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Journal articles on the topic 'Cell/net'

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Published: 4 June 2021
Last updated: 1 February 2022

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1

Hurtley, S. "CELL BIOLOGY: Caught in the NET." Science 315, no. 5811 (January 26, 2007): 438a. http://dx.doi.org/10.1126/science.315.5811.438a.

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2

Boucher, Thomas O., Mohsen A. Jafari, and Glenn A. Meredith. "Petri net control of an automated manufacturing cell." Computers & Industrial Engineering 17, no. 1-4 (January 1989): 459–63. http://dx.doi.org/10.1016/0360-8352(89)90105-8.

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3

Vitali, Eleonora, Ilena Boemi, Giulia Tarantola, Sara Piccini, Alessandro Zerbi, Giulia Veronesi, Roberto Baldelli, et al. "Metformin and Everolimus: A Promising Combination for Neuroendocrine Tumors Treatment." Cancers 12, no. 8 (August 2, 2020): 2143. http://dx.doi.org/10.3390/cancers12082143.

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Introduction: Treatment options for neuroendocrine tumors (NETs) are rarely curative, as NETs frequently show resistance to medical therapy. The use of everolimus, an mTOR inhibitor, is limited by the development of resistance, probably due to the activation of Akt signaling. In this context, the antidiabetic drug metformin is able to inhibit mTOR, providing a rationale for the use of metformin and everolimus in combination. Methods: We investigated the effects of the metformin and everolimus combination on NET cell proliferation, apoptosis, colony formation, cell viability, NET spheroids growth and the involvement of the Akt and mTOR pathways, and also developed everolimus-resistant NET cells to further study this combination. Results: Metformin and everolimus in combination are more effective than monotherapy in inhibiting pancreatic NET (PAN-NET) cell proliferation (−71% ± 13%, p < 0.0001 vs. basal), whereas no additive effects were observed on pulmonary neuroendocrine tumor (PNT) cell proliferation. The combinatorial treatment is more effective than monotherapy in inhibiting colony formation, cell viability, NET spheroids growth rate and mTOR phosphorylation in both NET cell lines. In a PAN-NET cell line, metformin did not affect Akt phosphorylation; conversely, it significantly decreased Akt phosphorylation in a PNT cell line. Using everolimus-resistant NET cells, we confirmed that metformin maintained its effects, acting by two different pathways: Akt-dependent or independent, depending on the cell type, with both leading to mTOR suppression. Conclusions: Considering the promising effects of the everolimus and metformin combination in NET cells, our results provide a rationale for its use in NET patients.
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4

Chen, D. S., H. C. Chen, and J. M. Park. "An improved ART neural net for machine cell formation." Journal of Materials Processing Technology 61, no. 1-2 (August 1996): 1–6. http://dx.doi.org/10.1016/0924-0136(96)02457-0.

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5

Jin, Xi-Feng, Gerald Spöttl, Julian Maurer, Svenja Nölting, and Christoph Josef Auernhammer. "Inhibition of Wnt/β-Catenin Signaling in Neuroendocrine Tumors In Vitro: Antitumoral Effects." Cancers 12, no. 2 (February 4, 2020): 345. http://dx.doi.org/10.3390/cancers12020345.

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Background and aims: Inhibition of Wnt/β-catenin signaling by specific inhibitors is currently being investigated as an antitumoral strategy for various cancers. The role of Wnt/β-catenin signaling in neuroendocrine tumors still needs to be further investigated. Methods: This study investigated the antitumor activity of the porcupine (PORCN) inhibitor WNT974 and the β-catenin inhibitor PRI-724 in human neuroendocrine tumor (NET) cell lines BON1, QGP-1, and NCI-H727 in vitro. NET cells were treated with WNT974, PRI-724, or small interfering ribonucleic acids against β-catenin, and subsequent analyses included cell viability assays, flow cytometric cell cycle analysis, caspase3/7 assays and Western blot analysis. Results: Treatment of NET cells with WNT974 significantly reduced NET cell viability in a dose- and time-dependent manner by inducing NET cell cycle arrest at the G1 and G2/M phases without inducing apoptosis. WNT974 primarily blocked Wnt/β-catenin signaling by the dose- and time-dependent downregulation of low-density lipoprotein receptor-related protein 6 (LRP6) phosphorylation and non-phosphorylated β-catenin and total β-catenin, as well as the genes targeting the latter (c-Myc and cyclinD1). Furthermore, the WNT974-induced reduction of NET cell viability occurred through the inhibition of GSK-3-dependent or independent signaling (including pAKT/mTOR, pEGFR and pIGFR signaling). Similarly, treatment of NET cells with the β-catenin inhibitor PRI-724 caused significant growth inhibition, while the knockdown of β-catenin expression by siRNA reduced NET tumor cell viability of BON1 cells but not of NCI-H727 cells. Conclusions: The PORCN inhibitor WNT974 possesses antitumor properties in NET cell lines by inhibiting Wnt and related signaling. In addition, the β-catenin inhibitor PRI-724 possesses antitumor properties in NET cell lines. Future studies are needed to determine the role of Wnt/β-catenin signaling in NET as a potential therapeutic target.
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6

Matsui, Mika, Sachie Fujita, Shunichi Suzuki, Hiroshi Matsuno, and Satoru Miyano. "Simulated Cell Division Processes of the Xenopus Cell Cycle Pathway by Genomic Object Net." Journal of Integrative Bioinformatics 1, no. 1 (December 1, 2004): 27–37. http://dx.doi.org/10.1515/jib-2004-3.

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Summary Matsuno et al.[1] modeled and simulated that multicellular patterning by the Drosophila Delta-Notch signaling pathway by using the software “Genomic Object Net” which was developed based on hybrid functional Petri net (HFPN) architecture. In this model, cellular formation is fixed throughout the simulation. This paper constructs an HFPN model of the Xenopus cell cycle pathway, which includes the mechanism for cell division control as well as checkpoint processes. This model simulates dynamic cell division processes of the early Xenopus embryo, including the changes in cell division cycles from synchronous to asynchronous.
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7

Krieger, Nancy S., Walter R. Parker, Kristen M. Alexander, and David A. Bushinsky. "Prostaglandins regulate acid-induced cell-mediated bone resorption." American Journal of Physiology-Renal Physiology 279, no. 6 (December 1, 2000): F1077—F1082. http://dx.doi.org/10.1152/ajprenal.2000.279.6.f1077.

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Metabolic acidosis induces bone calcium efflux initially by physicochemical dissolution and subsequently by cell-mediated mechanisms involving inhibition of osteoblasts and stimulation of osteoclasts. In rat kidney, acidosis increases endogenous prostaglandin synthesis, and in bone, prostaglandins are important mediators of resorption. To test the hypothesis that acid-induced bone resorption is mediated by prostaglandins, we cultured neonatal mouse calvariae in neutral or physiologically acidic medium with or without 0.56 μM indomethacin to inhibit prostaglandin synthesis. We measured net calcium efflux and medium PGE2 levels. Compared with neutral pH medium, acid medium led to an increase in net calcium flux and PGE2 levels after both 48 h and 51 h, a time at which acid-induced net calcium flux is predominantly cell mediated. Indomethacin inhibited the acid-induced increase in both net calcium flux and PGE2. Net calcium flux was correlated directly with medium PGE2 ( r = 0.879, n = 29, P < 0.001). Exogenous PGE2, at a level similar to that found after acid incubation, induced net calcium flux in bones cultured in neutral medium. Acid medium also stimulated an increase in PGE2levels in isolated bone cells (principally osteoblasts), which was again inhibited by indomethacin. Thus acid-induced stimulation of cell-mediated bone resorption appears to be mediated by endogenous osteoblastic PGE2 synthesis.
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8

Mura, Ivan, and Attila Csikász-Nagy. "Stochastic Petri Net extension of a yeast cell cycle model." Journal of Theoretical Biology 254, no. 4 (October 2008): 850–60. http://dx.doi.org/10.1016/j.jtbi.2008.07.019.

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9

Falk, Thorsten, Dominic Mai, Robert Bensch, Özgün Çiçek, Ahmed Abdulkadir, Yassine Marrakchi, Anton Böhm, et al. "U-Net: deep learning for cell counting, detection, and morphometry." Nature Methods 16, no. 1 (December 17, 2018): 67–70. http://dx.doi.org/10.1038/s41592-018-0261-2.

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10

Dunlop, Stuart, Ben Jones, and Duncan McFarlane. "Petri Net Based Design and Diagnosis for an Assembly Cell." IFAC Proceedings Volumes 30, no. 18 (August 1997): 1107–12. http://dx.doi.org/10.1016/s1474-6670(17)42544-4.

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11

Pasquale, Elena B. "Eph receptor signalling casts a wide net on cell behaviour." Nature Reviews Molecular Cell Biology 6, no. 6 (June 1, 2005): 462–75. http://dx.doi.org/10.1038/nrm1662.

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12

Chang, Zhaoyu, Jian Zhang, Wanyuan Dong, Xiangqi Meng, Hualei Wang, Dongzhi Wei, and Yuhong Ren. "Cadmium sulfide net framework nanoparticles for photo-catalyzed cell redox." RSC Advances 10, no. 62 (2020): 37820–25. http://dx.doi.org/10.1039/d0ra08235j.

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CdS net framework (CdS-NF) nanoparticles were synthesized under mild reaction conditions and used to construct an Escherichia coli–CdS-NF hybrid system which used NADH regeneration to promote the redox reaction.
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13

MAŁEK, Arkadiusz. "Adaptive search for a PEM fuel cell maximum net power." Combustion Engines 145, no. 2 (May 1, 2011): 49–57. http://dx.doi.org/10.19206/ce-117101.

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Supply method of the fuel cell cathode side significantly affects the durability and efficiency of the hydrogen energy conversion. A fuel cell is a stochastic object. The paper presents air flow control of the PEM fuel cell in order to find and hold the maximum value of the net power produced by the fuel cell stack, regardless of changes of the parameters of the object of control and its outer environment. The Application of an adaptive extremum control with bi-parameter identification provide automatic adjustment of the parameters of a controller to the changing characteristics of an object. The adaptive algorithm contains a number of variables and signals that support the estimation process. The quality and speed of finding an optimal point depends on their values.
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14

Koide, Tetsushi, Takeshi Suzuki, Shin'Ichi Wakabayashi, and Noriyoshi Yoshida. "A standard cell global routing algorithm with net selection for over-the-cell routing." Electronics and Communications in Japan (Part III: Fundamental Electronic Science) 78, no. 12 (December 1995): 102–15. http://dx.doi.org/10.1002/ecjc.4430781211.

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15

Law, Jade, Alex Zhornitskiy, James H. Tabibian, and Armine Baltayan. "1409 Casting a Wide Net to Find a Rare NET: A Case of Gallbladder Large Cell Neuroendocrine Carcinoma." American Journal of Gastroenterology 114, no. 1 (October 2019): S781—S782. http://dx.doi.org/10.14309/01.ajg.0000595164.54499.73.

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16

Brady, H. R., B. C. Kone, and S. R. Gullans. "Extracellular Na+ electrode for monitoring net Na+ flux in cell suspensions." American Journal of Physiology-Cell Physiology 256, no. 5 (May 1, 1989): C1105—C1110. http://dx.doi.org/10.1152/ajpcell.1989.256.5.c1105.

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A computer-linked extracellular sodium-sensitive electrode system is described that is suitable for the routine measurement of net Na+ transport in cell suspensions. The commercially available Na+ electrode exhibited high selectivity for Na+ over other cations and a rapid response time (less than 3 s). This system resolved changes of 0.4 mM in the presence of 147 mM extracellular Na+. Measurements of Na+ transport in suspensions of rabbit proximal tubules showed that ouabain caused a dose-dependent net Na+ influx with an inhibitor constant (Ki) of 2.5 +/- 0.2 microM and a maximal velocity (Vmax) of 229 +/- 7 nmol Na+.min-1.mg protein-1. This compared favorably with the ouabain-induced K+ efflux (Ki = 2.4 microM; Vmax = 160 +/- 3.3 nmol K+.min-1.mg protein-1) and the ouabain-induced inhibition of respiration (Ki = 3.3 microM; Vmax = 11.8 nmol O2.min-1.mg protein-1). In addition, Ba2+, a K+ channel blocker known to depolarize the cell, caused a net Na+ efflux, whereas glucose, a Na+-cotransported solute, promoted a net Na+ influx. This system should be a powerful tool for continuous monitoring of net Na+ fluxes in cell suspensions.
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17

Pugliese, F., G. A. Cinotti, and P. Menè. "Regulation of cultured human mesangial cell growth by ionized macromolecules." Journal of the American Society of Nephrology 2, no. 10 (April 1992): S95. http://dx.doi.org/10.1681/asn.v210s95.

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We evaluated the importance of the net charge of polyionic macromolecules in the regulation of cultured human mesangial cell growth. Structurally unrelated polyanionic compounds, i.e., heparin, suramin, poly-L-aspartic acid, and poly-L-glutamic acid, strongly inhibited 10% fetal bovine serum-stimulated cell proliferation. On the other hand, two polycations, protamin sulfate and poly-L-lysine, were equally effective in inhibiting cell growth. The antiproliferative activity of each compound was neutralized by molecules with opposite net charge. These data indicate that both anionic and cationic macromolecules exert an antimitogenic effect on cultured human mesangial cells. This inhibitory effect is dependent upon charge density rather than on the net electric charge of each compound.
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18

Pagliassotti, M. J., and C. M. Donovan. "Role of cell type in net lactate removal by skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 258, no. 4 (April 1, 1990): E635—E642. http://dx.doi.org/10.1152/ajpendo.1990.258.4.e635.

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Net lactate uptake and subsequent pathways for removal were studied in three rabbit skeletal muscle preparations of distinct fiber type composition, i.e., glycolytic (99.1 +/- 0.2% type IIb fibers), oxidative (97.5 +/- 0.6% type I fibers), and mixed (type I, IIa, and IIb fibers). Single-pass perfusions were carried out for 3 h in the presence of glucose, lactate, and [U-14C]lactate. Lactate levels, initially set at either 1 mM (n = 4/prep) or 2 mM (n = 4/prep), were elevated twice during the perfusion at 60 and 120 min. Net lactate uptake (mumol.100 g-1.min-1) was first observed in the oxidative preparation, 1.4 +/- 0.2, at an arterial lactate concentration of approximately 2.5 mM, whereas net lactate uptake in the glycolytic, 0.7 +/- 0.2, and mixed preparations, 7.0 +/- 0.5, was first observed at 4 mM. Net lactate balance, [14C]lactate removal, and 14CO2 release demonstrated strong linear correlations (r = 0.94-0.98) with arterial lactate concentration. To quantify the fate of [14C]lactate, preparations were perfused at a single elevated lactate concentration (approximately 8 mM) for 2 h. Oxidation was the primary means of disposal in the oxidative and mixed preparations, whereas glyconeogenesis dominated removal in the glycolytic preparation. The arterial lactate concentration at which a given muscle switches from net production to net removal, the rate of removal, and subsequent pathway(s) for disposal are a function of that muscle's fiber type composition.
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19

Jitsukawa, Mitsuru, Pauline N. Kawamoto, and Yasunari Shidama. "Formulation of Cell Petri Nets." Formalized Mathematics 21, no. 4 (December 1, 2013): 241–47. http://dx.doi.org/10.2478/forma-2013-0026.

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Abstract Based on the Petri net definitions and theorems already formalized in the Mizar article [13], in this article we were able to formalize the definition of cell Petri nets. It is based on [12]. Colored Petri net has already been defined in [11]. In addition, the conditions of the firing rule and the colored set to this definition, that defines the cell Petri nets are further extended to CPNT.i further. The synthesis of two Petri nets was introduced in [11] and in this work the definition is extended to produce the synthesis of a family of colored Petri nets. Specifically, the extension to a CPNT family is performed by specifying how to link the outbound transitions of each colored Petri net to the place elements of other nets to form a neighborhood relationship. Finally, the activation of colored Petri nets was formalized.
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20

Hendifar, Andrew Eugene, Harris S. Soifer, Mason Israel, and Catherine A. Schnabel. "Molecular classification of neuroendocrine tumors: Clinical experience with the 92-gene assay in >24,000 cases." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): e15700-e15700. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e15700.

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e15700 Background: Histological diagnosis of metastatic neuroendocrine tumors (NET) can be straightforward, but identification of the specific NET tumor type/subtype is often challenging based on morphology alone. Accurate identification of tumor type/subtype in NETs of unknown primary has implications for grading, staging, and treatment decision-making as availability of targeted therapies increases. The 92-gene assay (CancerTYPE ID) is a validated gene expression classifier of 50 tumor type/subtypes (including 7 NET subtypes) for patients with unknown/uncertain diagnoses. In this study, 92-gene assay results from cases submitted for clinical testing with molecular diagnoses of NET were evaluated. Methods: A de-identified database was created under an IRB approved protocol that contains clinical and molecular information from consecutive cases submitted for clinical testing with the 92-gene assay with sufficient tissue for testing. In this analysis, patient demographics and distribution of molecular diagnoses were analyzed based on biopsy site, age, and gender. Chi-squared tests were used to compare between subgroups. Results: Analysis included 24,484 patients. Median age was 65y (51% female). The 92-gene assay rendered a molecular diagnosis of NET in 6.3% of cases (n = 1551). Small/large cell lung carcinoma (50%) was the most common NET molecular diagnosis, followed by GI carcinoid (14%), islet cell (14%), Merkel cell (10%), and lung carcinoid (9%). In liver biopsies (39% of cases), all 7 NET subtypes were identified by the 92-gene assay. The proportion of molecular diagnoses classified as small/large cell lung NET increased with age, from 25% in < 40y to 45% in 40-65y and 55% in > 65y, and the proportion of islet cell NET decreased with age (p < 0.0001). Men had a higher proportion of molecular diagnoses that were small/large cell lung NET (53%) vs women (46%; p < 0.0001). Conclusions: These findings highlight the utility of molecular classification to identify distinct NET tumor types/subtypes to improve diagnostic precision and treatment decision-making. In addition, significant differences in the distribution of molecular diagnoses of NET subtype by age and gender were identified.
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21

Jin, Xi-Feng, Gerald Spöttl, Julian Maurer, Svenja Nölting, and Christoph Josef Auernhammer. "Antitumoral Activity of the MEK Inhibitor Trametinib (TMT212) Alone and in Combination with the CDK4/6 Inhibitor Ribociclib (LEE011) in Neuroendocrine Tumor Cells In Vitro." Cancers 13, no. 6 (March 23, 2021): 1485. http://dx.doi.org/10.3390/cancers13061485.

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Objectives: This study assessed the antitumoral activity of the MEK inhibitor trametinib (TMT212) and the ERK1/2 inhibitor SCH772984, alone and in combination with the CDK4/6 inhibitor ribociclib (LEE011) in human neuroendocrine tumor (NET) cell lines in vitro. Methods: Human NET cell lines BON1, QGP-1, and NCI-H727 were treated with trametinib or SCH772984, alone and in combination with ribociclib, to assess cell proliferation, cell cycle distribution, and protein signaling using cell proliferation, flow cytometry, and Western blot assays, respectively. Results: Trametinib and SCH772984, alone and in combination with ribociclib, significantly reduced NET cell viability and arrested NET cells at the G1 phase of the cell cycle in all three cell lines tested. In addition, trametinib also caused subG1 events and apoptotic PARP cleavage in QGP1 and NCI-H727 cells. A western blot analysis demonstrated the use of trametinib alone and trametinib in combination with ribociclib to decrease the expression of pERK, cMyc, Chk1, pChk2, pCDK1, CyclinD1, and c-myc in a time-dependent manner in NCI-H727 and QGP-1 cells. Conclusions: MEK and ERK inhibition causes antiproliferative effects in human NET cell lines in vitro. The combination of the MEK inhibitor trametinib (TMT212) with the CDK4/6 inhibitor ribociclib (LEE011) causes additive antiproliferative effects. Future preclinical and clinical studies of MEK inhibition in NETs should be performed.
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22

Zitzmann, Kathrin, George Vlotides, Stephan Brand, Harald Lahm, Gerald Spöttl, Burkhard Göke, and Christoph J. Auernhammer. "Perifosine-mediated Akt inhibition in neuroendocrine tumor cells: role of specific Akt isoforms." Endocrine-Related Cancer 19, no. 3 (April 12, 2012): 423–34. http://dx.doi.org/10.1530/erc-12-0074.

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The majority of neuroendocrine tumors (NETs) of the gastroenteropancreatic system show aberrant Akt activity. Several inhibitors of the phosphoinositide 3-kinase (PI(3)K)–Akt–mTOR signaling pathway are currently being evaluated in clinical phase II and III studies for the treatment of NETs with promising results. However, the molecular mechanisms and particularly the role of different Akt isoforms in NET signaling are not fully understood. In this study, we examine the effect of Akt inhibition on NET cells of heterogeneous origin. We show that the Akt inhibitor perifosine effectively inhibits Akt phosphorylation and cell viability in human pancreatic (BON1), bronchus (NCI-H727), and midgut (GOT1) NET cells. Perifosine treatment suppressed the phosphorylation of Akt downstream targets such as GSK3α/β, MDM2, and p70S6K and induced apoptosis. To further investigate the role of individual Akt isoforms for NET cell function, we specifically blocked Akt1, Akt2, and Akt3 via siRNA transfection. In contrast to Akt2 knockdown, knockdown of Akt isoforms 1 and 3 decreased phosphorylation levels of GSK3α/β, MDM2, and p70S6K and suppressed NET cell viability and colony-forming capacity. The inhibitory effect of simultaneous downregulation of Akt1 and Akt3 on tumor cell viability was significantly stronger than that caused by downregulation of all Akt isoforms, suggesting a particular role for Akt1 and Akt3 in NET signaling. Akt3 siRNA-induced apoptosis while all three isoform-specific siRNAs impaired BON1 cell invasion. Together, our data demonstrate potent antitumor effects of the pan-Akt inhibitor perifosine on NET cells in vitro and suggest that selective targeting of Akt1 and/or Akt3 might improve the therapeutic potential of Akt inhibition in NET disease.
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23

Yin, Fei, Shiqi Yang, Shan Hu, Shihuan Kuang, and Qingyou Han. "Enhanced human osteoblast cell functions by “net-like” nanostructured cell-substrate interface in orthopedic applications." Materials Letters 189 (February 2017): 275–78. http://dx.doi.org/10.1016/j.matlet.2016.11.077.

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24

MOORMAN, MARK A., CAITLIN A. THELEMANN, SHENGYING ZHOU, JAMES J. PESTKA, JOHN E. LINZ, and ELLIOT T. RYSER. "Altered Hydrophobicity and Membrane Composition in Stress-Adapted Listeria innocua." Journal of Food Protection 71, no. 1 (January 1, 2008): 182–85. http://dx.doi.org/10.4315/0362-028x-71.1.182.

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Exposure of Listeria innocua to acid and starvation stress decreases sensitivity to the quaternary ammonium compound cetrimide, whereas exposure to cold and heat stress increases sensitivity to this compound. Changes in membrane lipids occur in response to certain types of stress, and these changes likely impact cell sensitivity to chemical sanitizers. The present study included an assessment of the effects of acid, starvation, cold, and heat stress on net cell hydrophobicity and fatty acid composition in L. innocua. Net cell hydrophobicity was determined by measuring absorbance of stress-adapted cell suspensions after partitioning with the nonpolar solvent n-hexadecane. Free fatty acids extracted from stress-adapted suspensions were analyzed by gas chromatography. Adaptation to acid and starvation increased net cell hydrophobicity and decreased membrane fluidity, which was correlated with reductions in anteiso fatty acids and in ratios of anteiso to iso fatty acids. Conversely, cold-stressed populations exhibited decreased net cell hydrophobicity and increased membrane fluidity with a corresponding increase in C15:C17 and anteiso:iso ratios and in C18 unsaturated fatty acids. No significant changes in net cell hydrophobicity or membrane fluidity were observed in heat-stressed cells, which exhibited increased sensitivity to cetrimide, suggesting another mechanism for altered cell sensitivity. These findings indicate that the efficacy of cetrimide against Listeria is partially dependent on the physiological state of the organism following exposure to various environmental stresses.
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Dadhwal, Rohit, Siddharth Jain, Amlesh Seth, and Chandra Shekhar Bal. "Neuroendocrine tumour of urinary bladder: a rare case of aggressively behaving primary well-differentiated neuroendocrine tumour with review of literature." BMJ Case Reports 12, no. 11 (November 2019): e231061. http://dx.doi.org/10.1136/bcr-2019-231061.

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Neuroendocrine tumour (NET) of the urinary bladder (UB) is a rare entity and comprises of well-differentiated, small cell and large cell types. Small and large cell NET like that in lung and gastrointestinal tract have an aggressive nature and are considered high-grade disease. Well-differentiated NET has been thought to be localised and having a good prognosis. We report the first case of metastatic well-differentiated NET of the UB. Our case is a 44-year-old man with well-differentiated NET of UB presented with hepatic and peritoneal metastases on initial diagnosis. He was treated with metaiodobenzylguanidine (MIBG) therapy and had a modest survival of 16 months. The primary well-differentiated NETs can present as a metastatic disease with an aggressive nature. MIBG therapy can be considered as a useful option but overall prognosis is poor. Further research is needed for better understanding and better treatment protocol.
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26

O’Rourke, Judith, Murat Arcak, and Manikandan Ramani. "Real-time optimization of net power in a fuel cell system." Journal of Power Sources 187, no. 2 (February 2009): 422–30. http://dx.doi.org/10.1016/j.jpowsour.2008.11.060.

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27

Zhou, M., K. McDermott, and P. A. Patel. "Petri net synthesis and analysis of a flexible manufacturing system cell." IEEE Transactions on Systems, Man, and Cybernetics 23, no. 2 (1993): 523–31. http://dx.doi.org/10.1109/21.229464.

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28

Pasquale, Elena B. "Erratum: Eph receptor signalling casts a wide net on cell behaviour." Nature Reviews Molecular Cell Biology 6, no. 7 (July 2005): 589. http://dx.doi.org/10.1038/nrm1690.

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29

D'Cruz, Akshay A., Mary Speir, Meghan Bliss-Moreau, Sylvia Dietrich, Alyce A. Chen, Mathilde Gavillet, Kate E. Lawlor, et al. "Padi4 Regulates NET Formation and Inflammatory Cell Death Downstream of Mlkl." Blood 132, Supplement 1 (November 29, 2018): 276. http://dx.doi.org/10.1182/blood-2018-99-110051.

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Abstract Neutrophil extracellular trap (NET) formation can generate short-term functional anucleate cytoplasts and can trigger loss of cell viability. We examined the role of non-apoptotic cell death signaling in NET formation by studying necroptotic human and mouse neutrophils. Necroptotic cell death signaling was activated by caspase-8 inhibition and pharmacological targeting of inhibitor of apoptosis proteins (IAPs). The specificity of cell death was confirmed using neutrophils from mice deficient in receptor-interacting protein kinase-3 (Ripk3), Ripk1 kinase activity (Ripk1D138N/D138N), caspase-8, or the plasma membrane-disrupting effector protein mixed lineage kinase domain-like (Mlkl). NETs were investigated with a combination of imaging and quantitative flow cytometry, immunogold electron microscopy, immunofluorescence microscopy, and ex vivo microbicidal assays to demonstrate functionality of NETs. In response to necroptotic stimuli, Mlkl translocates to the plasma membrane in neutrophils, and is required for downstream NADPH oxidase-independent reactive oxygen species production, loss of cytoplasmic granules, breakdown of the nuclear membrane, chromatin decondensation, histone hypercitrullination, and extrusion of bacteriostatic NETs. Neutrophils expressing a kinase-dead form of Ripk1 (Ripk1D138N/D138N) were unable to generate Ripk3/Mlkl-dependent NETs, or to undergo necroptosis or caspase-8-dependent apoptosis. NET formation that is triggered by necroptotic stimuli is dependent on TNF production, can be differentially modulated by the actions of G-CSF and IFNγ, and occurs concomitantly with the production, processing and release of IL-1α/β. Human necroptotic neutrophils also release NETs that kill S.aureus. Necroptotic NETs contain components of canonical NETs including dsDNA, hypercitrullinated histones, and neutrophil elastase, but also non-canonical components including Mlkl and membranes. Peptidylarginine deiminase 4 (Padi4) is required for extrusion of necroptotic NETs but not for chromatin decondensation. Padi4-deficient neutrophils are hypersensitive to necroptotic stimuli despite normal levels of phosphorylated Mlkl, indicating that Padi4 acts downstream of Mlkl activation. The failure of Padi4-deficient neutrophils to generate necroptotic NETs in the presence of membrane-associated Mlkl, suggests that the removal of Mlkl membrane-disrupting complexes by NETs can facilitate membrane repair and control the kinetics of neutrophil necroptosis. This work defines a distinct cell death signaling network downstream of Mlkl that promotes Padi4-dependent necroptotic NET release. Disclosures No relevant conflicts of interest to declare.
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Yousefi⁎, S., E. Kozlowski, I. Schmid, and H.-U. Simon. "Neutrophil Extracellular Trap (NET) formation in the absence of cell death." Free Radical Biology and Medicine 53 (September 2012): S13. http://dx.doi.org/10.1016/j.freeradbiomed.2012.08.096.

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Wang, L.-C. "The development of an object-oriented Petri net cell control model." International Journal of Advanced Manufacturing Technology 11, no. 1 (January 1996): 59–69. http://dx.doi.org/10.1007/bf01177185.

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32

Nall, Duncan L., and Paul R. Selvin. "Live Cell Storm Studies on the Perineuronal Net in Cultured Neurons." Biophysical Journal 118, no. 3 (February 2020): 290a. http://dx.doi.org/10.1016/j.bpj.2019.11.1650.

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33

Pouyan, Ali A., Heydar Toossian Shandiz, and Soheil Arastehfar. "Synthesis a Petri net based control model for a FMS cell." Computers in Industry 62, no. 5 (June 2011): 501–8. http://dx.doi.org/10.1016/j.compind.2011.01.001.

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34

Busse, Antonia, Liliana H. Mochmann, Christiane Spenke, Ruza Arsenic, Franziska Briest, Korinna Jöhrens, Hedwig Lammert, et al. "Immunoprofiling in Neuroendocrine Neoplasms Unveil Immunosuppressive Microenvironment." Cancers 12, no. 11 (November 19, 2020): 3448. http://dx.doi.org/10.3390/cancers12113448.

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Checkpoint inhibitors have shown promising results in a variety of tumors; however, in neuroendocrine tumors (NET) and neuroendocrine carcinomas (NEC), low response rates were reported. We aimed herein to investigate the tumor immune microenvironment in NET/NEC to determine whether checkpoint pathways like programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) might play a role in immune escape and whether other escape mechanisms might need to be targeted to enable a functional antitumor response. Forty-eight NET and thirty NEC samples were analyzed by immunohistochemistry (IHC) and mRNA immunoprofiling including digital spatial profiling. Through IHC, both NET/NEC showed stromal, but less intratumoral CD3+ T cell infiltration, although this was significantly higher in NEC compared to NET. Expression of PD1, PD-L1, and T cell immunoglobulin and mucin domain-containing protein 3 (TIM3) on immune cells was low or nearly absent. mRNA immunoprofiling revealed low expression of IFNγ inducible genes in NET and NEC without any spatial heterogeneity. However, we observed an increased mRNA expression of chemokines, which attract myeloid cells in NET and NEC, and a high abundance of genes related to immunosuppressive myeloid cells and genes with immunosuppressive functions like CD47 and CD74. In conclusion, NET and NEC lack signs of an activation of the adaptive immune system, but rather show abundance of several immunosuppressive genes that represent potential targets for immunomodulation.
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Seeger, Harald, Diethelm Wallwiener, and Alfred O. Mueck. "Comparison of the Effect of Progesterone, Medroxyprogesterone Acetate and Norethisterone on the Proliferation of Human Breast Cancer Cells." British Menopause Society Journal 9, no. 1 (March 2003): 36–38. http://dx.doi.org/10.1177/136218070300900111.

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Objective To investigate in vitro the influence of the three most used progestogens in continuous combined HRT on cell proliferation of the human breast cancer cell line MCF-7. Study design Progesterone (P), medroxyprogesterone acetate (MPA) and norethisterone (NET) were investigated in the range of 0.01 nM to 10 μM alone and in combination with 10 nM oestradiol. Cell proliferation was measured after seven days using the ATP-chemosensitivity test. Results P alone reduced cell proliferation by 20 and 40% at 10−7 and 10−5 M. MPA and NET displayed a significant inhibition of cell proliferation between 20 and 25% for MPA and 23 and 41% for NET over the whole concentration range tested. The effect was greatest at 10−7 M for MPA and at 10−9 M for NET. In combination with oestradiol, P still significantly reduced cell proliferation, the values being between 12 and 61%. For MPA too an inhibitory effect between 20 and 40% was found, whereas for NET the values were between 23 and 38%. Conclusions Our in vitro results indicate that the influence on breast cancer risk using HRT in postmenopausal women may depend on the type of progestogen used as well as on the regimen applied. However, the inhibitory in vitro net effect of the progestogens at clinically relevant dosages is rather minimal and it remains uncertain as to whether progestogens generally may reduce breast cancer risk in long-term treatment. Further clinical trials are urgently required to determine the appropriate choice - if any - of progestogen to complement HRT.
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Buchwalter, Gilles, Christian Gross, and Bohdan Wasylyk. "The Ternary Complex Factor Net Regulates Cell Migration through Inhibition of PAI-1 Expression." Molecular and Cellular Biology 25, no. 24 (December 15, 2005): 10853–62. http://dx.doi.org/10.1128/mcb.25.24.10853-10862.2005.

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ABSTRACT Net, Elk-1, and Sap-1 are members of the ternary complex factor (TCF) subfamily of Ets transcription factors. They form ternary complexes with serum response factor (SRF) on serum response elements of immediate early genes such as c-fos and egr-1 and mediate responses to growth factors and mitogen-activated protein kinase signaling. Although the TCFs have been extensively studied as intermediates in signaling cascades, surprisingly little is known about their different target genes and physiological functions. We report that Net homozygous mutant mouse embryonic fibroblasts have a defect in cell migration. This defect results at least in part from increased expression of plasminogen activator inhibitor type 1 (PAI-1), a serine protease inhibitor (serpin) that controls extracellular proteolysis and cell matrix adhesion. The defect in cell migration can be reverted by the addition of a PAI-1 blocking antibody. Net represses PAI-1 promoter activity and binds to a specific region of the promoter containing Ets binding sites in the absence of SRF. We conclude that Net is a negative regulator of PAI-1 expression and is thereby involved in cell migration.
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Höpfner, Michael, Viola Baradari, Alexander Huether, Christof Schöfl, and Hans Scherübl. "The insulin-like growth factor receptor 1 is a promising target for novel treatment approaches in neuroendocrine gastrointestinal tumours." Endocrine-Related Cancer 13, no. 1 (March 2006): 135–49. http://dx.doi.org/10.1677/erc.1.01090.

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Gastrointestinal neuroendocrine tumours (NET) represent a heterogeneous tumour entity. The anti-neoplastic therapy of advanced NET disease is still unsatisfactory and innovative therapeutic approaches are needed. As NET frequently express insulin-like growth factors (IGFs) and their receptors (IGFR), known to promote survival, oncogenic transformation, tumour growth and spreading, the inhibition of the IGF/IGF-receptor system may offer possibilities for novel targeted treatment strategies of NET. Here, we studied the anti-neoplastic effects of an inhibition of the IGF-I receptor (IGF-1R) signalling in NET cells by the novel IGF-1R tyrosine kinase (TK) inhibitor NVP-AEW541, whose anti-neoplastic potency has not yet been tested in NET disease. Using two human NET cell lines with different growth characteristics, we demonstrated that NVP-AEW541 dose-dependently inhibited the proliferation of NET cells by inducing apoptosis and cell cycle arrest. Anti-neoplastic effects of NVP-AEW541 were also detected in primary cultures of human neuroendocrine gastrointestinal tumours. Apoptosis was characterized by activation of the apoptotic key enzyme, caspase-3, as well as by detection of changes in the expression of the pro- and anti-apoptotic proteins, BAX and Bcl-2, after NVP-AEW541 treatment. Cell cycle was arrested at the G1/S checkpoint. The anti-neoplastic effects of NVP-AEW541 involved the inactivation of ERK1/2. Induction of immediate cytotoxicity did not account for the anti-neoplastic effects of NVP-AEW541, as shown by measurement of lactate dehydrogenase release. Moreover, additive anti-neoplastic effects were observed when NVP-AEW541 was combined with cytostatics such as doxorubicin or the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, fluvastatin. This is the first report on the induction of apoptosis and cell cycle arrest by the IGF-1R-TK inhibitor, NVP-AEW541, in NET cells. The inhibition of the IGF/IGFR system appears to be a promising novel approach for future treatment strategies of NET disease.
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Whittaker, Scott D. "Net Notes." Microscopy and Microanalysis 4, no. 3 (June 1998): 349. http://dx.doi.org/10.1017/s1431927698250355.

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Well it's time again for another edition of Net Notes. This edition is for you biological science technicians out there. Maybe this discussion can speed up cell and bacterial processing for SEM so you can take longer lunches. This discussion is archived in full at the Tips & Tricks site located at www.biotech.ufl.edu/~emcl. Good luck.
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Hutchinson, T. C., C. Soto, and J. A. Hellebust. "Effect of naphthalene and aqueous crude-oil extracts on the green flagellate Chlamydomonas angulosa. VI. Phosphate uptake and retention." Canadian Journal of Botany 63, no. 4 (April 1, 1985): 829–33. http://dx.doi.org/10.1139/b85-106.

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Chlamydomonas angulosa when grown in normal Bold's basal medium (BBM) (1.7 mM Pi) has a very high cell P content (120 fg-at. P∙cell−1) and low C: P atomic ratio (35: 1) and is only able to show net Pi uptake in media with Pi concentrations higher than 0.1 mM when grown in the light. The presence of light enhances net phosphate uptake or decreases net phosphate loss under all external Pi concentrations. Cells transferred to low-Pi media will, however, grow rapidly while reducing their cell P to almost 1/10 of the initial level, indicating that most of the cell P in cells grown in high-P media represents reserve P, probably in the form of polyphosphates. The presence of naphthalene and crude-oil components in the culture media decreases net uptake of Pi at high external Pi concentrations and increases the rate of Pi loss at low external concentrations. Naphthalene present at 100% saturation level in BBM causes rapid loss of a large fraction of cell P under all conditions tested. The phosphorus lost appears as reactive phosphorus in the medium, suggesting that cell polyphosphates are rapidly converted to Pi, which then leaks out of the cells in response to the presence of saturating naphthalene concentrations in the medium. BBM with 50% naphthalene saturation causes much less loss of cell P under most of the incubation conditions, and net uptake can take place at the highest external Pi concentrations tested in the light. Media saturated with crude oil are even less effective than 50% naphthalene saturated media in causing P efflux, or in reducing net Pi uptake, although at low external P concentrations, uptake of P is decreased compared with the control.
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40

Cooke, Keegan, Juan Estrada, Jinghui Zhan, Jonathan Werner, Fei Lee, Aditya Shetty, Marie-Anne Damiette Smit, Mark Salvati, and Julie Bailis. "627 The DLL3-targeted half-life extended bispecific T cell engager (HLE BiTE®) immune-oncology therapy AMG 757 has potent antitumor activity in neuroendocrine cancer." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (November 2020): A663. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0627.

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BackgroundNeuroendocrine tumors (NET), including small cell lung cancer (SCLC), have poor prognosis and limited therapeutic options. AMG 757 is an HLE BiTE® immune therapy designed to redirect T cell cytotoxicity to NET cells by binding to Delta-like ligand 3 (DLL3) expressed on the tumor cell surface and CD3 on T cells.MethodsWe evaluated activity of AMG 757 in NET cells in vitro and in mouse models of neuroendocrine cancer in vivo. In vitro, co-cultures of NET cells and human T cells were treated with AMG 757 in a concentration range and T cell activation, cytokine production, and tumor cell killing were assessed. In vivo, AMG 757 antitumor efficacy was evaluated in xenograft NET and in orthotopic models designed to mimic primary and metastatic SCLC lesions. NSG mice bearing established NET were administered human T cells and then treated once weekly with AMG 757 or control HLE BiTE molecule; tumor growth inhibition was assessed. Pharmacodynamic effects of AMG 757 in tumors were also evaluated in SCLC models following a single administration of human T cells and AMG 757 or control HLE BiTE molecule.ResultsAMG 757 induced T cell activation, cytokine production, and potent T cell redirected killing of DLL3-expressing SCLC, neuroendocrine prostate cancer, and other DLL3-expressing NET cell lines in vitro. AMG 757-mediated redirected lysis was specific for DLL3-expressing cells. In patient-derived xenograft and orthotopic models of SCLC, single-dose AMG 757 effectively engaged human T cells administered systemically, leading to a significant increase in the number of human CD4+ and CD8+ T cells in primary and metastatic tumor lesions. Weekly administration of AMG 757 induced significant tumor growth inhibition of SCLC (figure 1) and other NET, including complete regression of established tumors and clearance of metastatic lesions. These findings warranted evaluation of AMG 757 (NCT03319940); the phase 1 study includes dose exploration (monotherapy and in combination with pembrolizumab) and dose expansion (monotherapy) in patients with SCLC (figure 2). A study of AMG 757 in patients with neuroendocrine prostate cancer is under development based on emerging data from the ongoing phase 1 study.Abstract 627 Figure 1AMG 757 Significantly reduced tumor growth in orthotopic SCLC mouse modelsAbstract 627 Figure 2AMG 757 Phase 1 study designConclusionsAMG 757 engages and activates T cells to kill DLL3-expressing SCLC and other NET cells in vitro and induces significant antitumor activity against established xenograft tumors in mouse models. These preclinical data support evaluation of AMG 757 in clinical studies of patients with NET.Ethics ApprovalAll in vivo work was conducted under IACUC-approved protocol #2009-00046.
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McInturff, Alison M., Mark J. Cody, Elizabeth A. Elliott, Jared W. Glenn, Jesse W. Rowley, Matthew T. Rondina, and Christian C. Yost. "Mammalian target of rapamycin regulates neutrophil extracellular trap formation via induction of hypoxia-inducible factor 1 α." Blood 120, no. 15 (October 11, 2012): 3118–25. http://dx.doi.org/10.1182/blood-2012-01-405993.

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Abstract Neutrophils are highly specialized innate immune effector cells that evolved for antimicrobial host defense. In response to inflammatory stimuli and pathogens, they form neutrophil extracellular traps (NETs), which capture and kill extracellular microbes. Deficient NET formation predisposes humans to severe infection, but, paradoxically, dysregulated NET formation contributes to inflammatory vascular injury and tissue damage. The molecular pathways and signaling mechanisms that control NET formation remain largely uncharacterized. Using primary human neutrophils and genetically manipulated myeloid leukocytes differentiated to surrogate neutrophils, we found that mammalian target of rapamycin (mTOR) regulates NET formation by posttranscriptional control of expression of hypoxia-inducible factor 1 α (HIF-1α), a critical modulator of antimicrobial defenses. Next-generation RNA sequencing, assays of mRNA and protein expression, and analysis of NET deployment by live cell imaging and quantitative histone release showed that mTOR controls NET formation and translation of HIF-1α mRNA in response to lipopolysaccharide. Pharmacologic and genetic knockdown of HIF-1α expression and activity inhibited NET deployment, and inhibition of mTOR and HIF-1α inhibited NET-mediated extracellular bacterial killing. Our studies define a pathway to NET formation involving 2 master regulators of immune cell function and identify potential points of molecular intervention in strategies to modify NETs in disease.
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42

Finegood, D. T., M. D. McArthur, D. Kojwang, M. J. Thomas, B. G. Topp, T. Leonard, and R. E. Buckingham. "-Cell Mass Dynamics in Zucker Diabetic Fatty Rats: Rosiglitazone Prevents the Rise in Net Cell Death." Diabetes 50, no. 5 (May 1, 2001): 1021–29. http://dx.doi.org/10.2337/diabetes.50.5.1021.

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43

Ahn, Mi-Hyun, Jae Ho Han, Young-Jun Chwae, Ju-Yang Jung, Chang-Hee Suh, Ji Eun Kwon, and Hyoun-Ah Kim. "Neutrophil Extracellular Traps May Contribute to the Pathogenesis in Adult-onset Still Disease." Journal of Rheumatology 46, no. 12 (May 1, 2019): 1560–69. http://dx.doi.org/10.3899/jrheum.181058.

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Objective.Release of neutrophil extracellular traps (NET) has been described as an effector mechanism of polymorphonuclear neutrophils in several inflammatory diseases. Thus, this study was performed to evaluate the role of NET in the pathogenesis of adult-onset Still disease (AOSD).Methods.We determined the serum levels of NET molecules and investigated their associations with clinical disease activities in patients with AOSD. Further, we analyzed the differences in the NETosis response in AOSD patients compared to healthy controls (HC). To explore the in vivo involvement of NET in AOSD, we performed immunohistochemical analysis of skin and lymph node (LN) biopsies for proteins related to NET in patients with active AOSD.Results.Serum levels of cell-free DNA, myeloperoxidase (MPO)-DNA complex, and α-defensin were significantly increased in patients with AOSD compared to HC. Serum levels of the NET molecules, cell-free DNA, MPO-DNA, and α-defensin were correlated with several disease activity markers for AOSD. In followup of patients with AOSD after treatment with corticosteroid, the levels of cell-free DNA and α-defensin decreased significantly. On immunohistochemistry, neutrophil elastase–positive and MPO-positive inflammatory cells were detected in skin and LN of patients with AOSD, and were expressed in fiber form in the lesions. The serum from patients with active AOSD induced NETosis in neutrophils from HC. NET molecules induced interleukin 1β production in monocytes, representing a novel mechanism in the pathogenesis of AOSD.Conclusion.The findings presented here suggest that NET may contribute to the inflammatory response and pathogenesis in AOSD.
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Lemus, Ana E., Juana Enríquez, Ángeles Hernández, René Santillán, and Gregorio Pérez-Palacios. "Bioconversion of norethisterone, a progesterone receptor agonist into estrogen receptor agonists in osteoblastic cells." Journal of Endocrinology 200, no. 2 (November 10, 2008): 199–206. http://dx.doi.org/10.1677/joe-08-0166.

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A number of clinical studies have demonstrated that norethisterone (NET), a potent synthetic progestin, restores postmenopausal bone loss, although its mode of action on bone cells is not fully understood, while the effect of naturally occurring progesterone in bone has remained controversial. A recent report claims that the potent effects of NET on osteoblastic cell proliferation and differentiation, mimicking the action of estrogens, are mediated by non-phenolic NET derivatives. To determine whether osteoblasts possess the enzymes required to bioconvert a progesterone receptor (PR) agonist into A-ring reduced metabolites with affinity to bind estrogen receptor (ER), we studied the in vitro metabolism of [3H]-labeled NET in cultured neonatal rat osteoblasts and the interaction of its metabolic conversion products with cytosolic –osteoblast ER, employing a competition analysis. Results indicated that NET was extensively bioconverted (36.4%) to 5α-reduced metabolites, including 5α-dihydro NET, 3α,5α-tetrahydro NET (3α,5α-NET) and 3β,5α-tetrahydro NET (3β,5α-NET), demonstrating the activities of 5α-steroid reductase and two enzymes of the aldo-keto reductases family. Expression of Srd5a1 in neonatal osteoblast was well demonstrated, whereas Srd5a2 expression was not detected. The most striking finding was that 3β,5α-NET and 3α,5α-NET were efficient competitors of [3H]-estradiol for osteoblast ER binding sites, exhibiting affinities similar to that of estradiol. The results support the concept that the interplay of 5α-steroid reductase and aldo-keto reductases in osteoblastic cells, acting as an intracrine modulator system is capable to bioconvert a PR agonist into ER agonists, offering an explanation of the molecular mechanisms NET uses to enhance osteoblastic cell activities.
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45

Gillette, Amani A., Christopher P. Babiarz, Ava R. VanDommelen, Cheri A. Pasch, Linda Clipson, Kristina A. Matkowskyj, Dustin A. Deming, and Melissa C. Skala. "Autofluorescence Imaging of Treatment Response in Neuroendocrine Tumor Organoids." Cancers 13, no. 8 (April 14, 2021): 1873. http://dx.doi.org/10.3390/cancers13081873.

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Gastroenteropancreatic neuroendocrine tumors (GEP-NET) account for roughly 60% of all neuroendocrine tumors. Low/intermediate grade human GEP-NETs have relatively low proliferation rates that animal models and cell lines fail to recapitulate. Short-term patient-derived cancer organoids (PDCOs) are a 3D model system that holds great promise for recapitulating well-differentiated human GEP-NETs. However, traditional measurements of drug response (i.e., growth, proliferation) are not effective in GEP-NET PDCOs due to the small volume of tissue and low proliferation rates that are characteristic of the disease. Here, we test a label-free, non-destructive optical metabolic imaging (OMI) method to measure drug response in live GEP-NET PDCOs. OMI captures the fluorescence lifetime and intensity of endogenous metabolic cofactors NAD(P)H and FAD. OMI has previously provided accurate predictions of drug response on a single cell level in other cancer types, but this is the first study to apply OMI to GEP-NETs. OMI tested the response to novel drug combination on GEP-NET PDCOs, specifically ABT263 (navitoclax), a Bcl-2 family inhibitor, and everolimus, a standard GEP-NET treatment that inhibits mTOR. Treatment response to ABT263, everolimus, and the combination were tested in GEP-NET PDCO lines derived from seven patients, using two-photon OMI. OMI measured a response to the combination treatment in 5 PDCO lines, at 72 h post-treatment. In one of the non-responsive PDCO lines, heterogeneous response was identified with two distinct subpopulations of cell metabolism. Overall, this work shows that OMI provides single-cell metabolic measurements of drug response in PDCOs to guide drug development for GEP-NET patients.
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46

D’Cruz, Akshay A., Mary Speir, Meghan Bliss-Moreau, Sylvia Dietrich, Shu Wang, Alyce A. Chen, Mathilde Gavillet, et al. "The pseudokinase MLKL activates PAD4-dependent NET formation in necroptotic neutrophils." Science Signaling 11, no. 546 (September 4, 2018): eaao1716. http://dx.doi.org/10.1126/scisignal.aao1716.

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Neutrophil extracellular trap (NET) formation can generate short-term, functional anucleate cytoplasts and trigger loss of cell viability. We demonstrated that the necroptotic cell death effector mixed lineage kinase domain–like (MLKL) translocated from the cytoplasm to the plasma membrane and stimulated downstream NADPH oxidase–independent ROS production, loss of cytoplasmic granules, breakdown of the nuclear membrane, chromatin decondensation, histone hypercitrullination, and extrusion of bacteriostatic NETs. This process was coordinated by receptor-interacting protein kinase-1 (RIPK1), which activated the caspase-8–dependent apoptotic or RIPK3/MLKL-dependent necroptotic death of mouse and human neutrophils. Genetic deficiency of RIPK3 and MLKL prevented NET formation but did not prevent cell death, which was because of residual caspase-8–dependent activity. Peptidylarginine deiminase 4 (PAD4) was activated downstream of RIPK1/RIPK3/MLKL and was required for maximal histone hypercitrullination and NET extrusion. This work defines a distinct signaling network that activates PAD4-dependent NET release for the control of methicillin-resistant Staphylococcus aureus (MRSA) infection.
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47

Nakade, Koji, Hong Zheng, Gitali Ganguli, Gilles Buchwalter, Christian Gross, and Bohdan Wasylyk. "The Tumor Suppressor p53 Inhibits Net, an Effector of Ras/Extracellular Signal-Regulated Kinase Signaling." Molecular and Cellular Biology 24, no. 3 (February 1, 2004): 1132–42. http://dx.doi.org/10.1128/mcb.24.3.1132-1142.2004.

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ABSTRACT The tumor suppressor function of p53 is linked to its ability to repress gene expression, but the mechanisms of specific gene repression are poorly understood. We report that wild-type p53 inhibits an effector of the Ras oncogene/mitogen-activated protein (MAP) kinase pathway, the transcription factor Net. Tumor-associated mutant p53s are less efficient inhibitors. p53 inhibits by preventing phosphorylation of Net by MAP kinases. Loss of p53 in vivo leads to increased Net phosphorylation in response to wound healing and UV irradiation of skin. Our results show that p53 can repress specific gene expression by inhibiting Net, a factor implicated in cell cycle entry.
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Yang, Yang, Xiaoxia Sun, Mingliang Zhu, Xuan Luo, and Shan Zheng. "Estimating the carbon biomass of marine net phytoplankton from abundance based on samples from China seas." Marine and Freshwater Research 68, no. 1 (2017): 106. http://dx.doi.org/10.1071/mf15298.

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The relationship between carbon biomass and cell abundance in net phytoplankton was determined to improve standing stock research in marine ecology. Based on samples from six cruises in the Yellow Sea and the East China Sea, significant regression equations for all net phytoplankton cells, diatoms, dinoflagellates and each dominant genus were obtained. The relationships could be described by the equation log10y=k×log10x+b, where x represents cell abundance based on cell counts (cells m–3), y represents carbon biomass (μgCm–3), and k and b are constants. The values of k and b were 0.48 and 0.49 respectively for total net phytoplankton, 0.75 and –1.46 respectively for diatoms in summer, 0.54 and –0.11 respectively for diatoms in spring and autumn, and 0.92 and –0.90 respectively for dinoflagellates. Regression equations for Chaetoceros, Coscinodiscus, Pseudo-nitzschia, Skeletonema, Ceratium, Protoperidinium and Pyrophacus were also obtained. We suggest using these carbon biomass:cell abundance relationships established for net phytoplankton to assess phytoplankton standing stocks and for reanalysing historical data.
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Wollmann, T., M. Gunkel, I. Chung, H. Erfle, K. Rippe, and K. Rohr. "GRUU-Net: Integrated convolutional and gated recurrent neural network for cell segmentation." Medical Image Analysis 56 (August 2019): 68–79. http://dx.doi.org/10.1016/j.media.2019.04.011.

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50

Lucas, Madhuri, and Theodore Mazzone. "Cell Surface Proteoglycans Modulate Net Synthesis and Secretion of Macrophage Apolipoprotein E." Journal of Biological Chemistry 271, no. 23 (June 7, 1996): 13454–60. http://dx.doi.org/10.1074/jbc.271.23.13454.

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