Urban–rural difference in the costs of disability and its effects on poverty among people with disabilities in China

The urban–rural difference in poverty is an important issue in China, particularly for people with disabilities. The extra costs of disability render this population susceptible to falling into poverty, where this can exacerbate the inequality among people with disabilities between urban and rural areas of the country. Previous studies have provided empirical evidence for the extra costs of disabilities in certain countries, but little scholarly attention has been devoted to the urban–rural gap in the costs of disability, particularly in countries like China that have a dual urban–rural system. This study explores changes in the extra costs of disability in China between urban and rural households with disabled members from 2008 to 2018 by using the standard of living approach. We apply the Foster–Greer–Thorbecke Poverty Index to measure the rates of poverty in urban and rural households with disabilities after considering the costs of disability. The results reveal that the costs of disability were not always lower for rural households than for urban households. At the same time, many rural households with disabled people were found to suffer from severe poverty owing to the high costs of their disabilities. The difference in health insurance and rehabilitation services between urban and rural China have led to an urban-rural gap in the costs of disability. This suggests that supplying more goods and services for disabled people in rural areas, especially free services, and raising the reimbursement due to them from their health insurance can help improve their standard of living

Monodansylpentane as a Blue-Fluorescent Lipid-Droplet Marker for Multi-Color Live-Cell Imaging

Lipid droplets (LDs) are dynamic cellular organelles responsible for the storage of neutral lipids, and are associated with a multitude of metabolic syndromes. Here we report monodansylpentane (MDH) as a high contrast blue-fluorescent marker for LDs. The unique spectral properties make MDH easily combinable with other green and red fluorescent reporters for multicolor fluorescence imaging. MDH staining does not apparently affect LD trafficking, and the dye is extraordinarily photo-stable. Taken together MDH represents a reliable tool to use for the investigation of dynamic LD regulation within living cells using fluorescence microscopy

Dimethyl 2,2-bis­(2-cyano­ethyl)malonate

The asymmetric unit of the title compound, C11H14N2O4, contains one half-mol­ecule; a twofold rotation axis passes through the central C atom. Inter­molecular C—H⋯N hydrogen bonds link the mol­ecules into a one-dimensional supra­molecular structure

2,2′-Hexamethyl­enedi-1,3-benzothia­zole

The title compound, C20H20N2S2, was prepared by the reaction of suberic acid and 2-amino­thio­phenol under microwave irradiation. The mol­ecule lies on an inversion center

Bis(μ-2-phenyl­acetato-κ2 O:O)bis­[(2,2′-bipyridyl-κ2 N,N′)(2-phenyl­acetato-κO)copper(II)] dihydrate

The mol­ecule of the binuclear title complex, [Cu2(C8H7O2)4(C10H8N2)2]·2H2O, is located on an inversion centre. The Cu atoms are bridged by two O atoms of the monodentate phenyl­acetate groups [Cu—O = 1.9808 (14) and 2.3668 (14) Å]. The longer of the two bridging Cu—O bonds takes the apical position of the distorted square-pyramidal environment of the Cu atom, which is completed by two N atoms of the chelate 2,2′-bipyridine ligand [Cu—N = 2.0107 (17) and 2.0234 (16) Å]. The mol­ecules are assembled into stacks along [100] through π–π inter­actions with inter­planar distances of 3.630 (4) and 3.407 (3) Å; the resulting stacks are further connected into a three-dimensional supra­molecular architecture by O—H⋯O and C—H⋯O hydrogen-bonding inter­actions

Silencing of c-Ski augments TGF-b1-induced epithelial-mesenchymal transition in cardiomyocyte H9C2 cells

Background: The shRNA lentiviral vector was constructed to silence c-Ski expression in cardiac mus-  cle cells, with the aim of exploring the role of c-Ski in transforming growth factor b1 (TGF-b1)-induced epithelial-mesenchymal transitions (EMT) in H9C2 cells. Methods: Real-time polymerase chain reaction (RT-PCR) and western blot were used to detect c-Ski ex- pression at protein and messenger ribonucleic acid (mRNA) levels in 5 different cell lines. Then, lentiviral vector was constructed to silence or overexpress c-Ski in H9C2 cells. MTT and/or soft agar assay and tran- swell assay were used to detect cell proliferation and migration, respectively. The expression levels of c-Ski under different concentrations of TGF-b1 stimulation were detected by RT-qPCR and immunocytochemi- cal analysis. In the presence or absence of TGF-b1 stimulation, the proteins’ expression levels of a-SMA, FN and E-cadherin, which are closely correlated with the process of EMT, were measured by western blot after c-Ski silencing or overexpression. Meanwhile, the effect of c-Ski on Samd3 phosphorylation with TGF-b1 stimulation was investigated.  Results: There is a high expression of c-Ski at protein and mRNA levels in H9C2 cell line, which first demonstrated the presence of c-Ski expression in H9C2 cells. Overexpression of c-Ski significantly increased H9C2 cell proliferation. The ability of c-Ski gene silencing to suppress cell proliferation was gradually enhanced, and inhibition efficiency was the highest after 6 to 7 d of transfection. Moreover, H9C2 cells with c-Ski knockdown gained significantly aggressive invasive potential when compared with the control group. TGF-b1 stimulation could dose-independently reduce c-Ski expression in H9C2 cells and lead to obvious down-regulated expression of E-cadherin. Interestingly, c-Ski could restore E-cadherin expression while suppressing a-SMA and/or FN expression stimulated by TGF-b1. How- ever, shRNA-induced c-Ski knockdown aggravated only the TGF-b1-induced EMT. Moreover, c-Ski- -shRNA also promoted the phosphorylation of Samd3 induced by TGF-b1.  Conclusions: c-Ski expression in cardiac muscle cells could be down-regulated by TGF-b1. Silencing of c-Ski gene was accompanied by down-regulation of E-cadherin, up-regulation of a-SMA and/or FN and Smad3 phosphorylation induced by TGF-b1, promoting EMT process. Therefore, c-Ski may be closely associated with TGF-b1-induced EMT and play an important role in cardiac fibrosis develop- ment and progression.

The First Sinomastodon (Gomphotheriidae, Proboscidea) Skull From the Quaternary in China

The first Sinomastodon (Gomphotheriidae, Proboscidea) skull of the Early Pleistocene, collected from the Renzidong Cave deposits in Anhui Province, Eastern China, is described here as S. jiangnanensis sp. nov. As the only brevirostrine trilophodont gomphotheriid known from the Old World, Sinomastodon was mainly indigenous to China from the Early Pliocene to the Pleistocene. Compared with a few single Pleistocene teeth previously found in China, S. jiangnanensis sp. nov. is represented by a relatively complete skull, mandible and dentition, which is the first discovery of a Quaternary Sinomastodon skull from China. With a brevirostrine, elephant-like skull, no lower tusks, and simple bunodont and trilophodont intermediate molars, the new species is morphologically distinct from other gomphotheres and should belong to the genus Sinomastodon. The new species is more progressive than S. hanjiangensis and the Pliocene type species S. intermedius in its skull and mandible morphology, but is evidently more primitive than the Pleistocene S. yangziensis in its molar morphology. The faunal analysis suggests that the emergence of S. jiangnanensis sp. nov. in Jiangnan area and its southward migration may have been related to a cooling event at the beginning of the Quaternary in Eastern China