Political connection and business transformation in family firms:evidence from China

We investigate the impact of family ownership on core business transformation and the moderating role of political connections in this relation through a Probit model, conditional Logit model, and Heckman selection model with instrumental variable using data from Chinese listed companies covering 2001–2010. The results demonstrate that, compared with non-family firms, family firms are more likely to transform their core business, enter strongly correlative industries and non-regulated industries, and adopt a mergers and acquisitions (M&A) mode. Furthermore, compared with politically non-connected family firms, family firms with political connections are more likely to conduct business transformation and adopt M&A rather than an internal cultivation mode to realize transformation. In addition, political connections make family firms more likely to enter weakly correlative industries and increase their chances of entering government-regulated industries

Energy price slump and policy response in the coal-chemical industry district:a case study of Ordos with a system dynamics model

We employ system dynamics method towards a coal-chemical industry district economy evolution model, using coal industry, the coal-chemical industry, their downstream industries, and the manufacture-related service industry. Moreover, we construct energy price and policy response scenarios based on Ordos’ management experience. The results show that the energy price slump had a negative impact on the overall economic development of the coal-chemical industry district, despite promoting non-resource industries. Furthermore, policies had different effects on the industry's output value and profit. In the long-term, developing alternative industries (AI) helps increase the industrial output value and profit. Decreasing value added tax (VAT) has immediate results and a distinctive effect on industrial short-term production value and profit, its long-term effect being limited. The effect of production limit (PL) on industrial profit is stronger than output value, and financial support (FS) is more conducive to improve the latter. However, coal mining and coal-chemical loan increases decrease the gross industrial profit level. Technology innovation (TI) has the best individual policy overall effect on production value and profits. Furthermore, the simultaneous implementation of PL, TI and AI can generate the synergy effect for each of them. And the simultaneous implementation of VAT and one or couple of other policies will generate the crowding-out effect both for VAT and other policies

Coal overcapacity in China:Multiscale analysis and prediction

Gaining a quantitative understanding of the causes of coal overcapacity and accurately predicting it are important for both government agencies and coal enterprises. Following the decomposition-reconstruction-prediction concept, a combined Ensemble Empirical Mode Decomposition-Least Square Support Vector Machine-Autoregressive Integrated Moving Average (EEMD-LSSVM-ARIMA) model is proposed for quantitatively analyzing and forecasting coal overcapacity in China. The results show that the main causes of coal overcapacity in China include insufficient demand, market failure, and institutional distortion. Institutional distortion, with an influence degree of 73.75%, is the most fundamental and influential factor. From 2017 to 2019, the scale of coal overcapacity in China will reach between 1.721and 1.819 billion tons, suggesting that coal overcapacity will remain a serious problem. The rate of coal overcapacity caused by insufficient demand will fluctuate slightly, while coal overcapacity caused by market failure will trend downward, but the impact of institutional distortion on coal overcapacity will be exacerbated. A statistical analysis demonstrates that the EEMD-LSSVM-ARIMA model significantly outperformed other widely developed baselines (e.g. ARIMA, LSSVM, EEMD-ARIMA, and EEMD-LSSVM)

Assessing industrial ecosystem vulnerability in the coal mining area under economic fluctuations

In the context of the depth adjustment of the global economy and wild fluctuations in energy prices, the vulnerability issue of the coal mining industrial ecosystem (CMIES) has seriously affected the sustainable development of the regional economy. Comparisons of CMIES health status at a regional level are worthy of being conducted. This not only contributes to understanding a particular coal mining area's situation in regards to CMIES vulnerability, but also helps to discover a meaningful benchmark to learn the experiences in terms of action programmes formulation. In this study, based on the analysis of the vulnerability response mechanism of CMIES to economic fluctuations, an initial indicator system for vulnerability assessment of CMIES was constructed. Ultimately, 14 vulnerability-evaluating indicators and their weights were obtained using rough set attribute reduction. Based on a composite CMIES Vulnerability Index (CVI), the Rough Set-Technique for Order Preference by Similarity to Ideal Solution-Rank-sum Ratio (RS-TOPSIS-RSR) methodology is proposed to conduct the CMIES vulnerability assessment process from an overall perspective. Using this methodology, 33 coal mining areas in China are ranked as well as grouped into three specific groups based on the CVI score. The results demonstrate the feasibility of the proposed method as a valuable tool for decision making and performance evaluation with multiple alternatives and criteria

Comparing the vulnerability of different coal industrial symbiosis networks under economic fluctuations

We establish a vulnerability analytical framework of CISN, and illustrate the impact path of economic fluctuation on CISN performance. Based on this, we propose an improved cascading failure model with directed weighted network, and design five network performance indicators (i.e., relative value of cascading failure, average path length, relative value of maximal connected sub-graphs, network efficiency, and structure entropy). Taking three coal eco-industrial parks in China as cases, we simulate and compare the impacts on CISN vulnerability (i.e., equality-based, dependent-based, and nested-based CISNs) of economic fluctuation. The results indicate that the interaction between economic fluctuation and network structure is the key factor in determining system vulnerability. Concerning overall vulnerability, equality-based CISN is highest, dependent-based CISN is next, and nested-based CISN is lowest. Regarding disturbance type, the changes in the five performance indicators of the three types of CISN are more intense under energy price shocks than with declining demand. Moreover, the cascading failure scale of equality-based CISN is greatest with declining demand, while the other two kinds of CISN’s is greatest under energy price shocks. Concerning disturbance intensity, equality-based CISN shows initial value sensitivity to economic fluctuation, and nested-based CISN has the strongest tolerances for economic fluctuation. From the network performance perspective, the performance of nested-based CISN is superior to that of dependent-based and equality-based CISNs. Due to longer average path length and lower network efficiency, the failure diffusion trend of equality-based CISN shows the curve of Type-S, and the diffusion rate is smooth and slow. Contrariwise, the initial diffusion rate of dependent-based CISN is the highest, indicating that the loss of system efficiency can somewhat improve the system’s anti-risk ability

Retinal basal laminar deposits in complement fH/fP mouse model of dense deposit disease

Purpose: Dense deposit disease (DDD) is caused by dysregulation of the alternative pathway of the complement cascade and characterized by electron-dense deposits in the kidney glomerular basement membrane (GBM) and drusen in Bruch's membrane (BrM). Complement factor H (fH) and factor properdin (fP) regulate complement activation; fH inhibits alternative pathway (AP) activation, whereas fP promotes it. We report pathologic changes in eyes of an fH and fP double-mutant mouse, which we previously showed have dense deposits in the GBM and early mortality from nephropathy.Methods: fHm/m, fP−/−, and fHm/m/fP−/− mice were generated on a C57BL/6–129J background. Fundus imaging at 8 weeks of age was followed by analysis via light and electron microscopy. Retinal function was assessed by electroretinography (ERG). Complement levels and localization were tested by immunohistochemistry and ELISA. Retinas of fHm/m/fP−/− mice treated with intraperitoneal injections of an anti-C5 antibody were compared to those of age- and genotype-matched mice injected with an isotype control antibody.Results: fHm/m/fP−/− mice suffered early-onset retinal hypopigmented spots detected using in vivo retinal photography, and histologic examination showed basal laminar deposits (BLamD), degeneration of the photoreceptors, and RPE vacuolization. ERG showed diminished retinal function. The anti-C5 antibody was retina-protective.Conclusions: This unique mouse represents a new model of complement-mediated rapid-onset DDD, and could be useful in exploring the pathologic changes associated with BLamD in age-related macular degeneration

Complement Factor H Mutation W1206R Causes Retinal Thrombosis and Ischemic Retinopathy in Mice

© 2019 American Society for Investigative Pathology Single-nucleotide polymorphisms and rare mutations in factor H (FH; official name, CFH) are associated with age-related macular degeneration and atypical hemolytic uremic syndrome, a form of thrombotic microangiopathy. Mice with the FH W1206R mutation (FH R/R ) share features with human atypical hemolytic uremic syndrome. Herein, we report that FH R/R mice exhibited retinal vascular occlusion and ischemia. Retinal fluorescein angiography demonstrated delayed perfusion and vascular leakage in FH R/R mice. Optical coherence tomography imaging of FH R/R mice showed retinal degeneration, edema, and detachment. Histologic analysis of FH R/R mice revealed retinal thinning, vessel occlusion, as well as degeneration of photoreceptors and retinal pigment epithelium. Immunofluorescence showed albumin leakage from blood vessels into the neural retina, and electron microscopy demonstrated vascular endothelial cell irregularity with narrowing of retinal and choroidal vessels. Knockout of C6, a component of the membrane attack complex, prevented the aforementioned retinal phenotype in FH R/R mice, consistent with membrane attack complex–mediated pathogenesis. Pharmacologic blockade of C5 also rescued retinas of FH R/R mice. This FH R/R mouse strain represents a model for retinal vascular occlusive disorders and ischemic retinopathy. The results suggest complement dysregulation can contribute to retinal vascular occlusion and that an anti-C5 antibody might be helpful for C5-mediated thrombotic retinal diseases

CD1 Mouse Retina Is Shielded From Iron Overload Caused by a High Iron Diet

Citation: Bhoiwala DL, Song Y, Cwanger A, et al. CD1 mouse retina is shielded from iron overload caused by a high iron diet. Invest Ophthalmol Vis Sci. 2015;56:5344-5352. DOI:10.1167/iovs.15-17026 PURPOSE. High RPE iron levels have been associated with age-related macular degeneration. Mutation of the ferroxidase ceruloplasmin leads to RPE iron accumulation and degeneration in patients with aceruloplasminemia; mice lacking ceruloplasmin and its homolog hephaestin have a similar RPE degeneration. To determine whether a high iron diet (HID) could cause RPE iron accumulation, possibly contributing to RPE oxidative stress in AMD, we tested the effect of dietary iron on mouse RPE iron. METHODS. Male CD1 strain mice were fed either a standard iron diet (SID) or the same diet with extra iron added (HID) for either 3 months or 10 months. Mice were analyzed with immunofluorescence and Perls' histochemical iron stain to assess iron levels. Levels of ferritin, transferrin receptor, and oxidative stress gene mRNAs were measured by quantitative PCR (qPCR) in neural retina (NR) and isolated RPE. Morphology was assessed in plastic sections. RESULTS. Ferritin immunoreactivity demonstrated a modest increase in the RPE in 10-month HID mice. Analysis by qPCR showed changes in mRNA levels of iron-responsive genes, indicating moderately increased iron in the RPE of 10-month HID mice. However, even by age 18 months, there was no Perls' signal in the retina or RPE and no retinal degeneration. CONCLUSIONS. These findings indicate that iron absorbed from the diet can modestly increase the level of iron deposition in the wild-type mouse RPE without causing RPE or retinal degeneration. This suggests regulation of retinal iron uptake at the blood-retinal barriers

Persistent and Progressive Outer Retina Thinning in Frontotemporal Degeneration

ObjectiveWhile Alzheimer’s disease is associated with inner retina thinning measured by spectral-domain optical coherence tomography (SD-OCT), our previous cross-sectional study suggested outer retina thinning in frontotemporal degeneration (FTD) patients compared to controls without neurodegenerative disease; we sought to evaluate longitudinal changes of this potential biomarker.MethodsSD-OCT retinal layer thicknesses were measured at baseline and after 1–2 years. Clinical criteria, genetic analysis, and a cerebrospinal fluid biomarker (total tau: β-amyloid) to exclude likely underlying Alzheimer’s disease pathology were used to define a subgroup of predicted molecular pathology (i.e., tauopathy). Retinal layer thicknesses and rates of change in all FTD patients (n = 16 patients, 30 eyes) and the tauopathy subgroup (n = 9 patients,16 eyes) were compared to controls (n = 30 controls, 47 eyes) using a generalized linear model accounting for inter-eye correlation and adjusting for age, sex, and race. Correlations between retinal layer thicknesses and Mini-Mental State Examinations (MMSE) were assessed.ResultsCompared to controls, returning FTD patients (143 vs. 130 μm, p = 0.005) and the tauopathy subgroup (143 vs. 128 μm, p = 0.03) had thinner outer retinas but similar inner layer thicknesses. Compared to controls, the outer retina thinning rate was not significant for all FTD patients (p = 0.34), but was significant for the tauopathy subgroup (−3.9 vs. 0.4 μm/year, p = 0.03). Outer retina thickness change correlated with MMSE change in FTD patients (Spearman rho = 0.60, p = 0.02) and the tauopathy subgroup (rho = 0.73, p = 0.04).ConclusionOur finding of FTD outer retina thinning persists and longitudinally correlates with disease progression. These findings were especially seen in probable tauopathy patients, which showed progressive outer retina thinning

A Murine Rp1 Missense Mutation Causes Protein Mislocalization and Slowly Progressive Photoreceptor Degeneration

Mutations in the RP1 gene can cause retinitis pigmentosa. We identified a spontaneous L66P mutation caused by two adjacent point mutations in the Rp1 gene in a colony of C57BL/6J mice. Mice homozygous for the L66P mutation exhibited slow, progressive photoreceptor degeneration throughout their lifespan. Optical coherence tomography imaging found abnormal photoreceptor reflectivity at 1 month of age. Histology found shortening and disorganization of the photoreceptor inner and outer segments and progressive thinning of the outer nuclear layer. Electroretinogram a- and b-wave amplitudes were decreased with age. Western blot analysis found that the quantity and size of the mutated retinitis pigmentosa 1 (RP1) protein were normal. However, immunohistochemistry found that the mutant Rp1 protein partially mislocalized to the transition zone of the shortened axonemes. This mutation disrupted colocalization with cytoplasmic microtubules in vitro. In conclusion, the L66P mutation in the first doublecortin domain of the Rp1 gene impairs Rp1 protein localization and function, leading to abnormalities in photoreceptor outer segment structure and progressive photoreceptor degeneration. This is the first missense mutation in Rp1 shown to cause retinal degeneration. It provides a unique, slowly progressive photoreceptor degeneration model that mirrors the slow degeneration kinetics in most patients with retinitis pigmentosa