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An anion exchanger from rice straw was used to remove Cr (VI) from synthetic wastewater and electroplating effluent. The exchanger was characterized using Fourier transform infrared (FTIR) spectrum and scanning electron microscopy (SEM), and it was found that the quaternary amino group and hydroxyl group are the main functional groups on the fibrous surface of the exchanger. The effect of contact time, initial concentration and pH on the removal of Cr (VI), and adsorption isotherms at different temperature, was investigated. The results showed that the removal of Cr (VI) was very rapid and was significantly affected by the initial pH of the solution. Although acidic conditions (pH=2−− 6) facilitated Cr (VI) adsorption, the exchanger was effective in neutral solution and even under weak base conditions. The equilibrium data fitted well with Langmuir adsorption model, and the maximum Cr (VI) adsorption capacities at pH 6.4 were 0.35, 0.36 and 0.38 mmol/g for 15, 25 and 35°C, respectively. The exchanger was finally tested with real electroplating wastewater, and at sorbent dosage of 10 g/L, the removal efficiencies for Cr (VI) and total Cr were 99.4% and 97.8%, respectively. In addition, the positive relationship between adsorbed Cr (VI) and desorbed Cl−suggested that Cr (VI) was mainly removed by ion exchange with chlorine. [ABSTRACT FROM PUBLISHER]

The article presents a summary of the academic dissertation "Real Wages and Wage Inequality in China, 1858-1936," by Se Yan of Peking University. An overview of the chapter-by-chapter structure and contents is given, noting its construction of a nominal wage series of employees in the Chinese Maritime Customs service in multiple cities. Additional subjects addressed by the work include the changes of skill premiums in Chinese workers over the period, the dynamics of the wage gap between skilled and unskilled workers, and the creation of a cost of living index.

The article seeks to provide information on the price of salt in China towards the end of the Ch'ing (Qing) dynasty, emphasizing the impact such prices had on the lives of China's poor. The price of salt is compared to the average wages received by Chinese unskilled laborers, or coolies. The retail price of salt is also compared to the retail price of rice in order to make conclusions about salt's real price during this time. The authors conclude that the price of salt was not exorbitantly large, and only caused economic difficulties in China's Yangtse valley. Various economic reports concerning these prices are analyzed by the authors.

An abstract of the article "Economic Openness, industrial Development and income Distribution in China, 1860-1936: Evidence from China Maritime Custom Archives," by Se Yan is presented.

This paper provides the first estimates of housing price movements for Beijing in late pre-modern China. We hand-collect from archival sources transaction prices and other house attribute information from the 498 surviving house sale contracts for Beijing during the first two centuries of the Qing Dynasty ( 1644-1840), a long period without major wars, political turmoil, or significant institutional change in the Chinese capital. We use hedonic methods to construct a real estate price index for Beijing for the period. The regression analysis explains a major proportion of the variance of housing prices. We find that house prices grew steadily for the first half-century of the Qing Dynasty and declined afterwards in both nominal and real terms through the late eighteenth century. Nominal prices grew starting in the late eighteenth century and declined from the early nineteenth century through 1840. But these price changes occurred with contemporaneous price changes in basic measures of the cost of living: there was little change in real tenns to the end of our period. [ABSTRACT FROM AUTHOR]

Our paper provides a comparative perspective on the development of public primary education in four of the largest developing economies circa 1910: Brazil, Russia, India and China (BRIC). These four countries encompassed more than 50% of the world's population in 1910, but remarkably few of their citizens attended any school by the early 20th century. We present new, comparable data on school inputs and outputs for BRIC drawn from contemporary surveys and government documents. Recent studies emphasize the importance of political decentralization, and relatively broad political voice for the early spread of public primary education in developed economies. We identify the former and the lack of the latter to be important in the context of BRIC, but we also outline how other factors such as factor endowments, colonialism, serfdom, and, especially, the characteristics of the political and economic elite help explain the low achievement levels of these four countries and the incredible amount of heterogeneity within each of them. [ABSTRACT FROM AUTHOR]

Capillary morphogenesis gene 2 (CMG2/ANTXR2) is a cell surface receptor for both collagen VI and anthrax toxin. Biallelic loss-of-function mutations in CMG2 lead to a severe condition, hyaline fibromatosis syndrome (HFS). We have here dissected a network of dynamic interactions between CMG2 and various actin interactors and regulators, describing a different behavior from other extracellular matrix receptors. CMG2 binds talin, and thereby the actin cytoskeleton, only in its ligand-free state. Extracellular ligand binding leads to src-dependent talin release and recruitment of the actin cytoskeleton regulator RhoA and its effectors. These sequential interactions of CMG2 are necessary for the control of oriented cell division during fish development. Finally, we demonstrate that effective switching between talin and RhoA binding is required for the intracellular degradation of collagen VI in human fibroblasts, which explains why HFS mutations in the cytoskeleton-binding domain lead to dysregulation of extracellular matrix homeostasis., Competing Interests: Declaration of Interests The authors declare no competing interests., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Hyaline fibromatosis syndrome is an autosomal recessive disease caused by mutations in ANTXR2, a gene involved in extracellular matrix homeostasis. Sixty percent of patients carry frameshift mutations at a mutational hotspot in exon 13. We show in patient cells that these mutations lead to low ANTXR2 mRNA and undetectable protein levels. Ectopic expression of the proteins encoded by the mutated genes reveals that a two base insertion leads to the synthesis of a protein that is rapidly targeted to the ER-associated degradation pathway due to the modified structure of the cytosolic tail, which instead of being hydrophilic and highly disordered as in wild type ANTXR2, is folded and exposes hydrophobic patches. In contrast, one base insertion leads to a truncated protein that properly localizes to the plasma membrane and retains partial function. We next show that targeting the nonsense mediated mRNA decay pathway in patient cells leads to a rescue of ANTXR2 protein in patients carrying one base insertion but not in those carrying two base insertions. This study highlights the importance of in-depth analysis of the molecular consequences of specific patient mutations, which even when they occur at the same site can have drastically different consequences., (© 2013 WILEY PERIODICALS, INC.)

The aim of the present study was to evaluate the impact of the UCP2-866 G/A polymorphism on the efficacy of repaglinide in treating patients with diabetes mellitus type 2 (T2DM). 370 patients with T2DM and 166 healthy volunteers were enrolled to identify UCP2-866 G/A genotypes. 16 patients with GG genotype, 14 with GA genotype and 11 with AA genotype of UCP2-866 G/A underwent an 8-week repaglinide treatment regimen. There were no differences in allele frequency of UCP2-866 G/A between T2DM patients and control subjects. The patient with AA genotype of UCP2-866 G/A had higher levels of fasting plasma glucose (FPG), 30-min and 2-h postload plasma glucose, glycated haemoglobin (HbA1c), and lower concentrations of 30-min and 2-h postload plasma insulin, homeostasis model assessment of beta cell function (HOMA-beta), deltaI30/deltaG30 compared with GG genotype. After repaglinide treatment for 8 consecutive weeks, we found that A allele carriers of UCP2 in the T2DM patients had smaller decrease in FPG (P < 0.05) and HbA1c (P < 0.05), and smaller increase in 30-min postload plasma insulin (P < 0.01) compared with GG genotypes. We demonstrated that UCP2-866 G/A polymorphism is associated with the therapeutic efficacy of repaglinide in Chinese T2DM patients.

Previous studies showed that cocaine exposure decreased brain-derived neurotrophic factor (BDNF) function and resulted in neuronal cell death. To investigate a role of BDNF in cocaine's cytotoxicity, an RNA interference (RNAi) approach was used. Transfection of neuroblastoma SK-N-AS cells or primary rat hippocampal neurons with the small double-stranded interfering RNA (siRNA) targeting BDNF mRNA, but not the scrambled siRNA, resulted in reductions in levels of BDNF mRNA and proteins by more than 70% in the transfected cells as compared with the control group, suggesting an RNAi-mediated, sequence-specific gene silencing. The results also showed that cocaine-induced cytotoxicity, assessed by the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazodium bromide) assay, was more pronounced in the cells transfected with the siRNA than in the cells transfected with the scrambled siRNA or in the cells treated with Lipofectamine 2000 alone (the control group), suggesting that inhibition of BDNF expression enhances cocaine's cytotoxicity. Together with previous studies showing that cocaine suppresses BDNF expression, the present data suggest that the drug-induced reduction of BDNF productions may make neurons more vulnerable to cocaine's toxic effects and precipitate cocaine-induced central nervous system damages.

Previous studies showed that prenatal cocaine in an animal model decreased brain-derived neurotrophic factor (BDNF) activity in offspring's brain. Since BDNF is one of target genes of cAMP response element-binding protein (CREB), this study examined effects of cocaine on CREB activities in a human neuroblastoma (SK-N-AS) cell line. The MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazodium bromide) assay indicated that cocaine exposure at 5 microM for 24 h had no significant influences on cell viability. However, a 24-h exposure to cocaine at the same concentration significantly decreased the level of phosphorylated CREB, although no significant changes in total CREB proteins were observed. Consistent with reduced CREB phosphorylation, the electrophoretic mobility shift assay showed that exposure to 5 microM of cocaine for 24 h also inhibited CREB binding activity and significantly decreased BDNF mRNA expression. In addition, exposure to 5 microM cocaine for 24 h attenuated the glutamic acid-evoked increase in the intracellular Ca2+ concentration. Taken together, these findings suggest that cocaine exposure at the sublethal concentration downregulates CREB functions in the cultured SK-N-AS cell line, and that diminished intracellular Ca2+ responses may be associated in part with cocaine-induced downregulation of CREB activity.

Evidence suggests that 5-hydroxytriptamine-1B (5-HT1B) receptors play a role in modifying ethanol's reinforcing effects and voluntary intake, and that 5-HT1B receptors within the ventral tegmental area (VTA) are involved in regulation of mesolimbic dopaminergic neuronal activity. Since increased mesolimbic dopaminergic transmission has been implicated in ethanol's reinforcing properties, this study was designed to assess the involvement of VTA 5-HT1B receptors in mediating the stimulatory effects of ethanol on VTA dopaminergic neurons. Dual-probe microdialysis was performed in freely moving adult Sprague-Dawley rats with one probe within the VTA and the other within the ipsilateral nucleus accumbens (NACC). Dopamine (DA) levels in dialysates from both areas, as the index of the activity of mesolimbic DA neurons, were measured simultaneously. The results showed that intraperitoneal injection of ethanol at the doses of 1 and 2 g/kg increased extracellular DA concentrations in both the VTA and the NACC, suggesting increased DA neuronal activity. These ethanol-induced increases of the DA release in the VTA and the NACC were significantly attenuated by intra-tegmental infusion of SB 216641 (a 5-HT(1B) receptor antagonist), but not BRL 15572 (a 5-HT(1D/1A) receptor antagonist) or WAY 100635 (a 5-HT1A receptor antagonist). Administration of ethanol at the same doses did not significantly alter extracellular levels of GABA in the VTA. The results also showed that intra-tegmental infusion of CP 94253, a 5-HT1B receptor agonist, significantly prolonged the effects of ethanol on NACC DA. The results suggest that blockade and activation of VTA 5-HT1B receptors attenuates and potentiates the neurochemical effects of ethanol, respectively, and support the suggestion that VTA 5-HT(1B) receptors may be involved in part in mediating the activating effects of ethanol on mesolimbic DA neurons.

Prenatal alcohol exposure produces many developmental defects in the central nervous system. The underlying molecular mechanism, however, has not been fully understood. The present study was undertaken to examine the effects of prenatal alcohol exposure on brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB) in offspring. The pregnant Sprague-Dawley rats received 1 or 3 g/kg of alcohol or an isocaloric solution by intragastric intubation once a day from gestational day (GD) 5 to GD 20. On postnatal day 7-8, pups were killed and the hippocampus, striatum, cortex, and cerebellum dissected out. Levels of BDNF mRNA and proteins, total TrkB proteins and receptor phosphorylation were measured. The results showed that prenatal alcohol exposure at the dose of 1 g/kg/day did not significantly affect BDNF protein levels in any region examined. However, administration of alcohol at the dose of 3 g/kg/day markedly reduced levels of BDNF protein and mRNA in the cortex and hippocampus of offspring. Western blotting showed that prenatal alcohol exposure at the dose of 3 g/kg/day also inhibited TrkB phosphorylation in the hippocampus although no changes in total TrkB protein levels were observed in any region examined. Our data suggest that prenatal alcohol exposure alters both presynaptic and postsynaptic BDNF function in certain brain areas of offspring. These alterations in BDNF function may contribute to the development of alcohol-related birth defects.

Recent studies suggest that the gene that encodes brain-derived neurotrophic factor (BDNF) might be linked with vulnerability to alcohol abuse. We have now compared BDNF protein levels in several brain regions between alcohol-naive alcohol-preferring (P) and -nonpreferring (NP) rats using the enzyme-linked immunosorbent assay (ELISA) procedure. The results showed that BDNF levels in the nucleus accumbens of the P rats were significantly lower than those of the NP rats, suggesting that this innate difference may contribute to the disparate alcohol drinking behavior of the P and NP rats.

This study was designed to assess the involvement of 5-HT1B receptors within the ventral tegmental area (VTA) in the regulation of mesolimbic dopaminergic transmission. Dual-probe microdialysis was performed in freely moving adult Sprague-Dawley rats with one probe within the VTA and the other within the ipsilateral nucleus accumbens (NACC). Drugs were administered into the VTA via retrograde dialysis. Dialysates from both the VTA and the NAC were collected for determination of dopamine (DA) and gamma-aminobutyric acid (GABA) by high-performance liquid chromatography with electrochemical detection. Intra-tegmental infusion of CP 93129 (20, 40, and 80 microM), a 5-HT1B receptor agonist, increased extracellular DA concentrations in a concentration-dependent manner not only in the NACC but also in the VTA, indicating increased mesolimbic DA neuron activity. Administration of CP 93129 at 80 microM into the VTA also significantly decreased extracellular GABA concentrations in this region. Co-infusion of the 5-HT1B receptor antagonist SB 216641 (10 microM), but not the 5-HT1A receptor antagonist WAY 100635 (10 microM) or the 5-HT1D/1A receptor antagonist BRL 15572 (10 microM), antagonized not only the effects of intra-tegmental CP 93129 (80 microM) on VTA DA and NAC DA but also on VTA GABA. The results suggest that activation of VTA 5-HT1B receptors increases mesolimbic DA neuron activities. The increased DA neuron activity may be associated, at least in part, with the 5-HT1B receptor-mediated inhibition of VTA GABA release.

The pregnant rats received daily sc injections of cocaine (30 mg/kg) or saline from the gestational day (GD) 7 to GD 20. At 1 week postnatal, all pups were killed and the hippocampus, cortex and striatum were dissected out. Levels of brain-derived neurotrophic factor (BDNF) under the basal condition and depolarization with high potassium (40 mM) were measured. The results showed that hippocampal BDNF levels under basal and depolarization conditions were all significantly lower in the pups prenatally exposed to cocaine than those exposed to saline. There were no significant differences in basal BDNF levels between the cocaine and saline groups in the cortex or striatum. However, the prenatally cocaine-treated pups showed significantly less BDNF release following high potassium depolarization than the saline-treated animals did in both these regions. The results support the suggestion that prenatal cocaine exposure decreases BDNF expression in the offspring.

In order to assess a role of 5-HT(1B) receptors for regulation of GABA transmission in the ventral tegmental area (VTA), VTA slices from the rat were incubated with [(3)H]GABA and beta-alanine, and superfused in the presence of nipecotic acid and aminooxyacetic acid. [(3)H]GABA release was induced by exposures to the medium containing 30 mM potassium for 2 min. The results showed that high potassium-evoked [(3)H]GABA release was sensitive to calcium withdrawal or blockade of sodium channels by tetrodotoxin, suggesting that tritium overflow induced by high potassium derived largely from neuronal stores. Administration of CP 93129 (0.15 and 0.45 microM), a 5-HT(1B) receptor agonist, or RU 24969 (0.15 and 0.45 microM), a 5-HT(1B/1A) receptor agonist, but not 8-OH-DPAT (0.45 microM), a 5-HT(1A) receptor agonist, inhibited high potassium-evoked [(3)H]GABA release in a concentration-related manner. The RU 24969-induced inhibition of [(3)H]GABA release was antagonized by either SB 216641, a 5-H(1B) receptor antagonist, or cyanopindolol, a 5-HT(1B/1A) receptor antagonist, but not by WAY 100635, a 5-HT(1A) receptor antagonist. Pre-treatment with SB 216641 also antagonized CP 93129-induced inhibition of [(3)H]GABA release. The results support the hypothesis that 5-HT(1B) receptors within the VTA can function as heteroreceptors to inhibit GABA release.

This study was designed to investigate the role of 5-hydroxytryptamine (5-HT)(1B) receptors located in the ventral tegmental area and nucleus accumbens in the modulation of accumbal dopaminergic transmission. The selective 5-HT(1B) receptor agonist CP 93129 [3-(1,2,5,6-tetrahydro-4-pyridyl)pyrrolo[3,2-b]pyrid-5-one] was administered into the ventral tegmental area or nucleus accumbens of freely moving Sprague-Dawley rats via retrograde microdialysis. The effects of intra-accumbal and intra-tegmental CP 93129 on extracellular dopamine levels in the nucleus accumbens were measured using one- and dual-probe microdialysis, respectively. For dual-probe microdialysis, one probe was in the ventral tegmental area for drug administration and the other in the ipsilateral nucleus accumbens for dopamine measurement. The results show that infusion of CP 93129 (2, 5 and 10 microM) into the nucleus accumbens increased local dopamine levels in a concentration-related manner. Infusion of CP 93129 (10 and 20 microM) into the ventral tegmental area also increased dopamine levels in the ipsilateral nucleus accumbens. The increased dopamine release in the nucleus accumbens produced by intra-accumbal or intra-tegmental CP 93129 was antagonized by co-infusion of cyanopindolol (5 microM), a 5-HT(1B/1A) receptor antagonist, but not by WAY-100635 [N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-2-pyridinyl-cyclohexanecarboxamide] (5 microM), a highly selective 5-HT(1A) receptor antagonist. In addition, augmentations of dopamine release in the nucleus accumbens induced by intra-accumbal CP 93129 were sensitive to Na(+) channel blockade with tetrodotoxin. These results are not in opposition to the concept that 5-HT(1B) receptors within the ventral tegmental area and nucleus accumbens are all involved in the modulation of dopamine release in the terminal area of the mesolimbic dopamine system.