Japanese current Situation of Care Service Industry and Labor Productivity

日本介護保険制度が実行されてから，介護費用が膨らみ，介護財政を圧迫し，第1，2号被保険者は保険料負担の増加を強いられている。今後の負担は更に重くなる。一方，介護サービス業は国民経済におけるパフォーマンスを確実に増している。投入構造で確認できた介護サービス業は粗付加価値投入であり，そのなかで雇用者所得は93.5%に達している。介護保険三施設の長期労働生産性を計測した結果，全産業平均を大きく下回っている。同部門は日本の産業部門においても有数の成長部門であり，労働・資本等の生産要素がこの部門に集約しつつある。しかし，低労働生産であり，資源配分を歪める恐れもある。また，労働生産性と賃金の間には密接な関係が確認されている。介護サービス業の低労働生産性は必然的に賃金に影響する。つまり低労働生産性から低賃金へという成り行きは従業員の高離職率，低い定着率をもたらす。結局，介護サービス業は人手不足という事態に直面する。賃金を引き上げるには，公定価格の介護報酬のもとでいかに労働生産性を上昇させるかが重要な課題である

Telomerase therapy reverses vascular senescence and extends lifespan in progeria mice

AIMS: Hutchinson-Gilford progeria syndrome (HGPS) is an accelerated ageing syndrome associated with premature vascular disease and death due to heart attack and stroke. In HGPS a mutation in lamin A (progerin) alters nuclear morphology and gene expression. Current therapy increases the lifespan of these children only modestly. Thus, greater understanding of the underlying mechanisms of HGPS is required to improve therapy. Endothelial cells (ECs) differentiated from induced pluripotent stem cells (iPSCs) derived from these patients exhibit hallmarks of senescence including replication arrest, increased expression of inflammatory markers, DNA damage, and telomere erosion. We hypothesized that correction of shortened telomeres may reverse these measures of vascular ageing. METHODS AND RESULTS: We generated ECs from iPSCs belonging to children with HGPS and their unaffected parents. Telomerase mRNA (hTERT) was used to treat HGPS ECs. Endothelial morphology and functions were assessed, as well as proteomic and transcriptional profiles with attention to inflammatory markers, DNA damage, and EC identity genes. In a mouse model of HGPS, we assessed the effects of lentiviral transfection of mTERT on measures of senescence, focusing on the EC phenotype in various organs. hTERT treatment of human HGPS ECs improved replicative capacity; restored endothelial functions such as nitric oxide generation, acetylated low-density lipoprotein uptake and angiogenesis; and reduced the elaboration of inflammatory cytokines. In addition, hTERT treatment improved cellular and nuclear morphology, in association with a normalization of the transcriptional profile, effects that may be mediated in part by a reduction in progerin expression and an increase in sirtuin 1 (SIRT1). Progeria mice treated with mTERT lentivirus manifested similar improvements, with a reduction in inflammatory and DNA damage markers and increased SIRT1 in their vasculature and other organs. Furthermore, mTERT therapy increased the lifespan of HGPS mice. CONCLUSION: Vascular rejuvenation using telomerase mRNA is a promising approach for progeria and other age-related diseases

Epidemiological Survey of Dyslipidemia in Civil Aviators in China from 2006 to 2011

Aim. This study aimed to analyze blood lipid levels, temporal trend, and age distribution of dyslipidemia in civil aviators in China. Methods. The 305 Chinese aviators were selected randomly and followed up from 2006 to 2011. Their total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) levels were evaluated annually. Mean values for each parameter by year were compared using a linear mixed-effects model. The temporal trend of borderline high, high, and low status for each index and of overall borderline high, hyperlipidemia, and dyslipidemia by year was tested using a generalized linear mixed model. Results. The aviators' TC (F=4.33, P<0.01), HDL-C (F=23.25, P<0.01), and LDL-C (F=6.13, P<0.01) values differed across years. The prevalence of dyslipidemia (F=5.53, P<0.01), borderline high (F=6.52, P<0.01), and hyperlipidemia (F=3.90, P<0.01) also differed across years. The prevalence rates for hyperlipidemia and dyslipidemia were the highest in the 41–50-year-old and 31–40-year-old groups. Conclusions. Civil aviators in China were in high dyslipidemia and borderline high level and presented with dyslipidemia younger than other Chinese populations

An epigenetic switch induced by Shh signalling regulates gene activation during development and medulloblastoma growth

The Sonic hedgehog (Shh) signalling pathway plays important roles during development and in cancer. Here we report a Shh-induced epigenetic switch that cooperates with Gli to control transcription outcomes. Before induction, poised Shh target genes are marked by a bivalent chromatin domain containing a repressive histone H3K27me3 mark and an active H3K4me3 mark. Shh activation induces a local switch of epigenetic cofactors from the H3K27 methyltransferase polycomb repressive complex 2 (PRC2) to an H3K27me3 demethylase Jmjd3/Kdm6b-centred coactivator complex. We also find that non-enzymatic activities of Jmjd3 are important and that Jmjd3 recruits the Set1/MLL H3K4 methyltransferase complexes in a Shh-dependent manner to resolve the bivalent domain. In vivo, changes of the bivalent domain accompanied Shh-activated cerebellar progenitor proliferation. Overall, our results reveal a regulatory mechanism that underlies the activation of Shh target genes and provides insight into the causes of various diseases and cancers exhibiting altered Shh signalling