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Статті в журналах з теми "Restores human"

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Автор: Grafiati

Опубліковано: 30 травня 2022

Оновлено: 31 травня 2022

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1

DRAGO, FRÉDÉRIC, and NORISHIGE CHIBA. "LOCALLY ADAPTIVE CHROMATIC RESTORATION OF DIGITALLY ACQUIRED PAINTINGS." International Journal of Image and Graphics 05, no. 03 (July 2005): 617–37. http://dx.doi.org/10.1142/s0219467805001914.

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This article presents a semi-automatic procedure to restore the visual appearance of aged paintings converted to a digital form. The innovative implementation of an image-processing algorithm based on the Retinex theory of human vision alleviates layers of yellowed varnish and dust, restores chromatic balance and contrast, and recovers some of the original painted details. This virtual cleaning of artwork is totally non-intrusive and can be applied automatically to color images of paintings or ancient illustrations. Cleaned virtual reproductions help art historians and restorers in their research and classification work, and also show the artwork in good condition to a wide audience while avoiding an always costly and dangerous manual restoration.

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2

Tversky, J., A. Bieneman, and J. Schroeder. "Allergen Immunotherapy Restores Human Dendritic Cell Innate Immune Function." Journal of Allergy and Clinical Immunology 123, no. 2 (February 2009): S127. http://dx.doi.org/10.1016/j.jaci.2008.12.469.

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3

Agalakova, Natalia I., Yulia N. Grigorova, Ivan A. Ershov, Vitaly A. Reznik, Elena V. Mikhailova, Olga V. Nadei, Leticia Samuilovskaya, et al. "Canrenone Restores Vasorelaxation Impaired by Marinobufagenin in Human Preeclampsia." International Journal of Molecular Sciences 23, no. 6 (March 19, 2022): 3336. http://dx.doi.org/10.3390/ijms23063336.

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Previous studies implicated cardiotonic steroids, including Na/K-ATPase inhibitor marinobufagenin (MBG), in the pathogenesis of preeclampsia (PE). Recently, we demonstrated that (i) MBG induces fibrosis in rat tissues via a mechanism involving Fli1, a negative regulator of collagen-1 synthesis, and (ii) MBG sensitive Na/K-ATPase inhibition is reversed by mineralocorticoid antagonists. We hypothesized that in human PE elevated MBG level is associated with the development of fibrosis of the umbilical arteries and that this fibrosis can be attenuated by canrenone. Fifteen patients with PE (mean BP = 118 ± 4 mmHg; 34 ± 2 years; 38 ± 0.3 weeks gest. age) and twelve gestational age-matched normal pregnant subjects (mean BP = 92 ± 2 mmHg; 34 ± 1 years; 39 ± 0.2 weeks gest. age) were enrolled in the study. PE was associated with a higher plasma MBG level, with a four-fold decrease in Fli1 level and a three-fold increase in collagen-1 level in the PE umbilical arteries vs. those from the normal subjects (p < 0.01). Isolated rings of umbilical arteries from the subjects with PE exhibited impaired responses to the relaxant effect of sodium nitroprusside vs. control vessels (EC50 = 141 nmol/L vs. EC50 = 0.9 nmol/L; p < 0.001). The effects of PE on Fli1 and collagen-1 were blocked by the in vitro treatment of umbilical arteries by 10 μmol/L canrenone. Similar results were obtained for umbilical arteries pretreated with MBG. These data demonstrate that elevated MBG level is implicated in the development of the fibrosis of umbilical arteries in PE, and that this could be blocked by mineralocorticoid antagonists.

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4

Whidden, David L. "Sin and the structure of Anselm's Cur Deus homo." Scottish Journal of Theology 75, no. 1 (February 2022): 23–32. http://dx.doi.org/10.1017/s003693062100079x.

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AbstractThe hypothesis of this article is that Anselm describes two consequences of sin for the human will in De casu diaboli, and these two consequences structure Anselm's later account of human salvation in the Cur Deus homo. First, sin causes us to deserve punishment for injustice; and, second, sin removes the grace by which humans were able to attain the goal of their creation, which is the happiness of heaven. Book 1 of the Cur Deus homo, then, deals with the need for satisfaction in the face of punishment, while book 2 addresses the need for a supererogatory gift that elevates human nature and restores it to its heavenly end. The article argues that, for Anselm, only a God-man can provide both the satisfaction and supererogatory gift necessary to restore humans to their original divine purpose.

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5

Feng, Qi, Ji Ma, Xin Li, Ming Hou, and Jun Peng. "Human Leukocyte Antigen-G Restores Immune Tolerance in Immune Thrombocytopenia." Blood 132, Supplement 1 (November 29, 2018): 3751. http://dx.doi.org/10.1182/blood-2018-99-115713.

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Abstract Immune thrombocytopenia (ITP) is a common autoimmune bleeding disorder in which loss of immune tolerance leads to platelet destruction. Human leukocyte antigen-G (HLA-G) is a non-classical major histocompatibility complex class I antigen including four membrane-bound (mHLA-G, HLA-G1 to -G4) and three soluble (sHLA-G, HLA-G5 to -G7) isoforms due to alternative splicing of the HLA-G primary transcript. HLA-G exerts immunosuppressive functions by interacting with its inhibitory receptors, immunoglobulin-like transcripts (ILTs), expressing differentially on natural killer cells, T cells, and antigen presenting cells. Upon binding to ILTs, HLA-G suppressed lymphocyte proliferation, promoted apoptosis of cytotoxic lymphocytes and natural killer cells, inhibited antibody secretion from activated B cells, and induced expansion of suppressive T cells, tolerogenic dendritic cells and myeloid-derived suppressor cells. HLA-G supports immune escape, and high level of HLA-G is associated with unfavorable outcomes in cancer patients. Meanwhile, HLA-G-induced tolerance can benefit human allotransplantation and autoimmune diseases, such as rheumatoid arthritis and systemic lupus erythematosus, but the role of HLA-G in the treatment of ITP is still unclear. Here we observed significantly less soluble HLA-G in plasma from ITP patients positive for anti-glycoprotein (GP) IIb/IIIa and/or anti-GPIb/IX autoantibodies compared with autoantibody-negative patients or healthy controls. However, no significant difference was found in the sHLA-G levels between anti-glycoprotein (GP) IIbIIIa and anti-GPIb-IX autoantibodies groups. Interestingly, sHLA-G is positively correlated with platelet counts in ITP patients both with and without autoantibodies, suggesting that HLA-G can also protect platelets from destruction through other mechanisms. To elucidate this, we then analyzed both expression of membrane HLA-G and ILTs on PBMCs. Our data found less membrane-bound HLA-G and ILTs on CD4+T cells and CD14+cells in ITP patients. Moreover, recombinant human HLA-G (rhHLA-G) upregulated expression of ILT2 on CD4+and ILT4 on CD14+cells. The upregulation of ILT by rhHLA-G indicates that sHLA-G might also benefit ITP patients negative for anti-platelet autoantibodies. To determine whether rhHLA-G affects T cell differentiation, we tested 17 cytokines by ELISA to investigate the immune environment with or without rhHLA-G, and found that rhHLA-G upregulated Interleukin (IL)-4 and IL-10, and downregulated tumor necrosis factor-α, IL-12, and IL-17 secreted by ITP patient peripheral blood mononuclear cells (PBMCs), indicating a promotion of helper T(Th)2 and inhibition of Th1 and Th17 differentiation. However, our results indicated that rhHLA-G did not expand the CD4+CD25+Foxp3+regulatory T cells(Tregs). In addition, rhHLA-G exerted their immunosuppressive effects by upregulating IL-1β, IL-2, Granulocyte colony-stimulating factor (G-CSF), and granulocyte-macrophage colony stimulating factor (GM-CSF). By reprogramming the cytokine profile in ITP patients, HLA-G established an optimal environment for the impaired cell populations, such as dendritic cells (DCs), to regain their tolerogenic function. Our results showed that rhHLA-G inhibited monocyte-derived DCs maturation by downregulating CD80 and CD86 expression. To further assess whether the rhHLA-G modulated-DCs were functionally tolerogenic, PBMCs were then cocultured with rhHLA-G modulated-DCs. Our results showed that rhHLA-G-modulated DCs from ITP patients suppressed CD4+T cell proliferation by 38.8% compared to unmodulated cells. Besides, PBMCs exposed to rhHLA-G were less cytotoxic toward plateletsfrom ITP patients or healthy subjects. This study provides a potential strategy to protect exogenous platelets from destruction in ITP patients. In conclusion, our data demonstrated that impaired expression of HLA-G and/or ILT is involved in the pathogenesis of ITP, and recombinant human HLA-G can restore immune tolerance in ITP patients via upregulation of ILTs, which indicates that HLA-G can be a diagnostic marker and also a therapeutic option for ITP treatment. Disclosures No relevant conflicts of interest to declare.

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6

Herbert, Katharine J., Anthony L. Cook, and Elizabeth T. Snow. "SIRT1 inhibition restores apoptotic sensitivity in p53-mutated human keratinocytes." Toxicology and Applied Pharmacology 277, no. 3 (June 2014): 288–97. http://dx.doi.org/10.1016/j.taap.2014.04.001.

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7

Zhu, Shao-Fang, Hong-Bo Hu, Hong-Yan Xu, Xia-Fei Fu, Dong-Xian Peng, Wei-Yan Su, and Yuan-Li He. "Human umbilical cord mesenchymal stem cell transplantation restores damaged ovaries." Journal of Cellular and Molecular Medicine 19, no. 9 (April 29, 2015): 2108–17. http://dx.doi.org/10.1111/jcmm.12571.

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8

Kubo, Toshihiko, Eduardo R. Azevedo, Gary E. Newton, Peter Picton, John D. Parker, and John S. Floras. "Beta-Blockade Restores Muscle Sympathetic Rhythmicity in Human Heart Failure." Circulation Journal 75, no. 6 (2011): 1400–1408. http://dx.doi.org/10.1253/circj.cj-10-0751.

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9

Herebian, Diran, Annette Seibt, Sander H. J. Smits, Richard J. Rodenburg, Ertan Mayatepek, and Felix Distelmaier. "4-Hydroxybenzoic acid restores CoQ10 biosynthesis in human COQ2 deficiency." Annals of Clinical and Translational Neurology 4, no. 12 (October 17, 2017): 902–8. http://dx.doi.org/10.1002/acn3.486.

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10

Schmidt, Ulrich, Robert H. G. Schwinger, and Michael Bohm. "Halothane Restores the Altered Force-Frequency Relationship in Failing Human Myocardium." Anesthesiology 82, no. 6 (June 1, 1995): 1456–62. http://dx.doi.org/10.1097/00000542-199506000-00017.

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Анотація:

Background The terminally failing human myocardium exerts a negative force-frequency relationship (FFR), whereas a positive FFR occurs in nonfailing myocardium. To study the possibility of pharmacologically influencing this defect of the failing human heart, the effect of halothane on the basal FFR and the FFR in the presence of isoproterenol and ouabain was investigated. Methods Experiments were performed on isolated, electrically driven (0.5-2 Hz, 37 degrees C, Ca2+ 1.8 mmol/l) ventricular preparations. Myocardium from human failing and nonfailing hearts was obtained at cardiac surgery. To further characterize the studied myocardium, the positive inotropic effect of isoproterenol and the density of beta-adrenoceptors were measured using the radioligand 125I-CYP. Results Halothane produced a negative inotropic effect. The anesthetic (0.38 mmol/l) reversed the negative FFR in failing myocardium, antagonized the effect of isoproterenol (0.1 mumol/l) on FFR, and restored the FFR in the presence of ouabain. Conclusions Halothane restores the FFR in human failing myocardium possibly by influencing the intracellular Ca2+ homeostasis. These findings provide evidence that pharmacologic interventions, e.g., during anesthesia, may influence contractility also as a result of a depressed or enhanced FFR.

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11

SCHNEYER, ALAN, and MELISSA BROWN. "FSTL3 Inhibition Restores Glucose Responsive Insulin Secretion in Nonfunctional Human Islets." Diabetes 67, Supplement 1 (May 2018): 2153—P. http://dx.doi.org/10.2337/db18-2153-p.

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12

Shimato, Shinji, Lisa M. Anderson, Martin Asslaber, Jeffrey N. Bruce, Peter Canoll, David E. Anderson, and Richard C. E. Anderson. "Inhibition of Caveolin-1 Restores Myeloid Cell Function in Human Glioblastoma." PLoS ONE 8, no. 10 (October 9, 2013): e77397. http://dx.doi.org/10.1371/journal.pone.0077397.

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13

Li, Jiao, Jun Dong, Zhen‐hui Zhang, Dong‐Cheng Zhang, Xiang‐Yu You, Yun Zhong, Min‐Sheng Chen, and Shi‐Ming Liu. "miR‐10a restores human mesenchymal stem cell differentiation by repressing KLF4." Journal of Cellular Physiology 228, no. 12 (August 23, 2013): 2324–36. http://dx.doi.org/10.1002/jcp.24402.

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14

Iriti, Marcello, Robert Kubina, Andrea Cochis, Rita Sorrentino, Elena M. Varoni, Agata Kabała-Dzik, Barbara Azzimonti, Arkadiusz Dziedzic, Lia Rimondini, and Robert D. Wojtyczka. "Rutin, a Quercetin Glycoside, Restores Chemosensitivity in Human Breast Cancer Cells." Phytotherapy Research 31, no. 10 (July 28, 2017): 1529–38. http://dx.doi.org/10.1002/ptr.5878.

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15

Danks, Lynett, Sarita Workman, David Webster, and Nicole J. Horwood. "Elevated cytokine production restores bone resorption by human Btk-deficient osteoclasts." Journal of Bone and Mineral Research 26, no. 1 (December 22, 2010): 182–92. http://dx.doi.org/10.1002/jbmr.210.

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16

Youl, B. D., S. D. T. White, M. Cadogan, and A. G. Dalgleish. "Goat serum product restores conduction in demyelinated human optic nerve fibres." Clinical Neurophysiology 118, no. 5 (May 2007): e158. http://dx.doi.org/10.1016/j.clinph.2006.07.243.

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17

Schwinger, Robert H. G., Michael Böhm, Rainer Uhlmann, Ulridi Schmid, Peter Übertuhr, Eckhart Kreuzer, Bruno Reichart, and Erland Erdmann. "Magnesium restores the altered force-frequency relationship in failing human myocardium." American Heart Journal 126, no. 4 (October 1993): 1018–21. http://dx.doi.org/10.1016/0002-8703(93)90731-n.

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18

Ou, Yen-Chuan, Jian-Ri Li, Jiaan-Der Wang, Wen-Ying Chen, Yu-Hsiang Kuan, Ching-Ping Yang, Su-Lan Liao, Hsi-Chi Lu, and Chun-Jung Chen. "Aspirin restores ABT-737-mediated apoptosis in human renal carcinoma cells." Biochemical and Biophysical Research Communications 502, no. 2 (July 2018): 187–93. http://dx.doi.org/10.1016/j.bbrc.2018.05.142.

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19

Behar, Jose, Byung Y. Rhim, William Thompson, and Piero Biancani. "Inositol trisphosphate restores impaired human gallbladder motility associated with cholesterol stones." Gastroenterology 104, no. 2 (February 1993): 563–68. http://dx.doi.org/10.1016/0016-5085(93)90427-e.

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20

Tominaga, Kana, Naoomi Tominaga, Eric O. Williams, Laura Rufibach, Verena Schöwel, Simone Spuler, Mohan Viswanathan, and Leonard P. Guarente. "4-Phenylbutyrate restores localization and membrane repair to human dysferlin mutations." iScience 25, no. 1 (January 2022): 103667. http://dx.doi.org/10.1016/j.isci.2021.103667.

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21

Khan, Mahfuz, Minerva Garcia-Barrio, and Michael D. Powell. "Treatment of Human Immunodeficiency Virus Type 1 Virions Depleted of Cyclophilin A by Natural Endogenous Reverse Transcription Restores Infectivity." Journal of Virology 77, no. 7 (April 1, 2003): 4431–34. http://dx.doi.org/10.1128/jvi.77.7.4431-4434.2003.

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ABSTRACT We have previously shown that virions with nef deleted can be restored to wild-type infectivity by treatment to induce natural endogenous reverse transcription (NERT). Since Nef and cyclophilin A (CyPA) appear to act in similar ways on postentry events, we determined whether NERT treatment would restore infectivity to virions depleted of CyPA. Our results show that the infectivity of virions depleted of CyPA by treatment with cyclosporine A could be restored by NERT treatment, while mutants in the CyPA binding loop of capsid could only be partially restored. These results suggest that CyPA is involved in some aspect of the uncoating process.

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22

Davey, S., and D. Beach. "RACH2, a novel human gene that complements a fission yeast cell cycle checkpoint mutation." Molecular Biology of the Cell 6, no. 10 (October 1995): 1411–21. http://dx.doi.org/10.1091/mbc.6.10.1411.

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We have identified a novel human gene by virtue of its ability to complement the rad1-1 checkpoint mutant of Schizosaccharomyces pombe. This gene, called RACH2, rescues the temperature-sensitive lethality of a rad1-1 wee1-50 double mutant of S. pombe. Expression of RACH2 in S. pombe rad1-1 strains partially restores UV resistance to the rad1-1 mutant strain. Expression of RACH2 in a rad1-1 cdc25-22 double mutant partially restores the dose-dependent delay in mitotic entry after irradiation that is lost in rad1-1 checkpoint-deficient mutants. Overexpression of RACH2 in human tissue culture cells induces apoptosis.

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23

Zhu, Guang-Jie, Sihao Gong, Deng-Bin Ma, Tao Tao, Wei-Qi He, Linqing Zhang, Fang Wang, et al. "Aldh inhibitor restores auditory function in a mouse model of human deafness." PLOS Genetics 16, no. 9 (September 24, 2020): e1009040. http://dx.doi.org/10.1371/journal.pgen.1009040.

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24

Graf, Laszloa, Christoper H. K. Cheng, and Choh Hao Li. "HUMAN SOMATOTROPIN: Noncovalent Interaction of Two Thrombin Fragments Restores Receptor-Binding Activity*." International Journal of Peptide and Protein Research 18, no. 4 (January 12, 2009): 409–12. http://dx.doi.org/10.1111/j.1399-3011.1981.tb02999.x.

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25

LIU, JIANYING, SEUNGHUN P. LEE, TONYA MARTIN, BRIAN RADY, SANATH MEEGALLA, HUI HUANG, MICHAEL P. WINTERS, et al. "FFAR1 Agonism Restores Insulin Secretion in Rodents, Human Islets, and Diabetic Monkeys." Diabetes 67, Supplement 1 (May 2018): 609—P. http://dx.doi.org/10.2337/db18-609-p.

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26

Toyama, Yasuyuki, Ken-ichiro Sasaki, Katsuro Tachibana, Takafumi Ueno, Hidemi Kajimoto, Shinji Yokoyama, Masanori Ohtsuka, et al. "Ultrasound stimulation restores impaired neovascularization-related capacities of human circulating angiogenic cells." Cardiovascular Research 95, no. 4 (May 28, 2012): 448–59. http://dx.doi.org/10.1093/cvr/cvs173.

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27

Olsson, Richard, Stefan Hagelberg, Olle Ringdén, Lennart Truedsson, and Anders Ahlin. "Allogeneic bone marrow transplantation restores complement function in human hereditary C1q deficiency." Immunobiology 217, no. 11 (November 2012): 1136. http://dx.doi.org/10.1016/j.imbio.2012.08.022.

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28

Rotondo, Rossella, Salvatore Castaldo, Maria Antonietta Oliva, and Antonietta Arcella. "Gymnema sylvestre Extract Restores the Autophagic Pathway in Human Glioblastoma Cells U87Mg." Biology 10, no. 9 (September 4, 2021): 870. http://dx.doi.org/10.3390/biology10090870.

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Glioblastoma is a brain tumour, characterised by recurrent or innate resistance to conventional chemoradiotherapy. Novel natural molecules and phyto-extracts have been proposed as adjuvants to sensitise the response to Temozolomide (TMZ). In this study, we investigated the effect of GS extract on human glioblastoma cells U87Mg. According to the IC50-values, GS extract displayed a significant cytotoxicity. This was confirmed by cell growth inhibition and alteration in metabolic activity evaluated by cell count and MTT assay. GS induced reduction in Pro-caspase 9, 3, but not PARP cleavage nor DNA fragmentation. Thus, in GS-induced cytotoxicity, cell death is not associated with apoptosis. In this context, short-term treatment of U87Mg cells with GS extract (1 mg/mL) reduced the phosphorylation levels of mTOR and of its downstream target P70 S6 kinase, highlighting the role of GS extract into autophagy induction. The activation of autophagic flux by GS extract was confirmed by Western blot analysis, which revealed the reduction in p62 and the concomitant increase in LC3B II/I ratio. Immunofluorescence evidenced the accumulation of LC3B puncta in U87Mg cells pretreated with autophagy inhibitor Bafilomycin A1. Furthermore, as main key regulators of type II programmed cell death, p53, p21 and CDK4 were also investigated and were inhibited by GS treatment. In conclusion, GS extract could be considered as an autophagy inducer in glioblastoma cells U87Mg.

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SALVIATI, Leonardo, Evelyn HERNANDEZ-ROSA, Winsome F. WALKER, Sabrina SACCONI, Salvatore DiMAURO, Eric A. SCHON, and Mercy M. DAVIDSON. "Copper supplementation restores cytochrome c oxidase activity in cultured cells from patients with SCO2 mutations." Biochemical Journal 363, no. 2 (April 8, 2002): 321–27. http://dx.doi.org/10.1042/bj3630321.

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Human SCO2 is a nuclear-encoded Cu-binding protein, presumed to be responsible for the insertion of Cu into the mitochondrial cytochrome c oxidase (COX) holoenzyme. Mutations in SCO2 are associated with cardioencephalomyopathy and COX deficiency. Studies in yeast and bacteria have shown that Cu supplementation can restore COX activity in cells harbouring mutations in genes involving Cu transport. Therefore we investigated whether Cu supplementation could restore COX activity in cultured cells from patients with SCO2 mutations. Our data demonstrate that the COX deficiency observed in fibroblasts, myoblasts and myotubes from patients with SCO2 mutations can be restored to almost normal levels by the addition of CuCl2 to the growth medium.

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Zhang, Xinyu, Shune Xiao, Bingcheng Liu, Yong Miao, and Zhiqi Hu. "Use of extracellular matrix hydrogel from human placenta to restore hair-inductive potential of dermal papilla cells." Regenerative Medicine 14, no. 8 (August 2019): 741–51. http://dx.doi.org/10.2217/rme-2018-0112.

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Aim: To explore the feasibility of human placenta extracellular matrix (HPECM) hydrogel in restoring the hair-inductive capacity of high-passaged (P8) dermal papilla cells (DPCs) for hair follicle regeneration. Materials & methods: HPECM hydrogel was prepared following decellularization and enzymatic solubilization treatment. DPCs isolated from human scalp were cultured in 2D and 3D environments. The hair-inductive ability of DPCs was assessed by quantitative RT-PCR, immunofluorescence staining, immunoblotting and patch assay. Results: DPCs (P8) formed spheres when cultured on the HPECM hydrogel. The expression levels of Versican, ALP, and β-catenin were restored in the DP spheres. HPECM hydrogel-cultured DP spheres co-grafted with newborn mouse epidermal cells regenerated new hair follicle. Conclusion: HPECM hydrogel successfully restores the hair-inductive capacity of high-passaged DPCs.

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31

Chen, Jie, Thomas C. Cesario, Runze Li, Ali O. Er, and Peter M. Rentzepis. "The low photo-inactivation rate of bacteria in human plasma II. Inhibition of methylene blue bleaching in plasma and effective bacterial destruction by the addition of dilute acetic acid to human plasma." Photochemical & Photobiological Sciences 14, no. 10 (2015): 1880–87. http://dx.doi.org/10.1039/c5pp00042d.

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32

Rankin, T. L., Z. B. Tong, P. E. Castle, E. Lee, R. Gore-Langton, L. M. Nelson, and J. Dean. "Human ZP3 restores fertility in Zp3 null mice without affecting order-specific sperm binding." Development 125, no. 13 (July 1, 1998): 2415–24. http://dx.doi.org/10.1242/dev.125.13.2415.

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The mammalian zona pellucida surrounding ovulated eggs mediates sperm binding at fertilization, provides a postfertilization block to polyspermy, and facilitates passage of pre-implantation embryos down the oviduct. Although the three zona proteins (ZP1, ZP2, ZP3) are well conserved, mammalian fertilization is relatively specific and human sperm do not bind to the mouse zona pellucida. There are considerable in vitro data that ZP3 acts as a primary sperm adhesion molecule in mice and, by analogy, a similar role has been postulated for human ZP3. Genetically altered mice lacking ZP3 (Zp3(tm/tm)) do not form a zona pellucida and are infertile. To rescue this phenotype, transgenic mice expressing human ZP3 (67% identical to mouse ZP3) were produced and bred with Zp3(tm/tm) null mice. The resultant human ZP3 rescue females had chimeric zonae pellucidae composed of mouse ZP1, mouse ZP2 and human ZP3. Human ZP3 expressed in mouse oocytes had an apparent mass (64 kDa) indistinguishable from native human ZP3 and distinct from mouse ZP3 (83 kDa). Despite the presence of human ZP3, human sperm did not bind to the chimeric zona pellucida, and notwithstanding the absence of mouse ZP3, mouse sperm bound to ovulated eggs in vitro and fertility was restored in vivo. These data have implications regarding the molecular basis of mouse and human sperm binding to their respective zonae pellucidae.

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33

Soma, Shivatheja, Andrew J. Latimer, Haarin Chun, Alison C. Vicary, Shrishiv A. Timbalia, Aren Boulet, Jennifer J. Rahn, et al. "Elesclomol restores mitochondrial function in genetic models of copper deficiency." Proceedings of the National Academy of Sciences 115, no. 32 (July 23, 2018): 8161–66. http://dx.doi.org/10.1073/pnas.1806296115.

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Copper is an essential cofactor of cytochrome c oxidase (CcO), the terminal enzyme of the mitochondrial respiratory chain. Inherited loss-of-function mutations in several genes encoding proteins required for copper delivery to CcO result in diminished CcO activity and severe pathologic conditions in affected infants. Copper supplementation restores CcO function in patient cells with mutations in two of these genes, COA6 and SCO2, suggesting a potential therapeutic approach. However, direct copper supplementation has not been therapeutically effective in human patients, underscoring the need to identify highly efficient copper transporting pharmacological agents. By using a candidate-based approach, we identified an investigational anticancer drug, elesclomol (ES), that rescues respiratory defects of COA6-deficient yeast cells by increasing mitochondrial copper content and restoring CcO activity. ES also rescues respiratory defects in other yeast mutants of copper metabolism, suggesting a broader applicability. Low nanomolar concentrations of ES reinstate copper-containing subunits of CcO in a zebrafish model of copper deficiency and in a series of copper-deficient mammalian cells, including those derived from a patient with SCO2 mutations. These findings reveal that ES can restore intracellular copper homeostasis by mimicking the function of missing transporters and chaperones of copper, and may have potential in treating human disorders of copper metabolism.

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34

OTA, Ichiro, Katsunari YANE, Kazue YUKI, Hirokazu KANATA, Hiroshi HOSOI, and Hiroshi MIYAHARA. "GLYCEROL RESTORES THE P53 FUNCTION IN HUMAN LINGUAL CANCER CELLS BEARING MUTANT P53." Japanese jornal of Head and Neck Cancer 27, no. 3 (2001): 639–43. http://dx.doi.org/10.5981/jjhnc1974.27.639.

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35

Yamaguchi, Tamio, Scott J. Hempson, Gail A. Reif, Anne-Marie Hedge, and Darren P. Wallace. "Calcium Restores a Normal Proliferation Phenotype in Human Polycystic Kidney Disease Epithelial Cells." Journal of the American Society of Nephrology 17, no. 1 (November 30, 2005): 178–87. http://dx.doi.org/10.1681/asn.2005060645.

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36

Ragin, Richard C., Patricia K. Donahoe, Mary K. Kenneally, Mir F. Ahmad, and David T. MacLaughlin. "Human Müllerian inhibiting substance: Enhanced purification imparts biochemical stability and restores antiproliferative effects." Protein Expression and Purification 3, no. 3 (June 1992): 236–45. http://dx.doi.org/10.1016/1046-5928(92)90020-w.

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37

Hunze, E. M., T. Barbour, N. Sheerin, M. C. Pickering та K. Marchbank. "Human FHΔ6–17 (a mini-FH) restores serum C3 levels in FH−/− mice". Molecular Immunology 56, № 3 (грудень 2013): 265–66. http://dx.doi.org/10.1016/j.molimm.2013.05.077.

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38

Mwamburi, D. Mkaya, Jül Gerrior, Ira B. Wilson, Hong Chang, Ed Scully, Shiva Saboori, Laurel Miller, Janet Forfia, Mary Albrecht, and Christine A. Wanke. "Combination Megestrol Acetate, Oxandrolone, and Dietary Advice Restores Weight in Human Immunodeficiency Virus." Nutrition in Clinical Practice 19, no. 4 (August 2004): 395–402. http://dx.doi.org/10.1177/0115426504019004395.

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39

Wang, Ding, Caiyun Fang, Nobel C. Zong, David A. Liem, Martin Cadeiras, Sarah B. Scruggs, Hongxiu Yu, et al. "Regulation of Acetylation Restores Proteolytic Function of Diseased Myocardium in Mouse and Human." Molecular & Cellular Proteomics 12, no. 12 (September 15, 2013): 3793–802. http://dx.doi.org/10.1074/mcp.m113.028332.

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40

Shen, Bing, Xiang Li, Fei Wang, Xiaoqiang Yao, and Dan Yang. "A Synthetic Chloride Channel Restores Chloride Conductance in Human Cystic Fibrosis Epithelial Cells." PLoS ONE 7, no. 4 (April 13, 2012): e34694. http://dx.doi.org/10.1371/journal.pone.0034694.

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41

Donetti, Elena, Alice Gualerzi, Federica Ricceri, Leonardo Pescitelli, Marzia Bedoni, and Francesca Prignano. "Etanercept restores a differentiated keratinocyte phenotype in psoriatic human skin: a morphological study." Experimental Dermatology 21, no. 7 (June 20, 2012): 549–51. http://dx.doi.org/10.1111/j.1600-0625.2012.01518.x.

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42

Guasch, Antonio, Carlos F. Zayas, and Kamal F. Badr. "MK-591 acutely restores glomerular size selectivity and reduces proteinuria in human glomerulonephritis." Kidney International 56, no. 1 (July 1999): 261–67. http://dx.doi.org/10.1046/j.1523-1755.1999.00537.x.

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43

Mojiri, A., G. Matrone, B. Walther, and J. Cooke. "HUMAN TELOMERASE M-RNA TREATMENT RESTORES FUNCTIONS IN PROGERIA IPSC- DERIVED ENDOTHELIAL CELLS." Canadian Journal of Cardiology 35, no. 10 (October 2019): S85. http://dx.doi.org/10.1016/j.cjca.2019.07.191.

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44

Erdogdu, Özlem, Linnéa Eriksson, Thomas Nyström, Åke Sjöholm, and Qimin Zhang. "Exendin-4 restores glucolipotoxicity-induced gene expression in human coronary artery endothelial cells." Biochemical and Biophysical Research Communications 419, no. 4 (March 2012): 790–95. http://dx.doi.org/10.1016/j.bbrc.2012.02.106.

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45

Yin, Liyuan, Yi Zhang, Lijuan Yin, Yan Ou, Michael S. Lewis, Ruoxiang Wang, Haiyen E. Zhau, Qinghua Zhou, and Leland W. K. Chung. "Novel Mitochondria-Based Targeting Restores Responsiveness in Therapeutically Resistant Human Lung Cancer Cells." Molecular Cancer Therapeutics 20, no. 12 (September 28, 2021): 2527–38. http://dx.doi.org/10.1158/1535-7163.mct-20-1095.

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46

Martínez-Escardó, Laura, Montse Alemany, María Sánchez-Osuna, Alejandro Sánchez-Chardi, Meritxell Roig-Martínez, Salvio Suárez-García, Daniel Ruiz-Molina, et al. "Gossypol Treatment Restores Insufficient Apoptotic Function of DFF40/CAD in Human Glioblastoma Cells." Cancers 13, no. 21 (November 8, 2021): 5579. http://dx.doi.org/10.3390/cancers13215579.

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Glioblastoma (GBM) is a highly aggressive brain tumor and almost all patients die because of relapses. GBM-derived cells undergo cell death without nuclear fragmentation upon treatment with different apoptotic agents. Nuclear dismantling determines the point-of-no-return in the apoptotic process. DFF40/CAD is the main endonuclease implicated in apoptotic nuclear disassembly. To be properly activated, DFF40/CAD should reside in the cytosol. However, the endonuclease is poorly expressed in the cytosol and remains cumulated in the nucleus of GBM cells. Here, by employing commercial and non-commercial patient-derived GBM cells, we demonstrate that the natural terpenoid aldehyde gossypol prompts DFF40/CAD-dependent nuclear fragmentation. A comparative analysis between gossypol- and staurosporine-treated cells evidenced that levels of neither caspase activation nor DNA damage were correlated with the ability of each compound to induce nuclear fragmentation. Deconvoluted confocal images revealed that DFF40/CAD was almost completely excluded from the nucleus early after the staurosporine challenge. However, gossypol-treated cells maintained DFF40/CAD in the nucleus for longer times, shaping a ribbon-like structure piercing the nuclear fragments and building a network of bridged masses of compacted chromatin. Therefore, GBM cells can fragment their nuclei if treated with the adequate insult, making the cell death process irreversible.

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47

Fry, Terry J., Barbara L. Christensen, Kristin L. Komschlies, Ronald E. Gress, and Crystal L. Mackall. "Interleukin-7 restores immunity in athymic T-cell–depleted hosts." Blood 97, no. 6 (March 15, 2001): 1525–33. http://dx.doi.org/10.1182/blood.v97.6.1525.

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Thymic-deficient hosts rely primarily on antigen-driven expansion to restore the peripheral T-cell compartment following T-cell depletion (TCD). The degree to which this thymic-independent pathway can restore immune competence remains poorly understood but has important implications for a number of clinical conditions including stem cell transplantation and human immunodeficiency virus (HIV) infection. A model of HY-mediated skin graft rejection by athymic, TCD mice was used to show that restoration of naive and recall responses via peripheral expansion requires transfer of only 25 × 106 lymph node (LN) cells representing approximately 10% of the T-cell repertoire. Consitutive expression of bcl-2 in the expanding inocula restored recall responses to HY at a substantially lower LN cell dose (1 × 106), which is normally insufficient to induce HY-mediated graft rejection in athymic hosts. Interestingly, bcl-2 had no effect on primary responses. Interleukin-7 (IL-7) potently enhanced thymic-independent peripheral expansion and led to HY graft rejection using an LN cell dose of 1 × 106 in both primary and recall models. The restoration of immune competence by IL-7 appeared to be mediated through a combination of programmed cell death inhibition, improved costimulation, and modulation of antigen-presenting cell (APC) function. These results show that immune competence for even stringent antigens such as HY can be restored in the absence of thymic function and identify IL-7 as a potent modulator of thymic-independent T-cell regeneration.

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48

Hubbard, Nicholas, David Hagin, Karen Sommer, Yumei Song, Iram Khan, Courtnee Clough, Hans D. Ochs, David J. Rawlings, Andrew M. Scharenberg, and Troy R. Torgerson. "Targeted gene editing restores regulated CD40L function in X-linked hyper-IgM syndrome." Blood 127, no. 21 (May 26, 2016): 2513–22. http://dx.doi.org/10.1182/blood-2015-11-683235.

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Key PointsThe CD40LG locus can be specifically targeted and repaired in primary human T cells by insertion of a spliced CD40LG complementary DNA. Gene editing restores regulated CD40L expression in X-HIGM T cells, reconstituting B-cell immunoglobulin class switching.

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49

An, Sugyun, Si-Young Cho, Junsoo Kang, Soobeom Lee, Hyung-Su Kim, Dae-Jin Min, EuiDong Son, and Kwang-Hyun Cho. "Inhibition of 3-phosphoinositide–dependent protein kinase 1 (PDK1) can revert cellular senescence in human dermal fibroblasts." Proceedings of the National Academy of Sciences 117, no. 49 (November 23, 2020): 31535–46. http://dx.doi.org/10.1073/pnas.1920338117.

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Cellular senescence is defined as a stable, persistent arrest of cell proliferation. Here, we examine whether senescent cells can lose senescence hallmarks and reenter a reversible state of cell-cycle arrest (quiescence). We constructed a molecular regulatory network of cellular senescence based on previous experimental evidence. To infer the regulatory logic of the network, we performed phosphoprotein array experiments with normal human dermal fibroblasts and used the data to optimize the regulatory relationships between molecules with an evolutionary algorithm. From ensemble analysis of network models, we identified 3-phosphoinositide–dependent protein kinase 1 (PDK1) as a promising target for inhibitors to convert the senescent state to the quiescent state. We showed that inhibition of PDK1 in senescent human dermal fibroblasts eradicates senescence hallmarks and restores entry into the cell cycle by suppressing both nuclear factor κB and mTOR signaling, resulting in restored skin regeneration capacity. Our findings provide insight into a potential therapeutic strategy to treat age-related diseases associated with the accumulation of senescent cells.

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50

Law, Y. M., R. S. Yeung, C. Mamalaki, D. Kioussis, T. W. Mak, and R. A. Flavell. "Human CD4 restores normal T cell development and function in mice deficient in murine CD4." Journal of Experimental Medicine 179, no. 4 (April 1, 1994): 1233–42. http://dx.doi.org/10.1084/jem.179.4.1233.

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The ability of a human coreceptor to function in mice was investigated by generating human CD4 (hCD4)-expressing transgenic mice on a mouse CD4-deficient (mCD4-/-) background. From developing thymocyte to matured T lymphocyte functions, hCD4 was shown to be physiologically active. By examining the expansion and deletion of specific V beta T cell families in mutated mice with and without hCD4, it was found that hCD4 can participate in positive and negative selection. Mature hCD4 single positive cells also were found in the periphery and they were shown to restore MHC class II-restricted alloreactive and antigen-specific T cell responses that were deficient in the mCD4 (-/-) mice. In addition, these hCD4 reconstituted mice can generate a secondary immunoglobulin G humoral response matching that of mCD4 wild-type mice. The fact that human CD4 is functional in mice and can be studied in the absence of murine CD4 should facilitate studies of human CD4 activity in general and human immunodeficiency virus 1 gp120-mediated pathogenesis in acquired immune deficiency syndrome specifically.

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