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Transplantation of human umbilical cord blood mesenchymal stem cells to treat a rat model of traumatic brain injury.

Neural regeneration research

Zhao J, Chen N, Shen N, Zhao H, Wang D, Shi J, Wang Y, Cui X, Yan Z, Xue H.
PMID: 25737696
Neural Regen Res. 2012 Apr 05;7(10):741-8. doi: 10.3969/j.issn.1673-5374.2012.10.004.

In the present study, human umbilical cord blood mesenchymal stem cells were injected into a rat model of traumatic brain injury via the tail vein. Results showed that 5-bromodeoxyuridine-labeled cells aggregated around the injury site, surviving up to 4...

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Zhao J, Chen N, Shen N, et al. Transplantation of human umbilical cord blood mesenchymal stem cells to treat a rat model of traumatic brain injury. Neural Regen Res. 2012;7(10):741-8doi: 10.3969/j.issn.1673-5374.2012.10.004.
Zhao, J., Chen, N., Shen, N., Zhao, H., Wang, D., Shi, J., Wang, Y., Cui, X., Yan, Z., & Xue, H. (2012). Transplantation of human umbilical cord blood mesenchymal stem cells to treat a rat model of traumatic brain injury. Neural regeneration research, 7(10), 741-8. https://doi.org/10.3969/j.issn.1673-5374.2012.10.004
Zhao, Junjian, et al. "Transplantation of human umbilical cord blood mesenchymal stem cells to treat a rat model of traumatic brain injury." Neural regeneration research vol. 7,10 (2012): 741-8. doi: https://doi.org/10.3969/j.issn.1673-5374.2012.10.004
Zhao J, Chen N, Shen N, Zhao H, Wang D, Shi J, Wang Y, Cui X, Yan Z, Xue H. Transplantation of human umbilical cord blood mesenchymal stem cells to treat a rat model of traumatic brain injury. Neural Regen Res. 2012 Apr 05;7(10):741-8. doi: 10.3969/j.issn.1673-5374.2012.10.004. PMID: 25737696; PMCID: PMC4345655.
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Deoxycytidine reverses the suppression of nucleolar organizer regions' activity caused by BrdU.

TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik

Yongshan Y, Jin Q, Xiahui X.
PMID: 24258947
Theor Appl Genet. 1984 May;68(1):81-5. doi: 10.1007/BF00252317.

In this article we report that 5'-bromodeoxyuridine (BrdU) significantly suppresses the nucleolar organizer regions (NORs) activity of Chinese hamster cells (both dipliod cells and cell line Wg3-h) (P

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Yongshan Y, Jin Q, Xiahui X. Deoxycytidine reverses the suppression of nucleolar organizer regions' activity caused by BrdU. Theor Appl Genet. 1984;68(1):81-5doi: 10.1007/BF00252317.
Yongshan, Y., Jin, Q., & Xiahui, X. (1984). Deoxycytidine reverses the suppression of nucleolar organizer regions' activity caused by BrdU. TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik, 68(1), 81-5. https://doi.org/10.1007/BF00252317
Yongshan, Y, et al. "Deoxycytidine reverses the suppression of nucleolar organizer regions' activity caused by BrdU." TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik vol. 68,1 (1984): 81-5. doi: https://doi.org/10.1007/BF00252317
Yongshan Y, Jin Q, Xiahui X. Deoxycytidine reverses the suppression of nucleolar organizer regions' activity caused by BrdU. Theor Appl Genet. 1984 May;68(1):81-5. doi: 10.1007/BF00252317. PMID: 24258947.
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Differential S-phase progression after irradiation of p53 functional versus non-functional tumour cells.

Radiology and oncology

Zölzer F, Mußfeldt T, Streffer C.
PMID: 25435848
Radiol Oncol. 2014 Nov 05;48(4):354-60. doi: 10.2478/raon-2014-0032. eCollection 2014 Dec.

BACKGROUND: Many pathways seem to be involved in the regulation of the intra-S-phase checkpoint after exposure to ionizing radiation, but the role of p53 has proven to be rather elusive. Here we have a closer look at the progression...

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Zölzer F, Mußfeldt T, Streffer C. Differential S-phase progression after irradiation of p53 functional versus non-functional tumour cells. Radiol Oncol. 2014;48(4):354-60doi: 10.2478/raon-2014-0032.
Zölzer, F., Mußfeldt, T., & Streffer, C. (2014). Differential S-phase progression after irradiation of p53 functional versus non-functional tumour cells. Radiology and oncology, 48(4), 354-60. https://doi.org/10.2478/raon-2014-0032
Zölzer, Friedo, et al. "Differential S-phase progression after irradiation of p53 functional versus non-functional tumour cells." Radiology and oncology vol. 48,4 (2014): 354-60. doi: https://doi.org/10.2478/raon-2014-0032
Zölzer F, Mußfeldt T, Streffer C. Differential S-phase progression after irradiation of p53 functional versus non-functional tumour cells. Radiol Oncol. 2014 Nov 05;48(4):354-60. doi: 10.2478/raon-2014-0032. eCollection 2014 Dec. PMID: 25435848; PMCID: PMC4230555.
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DNA replication in soybean protoplasts and suspension-cultured cells: Comparison of exponential and fluorodeoxyuridine synchronized cultures.

Planta

Cress DE, Jackson PJ, Kadouri A, Chu YE, Lark KG.
PMID: 24408461
Planta. 1978 Jan;143(3):241-53. doi: 10.1007/BF00391994.

Cell-suspension cultures of soybean (Glycine max (L.) Merr., line SB-1) have been used to study DNA replication. Cells or protoplasts incorporate either radioactive thymidine or 5-bromodeoxyuridine (BUdR) into DNA. The DNA has been extracted as large molecules which can...

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Cress DE, Jackson PJ, Kadouri A, et al. DNA replication in soybean protoplasts and suspension-cultured cells: Comparison of exponential and fluorodeoxyuridine synchronized cultures. Planta. 1978;143(3):241-53doi: 10.1007/BF00391994.
Cress, D. E., Jackson, P. J., Kadouri, A., Chu, Y. E., & Lark, K. G. (1978). DNA replication in soybean protoplasts and suspension-cultured cells: Comparison of exponential and fluorodeoxyuridine synchronized cultures. Planta, 143(3), 241-53. https://doi.org/10.1007/BF00391994
Cress, D E, et al. "DNA replication in soybean protoplasts and suspension-cultured cells: Comparison of exponential and fluorodeoxyuridine synchronized cultures." Planta vol. 143,3 (1978): 241-53. doi: https://doi.org/10.1007/BF00391994
Cress DE, Jackson PJ, Kadouri A, Chu YE, Lark KG. DNA replication in soybean protoplasts and suspension-cultured cells: Comparison of exponential and fluorodeoxyuridine synchronized cultures. Planta. 1978 Jan;143(3):241-53. doi: 10.1007/BF00391994. PMID: 24408461.
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Genome-wide localization of Rrm3 and Pif1 DNA helicases at stalled active and inactive DNA replication forks of Saccharomyces cerevisiae.

Genomics data

Rossi SE, Carotenuto W, Giannattasio M.
PMID: 26981397
Genom Data. 2015 Dec 01;7:162-5. doi: 10.1016/j.gdata.2015.11.024. eCollection 2016 Mar.

The genome of the budding yeast Saccharomyces cerevisiae is sequenced and the location and dynamic of activation of DNA replication origins are known. G1 synchronized yeast cells can be released into S-phase in the presence of hydroxyurea (HU) (1),...

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Rossi SE, Carotenuto W, Giannattasio M. Genome-wide localization of Rrm3 and Pif1 DNA helicases at stalled active and inactive DNA replication forks of Saccharomyces cerevisiae. Genom Data. 2015;7:162-5doi: 10.1016/j.gdata.2015.11.024.
Rossi, S. E., Carotenuto, W., & Giannattasio, M. (2016). Genome-wide localization of Rrm3 and Pif1 DNA helicases at stalled active and inactive DNA replication forks of Saccharomyces cerevisiae. Genomics data, 7162-5. https://doi.org/10.1016/j.gdata.2015.11.024
Rossi, Silvia Emma, et al. "Genome-wide localization of Rrm3 and Pif1 DNA helicases at stalled active and inactive DNA replication forks of Saccharomyces cerevisiae." Genomics data vol. 7 (2016): 162-5. doi: https://doi.org/10.1016/j.gdata.2015.11.024
Rossi SE, Carotenuto W, Giannattasio M. Genome-wide localization of Rrm3 and Pif1 DNA helicases at stalled active and inactive DNA replication forks of Saccharomyces cerevisiae. Genom Data. 2015 Dec 01;7:162-5. doi: 10.1016/j.gdata.2015.11.024. eCollection 2016 Mar. PMID: 26981397; PMCID: PMC4778647.
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Co-Ultramicronized Palmitoylethanolamide/Luteolin Promotes Neuronal Regeneration after Spinal Cord Injury.

Frontiers in pharmacology

Crupi R, Impellizzeri D, Bruschetta G, Cordaro M, Paterniti I, Siracusa R, Cuzzocrea S, Esposito E.
PMID: 27014061
Front Pharmacol. 2016 Mar 08;7:47. doi: 10.3389/fphar.2016.00047. eCollection 2016.

Spinal cord injury (SCI) stimulates activation of astrocytes and infiltration of immune cells at the lesion site; however, the mechanism that promotes the birth of new neurons is still under debate. Neuronal regeneration is restricted after spinal cord injury,...

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Crupi R, Impellizzeri D, Bruschetta G, et al. Co-Ultramicronized Palmitoylethanolamide/Luteolin Promotes Neuronal Regeneration after Spinal Cord Injury. Front Pharmacol. 2016;7:47doi: 10.3389/fphar.2016.00047.
Crupi, R., Impellizzeri, D., Bruschetta, G., Cordaro, M., Paterniti, I., Siracusa, R., Cuzzocrea, S., & Esposito, E. (2016). Co-Ultramicronized Palmitoylethanolamide/Luteolin Promotes Neuronal Regeneration after Spinal Cord Injury. Frontiers in pharmacology, 747. https://doi.org/10.3389/fphar.2016.00047
Crupi, Rosalia, et al. "Co-Ultramicronized Palmitoylethanolamide/Luteolin Promotes Neuronal Regeneration after Spinal Cord Injury." Frontiers in pharmacology vol. 7 (2016): 47. doi: https://doi.org/10.3389/fphar.2016.00047
Crupi R, Impellizzeri D, Bruschetta G, Cordaro M, Paterniti I, Siracusa R, Cuzzocrea S, Esposito E. Co-Ultramicronized Palmitoylethanolamide/Luteolin Promotes Neuronal Regeneration after Spinal Cord Injury. Front Pharmacol. 2016 Mar 08;7:47. doi: 10.3389/fphar.2016.00047. eCollection 2016. PMID: 27014061; PMCID: PMC4782663.
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miR-33a is downregulated in melanoma cells and modulates cell proliferation by targeting PCTAIRE1.

Oncology letters

Tian F, Wei H, Tian H, Qiu Y, Xu J.
PMID: 27073545
Oncol Lett. 2016 Apr;11(4):2741-2746. doi: 10.3892/ol.2016.4321. Epub 2016 Mar 09.

MicroRNA-33a (miR-33a) was previously identified as a lipid regulator that controls the cellular balance between cholesterol and fatty acid metabolism. However, its role in tumor progression is largely unknown. The present study identified that miR-33a acts as a tumor...

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Tian F, Wei H, Tian H, et al. miR-33a is downregulated in melanoma cells and modulates cell proliferation by targeting PCTAIRE1. Oncol Lett. 2016;11(4):2741-2746doi: 10.3892/ol.2016.4321.
Tian, F., Wei, H., Tian, H., Qiu, Y., & Xu, J. (2016). miR-33a is downregulated in melanoma cells and modulates cell proliferation by targeting PCTAIRE1. Oncology letters, 11(4), 2741-2746. https://doi.org/10.3892/ol.2016.4321
Tian, Fangzhen, et al. "miR-33a is downregulated in melanoma cells and modulates cell proliferation by targeting PCTAIRE1." Oncology letters vol. 11,4 (2016): 2741-2746. doi: https://doi.org/10.3892/ol.2016.4321
Tian F, Wei H, Tian H, Qiu Y, Xu J. miR-33a is downregulated in melanoma cells and modulates cell proliferation by targeting PCTAIRE1. Oncol Lett. 2016 Apr;11(4):2741-2746. doi: 10.3892/ol.2016.4321. Epub 2016 Mar 09. PMID: 27073545; PMCID: PMC4812543.
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Tissue specific loss of proliferative capacity of parthenogenetic cells in fetal mouse chimeras.

Roux's archives of developmental biology : the official organ of the EDBO

Bender R, Fundele R, Surani MA, Li LL, Kothary R, Fürst DO, Christ B.
PMID: 28305863
Rouxs Arch Dev Biol. 1995 Aug;204(7):436-443. doi: 10.1007/BF00360851.

Parthenogenetic cells are lost from fetal chimeras. This may be due to decreased proliferative potential. To address this question, we have made use of combined cell lineage and cell proliferation analysis. Thus, the incorporation of bromodeoxyuridine in S-phase was...

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Bender R, Fundele R, Surani MA, et al. Tissue specific loss of proliferative capacity of parthenogenetic cells in fetal mouse chimeras. Rouxs Arch Dev Biol. 1995;204(7):436-443doi: 10.1007/BF00360851.
Bender, R., Fundele, R., Surani, M. A., Li, L. L., Kothary, R., Fürst, D. O., & Christ, B. (1995). Tissue specific loss of proliferative capacity of parthenogenetic cells in fetal mouse chimeras. Roux's archives of developmental biology : the official organ of the EDBO, 204(7), 436-443. https://doi.org/10.1007/BF00360851
Bender, R, et al. "Tissue specific loss of proliferative capacity of parthenogenetic cells in fetal mouse chimeras." Roux's archives of developmental biology : the official organ of the EDBO vol. 204,7 (1995): 436-443. doi: https://doi.org/10.1007/BF00360851
Bender R, Fundele R, Surani MA, Li LL, Kothary R, Fürst DO, Christ B. Tissue specific loss of proliferative capacity of parthenogenetic cells in fetal mouse chimeras. Rouxs Arch Dev Biol. 1995 Aug;204(7):436-443. doi: 10.1007/BF00360851. PMID: 28305863.
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The effects of bromodeoxyuridine and bromouracil on regeneration inHydra.

Wilhelm Roux' Archiv fur Entwicklungsmechanik der Organismen

Goyns MH, Stanisstreet M.
PMID: 28304714
Wilhelm Roux Arch Entwickl Mech Org. 1974 Jun;175(2):87-90. doi: 10.1007/BF00574294.

The effects on tentacle regeneration inHydra of two DNA-antimetabolites, bromouracil and bromodeoxyuridine, have been studied. Bromouracil inhibits tentacle regeneration inH. vulgaris andH. viridis; bromodeoxynridine inhibits tentacle regeneration inH. vulgaris but notH. viridis over the range of concentrations studied. Thus...

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Goyns MH, Stanisstreet M. The effects of bromodeoxyuridine and bromouracil on regeneration inHydra. Wilhelm Roux Arch Entwickl Mech Org. 1974;175(2):87-90doi: 10.1007/BF00574294.
Goyns, M. H., & Stanisstreet, M. (1974). The effects of bromodeoxyuridine and bromouracil on regeneration inHydra. Wilhelm Roux' Archiv fur Entwicklungsmechanik der Organismen, 175(2), 87-90. https://doi.org/10.1007/BF00574294
Goyns, M H, and Stanisstreet, M. "The effects of bromodeoxyuridine and bromouracil on regeneration inHydra." Wilhelm Roux' Archiv fur Entwicklungsmechanik der Organismen vol. 175,2 (1974): 87-90. doi: https://doi.org/10.1007/BF00574294
Goyns MH, Stanisstreet M. The effects of bromodeoxyuridine and bromouracil on regeneration inHydra. Wilhelm Roux Arch Entwickl Mech Org. 1974 Jun;175(2):87-90. doi: 10.1007/BF00574294. PMID: 28304714.
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GIT1 is a novel prognostic biomarker and facilitates tumor progression via activating ERK/MMP9 signaling in hepatocellular carcinoma.

OncoTargets and therapy

Chen J, Yang P, Yang J, Wen Z, Zhang B, Zheng X.
PMID: 26719701
Onco Targets Ther. 2015 Dec 15;8:3731-42. doi: 10.2147/OTT.S96715. eCollection 2015.

AIM: Multiple studies have revealed that G-protein-coupled receptor kinase-interacting protein 1 (GIT1) is overexpressed in many cancers and facilitates tumor progression. However, the role of GIT1 in hepatocellular carcinoma (HCC) remains unclear.METHODS: GIT1 expression was detected in cell lines...

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Chen J, Yang P, Yang J, et al. GIT1 is a novel prognostic biomarker and facilitates tumor progression via activating ERK/MMP9 signaling in hepatocellular carcinoma. Onco Targets Ther. 2015;8:3731-42doi: 10.2147/OTT.S96715.
Chen, J., Yang, P., Yang, J., Wen, Z., Zhang, B., & Zheng, X. (2015). GIT1 is a novel prognostic biomarker and facilitates tumor progression via activating ERK/MMP9 signaling in hepatocellular carcinoma. OncoTargets and therapy, 83731-42. https://doi.org/10.2147/OTT.S96715
Chen, Junyi, et al. "GIT1 is a novel prognostic biomarker and facilitates tumor progression via activating ERK/MMP9 signaling in hepatocellular carcinoma." OncoTargets and therapy vol. 8 (2015): 3731-42. doi: https://doi.org/10.2147/OTT.S96715
Chen J, Yang P, Yang J, Wen Z, Zhang B, Zheng X. GIT1 is a novel prognostic biomarker and facilitates tumor progression via activating ERK/MMP9 signaling in hepatocellular carcinoma. Onco Targets Ther. 2015 Dec 15;8:3731-42. doi: 10.2147/OTT.S96715. eCollection 2015. PMID: 26719701; PMCID: PMC4689273.
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The ret-Activating Ligand GDNF Is Differentiative and Not Mitogenic for Normal and Neoplastic Human Chromaffin Cells In Vitro.

Endocrine pathology

Powers JF, Tsokas P, Tischler AS.
PMID: 12114780
Endocr Pathol. 1998;9(1):325-331. doi: 10.1007/BF02739692.

Activating mutations of the receptor tyrosine kinase, ret, are associated with multiple endocrine neoplasia type 2A (MEN 2A). However, the mechanisms leading to tumor development are unclear. Glial-derived neurotrophic factor (GDNF) activates wild-type ret via interaction with a second...

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Powers JF, Tsokas P, Tischler AS. The ret-Activating Ligand GDNF Is Differentiative and Not Mitogenic for Normal and Neoplastic Human Chromaffin Cells In Vitro. Endocr Pathol. 1998;9(1):325-331doi: 10.1007/BF02739692.
Powers, J. F., Tsokas, P., & Tischler, A. S. (1998). The ret-Activating Ligand GDNF Is Differentiative and Not Mitogenic for Normal and Neoplastic Human Chromaffin Cells In Vitro. Endocrine pathology, 9(1), 325-331. https://doi.org/10.1007/BF02739692
Powers, James F., et al. "The ret-Activating Ligand GDNF Is Differentiative and Not Mitogenic for Normal and Neoplastic Human Chromaffin Cells In Vitro." Endocrine pathology vol. 9,1 (1998): 325-331. doi: https://doi.org/10.1007/BF02739692
Powers JF, Tsokas P, Tischler AS. The ret-Activating Ligand GDNF Is Differentiative and Not Mitogenic for Normal and Neoplastic Human Chromaffin Cells In Vitro. Endocr Pathol. 1998;9(1):325-331. doi: 10.1007/BF02739692. PMID: 12114780.
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Is the capacity for optic nerve regeneration related to continued retinal ganglion cell production in the frog?.

The European journal of neuroscience

Taylor JS, Jack JL, Easter SS.
PMID: 12106120
Eur J Neurosci. 1989;1(6):626-38. doi: 10.1111/j.1460-9568.1989.tb00368.x.

In the central nervous system of fish and frogs, some, but not all, axons can regenerate. Retinal ganglion cells are among those that can. The retinae of fish and frogs produce new retinal neurons, including ganglion cells, for months...

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Taylor JS, Jack JL, Easter SS. Is the capacity for optic nerve regeneration related to continued retinal ganglion cell production in the frog?. Eur J Neurosci. 1989;1(6):626-38doi: 10.1111/j.1460-9568.1989.tb00368.x.
Taylor, J. S., Jack, J. L., & Easter, S. S. (1989). Is the capacity for optic nerve regeneration related to continued retinal ganglion cell production in the frog?. The European journal of neuroscience, 1(6), 626-38. https://doi.org/10.1111/j.1460-9568.1989.tb00368.x
Taylor, J S, et al. "Is the capacity for optic nerve regeneration related to continued retinal ganglion cell production in the frog?." The European journal of neuroscience vol. 1,6 (1989): 626-38. doi: https://doi.org/10.1111/j.1460-9568.1989.tb00368.x
Taylor JS, Jack JL, Easter SS. Is the capacity for optic nerve regeneration related to continued retinal ganglion cell production in the frog?. Eur J Neurosci. 1989;1(6):626-38. doi: 10.1111/j.1460-9568.1989.tb00368.x. PMID: 12106120.
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