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Areas subjected to frequent winds show severe farmland degradation and air pollution caused by wind erosion and particulate matter emissions. Biological soil crust (BCS) coverage can inhibit wind erosion. This study used wind tunnels to analyze the wind erosion and particulate matter emissions of algae crusts and moss crusts for different wind speeds and coverage conditions, providing the proportion of particulate matter emission of the total wind erosion under different conditions. Wind erosion of algae crusts was 33% higher than that of moss crusts, and the average emissions of total suspended particles (TSP), PM10, PM2.5, and PM1 were 51%, 64%, 149%, and 167% higher than those of moss crusts. The wind erosion process pairs of the two biological soil crusts both had strong responses to wind speed and coverage, and particulate matter emissions were particularly sensitive to coverage. The average aerodynamic roughness length of moss crusts was 164% higher than that of algae crusts; with increasing wind speed, the aerodynamic roughness length of algae crusts decreased 60% faster than that of moss crusts. The proportion of particulate matter emissions from biological soil crusts in wind erosion was inversely proportional to wind speed and coverage. The particle emission capacity of moss crusts was directly proportional to the particle size and inversely proportional to the coverage. In contrast, the particle emission capacity of algae crust particles was proportional to the particle size. This study provides information for the management of farmland wind erosion and particulate matter emission. [ABSTRACT FROM AUTHOR]

Copyright of Irrigation & Drainage is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Irrigation & Drainage is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The transcription factor nuclear factor erythroid 2-like 2 ( NFE2L2) is essential for preventing type 2 diabetes mellitus (T2 DM)-induced complications in animal models. This case and control study assessed genetic variants of NFE2L2 for associations with T2 DM and its complications in Han Chinese volunteers. T2 DM patients with ( n = 214) or without ( n = 236) complications, or healthy controls ( n = 359), were genotyped for six NFE2L2 single nucleotide polymorphisms ( SNPs: rs2364723, rs13001694, rs10497511, rs1806649, rs1962142 and rs6726395) with TaqMan Pre-Designed SNP Genotyping and Sequence System. Serum levels of heme oxygenase-1 ( HMOX1) were determined through enzyme-linked immunosorbent assay. Informative data were obtained for 341 cases and 266 controls. Between T2 DM patients and controls, the genotypic and allelic frequencies and haplotypes of the SNPs were similar. However, there was a significant difference in genotypic and allelic frequencies of rs2364723, rs10497511, rs1962142 and rs6726395 between T2 DM patients with and without complications, including peripheral neuropathy, nephropathy, retinopathy, foot ulcers and microangiopathy. Furthermore, HMOX1 levels were significantly higher in T2 DM patients with complications than in controls. Multiple logistic regression analysis, however, showed that only rs2364723 significantly reduced levels of serum HMOX1 in T2 DM patients for the GG genotype carriers compared with participants with CG+ CC genotype. The data suggest that although NFE2L2 rs2364723, rs10497511, rs1962142 and rs6726395 were not associated with T2 DM risk, they were significantly associated with complications of T2 DM. In addition, only for rs2364723 higher serum HMOX1 levels were found in the T2 DM patients with CG+ CC than those with GG genotype. [ABSTRACT FROM AUTHOR]

Overexpression of gonadotropin‐releasing hormone (GnRH) receptor in many tumors but not in normal tissues makes it possible to use GnRH analogs as targeting peptides for selective delivery of cytotoxic agents, which may help to enhance the uptake of anticancer drugs by cancer cells and reduce toxicity to normal cells. The GnRH analogs [d‐Cys6, desGly10, Pro9‐NH2]‐GnRH, [d‐Cys6, desGly10, Pro9‐NHEt]‐GnRH, and [d‐Cys6, α‐aza‐Gly10‐NH2]‐GnRH were conjugated with doxorubicin (Dox), respectively, through N‐succinimidyl‐3‐maleimidopropionate as a linker to afford three new GnRH‐Dox conjugates. The metabolic stability of these conjugates in human serum was determined by RP‐HPLC. The antiproliferative activity of the conjugates was examined in GnRH receptor‐positive MCF‐7 human breast cancer cell line by MTT assay. The three GnRH‐Dox conjugates showed improved metabolic stability in human serum in comparison with AN‐152. The antiproliferative effect of conjugate II ([d‐Cys6, desGly10, Pro9‐NHEt]‐GnRH‐Dox) on MCF‐7 cells was higher than that of conjugate I ([d‐Cys6, desGly10, Pro9‐NH2]‐GnRH‐Dox) and conjugate III ([d‐Cys6, α‐aza‐Gly10‐NH2]‐GnRH‐Dox), and the cytotoxicity of conjugate II against GnRH receptor‐negative 3T3 mouse embryo fibroblast cells was decreased in comparison with free Dox. GnRH receptor inhibition test suggested that the antiproliferative activity of conjugate II might be due to the cellular uptake mediated by the targeting binding of [d‐Cys6‐des‐Gly10‐Pro9‐NHEt]‐GnRH to GnRH receptors. Our study indicates that targeting delivery of conjugate II mediated by [d‐Cys6‐des‐Gly10‐Pro9‐NHEt]‐GnRH is a promising strategy for chemotherapy of tumors that overexpress GnRH receptors. A novel [d‐Cys6, des‐Gly10, Pro9‐NHEt]‐GnRH‐Doxorubicin conjugate was designed and synthesized. It showed improved human serum stability and targeting antiproliferative effect on GnRH receptor positive MCF‐7 human breast cancer cells. [ABSTRACT FROM AUTHOR]