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This paper makes a systematic overview of the development process of evaluation on China river health growing out of nothing and summarizes the explanations of the river health concept made by famous experts and scholars in China to obtain the essence of river health evaluation. This paper compares the domestic typical evaluation methods and summarizes the common advantages and disadvantages of these methods. Based on the above-mentioned summary, this paper concludes that the research direction of health evaluation is the urban river health evaluation, biological habitat evaluation, research on the river ecological base flow and evaluation on the influence of inter-basin water transfer. Finally, this paper gives a brief prospect of China’s river health evaluation work in the future.

Bilinear derivative method is widely used in calculating multi-soliton solutions of some nonlinear evolution equation. The paper proves some frequently used properties of bilinear derivative from the perspective of the definition of bilinear derivative, hoping to be useful for learning and teaching in nonlinear science.

In order to evaluate the ecological health condition of Zhanghe River Watershed, an adapted Benthic Index of Biotic Integrity (B-IBI) was developed. Macro-invertebrates were sampled at 12 monitoring stations which were grouped into two condition categories (reference and impaired stations) according to the level of degradation. A total of 47 benthic macroinvertebrates taxa were identified, in which aquatic insects 33 taxa, Mollusca 8, Annalida 3 and Crustacea 3 taxa. Based on macro-invertebrate assemblages characters of this area, 18 candidate biological metrics in four categories, including taxonomic richness, community composition, pollution tolerance, trophic guild, and value distribution, were chosen. In which, four metrics were excluded because of low values or narrow distribution range. Discriminatory power between reference and impaired stations was analysed using box-plots, and six metrics were excluded because the medians of the box-plot inside the inter quartile range. Of all the rest eight metrics, four were not suitable for B-IBI index system because of their high Pearson correlation (| r | 0.75). Finally, total taxa, percentage of Crustacea and Mollusca, percentage of tolerant taxa and percentage of predators were screened out to form a B-IBI index system. Ratio scoring method for B-IBI index was used to get a uniform score. Evaluation criterion was established based on the 25 percentiles value of reference stations. Assessment results using B-IBI showed 5 of sampling stations were in ‘healthy’ and ‘sub-healthy’ state, 3 were in ‘fair’ state, and 4 were in ‘poor’ or ‘very poor’ state of the whole watershed.

To further our understanding of the effects of nicotine on the molecular responses of macrophages during virus or virus-like infections, poly(I:C)-stimulated macrophage-like RAW264.2 cells or mouse primary peritoneal macrophages were challenged with nicotine; and their molecular responses were evaluated using a qRT-PCR array, antibody array, ELISA, Western blotting, and Ca(2+) imaging. Of 51 genes expressed in the Toll-like receptor (TLR) and RIG-I-like receptor (RLR) pathways, mRNA expression of 15 genes in RAW264.7 cells was attenuated by nicotine, of which mRNA expression of IL-6, TNF-α, and IL-1β was confirmed to be attenuated in peritoneal macrophages. Concurrently, nicotine treatment attenuated the release of IL-6 and TNF-α from poly(I:C)-stimulated macrophages. However, when poly(I:C)-stimulated macrophages were challenged with nicotine plus α-bungarotoxin (α-BTX), secretion of IL-6 and TNF-α was found to be in a level seen with poly(I:C) stimulation only, indicating that α7-nAChR, a highly Ca(2+) permeable ion channel sensitive to blockade by α-BTX, is involved in this process. Furthermore, results from an antibody array indicated that nicotine treatment attenuated the phosphorylation of 82 sites, including Thr286 on CaMKIIα, from poly(I:C)-stimulated RAW264.7 cells, of which 28 are expressed in the downstream cascade of Ca(2+) signaling. Coincidentally, poly(I:C)-stimulated macrophages showed attenuated expression of phosphorylated CaMKIIα when pretreated with nicotine. In addition, nicotine attenuated intracellular Ca(2+) signal from poly(I:C)-stimulated RAW264.7 cells. Collectively, these results indicate that poly(I:C)-induced molecular responses of macrophages could be significantly attenuated by nicotine.

Using pavement thickness layered system computational theories and methods that current design criteria proposed, according to the result of the calculating example, this paper analyzed the influence of different soil base and the base stiffness of highway asphalt pavement for base thickness, and pointed out that thickness of pavement base decreased with increase of the soil base and the base stiffness. Therefore, optimum selecting fillers in constructing road bed beside the upper part of the roadbed, strengthening the subgrade and compacting by layer, to improve the mechanical properties of subgrade. Meanwhile, it has important significance in obtaining the obvious economic effect on decreasing thickness of pavement structure by properly using base material of high stiffness. Besides, this result indicate that the base course underside stresses increased with the base stiffness, therefore, the base course underside stresses should be checked, to ensure the corresponding the tensile strength of base material.

Genome-wide association studies have identified susceptibility loci for esophageal squamous cell carcinoma (ESCC). We conducted a meta-analysis of all single-nucleotide polymorphisms (SNPs) that showed nominally significant P-values in two previously published genome-wide scans that included a total of 2961 ESCC cases and 3400 controls. The meta-analysis revealed five SNPs at 2q33 with P5 × 10(-8), and the strongest signal was rs13016963, with a combined odds ratio (95% confidence interval) of 1.29 (1.19-1.40) and P= 7.63 × 10(-10). An imputation analysis of 4304 SNPs at 2q33 suggested a single association signal, and the strongest imputed SNP associations were similar to those from the genotyped SNPs. We conducted an ancestral recombination graph analysis with 53 SNPs to identify one or more haplotypes that harbor the variants directly responsible for the detected association signal. This showed that the five SNPs exist in a single haplotype along with 45 imputed SNPs in strong linkage disequilibrium, and the strongest candidate was rs10201587, one of the genotyped SNPs. Our meta-analysis found genome-wide significant SNPs at 2q33 that map to the CASP8/ALS2CR12/TRAK2 gene region. Variants in CASP8 have been extensively studied across a spectrum of cancers with mixed results. The locus we identified appears to be distinct from the widely studied rs3834129 and rs1045485 SNPs in CASP8. Future studies of esophageal and other cancers should focus on comprehensive sequencing of this 2q33 locus and functional analysis of rs13016963 and rs10201587 and other strongly correlated variants.

Although nicotine has a broad impact on both the central and peripheral nervous systems, the molecular mechanisms remain largely unknown, especially at the signaling pathway level. To investigate that aspect, we employed both conventional molecular techniques, such as quantitative real-time PCR and Western blotting analysis, and high-throughput microarray approach to identify the genes and signaling pathways that are modulated by nicotine. We found 14 pathways significantly altered in SH-SY5Y neuroblastoma cells. Of these, the Toll-like receptor pathway (TLR; p = 2.57 × 10(-4)) is one of the most important innate immune pathways. The death receptor pathway (DR; p = 8.71 × 10(-4)), whose transducers coordinate TLR signals and help conduct the host immune response to infection, was also significantly changed by nicotine. Furthermore, we found that several downstream pathways of TLR and DR signaling, such as PI3K/AKT signaling (p = 9.55 × 10(-6)), p38 signaling (p = 2.40 × 10(-6)), and ERK signaling (p = 1.70 × 10(-4)), were also significantly modulated by nicotine. Interestingly, most of the differentially expressed genes in these pathways leading to nuclear factor κB (NF-κB) activation and those important inhibitors of pathways leading to apoptosis, including FLIP and Bcl-2, were up-regulated by nicotine. Taken together, our findings demonstrate that nicotine can regulate multiple innate immune-related pathways, and our data thus provide new clues to the molecular mechanisms underlying nicotine's regulatory effects on neurons.

Both nicotine and alcohol addictions are common chronic brain disorders that are of great concern to individuals and society. Although genetics contributes significantly to these disorders, the susceptibility genes and variants underlying them remain largely unknown. Many years of genome-wide linkage and association studies have implicated a number of genes and pathways in the etiology of nicotine and alcohol addictions. In this communication, we focus on current evidence, primarily from human genetic studies, supporting the involvement of genes and variants in the GABAergic signaling system in the etiology of nicotine dependence and alcoholism based on linkage, association, and gene-by-gene interaction studies. Current efforts aim not only to replicate these findings in independent samples, but also to identify which variant contributes to the detected associations and through what molecular mechanisms.

Diseases related to smoking are the second leading cause of death in the world. Cigarette smoking is a risk factor for several diseases such as cancer and cardiovascular and respiratory disorders. Despite increasing evidence of genetic determination, the susceptibility genes and loci underlying various aspects of smoking behavior are largely unknown. Moreover, almost all reported genome-wide association studies (GWASs) have been performed on samples of European origin, limiting the applicability of the results to other ethnic populations. In this first GWAS on smoking behavior in an Asian population, after analyzing 8,842 DNA samples from the Korea Association Resource project with 352,228 single nucleotide polymorphisms (SNPs) genotyped for each sample, we identified 8 SNPs significantly associated with smoking initiation (SI) and 4 with nicotine dependence (ND). Because of the current unavailability of an independent Asian smoking sample, we replicated the discoveries in independent samples of European-American and African-American origin. Of the 12 SNPs examined in the replicated samples, we identified two SNPs, in the regulator of G-protein signaling 17 gene (rs7747583, p value(meta) = 6.40 × 10(-6); rs2349433, p value(meta) = 5.57 × 10(-6)), associated with SI. Also, we found two SNPs significantly associated with ND; one in the FERM domain containing 4A (rs4424567, p value(meta) = 2.30 × 10(-6)) and the other at 7q31.1 (rs848353, p value(meta) = 9.16 × 10(-8)). These SNPs represent novel targets for examination of smoking behavior and warrant further investigation using independent samples.

Li Dong Wang and colleagues report a genome wide association study for esophageal squamous cell carcinoma in the Chinese population. They identify two risk loci at PLCE1 and C20orf54.

The major addictive component of tobacco, nicotine, exerts anti-inflammatory effects in multiple cell types and may benefit neurons in various degenerative disorders, such as Alzheimer's and Parkinson's disease, in which an inflammation-related mechanism is implicated. Among the various nicotinic acetylcholine receptors, α7, which has been identified in both neurons and immune cells and has high permeability to calcium, is believed to contribute significantly to nicotinic anti-inflammatory and neuron-protective effects. Although nicotine has been used in clinical trials for the treatment of some inflammatory diseases such as ulcerative colitis, the molecular mechanisms of its actions are largely unknown. In this review, we provide current evidence for nicotine's modulation of multiple immune pathways via α7 nAChRs in both neurons and immune cells. Understanding the mechanism of the nicotinic anti-inflammatory effect and neuron-protective function may guide the development of novel medicines for infectious and neuron-degenerative diseases.

Choline acetyltransferase is critical in the synthesis of acetylcholine and regulation of cholinergic neuron functions. We recently reported association of the encoding gene ChAT with both smoking cessation and nicotine dependence (ND) in two independent European American (EA) samples; however, in the replication sample, only limited SNPs partially covering the gene were examined. In this study, we examined the association of 14 SNPs, which cover the entire gene, with ND, assessed by smoking quantity (SQ), heaviness of smoking index (HSI), and Fagerström Test for ND (FTND), in 2,037 subjects from 602 families of African American (AA) or EA origin. Individual SNP-based association analysis revealed that five SNPs showed nominal association with at least one ND measure in one of the samples (P = 0.022–0.042); none remained significant after correction for multiple testing. Haplotype-based association analysis revealed that haplotypes G–G–A–C, formed by rs1880676–rs3810950–rs10082479–rs8178990 (P = 0.005–0.0178), and G–G–T–C–G–C, formed by rs1880676–rs3810950–rs10082479–rs8178990–rs3793790–rs12266458 (P = 0.00247–0.00468), displayed significant association with all three ND measures in the AA sample, as did haplotype T–C–G–A–T, formed by rs12266458–rs11101191–rs8178991–rs4838544–rs4838547 (P = 0.00741–0.0103), in the EA sample. All these detected haplotype-based associations remained significant after correction for all major haplotypes for a given SNP combination. Together, our findings, in conjunction with the previous report of the association, warrant further investigation of ChAT in ND.

Although maternal smoking during pregnancy disrupts offspring development, it is not clear whether smoking before pregnancy has any effect on the next generation. Given that nicotine, the major psychoactive component in cigarettes, is toxic to many organs, we hypothesized that maternal smoking even before a pregnancy affects offspring development. Myelin is an important structure in the nervous system, and deficits in myelin are related to many psychiatric disorders and drug addiction. We therefore examined the effect of maternal exposure to nicotine on the expression of myelin genes in the offspring using zebrafish as a model.Female adult zebrafish were exposed to nicotine through water at a concentration of 1, 5, 10, 15, 20, 25, or 30 μM (nicotine base) for either 1 h or a continuous 24 h each day for 4 months. The nicotine-treated females were then bred with drug-naive males, and the embryos and larvae were grown in a nicotine-free environment. Maternal survival rates were calculated. Larvae of those exposed to nicotine at a dose of 1, 5, 10, 15, or 20 μM for 24 h each day were collected at 4, 7, or 14 days postfertilization (dpf). The mRNA expression of myelin-related genes was examined using quantitative RT-PCR.The mRNA expression of most genes encoding myelin major proteins increased with age. These genes were generally downregulated by maternal nicotine exposure in 4 dpf larvae, whereas they were upregulated in 14 dpf larvae. The expression of myelin-related transcription regulators correlated well with that of myelin major proteins.Prepregnancy nicotine exposure altered myelin gene expression in the offspring, implying that maternal smoking before pregnancy affects the next generation.

Persons infected with HIV-1 often develop neurologic disorders despite receiving highly active anti-retroviral therapy. Although the underlying mechanism is largely undetermined, our previous RNA-seq-based study showed that the expression of many genes was altered in the central nervous system (CNS) of HIV-1 transgenic (HIV-1Tg) rats. Because nicotine, a natural agonist of nicotinic acetylcholine receptors, exhibits a neuroprotective effect, we presently tested the hypothesis that nicotine restores the expression of altered genes in the CNS of HIV-1Tg rats. Adult male HIV-1Tg and F344 control strain rats were injected with either nicotine (0.25 mg/kg) or saline subcutaneously twice a day for 17 days. Gene expression in the prefrontal cortex (PFC), dorsal hippocampus (HIP), and dorsal striatum (STR) was evaluated using the RNA deep sequencing technique. We found that about 20% of the altered genes in the HIV-1Tg rat were affected by nicotine in each brain region, with the expression of most restored. Analysis of the restored genes showed distinct pathways corrected by nicotine in different brain regions of HIV-1Tg rats. Specifically, the two most significantly restored pathways were Wnt/β-catenin signaling and ephrin B signaling in the PFC, cAMP-responsive element-binding protein (CREB) signaling and glutathione metabolism pathway in the HIP, and tricarboxylic acid (TCA) cycle and calcium signaling in the STR. Together, our findings indicate that cholinergic modulators such as nicotine have beneficial effects on HIV-1-induced neurologic deficits.

Previous human and animal studies demonstrate that acute nicotine exposure has complicated influences on the function of the nervous system, which may lead to long-lasting effects on the behavior and physiology of the subject. To determine the genes and pathways that might account for long-term changes after acute nicotine exposure, a pathway-focused oligoarray specifically designed for drug addiction research was used to assess acute nicotine effect on gene expression in the neuron-like SH-SY5Y cells. Our results showed that 295 genes involved in various biological functions were differentially regulated by 1 h of nicotine treatment. Among these genes, the expression changes of 221 were blocked by mecamylamine, indicating that the majority of nicotine-modulated genes were altered through the nicotinic acetylcholine receptors (nAChRs)-mediated signaling process. We further identified 14 biochemical pathways enriched among the nicotine-modulated genes, among which were those involved in neural development/synaptic plasticity, neuronal survival/death, immune response, or cellular metabolism. In the genes significantly regulated by nicotine but blocked by mecamylamine, 13 enriched pathways were detected. Nine of these pathways were shared with those enriched in the genes regulated by nicotine, including neuronal function-related pathways such as glucocorticoid receptor signaling, p38 MAPK signaling, PI3K/AKT signaling, and PTEN signaling, implying that nAChRs play important roles in the regulation of these biological processes. Together, our results not only provide insights into the mechanism underlying the acute response of neuronal cells to nicotine but also provide clues to how acute nicotine exposure exerts long-term effects on the nervous system.

We performed a genome-wide association study of esophageal squamous cell carcinoma (ESCC) by genotyping 1,077 individuals with ESCC and 1,733 control subjects of Chinese Han descent. We selected 18 promising SNPs for replication in an additional 7,673 cases of ESCC and 11,013 control subjects of Chinese Han descent and 303 cases of ESCC and 537 control subjects of Chinese Uygur-Kazakh descent. We identified two previously unknown susceptibility loci for ESCC: PLCE1 at 10q23 (P(Han combined for ESCC) = 7.46 x 10(-56), odds ratio (OR) = 1.43; P(Uygur-Kazakh for ESCC) = 5.70 x 10(-4), OR = 1.53) and C20orf54 at 20p13 (P(Han combined for ESCC) = 1.21 x 10(-11), OR = 0.86; P(Uygur-Kazakh for ESCC) = 7.88 x 10(-3), OR = 0.66). We also confirmed association in 2,766 cases of gastric cardia adenocarcinoma cases and the same 11,013 control subjects (PLCE1, P(Han for GCA) = 1.74 x 10(-39), OR = 1.55 and C20orf54, P(Han for GCA) = 3.02 x 10(-3), OR = 0.91). PLCE1 and C20orf54 have important biological implications for both ESCC and GCA. PLCE1 might regulate cell growth, differentiation, apoptosis and angiogenesis. C20orf54 is responsible for transporting riboflavin, and deficiency of riboflavin has been documented as a risk factor for ESCC and GCA.

In this paper new kind of porphyrin compounds was prepared, which combined well the affinity of prophyrin to malignant tumour with anticancer of 5-fluorouracil porphyrin. The IR spectra of m- and p-chlorophenyl-5-fluorouracil prophyrin were obtained and analyzed. The IR absorption peaks were investigated and concluded in detail. The IR absorption rule of chloropenly-5-fluorouracil prophyrin which occurred when m-substitution and p-substitution appeared respectively on phenyl, and single substitution of N1 and double substitution of N1 appeared respectively on phenyl or N1 and N1, N3 positions on pyrimidine ring was also discussed. The results show that the relative intensity of nu c-o stretching vibration changed obviously by field-effect when the substitution was strong electro-negative group. Meanwhile, the IR spectral characteristics of the compounds mentioned above were revealed, and this can be used to deduce the stereochemistry structure of them.

Nat. Genet. 42, 759–763 (2010); published online 22 August 2010; corrected after print 27 August 2014 In contrast to the version of this article initially published, the authors now find no evidence to support association with esophageal squamous cell carcinoma susceptibility for rs13042395[T] at 20p13 in their original data, in two independent sets of cases and controls collected in other Chinese populations or in the joint analysis of these three studies.