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Whether China’s carbon emissions trading (CET) has an impact on the financial performance of the market players of carbon trading, i.e., firms, is crucial to the sustainable development of national economy and carbon trading market. Based on the panel data of the listed firms in the seven high energy-consuming industries in China during 2010–2017, this paper uses the DID model to study the impact of CET on the firms’ financial performance. The empirical results show that the impact of CET on firms’ financial performance presents obvious industrial heterogeneity; CET policy reduces the financial performance of firms in the nonferrous metal industry but improves that in the power industry. In addition, with the implementation of CET policy, its impact on the financial performance of firms in the nonferrous metal and power industries is increasingly intensifying. Finally, there is a lag of 2–4 years on the impact of CET on the firms’ financial performance in the chemical, paper and aviation industries, and the effects change from negative to positive over time. That is, CET policy can hardly ensure that all firms are profitable in the short term, but there is still the possibility of profitability in the long term.

Does environmental quality affect firms’ activities that might improve that quality? In this paper, we use China's public heating policy as a quasi-experiment to investigate the impact of exogenous pollution differences on green innovation behavior. We use a regression discontinuity model, and carry out a suite of robustness tests. We consistently find that firms located in cities with an exogenous source of heavy pollution tend to adopt green innovation at a lower rate while we find no difference in the rate at which they adopt non-green innovation. We find a strong causal effect: being north of the boundary, where pollution levels are higher, leads firms to adopt less green innovation. Firms located in the heating areas report roughly 1 less green innovation per billion RMB of assets, a substantial difference given the average number of green innovations per billion RMB of assets of northern firms is 0.641.

Grain boundary diffusion technique with TbH3 nanoparticles was applied to fabricate Tb-less sintered NdFe-B permanent magnets with high coercivity. The magnetic properties and microstructure of magnets were systematically studied. The coercivity and remanence of grain boundary diffusion magnet are improved by 112% and reduced by 26% compared with those of the original magnet, respectively. Meanwhile, both the remanence temperature coefficient（α） and the coercivity temperature coefficient（β） of the magnets are improved after diffusion treatment. Microstructure shows that Tb element enriches in the surface region of Nd2Fe（14）B grains and is expected to exist as（Nd,Tb）2Fe（14）B phase. Thus, the magneto-crystalline anisotropy field of the magnet improves remarkably. As a result, the sintered Nd-FeB magnets by grain boundary diffusion with TbH3 nanoparticles exhibit enhanced coercivity.

Background： Kearns-Sayre syndrome （KSS） is a mitochondrial DNA （mtDNA） deletion disorder characterized by a triad of onset before 20 years of age, ophthalmoplegia, and pigmentary retinopathy. The heart and central nervous system are commonly involved. We summarized clinical and brain magnetic resonance imaging （M RI） features of a cohort of Chinese KSS patients. Methods： Nineteen patients confirmed by muscle biopsy and mtDNA analysis were enrolled. We examined clinical profiles, mainly focusing on changes in electrocardiogram （ECG） and brain MRI. The correlation between genotype and phenotype was statistically analyzed. Results： The mean age of onset was 9.6 ＋ 4.3 years, with all developing the classic triad at the time of diagnosis. Heart conduction block was detected in 63.2%, with four initially presenting as bundle branch block and developing into complete atrioventricular block over 3-72 months. Brain MRI showed symmetric high-T2 signals in 100% of cerebral and cerebellar white matter, as well as brainstem, 46.7% of basal ganglia, and 53.3% of thalamus. There were two patterns of cerebral white matter involvements, one with selective subcortical U-fibers and the other with periventricular white matter. The size of mtDNA deletion did not significantly correlate with age of onset or percentage of ragged blue fibers on muscle pathology. Conclusions： The clinical features of KSS evolve dynamically, affecting the cardiac conduction system predominantly, highlighting the significance of ECG monitoring. Brain MRI showed changes involving both the white matter and deep gray nuclei. Clinical presentation or severity of muscle pathological changes is not related to the size of mtDNA deletions.

Aim： To investigate the changes of expression and function of P-glycoprotein （P-GP） in cerebral cortex, hippocampus, liver, intestinal mucosa and kidney of streptozocin-induced diabetic rats. Methods： Diabetic rats were prepared via a single dose of streptozocin （65 mg/kg, ip）. Abcbl/P-GP mRNA and protein expression levels in tissues were evaluated using quantitative real time polymerase chain reaction （QRT-PCR） analysis and Western blot, respectively. P-GP function was investigated via measuring tissue-to-plasma concentration ratios and body fluid excretion percentages of rhodamine 123. Results： In 5- and 8-week diabetic rats, Abcbla mRNA levels were significantly decreased in cerebral cortices and intestinal mucosa, but dramatically increased in hippocampus and kidney. In liver, the level was increased in 5-week diabetic rats, and decreased in 8-week diabetic rats. Abcblb mRNA levels were increased in cerebral cortex, hippocampus and kidney, but reduced in liver and intestinal mucosa in the diabetic rats. Western blot results were in accordance with the alterations ofAbcbla mRNA levels in most tissues examined. P-GP activity was markedly decreased in most tissues of diabetic rats, except kidney tissues. Conclusion： Alterations in the expression and function of Abcbl/P-GP under diabetic conditions are tissue specific, Abcbl specific and diabetic duration-dependent.

目的：探讨IL-10、IL-13、IL-4Rα、FcεRIβ、IFNGR2、CYP3A4基因多态性与中国西北地区汉族人群β-内酰胺类抗生素过敏易感性的关联性。创新点：首次在甘肃地区汉族人群中探讨10个单核苷酸多态性位点与β-内酰胺类抗生素过敏易感性的关联性,为该地区人群β-内酰胺类抗生素过敏患者提供了基因组学水平的诊断数据。方法：以β-内酰胺类抗生素过敏者为研究对象进行病例对照研究,采用Sequenom Mass ARRAY分子量阵列技术平台定制单核苷酸多态性（SNP）芯片检测10个单核苷酸多态性与甘肃地区汉族人群β-内酰胺类抗生素过敏易感性的关联性。应用SHEsis软件完成IL-10及IL-13的连锁不平衡分析及单倍型构建。结论：CYP3A4 rs2242480基因多态性与男性患者β-内酰胺类抗生素过敏有显著的相关性（P=0.022;OR=0.167,95%CI：0.032–0.867）。IL-13的CCT及CAC单倍型与中国西北地区汉族β-内酰胺类抗生素过敏的相关性有待进一步研究。

For preventing ecosystem degradation, protecting natural habitats and conserving biodiversity within the habitats, 2588 nature reserves have been established in China at the end of 2010. The total area is up to 149.44 million ha and covers over 15% of Chinese terrestrial surface. Land-cover change, as the primary driver of biodiversity change, directly impacts ecosystem structures and functions. In this paper, 180 National Nature Reserves （NNRs） are selected and their total area is 44.71 million ha, accounting for 29.9% of all NNRs in China. In terms of the ecosystem characteristics and their major protected object, all selected NNRs are classified into 7 types. A Positive and Negative Change Index of Land-cover （PNCIL） was developed to analyze the land-cover change of each NNRs type from the late 1980s to 2005. The results show that the land-cover of all selected NNRs types have degradated to a certain degree except the forest ecosystem reserves with a decreasing rate, but the rate of degrada tion alleviated gradually. The mean positive and negative change rates of land-cover in all core zones decreased by 0.69% and 0.16% respectively. The landscape pattern of land-cover in the core zones was more stable than that in the buffer zones and the experimental zones. Furthermore, the ecological diversity and patch connectivity of land-cover in selected NNRs increased generally. In short, the land-cover of 180 selected NNRs in China had a beneficial chan qe trend after NNRs established, especially between 1995 and 2005.

Background： Tenofovir disoproxil （TDF） is a promising salvage therapy for patients with chronic hepatitis B （CHB） who failed regimens of other nucleoside analogues （NAs）. In this study, we aimed to investigate the clinical efficacy and safety ofTDF monotherapy in Chinese CHB patients with genotypic resistance. Methods： A total of 33 CHB patients who had tailed treatment with other NAs and had genotypic resistance were switched to TDF monotherapy for 48 weeks. Patients＇ demographic data （age, sex, history of hepatitis B virus [HBV] therapy）, laboratory testing results （hepatitis B e antigen [HBeAg] status, HBV DNA levels, alanine aminotransferase [ALT] levels, serum creatinine, urinary protein, genotypic assay）, clinical symptoms, and liver color ultrasound examinations were collected for evaluation at day 0 （baseline） and the 12th, 24th, 36th, and 48th weeks after initiating treatment. Statistical analyses were carried out using rank sum test or rank correlation. Results： With regard to efficacy, the study found that all patients who switched to TDF monotherapy had undetectable HBV DNA levels after 48 weeks. In addition, patients with lower baseline HBV DNA levels realized earlier virological undetectability （r = 0.39, P = 0.030）. AET levels were normal in 30 of 33 patients （91%）. HBeAg negative conversion occurred in 7 of 25 patients （28%）, among whom HBeAg seroconversion （12%） and H BeAg seroclearance （16%） occurred. The time of complete virological response was significantly affected by the number of resistance loci （r = 0.36, P = 0.040）. Concerning safety, the study found that no adverse events were observed during the 48 weeks. Conclusion： TDF monotherapy is an effective and safe salvage treatment for CHB patients who are resistant to other NAs.

Background： X-linked Charcot-Marie-Tooth type 1 （CMT1 X） disease is one of the most common forms of inherited neuropathy caused by mutations in the gap junction beta-1 protein （GJB1） gene （also known as connexin 32）. This study presented the clinical and genetic features of a series of Chinese patients with GJB1 gene mutations. Methods： A total of 22 patients from unrelated families, who were referred to Department of Neurology, Peking University First Hospital from January 2005 to January 2016, were identified with GJBI mutations. Their clinical records and laboratory findings were retrospectively collected and reviewed. Mutations in the GJB1 gene were analyzed by targeted next-generation sequencing （NGS）. Nucleotide alternations were confirnled with Sanger sequencing. Results： The CMT1X patients predominantly showed distal muscle weakness of lower limbs with mild sensory disturbance. The mean age of onset was 15.6 ± 8.7 years （ranging from 1 year to 42 years）. The sudden onset of cerebral symptoms appeared in four patients （ 18.2%）： two were initial symptoms. One case had constant central nervous system （CNS） signs. There were 19 different heterozygous mutations, including 15 known mutations and tbur novel mutations （c. II5G〉T, c.380T〉A, c.263C〉A, and c.818_819insGGGCT）. Among the 22 Chinese patients with CMT1X, the frequency of the GJB1 mutation was 4.5% in transmembrane domain 1 （TM1）, 4.5% in TM2, 27.7% in TM3, 9.1% in TM4, 4.5% in extracellular 1 （EC1）, 27.3% in EC2, 9.1% in intracellular loop, 13.6% in the N-terminal domain, and 4.5% in the C-ternlinal domain. CMTIX with CNS impairment appeared in five （22.7%） of these patients. Conclusions： This study indicated that CNS impairment was not rare in Chinese CMT1X patients. Mutations in the EC2 domain of the GJBI gene were hotspot in Chinese CMT1X patients.

Objective： Dementia is the fourth most common cause of death in developed countries. The relationship between plasma lipids and cognitive function is complex and controversial. Due to the increasing life expectancy of the population, there is an urgent need to control vascular risk factors and to identify therapies to prevent and treat both cognitive impairment and dementia. Here, we reviewed the eff＇ects of plasma lipids and statins on cognitive function. Data Sources： We searched the PubMed database for research articles published through November 2017 with key words including ＂plasma lipids,＂ ＂hyperlipidemia,＂ ＂hypercholesterolemia,＂ ＂statins,＂ and ＂cognition function.＂ Study Selection： Articles were retrieved and reviewed to analyze the effects of plasma lipids and statins on cognitive function and the mechanisms underlying these effects. Results： Many studies have examined the relationship between plasma lipids and cognitive function, but no definitive conclusions can be drawn. The mechanisms involved may include blood-brain barrier injury, the influence on small blood vessels in the brain, the influence on amyloid deposition, and a neuroprotective effect. To date, most studies of statins and cognition have been observational, with few randomized controlled trials. Therefore, finn conclusions regarding whether mid- or long-term statin use affects cognition function and dementia remain elusive. However, increasing concern exists that statins may be a causative factor for cognitive problems. These adverse eff＇ects appear to be rare and likely represent a yet-to-be-defined vulnerability in susceptible individuals. Conclusions： The association between plasma lipids and cognition, the mechanism of the influence of plasma lipids on cognitive function, and the association between statins and cognitive function are complex issues and currently not fully understood. Future research aimed at identifying the mechanisms that underlie the effects of plasma lipids and statins on cognition will not only provide important insight into the causes and interdependencies of cognitive impairment and dementia, but also inspire novel strategies for treating and preventing these cognitive disorders.