Gotowe bibliografie tematyczne / Proliferation

Gotowa bibliografia na temat „Proliferation”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 7 lipca 2024

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Artykuły w czasopismach na temat "Proliferation"

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Fraser, Hamish M., Helen Wilson, Audrey Silvestri, Keith D. Morris i Stanley J. Wiegand. "The Role of Vascular Endothelial Growth Factor and Estradiol in the Regulation of Endometrial Angiogenesis and Cell Proliferation in the Marmoset". Endocrinology 149, nr 9 (22.05.2008): 4413–20. http://dx.doi.org/10.1210/en.2008-0325.

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The present studies explore the roles of vascular endothelial growth factor (VEGF) and estradiol on angiogenesis and stromal and epithelial cell proliferation in the marmoset endometrium during the proliferative phase of the ovulatory cycle. At the start of the proliferative phase, marmosets were 1) treated with vehicle, 2) treated with a VEGF inhibitor (VEGF Trap, aflibercept), 3) ovariectomized, 4) ovariectomized and given replacement estradiol, or 5) treated with VEGF Trap and given replacement estradiol. The uterus was examined 10 d later in the late proliferative phase. Changes in endothelial and epithelial cell proliferation were quantified using a volumetric density method after immunohistochemistry for bromodeoxyuridine to localize proliferating cells, CD31 to visualize endothelial cells, and dual staining to distinguish endothelial cell proliferation. Endothelial proliferation was elevated in late proliferative controls but virtually absent after VEGF Trap. Ovariectomy had a similar inhibitory effect, whereas angiogenesis was restored by estrogen replacement. Estradiol replacement in VEGF Trap-treated marmosets resulted in only a small increase in endothelial cell proliferation that remained significantly below control values. VEGF Trap treatment and ovariectomy also markedly reduced stromal cell proliferation but resulted in increased stromal cell density associated with a reduction in overall endometrial volume. Estrogen replacement in both ovariectomized and VEGF Trap-treated animals restored stromal proliferation rates and cell density. These results show that endometrial angiogenesis and stromal proliferation during the proliferative phase are driven by estradiol and that the effect of estrogen on angiogenesis is mediated largely by VEGF.
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Nishimura, R., i N. Arima. "Clinical significance of proliferative activity evaluated by MIB-1 in the treatment and postoperative follow-up of early breast cancer". Journal of Clinical Oncology 25, nr 18_suppl (20.06.2007): 21054. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.21054.

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21054 Background: To evaluate a clinical significance of proliferative activity in breast cancer, we studied relationships between proliferative activity and recurrence rate, the time of recurrence or adjuvant therapy. Methods: We analyzed 2448 patients with primary breast cancer between 1987 and 2004 in the Kumamoto City Hospital, and 437 cases out of the patients developed recurrence. Furthermore, the rate of recurrence before and after 1999 when postoperative adjuvant therapy (such as CEF or Taxanes) was started as standard treatment was investigated. Proliferative activity was judged by immunostaining for MIB-1. The fraction of proliferating cells was classified into 3 degrees (=19%, 20–49%, 50%=). Median observation period was 70 months. Results: 1) Distribution of patients by proliferation was as follows; =19%:1215 cases(50%), 20–49%: 870 cases(35%), or 50%=: 363 cases(15%). There was a significant relationship between proliferative activity and tumor size, nodal status, ER, PgR, p53 or HER2 status. 2) Multivariate analysis for disease-free survival revealed that a proliferative activity was one of significant factors in node-negative and positive cases. Recurrence rate was 11.6% in cases with low proliferation and 31.0% in high proliferation. The mean period from operation to recurrence in cases with low proliferation was 50.2 months, whereas 19.9 months in high proliferation (p<0.0001). Moreover, 74% of recurrent cases with high proliferation recurred within 2 years after operation, and there were few recurrences from the fifth year. 3) Patients with low proliferation frequently developed bone metastasis. In local recurrence, diffuse skin recurrence was often seen in cases with high proliferation. 4) The prognosis of patients in the later period (standard therapy group) was significantly better than that of patients in the earlier period, especially in high proliferation group. Conclusions: Proliferative activity might reflect aggressive behavior of breast cancer and predict the time of recurrence. The standard adjuvant therapy was effective in inhibiting early recurrence with high proliferation. It is important to take proliferative activity into consideration in the treatment and follow-up of breast cancer. No significant financial relationships to disclose.
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Bocheński, Szymon. "Proliferation Security Initiative: A New Formula for WMD Counter-Proliferation Efforts?" Connections: The Quarterly Journal 06, nr 4 (2007): 64–83. http://dx.doi.org/10.11610/connections.06.4.05.

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Hernández-Núñez, Ismael, Ana Quelle-Regaldie, Laura Sánchez, Fátima Adrio, Eva Candal i Antón Barreiro-Iglesias. "Decline in Constitutive Proliferative Activity in the Zebrafish Retina with Ageing". International Journal of Molecular Sciences 22, nr 21 (28.10.2021): 11715. http://dx.doi.org/10.3390/ijms222111715.

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It is largely assumed that the teleost retina shows continuous and active proliferative and neurogenic activity throughout life. However, when delving into the teleost literature, one finds that assumptions about a highly active and continuous proliferation in the adult retina are based on studies in which proliferation was not quantified in a comparative way at the different life stages or was mainly studied in juveniles/young adults. Here, we performed a systematic and comparative study of the constitutive proliferative activity of the retina from early developing (2 days post-fertilisation) to aged (up to 3–4 years post-fertilisation) zebrafish. The mitotic activity and cell cycle progression were analysed by using immunofluorescence against pH3 and PCNA, respectively. We observed a decline in the cell proliferation in the retina with ageing despite the occurrence of a wave of secondary proliferation during sexual maturation. During this wave of secondary proliferation, the distribution of proliferating and mitotic cells changes from the inner to the outer nuclear layer in the central retina. Importantly, in aged zebrafish, there is a virtual disappearance of mitotic activity. Our results showing a decline in the proliferative activity of the zebrafish retina with ageing are of crucial importance since it is generally assumed that the fish retina has continuous proliferative activity throughout life.
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Lawrence, Ben, Simon Schimmack, Bernhard Svejda, Ignat Drozdov, Daniele Alaimo, Barton Kenney, Mark Kidd i Irvin M. Modlin. "Prognostication by multigene proliferative marker panel compared with Ki-67 in small-intestinal NENs." Journal of Clinical Oncology 30, nr 4_suppl (1.02.2012): 242. http://dx.doi.org/10.1200/jco.2012.30.4_suppl.242.

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242 Background: Ki-67 is the major proliferative marker in clinical use to determine neuroendocrine neoplasm (NEN) prognosis. Ki-67 is unable to predict the outcome of SI-NENs, as the majority have a low (≤2) Ki-67%. Therefore, we aimed to identify a sensitive panel of proliferative markers using qRT-PCR to more accurately define the proliferation of these slow growing tumors. Methods: We identified genes with a mechanistic function in cell cycle progression that were over-expressed in RNA microarrays of SI-NENs (n=8) compared to adjacent normal tissue (n=4) (dCHIP, annotation databases). Timing of marker gene expression (qRT-PCR) in proliferating cell-cycle phases (S, G2, M) was determined in flow-sorted SI-NEN cell lines (KRJ-1, H-STS) after propidium iodide staining. RNA expression of candidate proliferative markers was then investigated using an in vivo model and two independent tumor datasets, and transcript level compared to Ki-67% protein expression (immunohistochemical staining). Results: Twenty genes with a mechanistic role in proliferation were identified and 17 confirmed to be expressed in proliferating cell cycle phases. Each tumor expressed a unique profile of the 17 proliferative markers. Both Ki-67 protein and Ki-67 RNA transcript levels failed to differentiate in vivo SI-NEN models or patient samples despite variable proliferative capacity (e.g., WDNETs versus WDNECs). Although most tumors showed low levels of Ki-67 expression, the tumors expressed high levels of select alternative proliferative markers. Hierarchical clustering provided a novel and clinically meaningful prognostic classification. Conclusions: Proliferation of individual SI-NENs is regulated by unique combinations of multiple genes with a mechanistic role in cell-cycle progression. Regulation of proliferation in SI-NENs is therefore complex and cannot accurately be defined by Ki-67 as a single marker. A panel of proliferative RNA markers has potential to significantly improve prognostication in patients with SI-NENs.
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Marlatt, Michael W., Jan Bauer, Eleonora Aronica, Elise S. van Haastert, Jeroen J. M. Hoozemans, Marian Joels i Paul J. Lucassen. "Proliferation in the Alzheimer Hippocampus Is due to Microglia, Not Astroglia, and Occurs at Sites of Amyloid Deposition". Neural Plasticity 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/693851.

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Microglia and astrocytes contribute to Alzheimer’s disease (AD) etiology and may mediate early neuroinflammatory responses. Despite their possible role in disease progression and despite the fact that they can respond to amyloid deposition in model systems, little is known about whether astro- or microglia can undergo proliferation in AD and whether this is related to the clinical symptoms or to local neuropathological changes. Previously, proliferation was found to be increased in glia-rich regions of the presenile hippocampus. Since their phenotype was unknown, we here used two novel triple-immunohistochemical protocols to study proliferation in astro- or microglia in relation to amyloid pathology. We selected different age-matched cohorts to study whether proliferative changes relate to clinical severity or to neuropathological changes. Proliferating cells were found across the hippocampus but never in mature neurons or astrocytes. Almost all proliferating cells were colabeled with Iba1+, indicating that particularly microglia contribute to proliferation in AD. Proliferating Iba1+ cells was specifically seen within the borders of amyloid plaques, indicative of an active involvement in, or response to, plaque accumulation. Thus, consistent with animal studies, proliferation in the AD hippocampus is due to microglia, occurs in close proximity of plaque pathology, and may contribute to the neuroinflammation common in AD.
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Kabraji, Sheheryar Kairas, Giorgio Gaglia, Danae Argyropoulou, Yang Dai, Shu Wang, Johann Bergholz, Shannon Coy i in. "Temporal and spatial topography of cell proliferation in cancer." Journal of Clinical Oncology 39, nr 15_suppl (20.05.2021): 3122. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.3122.

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3122 Background: Tumors are complex ecosystems where exogenous and endogenous cues are integrated to either stimulate or inhibit cancer cell proliferation. However, the nature of these complex cell cycle states, their spatial organization, response to perturbation, and implications for clinical outcomes, are poorly characterized in tumor tissues. Methods: We used multiplexed tissue imaging to develop a robust classifier of proliferation, the multivariate proliferation index (MPI), using 513 unique tumors across five cancer types. Next, we used dimensionality reduction analysis to assess how the patterns of cell cycle protein expression in tumors were altered in response to perturbation. Results: The MPI outperforms single markers, like Ki67, when classifying proliferative index across diverse tumor types and reveals the proliferative architecture of tumors in situ. We find that proliferative and non-proliferative cancer cells are organized across microscopic (cell-to-cell) and macroscopic (tissue-level) scales. Both domains are reshaped by therapy, and local clusters of proliferative and non-proliferative tumor cells preferentially neighbor distinct tumor-infiltrating immune cells. We further phenotyped non-proliferating cancer cells using markers of quiescent cancer cells, cancer stem cells, and dormant cancer cells. We found that these types of non-proliferating cancer cells can occupy distinct regions within the same primary tumor. In high-dimensional marker space, populations of proliferative cancer cells express canonical patterns of cell cycle protein markers, a property we refer to as “cell cycle coherence”. Untreated tumors exist in a continuum of coherence states, ranging from optimal coherence, akin to freely cycling cells in culture, to reduced coherence characterized by either cell cycle polarization or non-canonical marker expression. Coherence can be stereotypically altered by induction and abrogation of mitogen signaling in a HER2-driven model of breast cancer. Cell cycle coherence is modulated by neoadjuvant therapy in patients with localized breast cancer, and coherence is associated with disease-free survival after adjuvant therapy in patients with colorectal cancer, mesothelioma and glioblastoma. Conclusions: The MPI robustly defines proliferating and non-proliferating cells in tissues, with immediate implications for clinical practice and research. The coherence metrics capture the diversity of post-treatment cell cycle states directly in clinical samples, a fundamental step in advancing precision medicine. More broadly, replacing binary metrics with multivariate traits provides a quantitative framework to study temporal processes from fixed static images and to investigate the rich spatial biology of human cancers.
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Levine, Richard, Magnus S. Agren i Patricia M. Mertz. "Effect of Occlusion on Cell Proliferation during Epidermal Healing". Journal of Cutaneous Medicine and Surgery 2, nr 4 (kwiecień 1998): 193–98. http://dx.doi.org/10.1177/120347549800200403.

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Background: Occlusive dressings influence epithelization of superficial wounds by some unknown mechanism(s). Objective: The effects of occlusion on epidermal cell proliferation in two types of wounds were examined. Methods: Partial-thickness wounds and tape-stripped skin wounds were compared. An immunohistochemical technique, employing PC10 — a monoclonal antibody against proliferating cell nuclear antigen (PCNA) — was applied to formalin-fixed, paraffin-embedded porcine tissue sections. Results: The number of PC10-positive cells was low during the migratory phase, then increased to a peak of proliferation 2 to 3 days after resurfacing. An overall increased proliferative response (mean = 21%) was seen in occluded compared to control partial-thickness wounds (day 10 postoperatively); an opposite effect of occlusion on epidermal proliferation was seen in tape-stripped skin. Occlusion decreased the proliferative response (mean = 42%) compared to air-exposure. Conclusion: Occlusion increased epidermal cell proliferation in wounds (where the entire surface epithelium and papillary dermis was removed), whereas an opposite effect was seen in tape-stripped skin from which only the stratum corneum had been removed.
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Sambasiva Rao, M., i Janardan K. Reddy. "The Relevance of Peroxisome Proliferation and Cell Proliferation in Peroxisome Proliferator-Induced Hepatocarcinogenesis". Drug Metabolism Reviews 21, nr 1 (styczeń 1989): 103–10. http://dx.doi.org/10.3109/03602538909029957.

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Shayan, Katayoon, Michael Ho, Vernon Edwards, Ronald Laxer i Paul S. Thorner. "Synovial Pathology in Camptodactyly-Arthropathy-Coxa Vara-Pericarditis Syndrome". Pediatric and Developmental Pathology 8, nr 1 (styczeń 2005): 26–33. http://dx.doi.org/10.1007/s10024-004-3035-z.

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At least 25 families with camptodactyly-arthropathy-coxa vara-pericarditis (CACP syndrome) have been reported, with descriptions of a distinctive synovial pathology based largely on light microscopy. Although described as “proliferative,” with numerous multinucleated giant cells, the natures of proliferating cells and giant cells have not been determined. To clarify the pathogenesis of this disorder, we studied 3 patients who had CACP syndrome and underwent synovial biopsy. Cells in the biopsies were studied by immunohistochemistry and electron microscopy. Giant cells were identified as macrophage in origin based on CD68 expression and electron microscopic features of macrophages. Most cells in the synovium were CD68 positive, in keeping with macrophages. The degree of proliferation in synovial biopsies was estimated by MIB1 immunostaining, which showed that up to 30% of cells were cycling compared with fewer than 10% in control synovial biopsies. None of the giant cells was cycling. By double immunostaining, proliferating cells were determined to be fibroblastic synoviocytes rather than macrophages. Thus the proliferative synovitis in this CACP syndrome can be more accurately thought of as hypercellularity by infiltrating macrophages with a contribution by proliferating fibroblastic synoviocytes. The synoviocyte proliferation is likely a response to the underlying genetic mutations involving the proteogly-can-4 (or CACP) gene. The encoded protein normally acts as a lubricant and possibly controls cell proliferation. Loss of one or another of these functions may be a possible mechanism that leads to synoviocyte proliferation in this disease, but the exact pathophysiology leading to this change requires further study.
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Rozprawy doktorskie na temat "Proliferation"

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Cheng, Wai. "The relationship between peroxisome proliferator-activated receptors (PPARs) and cell proliferation /". View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36433937.

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Cheng, Wai, i 鄭蔚. "The relationship between peroxisome proliferator-activated receptors (PPARs) and cell proliferation". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45010614.

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Jemec, Barbara. "Proliferation and action of an anti-proliferative agent in Dupuytren's fibroblast cultures". Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343601.

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Veerapen, Pierce Elaine. "Proliferation in astrocytomas". Thesis, University of Greenwich, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245348.

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Green, Daniel M. "Monitoring technology proliferation: an open source methodology for generating proliferation intelligence". Thesis, Monterey, California. Naval Postgraduate School, 1993. http://hdl.handle.net/10945/39686.

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Approved for public release; distribution is unlimited.
This thesis develops a methodology to monitor technology proliferation. It is designed to provide proliferation intelligence on specific threat technologies and can be used to augment export controls or enhance counter proliferation initiatives. A high-te
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Miller, Nicholas L. (Nicholas LeSuer). "Hegemony and nuclear proliferation". Thesis, Massachusetts Institute of Technology, 2014. http://hdl.handle.net/1721.1/95553.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Political Science, 2014.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 277-292).
Contrary to longstanding of predictions of nuclear tipping points, the number of states interested in nuclear weapons has sharply declined in recent decades. In contrast to existing explanations, this dissertation argues that the decline is largely attributable to US nonproliferation policies, in particular the threat of sanctions that was instituted in the late 1970s. By credibly threatening to cut off economic and military support to countries pursuing nuclear weapons, I argue that this threat of sanctions deters states within the US sphere of influence from proliferating, reducing the overall rate of proliferation and also explaining why recent nuclear aspirants have exclusively been "rogue" states outside the US sphere of influence. Because states that depend on the United States have been deterred from proliferating in recent decades, the observed success rate of sanctions should be low, since they will generally be targeted at states that do not rely on US resources. This dissertation also offers a theory of the sources of US nonproliferation policy, arguing that fears of nuclear domino effects are necessary to explain (1) why US policy strengthened so dramatically in the wake of Chinese and Indian nuclear tests in the 1960s and 1970s, and (2) why the US abandoned a selective nonproliferation policy and decided to enforce nonproliferation across the board. To test these two arguments, this dissertation employs a mix of quantitative and qualitative methods. First, I draw on archival documents to show that fears of nuclear domino effects motivated US nonproliferation policy advances in the 1960s and 1970s, and that this motivation was prominent in individual cases of nonproliferation. Second, I show quantitatively that states dependent on the United States have been less likely to pursue nuclear weapons since sanctions policies were instituted in the late 1970s, that observed cases of sanctions have been largely ineffective, and that the deterrent effect of sanctions largely accounts for the temporal decline in proliferation. Case studies of US policy toward Pakistan and Taiwan demonstrate that a credible threat of sanctions can arrest ongoing nuclear programs when the proliferator is dependent on the United States and underestimated the likelihood of sanctions.
by Nicholas L. Miller.
Ph. D.
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Li, Xiaoling. "Peroxisome proliferation and division". Available to US Hopkins community, 2002. http://wwwlib.umi.com/dissertations/dlnow/3080712.

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Renda, Guido. "Resisting Nuclear Proliferation Through Design : a Systems Approach to Nuclear Proliferation Resistance Assessment". Thesis, University of Bristol, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.520167.

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Du, Zhenjian Cheung H. Tak. "Febrile condition and lymphocyte proliferation". Normal, Ill. Illinois State University, 1991. http://wwwlib.umi.com/cr/ilstu/fullcit?p9203029.

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Thesis (Ph. D.)--Illinois State University, 1991.
Title from title page screen, viewed December 8, 2005. Dissertation Committee: H. Tak Cheung (chair), Herman E. Brockman, Lynne A. Lucher, Anthony J. Otsuka, Alan J. Katz. Includes bibliographical references (leaves 99-110) and abstract. Also available in print.
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Ashagbley, Anthony J. "Ethanolamine requirement and cell proliferation". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq23203.pdf.

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Książki na temat "Proliferation"

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Harris, Joseph. Nuclear proliferation. Pleasantville, NY: Gareth Stevens Pub., 2010.

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Flamini, Roland. Nuclear Proliferation. 2455 Teller Road, Thousand Oaks California 91320 United States: CQ Press, 2007. http://dx.doi.org/10.4135/cqrglobal20070100.

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Griffin, Rodman D. Nuclear Proliferation. 2455 Teller Road, Thousand Oaks California 91320 United States: CQ Press, 1992. http://dx.doi.org/10.4135/cqrglobal19920605.

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Patrick, Keatinge, i Rotblat Joseph, red. Nuclear Non-Proliferation: And the Non-Proliferation Treaty. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990.

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1940-, Fry M. P., Keatinge Patrick 1939- i Rotblat Joseph 1908-, red. Nuclear non-proliferation and the non-proliferation treaty. Berlin: Springer-Verlag, 1990.

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Santoro, David. Treating Weapons Proliferation. New York: Palgrave Macmillan US, 2010. http://dx.doi.org/10.1057/9780230105713.

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Security, Canadian Institute for International Peace and. Ballistic missile proliferation. [Ottawa: CIIPS], 1990.

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Fry, Michael P., Patrick Keatinge i Joseph Rotblat, red. Nuclear Non-Proliferation. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75105-9.

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United States. Congress. House. Committee on Foreign Affairs. Subcommittee on Arms Control, International Security, and Science., United States. Congress. House. Committee on Foreign Affairs. Subcommittee on International Economic Policy and Trade., United States. Congress. Senate. Committee on Governmental Affairs. Subcommittee on Energy, Nuclear Proliferation, and Government Processes. i Library of Congress. Environment and Natural Resources Policy Division., red. Nuclear proliferation factbook. Washington: U.S. G.P.O., 1985.

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Dunn, Lewis A. Containing nuclear proliferation. London: Brassey's for the International Institute for Strategic Studies, 1991.

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Części książek na temat "Proliferation"

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Cottey, Andrew. "Proliferation". W Security in 21st Century Europe, 175–201. London: Macmillan Education UK, 2013. http://dx.doi.org/10.1007/978-1-137-00647-9_8.

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Klinghoffer, Arthur Jay, i Judith Apter Klinghoffer. "Proliferation". W International Citizens’ Tribunals, 163–85. New York: Palgrave Macmillan US, 2002. http://dx.doi.org/10.1057/9780312299163_15.

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Gold, John R., i Margaret M. Gold. "Proliferation". W Festival Cities, 209–39. Abingdon, Oxon ; New York, NY : Routledge, 2021. | Series: Planning, history and environment: Routledge, 2020. http://dx.doi.org/10.4324/9781003130802-7.

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Lidington, Tony. "Proliferation". W “Don't Forget the Pierrots!” The Complete History of British Pierrot Troupes and Concert Parties, 109–57. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003043539-6.

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Eidemüller, Dirk. "Proliferation". W Nuclear Power Explained, 173–93. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72670-6_9.

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Bährle-Rapp, Marina. "proliferation". W Springer Lexikon Kosmetik und Körperpflege, 453. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_8516.

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Bährle-Rapp, Marina. "Proliferation". W Springer Lexikon Kosmetik und Körperpflege, 453. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_8517.

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Rees, Wyn. "Nuclear Non-Proliferation and Counter-Proliferation". W The US-EU Security Relationship, 130–52. London: Macmillan Education UK, 2011. http://dx.doi.org/10.1007/978-1-137-28556-0_7.

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Armstrong, Carol L. "Endothelial Proliferation". W Encyclopedia of Clinical Neuropsychology, 953. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_106.

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Hangay, George, Severiano F. Gayubo, Marjorie A. Hoy, Marta Goula, Allen Sanborn, Wendell L. Morrill, Gerd GÄde i in. "Apple Proliferation". W Encyclopedia of Entomology, 261. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_10313.

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Streszczenia konferencji na temat "Proliferation"

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Tatum, Jim. "VCSEL proliferation". W Integrated Optoelectronic Devices 2007, redaktorzy Kent D. Choquette i James K. Guenter. SPIE, 2007. http://dx.doi.org/10.1117/12.715082.

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Tsomartova, Dibakhan Aslanbekovna, Nataliya Valentinovna Yaglova i Sergey Stanislavovich Obernikhin. "ALTERED PROLIFERATION OF THYMIC LYMPHOCYTES IN PUBERTAL RATS EXPOSED TO LOW DOSES OF DDT". W International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.14.

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Low-dose developmental exposure to DDT alters proliferative activity of thymic lymphocytes of rats. Higher proliferation rate and low differentiated lymphoblast content are found in rat thymus during puberty.
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Nazimova, Svetlana Vladimirovna, Nataliya Valentinovna Yaglova, Dibakhan Aslanbekovna Tsomartova, Sergey Stanislavovich Obernikhin i Valentin Vasilyevich Yaglov. "REGULATION OF ADRENAL RETICULARIS CELL’S PROLIFERATION IN ORGANISM DEVELOPMENTALLY EXPOSED TO LOW DOSES OF DDT". W International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.10.

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Altered patterns of cell proliferation in adrenal zona reticularis during postnatal development and regulation of proliferative activity by transcriptional factor PRH were revealed in rats exposed to endocrine disrupter DDT.
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Tsomartova, Dibakhan, Ekaterina Timokhina, Nataliya Yaglova, Sergey Obernikhin i Valentin Yaglov. "MITOTIC ACTIVITY OF LYMPHOCYTES IN PREPUBERTAL RATS EXPOSED TO LOW DOSES OF DDT". W NEW TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2021. http://dx.doi.org/10.47501/978-5-6044060-1-4.13.

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Low-dose developmental exposure to DDT results in inhibited mitotic activity of thymic lymphocytes in prepubertal rats. Decreased number of proliferating cells in deeper layers of the cortex and in the medulla, not subcapsular lymphoblasts, contributes to lowered proliferation rate.
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CANAVAN, GREGORY H. "MISSILE DEFENSE AND PROLIFERATION". W International Seminar on Nuclear War and Planetary Emergencies 25th Session. Singapore: World Scientific Publishing Co. Pte. Ltd., 2001. http://dx.doi.org/10.1142/9789812797001_0035.

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King Liu, T. J. "Electronics Proliferation through Diversification". W 2011 International Conference on Solid State Devices and Materials. The Japan Society of Applied Physics, 2011. http://dx.doi.org/10.7567/ssdm.2011.pl-2-2.

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KAMAL, AHMAD. "THE NUCLEAR NON-PROLIFERATION DEBATE". W International Seminar on Nuclear War and Planetary Emergencies 34th Session. WORLD SCIENTIFIC, 2006. http://dx.doi.org/10.1142/9789812773890_0044.

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Schuppen, A., M. Tortschanoff, J. Berntgen, P. Maier, D. Zerrweck, H. von der Ropp, J. Tolonics i K. Burger. "The Proliferation of Silicon Germanium". W 30th European Solid-State Device Research Conference. IEEE, 2000. http://dx.doi.org/10.1109/essderc.2000.194723.

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Gorain, S., A. Kumar i L. Reddy. "Prediction of Facies & Reservoir Properties in Carbonate Reservoir through Geo-body Modelling: Mumbai Offshore Case Study". W EAGE Workshop on Innovative Reservoir Modeling into Digital Proliferation. European Association of Geoscientists & Engineers, 2022. http://dx.doi.org/10.3997/2214-4609.202273004.

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Uli, D., D. J. Shield, M. F. Abdul Kadir i Z. Z. Tuan Harith. "Derisking Well Placement through Innovative Geological Driven Modeling for Greenfield Deepwater Turbidite in NW of Borneo". W EAGE Workshop on Innovative Reservoir Modeling into Digital Proliferation. European Association of Geoscientists & Engineers, 2022. http://dx.doi.org/10.3997/2214-4609.202273026.

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Raporty organizacyjne na temat "Proliferation"

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Lindsey, Nicholas C. Printed Proliferation: The Implications of Additive Manufacturing and Nuclear Weapons Proliferation. Office of Scientific and Technical Information (OSTI), styczeń 2016. http://dx.doi.org/10.2172/1413398.

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Bailey, Kathleen C. Director's Series on Proliferation. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 1993. http://dx.doi.org/10.21236/ada338763.

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Sullivan, Peter. Iraq's Enduring Proliferation Threat. Fort Belvoir, VA: Defense Technical Information Center, listopad 1996. http://dx.doi.org/10.21236/ada385717.

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Bailey, K. C., i M. E. Price. Director`s series on proliferation. Office of Scientific and Technical Information (OSTI), grudzień 1994. http://dx.doi.org/10.2172/10108550.

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Zentner, Michael D., Garill A. Coles i Robert J. Talbert. Nuclear Proliferation Technology Trends Analysis. Office of Scientific and Technical Information (OSTI), październik 2005. http://dx.doi.org/10.2172/885472.

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Bailey, K. C., i M. E. Price. Director`s series on proliferation. Office of Scientific and Technical Information (OSTI), listopad 1995. http://dx.doi.org/10.2172/216294.

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Bailey, K. C. Director`s series on proliferation. Office of Scientific and Technical Information (OSTI), wrzesień 1993. http://dx.doi.org/10.2172/10188542.

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Bailey, K. C., i M. E. Price. Director`s series on proliferation. Office of Scientific and Technical Information (OSTI), październik 1994. http://dx.doi.org/10.2172/10190132.

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Gray, L., K. Moody, K. Bradley i H. Lorenzana. Proliferation Resistant Nuclear Reactor Fuel. Office of Scientific and Technical Information (OSTI), luty 2011. http://dx.doi.org/10.2172/1021549.

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Hinton, J. P., R. W. Barnard i D. E. Bennett. Proliferation Vulnerability Red Team report. Office of Scientific and Technical Information (OSTI), październik 1996. http://dx.doi.org/10.2172/437625.

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Możesz być także zainteresowany rozszerzonymi bibliografiami na temat „Proliferation” dla poszczególnych typów źródeł:
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