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1

Velegrakis, Alexandros, Maria Sfakiotaki, and Stavros Sifakis. "Human placental growth hormone in normal and abnormal fetal growth." Biomedical Reports 7, no. 2 (2017): 115–22. http://dx.doi.org/10.3892/br.2017.930.

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2

Khong, TY, and IH Sawyer. "The human placental bed in health and disease." Reproduction, Fertility and Development 3, no. 4 (1991): 373. http://dx.doi.org/10.1071/rd9910373.

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The morphology of the human placental bed is reviewed. The pathological features seen in spontaneous abortion, pregnancy-induced hypertension, intrauterine growth retardation, placenta accreta and postpartum haemorrhage suggest that abnormal placentation may be a common feature. A defect in the normal materno-trophoblastic interaction is implicated in the pathogenesis of abnormal placentation.
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3

Kim, Soung Min, Young Joon Lee, Sang Shin Lee, et al. "Abnormal Maxillary Trapezoid Pattern in Human Fetal Cleft Lip and Palate." Cleft Palate-Craniofacial Journal 45, no. 2 (2008): 131–40. http://dx.doi.org/10.1597/06-077.1.

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Objective: To elucidate abnormal growth patterns of human fetal maxillae with cleft lip and palate (CLP). Subject: A total of 71 fetal maxillae with CLP were obtained from aborted human fetuses. Method: Dimensions of the maxillary trapezoid (MT), formed by the maxillary primary growth centers (MxPGC), were taken from radiographic images. The CLP dimensions were compared with maxillary trapezoid dimensions of normal fetuses from a previous study (Lee et al., 1992). Main Outcome Measures: Cleft lip subjects without a cleft palate, unilateral cleft lip-alveolar cleft or cleft palate (UCL+A/UCLP),
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4

Schulman, S., E. F. Roth, B. Cheng, et al. "Growth of Plasmodium falciparum in human erythrocytes containing abnormal membrane proteins." Proceedings of the National Academy of Sciences 87, no. 18 (1990): 7339–43. http://dx.doi.org/10.1073/pnas.87.18.7339.

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5

Bonkhoff, H., and Klaus Remberger. "Morphogenetic concepts of normal and abnormal growth in the human prostate." Virchows Archiv 433, no. 3 (1998): 195–202. http://dx.doi.org/10.1007/s004280050236.

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6

Lewis, Aaron M., Melissa Yu, Stephen J. DeArmond, William P. Dillon, Bruce L. Miller, and Michael D. Geschwind. "Human Growth Hormone–Related Iatrogenic Creutzfeldt-Jakob Disease With Abnormal Imaging." Archives of Neurology 63, no. 2 (2006): 288. http://dx.doi.org/10.1001/archneur.63.2.288.

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7

Murthi, Padma, Gayathri Rajaraman, Shaun Patrick Brennecke, and Bill Kalionis. "The Role of Placental Homeobox Genes in Human Fetal Growth Restriction." Journal of Pregnancy 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/548171.

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Fetal growth restriction (FGR) is an adverse pregnancy outcome associated with significant perinatal and paediatric morbidity and mortality, and an increased risk of chronic disease later in adult life. One of the key causes of adverse pregnancy outcome is fetal growth restriction (FGR). While a number of maternal, fetal, and environmental factors are known causes of FGR, the majority of FGR cases remain idiopathic. These idiopathic FGR pregnancies are frequently associated with placental insufficiency, possibly as a result of placental maldevelopment. Understanding the molecular mechanisms of
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8

Tsitsiloni, O. E., J. Stiakakis, A. Koutselinis, et al. "Expression of alpha-thymosins in human tissues in normal and abnormal growth." Proceedings of the National Academy of Sciences 90, no. 20 (1993): 9504–7. http://dx.doi.org/10.1073/pnas.90.20.9504.

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9

Einstein, Francine, Reid F. Thompson, Hye Heo, et al. "600: Abnormal intrauterine growth induces global epigenetic changes in human stem cells." American Journal of Obstetrics and Gynecology 199, no. 6 (2008): S173. http://dx.doi.org/10.1016/j.ajog.2008.09.630.

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10

Vijayakumar, Soundarapandian, Suparna Dang, M. Peter Marinkovich, et al. "Aberrant expression of laminin-332 promotes cell proliferation and cyst growth in ARPKD." American Journal of Physiology-Renal Physiology 306, no. 6 (2014): F640—F654. http://dx.doi.org/10.1152/ajprenal.00104.2013.

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Basement membrane abnormalities have often been observed in kidney cysts of polycystic kidney disease (PKD) patients and animal models. There is an abnormal deposition of extracellular matrix molecules, including laminin-α3,β3,γ2 (laminin-332), in human autosomal dominant PKD (ADPKD). Knockdown of PKD1 paralogs in zebrafish leads to dysregulated synthesis of the extracellular matrix, suggesting that altered basement membrane assembly may be a primary defect in ADPKD. In this study, we demonstrate that laminin-332 is aberrantly expressed in cysts and precystic tubules of human autosomal recessi
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11

Borg, A. J., H. E. J. Yong, M. Lappas, et al. "Decreased STAT3 in human idiopathic fetal growth restriction contributes to trophoblast dysfunction." REPRODUCTION 149, no. 5 (2015): 523–32. http://dx.doi.org/10.1530/rep-14-0622.

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Abnormal trophoblast function is associated with fetal growth restriction (FGR). The JAK–STAT pathway is one of the principal signalling mechanisms by which cytokines and growth factors modulate cell proliferation, differentiation, cell migration and apoptosis. The expression of placental JAK–STAT genes in human idiopathic FGR is unknown. In this study, we propose the hypothesis that JAK–STAT pathway genes are differentially expressed in idiopathic FGR-affected pregnancies and contribute to abnormal feto-placental growth by modulating the expression of the amino acid transporter SNAT2, differe
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12

Filonenko, T.G., A.A. Davydova, Yu.A. Ermola, et al. "Placental growth factor and apoptosis as early prognostic factor of placental insufficiency." Journal of Education, Health and Sport 5, no. 1 (2015): 69–74. https://doi.org/10.5281/zenodo.13990.

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<strong>Filonenko T.G., Davydova A.A., Ermola Yu.A., Nechiporenko G.V., Shalanin V.V., Syurina N.A., Menshikova O.P., Kuzmin M.N., Fedotov&nbsp;V.V., Beketov A.A. Placental growth factor and apoptosis as early prognostic factor of placental insufficiency. </strong><strong>Journal of Education, Health and Sport. </strong><strong>2015;5(1):69-74. </strong><strong>ISSN 2391-8306</strong><strong>. </strong><strong>DOI: 10.5281/zenodo.13990</strong> <strong>http://ojs.ukw.edu.pl/index.php/johs/article/view/2015%3B5%281%29%3A69-74</strong> <strong>https://pbn.nauka.gov.pl/works/527851</strong> <stro
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13

Wilson, Patricia D., David Hreniuk, and Patricia A. Gabow. "Abnormal extracellular matrix and excessive growth of human adult polycystic kidney disease epithelia." Journal of Cellular Physiology 150, no. 2 (1992): 360–69. http://dx.doi.org/10.1002/jcp.1041500220.

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14

Coffin, J. D., R. Z. Florkiewicz, J. Neumann, et al. "Abnormal bone growth and selective translational regulation in basic fibroblast growth factor (FGF-2) transgenic mice." Molecular Biology of the Cell 6, no. 12 (1995): 1861–73. http://dx.doi.org/10.1091/mbc.6.12.1861.

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Basic fibroblast growth factor (FGF-2) is a pleiotropic growth factor detected in many different cells and tissues. Normally synthesized at low levels, FGF-2 is elevated in various pathologies, most notably in cancer and injury repair. To investigate the effects of elevated FGF-2, the human full-length cDNA was expressed in transgenic mice under control of a phosphoglycerate kinase promoter. Overexpression of FGF-2 caused a variety of skeletal malformations including shortening and flattening of long bones and moderate macrocephaly. Comparison by Western blot of FGF-2 transgenic mice to nontra
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15

Bergant, Kaja, Katja Valjavec, Matej Janežič, Marija Sollner Dolenc та Andrej Perdih. "3,5-Substituted Oxadiazoles as Catalytic Inhibitors of the Human Topoisomerase IIα Molecular Motor". Proceedings 22, № 1 (2019): 78. http://dx.doi.org/10.3390/proceedings2019022078.

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16

Rosario, Fredrick J., Kris Genelyn Dimasuay, Yoshikatsu Kanai, Theresa L. Powell, and Thomas Jansson. "Regulation of amino acid transporter trafficking by mTORC1 in primary human trophoblast cells is mediated by the ubiquitin ligase Nedd4-2." Clinical Science 130, no. 7 (2016): 499–512. http://dx.doi.org/10.1042/cs20150554.

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We demonstrate that mTOR complex 1 modulates amino acid transport in primary human trophoblast cells by regulating Nedd4-2 mediated ubiquitination and plasma membrane trafficking of specific transporter isoforms, which may constitute a molecular mechanisms underlying abnormal human fetal growth.
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17

Chitnis, Kshitij, Jasdev Singh Tuteja, and Priti Patidar. "Molecular Docking of Combretastatin Derivatives to Combat Human Cancer Cells." Journal of the Scientific Society 51, no. 1 (2023): 27–31. http://dx.doi.org/10.4103/jss.jss_82_23.

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Abstract Cancer is defined as the group of diseases which involve abnormal cell growth or controlled growth of abnormal cells that are present in any part of the body. The causative agents of cancer are chemical, environmental, viral, and mutagenic, which lead to the mutation of genes into oncogenes, which provoke or demean regulatory biochemicals, resulting in accelerated cellular growth. Combretastatin was selected as the candidate because it is a water-soluble prodrug which is quickly converted into combretastatin A4, a cancer-fighting substance. It has longer circulation, better drug targe
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18

&NA;. "Somatropin [human growth hormone] therapy reduces the abnormal central fat accumulation in patients with somatotropin (growth hormone) deficiency,." Inpharma Weekly &NA;, no. 1566 (2006): 17. http://dx.doi.org/10.2165/00128413-200615660-00042.

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19

Giudice, Linda C. "The insulin-like growth factor system in normal and abnormal human ovarian follicle development." American Journal of Medicine 98, no. 1 (1995): S48—S54. http://dx.doi.org/10.1016/s0002-9343(99)80059-x.

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20

Rücker-Martin, Catherine, Françoise Pecker, David Godreau, and Stéphane N. Hatem. "Dystrophic myocytes in fibrillating and dilated human atria: An abnormal adaptative and growth process." Journal of Molecular and Cellular Cardiology 33, no. 6 (2001): A103. http://dx.doi.org/10.1016/s0022-2828(01)90411-0.

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21

King, Roger A., Sotiria Bexis, Edward J. McMurchie, Sharon L. Burnard, Glen S. Patten, and Richard J. Head. "The Relationship Between Salivary Growth Factors, Electrolytes and Abnormal Sodium Transport in Human Hypertension." Blood Pressure 3, no. 1-2 (1994): 76–81. http://dx.doi.org/10.3109/08037059409101525.

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22

Lesch, Klaus-Peter, Gerd Laux, Heinrich M. Schulte, Hans Pfüller, and Helmut Beckmann. "Abnormal responsiveness of growth hormone to human corticotropin-releasing hormone in major depressive disorder." Journal of Affective Disorders 14, no. 3 (1988): 245–50. http://dx.doi.org/10.1016/0165-0327(88)90041-9.

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23

Hammond, WP, GS Chatta, RG Andrews, and DC Dale. "Abnormal responsiveness of granulocyte-committed progenitor cells in cyclic neutropenia." Blood 79, no. 10 (1992): 2536–39. http://dx.doi.org/10.1182/blood.v79.10.2536.2536.

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Abstract The mechanism(s) driving cyclic hematopoiesis in human cyclic neutropenia remains unknown. Clinical trials suggest that an abnormal responsiveness of bone marrow progenitor cells to hematopoietic growth factors might cause oscillatory blood counts. Studies were performed to determine whether an abnormal responsiveness to multiple growth factors exists in this disorder and whether the defect could be shown in highly enriched populations of marrow progenitor cells. Bone marrow mononuclear cells from patients with congenital cyclic neutropenia required higher concentrations of added gran
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24

Hammond, WP, GS Chatta, RG Andrews, and DC Dale. "Abnormal responsiveness of granulocyte-committed progenitor cells in cyclic neutropenia." Blood 79, no. 10 (1992): 2536–39. http://dx.doi.org/10.1182/blood.v79.10.2536.bloodjournal79102536.

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The mechanism(s) driving cyclic hematopoiesis in human cyclic neutropenia remains unknown. Clinical trials suggest that an abnormal responsiveness of bone marrow progenitor cells to hematopoietic growth factors might cause oscillatory blood counts. Studies were performed to determine whether an abnormal responsiveness to multiple growth factors exists in this disorder and whether the defect could be shown in highly enriched populations of marrow progenitor cells. Bone marrow mononuclear cells from patients with congenital cyclic neutropenia required higher concentrations of added granulocyte-c
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25

Li, Yingchun, Ramón A. Lorca, and Emily J. Su. "Molecular and cellular underpinnings of normal and abnormal human placental blood flows." Journal of Molecular Endocrinology 60, no. 1 (2018): R9—R22. http://dx.doi.org/10.1530/jme-17-0139.

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Abnormal placental function is well-established as a major cause for poor pregnancy outcome. Placental blood flow within the maternal uteroplacental compartment, the fetoplacental circulation or both is a vital factor in mediating placental function. Impairment in flow in either or both vasculatures is a significant risk factor for adverse pregnancy outcome, potentially impacting maternal well-being, affecting immediate neonatal health and even influencing the long-term health of the infant. Much remains unknown regarding the mechanistic underpinnings of proper placental blood flow. This revie
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26

Yousef, George, and Eleftherios Diamandis. "Tissue kallikreins: new players in normal and abnormal cell growth?" Thrombosis and Haemostasis 90, no. 07 (2003): 7–16. http://dx.doi.org/10.1055/s-0037-1613593.

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SummarySerine proteases are proteolytic enzymes with an active serine residue in their catalytic site. Kallikreins are a subgroup of the serine protease family and are known to have diverse physiological functions. The human tissue kallikrein gene family has now been fully characterized and includes 15 members, clustered in a 300 kb region on chromosome 19q13.4. In this review, we discuss the common structural features of kallik-reins at the DNA, mRNA and protein levels. Kallikreins are secreted as inactive zymogens and are activated by cleavage of an N-terminal peptide. Some kallikreins can u
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27

Kwan, Kin Ming, Michael K. M. Pang, Sheila Zhou, et al. "Abnormal Compartmentalization of Cartilage Matrix Components in Mice Lacking Collagen X: Implications for Function." Journal of Cell Biology 136, no. 2 (1997): 459–71. http://dx.doi.org/10.1083/jcb.136.2.459.

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There are conflicting views on whether collagen X is a purely structural molecule, or regulates bone mineralization during endochondral ossification. Mutations in the human collagen α1(X) gene (COL10A1) in Schmid metaphyseal chondrodysplasia (SMCD) suggest a supportive role. But mouse collagen α1(X) gene (Col10a1) null mutants were previously reported to show no obvious phenotypic change. We have generated collagen X deficient mice, which shows that deficiency does have phenotypic consequences which partly resemble SMCD, such as abnormal trabecular bone architecture. In particular, the mutant
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28

Kelnar, CJH, LE Bath, PC Midgley, and AA Toogood. "Growth hormone therapy in children and adults." Journal of the Royal College of Physicians of Edinburgh 35, no. 2 (2005): 132–38. https://doi.org/10.1177/1478271520053502010.

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Growth hormone is responsible for growth in childhood after the first one to two years, and its deficiency results in short stature. Use of GH has been restricted over the years, initially due to scarcity of supply (human pituitary GH), and thereafter due to expense of the drug (synthetic GH). In the UK, GH is licensed for the treatment of children with GHD, TS, PWS, CRI, and those born SGA who fail to catch up in growth. In some countries GH is used for other indications, and it is also used off-license in the UK for treatment of other conditions (primarily ‘short stature syndromes’). Growth
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29

Bale, James F., Charles F. Contant, Bhuwan Garg, Ann Tilton, David M. Kaufman, and Warren Wasiewski. "Neurologic History and Examination Results and Their Relationship to Human Immunodeficiency Virus Type 1 Serostatus in Hemophilic Subjects: Results From the Hemophilia Growth and Development Study." Pediatrics 91, no. 4 (1993): 736–41. http://dx.doi.org/10.1542/peds.91.4.736.

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In a prospective study of the growth and neuropsychologic function of hemophilic subjects, 333 boys, median age of 12.3 years, had baseline neurologic examinations. The study population included 207 individuals (62%) who were seropositive for human immunodeficiency virus type 1 (HIV-1). Overall results indicated that 11% had abnormalities of cranial nerve function, 17% had abnormal deep tendon reflexes, 23% had abnormal strength, 25% had abnormal coordination, and 31% had abnormal tone, bulk, or range of motion. By contrast, 2% or fewer displayed abnormal movements or had abnormal pain or vibr
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30

Sugita, T., T. Totsuka, M. Saito, et al. "Functional murine interleukin 6 receptor with the intracisternal A particle gene product at its cytoplasmic domain. Its possible role in plasmacytomagenesis." Journal of Experimental Medicine 171, no. 6 (1990): 2001–9. http://dx.doi.org/10.1084/jem.171.6.2001.

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Two species of the cDNAs encoding murine IL-6-R (one is abnormal and the other authentic) have been cloned from a plasmacytoma cell line, P3U1, and BALB/c mouse spleen cDNA libraries. In the cDNA encoding the abnormal IL-6-R, the region corresponding to an intracytoplasmic domain was replaced with a part of the long terminal repeat of the intracisternal A particle gene (IAP-LTR). The authentic IL-6-R consists of 460 amino acids with the domain of the Ig superfamily. The overall homology between murine and human IL-6-R was 69 and 54% at DNA and protein levels, respectively. The extracellular do
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31

Kobayashi, M., C. Yumiba, Y. Kawaguchi, et al. "Abnormal responses of myeloid progenitor cells to recombinant human colony-stimulating factors in congenital neutropenia." Blood 75, no. 11 (1990): 2143–49. http://dx.doi.org/10.1182/blood.v75.11.2143.2143.

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Abstract The effects of recombinant human interleukin-3 (IL-3) and recombinant human granulocyte colony-stimulating factor (G-CSF) on the growth of myeloid progenitor cells (CFU-C) in semisolid agar culture were studied in two patients with Kostmann-type congenital neutropenia. CFU-C growth in bone marrow cells from patients was significantly reduced in response to various concentrations of either IL-3 or G-CSF alone, compared with that from normal subjects. There was no inhibitory effect of bone marrow cells from patients on normal CFU-C formation supported by IL-3 or G-CSF. However, the simu
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32

Kobayashi, M., C. Yumiba, Y. Kawaguchi, et al. "Abnormal responses of myeloid progenitor cells to recombinant human colony-stimulating factors in congenital neutropenia." Blood 75, no. 11 (1990): 2143–49. http://dx.doi.org/10.1182/blood.v75.11.2143.bloodjournal75112143.

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The effects of recombinant human interleukin-3 (IL-3) and recombinant human granulocyte colony-stimulating factor (G-CSF) on the growth of myeloid progenitor cells (CFU-C) in semisolid agar culture were studied in two patients with Kostmann-type congenital neutropenia. CFU-C growth in bone marrow cells from patients was significantly reduced in response to various concentrations of either IL-3 or G-CSF alone, compared with that from normal subjects. There was no inhibitory effect of bone marrow cells from patients on normal CFU-C formation supported by IL-3 or G-CSF. However, the simultaneous
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33

Mayhew, T. M. "Patterns of villous and intervillous space growth in human placentas from normal and abnormal pregnancies." European Journal of Obstetrics & Gynecology and Reproductive Biology 68 (September 1996): 75–82. http://dx.doi.org/10.1016/0301-2115(96)02486-4.

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34

Du, J., and P. D. Wilson. "Abnormal polarization of EGF receptors and autocrine stimulation of cyst epithelial growth in human ADPKD." American Journal of Physiology-Cell Physiology 269, no. 2 (1995): C487—C495. http://dx.doi.org/10.1152/ajpcell.1995.269.2.c487.

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The underlying mechanism of the hyperproliferative response of human autosomal dominant polycystic kidney disease (ADPKD) epithelia was studied. Epidermal growth factor (EGF) protein is highly expressed in ADPKD cyst epithelia in vivo, and primary cultures are hyperesponsive to mitogenic stimulation by EGF in vitro. Doses of &gt; 1 ng/ml EGF were highly mitogenic to ADPKD epithelia. 3H-labeled thymidine proliferation assays showed that cyst fluids and ADPKD epithelial cell-conditioned media also stimulated renal epithelial cell proliferation and contained EGF immunoreactivity (6, 30, and 37 kD
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35

Puy, Libertad A., Gioconda Lo Castro, Jesùs E. Olcese, Héctor O. Lotfi, Hugo R. Brandi, and Daniel R. Ciocca. "Analysis of a 24-kilodalton (KD) protein in the human uterine cervix during abnormal growth." Cancer 64, no. 5 (1989): 1067–73. http://dx.doi.org/10.1002/1097-0142(19890901)64:5<1067::aid-cncr2820640518>3.0.co;2-h.

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36

Her, Kyu Hee. "Transforming Growth Factor-β signaling on tumorigenesis". Journal of Medicine and Life Science 4, № 1 (2006): 21–39. http://dx.doi.org/10.22730/jmls.2006.4.1.21.

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Transforming growth factor beta (TGF-β ) is a ubiquitous multifunctional polypetide and essential regulator of cellular and physiologic processes including proliferation, differentiation, adhesion, migration, apoptosis, angiogenesis and immunosurveillance. Abnormal activation or inhibition of these TGF-β signaling pathway, including mutation or deletion of members of the signaling pathway and resistance to TGF-β -mediated inhibition of proliferation are frequently observed in human cancers. Although these alterations define a tumor suppressor role for the TGF-β pathway in human cancer, TGF-β a
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37

Stolfi, Carmine. "Editorial for the Special Issue “Latest Review Papers in Molecular Oncology 2023”." International Journal of Molecular Sciences 25, no. 6 (2024): 3257. http://dx.doi.org/10.3390/ijms25063257.

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Human cancers are products of multistep processes resulting in abnormal cell growth and differentiation, along with a loss of apoptotic function, leading to the uncontrolled expansion of neoplastic cells and their spread to surrounding tissues and, ultimately, distant parts of the body [...]
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38

Miller, Tracie L. "Nutrition in paediatric human immunodeficiency virus infection." Proceedings of the Nutrition Society 59, no. 1 (2000): 155–62. http://dx.doi.org/10.1017/s0029665100000185.

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The nutritional condition of children with human immunodeficiency virus (HIV) infection continues to be a problem both in developed and developing countries. HIV-infected children grow below normal standards in both height and weight when compared with HIV-exposed non-infected children. These patterns persist over time. It is possible that acute infectious episodes and increased HIV viral burden contribute to decrements in all growth variables. Potential aetiologies for abnormal growth include inadequate dietary intake, gastrointestinal malabsorption, increased energy utilization and psycho-so
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39

Angelini, Ines, Mariangela Centrone, Giusy Rita Caponio, et al. "MOMAST® Downregulates AQP3 Expression and Function in Human Colon Cells." Antioxidants 14, no. 1 (2024): 26. https://doi.org/10.3390/antiox14010026.

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The water channel AQP3 is an aquaglyceroporin expressed in villus epithelial cells, and it plays a role in water transport across human colonic surface cells. Beyond water, AQP3 can mediate glycerol and H2O2 transport. Abnormal expression and function of AQP3 have been found in various diseases often characterized by altered cell growth and proliferation. Here, the beneficial effects of MOMAST® have been evaluated. MOMAST® is an antioxidant-patented natural phenolic complex obtained from olive wastewater (OWW) of the Coratina cultivar. Treatment of human colon HCT8 cells with MOMAST® reduced c
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40

Caufriez, A., F. Frankenne, G. Hennen, and G. Copinschi. "Regulation of maternal IGF-I by placental GH in normal and abnormal human pregnancies." American Journal of Physiology-Endocrinology and Metabolism 265, no. 4 (1993): E572—E577. http://dx.doi.org/10.1152/ajpendo.1993.265.4.e572.

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Throughout gestation, maternal insulin-like growth factor I (IGF-I) increases progressively despite suppressed pituitary growth hormone (GH) secretion. We have previously shown that in normal pregnancy, a specific placental GH variant, rather than human placental lactogen (hPL), substitutes for pituitary GH in the regulation of maternal IGF-I. We studied the maternal IGF-I secretion in a cohort of 286 normal and abnormal pregnancies (617 blood samples). Regardless of pathology and gestational age, IGF-I values correlated with corresponding placental GH but not with hPL values. Similar correlat
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41

Mossberg, Kurt A., William J. Durham, Dennis J. Zgaljardic, et al. "Functional Changes after Recombinant Human Growth Hormone Replacement in Patients with Chronic Traumatic Brain Injury and Abnormal Growth Hormone Secretion." Journal of Neurotrauma 34, no. 4 (2017): 845–52. http://dx.doi.org/10.1089/neu.2016.4552.

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42

Malila, Yuwares, Sunitta Saensa-ard, Chanikarn Kunyanee, et al. "Influences of Growth-Related Myopathies on Peptide Patterns of In Vitro Digested Cooked Chicken Breast and Stress-Related Responses in an Intestinal Caco-2 Cell Model." Foods 13, no. 24 (2024): 4042. https://doi.org/10.3390/foods13244042.

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The objective of this study was to determine the effects of growth-related myopathies, i.e., normal, wooden breast (WB), white striping (WS), and the combined lesions of WS and WB (WS + WB), on the molecular response of Caco-2 cells. A total of 24 cooked chicken breasts (n = 6 per myopathy) was subjected to an in vitro digestion using an enzymatic process mimicking human gastrointestinal digestion. Based on peptidomics, in vitro protein digestion of the abnormal samples, particularly WB meat, resulted in more peptides with lower molecular mass relative to those of normal samples. The cooked me
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43

Takauji, Yuki, Ikuru Kudo, Atsuki En та ін. "GNG11 (G-protein subunit γ 11) suppresses cell growth with induction of reactive oxygen species and abnormal nuclear morphology in human SUSM-1 cells". Biochemistry and Cell Biology 95, № 4 (2017): 517–23. http://dx.doi.org/10.1139/bcb-2016-0248.

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Enforced expression of GNG11, G-protein subunit γ 11, induces cellular senescence in normal human diploid fibroblasts. We here examined the effect of the expression of GNG11 on the growth of immortalized human cell lines, and found that it suppressed the growth of SUSM-1 cells, but not of HeLa cells. We then compared these two cell lines to understand the molecular basis for the action of GNG11. We found that expression of GNG11 induced the generation of reactive oxygen species (ROS) and abnormal nuclear morphology in SUSM-1 cells but not in HeLa cells. Increased ROS generation by GNG11 would
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Bossis, Ioannis, and Constantine A. Stratakis. "Minireview: PRKAR1A: Normal and Abnormal Functions." Endocrinology 145, no. 12 (2004): 5452–58. http://dx.doi.org/10.1210/en.2004-0900.

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Abstract The type 1α regulatory subunit (RIα) of cAMP-dependent protein kinase (PKA) (coded by the PRKAR1A gene) is the main component of type I PKA, which regulates most of the serine-threonine kinase activity catalyzed by the PKA holoenzyme in response to cAMP. Carney complex (CNC), or the complex of spotty skin pigmentation, myxomas, and endocrine overactivity, is a multiple endocrine (and not only) neoplasia syndrome that is due to PRKAR1A-inactivating mutations. The R1α protein and PRKAR1A mRNA have been found to be up-regulated in a series of cell lines and human and rodent neoplasms, su
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McClure, F., T. Dawson, and D. Wynford-Thomas. "Construction of an ecotropic retroviral vector expressing human insulin-like growth factor-I." Journal of Molecular Endocrinology 11, no. 1 (1993): 49–57. http://dx.doi.org/10.1677/jme.0.0110049.

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ABSTRACT There is increasing evidence that IGF-I plays an autocrine role in a wide range of human tumours, including, in particular, adenomas of the thyroid epithelium. To investigate this further, we set out to generate a retrovirus vector which would permit experimental manipulation of the expression of IGF-I in normal and neoplastic epithelial cells. We describe here the construction and validation of a high-titre ecotropic vector which transduces stable expression and secretion of human IGF-IA, as shown by analysis of mRNA and conditioned medium from rodent epithelial target cells. This ve
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Pocoví, Coloma, Celia Conesa, Chockry Barbana, María D Pérez, Miguel Calvo, and Lourdes Sánchez. "Comparison of the activity of human and bovine milk on two cell lines." Journal of Dairy Research 76, no. 3 (2009): 308–16. http://dx.doi.org/10.1017/s0022029909004051.

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The activity of human milk on cell growth has been evaluated on two cell lines, MDCK and Caco-2. The proportion of human milk samples that reduced by half the growth of MDCK cells was of 36%. This inhibitory activity was associated with casein and not the whey fraction. Great variability was found in the degree of inhibitory activity depending on the milk sample. The susceptibility of Caco-2 cells to milk inhibitory activity was lower than that of MDCK. Bovine milk did not have any effect on cell growth, either as skimmed milk or as whey or casein. Morphology of cells incubated with active hum
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Monni, Giovanni, and Ulrich Honemeyer. "Normal and Abnormal Early Pregnancy." Donald School Journal of Ultrasound in Obstetrics and Gynecology 5, no. 4 (2011): 356–84. http://dx.doi.org/10.5005/jp-journals-10009-1214.

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ABSTRACT The first trimester, mostly defined as the first 100 days of pregnancy, is characterized by many important landmarks heralding the ultimate outcome of pregnancy. Woman becomes aware of her pregnancy after missing her period, being already two weeks postconception at that time. A positive pregnancy test opens Pandora's Box, raising more questions than giving answers. Although a positive pregnancy test most likely suggests an intrauterine pregnancy, production of human chorionic gonadotropin (hCG) occurs as well in tumors (dysgerminoma, choriocarcinoma) or maldeveloped pregnancies, such
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Jabbour, Mark N., James B. Elder, Christian G. Samuelson, et al. "ABERRANT ANGIOGENIC CHARACTERISTICS OF HUMAN BRAIN ARTERIOVENOUS MALFORMATION ENDOTHELIAL CELLS." Neurosurgery 64, no. 1 (2009): 139–48. http://dx.doi.org/10.1227/01.neu.0000334417.56742.24.

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Abstract OBJECTIVE To identify and characterize the phenotypic and functional differences of endothelial cells derived from cerebral arteriovenous malformations (AVM), as compared with endothelial cells derived from a normal brain. METHODS Isolated AVM brain endothelial cells and control brain endothelial cells were evaluated immunohistochemically for expression of the endothelial cell markers von Willebrand factor and CD31, as well as angiogenic factors including vascular endothelial growth factor A, interleukin-8, and endothelin-1. Vascular endothelial growth factor receptors 1 and 2 were al
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Ambrus, Julian L., Susan Haneiwich, Laura Chesky, Patrick McFarland, Marion G. Peters, and Renata J. Engler. "Abnormal response to a human B cell growth factor in patients with common variable immunodeficiency (CVI)." Journal of Allergy and Clinical Immunology 87, no. 6 (1991): 1138–49. http://dx.doi.org/10.1016/0091-6749(91)92160-3.

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D'Angio, Carl T., and Rita M. Ryan. "Animal models of bronchopulmonary dysplasia. The preterm and term rabbit models." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 12 (2014): L959—L969. http://dx.doi.org/10.1152/ajplung.00228.2014.

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Bronchopulmonary dysplasia (BPD) is an important lung developmental pathophysiology that affects many premature infants each year. Newborn animal models employing both premature and term animals have been used over the years to study various components of BPD. This review describes some of the neonatal rabbit studies that have contributed to the understanding of BPD, including those using term newborn hyperoxia exposure models, premature hyperoxia models, and a term newborn hyperoxia model with recovery in moderate hyperoxia, all designed to emulate aspects of BPD in human infants. Some invest
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