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As an extension of the classical job shop scheduling problem, the flexible job shop scheduling problem (FJSP) plays an important role in real production systems. In FJSP, an operation is allowed to be processed on more than one alternative machine. It has been proven to be a strongly NP-hard problem. Ant colony optimization (ACO) has been proven to be an efficient approach for dealing with FJSP. However, the basic ACO has two main disadvantages including low computational efficiency and local optimum. In order to overcome these two disadvantages, an improved ant colony optimization (IACO) is proposed to optimize the makespan for FJSP. The following aspects are done on our improved ant colony optimization algorithm: select machine rule problems, initialize uniform distributed mechanism for ants, change pheromone’s guiding mechanism, select node method, and update pheromone’s mechanism. An actual production instance and two sets of well-known benchmark instances are tested and comparisons with some other approaches verify the effectiveness of the proposed IACO. The results reveal that our proposed IACO can provide better solution in a reasonable computational time.

W i l l i a m V. B l e i s c h , P a u l J. B u z z a r d , H u i b i n Z h a n g , D o n g h u a X Ü , Z h i h u L i u W e i d o n g L i and H o w m a n W o n g Abstract Females in most populations of chiru or Tibetan antelope Pantholops hodgsonii migrate each year up to 350 km to summer calving grounds, and these migrations characterize the Tibet/Qinghai Plateau. We studied the migratory chiru population at the Ullughusu calving grounds southwest of the Arjinshan Nature Reserve in Xinjiang, China. The 750-1,000 km 2 of suitable habitat at Ullughusu is at 4,500-5,000 m with sparse vegetation. We used direct methods (block counts, vehicle and walking transects and radial point sampling) and an indirect method (pellet counts) during six summers to assess population density. We also witnessed and stopped two major poaching events, in 1998 and 1999 (103 and 909 carcasses, respectively). Surveys suggested a drop in population density from 1999 to 2000. Poaching was not seen during summer monitoring after 1999, and surveys in 2001 and 2006 suggest that the population density is stable or recovering. We compare the Ullughusu calving grounds with those in the western Kunlun and discuss possible routes for migrating females.

Background5-Fluorouracil (5-FU)-based chemotherapy is a conventional therapeutic approach for the treatment of patients with colorectal cancer (CRC). However, development of 5-FU resistance frequently occurs. We explored a potential method for regulating the sensitivity to 5-FU-based chemotherapy in CRC patients.Material/MethodsCell viability was determined by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Gene expression levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Protein expression levels were evaluated by Western blot. TargetScan was used for the prediction of binding sites for miRNA in mRNAs. The interaction between mRNA 3′UTR and miRNA was verified by dual luciferase reporter assay. Tissue samples were obtained from 33 CRC patients who received surgery at Xingtai People’s Hospital.ResultsmiR-106a level was associated with 5-FU sensitivity in CRC cells. Overexpression of miR-106a reduced 5-FU sensitivity of HCT116 and SW620 cells, and antagonist of miR-106a sensitized HCT116 and SW620 towards 5-FU. miR-106a overexpression decreased dual-specificity phosphatases 2 (DUSP2) expression at mRNA and protein levels in HCT116 and SW620 cells. Through downregulation of DUSP2, miR-106a elevation increased COX-2 expression and stemness-maintenance genes (SOX2 and OCT4). Furthermore, we predicted that miR-106a directly binds to 3′UTR of DUSP2 mRNA, which was confirmed by dual luciferase assay. Silencing of DUSP2 reversed elevated 5-FU sensitivity induced by miR-106a antagonist in HCT116 cells. A negative correlation was discovered between miR-106a and DUSP2 in tumor samples of CRC patients.ConclusionsmiR-106a plays an important role in mediating response to 5-FU-based chemotherapy in CRC and could serve as a potential target for CRC patients.

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Koslov's pika, Ochotona koslowi (Büchner), was surveyed in western China. This endangered species is poorly known. We determined that it is a burrowing pika, and lives in social family groups at high densities. It primarily occupies high-elevation cold grassland vegetation. It appears to have a high reproductive rate. More emphasis should be placed on research into this unique species in China.

Chemotherapy resistance poses a major challenge for the clinical treatment of colorectal cancer, therefore, the aim of the present study was to examine its underlying mechanisms. Reverse transcription-quantitative polymerase chain reaction and western blot analysis were used to determine the microRNA (miRNA)/mRNA and protein expression levels, respectively. A dual luciferase assay was conducted for verification of the interaction between miR-106a and 3′untranslated region (UTR) of Forkhead box Q1 (FOXQ1). Cell viability was assessed using an MTT assay. In the present study, it was demonstrated that miR-106a is involved in regulating oxaliplatin sensitivity of colorectal cancer. Transfection of miR-106a mimics slightly inhibited colorectal cancer cell growth and sensitized colorectal cancer cells to oxaliplatin exposure. In addition, miR-106a overexpression induced a decrease of FOXQ1 at mRNA and protein levels in colorectal cancer cells. The enhanced expression of miR-106a also increased the expression of Wnt target genes, including vascular endothelial growth factor-A and matrix metallopeptidase 2, which were reported to be regulated by FOXQ1. It was predicted and validated that miR-106a could repress FOXQ1 expression via direct binding to 3′UTR. Elevation of miR-106a and a decrease of FOXQ1 expression levels were detected in tumor tissues from patients with oxaliplatin-sensitive colorectal cancer, compared with patients with oxaliplatin-resistant colorectal cancer. Furthermore, there was a significant association between miR-106a and FOXQ1 mRNA levels. In conclusion, the present study demonstrated that miR-106a increased oxaliplatin sensitivity of colorectal cancer cells through direct repression of FOXQ1 expression.