Relevant bibliographies by topics / Transforming growth factor-P

Academic literature on the topic 'Transforming growth factor-P'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Transforming growth factor-P"

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Tremollieres, Florence A., Donna D. Strong, David J. Baylink, and Subburaman Mohan. "Insulin-like growth factor II and transforming growth factor β1 regulate insulin-like growth factor I secretion in mouse bone cells." Acta Endocrinologica 125, no. 5 (November 1991): 538–46. http://dx.doi.org/10.1530/acta.0.1250538.

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Abstract. Bone cells in culture produce and respond to growth factors, suggesting that local as well as systemic factors regulate bone volume. Previous studies have shown that IGF-I is the major mitogen produced by mouse bone cells and that its production is regulated by systemic agents such as PTH and estrogen. Because IGF-II and transforming growth factor β1 have been shown, respectively, to increase and decrease MC3T3-E1 cell proliferation, we tested the hypothesis that these two growth factors modulate the production of IGF-I in this cell line. In order to eliminate artifacts owing to IGF binding proteins, conditioned media samples were pretreated with IGF-II before measurement of IGF-I by RIA. After 24 h treatment at a density of 2.5× 104 cells/cm2, IGF-II (10 μg/l) induced a 2.2-fold increase compared with untreated control (9.5±1.5 vs 4.2±0.44 pg/μg protein, p<0.001), whereas transforming growth factor β1 (1 μg/l) caused a 66% decrease in IGF-I production (1.5±0.3 vs 4.2±0.44 pg/μg protein, p<0.001). Both IGF-II and transforming growth factor β1 regulated IGF-I production in a dose-, time- and cell density-dependent manner. The lowest effective doses for IGF-II and transforming growth factor β1 were 1 and 0.01 μg/l, respectively. These results support a role for IGF-II and transforming growth factor β1 as potent modulators of IGF-I secretion in mouse bone cells. Furthermore, regulation of IGF-I production in bone cells by IGF-II and transforming growth factor β1 in an autocrine/paracrine manner could represent a component part of the mechanism whereby the skeleton locally adapts in reponse to external stimuli.
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Peña-Ortiz, Miguel Ángel, Liliana Germán-Castelán, and Aliesha González-Arenas. "Growth factors and kinases in glioblastoma growth." Advances in Modern Oncology Research 2, no. 5 (October 19, 2016): 248. http://dx.doi.org/10.18282/amor.v2.i5.100.

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<p>Glioblastoma multiforme (GBM) is the most aggressive type of brain cancer, having the highest invasion, migration, proliferation, and angiogenesis rates. Several signaling pathways are involved in the regulation of these processes including growth factors and their tyrosine kinase receptors, such as vascular endothelial growth factor (VEGF), transforming growth factor beta (TGFβ), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), and insulin-like growth factor–I (IGF–I). Different kinases and regulators also participate in signaling pathways initiated by growth factors, such as mitogen-activated kinases (MAPK), protein kinases C (PKC), phosphatidylinositol-3 kinases (PI3K), protein kinase B (PKB or Akt), glycogen synthase kinase 3β (GSK3β), the mTOR complex, and Bcl-2. In this review, we will focus on the role of these proteins as possible therapeutic targets in GBM.</p>
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KIRA, S. "P-481 Expression of transforming growth factor alpha and epidermal growth factor receptor in human hepatocellular carcinoma." International Hepatology Communications 3 (July 1995): S157. http://dx.doi.org/10.1016/0928-4346(95)90778-6.

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Zhang, Nan, Tingting Zhao, Meirong Bi, Xuejia He, Yamin Zhang, and Weiwei Zhu. "Hyperin Ameliorates Proliferation, Migration, and Extracellular Matrix Formation in Airway Smooth Muscle Cells by Inhibiting Transforming Growth Factor-β1-Induced Nuclear Factor-κB Activation." Current Topics in Nutraceutical Research 19, no. 2 (September 28, 2020): 222–27. http://dx.doi.org/10.37290/ctnr2641-452x.19:222-227.

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We have explored the role of hyperin remodeling of airway smooth muscle cells during asthma. To this end, airway smooth muscle cells were isolated from tracheae and bronchi of mice, treated with transforming growth factor-β1 and increasing concentrations of hyperin followed by analysis of cell viability, proliferation, and migration. The levels of extracellular matrix formation were evaluated by analysis of fibronectin and type I collagen. Western blot analysis was used to assess the function of the downstream pathway of nuclear factor-kappa B. Transforming growth factor-β1 treatment led to a dose-dependent increase in type I collagen and fibronectin that was reversed by hyperin. Transforming growth factor-β1 promoted activation of nuclear factor-kappa B pathway with reduced IκBα and enhanced phospho (p)-p65 and p-IκBα. However, hyperin treatment upregulated IκBα and downregulated p-p65/p-IκBα to inactivate NF-κB pathway. In conclusion, hyperin ameliorates proliferation, migration, and extracellular matrix formation in airway smooth muscle cells by inhibiting transforming growth factor-β1-induced nuclear factor-kappa B activation suggesting potential prevention of airway remodeling during asthma.
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Looney, Micheal, Peter Doran, and Donal J. Buggy. "Effect of Anesthetic Technique on Serum Vascular Endothelial Growth Factor C and Transforming Growth Factor β in Women Undergoing Anesthesia and Surgery for Breast Cancer." Anesthesiology 113, no. 5 (November 1, 2010): 1118–25. http://dx.doi.org/10.1097/aln.0b013e3181f79a69.

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Background In breast cancer, vascular endothelial growth factor C, transforming growth factor β, placental growth factor, and fibroblast growth factor (acidic and basic) promote angiogenesis and metastases. We tested the hypothesis that a propofol-paravertebral anesthetic (PPA) technique would attenuate postoperative changes in these angiogenic factors to a greater extent than balanced general anesthesia (GA) and morphine analgesia in women undergoing surgery for primary breast cancer. Method Forty women with primary breast cancer undergoing surgical excision were randomized to receive either standard GA or PPA technique. Venous blood was sampled before and at 24 h after surgery and serum analyzed. The primary endpoint was a preoperative versus postoperative change in vascular endothelial growth factor C and transforming growth factor β concentrations. Results Using a visual analog scale (median [25-75% interquartile range]), PPA patients (1 [0-2]) had less pain at 2 h (P = 0.02) than did GA patients (3 [2-5]). The mean postoperative change in vascular endothelial growth factor C concentrations among GA patients was 733 versus 27 pg/ml for PPA patients (difference, 706 [97.5% CI, 280-1,130] pg/ml, P = 0.001). In contrast, the mean postoperative change in transforming growth factor β concentration among GA patients was -163 versus 146 pg/ml for PPA patients (difference, 309 [97.5% CI, -474 to -143] pg/ml, P = 0.005). Concentrations of placental growth factor and fibroblast growth factor, both acidic and basic, were undetectable in serum. Conclusion Anesthetic technique influences serum concentrations of factors associated with angiogenesis in primary breast cancer surgery.
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Barcellos-Hoff, M. "SP-0269 THERAPEUTIC BENEFIT FROM TRANSFORMING GROWTH FACTOR p INHIBITION DURING RADIOTHERAPY." Radiotherapy and Oncology 103 (May 2012): S105—S106. http://dx.doi.org/10.1016/s0167-8140(12)70608-4.

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Choi, I. G., H. W. Kim, Y. C. Kim, C. H. Han, B. C. Lee, B. J. Ham, and B. H. Yang. "P.6.b.001 Increased transforming growth factor-beta1 in alcohol dependence." European Neuropsychopharmacology 17 (October 2007): S547. http://dx.doi.org/10.1016/s0924-977x(07)70848-9.

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Korah, J., N. Falah, and J. J. Lebrun. "1023 POSTER Role of the E2F1 Transcription Factor in Transforming Growth Factor-p-mediated Apoptosis." European Journal of Cancer 47 (September 2011): S103. http://dx.doi.org/10.1016/s0959-8049(11)70666-9.

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Blanco, F. F., S. Sanduja, N. G. Deane, P. J. Blackshear, and D. A. Dixon. "Transforming Growth Factor Regulates P-Body Formation through Induction of the mRNA Decay Factor Tristetraprolin." Molecular and Cellular Biology 34, no. 2 (November 4, 2013): 180–95. http://dx.doi.org/10.1128/mcb.01020-13.

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Brahmatewari, Just, Anton Serafini, Victoria Serralta, Patricia M. Mertz, and William H. Eaglstein. "The Effects of Topical Transforming Growth Factor-β2 and Anti-Transforming Growth Factor-β2,3 on Scarring in Pigs." Journal of Cutaneous Medicine and Surgery 4, no. 3 (July 2000): 126–31. http://dx.doi.org/10.1177/120347540000400303.

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Background: Transforming growth factor-β2 (TGF-β2) has been implicated in the inflammatory response and subsequent scarring during wound healing. Objective: The experiment was designed to study the effects of a topical application of TGF-β2 and mouse monoclonal anti-TGF-β2,3 neutralizing antibody (and TGF-β2,3) on the development of fibrosis during healing. Methods: Sixteen full-thickness excision wounds were made in the paravertebral and thoracic area of four domestic pigs. On day 0, three wounds each were treated with: a) 5 μg of TGF-β2, b) 5 μg of 2% methylcellulose (mc), or c) 1.2 mg of anti-TGF-β2,3. As a vehicle for treatment of each wound methylcellulose 2% was used. Four wounds served as the untreated air-exposed control. Wounds were biopsied and the tissue sectioned and stained with hematoxylin and eosin on days 7, 14, and 45. Three blinded observers evaluated the wound specimens. Results: Using computer-aided point count stereology on days 7, 14, and 45, we found a statistically significant increase (p < .05) in the number of nucleated cells in the TGF-β2-treated wounds as compared to the other control wounds. Wounds treated with anti-TGF-β2,3 had significantly (p < .05) fewer nucleated cells on days 7,14, and 45. Microscopically, the TGF-β2-treated wounds had a larger scar area as compared to anti-TGF-β2,3 and controls. Conclusion: Treating wounds with an antibody directed against TGF-β2 might be a useful clinical approach to reduce fibrosis.
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Dissertations / Theses on the topic "Transforming growth factor-P"

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Fong, Gloria. "Influence of neuromodulators and mechanical loading on pathological cell and tissue characteristics in tendinosis." Doctoral thesis, Umeå universitet, Institutionen för integrativ medicinsk biologi (IMB), 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-131390.

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Background: Tendinosis is a painful chronic, degenerative condition characterized by objective changes in the tissue structure of a tendon. Hallmark features in tendinosis tendons include increased number of cells (hypercellularity), extracellular matrix (ECM) degradation and disorganized collagen. The progression of these pathological changes seen in tendinosis is neither well characterized nor fully understood. Studies have suggested that there are biochemical and mechanical elements involved in tendinosis. From a biochemical perspective, studies have shown that the tendon cells, tenocytes, produce a number of neuronal signal substances/neuromodulators, such as substance P (SP) and acetylcholine (ACh), traditionally thought to be confined to the nervous system. Furthermore, it has been shown that the expression of these neuromodulators is elevated in tendinosis tendons as compared to normal healthy tendons. Interestingly, studies on other tissue types have revealed that both SP and ACh can induce tissue changes seen in tendinosis, such as hypercellularity and collagen disorganization. From a mechanical angle, it has been suggested that overload of tendons, including extensive strain on the primary tendon cells (tenocytes), causes the degenerative processes associated with tendinosis. In vivo studies have shown that in overloaded tendons, the presence of neuromodulators is elevated, not least SP, which also precedes the development of the tissue changes seen in tendinosis. This further supports the importance of combining biochemical factors and mechanical factors in the pathogenesis of tendinosis. Hypotheses: In this thesis project, we hypothesize: 1) that neuromodulators, such as SP and ACh when stimulating their preferred receptors, the neurokinin 1 (NK-1 R) and muscarinic receptors (mAChRs), respectively, can cause increased tenocyte proliferation; 2) that the effects of SP and ACh on tenocyte proliferation converge mechanistically via a shared signalling pathway; 3) that mechanical loading of tenocytes results in increased production of SP by the tenocytes; and 4) that SP enhances collagen remodelling by tenocytes via NK-1 R. Model system: In vitro studies offer insight into the function of healthy tendon matrix and the etiology of tendinopathy. Using a cell culture model of human primary tendon cells, highly controlled experiments were performed in this thesis project to study a subset of biological and mechanical parameters that are implicated in tendinosis. The FlexCell® Tension System was used to study the influence of mechanical loading on tenocytes. As well, a collagen gel contraction assay was used to examine the intrinsic ability of tenocytes to reorganise type I collagen matrices under the influence of the neuromodulator SP. Results: The studies showed that exogenous administration of SP and ACh results in increased tenocyte proliferation that is mediated via activation of the ERK1/2 mitogenic pathway when the preferred receptors of SP and ACh, the NK-1 R and mAChRs, respectively, are stimulated. Furthermore, the studies resulted in the novel finding that SP and ACh both converge mechanistically via transforming growth factor (TGF)-β1 and that a negative feedback mechanism is present in which TGF-β1 downregulates the expression of mAChRs and NK-1 R. The studies also showed that SP can increase collagen remodelling and upregulate expression of genes related to tendinosis. Finally, it was established that tenocytes are mechanoresponsive by showing that cyclic mechanical loading increases the expression of SP by human tenocytes. Conclusions: This thesis work concludes that stimulation of NK-1 R and mAChRs results in proliferation of human tenocytes, which both involve the ERK1/2 signalling pathway. It also shows that SP and ACh converge mechanistically via TGF-β1 in their contribution to tenocyte proliferation. The role of hypercellularity in tendinosis tissue is unknown. Possibly, it has different roles at different stages of the disease. The findings also show that SP increases collagen remodelling, suggesting that increased SP not only results in hypercellularity but also contributes to the collagen morphology in tendinosis.
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Jia, Kailiang. "Daf-9, a cytochrome P450 regulating C. elegans larval development and adult longevity /." free to MU campus, to others for purchase, 2000. http://wwwlib.umi.com/cr/mo/fullcit?p9998488.

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Ryseck, Ilona [Verfasser], H. J. [Gutachter] Thiel, M. [Gutachter] Wiederholt, and P. [Gutachter] Rieck. "Modulation von Proliferation und Migration boviner kornealer Endothelzellen in Kultur durch humanes Kammerwasser, Transforming Groth Factor-Beta 2 und Ascorbinsäure / Ilona Ryseck ; Gutachter: H.-J. Thiel, M. Wiederholt, P. Rieck." Berlin : Humboldt-Universität zu Berlin, 2000. http://d-nb.info/120763493X/34.

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Sieprath, Sonja. "Die Rolle von p38 in der TGF-β- induzierten Transdifferenzierung humaner Tenonfibroblasten zu Myofibroblasten." Doctoral thesis, 2010. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-54542.

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Hintergrund dieser Arbeit ist eine Charakterisierung der zellulären Signalkaskaden innerhalb von Tenonfibroblasten, die an einer überschießenden Wundheilung mit Vernarbung nach filtrierender Glaukomchirurgie beteiligt sind. Ein besseres Verständnis der zellinternen Abläufe soll neue Ansatzpunkte zur Vernarbungshemmung nach Trabekulektomie eröffnen. Die Ergebnisse dieser Arbeit weisen auf eine zentrale Rolle des p38-Signalweges für die Übermittlung der TGF-β-induzierten Transdifferenzierung humaner Tenonfibroblasten hin. Die Transdifferenzierung der HTF ist durch die nach 48 Stunden einsetzende Expression von Markerproteinen wie αSMA, der vermehrten Synthese von Matrixproteinen wie Collagen Iα1 und Fibronectin sowie Veränderungen der Zellmorphologie charakterisiert. Im Rahmen der Arbeit wurde die Aktivierung der p38 MAPK im Zeitverlauf betrachtet und verschiedene Aktivierungsformen von p38 herausgearbeitet: Die schnell einsetzende Aktivierung einer „hohen“ schweren p38-Isoform war meist nicht durch TGF-β an sich, sondern vielmehr durch eine mechanische Stimulation der Zellen bei Mediumwechsel zur Zugabe des Wachstumsfaktors bedingt. Demgegenüber war eine späte nach etwa 12 Stunden zu beobachtende Aktivierung einer „tiefen“ leichten p38-Isoform streng von der TGF-β-Stimulation sowie einem funktionsfähigen TGF-β-Rezeptor Typ I abhängig. Diese p38-Spätaktivierung ist zeitlich mit der TGF-β-induzierten αSMA-Expression assoziiert. Da die TGF-β-induzierte αSMA-Transkription durch Blockade der Proteinbiosynthese verhindert wird und eine zeitliche Lücke bis zur relevanten p38-Spätaktivierung besteht, ist offenbar die Synthese eines Zwischenboten notwendig. Als möglicher Kandidat für einen solchen Intermediator kam nach Literaturlage GADD45β in Frage: GADD45β konnte schließlich sowohl qualitativ als auch quantitativ nach TGF-β-Exposition in HTF nachgewiesen werden: Es wird mit einem deutlichen Maximum innerhalb der ersten Stunde für einige Stunden synthetisiert. Die beobachtete rasche SMAD2-Aktivierung in HTF, die in keinem direkten zeitlichen Zusammenhang zur αSMA-Expression steht, könnte verantwortlich für die Induktion von GADD45β sein und damit über Aktivierung von p38 zur Transdifferenzierung der Tenonfibroblasten zu Myofibroblasten beitragen. Für den weitergehenden Nachweis der Bedeutung von GADD45β ist dessen spezifische Blockade durch antisense-Überexpression mittels viralen Vektoren oder RNA-Interferenz anzustreben. Die durchgeführten Untersuchungen zeigen, dass GADD45β neben der p38 MAPK ein potentielles Ziel zur therapeutischen Modulation der TGF-β-vermittelten Transdifferenzierung von humanen Tenonfibroblasten darstellen kann
Main problem after trabeculectomy in therapy of glaucoma is scarring. In search of new targets in modification of wound healing, a better understanding of cellular signal cascades of human tenonfibroblasts in transdifferentiation to myofibroblasts is aspired. TGF-β induces transdifferentiation of tenonfibroblasts, characterised by increased expression of marker proteins like αSMA and synthesis of matrix proteins like Collagen Iα1 and Fibronectin. Intracellular signal transducing of TGF-β by p38 seems to be essential. The time course of activation of the p38 MAPK was observed and a relevant late activation after 12 hours was found. Furthermore a mediatior in the meantime of the first hours was identified: GADD45β is induced in a chronological correlation. P38 and GADD45β could both be potential targets in modification of scarring after trabeculectomy
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Book chapters on the topic "Transforming growth factor-P"

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Mostert, V., I. Dreher, J. Köhrle, and J. Abel. "Transforming Growth Factor-β1 Inhibits Selenoprotein P Expression in Cultured Human Liver Cells." In Trace Elements in Man and Animals 10, 899–900. New York, NY: Springer US, 2002. http://dx.doi.org/10.1007/0-306-47466-2_284.

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"EVIDENCE OF A ROLE FOR VITAMIN D AND TRANSFORMING GROWTH FACTOR P IN OSTEOINDUCTION." In Vitamin D, 559–60. De Gruyter, 1991. http://dx.doi.org/10.1515/9783110850345-184.

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Conference papers on the topic "Transforming growth factor-P"

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Dillard, Joshua, Uzma Amir, Pawan Tyagi, and Vincent Lamberti. "Structural Stability of Magnetic Tunnel Junction Based Molecular Spintronics Devices (MTJMSD)." In ASME 2020 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/imece2020-24134.

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Abstract Harnessing the exotic properties of molecular level nanostructures to produce novel sensors, metamaterials, and futuristic computer devices can be technologically transformative. In addition, connecting the molecular nanostructures to ferromagnetic electrodes bring the unprecedented opportunity of making spin property based molecular devices. We have demonstrated that magnetic tunnel junction based molecular spintronics device (MTJMSD) approach to address numerous technological hurdles that have been inhibiting this field for decades (P. Tyagi, J. Mater. Chem., Vol. 21, 4733). MTJMSD approach is based on producing a capacitor like a testbed where two metal electrodes are separated by an ultrathin insulator and subsequently bridging the molecule nanostructure across the insulator to transform a capacitor into a molecular device. Our prior work showed that MTJMSDs produced extremely intriguing phenomenon such as room temperature current suppression by six orders, spin photovoltaic effect, and evolution of new forms of magnetic metamaterials arising due to the interaction of the magnetic a molecule with two ferromagnetic thin films. However, making robust and reproducible electrical connections with exotic molecules with ferromagnetic electrodes is full of challenges and requires attention to MTJMSD structural stability. This paper focuses on MTJMSD stability by describing the overall fabrication protocol and the associated potential threat to reliability. MTJMSD is based on microfabrication methods such as (a) photolithography for patterning the ferromagnetic electrodes, (b) sputtering of metallic thin films and insulator, and (c) at the end electrochemical process for bridging the molecules between two ferromagnetic films separated by ∼ 2nm insulating gap. For the successful MTJMSD fabrication, the selection of ferromagnetic metal electrodes and thickness was found to be a deterministic factor in designing the photolithography, thin film deposition strategy, and molecular bridging process. We mainly used isotropic NiFe soft magnetic material and anisotropic Cobalt (Co) with significant magnetic hardness. We found Co was susceptible to chemical etching when directly exposed to photoresist developer and aged molecular solution. However, NiFe was very stable against the chemicals we used in the MTJMSD fabrication. As compared to NiFe, the Co films with &gt; 10nm thickness were susceptible to mechanical stress-induced nanoscale deformities. However, cobalt was essential to produce (a) low leakage current before transforming the capacitor from the magnetic tunnel junction into molecular devices and (b) tailoring the magnetic properties of the ferromagnetic electrodes. This paper describes our overall MTJMSD fabrication scheme and process optimization to overcome various challenges to produce stable and reliable MTJMSDs. We also discuss the role of mechanical stresses arising during the sputtering of the ultrathin insulator and how to overcome that challenge by optimizing the insulator growth process. This paper will benefit researchers striving to make nanoscale spintronics devices for solving grand challenges in developing advanced sensors, magnetic metamaterials, and computer devices.
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