanied with attenuated downregulation of aquaporin-2 and Na+-K+-2Cl− cotransporter protein. The protective effect of CQ on aquaporin-2 protein abundance was confirmed in cultured cortical collecting duct cells. In addition, we found that lithium-induced proliferation of collecting duct cells was also suppressed by CQ as detected by proliferating cell nuclear antigen staining. Moreover, both phosphorylated mammalian target of rapamycin and β-catenin expression, which have been reported to be increased by lithium and associated with cell proliferation, were reduced by CQ. Taken together, our study demonstrated that CQ protected against lithium-induced NDI and collecting duct cell proliferation possibly through inhibiting autophagy.

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35

Gao, Yang, Melissa J. Romero-Aleshire, Qi Cai, Theodore J. Price, and Heddwen L. Brooks. "Rapamycin inhibition of mTORC1 reverses lithium-induced proliferation of renal collecting duct cells." American Journal of Physiology-Renal Physiology 305, no. 8 (October 15, 2013): F1201—F1208. http://dx.doi.org/10.1152/ajprenal.00153.2013.

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Nephrogenic diabetes insipidus (NDI) is the most common renal side effect in patients undergoing lithium therapy for bipolar affective disorders. Approximately 2 million US patients take lithium of whom ∼50% will have altered renal function and develop NDI ( 2 , 37 ). Lithium-induced NDI is a defect in the urinary concentrating mechanism. Lithium therapy also leads to proliferation and abundant renal cysts (microcysts), commonly in the collecting ducts of the cortico-medullary region. The mTOR pathway integrates nutrient and mitogen signals to control cell proliferation and cell growth (size) via the mTOR Complex 1 (mTORC1). To address our hypothesis that mTOR activation may be responsible for lithium-induced proliferation of collecting ducts, we fed mice lithium chronically and assessed mTORC1 signaling in the renal medulla. We demonstrate that mTOR signaling is activated in the renal collecting ducts of lithium-treated mice; lithium increased the phosphorylation of rS6 (Ser240/Ser244), p-TSC2 (Thr1462), and p-mTOR (Ser2448). Consistent with our hypothesis, treatment with rapamycin, an allosteric inhibitor of mTOR, reversed lithium-induced proliferation of medullary collecting duct cells and reduced levels of p-rS6 and p-mTOR. Medullary levels of p-GSK3β were increased in the renal medullas of lithium-treated mice and remained elevated following rapamycin treatment. However, mTOR inhibition did not improve lithium-induced NDI and did not restore the expression of collecting duct proteins aquaporin-2 or UT-A1.

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36

Chen, Peng‐Yu, Chong Yan, Pengyu Chen, Rui Zhang, Yu‐Xing Yao, Hong‐Jie Peng, Li‐Tang Yan, Stefan Kaskel, and Qiang Zhang. "Selective Permeable Lithium‐Ion Channels on Lithium Metal for Practical Lithium–Sulfur Pouch Cells." Angewandte Chemie International Edition 60, no. 33 (July 9, 2021): 18031–36. http://dx.doi.org/10.1002/anie.202101958.

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37

Chen, Peng‐Yu, Chong Yan, Pengyu Chen, Rui Zhang, Yu‐Xing Yao, Hong‐Jie Peng, Li‐Tang Yan, Stefan Kaskel, and Qiang Zhang. "Selective Permeable Lithium‐Ion Channels on Lithium Metal for Practical Lithium–Sulfur Pouch Cells." Angewandte Chemie 133, no. 33 (July 7, 2021): 18179–84. http://dx.doi.org/10.1002/ange.202101958.

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38

Fornai, Francesco, Michela Ferrucci, Paola Lenzi, Alessandra Falleni, Francesca Biagioni, Marina Flaibani, Gabriele Siciliano, Francesco Giannessi, and Antonio Paparelli. "Plastic Changes in the Spinal Cord in Motor Neuron Disease." BioMed Research International 2014 (2014): 1–14. http://dx.doi.org/10.1155/2014/670756.

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In the present paper, we analyze the cell number within lamina X at the end stage of disease in a G93A mouse model of ALS; the effects induced by lithium; the stem-cell like phenotype of lamina X cells during ALS; the differentiation of these cells towards either a glial or neuronal phenotype. In summary we found that G93A mouse model of ALS produces an increase in lamina X cells which is further augmented by lithium administration. In the absence of lithium these nestin positive stem-like cells preferentially differentiate into glia (GFAP positive), while in the presence of lithium these cells differentiate towards a neuron-like phenotype (βIII-tubulin, NeuN, and calbindin-D28K positive). These effects of lithium are observed concomitantly with attenuation in disease progression and are reminiscent of neurogenetic effects induced by lithium in the subependymal ventricular zone of the hippocampus.

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39

Kohari, Tazeen, Farah Malik, and Aftab Ahmad. "Decrement of the Purkinje Cells Diameter after Oral Intake of Lithium in Albino Rats." Pakistan Journal of Medical and Health Sciences 15, no. 8 (August 25, 2021): 1788–89. http://dx.doi.org/10.53350/pjmhs211581788.

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Background: The histology of Cerebellar gray matter consists of a middle Purkinje cells layer with flask shaped Purkinje cells. The field of Neurology has documented that different organic compounds and metals are lethal to the excitatory Purkinje Neurons. Researches have proved Lithium to be hazardous to nervous tissue and especially Cerebellum For the past sixty years Lithium is the favorable drug for treatment of Bipolar Disorder. Aim: To Analyse and record the changes of decrement of the size of Purkinje cell Diameter after chronic Lithium ingestion. Methods: Sixteen albino rats were selected and were treated with lithium for a period of fifteen days and the data for changes in Purkinje cells Diameter was observed. Results: The Observations of Our study showed highly significantly decreased diameter of the Purinje cells in Group B (Lithium Carbonate) animals as compared to Group A Animals which were on Lab Diet Conclusion: The Morphometric Data proved that Lithium Carbonate is Toxic to Purkinje cells, and it educated our Population to use Lithium with caution. Keywords: Purkinje cell Diameter, Gray matter, Hazardous

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40

Louli, A. J., A. Eldesoky, Jack deGooyer, Matt Coon, C. P. Aiken, Z. Simunovic, M. Metzger, and J. R. Dahn. "Different Positive Electrodes for Anode-Free Lithium Metal Cells." Journal of The Electrochemical Society 169, no. 4 (April 1, 2022): 040517. http://dx.doi.org/10.1149/1945-7111/ac62c4.

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With a potential to deliver 60% greater energy density than conventional lithium-ion batteries, the simple design of anode-free lithium metal cells with liquid electrolytes has generated significant research interest. However, without excess lithium, the short lifetime and safety concerns for cells cycling lithium metal with liquid electrolytes make the development of anode-free cells particularly challenging. Herein, we investigate the effect of four different positive electrode materials on the performance of anode-free cells—LiNi0.5Mn0.3Co0.2O2 (NMC532), LiNi0.8Mn0.1Co0.1O2 (NMC811), LiCoO2 (LCO), and LiFePO4 (LFP). In-situ electrochemical impedance spectroscopy and electrolyte degradation measurements were performed on cells with dual-salt LiDFOB/LiBF4 electrolyte to elucidate cell failure. Additional state-of-the-art electrolyte systems as well as other testing conditions (temperature, pressure, depth of discharge) were also explored, along with nail safety tests and calendar aging cycle-hold experiments. We show that the rate of lithium inventory loss and impedance growth differs amongst these cell chemistries, ultimately resulting in the shortest lifetime for NMC811 and the longest lifetime for LCO anode-free cells of 200 cycles.

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Tobe, Brian T. D., Andrew M. Crain, Alicia M. Winquist, Barbara Calabrese, Hiroko Makihara, Wen-ning Zhao, Jasmin Lalonde, et al. "Probing the lithium-response pathway in hiPSCs implicates the phosphoregulatory set-point for a cytoskeletal modulator in bipolar pathogenesis." Proceedings of the National Academy of Sciences 114, no. 22 (May 12, 2017): E4462—E4471. http://dx.doi.org/10.1073/pnas.1700111114.

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The molecular pathogenesis of bipolar disorder (BPD) is poorly understood. Using human-induced pluripotent stem cells (hiPSCs) to unravel such mechanisms in polygenic diseases is generally challenging. However, hiPSCs from BPD patients responsive to lithium offered unique opportunities to discern lithium's target and hence gain molecular insight into BPD. By profiling the proteomics of BDP–hiPSC-derived neurons, we found that lithium alters the phosphorylation state of collapsin response mediator protein-2 (CRMP2). Active nonphosphorylated CRMP2, which binds cytoskeleton, is present throughout the neuron; inactive phosphorylated CRMP2, which dissociates from cytoskeleton, exits dendritic spines. CRMP2 elimination yields aberrant dendritogenesis with diminished spine density and lost lithium responsiveness (LiR). The “set-point” for the ratio of pCRMP2:CRMP2 is elevated uniquely in hiPSC-derived neurons from LiR BPD patients, but not with other psychiatric (including lithium-nonresponsive BPD) and neurological disorders. Lithium (and other pathway modulators) lowers pCRMP2, increasing spine area and density. Human BPD brains show similarly elevated ratios and diminished spine densities; lithium therapy normalizes the ratios and spines. Consistent with such “spine-opathies,” human LiR BPD neurons with abnormal ratios evince abnormally steep slopes for calcium flux; lithium normalizes both. Behaviorally, transgenic mice that reproduce lithium's postulated site-of-action in dephosphorylating CRMP2 emulate LiR in BPD. These data suggest that the “lithium response pathway” in BPD governs CRMP2's phosphorylation, which regulates cytoskeletal organization, particularly in spines, modulating neural networks. Aberrations in the posttranslational regulation of this developmentally critical molecule may underlie LiR BPD pathogenesis. Instructively, examining the proteomic profile in hiPSCs of a functional agent—even one whose mechanism-of-action is unknown—might reveal otherwise inscrutable intracellular pathogenic pathways.

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Sgroi, Mauro Francesco. "Lithium-Ion Batteries Aging Mechanisms." Batteries 8, no. 11 (November 1, 2022): 205. http://dx.doi.org/10.3390/batteries8110205.

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Lithium batteries (including lithium-ion, lithium-sulfur and lithium-air cells) are considered a technology enabling industrial sectors, including electrified vehicles, consumer electronics and stationary energy storage [...]

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43

West, K., B. Zachau-Christiansen, T. Jacobsen, and S. Skaarup. "Solid-state sodium cells — An alternative to lithium cells?" Journal of Power Sources 26, no. 3-4 (May 1989): 341–45. http://dx.doi.org/10.1016/0378-7753(89)80144-2.

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Goldberg, H., P. Clayman, and K. Skorecki. "Mechanism of Li inhibition of vasopressin-sensitive adenylate cyclase in cultured renal epithelial cells." American Journal of Physiology-Renal Physiology 255, no. 5 (November 1, 1988): F995—F1002. http://dx.doi.org/10.1152/ajprenal.1988.255.5.f995.

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We investigated the mechanism for lithium-induced inhibition of vasopressin-stimulated adensoine 3',5'-cyclic monophosphate (cAMP) production in the renal epithelial cell line LLC-PK1. In LLC-PK1 membranes lithium caused direct inhibition of hormone-stimulated adenylate cyclase activity by competing with magnesium. Fifty percent inhibition occurred at 20 mM lithium. The maximum transport activity (Vmax) but not the activation constant (Ka) for activation by vasopressin was altered. Activation by GTP and its nonhydrolyzable analogues was also inhibited by lithium. Furthermore, kinetic studies revealed that the lag phase in the activation of adenylate cyclase by 5'-guanylimi-dotriphosphate [Gpp(NH)p] was prolonged from 1 to 3 min, suggesting an effect of lithium on magnesium-dependent activation of the stimulatory GTP binding protein Gs. The function of the corresponding inhibitory GTP-binding protein Gi, as assessed by GTP inhibition of vasopressin-stimulated adenylate cyclase activity in the presence and absence of pertussis toxin pretreatment, was unaffected. Intact LLC-PK1 cells incubated in 10 mM lithium (approximate urinary concentration in lithium-treated patients) attained an intracellular lithium concentration of 17 mM, which led to a 40% reduction in cAMP formation. Magnesium loading of intact cells with the ionophore A23187 reversed the inhibitory effect of lithium. It is concluded that lithium directly inhibits the activation of vasopressin-sensitive adenylate cyclase in renal epithelia by competing with magnesium for activation of Gs. This direct effect on Gs activation accounts for the inhibitory effect of lithium on cAMP production in the intact cell.

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45

Fateev, Sergei Anatol'evich, Elena Konstantinovna Tuseeva, and Aleksandr Mordukhaevich Skundin. "Current leads corrosion and the problem of diagnostics of fluorocarbon-lithium cells." Electrochemical Energetics 10, no. 4 (2010): 182–86. http://dx.doi.org/10.18500/1608-4039-2010-10-4-182-186.

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Corrosion behavior of niobium current leads of fluorocarbon-lithium cells are studied. Polarization measurements at plain niobium leads and at such leads in a contact with fluorocarbon cathode in an electrolyte of fluorocarbon-lithium cell were carried out. Besides, behavior of niobium lead directly in a feedthrough of real cells was studied. The contact of niobium with fluorocarbon cathode is shown to result in toughening of corrosion conditions and in possible niobium depassivation. Long-term cells storage at elevated temperature was shown to result in complete corrosion dissolution of niobium leads. Certain correlation between cell's OCV and corrosion intensity was obtained.

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Bartony, Maggie A., and Vincent S. Gallicchio. "Stem Cells, Lithium And Neuropsychiatric Disorders." Journal of Stem Cell Research 3, no. 1 (March 21, 2022): 1. http://dx.doi.org/10.52793/jscr.2022.3(1)-30.

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47

Tobishima, Shinichi, Katsuya Hayashi, K. Takei, Minoru Takahashi, and Yoji Sakurai. "Safety Characteristics of Lithium Ion Cells." Key Engineering Materials 216 (September 2001): 111–14. http://dx.doi.org/10.4028/www.scientific.net/kem.216.111.

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Tobishima, Shinichi, Y. Ogino, T. Kuryu, Yoshiyuki Saito, R. Sugawara, and M. Oura. "Storage Characteristics of Lithium Ion Cells." Key Engineering Materials 228-229 (September 2002): 293–98. http://dx.doi.org/10.4028/www.scientific.net/kem.228-229.293.

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Bugga, Ratnakumar V., Marshall C. Smart, and Larry Whitcanack. "Storage Characteristics of Lithium-Ion Cells." ECS Transactions 25, no. 36 (December 17, 2019): 297–306. http://dx.doi.org/10.1149/1.3393865.

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Takeda, Y., R. Kanno, T. Tanaka, and O. Yamamoto. "Lithium / V 9Mo6 O 40 Cells." Journal of The Electrochemical Society 134, no. 3 (March 1, 1987): 641–43. http://dx.doi.org/10.1149/1.2100522.

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