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Fanconi anaemia (FA) is an autosomal recessive disorder characterized by progressive pancytopaenia and predisposition to malignancy, often accompanied by congenital malformations. The cellular phenotype of FA includes increased chromosomal instability and accumulation in the G2 phase of the cell cycle, both of which are exacerbated by the hallmark sensitivity of FA cells to DNA crosslinking agents such as mitomycin C (MMC) and diepoxybutane (DEB). FA is genetically heterogeneous, consisting of at least eleven complementation groups, the genes for eight of which have been cloned. was the first gene causal for FA to be identified, and consequently has been the most intensively studied. Loss of function studies have demonstrated an important role for FANCC in the proliferation of germ cells and haematopoietic stem cells (HPCs). Together with the protein products of at least five other FA genes, FANCC participates in the formation of a nuclear protein complex, the formation of which is required for monoubiquitination of the FANCD2 protein. This cooperative action of the FA proteins fits well with the indistinguishable clinical presentation and universal cellular crosslinker sensitivity of the complementation groups. However, despite its ability to participate in a nuclear protein complex and possible involvement in nuclear activities such as DNA repair and transcriptional regulation, FANCC is unique among the FA proteins in having a predominandy cytoplasmic cellular localization. Investigation of possible cytoplasmic roles for FANCC have revealed it to be a multifunctional protein involved in the suppression of cell death in response to a wide range of stimuli including DNA-crosslinking agents, factor withdrawl, dsRNA, stimulatory cytokines and Fas ligation, as well as a having a possibly interrelated role in maintaining of the redox state of the cell.

Fanconi anaemia (FA) is an autosomal recessive disorder characterized by progressive pancytopaenia and predisposition to malignancy, often accompanied by congenital malformations. The cellular phenotype of FA includes increased chromosomal instability and accumulation in the G2 phase of the cell cycle, both of which are exacerbated by the hallmark sensitivity of FA cells to DNA crosslinking agents such as mitomycin C (MMC) and diepoxybutane (DEB). FA is genetically heterogeneous, consisting of at least eleven complementation groups, the genes for eight of which have been cloned. was the first gene causal for FA to be identified, and consequently has been the most intensively studied. Loss of function studies have demonstrated an important role for FANCC in the proliferation of germ cells and haematopoietic stem cells (HPCs). Together with the protein products of at least five other FA genes, FANCC participates in the formation of a nuclear protein complex, the formation of which is required for monoubiquitination of the FANCD2 protein. This cooperative action of the FA proteins fits well with the indistinguishable clinical presentation and universal cellular crosslinker sensitivity of the complementation groups. However, despite its ability to participate in a nuclear protein complex and possible involvement in nuclear activities such as DNA repair and transcriptional regulation, FANCC is unique among the FA proteins in having a predominandy cytoplasmic cellular localization. Investigation of possible cytoplasmic roles for FANCC have revealed it to be a multifunctional protein involved in the suppression of cell death in response to a wide range of stimuli including DNA-crosslinking agents, factor withdrawl, dsRNA, stimulatory cytokines and Fas ligation, as well as a having a possibly interrelated role in maintaining of the redox state of the cell.

Fanconi anaemia (FA) is an autosomal recessive disorder characterized by progressive pancytopaenia and predisposition to malignancy, often accompanied by congenital malformations. The cellular phenotype of FA includes increased chromosomal instability and accumulation in the G2 phase of the cell cycle, both of which are exacerbated by the hallmark sensitivity of FA cells to DNA crosslinking agents such as mitomycin C (MMC) and diepoxybutane (DEB). FA is genetically heterogeneous, consisting of at least eleven complementation groups, the genes for eight of which have been cloned. was the first gene causal for FA to be identified, and consequently has been the most intensively studied. Loss of function studies have demonstrated an important role for FANCC in the proliferation of germ cells and haematopoietic stem cells (HPCs). Together with the protein products of at least five other FA genes, FANCC participates in the formation of a nuclear protein complex, the formation of which is required for monoubiquitination of the FANCD2 protein. This cooperative action of the FA proteins fits well with the indistinguishable clinical presentation and universal cellular crosslinker sensitivity of the complementation groups. However, despite its ability to participate in a nuclear protein complex and possible involvement in nuclear activities such as DNA repair and transcriptional regulation, FANCC is unique among the FA proteins in having a predominandy cytoplasmic cellular localization. Investigation of possible cytoplasmic roles for FANCC have revealed it to be a multifunctional protein involved in the suppression of cell death in response to a wide range of stimuli including DNA-crosslinking agents, factor withdrawl, dsRNA, stimulatory cytokines and Fas ligation, as well as a having a possibly interrelated role in maintaining of the redox state of the cell.

Fanconi anaemia (FA) is an autosomal recessive disorder characterized by progressive pancytopaenia and predisposition to malignancy, often accompanied by congenital malformations. The cellular phenotype of FA includes increased chromosomal instability and accumulation in the G2 phase of the cell cycle, both of which are exacerbated by the hallmark sensitivity of FA cells to DNA crosslinking agents such as mitomycin C (MMC) and diepoxybutane (DEB). FA is genetically heterogeneous, consisting of at least eleven complementation groups, the genes for eight of which have been cloned. was the first gene causal for FA to be identified, and consequently has been the most intensively studied. Loss of function studies have demonstrated an important role for FANCC in the proliferation of germ cells and haematopoietic stem cells (HPCs). Together with the protein products of at least five other FA genes, FANCC participates in the formation of a nuclear protein complex, the formation of which is required for monoubiquitination of the FANCD2 protein. This cooperative action of the FA proteins fits well with the indistinguishable clinical presentation and universal cellular crosslinker sensitivity of the complementation groups. However, despite its ability to participate in a nuclear protein complex and possible involvement in nuclear activities such as DNA repair and transcriptional regulation, FANCC is unique among the FA proteins in having a predominandy cytoplasmic cellular localization. Investigation of possible cytoplasmic roles for FANCC have revealed it to be a multifunctional protein involved in the suppression of cell death in response to a wide range of stimuli including DNA-crosslinking agents, factor withdrawl, dsRNA, stimulatory cytokines and Fas ligation, as well as a having a possibly interrelated role in maintaining of the redox state of the cell.

Between 1957 and 1974 Jacob Mincer pioneered important new approaches to labor economics. In the years since these seminal discoveries, he, as well as generations of his students and colleagues at Columbia University and elsewhere, adopted these innovations to reach important conclusions about human wellbeing. In 1967 I was lucky enough to arrive as a graduate student at Columbia University, just at the peak of this research revolution. In this paper, I detail some of my recollections concerning Jacob Mincer and the hospitable research atmosphere at Columbia University that sparked so much of this path breaking research.

Fanconi anaemia (FA) is an autosomal recessive disorder characterized by progressive pancytopaenia and predisposition to malignancy, often accompanied by congenital malformations. The cellular phenotype of FA includes increased chromosomal instability and accumulation in the G2 phase of the cell cycle, both of which are exacerbated by the hallmark sensitivity of FA cells to DNA crosslinking agents such as mitomycin C (MMC) and diepoxybutane (DEB). FA is genetically heterogeneous, consisting of at least eleven complementation groups, the genes for eight of which have been cloned. was the first gene causal for FA to be identified, and consequently has been the most intensively studied. Loss of function studies have demonstrated an important role for FANCC in the proliferation of germ cells and haematopoietic stem cells (HPCs). Together with the protein products of at least five other FA genes, FANCC participates in the formation of a nuclear protein complex, the formation of which is required for monoubiquitination of the FANCD2 protein. This cooperative action of the FA proteins fits well with the indistinguishable clinical presentation and universal cellular crosslinker sensitivity of the complementation groups. However, despite its ability to participate in a nuclear protein complex and possible involvement in nuclear activities such as DNA repair and transcriptional regulation, FANCC is unique among the FA proteins in having a predominandy cytoplasmic cellular localization. Investigation of possible cytoplasmic roles for FANCC have revealed it to be a multifunctional protein involved in the suppression of cell death in response to a wide range of stimuli including DNA-crosslinking agents, factor withdrawl, dsRNA, stimulatory cytokines and Fas ligation, as well as a having a possibly interrelated role in maintaining of the redox state of the cell.

This paper studies forty years of New Home Economics (NHE), a school of household economics started by Jacob Mincer and Gary Becker at Columbia University in the early sixties. Household economics is defined as economic research concerning decisions that household members make regarding any allocation of resources. These decisions may regard consumption, labor supply, transportation, fertility, or health. From studying the history of the NHE we learn that its growth benefited from the concentration of talent at Columbia, the diversity of a student body that included many talented men and women, a relatively high concentration of married students who tended to be more interested in household production, the proximity of research organizations in New York, an avoidance of political controversy, and a pleasant workshop atmosphere.

Economic developments of the past 3 decades posed new questions to economists: What are the causes of fluctuations in rates of return to human capital? What is the relation between the changing skill-wage structure and changing overall wage inequality? Does the widening of the wage structure produce an equilibrating supply response? What are the causes, dimensions and implications of the “technological cycle” for wages, unemployment, and its “natural rate”? Why is the long term trend of human capital formation relentlessly upward?

My research of the past decade, among that of other economists, attempted to provide answers to these questions, as described above. In the course of the analysis several misconceptions are clarified: (1) The view of an increasing “wage gap” as a worsening “social divide” misses the incentive effects of the increased rates of return on furthering investments in human capital. These are empirically documented. (2) Growing overall wage inequality can conceal a declining inequality of opportunity as it did in recent decades. (3) Technological unemployment as an aggregate phenomenon appears to be a myth. (4) The concurrent supply response to increasing demand for human capital applies to investments, not to the stock. The accumulation of investments (such as enrollments) over time produces a lag in the response of the human capital stock. This lag is a basic cause of the “technological cycle”.

Finally, it is worth noting that a positive skill bias is not inherent in technological changes. These may sometimes carry a negative effect on the demand for human capital. The implications of “deskilling” (the assembly line is an example) would be the opposite of what we found for the recent decades (1970–2000). However the long-term growth of human capital suggests a positive skill bias in the long run.

In 1958, Jacob Mincer pioneered an important approach to understanding earnings distribution. In the years since Mincer’s seminal work, he as well as his students and colleagues extended the original human capital model, reaching important conclusions about a whole array of observations pertaining to human wellbeing. This line of research explained why education enhances earnings; why earnings rise at a diminishing rate throughout one’s life; why earnings growth is smaller for those anticipating intermittent labor force participation; why men earn more than women; why whites earn more than blacks; why occupational distributions differ by gender; why geographic and job mobility predominate among the young; why unemployment is lower among the skilled; and why numerous other labor market phenomena occur. This paper surveys the answers to these and other questions based on research emanating from Mincer’s original discovery. In addition, this paper provides new empirical evidence regarding Mincer’s concept of the “overtaking age” — a topic not currently well explored in the literature. In this latter vein, the paper shows that Mincer’s original finding of a U-shaped (log) variance of earnings over the life cycle is upheld in recent data, both for the U.S. as well as at least seven other countries.

This paper reviews Jacob Mincer’s contributions to the analyses of earnings and the distribution of earnings through his pioneering focus on labor market experience or on-the-job training. It begins with a brief discussion of the theoretical literature on the distribution of earnings in the pre-Mincer period, and then discusses his analysis of human capital and earnings developed in his 1957 doctoral dissertation and 1958 Journal of Political Economy (JPE) article. Further analyses of on-the-job training, and in particular estimates of the rate of return from on-the-job training, are presented in his 1962 JPE paper. The synergy between Mincer and Becker during the 1960s is discussed, as is the development of the schooling-earnings function by Becker and Chiswick (1966). Mincer (1974) extended this relationship by incorporating experience to form the “human capital earnings function” in his Schooling, Experience and Earnings (1974). Subsequent modifications, extensions, tests of robustness and the wide applicability of the human capital earnings functions are presented.