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Bücher zum Thema „NDDs“

Autor: Grafiati
Veröffentlicht am 30. Juni 2021
Zuletzt aktualisiert am 21. Juni 2025

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1

Society, National Deaf Children's, ed. NDCS technology services. NDCS, 2000.

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2

Minaev, B. A. NDS: Aktualʹnye voprosy. Glavbukh, 1999.

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3

Hughes, Jeffrey F. NDS for NT. IDG Books Worldwide, 1998.

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4

National Disaster Medical System (U.S.), ed. NDMS, catastrophic care for the nation. National Disaster Medical System, 1999.

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5

Luis, Hernández Otero Ricardo, ed. NDCS, nuevo diccionario cubano de seudónimos. Rogés Llibres, 2000.

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6

Jeffrey, Harris, ed. Administering NDS corporate edition. McGraw-Hill, 2000.

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7

Ukraine. NDS: Sbornik sistematizirovannogo zakonodatelʹstva. "Faktor", 2005.

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8

Andrew, Chris. Novell's NDS developer's guide. Novell Press, 1999.

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9

(Canada), NDSS Steering Committee. National Diabetes Surveillance System (NDSS) business plan. 3rd ed. Health Canada, 2000.

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10

Konstantinov, V. N. Ischislenie NDS predprii͡a︡tii͡a︡mi razlichnykh otrasleĭ. Glavbukh, 1998.

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11

Seleznev, A. P. Spravochnik platelʹshchika NDS: Zakonodatelʹnye terminy i opredelenii︠a︡, sistematizirovannyĭ ukazatelʹ osnovnykh polozheniĭ NDS, GNAU razʺi︠a︡sni︠a︡et, obzor konfliktnykh situat︠s︡iĭ, NDS i nalog na pribylʹ. "Prapor", 1998., 1998.

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12

Chatterjee, M. NDDP multi-stage flash desalination process simulator design. Bhabha Atomic Research Centre, 2006.

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13

Society, National Deaf Children's. Welcome to NDCS the National Deaf Children's Society. NDCS, 2000.

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14

Services, Canada National Dosimetry. Technology comparison, NDS-National Dosimetry Services. Health Canada, 2006.

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15

Hughes, Jeffrey F. Novell's four principles of NDS design. Novell Press, 1996.

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16

TVGAME360, ed. NDS/NDSL wu suo bu wan. Qi biao chu ban gu fen you xian gong si, 2007.

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17

Ltd, Kaif Informatics, and National Library of Canada, eds. Network directory service: NDS service definition. s.n., 1988.

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18

Stafford, Bruce. New Deal for Disabled People (NDDP): First synthesis report. Department for Work and Pensions Research Management, 2004.

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19

Association, American Forest &. Paper. NDS, national design specification for wood construction. The Association, 1997.

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20

Alexander, Milson, and Tofield Christopher, eds. Ha nds-on guide to clinical pharmacology. Blackwell Science, 2000.

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21

N, Sashi Kumar G., and Bhabha Atomic Research Centre, eds. NDDP multi-stage flash desalination process simulator design "process optimization". Bhabha Atomic Research Centre, 2009.

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22

Schweiger, Detlef. Sa[e]nds: Malerei Collage Zeichnung Grafik, 1995-1997. Artco, 1997.

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23

Makhrov, I. E. NDS po ėksportu: Vozmeshchenie iz bi︠u︡dzheta : kommentariĭ k zakonodatelʹstvu. I︠U︡stit︠s︡inform, 2002.

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24

Swaziland. National development strategy (NDS): "a twenty-five year vision". Kingdom of Swaziland, 1997.

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25

Cummings, Jeffrey L., and Jagan A. Pillai. Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0001.

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Neurodegenerative diseases (NDDs) are growing in frequency and represent a major threat to public health. Advances in scientific progress have made it clear that NDDs share many underlying processes, including shared intracellular mechanisms such as protein misfolding and aggregation, cell-to-cell prion-like spread, growth factor signaling abnormalities, RNA and DNA disturbances, glial cell changes, and neuronal loss. Transmitter deficits are shared across many types of disorders. Means of studying NDDs with human iPS cells and transgenic models are similar. The progression of NDDs through asymptomatic, prodromal, and manifest stages is shared across disorders. Clinical features of NDDs, including cognitive impairment, disease progression, age-related effects, terminal stages, neuropsychiatric manifestations, and functional disorders and disability, have many common elements. Clinical trials, biomarkers, brain imaging, and regulatory aspects of NDD can share information across NDDs. Disease-modifying and transmitter-based therapeutic interventions, clinical trials, and regulatory approaches to treatments for NDDs are also similar.
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26

Jay, Taylor R., Shane M. Bemiller, Lee E. Neilson, Paul J. Cheng-Hathaway, and Bruce T. Lamb. Neuroinflammation and Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0004.

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Neuroinflammation has long been associated with many neurodegenerative diseases (NDDs). Immune-related genetic and environmental risk factors have recently been identified for NDDs, suggesting that neuroinflammation can play an active role in modifying NDD pathologies. Immune cells that underlie this neuroinflammatory response can have both beneficial and detrimental roles in NDDs. These cells can engage in clearance of debris and provide important survival factors to neighboring neurons. However, these cells can also release inflammatory molecules that promote oxidative stress and excitotoxic damage in surrounding neurons, and aberrantly clear healthy cells and structures from the brain. In turn, the cells within the brain play important roles in determining the phenotype and function of these immune cells, and changes in the interaction among these cells in the context of disease can lead to detrimental immune cell activation. There has been recent interest in developing inflammation-related biomarkers to help diagnose NDDs and immune-targeted therapeutics.
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27

Cummings, Jeffrey L., and Kate Zhong. Clinical Trials and Drug Development in Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0018.

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This chapter describes the common therapeutic targets, approaches to clinical trial design, biomarkers, and therapeutic interventions across neurodegenerative disorders (NDDs). Each unique NDD-Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), etc.-has a unique phenotype associated with the regional cell population most affected. Each disease, however, is associated with protein misfolding, oxidation, inflammation, apoptosis, and cell death. If vulnerable cell populations include transmitter source nuclei, transmitter deficits also emerge (e.g. cholinergic abnormalities in AD and dopaminergic deficits in PD). Biomarkers show regionally appropriate brain atrophy or process-related cerebrospinal deficits. Clinical trial designs share features for symptomatic interventions (e.g. cholinesterase inhibitors in AD and dopamine agents in PD) and disease-modifying therapies. Biomarkers play similar roles in trials for NDD, including demonstrating target engagement and supporting disease modification. No disease-modifying therapies have been approved for any NDDs; all programs face similar pharmacokinetic, pharmacodynamic, and regulatory challenges in therapeutic development.
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28

Pillai, Jagan A., and Jeffrey L. Cummings. Conclusions on Neurodegenerative Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0019.

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Neurodegenerative diseases strip an individual of his or her cognitive powers, functional capacity, and autonomy while increasing dependence on others. They are an existential threat to an aging society in its ability to provide a meaningful and high quality of life to all its citizens. The classical view of neurodegenerative disorders (NDDs) emphasized the distinctness of each NDD ,with a definable clinical syndrome of neurological deficits, behavioral changes, and progressive functional decline, underpinned by inexorable neuronal loss that is pathological for the age of the subject. Neurodegenerative Disorders: Unifying Principles has covered each of these themes from multiple expert domains to basic science to clinical therapeutics. This detailed overview emphasizes the work recently accomplished to uncover shared themes across NDDs and further posits questions for the future.
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29

Pillai, Jagan A. Predementia Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0009.

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Neurodegenerative disorders (NDDs) are currently conceptualized as proteinopathies with a long trajectory of pathological changes preceding the onset of clinical symptoms by over a decade. Predementia, the stage of disease before onset of clinical symptoms and dementia where significant irreversible neuronal damage and cognitive decline have yet to occur, is seen as a promising stage to target for a new generation of therapeutic interventions. This chapter reviews the growing understanding of the predementia stages across NDDs and some of the developing challenges to the present clinical characterization of the predementia stage. It further surveys the clinical trials being currently undertaken across NDDs in this domain.
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30

Bekris, Lynn M., and James B. Leverenz. Genetics of Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0010.

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A great deal has been discovered about Neurodegenerative disorders (NDDs) including Alzheimer’s disease, Parkinson’s disease, frontotemporal dementia, dementia with Lewy bodies . This includes genetic variants associated with both sporadic and autosomal dominant NDDs. These findings have been crucial in our understanding the underlying factors that drive neuropathological changes and in clarifying the time line of biomarker changes in presymptomatic autosomal dominant mutation carriers. While much is still to be learned, these findings will play an important role in the future of neurodegenerative prediction, diagnosis, and treatment. This chapter summarizes the current genetic knowledge related to both the sporadic and autosomal dominant forms of neurodegenerative disease.
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31

Padilla, Claudia R., and Mario F. Mendez. Neuropsychiatric Features Across Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0006.

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Neuropsychiatric symptoms (NPS) are a major manifestation of neurodegenerative diseases(NDDs) including Alzheimer’s disease (AD), Dementia with Lewy Bodies (DLB) and frontotemporal dementia (FTD). NPS symptoms are a determining factor impacting economic and psychological costs for both the patient and their caregivers in these devastating illness. Recent developments in neuroscience have clarified the relationship of NPS with changes in brain structures, alterations in neural circuits and networks, and their neurotransmitter systems. It is increasingly recognized that NPS shared across different NDDs might have shared alterations in neural circuits and networks, and their neurotransmitter systems and ways to modulate them theraputcally. This chapter focuses on the more common NPS and their links to causative neurodegenerative processes that transcend specific diseases.
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32

Drouin-Ouellet, Janelle, and Roger A. Barker. Disease-Modifying Therapies in Neurodegenerative Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0016.

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The recent identification of the genetic basis of many neurodegenerative disorders (NDDs), coupled with a greater understanding of their pathophysiology, has enabled better therapeutic strategies to be identified and tried. This includes approaches that target critical specific nodes in the disease pathways, for example, agents that modulate levels of mutant huntingtin in Huntington’s disease. In addition to these highly specific targeted therapies, there is also a growing realization that more generic lifestyle therapies influencing whole brain health may also have merit in treating these conditions-such as diet and exercise. This chapter explores the different approaches and agents used to try to modify the course of a range of NDDs, and highlights their progress relative to the clinic and the patients suffering with these currently incurable conditions.
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33

Nakamura, Tomohiro, and Stuart A. Lipton. Neurodegenerative Diseases as Protein Misfolding Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0002.

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Neurodegenerative diseases (NDDs) often represent disorders of protein folding. Rather than large aggregates, recent evidence suggests that soluble oligomers of misfolded proteins are the most neurotoxic species. Emerging evidence points to small, soluble oligomers of misfolded proteins as the cause of synaptic dysfunction and loss, the major pathological correlate to disease progression in many NDDs including Alzheimer’s disease. The protein quality control machinery of the cell, which includes molecular chaperones as found in the endoplasmic reticulum (ER), the ubiquitin-proteasome system (UPS), and various forms of autophagy, can counterbalance the accumulation of misfolded proteins to some extent. Their ability to eliminate the neurotoxic effects of misfolded proteins, however, declines with age. A plausible explanation for the age-dependent deterioration of the quality control machinery involves compromise of these systems by excessive generation of reactive oxygen species (ROS), such as superoxide anion (O2-), and reactive nitrogen species (RNS), such as nitric oxide (NO). The resulting redox stress contributes to the accumulation of misfolded proteins. Here, we focus on aberrantly increased generation of NO-related species since this process appears to accelerate the manifestation of key neuropathological features, including protein misfolding. We review the chemical mechanisms of posttranslational modification by RNS such as protein S-nitrosylation of critical cysteine thiol groups and nitration of tyrosine residues, showing how they contribute to the pathogenesis of NDDs.
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34

Zetterberg, Henrik, and Jonathan M. Schott. Fluid Biomarkers Indicative of Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0008.

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A major unifying feature of neurodegenerative diseases (NDDs) is excessive neuronal loss. Depending on when and where this occurs, patients may express distinct neurological and psychiatric symptoms. Neurodegeneration is accompanied by protein aggregation, inflammation, and microglial activation that may be drivers of the disease or in some circumstances may be protective reactions to the neurodegenerative process. A key development over the past decade has been our ability to leverage these accompanying central nervous system changes to develop clinically impactful biomarkers of specific NDDs. This has been crucial in helping us develop an understanding the time line of progression of these diseases, in their early diagnosis and to help target patients appropriately in therapeutic clinical trials, This chapter gives an overview of both established and novel fluid biomarkers for neurodegeneration, protein accumulation, inflammation, and microglial activation across different neurodegenerative diseases. Common as well as disease-specific biomarker changes in cerebrospinal fluid and blood are emphasized.
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35

Nat, Roxana, and Andreas Eigentler. Cell Culture, iPS Cells and Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0013.

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Somatic reprogramming technology, which enables the conversion of adult human non-neural cells into neurons, has progressed rapidly in recent years. The derivation of patient-specific induced pluripotent stem (iPS) cells has become routine. The inherent broad differentiation potential of iPS cells makes possible the generation of diverse types of human neurons. This constitutes a remarkable step in facilitating the development of more appropriate and comprehensive preclinical human disease models, as well as for high throughput drug screenings and cell therapy. This chapter reviews recent progress in the human iPS cell culture models related to common and rare NDDs, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, spinal muscular atrophy, and degenerative ataxias. It focuses on the pathophysiological features revealed in cell cultures, and the neuronal subtypes most affected in NDDs. The chapter discusses the validity, limitation, and improvements of this system in faithfully and reproducibly recapitulating disease pathology.
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36

Holzmann, Robert. The ABCs of NDCs. World Bank, Washington, DC, 2019. http://dx.doi.org/10.1596/31627.

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37

Vern, Jules. CÆsar Cascabel: NDAS Digest. Independently Published, 2018.

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38

Martin, Doc. NDEs ETs and PTSD. Lulu Press, Inc., 2021.

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39

Homer, Blaine. Netware Printing: Managing Ndps. New Riders Pub, 1996.

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40

Homer, Blaine. Netware Printing With Ndps. New Riders Pub, 1996.

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41

Belikova, T. N. Vse ob NDS. Piter, 2006.

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42

Vern, Jules. Meridiana: Ndas Digest Print Edition. Independently Published, 2018.

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43

Persuasion: Ndas Digest Print Edition. Independently Published, 2018.

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44

Vern, Jules. Godfrey Morgan: Ndas Digest Print Edition. Independently Published, 2018.

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45

Vern, Jules. Fur Country: Ndas Digest Print Edition. Independently Published, 2018.

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46

Vern, Jules. Floating City: Ndas Digest Print Edition. Independently Published, 2018.

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47

Vern, Jules. Antarctic Mystery: Ndas Digest Print Edition. Independently Published, 2018.

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48

Vern, Jules. Green Ray: Ndas Digest Print Edition. Independently Published, 2018.

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49

Vern, Jules. Mathias Sandorf: Ndas Digest Print Edition. Independently Published, 2018.

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50

Vern, Jules. Claudius Bombarnac: Ndas Digest Print Edition. Independently Published, 2018.

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