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M1 (Tank) --- History.

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Microglia-mediated neuroinflammation is one of the shared prominent hallmarks among various forms of neurodegeneration. Depending on the milieu in which microglia become activated, the polarization of microglia shows to be heterogeneous with diverse functional phenotypes that range from pro-inflammatory phenotypes to immunosuppressive phenotypes. Therefore, targeting microglial polarization holds great promise for the treatment of neurodegeneration. This eBook focuses on the potential mechanisms of microglial polarization that are critically associated with a broad spectrum of neurodegenerative diseases, including Parkinson’s disease (PD), Alzheimer’s disease (AD), Amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), Traumatic brain injury (TBI), glaucomatous neurodegeneration and prion diseases. This topic also involves the therapeutic targeting of microglial polarization by nutritional and pharmacological modulators. Moreover, this topic describes advanced technologies employed for studying microglia. Age-related changes in microglia functions are also discussed. Overall, this eBook provides comprehensive understandings of microglial polarization in the course of neurodegeneration, linking with aging-related microglial alterations and technologies developed for microglial studies. Hopefully, it will also give comprehensive insights into various aspects of therapeutic treatment for neurodegeneration, through targeting microglial polarization.

M2 Microglia --- Microglial Polarization --- Neurodegenerative diseases --- M1 Microglia --- Aging --- Neuroinflammation --- M1/M2 Switch --- M2 Microglia --- Microglial Polarization --- Neurodegenerative diseases --- M1 Microglia --- Aging --- Neuroinflammation --- M1/M2 Switch

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Microglia-mediated neuroinflammation is one of the shared prominent hallmarks among various forms of neurodegeneration. Depending on the milieu in which microglia become activated, the polarization of microglia shows to be heterogeneous with diverse functional phenotypes that range from pro-inflammatory phenotypes to immunosuppressive phenotypes. Therefore, targeting microglial polarization holds great promise for the treatment of neurodegeneration. This eBook focuses on the potential mechanisms of microglial polarization that are critically associated with a broad spectrum of neurodegenerative diseases, including Parkinson’s disease (PD), Alzheimer’s disease (AD), Amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), Traumatic brain injury (TBI), glaucomatous neurodegeneration and prion diseases. This topic also involves the therapeutic targeting of microglial polarization by nutritional and pharmacological modulators. Moreover, this topic describes advanced technologies employed for studying microglia. Age-related changes in microglia functions are also discussed. Overall, this eBook provides comprehensive understandings of microglial polarization in the course of neurodegeneration, linking with aging-related microglial alterations and technologies developed for microglial studies. Hopefully, it will also give comprehensive insights into various aspects of therapeutic treatment for neurodegeneration, through targeting microglial polarization.

M2 Microglia --- Microglial Polarization --- Neurodegenerative diseases --- M1 Microglia --- Aging --- Neuroinflammation --- M1/M2 Switch

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Macrophages have unique and diverse functions necessary for survival. And, in humans (and other species), they are the most abundant leukocytes in tissues. The Innate functions of macrophages that are best known are their unusual ability to either “Kill” or “Repair”. Since killing is a destructive process and repair is a constructive process, it was stupefying how one cell could exhibit these 2 polar – opposite functions. However, in the late 1980’s, it was shown that macrophages have a unique ability to enzymatically metabolize Arginine to Nitric Oxide (NO, a gaseous non – specific killer molecule) or to Ornithine (a precursor of polyamines and collagen for repair). The dual Arginine metabolic capacity of macrophages provided a functional explanation for their ability to kill or repair. Macrophages predominantly producing NO are called M1 and those producing Ornithine are called M2. M1 and M2 – dominant responses occur in lower vertebrates, and in T cell deficient vertebrates being directly driven by Damage and Pathogen Associated Molecular Patterns (DAMP and PAMP). Thus, M1 and M2 are Innate responses that protect the host without Adaptive Immunity. In turn, M1/M2 is supplanting previous models in which T cells were necessary to “activate” or “alternatively activate” macrophages (the Th1/Th2 paradigm). M1 and M2 macrophages were named such because of the additional key findings that these macrophages stimulate Th1 and Th2 – like responses, respectively. So, in addition to their unique ability to kill or repair, macrophages also govern Adaptive Immunity.All of the foregoing would be less important if M1 or M2 – dominant responses were not observed in disease. But, they are. The best example to date is the predominance of M2 macrophages in human tumors where they act like wound repair macrophages and actively promote growth. More generally, humans have become M2 – dominant because sanitation, antibiotics and vaccines have lessened M1 responses. And, M2 dominance seems the cause of ever - increasing allergies in developed countries. Obesity represents a new and different circumstance. Surfeit energy (e.g., lipoproteins) causes monocytes to become M1 dominant in the vessel walls causing plaques.Because M1 or M2 dominant responses are clearly causative in many modern diseases, there is great potential in developing the means to selectively stimulate (or inhibit) either M1 or M2 responses to kill or repair, or to stimulate Th1 or Th2 responses, depending on the circumstance. The contributions here are meant to describe diseases of M1 or M2 dominance, and promising new methodologies to modulate the fungible metabolic machinery of macrophages for better health.

Microbiology & Immunology --- Biology --- Health & Biological Sciences --- Infection --- wound --- innate immunity --- M1 --- M2 --- Atherosclerosis --- macrophage --- Cancer

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As the average ages of Army weapon systems increase, it has been assumed that this is leading to increasing maintenance costs. However, it has proved difficult to quantitatively "validate" and estimate the actual effect of equipment age on costs. In particular, it has been noted that increases in costs may have been "hidden" by how Army budgets are structured or mitigated by adaptations in part-ordering practices that are not reflected in spending and budgets. This study examines the relationship between equipment age and spare part costs for M1 Abrams tanks through the use of part requisition data. The authors also examine the issue of adaptive practices by comparing actual part expenditures to an exchange price-based valuation of part demands. This work is closely related to a companion study on the effects of equipment age on mission critical failures, a key component of equipment readiness.

M1 (Tank) --- Spare parts --- Maintenance and repair --- Costs. --- United States. --- Equipment --- Maintenance and repair. --- Weapons systems