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Journal articles on the topic 'PSD-93'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 April 2022

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1

Tao, Feng, John Skinner, Ya Yang, and Roger A. Johns. "Effect of PSD-95/SAP90 and/or PSD-93/Chapsyn-110 Deficiency on the Minimum Alveolar Anesthetic Concentration of Halothane in Mice." Anesthesiology 112, no. 6 (2010): 1444–51. http://dx.doi.org/10.1097/aln.0b013e3181dcd3dc.

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Background The authors have previously shown that the clinically relevant concentrations of inhalational anesthetics dose-dependently inhibit the postsynaptic density protein (PSD)-95, Dlg, and ZO-1 domain-mediated protein interactions between N-methyl-d-aspartate receptors and PSD-95/synaptic-associated protein (SAP) 90 or PSD-93/Chapsyn-110 and that the knockdown of spinal PSD-95/SAP90 significantly reduces the minimum alveolar concentration (MAC) for isoflurane in rats. Methods The authors designed antisense oligodeoxynucleotides based on the mouse PSD-95/SAP90 and PSD-93/Chapsyn-110 messenger RNAs that correspond to their PSD-95, Dlg, and ZO-1 domain nucleotides and can specifically knock down the respective proteins. The authors intrathecally injected antisense oligodeoxynucleotides into wild-type and PSD-93/Chapsyn-110 knockout mice to investigate the effect of PSD-95/SAP90 and/or PSD-93/Chapsyn-110 deficiency on halothane anesthesia. Results Both PSD-95/SAP90 and PSD-93/Chapsyn-110 antisense oligodeoxynucleotides caused a dose-dependent and significant reduction in the MAC of halothane in wild-type mice. The intrathecal injection of PSD-95/SAP90 antisense oligodeoxynucleotide at different doses (25 and 50 microg) reduced halothane MAC by 40 and 55%, respectively, and intrathecal injection of PSD-93/Chapsyn-110 antisense oligodeoxynucleotide at different doses (12 and 24 microg) reduced halothane MAC by 25 and 53%, respectively. The PSD-95/SAP90 antisense oligodeoxynucleotide showed similar effect on halothane MAC in wild-type and PSD-93/Chapsyn-110 knockout mice, suggesting that the combination of PSD-95/SAP90 knockdown with PSD-93/Chapsyn-110 deletion did not have an additive effect on halothane anesthesia. Conclusions The current results indicate that PSD-95/SAP90 and PSD-93/Chapsyn-110 are involved in the molecular mechanisms of halothane anesthesia and that the functional role of PSD-95/SAP90 in halothane anesthesia is not enhanced after PSD-93/Chapsyn-110 deletion.

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2

Girard, Beatrice M., Laura A. Merriam, John D. Tompkins, Margaret A. Vizzard, and Rodney L. Parsons. "Decrease in neuronal nicotinic acetylcholine receptor subunit and PSD-93 transcript levels in the male mouse MPG after cavernous nerve injury or explant culture." American Journal of Physiology-Renal Physiology 305, no. 10 (2013): F1504—F1512. http://dx.doi.org/10.1152/ajprenal.00343.2013.

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Quantitative real-time PCR was used to test whether cavernous nerve injury leads to a decrease in major pelvic ganglia (MPG) neuronal nicotinic ACh receptor (nAChR) subunit and postsynaptic density (PSD)-93 transcript levels. Subunits α3, β4, and α7, commonly expressed in the MPG, were selected for analysis. After 72 h in explant culture, MPG transcript levels for α3, β4, α7, and PSD-93 were significantly depressed. Three days after cavernous nerve axotomy or crush in vivo, transcript levels for α3, β4, and PSD-93, but not for α7, were significantly depressed. Three days after dissection of the cavernous nerve free of underlying tissue and application of a 5-mm lateral stretch (manipulation), transcript levels for α3and PSD-93 were also significantly decreased. Seven days after all three surgical procedures, α3transcript levels remained depressed, but PSD-93 transcript levels were still decreased only after axotomy or nerve crush. At 30 days postsurgery, transcript levels for the nAChR subunits and PSD-93 had recovered. ACh-induced currents were significantly smaller in MPG neurons dissociated from 3-day explant cultured ganglia than from those recorded in neurons dissociated from acutely isolated ganglia; this observation provides direct evidence showing that a decrease in nAChR function was coincident with a decrease in nAChR subunit transcript levels. We conclude that a downregulation of nAChR subunit and PSD-93 expression after cavernous nerve injury, or even manipulation, could interrupt synaptic transmission within the MPG and thus contribute to the loss of neural control of urogenital organs after pelvic surgeries.

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3

DeGiorgis, Joseph A., James A. Galbraith, Ayse Dosemeci, Xiaobing Chen, and Thomas S. Reese. "Distribution of the scaffolding proteins PSD-95, PSD-93, and SAP97 in isolated PSDs." Brain Cell Biology 35, no. 4-6 (2006): 239–50. http://dx.doi.org/10.1007/s11068-007-9017-0.

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4

Löwel, Siegrid. "Yin und Yang beim Lernen im jungen Gehirn: Balance von PSD-95 und PSD-93." BIOspektrum 26, no. 2 (2020): 140–42. http://dx.doi.org/10.1007/s12268-020-1355-9.

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5

Tao, Yuan-Xiang, Frederick Kauer, David S. Bredt, and Roger A. Johns. "Reduction of Neuropathic Pain in Mice Lacking PSD-93." Anesthesiology 96, Sup 2 (2002): A829. http://dx.doi.org/10.1097/00000542-200209002-00829.

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6

Sun, Q., and G. G. Turrigiano. "PSD-95 and PSD-93 Play Critical But Distinct Roles in Synaptic Scaling Up and Down." Journal of Neuroscience 31, no. 18 (2011): 6800–6808. http://dx.doi.org/10.1523/jneurosci.5616-10.2011.

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7

Fiorentini, Monica, Ann Kallehauge Nielsen, Ole Kristensen, Jette S. Kastrup, and Michael Gajhede. "Structure of the first PDZ domain of human PSD-93." Acta Crystallographica Section F Structural Biology and Crystallization Communications 65, no. 12 (2009): 1254–57. http://dx.doi.org/10.1107/s1744309109043267.

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8

Carlisle, Holly J., Ann E. Fink, Seth G. N. Grant, and Thomas J. O’Dell. "Opposing effects of PSD-93 and PSD-95 on long-term potentiation and spike timing-dependent plasticity." Journal of Physiology 586, no. 24 (2008): 5885–900. http://dx.doi.org/10.1113/jphysiol.2008.163469.

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9

Guo, Ming-Lei, Bing Xue, Dao-Zhong Jin, Li-Min Mao, and John Q. Wang. "Interactions and phosphorylation of postsynaptic density 93 (PSD-93) by extracellular signal-regulated kinase (ERK)." Brain Research 1465 (July 2012): 18–25. http://dx.doi.org/10.1016/j.brainres.2012.05.026.

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10

LARSSON, Mårten, Göran HJÄLM, Amos M. SAKWE, et al. "Selective interaction of megalin with postsynaptic density-95 (PSD-95)-like membrane-associated guanylate kinase (MAGUK) proteins." Biochemical Journal 373, no. 2 (2003): 381–91. http://dx.doi.org/10.1042/bj20021958.

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Megalin is an integral membrane receptor belonging to the low-density lipoprotein receptor family. In addition to its role as an endocytotic receptor, megalin has also been proposed to have signalling functions. Using interaction cloning in yeast, we identified the membrane-associated guanylate kinase family member postsynaptic density-95 (PSD-95) as an interaction partner for megalin. PSD-95 and a truncated version of megalin were co-immunoprecipitated from HEK-293 cell lysates overexpressing the two proteins, which confirmed the interaction. The two proteins were found to be co-localized in these cells by confocal microscopy. Immunocytochemical studies showed that cells in the parathyroid, proximal tubuli of the kidney and placenta express both megalin and PSD-95. We found that the interaction between the two proteins is mediated by the binding of the C-terminus of megalin, which has a type I PSD-95/Drosophila discs-large/zona occludens 1 (PDZ)-binding motif, to the PDZ2 domain of PSD-95. The PSD-95-like membrane-associated guanylate kinase (‘MAGUK’) family contains three additional members: PSD-93, synapse-associated protein 97 (SAP97) and SAP102. We detected these proteins, apart from SAP102, in parathyroid chief cells, a cell type having a marked expression of megalin. The PDZ2 domains of PSD-93 and SAP102 were also shown to interact with megalin, whereas no interaction was detected for SAP97. The SAP97 PDZ2 domain differed at four positions from the other members of the PSD-95 subfamily. One of these residues was Thr389, located in the αB-helix and part of the hydrophobic pocket of the PDZ2 domain. Surface plasmon resonance experiments revealed that mutation of SAP97 Thr389 to alanine, as with the other PSD-95-like membrane-associated guanylate kinases, induced binding to megalin.

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11

Liu, Mingna, Rebecca Shi, Hongik Hwang, et al. "SAP102 regulates synaptic AMPAR function through a CNIH-2-dependent mechanism." Journal of Neurophysiology 120, no. 4 (2018): 1578–86. http://dx.doi.org/10.1152/jn.00731.2017.

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The postsynaptic density (PSD)-95-like, disk-large (DLG) membrane-associated guanylate kinase (PSD/DLG-MAGUK) family of proteins scaffold α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) complexes to the postsynaptic compartment and are postulated to orchestrate activity-dependent modulation of synaptic AMPAR functions. SAP102 is a key member of this family, present from early development, before PSD-95 and PSD-93, and throughout life. Here we investigate the role of SAP102 in synaptic transmission using a cell-restricted molecular replacement strategy, where SAP102 is expressed against the background of acute knockdown of endogenous PSD-95. We show that SAP102 rescues the decrease of AMPAR-mediated evoked excitatory postsynaptic currents (AMPAR eEPSCs) and AMPAR miniature EPSC (AMPAR mEPSC) frequency caused by acute knockdown of PSD-95. Further analysis of the mini events revealed that PSD-95-to-SAP102 replacement but not direct manipulation of PSD-95 increases the AMPAR mEPSC decay time. SAP102-mediated rescue of AMPAR eEPSCs requires AMPAR auxiliary subunit cornichon-2, whereas cornichon-2 knockdown did not affect PSD-95-mediated regulation of AMPAR eEPSC. Combining these observations, our data elucidate that PSD-95 and SAP102 differentially influence basic synaptic properties and synaptic current kinetics potentially via different AMPAR auxiliary subunits. NEW & NOTEWORTHY Synaptic scaffold proteins postsynaptic density (PSD)-95-like, disk-large (DLG) membrane-associated guanylate kinase (PSD-MAGUKs) regulate synaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) function. However, the functional diversity among different PSD-MAGUKs remains to be categorized. We show that distinct from PSD-95, SAP102 increase the AMPAR synaptic current decay time, and the effect of SAP102 on synaptic AMPAR function requires the AMPAR auxiliary subunit cornichon-2. Our data suggest that PSD-MAGUKs target and modulate different AMPAR complexes to exert specific experience-dependent modification of the excitatory circuit.

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12

Delint-Ramirez, I., E. Fernandez, A. Bayes, E. Kicsi, N. H. Komiyama, and S. G. N. Grant. "In Vivo Composition of NMDA Receptor Signaling Complexes Differs between Membrane Subdomains and Is Modulated by PSD-95 And PSD-93." Journal of Neuroscience 30, no. 24 (2010): 8162–70. http://dx.doi.org/10.1523/jneurosci.1792-10.2010.

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13

Chen, Xiaobing, Jonathan M. Levy, Austin Hou, et al. "PSD-95 family MAGUKs are essential for anchoring AMPA and NMDA receptor complexes at the postsynaptic density." Proceedings of the National Academy of Sciences 112, no. 50 (2015): E6983—E6992. http://dx.doi.org/10.1073/pnas.1517045112.

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The postsynaptic density (PSD)-95 family of membrane-associated guanylate kinases (MAGUKs) are major scaffolding proteins at the PSD in glutamatergic excitatory synapses, where they maintain and modulate synaptic strength. How MAGUKs underlie synaptic strength at the molecular level is still not well understood. Here, we explore the structural and functional roles of MAGUKs at hippocampal excitatory synapses by simultaneous knocking down PSD-95, PSD-93, and synapse-associated protein (SAP)102 and combining electrophysiology and transmission electron microscopic (TEM) tomography imaging to analyze the resulting changes. Acute MAGUK knockdown greatly reduces synaptic transmission mediated by α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors (AMPARs) and N-methyl-d-aspartate receptors (NMDARs). This knockdown leads to a significant rise in the number of silent synapses, diminishes the size of PSDs without changes in pre- or postsynaptic membrane, and depletes the number of membrane-associated PSD-95–like vertical filaments and transmembrane structures, identified as AMPARs and NMDARs by EM tomography. The differential distribution of these receptor-like structures and dependence of their abundance on PSD size matches that of AMPARs and NMDARs in the hippocampal synapses. The loss of these structures following MAGUK knockdown tracks the reduction in postsynaptic AMPAR and NMDAR transmission, confirming the structural identities of these two types of receptors. These results demonstrate that MAGUKs are required for anchoring both types of glutamate receptors at the PSD and are consistent with a structural model where MAGUKs, corresponding to membrane-associated vertical filaments, are the essential structural proteins that anchor and organize both types of glutamate receptors and govern the overall molecular organization of the PSD.

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14

Claudepierre, T., C. Dalloz, D. Mornet, K. Matsumura, J. Sahel, and A. Rendon. "Characterization of the intermolecular associations of the dystrophin-associated glycoprotein complex in retinal Muller glial cells." Journal of Cell Science 113, no. 19 (2000): 3409–17. http://dx.doi.org/10.1242/jcs.113.19.3409.

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The abnormal retinal neurotransmission observed in Duchenne muscular dystrophy patients has been attributed to altered expression of C-terminal products of the dystrophin gene in this tissue. Muller glial cells from rat retina express dystrophin protein Dp71, utrophin and the members of the dystrophin-associated glycoprotein complex (DGC), namely beta-dystroglycan, delta- and gamma-sarcoglycans and alpha1-syntrophin. The DGC could function in muscle as a link between the cystoskeleton and the extracellular matrix, as well as a signaling complex. However, other than in muscle the composition and intermolecular associations among members of the DGC are still unknown. Here we demonstrate that Dp71 and/or utrophin from rat retinal Muller glial cells form a complex with beta-dystroglycan, delta-sarcoglycan and alpha1-syntrophin. We also show that beta-dystroglycan is associated with alpha-dystrobrevin-1 and PSD-93 and that anti-PSD antibodies coimmunoprecipitated alpha-syntrophin with PSD-93. By overlay experiments we also found that Dp71and/or utrophin and alpha-dystroglycan from Muller cells could bind to actin and laminin, respectively. These results indicate that the DGC could have both structural and signaling functions in retina. On the basis of our accumulated evidence, we propose a hypothetical model for the molecular organization of the dystrophin-associated glycoprotein complex in retinal Muller glial cells, which would be helpful for understanding its function in the central nervous system.

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15

Rong, Rong, Hui Yang, Liangqun Rong, et al. "Proteomic analysis of PSD-93 knockout mice following the induction of ischemic cerebral injury." NeuroToxicology 53 (March 2016): 1–11. http://dx.doi.org/10.1016/j.neuro.2015.12.005.

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16

Fiorentini, Monica, Anders Bach, Kristian Strømgaard, Jette S. Kastrup, and Michael Gajhede. "Interaction partners of PSD-93 studied by X-ray crystallography and fluorescence polarization spectroscopy." Acta Crystallographica Section D Biological Crystallography 69, no. 4 (2013): 587–94. http://dx.doi.org/10.1107/s0907444912051839.

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17

Nada, Shigeyuki, Takaki Shima, Hiroyuki Yanai, et al. "Identification of PSD-93 as a Substrate for the Src Family Tyrosine Kinase Fyn." Journal of Biological Chemistry 278, no. 48 (2003): 47610–21. http://dx.doi.org/10.1074/jbc.m303873200.

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18

Yu, Linjie, Yi Liu, Hui Yang та ін. "PSD-93 Attenuates Amyloid-β-Mediated Cognitive Dysfunction by Promoting the Catabolism of Amyloid-β". Journal of Alzheimer's Disease 59, № 3 (2017): 913–27. http://dx.doi.org/10.3233/jad-170320.

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19

Zhang, Meijuan, Qingjie Li, Ling Chen, et al. "PSD-93 deletion inhibits Fyn-mediated phosphorylation of NR2B and protects against focal cerebral ischemia." Neurobiology of Disease 68 (August 2014): 104–11. http://dx.doi.org/10.1016/j.nbd.2014.04.010.

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20

Jiang, Xiangning, Dezhi Mu, R. Ann Sheldon, David V. Glidden, and Donna M. Ferriero. "Neonatal Hypoxia-Ischemia Differentially Upregulates MAGUKs and Associated Proteins in PSD-93–Deficient Mouse Brain." Stroke 34, no. 12 (2003): 2958–63. http://dx.doi.org/10.1161/01.str.0000102560.78524.9d.

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21

Zhang, Qingxiu, Hui Yang, Hong Gao, et al. "PSD-93 Interacts with SynGAP and Promotes SynGAP Ubiquitination and Ischemic Brain Injury in Mice." Translational Stroke Research 11, no. 5 (2020): 1137–47. http://dx.doi.org/10.1007/s12975-020-00795-z.

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22

Yang, Eddy, Daniel Scott, and Jess Nithianantharajah. "Investigating the Molecular and Functional Impact of a Novel DLG2 /PSD‐93 Mutation in Neurodevelopmental Disorders." FASEB Journal 34, S1 (2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.09279.

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23

Xu, Yun, Bosheng Zhang, Zichun Hua, Roger A. Johns, David S. Bredt, and Yuan-Xiang Tao. "Targeted disruption of PSD-93 gene reduces platelet-activating factor-induced neurotoxicity in cultured cortical neurons." Experimental Neurology 189, no. 1 (2004): 16–24. http://dx.doi.org/10.1016/j.expneurol.2004.05.013.

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24

Aoki, Chiye, Ilona Miko, Hysell Oviedo, et al. "Electron microscopic immunocytochemical detection of PSD-95, PSD-93, SAP-102, and SAP-97 at postsynaptic, presynaptic, and nonsynaptic sites of adult and neonatal rat visual cortex." Synapse 40, no. 4 (2001): 239–57. http://dx.doi.org/10.1002/syn.1047.

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25

Leyland, Mark L., and Caroline Dart. "An Alternatively Spliced Isoform of PSD-93/Chapsyn 110 Binds to the Inwardly Rectifying Potassium Channel, Kir2.1." Journal of Biological Chemistry 279, no. 42 (2004): 43427–36. http://dx.doi.org/10.1074/jbc.m407575200.

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26

Ibarahim, Najwa Adni, Nafisah Osman, and Mohd Azlan Mohd Ishak. "Particle Size Distribution of Cerate-Zirconate Powder Prepared via Three Different Methods." Advanced Materials Research 1108 (June 2015): 67–72. http://dx.doi.org/10.4028/www.scientific.net/amr.1108.67.

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Ceramics powder of BaCe0.54Zr0.36Y0.1O2.95 (BCZY) was synthesized using three different methods namely sol-gel (SG), supercritical fluid (SC) and sol-gel assisted supercritical fluids (SGSF).The respective prepared samples were denoted as S1, S2 and S3. The calcined powder (T= 1100 °C) was analyzed using particle size analyzer (PSA), Pcynometer and scanning electron microscope (SEM). PSA showed a single particle size distribution (PSD) for all samples except for S3 which exhibits bimodial particle distribution. PSD of the samples were in the range of 295-396 nm for the primary powder and 712-820 nm for secondary powder. High relative powder density for S1, S2, S3 were recorded at 95 %, 93 % and 99 %, respectively. Morphology of the calcined powders by SEM micrograph revealed that S1 is in spherical shape, S2 is in cubic structure and S3 showed a mixture of spherical and rod-like structure. It was found that SG and SC produce a single shape of powder with lower density compared with SGSF.

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Limperger, Verena, Gili Kenet, Christine Heller, et al. "Impact of SERPINC1, PROC and PROS1 Mutations on the Thrombotic Phenotype in Children with Venous Thromboembolism: An Observational Multicenter Cohort Study." Blood 124, no. 21 (2014): 583. http://dx.doi.org/10.1182/blood.v124.21.583.583.

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Abstract Background: Venous thromboembolism [TE] is a multifactorial disease and antithrombin [ATD] -, protein C [PCD] - or protein S [PSD] -deficiency constitutes a major risk factor. The objective of the present study was to i) evaluate the prevalence of ATD, PCD and PSD in a white Israeli-German cohort of children with TE, ii) the underlying gene mutations, and iii) the clinical presentation of ATD, PCD and PCS on symptomatic TE in children. Methods: In 367 unselected children (0.1-18 years) with TE recruited between July 1996 and December 2013 from Germany & Israel, a comprehensive thrombophilia screening was performed. Along with standardized plasma-based coagulation assays and the use of age-dependent reference values ATD, PCD and PSD were confirmed by family studies and/or molecular diagnosis [gene sequencing & multiplex ligation-dependent probe amplification]. Apart from descriptive analysis non-parametric statistics was performed. To compare the rates of deficiency phenotypes, locations of TE, spontaneous versus provoked TE, presence or absence of a positive family history of TE, Chi-square or Fisher’s exact test was applied. Results: 6.6% of children were ATD, 6.8% PCD including purpura fulminans (1.4%) and 8.2% patients carried PSD. Mean age at first TE was 13 years (range 0.1 to 18) with no statistically significant difference found between deficiency phenotypes (p=0.32). 38 children were male. 72 of 76 children (95%) showed type 1 deficiency, whereas in 4 cases [ATD] a type 2 deficiency was found (p=0.004). Underlying gene mutations were in the majority of cases missense mutations (SERPINC1: 75%; PROC: 93%; PROS1: 72%), with 24% presence of the Herleen polymorphism (CM951058) in children with PSD. Homozygous genotypes were found in 4 cases [ATD], 6 cases [PCD] and in one PSD carrier [p=0.07]. ATD co-occurred with the factor 5 mutation [F5] at rs6025 in one and the factor 2 susceptibility variant [F2] at rs1799963 in two children. PSD co-occurred with the F5 or the homozygous F2 in one case each. Apart from purpura fulminans which was seen only in neonates with homozygous PCD, thrombotic locations were similarly distributed (p=0.11): multiple veins (n=7), cerebral veins/stroke of venous origin (n=18), deep veins [DVT; n=38], DVT & pulmonary embolism (n=13). The rates of provoked TE were 57% [ATD], 48% [PCD] and 60% in PCD (p=0.06). A positive family history was present in 43% [ATD], 40% [PCD] and 57% [PSD; p=0.41]. After withdrawal of anticoagulation, - performed on an individual basis according to CHEST guidelines (updated according to year of publication) -, recurrence rates were 38% [ATD], 24% [PCD] and 6.6% in carriers of PSD (p=0.017). Conclusion: Given its clinical implication for patients and family members, thrombophilia testing should be performed and the benefit of medical or educational interventions should be evaluated in this high risk population Disclosures No relevant conflicts of interest to declare.

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Zhang, Qingxiu, Hongyu Cheng, Rong Rong, et al. "The Effect of PSD-93 Deficiency on the Expression of Early Inflammatory Cytokines Induced by Ischemic Brain Injury." Cell Biochemistry and Biophysics 73, no. 3 (2015): 695–700. http://dx.doi.org/10.1007/s12013-015-0666-9.

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Shah, Hemali, Paul Feustel, and Lindy Davis. "Survivorship care plans and adherence with surveillance schedule in patients with invasive melanoma." Journal of Clinical Oncology 39, no. 15_suppl (2021): e24079-e24079. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e24079.

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e24079 Background: Melanoma accounts for 5.5% of new cancer diagnoses in the United States, and the 5-year overall survival is 93%. Overall, 7% of patients develop a recurrence, and 4-8% develop a second primary melanoma. This study aimed to assess how the standards set by the American College of Surgeons Commission on Cancer (CoC) to provide survivorship care plans (SCP) to patients may improve adherence to surveillance visits. Methods: All patients treated for invasive melanoma at our institution between 8/2018-2/2020 were included. SCP containing stage, treatment summary, and surveillance plan were delivered in-person to patients and sent to primary providers and dermatologists as outlined by CoC Standards for Optimal Care. Psychosocial distress (PSD) screening was performed using the National Comprehensive Cancer Network Distress Thermometer, with scores > 4 requiring further evaluation by oncology social worker. SCP and PSD were provided during the initiation phase of our cancer care program, and half the patients received services. Surveillance adherence was determined from chart review. The two groups were compared by t-test for continuous or chi-square test for categorical variables. Multiple regression analysis with odds ratios were performed. Mann-Whitney analysis was performed to assess the impact of SCP on PSD. Results: Of 146 patients identified for our cohort, 73 received SCP and PSD screening. Stage IA was the most common diagnosis (44%), followed by IB (13%) and IIIC (9%). Ninety-eight patients (67%) were adherent to all surveillance visits, and 55 of these received SCPs. Most patients noted low distress without the need for further support (79%), and 12 (21%) scored ≥4, benefiting from emotional and financial support and appointment and health insurance navigation. High PSD score did not correlate with advanced stage. Reception of SCP (p = 0.036) and close distance to treating facility (p = 0.016) improved adherence to surveillance visits. For patients who did not receive SCP, likelihood to follow up decreased by a factor of 0.469 (95% CI 0.231 - 0.952). Sex, age, PSD score, and stage did not affect surveillance adherence (p = NS). There were 6 recurrences, of which 4 were physician-detected during surveillance, and 8 patients developed second primary melanomas, all physician-detected. Conclusions: Delivery of SCP, a component of which includes counseling regarding signs and symptoms of recurrence or possibility of second primary melanoma, leads to significantly higher rates of surveillance adherence. This was shown for all stages. Melanoma survivors require close clinical follow-up, as demonstrated by our study finding that even with patient education, most recurrences and all new primary melanomas were physician-detected. PSD among melanoma patients is common, and all patients regardless of stage should undergo screening, as even early-stage patients exhibited distress.

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Turkoglu, Ahmet, Zubeyir Bozdag, Metehan Gumus, et al. "Comparison of Crystallized Phenol Treatment and Simple Primary Closure Methods for Pilonidal Sinus Disease." International Surgery 103, no. 9-10 (2019): 424–28. http://dx.doi.org/10.9738/intsurg-d-15-00066.1.

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The objective of the study was to compare the results of the patients treated with crystallized phenol treatment (CPT) or simple primary closure (SPC) for pilonidal sinus disease (PSD). For PSD treatment, both SPC and CPT have the advantages of rapid recovery, minimal pain, and short hospital stay. Even though these two techniques can be used interchangeably in uncomplicated cases, there is not enough evidence about which method is superior. A total of 102 patients who underwent CPT (n = 57) and SPC (n = 45) for uncomplicated PSD were included in the study. In all of the cases, data were recorded and compared between CPT and SPC groups, including age, gender, duration of the symptoms, hospital stay, complications, healing time, and recurrence. The mean age was 25.6 years and the male-to-female ratio was 93:9. The SPC and CPT groups were similar in terms of age, gender, duration of symptoms, complications, and healing time. The CPT group did not require hospitalization or anesthetic procedure in addition to local anesthesia, but the SPC group required a median of 1 day (range, 1–3 days) of hospitalization, and 3 patients (6.7%) needed spinal anesthesia. During a median of 27.5 months' follow-up, the recurrence rate in the CPT group (6 patients; 10.5%) was lower than in the SPC group (13 patients; 28.9%). Both hospital stay and recurrence rates were better in the CPT group. Healing time and complication rates were similar in both methods. Based on these results, we suggest that CPT should be preferred to SPC in uncomplicated cases.

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Gursel, Gul, Kamil Inci, and Zenfira Alasgarova. "Can Diaphragm Dysfunction Be Reliably Evaluated with Pocket-Sized Ultrasound Devices in Intensive Care Unit?" Critical Care Research and Practice 2018 (2018): 1–6. http://dx.doi.org/10.1155/2018/5192647.

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Background. Diaphragm dysfunction (DD) is frequently seen in critically ill patients, and ultrasound could be a useful tool to detect it and to predict extubation success or failure in mechanically ventilated patients. Besides, it would also be useful in differential diagnosis of dyspnea and respiratory failure. The aim of this study is to evaluate usefulness and accuracy of pocket-sized ultrasound devices (PSDs) in assessment of DD in intensive care unit (ICU) patients in comparison with standard ultrasound devices (SD). Methods. In this prospective observational study, we compared the performance of PSD and SD in visualization of diaphragm, detection of paradoxical movement, measurement of tidal and maximal thickness, tidal and maximal excursion, and calculation of thickening fraction (TF) of the diaphragm. We used Bland and Altman test for agreement and bias analysis and intraclass correlation analysis to evaluate interobserver variability. Results. Thirty-nine patients were included in the study. In 93% of the patients, diaphragm was visualized with PSD. There was very good agreement between the measurements of the devices, and there was no proportional bias in the measurements of tidal inspiratory and expiratory thickness, tidal TF, tidal excursion, and maximal inspiratory thickness. In interobserver reliability analysis of all measurements for both devices, ICC coefficients were higher than 0.8. Total diaphragm examination times of the devices were similar (p>0.05). Conclusion. These results suggest that PSD can be useful in ICU patients for evaluating DD. But further studies are required to determine the exact place of these devices in evaluation of DD in ICU patients.

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Zhang, Qingxiu, Lei He, Mo Chen, et al. "PSD‐93 mediates the crosstalk between neuron and microglia and facilitates acute ischemic stroke injury by binding to CX3CL1." Journal of Neurochemistry 157, no. 6 (2021): 2145–57. http://dx.doi.org/10.1111/jnc.15324.

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Raspor, Eva, Peter K. Hahn, Tom Lancaster, et al. "S177. IMPACT OF NOS1AP AND ITS INTERACTION PARTNERS AT THE GLUTAMATERGIC SYNAPSE ON WORKING MEMORY NETWORKS - AN FMRI IMAGING GENETICS STUDY." Schizophrenia Bulletin 46, Supplement_1 (2020): S105. http://dx.doi.org/10.1093/schbul/sbaa031.243.

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Abstract Background N-methyl-D-aspartate receptor (NMDAR) hypofunction is an important pathophysiological mechanism in schizophrenia. At the postsynapse the NMDAR interacts with the post-synaptic density (PSD). Neuronal nitric oxide synthase 1 (NOS1) binds to the PSD scaffolding proteins PSD-93 and PSD-95, enabling NMDAR-mediated release of nitric oxide via NOS1. NOS1AP (adaptor of NOS1) is capable of disrupting the interactions between NOS1, PSD-93, and PSD95. Therefore, NOS1AP is closely involved in both glutamatergic and nitrinergic neurotransmission. NOS1AP has been implicated as a risk gene for schizophrenia and cognitive dysfunction. Its increased expression has been observed in dorsolateral prefrontal post-mortem brain tissue of patients with schizophrenia, and NOS1AP SNPs have been associated with established schizophrenia endophenotypes. These findings suggest that the influence of NOS1AP variants should be observable in neural systems implicated in schizophrenia. In the present study, we investigate the impact of NOS1AP and its interaction partners at the glutamatergic synapse on the cortical working memory (WM) networks using fMRI and a gene set analysis approach. Methods 97 right-handed individuals with no personal or family history of psychiatric disorders underwent fMRI in a 3T Siemens Trio scanner during the performance of a visuospatial change detection WM task. Data analysis in Brain Voyager QX 2.8 included standard data preprocessing. Additionally, a multiscale curvature driven cortex based alignment procedure was used to minimize macro-anatomical variability between subjects. Subsequently, data were analyzed using a random-effects multi-subject general linear model. We investigated 19 regions of interest (ROIs) within the core fronto-parietal WM network. We studied all phases of our WM paradigm (encoding, maintenance, retrieval), which were modeled by a total of 5 regressors (encoding, delays 1–3, retrieval). Genetic data was quality controlled and imputed using the RICOPILI pipeline. Gene-set analyses of the 19 ROIs were performed using MAGMA. Two gene sets were selected: 1) NOS1AP/NOS1; 2) NOS1AP/glutamatergic synapse. We applied a Bonferroni correction for the total of 19 ROIs and 5 regressors (95 tests) to both analyses. Results Both gene set analyses revealed multiple associations between brain activation in core fronto-parietal WM areas. For the NOS1/NOS1AP set, most associations were observed during the late maintenance phase (Delay 3) of our WM paradigm. One association was significant Bonferroni correction: a cluster in the left intraparietal sulcus during the late maintenance phase (Delay 3; β=2.2459, SD=0.0239, SE=0.6451, p=0,00025). For NOS1AP / glutamatergic synapse interaction partners, two associations were significant after Bonferroni correction: a cluster in the right IPS during the early maintenance phase (Delay 1; β=0.8525, SD=0.0257, SE=0.2127, p=0.0000308) and a cluster in a different part of the right IPS during the late maintenance phase (Delay 3; β=0.7186, SD=0.0216, SE=0.2119, p=0,000348). Discussion In our gene set analyses we observed multiple associations between brain activation during WM and NOS1AP and its interaction partners, which were most pronounced during the late maintenance phase of our WM task in bilateral areas within the IPS. Both the more constrained NOS1AP / NOS1 gene set and the NOS1AP / glutamatergic synapse gene set showed similar association patterns. Our results implicate the NOS1AP interactome and the glutamatergic system in information processing and brain function in a cognitive domain strongly impaired in schizophrenia. They also indicate that altered activation of parietal WM areas during the maintenance phase is most strongly affected.

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Gun'ko, V. M. "Features of the morphology and texture of silica and carbon adsorbents." Surface 13(28) (December 30, 2021): 127–65. http://dx.doi.org/10.15407/surface.2021.13.127.

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The morphological and textural characteristics of various silicas (93 fumed silicas and 56 porous silicas), different carbons (230), and porous polymers (53) are analyzed using probe (nitrogen, argon, benzene, n-decane, water) adsorption, small angle X-ray scattering (SAXS), and transition (TEM), scanning (SEM) electron and atom force (AFM) microscopies. There are certain correlations between pore volume (Vp) and specific surface area (SSA, SBET) for these materials. Synthesis and treatment temperatures affect this relationship since a linear Vp - SBET approximation scatter decreases with decreasing these temperatures. Silicas are composed of nonporous nanoparticles (NPNP), but activated carbons (AC) are composed of porous nanoparticles (PNP). For different materials, NP are weakly or strongly packed in secondary structures. However, there are general features of pore size distributions (PSD) for NP-based materials, e.g., minimal contribution of narrow mesopores of 3-5 nm in radius due NP-packing effects. For AC produced using the same chars and activation agents but with varied activation time, the textural characteristics demonstrate smooth changes with increasing burn-off degree: nanopores partially transform into narrow mesopores with opposite PSD shifts of broad mesopores and macropores. Comparison of adsorption (open pores accessible for probes) and SAXS (both open and closed pores) data for carbons shows that the difference decreases with increasing burn-off degree due to decreasing contribution of closed pores. Most clear pictures on the particulate morphology and texture could be obtained in parallel analysis using adsorption, SAXS, and microscopic methods with appropriate data treatments.

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McGee, Aaron W., J. Rick Topinka, Kouichi Hashimoto, et al. "PSD-93 Knock-Out Mice Reveal That Neuronal MAGUKs Are Not Required for Development or Function of Parallel Fiber Synapses in Cerebellum." Journal of Neuroscience 21, no. 9 (2001): 3085–91. http://dx.doi.org/10.1523/jneurosci.21-09-03085.2001.

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Zhang, Bosheng, Feng Tao, Wen-Jinn Liaw, David S. Bredt, Roger A. Johns та Yuan-Xiang Tao. "Effect of knock down of spinal cord PSD-93/chapsin-110 on persistent pain induced by complete Freundʼs adjuvant and peripheral nerve injury". Pain 106, № 1 (2003): 187–96. http://dx.doi.org/10.1016/j.pain.2003.08.003.

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Zhang, Aixiang, Yuanjie Qian, and Jian Qian. "MicroRNA-152-3p protects neurons from oxygen-glucose-deprivation/reoxygenation-induced injury through upregulation of Nrf2/ARE antioxidant signaling by targeting PSD-93." Biochemical and Biophysical Research Communications 517, no. 1 (2019): 69–76. http://dx.doi.org/10.1016/j.bbrc.2019.07.012.

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SINGH, SINAM AJITKUMAR, and SWANIRBHAR MAJUMDER. "CLASSIFICATION OF UNSEGMENTED HEART SOUND RECORDING USING KNN CLASSIFIER." Journal of Mechanics in Medicine and Biology 19, no. 04 (2019): 1950025. http://dx.doi.org/10.1142/s0219519419500258.

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Due to low physical workout, high-calorie intake, and bad behavioral character, people were affected by cardiological disorders. Every instant, one out of four deaths are due to heart-related ailments. Hence, the early diagnosis of a heart is essential. Most of the approaches for automated classification of the heart sound need segmentation of Phonocardiograms (PCG) signal. The main aim of this study was to decline the segmentation process and to estimate the utility for accurate and detailed classification of short unsegmented PCG recording. Based on wavelet decomposition, Hilbert transform, homomorphic filtering, and power spectral density (PSD), the features had been obtained using the beginning 5 second PCG recording. The extracted features were classified using nearest neighbors with Euclidean distances for different values of [Formula: see text] by bootstrapping 50% PCG recording for training and 50% for testing over 100 iterations. The overall accuracy of 100%, 85%, 80.95%, 81.4%, and 98.13% had been achieved for five different datasets using KNN classifiers. The classification performance for analyzing the whole datasets is 90% accuracy with 93% sensitivity and 90% specificity. The classification of unsegmented PCG recording based on an efficient feature extraction is necessary. This paper presents a promising classification performance as compared with the state-of-the-art approaches in short time less complexity.

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Votanopoulos, Konstantinos I., Greg B. Russell, Reese W. Randle, Perry Shen, John H. Stewart, and Edward Allen Levine. "Peritoneal surface disease (PSD) from appendiceal cancer treated with cytoreductive surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPEC): Overview of 481 cases." Journal of Clinical Oncology 32, no. 3_suppl (2014): 565. http://dx.doi.org/10.1200/jco.2014.32.3_suppl.565.

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565 Background: Appendiceal cancer PSD treated with CRS/HIPEC has shown significant variability in the obtained survival benefit. Methods: A prospective database of 1,069 procedures was reviewed for primary, grade, nodal and performance status, resection type, morbidity, mortality, and survival. Results: 481 CRS/HIPEC procedures, 317 (77.3%) for low grade (LGA) and 93 (22.7%) for high grade (HGA) appendiceal primaries, were identified. Median follow up was 44.4 months. 30 and 90 day major morbidity were 27.8% and 9.3% while the 30 and 90 day mortality was 2.7% and 5.6% respectively. Median ICU and hospital stay was 1 and 9 days. In multivariate analysis, Clavien III/IV complications, were related to incomplete CRS (p = 0.0037), involved nodes (p < 0.0001) and comorbidities (p = 0.003). Multivariate analysis of the LGA patients indicated survival to be dependent on nodal status (p = 0.003 HR 3.6), complete cytoreduction (p < 0.0001) and preoperative chemotherapy (p = 0.04 HR 2.2). The multivariate survival of HGA was dependent on complete cytoreduction (p = 0.0003 HR 3.8) and preoperative chemotherapy (p = 0.0064 HR 2.5). In patients with complete cytoreduction, median survival for node positive LGA and HGA patients was less than their node negative counterparts. (85 months vs. not reached (82% alive at 90 months) and 30 vs. 153 months respectively p < 0.0001). Conclusions: Positive nodes are associated with decreased survival not only in HGA but also in LGA patients even after a complete cytoreduction. Nodal status is superior to grade of disease as a prognostic indicator of survival. Node negative HGA primaries after complete CRS can obtain a comparable survival benefit to LGA counterparts.

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Banaszak, David, Dansen Brown, and David Laird. "Antonomous Environmental Definition of C-130 Flap Well Skin Panel." Journal of the IEST 48, no. 1 (2005): 50–61. http://dx.doi.org/10.17764/jiet.48.1.pw070l022uu28503.

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Air Force C-130 aircraft require numerous aluminum doubler repairs on the wing flap skin aft of the right-hand outboard engine. These repairs are costly and require riveting. Rivets often provide new areas of stress concentration, which causes new cracks to develop elsewhere. Boeing and the Air Force Research Laboratory (AFRL) are measuring the thermal and strain environment behind the right-hand outboard engine of a North Carolina Air National Guard (NCANG) operational C-130 aircraft (TN 93-1456) for use in design of a damped repair patch to prevent the growth of cracks in skin under the wing flap panel. During June 2003. AFRL engineers and technicians acquired data using an autonomous damage dosimeter during five operational C-130 flights. The damage dosimeter measures structural strains and temperatures on in-service aircraft to diagnose structural conditions that are difficult to analyze, such as acoustics and high cycle fatigue (HCF). The first flight was from Charlotte, North Carolina to Warner Robins Air Force Base (AFB), Georgia and returned to Charlotte. The last four flights were assault flights where the C-130 simulated cargo drops. Pilots logged the altitude and indicated airspeed, engine speed, and flap positions for the first four flights. Flap position settings were compared with dosimeter temperature and root mean square (rms) strain measurements. This paper presents typical third octave plots showing engine speed vibratory frequencies, rms time histories (TH), and correlation data for a flight. This paper also presents typical limited data in TH, probability density function (PDF), power spectral density (PSD), and rain flow formats.

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Xian, Yan-Fang, Chang Qu, Yue Liu, et al. "Magnolol Ameliorates Behavioral Impairments and Neuropathology in a Transgenic Mouse Model of Alzheimer’s Disease." Oxidative Medicine and Cellular Longevity 2020 (July 3, 2020): 1–17. http://dx.doi.org/10.1155/2020/5920476.

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Alzheimer’s disease (AD) is a common neurodegenerative disease characterized by progressive memory loss. Magnolol (MN), the main active ingredient of Magnolia officinalis, possesses anti-AD effects in several experimental models of AD. In this study, we aimed to explore whether MN could ameliorate the cognitive deficits in TgCRND8 transgenic mice and to elucidate its molecular mechanisms. Male TgCRND8 mice were orally administered with MN (20 and 40 mg/kg) daily for 4 consecutive months, followed by assessing the spatial learning and memory functions using the open-field, radial arm maze, and novel object recognition tests. The results demonstrated that MN (20 and 40 mg/kg) could markedly ameliorate the cognitive deficits in TgCRND8 mice. In addition, MN significantly increased the expression of postsynaptic density protein 93 (PSD93), PSD-95, synapsin-1, synaptotagmin-1, synaptophysin (SYN), and interleukin-10 (IL-10), while markedly reduced the protein levels of tumor necrosis factor alpha (TNF-α), IL-6, IL-1β, Aβ40, and Aβ42, and modulated the amyloid precursor protein (APP) processing and phosphorylation. Immunofluorescence showed that MN significantly suppressed the activation of microglia (Iba-1) and astrocytes (GFAP) in the hippocampus and cerebral cortex of TgCRND8 mice. Mechanistic studies revealed that MN could significantly increase the ratios of p-GSK-3β (Ser9)/GSK-3β, p-Akt (Ser473)/Akt, and p-NF-κB p65/NF-κB p65. These findings indicate that MN exerted cognitive deficits improving effects via suppressing neuroinflammation, amyloid pathology, and synaptic dysfunction through regulating the PI3K/Akt/GSK-3β and NF-κB pathways, suggesting that MN is a promising naturally occurring polyphenol worthy of further developing into a therapeutic agent for AD treatment.

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Rickhag, Mattias, William A. Owens, Marie-Therese Winkler, et al. "Membrane-permeable C-terminal Dopamine Transporter Peptides Attenuate Amphetamine-evoked Dopamine Release." Journal of Biological Chemistry 288, no. 38 (2013): 27534–44. http://dx.doi.org/10.1074/jbc.m112.441295.

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The dopamine transporter (DAT) is responsible for sequestration of extracellular dopamine (DA). The psychostimulant amphetamine (AMPH) is a DAT substrate, which is actively transported into the nerve terminal, eliciting vesicular depletion and reversal of DA transport via DAT. Here, we investigate the role of the DAT C terminus in AMPH-evoked DA efflux using cell-permeant dominant-negative peptides. A peptide, which corresponded to the last 24 C-terminal residues of DAT (TAT-C24 DAT) and thereby contained the Ca2+-calmodulin-dependent protein kinase IIα (CaMKIIα) binding domain and the PSD-95/Discs-large/ZO-1 (PDZ)-binding sequence of DAT, was made membrane-permeable by fusing it to the cell membrane transduction domain of the HIV-1 Tat protein (TAT-C24WT). The ability of TAT-C24WT but not a scrambled peptide (TAT-C24Scr) to block the CaMKIIα-DAT interaction was supported by co-immunoprecipitation experiments in heterologous cells. In heterologous cells, we also found that TAT-C24WT, but not TAT-C24Scr, decreased AMPH-evoked 1-methyl-4-phenylpyridinium efflux. Moreover, chronoamperometric recordings in striatum revealed diminished AMPH-evoked DA efflux in mice preinjected with TAT-C24WT. Both in heterologous cells and in striatum, the peptide did not further inhibit efflux upon KN-93-mediated inhibition of CaMKIIα activity, consistent with a dominant-negative action preventing binding of CaMKIIα to the DAT C terminus. This was further supported by the ability of a peptide with perturbed PDZ-binding sequence, but preserved CaMKIIα binding (TAT-C24AAA), to diminish AMPH-evoked DA efflux in vivo to the same extent as TAT-C24WT. Finally, AMPH-induced locomotor hyperactivity was attenuated following systemic administration of TAT-C24WT but not TAT-C24Scr. Summarized, our findings substantiate that DAT C-terminal protein-protein interactions are critical for AMPH-evoked DA efflux and suggest that it may be possible to target protein-protein interactions to modulate transporter function and interfere with psychostimulant effects.

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Alvarez, I., A. Modolell, J. I. Mayordomo, et al. "Biweekly nonpegylated liposomal doxorubicin (M) and docetaxel (T) as neoadjuvant treatment in patients with stage II-III breast cancer." Journal of Clinical Oncology 25, no. 18_suppl (2007): 11049. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.11049.

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11049 Background: We have previously reported (ASCO 2006) the efficacy and toxicity of 4 courses of M (75mg/m2) and T (75mg/m2) with G-CSF support in a 21 day schedule as neoadjuvant treatment in patients with resectable breast cancer. Aim: To evaluate the clinical and pathological response rate (RR) and toxicity of biweekly M and T given prior to surgery in patients with breast cancer. Methods: Patients with histological confirmation of breast cancer (stage II-III and inflammatory), age >18 years, left ventricular ejection fraction > 45% and adequate bone marrow, renal and hepatic function were included in the study. Prior systemic therapy, radiotherapy or surgery for breast cancer were not allowed. The treatment was: M (60 mg/m2) and T (60mg/m2) each in 1 hour infusion, with subcutaneous G-CSF (5 mcg/kg) support on days 4–9. Courses were repeated every 14 days. Patients received 6 courses prior to surgery. Results: To date 45 patients have been enrolled; 20 who have completed therapy and underwent surgery (except for patients with progression) were included in this interim analysis. Median age: 48 years (38–63), ECOG PS 0: 90%, ECOG PS1: 10%, postmenopausal: 35%. Histology was infiltrating ductal carcinoma in 80%. Patients received a total of 110 courses (median 6, range 2–6). Efficacy: Of 19 evaluable patients, 4 achieved a clinical complete response (cCR) (21%), 12 partial response (cPR) (63%), 1 stable disease (cSD) (5%) and 2 progressive disease (cPD) (10%), resulting in a clinical response rate (cRR) of 84%. Surgery was performed in 17 (85%) patients, 4 (23%) of them had pathological complete response (pCR), 12 (70%) partial response (pPR), 1 (6%) stable disease (pSD), resulting in a pathological RR of 93%. Median time to progression and overall survival have not been reached. Toxicity: Hematological grade III/IV toxicities per patient were neutropenia (10%), febrile neutropenia (10%) and thrombocytopenia (5%). Non-hematological grade III/IV toxicities per patient were mucositis (10%), nausea/vomiting (10%) and epigastralgia (10%) Conclusions: Six courses of T and M every 14 days with G- CSF support as induction treatment in stage II and III breast cancer are active and well tolerated. No significant financial relationships to disclose.

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Løvlie, Reidar. "Experimental determination of the relationship between magnetic moment and grain geometry of PSD magnetite grains." Physics of the Earth and Planetary Interiors 76, no. 1-2 (1993): 105–12. http://dx.doi.org/10.1016/0031-9201(93)90059-i.

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Abdel-Magid, Shaban. "MINQUE and PSD-MINQMBE in the two way cross classification random effect model without interaction." Microelectronics Reliability 35, no. 1 (1995): 97–99. http://dx.doi.org/10.1016/0026-2714(93)e0004-s.

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Woods, Daniel F., and Peter J. Bryant. "ZO-1, DlgA and PSD-95/SAP90: homologous proteins in tight, septate and synaptic cell junctions." Mechanisms of Development 44, no. 2-3 (1993): 85–89. http://dx.doi.org/10.1016/0925-4773(93)90059-7.

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Rimbault, Charlotte, Kashyap Maruthi, Christelle Breillat, et al. "Engineering selective competitors for the discrimination of highly conserved protein-protein interaction modules." Nature Communications 10, no. 1 (2019). http://dx.doi.org/10.1038/s41467-019-12528-4.

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Abstract Designing highly specific modulators of protein-protein interactions (PPIs) is especially challenging in the context of multiple paralogs and conserved interaction surfaces. In this case, direct generation of selective and competitive inhibitors is hindered by high similarity within the evolutionary-related protein interfaces. We report here a strategy that uses a semi-rational approach to separate the modulator design into two functional parts. We first achieve specificity toward a region outside of the interface by using phage display selection coupled with molecular and cellular validation. Highly selective competition is then generated by appending the more degenerate interaction peptide to contact the target interface. We apply this approach to specifically bind a single PDZ domain within the postsynaptic protein PSD-95 over highly similar PDZ domains in PSD-93, SAP-97 and SAP-102. Our work provides a paralog-selective and domain specific inhibitor of PSD-95, and describes a method to efficiently target other conserved PPI modules.

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Yang, Eddy, Daniel Scott, and Jess Nithianantharajah. "A Novel Missense Variant in DLG2 /PSD‐93 Disrupts Protein Folding and Binding In Neurodevelopmental Disorders." FASEB Journal 35, S1 (2021). http://dx.doi.org/10.1096/fasebj.2021.35.s1.04406.

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Qin, Xin-Ya, Qing-Hong Shan, Hui Fang, et al. "PSD-93 up-regulates the synaptic activity of corticotropin-releasing hormone neurons in the paraventricular nucleus in depression." Acta Neuropathologica, September 18, 2021. http://dx.doi.org/10.1007/s00401-021-02371-7.

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Zhang, Qingxiu, Lei He, Mo Chen, et al. "PSD-93 Mediates the Crosstalk between Neuron and Microglia and Facilitates Acute Ischemic Stroke Injury by Binding to CX3CL1." SSRN Electronic Journal, 2020. http://dx.doi.org/10.2139/ssrn.3666283.

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