Chapter 6 Challenges for the education system in the era of the Fourth Industrial Revolution

The fourth industrial revolution, characterized by digitization, artificial intelligence and augmented reality, and megatrends such as globalization, urbanization, demographic changes and the knowledge-based economy, will trigger a series of profound technological, economic, social and environmental changes that will permanently and irreversibly change the role of the state in meeting social needs. Industry 4.0 will also change the type, nature, and scope of public goods and how they are produced, financed, delivered, and consumed. This book redefines the current paradigm of public goods. It proposes a model of production and distribution of public goods that acknowledges the participation of entities from the public, private, and nonprofit sectors. The authors argue that these entities would participate in the production, financing, distribution, and consumption of such goods. From a theoretical point of view, such an inclusive approach involving the expansion of the classical state - market dichotomy with new entities, including citizens themselves, leads to a new conceptualization and approach towards public goods. The model assumes shared responsibility, subsidiarity, and paternalistic libertarianism, and it allows the state to create new entities of an educational or fiscal nature, while remaining the regulator of public services and distribution. Additionally, the book analyzes changes regarding the perception of public goods, in the era of the fourth industrial revolution, across selected sectors such as healthcare and pension systems, education, local public goods, and public utility services. The book is primarily addressed to researchers, scholars and students across social and technical sciences, and it will also be a useful guide for central and local administration bodies responsible for public policy

Mechanisms and consequences of paternally transmitted chromosomal abnormalities

Paternally transmitted chromosomal damage has been associated with pregnancy loss, developmental and morphological defects, infant mortality, infertility, and genetic diseases in the offspring including cancer. There is epidemiological evidence linking paternal exposure to occupational or environmental agents with an increased risk of abnormal reproductive outcomes. There is also a large body of literature on germ cell mutagenesis in rodents showing that treatment of male germ cells with mutagens has dramatic consequences on reproduction producing effects such as those observed in human epidemiological studies. However, we know very little about the etiology, transmission and early embryonic consequences of paternally-derived chromosomal abnormalities. The available evidence suggests that: (1) there are distinct patterns of germ cell-stage differences in the sensitivity of induction of transmissible genetic damage with male postmeiotic cells being the most sensitive; (2) cytogenetic abnormalities at first metaphase after fertilization are critical intermediates between paternal exposure and abnormal reproductive outcomes; and, (3) there are maternally susceptibility factors that may have profound effects on the amount of sperm DNA damage that is converted into chromosomal aberrations in the zygote and directly affect the risk for abnormal reproductive outcomes

High-Throughput Screening of Shape Memory Alloy Thin-Film Spreads using Nanoindentation

We have demonstrated the utility of nanoindentation as a rapid characterization tool for mapping shape memoryalloy compositions in combinatorial thin-film libraries. Nanoindentation was performed on Ni–Mn–Al ternary composition spreads. The indentation hardness and the reduced elastic modulus were mapped across a large fraction of the ternary phase diagram. The large shape memoryalloy composition region, located around the Heusler composition (Ni2MnAl), was found to display significant departure in these mechanical properties from the rest of the composition spread. In particular, the modulus and the hardness values are lower for the martensite region than those of the rest of the phase diagram

ETOPOSIDE INDUCES CHROMOSOMAL ABNORMALITIES IN SPERMATOCYTES AND SPERMATOGONIAL STEM CELLS

Etoposide (ET) is a chemotherapeutic agent widely used in the treatment of leukemia, lymphomas and many solid tumors, such as testicular and ovarian cancers, that affect patients in their reproductive years. The purpose of the study was to use sperm FISH analyses to characterize the long-term effects of ET on male germ cells. We used a mouse model to characterize the induction of chromosomal aberrations (partial duplications and deletions) and whole chromosomal aneuploidies in sperm of mice treated with a clinical dose of ET. Semen samples were collected at 25 and 49 days after dosing to investigate the effects of ET on meiotic pachytene cells and spermatogonial stem-cells, respectively. ET treatment resulted in major increases in the frequencies of sperm carrying chromosomal aberrations in both meiotic pachytene (27- to 578-fold) and spermatogonial stem-cells (8- to 16-fold), but aneuploid sperm were induced only after treatment of meiotic cells (27-fold) with no persistent effects in stem cells. These results demonstrate that male meiotic germ cells are considerably more sensitive to ET than spermatogonial stem-cell and that increased frequencies of sperm with structural aberrations persist after spermatogonial stem-cell treatment. These findings predict that patients who undergo chemotherapy with ET may have transient elevations in the frequencies of aneuploid sperm, but more importantly, may have persistent elevations in the frequencies of sperm with chromosomal aberrations, placing them at higher risk for abnormal reproductive outcomes long after the end of their chemotherapy

Early Brain Response to Low-Dose Radiation Exposure Involves Molecular Networks and Pathways Associated with Cognitive Functions, Advanced Aging and Alzheimer's Disease

Understanding the cognitive and behavioral consequences of brain exposures to low-dose ionizing radiation has broad relevance for health risks from medical radiation diagnostic procedures, radiotherapy, environmental nuclear contamination, as well as earth orbit and space missions. Analyses of transcriptome profiles of murine brain tissue after whole-body radiation showed that low-dose exposures (10 cGy) induced genes not affected by high dose (2 Gy), and low-dose genes were associated with unique pathways and functions. The low-dose response had two major components: pathways that are consistently seen across tissues, and pathways that were brain tissue specific. Low-dose genes clustered into a saturated network (p < 10{sup -53}) containing mostly down-regulated genes involving ion channels, long-term potentiation and depression, vascular damage, etc. We identified 9 neural signaling pathways that showed a high degree of concordance in their transcriptional response in mouse brain tissue after low-dose radiation, in the aging human brain (unirradiated), and in brain tissue from patients with Alzheimer's disease. Mice exposed to high-dose radiation did not show these effects and associations. Our findings indicate that the molecular response of the mouse brain within a few hours after low-dose irradiation involves the down-regulation of neural pathways associated with cognitive dysfunctions that are also down regulated in normal human aging and Alzheimer's disease