Статті в журналах: "Max"

1

Perkinson, Robert. "Mad Max." Punishment & Society 8, no. 1 (January 2006): 125–30. http://dx.doi.org/10.1177/1462474506059146.

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2

Malec, Bogusz. "Utopian Thinking in "Mad Max: Fury Road"." Annales Universitatis Mariae Curie-Sklodowska, sectio FF, Philologia 34, no. 2 (January 9, 2017): 137. http://dx.doi.org/10.17951/ff.2016.34.137.

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3

Malec, Bogusz. "Utopian Thinking in "Mad Max: Fury Road"." Annales Universitatis Mariae Curie-Sklodowska, sectio FF, Philologia 34, no. 2 (January 9, 2017): 137. http://dx.doi.org/10.17951/ff.2016.34.2.137.

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4

Andelman, David A. "Mad Max Redux." World Policy Journal 26, no. 1 (2009): 105–12. http://dx.doi.org/10.1162/wopj.2009.26.1.105.

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5

Lee, Haram. "Anthropocene Time in Max Frisch’s Man in the Holocene." Journal of English Studies in Korea 42 (June 15, 2022): 5–43. http://dx.doi.org/10.46562/jesk.42.1.

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6

Baydar, Gökçe. "Potential of Feminist Action Film: On Mad Max Fury Road." Moment Journal 2, no. 2 (December 15, 2015): 104–34. http://dx.doi.org/10.17572/mj2015.2.104134.

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7

Sharrett, Christopher. ": Mad Max beyond Thunderdome ." Film Quarterly 40, no. 3 (April 1987): 59. http://dx.doi.org/10.1525/fq.1987.40.3.04a00190.

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8

Sharrett, Christopher. "Mad Max beyond Thunderdome." Film Quarterly 40, no. 3 (April 1987): 59. http://dx.doi.org/10.2307/1212474.

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9

Hay, John. "The American Mad Max." Science Fiction Film & Television 10, no. 3 (October 2017): 307–27. http://dx.doi.org/10.3828/sfftv.2017.22.

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10

Kvyetnyy, R. N., S. G. Krivogubchenko, and Yu Yu Ivanov. "HARDWARE IMPLEMENTATION AND EXPERIMENTAL RESEARCHES OF MAX-LOG-MAP TURBO-DECODER." Information Technology And Computer Engineering 43, no. 3 (2018): 48–53. http://dx.doi.org/10.31649/1999-9941-2018-43-3-48-53.

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11

Nair, Satish K., and Stephen K. Burley. "X-Ray Structures of Myc-Max and Mad-Max Recognizing DNA." Cell 112, no. 2 (January 2003): 193–205. http://dx.doi.org/10.1016/s0092-8674(02)01284-9.

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12

Loo, K. K., K. Salman, T. Alukaidey, and S. A. Jimaa. "Parallelised max-Log-Map model." Electronics Letters 38, no. 17 (2002): 971. http://dx.doi.org/10.1049/el:20020663.

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13

Baudino, Troy A., and John L. Cleveland. "The Max Network Gone Mad." Molecular and Cellular Biology 21, no. 3 (February 1, 2001): 691–702. http://dx.doi.org/10.1128/mcb.21.3.691-702.2001.

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14

Urry, John. "Medieval worlds and Mad Max." postmedieval: a journal of medieval cultural studies 4, no. 2 (June 2013): 233–37. http://dx.doi.org/10.1057/pmed.2013.6.

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15

Scaff, Lawrence A. "Max Weber's Legacy." Annual review of sociology 2015, no. 28 (2015): 18–27. http://dx.doi.org/10.5690/kantoh.2015.18.

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16

Faiola, Francesco, Yi-Ting Wu, Songqin Pan, Kangling Zhang, Anthony Farina, and Ernest Martinez. "Max is acetylated by p300 at several nuclear localization residues." Biochemical Journal 403, no. 3 (April 12, 2007): 397–407. http://dx.doi.org/10.1042/bj20061593.

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Max is a ubiquitous transcription factor with a bHLHZip [basic HLH (helix–loop–helix) leucine zipper] DNA-binding/dimerization domain and the central component of the Myc/Max/Mad transcription factor network that controls cell growth, proliferation, differentiation and apoptotic cell death in metazoans. Max is the obligatory DNA-binding and dimerization partner for all the bHLHZip regulators of the Myc/Max/Mad network, including the Myc family of oncoproteins and the Mad family of Myc antagonists, which recognize E-box DNA elements in the regulatory regions of target genes. Max lacks a transcription regulatory domain and is the only member of the network that efficiently homodimerizes. Binding of Max homodimers to E-box elements suppresses the transcription regulatory functions of its network partners and of other non-network E-box-binding regulators. In contrast with its highly regulated partners, Max is a constitutively expressed and phosphorylated protein. Phosphorylation is, however, the only Max post-translational modification identified so far. In the present study, we have analysed Max posttranslational modifications by MS. We have found that Max is acetylated at several lysine residues (Lys-57, Lys-144 and Lys-145) in mammalian cells. Max acetylation is stimulated by inhibitors of histone deacetylases and by overexpression of the p300 co-activator/HAT (histone acetyltransferase). The p300 HAT also directly acetylates Max in vitro at these three residues. Interestingly, the three Max residues acetylated in vivo and in vitro by p300 are important for Max nuclear localization and Max-mediated suppression of Myc transactivation. These results uncover novel post-translational modifications of Max and suggest the potential regulation of specific Max complexes by p300 and reversible acetylation.

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17

KRIPPNER-HEIDENREICH, Anja, Robert V. TALANIAN, Renate SEKUL, Regine KRAFT, Hubert THOLE, Holger OTTLEBEN, and Bernhard LÜSCHER. "Targeting of the transcription factor Max during apoptosis: phosphorylation-regulated cleavage by caspase-5 at an unusual glutamic acid residue in position P1." Biochemical Journal 358, no. 3 (September 10, 2001): 705–15. http://dx.doi.org/10.1042/bj3580705.

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Max is the central component of the Myc/Max/Mad network of transcription factors that regulate growth, differentiation and apoptosis. Whereas the Myc and Mad genes and proteins are highly regulated, Max expression is constitutive and no post-translational regulation is known. We have found that Max is targeted during Fas-induced apoptosis. Max is first dephosphorylated and subsequently cleaved by caspases. Two specific cleavage sites for caspases in Max were identified, one at IEVE10↓S and one at SAFD135↓G near the C-terminus, which are cleaved in vitro by caspase-5 and caspase-7 respectively. Mutational analysis indicates that both sites are also used in vivo. Thus Max represents the first caspase-5 substrate. The unusual cleavage after a glutamic acid residue is observed only with full-length, DNA-binding competent Max protein but not with corresponding peptides, suggesting that structural determinants might be important for this activity. Furthermore, cleavage by caspase-5 is inhibited by the protein kinase CK2-mediated phosphorylation of Max at Ser-11, a previously mapped phosphorylation site in vivo. These findings suggest that Fas-mediated dephosphorylation of Max is required for cleavage by caspase-5. The modifications that occur on Max in response to Fas signalling affect the DNA-binding activity of Max/Max homodimers. Taken together, our findings uncover three distinct processes, namely dephosphorylation and cleavage by caspase-5 and caspase-7, that target Max during Fas-mediated apoptosis, suggesting the regulation of the Myc/Max/Mad network through its central component.

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18

Grinberg, Asya V., Chang-Deng Hu, and Tom K. Kerppola. "Visualization of Myc/Max/Mad Family Dimers and the Competition for Dimerization in Living Cells." Molecular and Cellular Biology 24, no. 10 (May 15, 2004): 4294–308. http://dx.doi.org/10.1128/mcb.24.10.4294-4308.2004.

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ABSTRACT Myc and Mad family proteins play opposing roles in the control of cell growth and proliferation. We have visualized the subcellular locations of complexes formed by Myc/Max/Mad family proteins using bimolecular fluorescence complementation (BiFC) analysis. Max was recruited to different subnuclear locations by interactions with Myc versus Mad family members. Complexes formed by Max with Mxi1, Mad3, or Mad4 were enriched in nuclear foci, whereas complexes formed with Myc were more uniformly distributed in the nucleoplasm. Mad4 was localized to the cytoplasm when it was expressed separately, and Mad4 was recruited to the nucleus through dimerization with Max. The cytoplasmic localization of Mad4 was determined by a CRM1-dependent nuclear export signal located near the amino terminus. We compared the relative efficiencies of complex formation among Myc, Max, and Mad family proteins in living cells using multicolor BiFC analysis. Max formed heterodimers with the basic helix-loop-helix leucine zipper (bHLHZIP) domain of Myc (bMyc) more efficiently than it formed homodimers. Replacement of two amino acid residues in the leucine zipper of Max reversed the relative efficiencies of homo- and heterodimerization in cells. Surprisingly, Mad3 formed complexes with Max less efficiently than bMyc, whereas Mad4 formed complexes with Max more efficiently than bMyc. The distinct subcellular locations and the differences between the efficiencies of dimerization with Max indicate that Mad3 and Mad4 are likely to modulate transcription activation by Myc at least in part through distinct mechanisms.

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19

Xiang, Yueming. "MAX-INJECTIVE, MAX-FLAT MODULES AND MAX-COHERENT RINGS." Bulletin of the Korean Mathematical Society 47, no. 3 (May 31, 2010): 611–22. http://dx.doi.org/10.4134/bkms.2010.47.3.611.

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20

Loužek, Marek. "Max Weber - an economist." Politická ekonomie 55, no. 1 (February 1, 2007): 91–105. http://dx.doi.org/10.18267/j.polek.592.

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21

Sarikakis, Katharine, and Francisco Seoane Pérez. "Media theory for Mad Max times." International Journal of Media & Cultural Politics 10, no. 2 (June 1, 2014): 125–28. http://dx.doi.org/10.1386/macp.10.2.125_2.

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22

Gordya, Andressa. "Mad Max e a feminilidade ativa." Ciência e Cultura 69, no. 1 (March 2017): 60–62. http://dx.doi.org/10.21800/2317-66602017000100020.

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23

Cohen, Charles Lloyd. "Mad Max (Weber) in New England." Reviews in American History 25, no. 1 (1997): 19–24. http://dx.doi.org/10.1353/rah.1997.0008.

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24

Hassler-Forest, Dan. "Mad Max: between apocalypse and utopia." Science Fiction Film & Television 10, no. 3 (October 2017): 301–6. http://dx.doi.org/10.3828/sfftv.2017.21.

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25

KRAUSE, Stefan W., Michael REHLI, Sven HEINZ, Reinhard EBNER, and Reinhard ANDREESEN. "Characterization of MAX.3 antigen, a glycoprotein expressed on mature macrophages, dendritic cells and blood platelets: identity with CD84." Biochemical Journal 346, no. 3 (March 7, 2000): 729–36. http://dx.doi.org/10.1042/bj3460729.

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MAX.3 is a monoclonal antibody that preferentially reacts with mature macrophages (MAC), monocyte-derived dendritic cells, megakaryocytes and platelets. In this study, we describe the characterization, purification and identification of the MAX.3 antigen. Immunoprecipitation and SDS/PAGE revealed different molecular masses of MAX.3 antigen in MAC (60-90 kDa) and platelets (58-64 kDa), whereas a similar size (45 kDa) was observed in both cell types after digestion with N-glycosidase F. Lectin affinity and sequential treatment with different glycosidases suggests complex type glycosylation of MAX.3 antigen in MAC and hybrid type glycosylation in platelets. Amino acid sequencing led to the identification of a corresponding cDNA clone and showed its identity to the sequence of the CD84 antigen, a member of the CD2 family of cell surface molecules. MAX.3/CD84 was further studied by immunohistochemistry and a variable expression was found on tissue MAC, confirming this antigen to be mainly a marker for MAC in situ.

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26

El Ghina, Miftah Fathi, Widawati Widawati, and Rizki Rahmawati Lestari. "Asupan Energi, Protein, Status Gizi, dan VO2 Max Atlet Futsal MAN 1 Pekanbaru." Jurnal Ilmu Gizi dan Dietetik 2, no. 3 (October 1, 2023): 175–81. http://dx.doi.org/10.25182/jigd.2023.2.3.175-181.

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Tujuan penelitian adalah menganalisis hubungan asupan gizi dan VO2 max atlet futsal MAN 1 Pekanbaru. Jenis penelitian ini adalah kuantitatif pendekatan analitik dengan desain penelitian cross sectional. Penelitian ini dilakukan di MAN 1 Pekanbaru pada 8-12 Maret 2023 dengan jumlah subjek 40 atlet diperoleh dengan teknik total sampling. Data asupan gizi diperoleh melalui wawancara food recall 2x24 jam, data status gizi diperoleh melalui pengukuran tinggi dan berat badan, data VO2 max diperoleh menggunakan metode Multystage Fitness Test (MFT). Analisa yang digunakan adalah univariat dan bivariat dengan uji Chi Square dan Fisher’s Exact Test. Hasil analisa univariat diperoleh 34 atlet (85%) asupan energi baik, 27 atlet (67,5%) asupan protein baik, 29 atlet (72,5%) status gizi baik dan 17 atlet (42,5%) VO2 max baik. Hasil analisa bivariat tidak terdapat hubungan antara asupan energi (p=0,17) dengan VO2 max, ada hubungan antara asupan protein (p=0,006) dan status gizi (p=0,009) dengan VO2 max atlet. Kesimpulan tidak terdapat hubungan antara asupan energi dengan VO2 max dan terdapat hubungan yang signifikan antara asupan protein dan status gizi dengan VO2 max atlet futsal MAN 1 Pekanbaru. Diharapkan kepada atlet selalu mengonsumsi cemilan sehat tinggi energi serta protein dan mampu memenuhi kebutuhan harian atlet untuk mencapai status gizi normal, meningkatkan intensitas latihan, untuk mencapai VO2 max yang maksimal.

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27

Ichinokawa, Yasutaka. "Max Weber in Japan." Annual review of sociology 2015, no. 28 (2015): 28–34. http://dx.doi.org/10.5690/kantoh.2015.28.

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28

Sanders, Jennifer A., and Philip A. Gruppuso. "Coordinated regulation of c-Myc and Max in rat liver development." American Journal of Physiology-Gastrointestinal and Liver Physiology 290, no. 1 (January 2006): G145—G155. http://dx.doi.org/10.1152/ajpgi.00545.2004.

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The processes of liver development and regeneration involve regulation of a key network of transcription factors, the c -myc/ max/ mad network. This network regulates the expression of genes involved in hepatocyte proliferation, growth, metabolism, and differentiation. In previous studies on the expression and localization of c-Myc in the fetal and adult liver, we made the unexpected observation that c-Myc content was similar in the two. However, c-Myc was localized predominantly to the nucleolus in the adult liver. On the basis of this finding, we went on to characterize the expression patterns of the other members of the network, max and mad, comparing their regulation during late fetal development with the proliferation of mature hepatocytes that is seen in liver regeneration. We found that Max content, rather than being constitutive, as predicted by other studies, was elevated in the fetal liver compared with the adult liver. Its content correlated with hepatocyte proliferation during the perinatal transition. In contrast, mad4 expression was decreased in the fetal liver compared with the adult liver. Nucleolar localization of c-Myc coincided with changes in Max content. To explore this relationship, we overexpressed Max in cultured adult hepatocytes. High levels of Max resulted in a shift in c-Myc localization from nucleolar to diffuse nuclear. In contrast, liver regeneration was associated with an increase in c-Myc content but no change in Max content. We conclude that the regulation of Max content during liver development and its potential role in determining c-Myc localization are means by which Max may control the biological activity of the c-Myc/Max/Mad network during liver development.

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29

Herman, Herman, and Muhammad Akbar Syafruddin. "Perbandingan Pengaruh Latihan Fartlek Dengan Latihan Sirkuit Training Terhadap Kapasitas Kerja Maksimal VO2 Max Pada Siswa MAN 1 Makassar." Jendela Olahraga 6, no. 1 (January 12, 2021): 139–49. http://dx.doi.org/10.26877/jo.v6i1.6933.

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This research is a descriptive study to determine (1) the effect of fartlek training on maximal working capacity of VO2 Max in MAN 1 Makassar (2) to determine the circuit training exercise on maximal working capacity of VO2 Max in MAN 1 Makassar (3) to determine differences in the effect of fartlek training with circuit training exercise on maximal working capacity of VO2 Max in MAN 2 Makassar. Population in this study were all students of MAN 1 Makassar while the sample in this study 40 students of class XI were taken by random sampling. The results of this study were (1) the data maximal work capacity (VO2max) through the end of the exercise test farlek obtained an average value of 40,872, a standard deviation of 5.6633, 29.8 minimum value, maximum value of 50.8, and 1634.9 total value of 35 samples (2) Data maximal work capacity (VO2max) obtained an average value of 44.562, a standard deviation of 21.575, 35.4 minimum value, maximum value of 52.2, and 1782.5 total value of 35 samples. Keywords: Effect of exercise training; Fartlek Training; circuit training; VO2Max.Abstrak Jenis penelitian ini adalah penelitian diskriptif untuk mengetahui (1) pengaruh latihan fartlek terhadap kapasitas kerja maksimal VO2 Max pada siswa MAN 1 Makassar (2) untuk mengetahui latihan circuit training terhadap kapasitas kerja maksimal VO2 Max pada siswa MAN 1 Makassar (3) untuk mengetahui perbedaan pengaruh latihan fartlek dengan latihan circuit training terhadap kapasitas kerja maksimal VO2 Max pada siswa MAN 1 Makassar. Populasi dalam penelitian ini adalah seluruh Siswa MAN 1 Makassar sedangkan sampel dalam penelitian ini 40 siswa kelas XI diambil dengan secara random sampling. Hasil penelitian ini adalah 1. Ada pengaruh yang signifikan latihan parlek terhadap kemampuan kerja maksimal (V O2 Max) (P < 0,05), 2. Ada pengaruh yang siknifikan latihan sirkuit terhadap kemampuan kerja maksimal (V O2 Max) (P < 0,05), 3. Ada perbedaan signifikan latihan parlek dan latihan sirkuit, dan 4. Latihan sirkuit lebih baik meningkatkan kemampuan kerja maksimal daripada latihan parlek (P < 0,05). Kata kunci: Pengaruh latihan; latihan fartlek; latihan circuit; VO 2Max

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30

Cultraro, C. M., T. Bino, and S. Segal. "Function of the c-Myc antagonist Mad1 during a molecular switch from proliferation to differentiation." Molecular and Cellular Biology 17, no. 5 (May 1997): 2353–59. http://dx.doi.org/10.1128/mcb.17.5.2353.

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Mad-Max heterodimers have been shown to antagonize Myc transforming activity by a mechanism requiring multiple protein-protein and protein-DNA interactions. However, the mechanism by which Mad functions in differentiation is unknown. Here, we present evidence that Mad functions by an active repression mechanism to antagonize the growth-promoting function(s) of Myc and bring about a transition from cellular proliferation to differentiation. We demonstrate that exogenously expressed c-Myc blocks inducer-mediated differentiation of murine erythroleukemia cells without disrupting the induction of endogenous Mad; rather, high levels of c-Myc prevent a heterocomplex switch from growth-promoting Myc-Max to growth-inhibitory Mad-Max. Cotransfection of a constitutive c-myc with a zinc-inducible mad1 results in clones expressing both genes, whereby a switch from proliferation to differentiation can be modulated. Whereas cells grown in N'N'-hexamethylene bisacetamide in the absence of zinc fail to differentiate, addition of zinc up-regulates Mad expression by severalfold and differentiation proceeds normally. Coimmunoprecipitation analysis reveals that Mad-Max complexes are in excess of Myc-Max in these cotransfectants. Moreover, we show that the Sin-binding, basic region, and leucine zipper motifs are required for Mad to function during a molecular switch from proliferation to differentiation.

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31

Ockert, Jason. "Max." Iowa Review 41, no. 1 (April 2011): 140–56. http://dx.doi.org/10.17077/0021-065x.7003.

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32

Capdvila, Max. "Max." Periferica, no. 20 (2019): 8–9. http://dx.doi.org/10.25267/periferica.2019.i20.02.

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33

Hunter, Wendy L. M., Victor C. Strasburger, David M. Snyder, and Martin T. Stein. "Max." Journal of Developmental & Behavioral Pediatrics 27, no. 6 (December 2006): 488–92. http://dx.doi.org/10.1097/00004703-200612000-00007.

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34

Kuokka, Daniel R. "MAX." ACM SIGART Bulletin 2, no. 4 (July 1991): 93–97. http://dx.doi.org/10.1145/122344.122363.

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35

Yap, Kok-KIONG, Vikram Srinivasan, and Mehul Motani. "MAX." ACM Transactions on Sensor Networks 4, no. 4 (August 2008): 1–34. http://dx.doi.org/10.1145/1387663.1387672.

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36

Litwin, Mark S. "Max." JAMA: The Journal of the American Medical Association 257, no. 16 (April 24, 1987): 2210. http://dx.doi.org/10.1001/jama.1987.03390160096036.

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37

King, Roy D., and Sandra L. Resodihardjo. "To max or not to max." Punishment & Society 12, no. 1 (December 17, 2009): 65–84. http://dx.doi.org/10.1177/1462474509349010.

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38

Farhangi, Hadi, Dincer Konur, and Cihan H. Dagli. "Combining Max-min and Max-max Approaches for Robust SoS Architecting." Procedia Computer Science 95 (2016): 103–10. http://dx.doi.org/10.1016/j.procs.2016.09.299.

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39

Zhang, Qiqiang, Yanchun Zhou, Xingyuan San, Wenbo Li, Yiwang Bao, Qingguo Feng, Salvatore Grasso, and Chunfeng Hu. "Zr2SeB and Hf2SeB: Two new MAB phase compounds with the Cr2AlC-type MAX phase (211 phase) crystal structures." Journal of Advanced Ceramics 11, no. 11 (November 2022): 1764–76. http://dx.doi.org/10.1007/s40145-022-0646-7.

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AbstractThe ternary or quaternary layered compounds called MAB phases are frequently mentioned recently together with the well-known MAX phases. However, MAB phases are generally referred to layered transition metal borides, while MAX phases are layered transition metal carbides and nitrides with different types of crystal structure although they share the common nano-laminated structure characteristics. In order to prove that MAB phases can share the same type of crystal structure with MAX phases and extend the composition window of MAX phases from carbides and nitrides to borides, two new MAB phase compounds Zr2SeB and Hf2SeB with the Cr2AlC-type MAX phase (211 phase) crystal structure were discovered by a combination of first-principles calculations and experimental verification in this work. First-principles calculations predicted the stability and lattice parameters of the two new MAB phase compounds Zr2SeB and Hf2SeB. Then they were successfully synthesized by using a thermal explosion method in a spark plasma sintering (SPS) furnace. The crystal structures of Zr2SeB and Hf2SeB were determined by a combination of the X-ray diffraction (XRD), scanning electron microscopy (SEM), and high-resolution transmission electron microscopy (HRTEM). The lattice parameters of Zr2SeB and Hf2SeB are a = 3.64398 Å, c = 12.63223 Å and a = 3.52280 Å, c = 12.47804 Å, respectively. And the atomic positions are M at 4f (1/3, 2/3, 0.60288 [Zr] or 0.59889 [Hf]), Se at 2c (1/3, 2/3, 1/4), and B at 2a (0, 0, 0). And the atomic stacking sequences follow those of the Cr2AlC-type MAX phases. This work opens up the composition window for the MAB phases and MAX phases and will trigger the interests of material scientists and physicists to explore new compounds and properties in this new family of materials.

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40

Hopewell, R., and E. B. Ziff. "The nerve growth factor-responsive PC12 cell line does not express the Myc dimerization partner Max." Molecular and Cellular Biology 15, no. 7 (July 1995): 3470–78. http://dx.doi.org/10.1128/mcb.15.7.3470.

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Heterodimerization of Max with the nuclear oncoprotein Myc and the differentiation-associated proteins Mad and Mxi1 enables these factors to bind E-box sites in DNA and control genes implicated in cell proliferation and differentiation. We show that in the PC12 pheochromocytoma tumor cell line, functional Max protein is not expressed because of the synthesis of a mutant max transcript. This transcript encodes a protein incapable of homo- or heterodimerization. Furthermore, the mutant Max protein, unlike wild-type Max, is incapable of repressing transcription from an E-box element. Synthesis of mutant max transcripts appears to be due to a homozygous chromosomal alteration within the max gene. Reintroduction of max into PC12 cells results in repression of E-box-dependent transcription and a reduction in growth rate, which may explain the loss of Max expression either during the growth of the pheochromocytoma or in subsequent passage of the PC12 cell line in vitro. Finally, the ability of these cells to divide, differentiate, and apoptose in the absence of Max demonstrates for the first time that these processes can occur via Max- and possibly Myc-independent mechanisms.

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41

Zada, A. Peer, J. Pulikkan, D. Bararia, M. Geletu, A. Trivedi, M. Balkhi, and G. Behre. "Proteomic Discovery of Max as a Novel Interacting Partner of C/EBPa: A Myc/Max/Mad Link." Blood 108, no. 11 (November 16, 2006): 1175. http://dx.doi.org/10.1182/blood.v108.11.1175.1175.

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Abstract In the present study, we sought to identify novel C/EBPa interacting proteins in vivo through immunoprecipitation using mass spectrometry-based proteomic techniques. We identified Max, a heterodimeric partner of Myc, as one of the interacting proteins of C/EBPa in our screen. We confirmed the in vivo interaction of C/EBPa with Max and showed that this interaction involves the basic region of C/EBPa. Endogenous C/EBPa and Max, but not Myc and Max co-localize in intranuclear structures during granulocytic differentiation of myeloid U937 cells. Max enhanced the transactivation capacity of C/EBPa on a minimal promoter. A chromatin-immunoprecipitation assay revealed occupancy of the human C/EBPa promoter in vivo by Max under cellular settings and by C/EBPa and Max under retinoic acid induced granulocytic differentiation. Interestingly, enforced expression of Max and C/EBPa, results in granulocytic differentiation of the human hematopoietic CD34+ cells as evidenced by CD11b and CD15 expression and by real-time PCR for various genes. Silencing of Max by short hairpin RNA in CD34+ and U937 cells strongly reduced the differentiation-inducing potential of C/EBPa, indicating the importance of C/EBPa-Max in myeloid progenitor differentiation. Taken together, our data reveal Max as a novel co-activator of C/EBPa functions thereby suggesting a possible link between CEBPa and Myc-Max-Mad network.

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42

Horne, G. "Max Yergan: Race Man, Internationalist, Cold Warrior." Journal of American History 93, no. 3 (December 1, 2006): 925–26. http://dx.doi.org/10.2307/4486530.

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43

Tranter, Kieran. "Mad Max: The Car and Australian Governance." National Identities 5, no. 1 (March 2003): 67–81. http://dx.doi.org/10.1080/14608940307120.

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44

Stebbing, Nicolas. "Max Yergan: Race Man, Internationalist, Cold Warrior." Journal of Religion in Africa 38, no. 1 (2008): 81–82. http://dx.doi.org/10.1163/157006608x262764.

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45

Graef, Nils, Joachim Hammerschmidt, and Carl-Erik Sundberg. "A low-complexity max-log-MAP detector." IEEE Transactions on Communications 57, no. 8 (August 2009): 2251–54. http://dx.doi.org/10.1109/tcomm.2009.08.070126.

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46

Vogt, J., and A. Finger. "Improving the max-log-MAP turbo decoder." Electronics Letters 36, no. 23 (2000): 1937. http://dx.doi.org/10.1049/el:20001357.

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47

Ravi, S., and TS Mavitha. "THE INTERPLAY BETWEEN I-MAX, I-MIN, P-MAX AND P-MIN STABLE DISTRIBUTIONS." Mathematical Journal of Interdisciplinary Sciences 4, no. 1 (September 1, 2015): 49–53. http://dx.doi.org/10.15415/mjis.2015.41006.

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48

Peters, M. A., K. G. Sollenberger, T. L. Kao, and E. J. Taparowsky. "A minimal regulatory region maintains constitutive expression of the max gene." Molecular and Cellular Biology 17, no. 3 (March 1997): 1037–48. http://dx.doi.org/10.1128/mcb.17.3.1037.

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Max is a basic helix-loop-helix/leucine zipper protein that forms heterodimers with the Myc family of proteins to promote cell growth and with the Mad/Mxi1 family of proteins to inhibit cell growth. The role of Max as the obligate binding partner for these two protein families necessitates the observed constitutive expression and relatively long half-life of the max mRNA under a variety of growth conditions. In this study, we have used the chicken max gene to map DNA elements maintaining max gene expression in vertebrate cells. We have identified a minimal regulatory region (MRR) that resides within 115 bp of the max translation initiation site and that possesses an overall structure typical of TATA-less promoters. Within the MRR are two consensus binding sites for Sp1, a ubiquitously expressed transcription factor that plays a role in the expression of many constitutive genes. Interestingly, we show that direct binding by Sp1 to these sites is not required for MRR-mediated transcription. Instead, the integrity of a 20-bp DNA element in the MRR is required for transcriptional activity, as is the interaction of this DNA element with a 90-kDa cellular protein. Our data suggest that it is the persistence of this 90-kDa protein in vertebrate cells which drives max gene expression, insulates the max promoter from the dramatic changes in transcription that accompany cell growth and development, and ensures that adequate levels of Max will be available to facilitate the function of the Myc, Mad, and Mxi1 families of proteins.

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49

Andreesen, R., KJ Bross, J. Osterholz, and F. Emmrich. "Human macrophage maturation and heterogeneity: analysis with a newly generated set of monoclonal antibodies to differentiation antigens." Blood 67, no. 5 (May 1, 1986): 1257–64. http://dx.doi.org/10.1182/blood.v67.5.1257.1257.

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Abstract We have analyzed the expression of late differentiation antigens during terminal in vitro maturation of human macrophages (M phi) from blood monocytes (MO) in comparison to their distribution among mature M phi residing in various tissue sites. By immunizing mice with M phi derived from blood MO by culture on hydrophobic Teflon foils, monoclonal antibodies (mAbs) were developed (MAX.1, MAX.2, MAX.3, MAX.11) that reacted with lineage-restricted differentiation antigens. These antigens were expressed exclusively on M phi or were markedly increased after in vitro differentiation. The only overlap to another hemopoietic cell lineage was observed with MAX.3, which is shared by platelets and megakaryocytes. In the course of M phi maturation in vitro, the MAX.1 and MAX.3 antigens are detected within the cytoplasm two days before they appear on the cell surface. In contrast, the MAX.11 antigen is expressed simultaneously in the cytoplasm and at the cell surface, is found in varying degrees on a minor portion of blood MO and U937 cells, and is expressed rapidly at high density during early M phi differentiation in vitro. Among conventional mAbs that do not react with MO we found those against the transferrin (TF)-receptor, the BA-2, and the PCA1 antigen to label M phi. M phi matured in vivo and isolated from body fluids were positive with some but not all MAX mAbs. Distinctive patterns were observed with pulmonary M phi, exudate M phi from pleural and peritoneal effusions, synovial fluids, and early lactation milk. M phi from the alveolar space, for example, constantly expressed the MAX.2 antigen but not the MAX.3 antigen. Pleural effusion M phi, however, did not react with the MAX.1 mAb, but in most cases, it did react with the MAX.3 mAb. The detection of novel differentiation antigens, all expressed on monocyte-derived M phi but differently expressed on site-specific M phi in situ, underlines the remarkable heterogeneity among human M phi. The expression of these antigens is flexible because those MAX antigens that were not expressed in situ could be induced if cells from distinct tissue sites were cultured in vitro for several days. MAX mAbs may be of potential value to study both the sequential stages of maturation within the M phi lineage as well as differential developments induced by various culture conditions in parallel to environmental factors in vivo.

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50

Andreesen, R., KJ Bross, J. Osterholz, and F. Emmrich. "Human macrophage maturation and heterogeneity: analysis with a newly generated set of monoclonal antibodies to differentiation antigens." Blood 67, no. 5 (May 1, 1986): 1257–64. http://dx.doi.org/10.1182/blood.v67.5.1257.bloodjournal6751257.

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We have analyzed the expression of late differentiation antigens during terminal in vitro maturation of human macrophages (M phi) from blood monocytes (MO) in comparison to their distribution among mature M phi residing in various tissue sites. By immunizing mice with M phi derived from blood MO by culture on hydrophobic Teflon foils, monoclonal antibodies (mAbs) were developed (MAX.1, MAX.2, MAX.3, MAX.11) that reacted with lineage-restricted differentiation antigens. These antigens were expressed exclusively on M phi or were markedly increased after in vitro differentiation. The only overlap to another hemopoietic cell lineage was observed with MAX.3, which is shared by platelets and megakaryocytes. In the course of M phi maturation in vitro, the MAX.1 and MAX.3 antigens are detected within the cytoplasm two days before they appear on the cell surface. In contrast, the MAX.11 antigen is expressed simultaneously in the cytoplasm and at the cell surface, is found in varying degrees on a minor portion of blood MO and U937 cells, and is expressed rapidly at high density during early M phi differentiation in vitro. Among conventional mAbs that do not react with MO we found those against the transferrin (TF)-receptor, the BA-2, and the PCA1 antigen to label M phi. M phi matured in vivo and isolated from body fluids were positive with some but not all MAX mAbs. Distinctive patterns were observed with pulmonary M phi, exudate M phi from pleural and peritoneal effusions, synovial fluids, and early lactation milk. M phi from the alveolar space, for example, constantly expressed the MAX.2 antigen but not the MAX.3 antigen. Pleural effusion M phi, however, did not react with the MAX.1 mAb, but in most cases, it did react with the MAX.3 mAb. The detection of novel differentiation antigens, all expressed on monocyte-derived M phi but differently expressed on site-specific M phi in situ, underlines the remarkable heterogeneity among human M phi. The expression of these antigens is flexible because those MAX antigens that were not expressed in situ could be induced if cells from distinct tissue sites were cultured in vitro for several days. MAX mAbs may be of potential value to study both the sequential stages of maturation within the M phi lineage as well as differential developments induced by various culture conditions in parallel to environmental factors in vivo.

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