As China continues to age rapidly, whether the country should adjust the official retirement age, and if so, when and how, are currently major policy concerns. We examine the impact of postponing the retirement age on the human capital of China in the next four decades. Two critical aspects of human capitalhealth and education-are incorporated to account for the quality of the work force. Our projections reveal the impact of nine scenarios on the Chinese labor force in the next few decades, highlighting the changes in ''the high human capital workforce''-those with good health and education. We show substantial impact with added work force ranging from 28 to 92 million per year depending on which scenarios are implemented. Furthermore, the retained workers are increasingly better educated. The gain in female workers is particularly significant, reaping the benefits of the education expansion since the 1990s.Electronic supplementary material The online version of this article (https://doi.org/10.1007/s10680-018-9467-3) contains supplementary material, which is available to authorized users.

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Cell apoptosis induced by heat stress is regulated by a complex signaling network. We previously reported that a p53-dependent pathway is involved. Here, we present evidence that NF-κB signaling plays a crucial role in preventing heat stress-induced early apoptosis. Human umbilical vein endothelial cells (HUVECs) were examined and increased phosphorylation of p65 and IκBα were detected, without IκBα degradation. When NF-κB signaling was inhibited by BAY11-7082, or a small interference RNA (siRNA) targeting p65, a significant increase in cell apoptosis and caspase-3 activity was observed, as well as reduced expression and translocation of HSP27 into the nucleus, an accumulation of reactive oxygen species, and prolonged phosphorylation of mitogen-activated protein kinases (MAPKs). In addition, an association between HSP27 and p65 was identified which may enhance NF-κB activation. When HSP27 was overexpressed, pretreatment of HUVECs with the antioxidant, apocynin, or N-acetyl cysteine, suppressed apoptosis. Similarly, inhibition of JNK and p38 with SP600125 and SB203580, respectively, also suppressed apoptosis, whereas siRNA-mediated HSP27 knockdown and treatment with the ERK 1/2 inhibitor PD98059 did otherwise. In conclusion, these findings suggest a novel role for an NF-κB signaling pathway involving HSP27, ROS, and MAPKs that confers a protective effect against heat stress-induced cell apoptosis.

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