Economic growth and household energy footprint inequality in China.

There are significant differences in energy footprints among individual households. This study uses an environmentally extended input-output approach to estimate the per capita household energy footprint (PCHEF) of 10 different income groups in China's 30 provinces and analyzes the heterogeneity of household consumption categories, and finally measures the energy equality of households in each province by measuring the energy footprint Gini coefficient (EF-Gini). It is found that the energy footprint of the top 10% income households accounted for about 22% of the national energy footprint in 2017, while the energy footprint of the bottom 40% income households accounted for only 24%. With the growth of China's economy, energy footprint inequality has declined spatially and temporally. Firstly, wealthier coastal regions have experienced greater convergence in their energy footprint than poorer inland regions. Secondly, China's household EF-Gini has declined from 0.38 in 2012 to 0.36 in 2017. This study shows that China's economic growth has not only raised household income levels, but also reduced energy footprint inequality.

Histone deacetylase 4 deletion results in abnormal chondrocyte hypertrophy and premature ossification from collagen type 2α1­expressing cells.

Histone deacetylase 4 (HDAC4) plays a vital role in chondrocyte hypertrophy and bone formation. To investigate the function of HDAC4 in postnatal skeletal development, the present study developed lineage­specific HDAC4­knockout mice [collagen type 2α1 (Col2α1)­Cre, HDAC4d/d mice] by crossing transgenic mice expressing Cre recombinase. Thus, a specific ablation of HDAC4 was performed in Col2α1­expressing mice cells. The knee joints of HDAC4fl/fl and Col2α1­Cre, HDAC4d/d mice were analyzed at postnatal day (P)2­P21 using an in vivo bromodeoxyuridine (BrdU) assay, and Safranin O, Von Kossa and whole­body staining were used to evaluate the developmental growth plate, hypertrophic differentiation, mineralization and skeletal mineralization patterns. The trabecular bone was analyzed using microcomputed tomography. The expressions of BrdU, proliferating cell nuclear antigen (PCNA), matrix metalloproteinase (MMP)­13, runt­related transcription factor (Runx)­2, osteoprotegerin (OPG), CD34, type X collagen (ColX), osteocalcin and Wnt5a were determined using immunohistochemistry, in situ hybridization (ISH) and reverse transcription­quantitative (RT­q)PCR. The results demonstrated that HDAC4­null mice (HDAC4d/d mice) were severely runted; these mice had a shortened hypertrophic zone (histopathological evaluation), accelerated vascular invasion and articular mineralization (Von Kossa staining), elevated expressions of MMP­13, Runx2, OPG and CD34 (RT­qPCR and immunohistochemistry), downregulated expression of the proliferative marker BrdU and PCNA (immunohistochemistry), increased expression of ColX and decreased expression of Wnt5a (ISH). In conclusion, chondrocyte­derived HDAC4 was responsible for regulating chondrocyte proliferation and differentiation as well as endochondral bone formation.