一个考虑扩散的Holling-Tanner捕食-食饵模型研究

研究了一个在齐次Neumann边界条件下考虑扩散的Holling-Tanner捕食-食饵模型.首先,得到了系统的全局吸引子和持久性;然后,讨论了系统正常数平衡解的全局渐进稳定性;最后,研究了系统的Turning失稳性质.

Modeling and multi-response optimization of machining performance while turning hardened steel with self-propelled rotary tool

There are many advanced tooling approaches in metal cutting to enhance the cutting tool performance for machining hard-to-cut materials. The self propelled rotary tool （SPRT） is one of the novel approaches to improve the cutting tool performance by providing cutting edge in the form of a disk, which rotates about its principal axis and provides a rest period for the cutting edge to cool and allow engaging a fresh cutting edge with the work piece. This paper aimed to present the cutting performance of SPRT while turning hardened EN24 steel and optimize the machining conditions. Surface roughness （Ra） and metal removal rate （rMMR） are considered as machining perfor- mance parameters to evaluate, while the horizontal incli- nation angle of the SPRT, depth of cut, feed rate and spindle speed are considered as process variables. Initially, design of experiments （DOEs） is employed to minimize the number of experiments. For each set of chosen process variables, the machining experiments are conducted on computer numerical control （CNC） lathe to measure the machining responses. Then, the response surface method- ology （RSM） is used to establish quantitative relationships for the output responses in terms of the input variables. Analysis of variance （ANOVA） is used to check the adequacy of the model. The influence of input variables on the output responses is also determined. Consequently, these models are formulated as a multi-response optimi- zation problem to minimize the Ra and maximize the rMMR simultaneously. Non-dominated sorting genetic algorithm-II （NSGA-II） is used to derive the set of Pareto-optimal solutions. The optimal results obtained through the pro- posed methodology are also compared with the results of validation experimental runs and good correlation is found between them.

A Novel Tetraphenylethylene-Based“Turn On”Fluorescent Sensor with Highly Sensitive Response to Mercury Ions

A novel 4-tert-butyl-N’-(4-(1,2,2-triphenylvinyl)benzylidene)benzohydrazide(TBB)was successfully synthesized in simple one-step process.It was characterized by FT-IR,1H NMR,13C NMR and HRMS.Its fluorescence sensing ability to 15 metal ions was investigated.Weak emission from TBB could be efficiently increased by trace Hg^2+,through coordination reaction between TBB and Hg^2+ with"turn on"character.The fluorescence intensity of TBB/Hg^2+([TBB]=3.0×10^–6 mol/L,[Hg2+]=1.3×10^–4 mol/L)was 7.5 times higher than that of TBB.This TBB sensor exhibited high selectivity for Hg^2+ and other metal ions did not interfere in this determination.The limit of detection was 0.566μmol/L(S/N=3).The experimental results showed that this TBB sensor could sensitively respond to Hg^2+ within concentration range(from 5×10–6 mol/L to 1.3×10^–4 mol/L).

Epigenetic Enabled Normal Human Cells, Lead to <i>First Cell</i>’s Unique Division System, Driving Tumorigenesis Evolution

Normal cells must become cancer-enabling before anything else occurs, according to latest literature. The goal in this mini-review is to demonstrate special tetraploidy in the enabling process. This we have shown from genomic damage, DDR (DNA Damage Response) activity with skip of mitosis leading to diploid G2 cells at the G1 border in need of chromatin repair for continued cell cycling to the special tetraploid division system. In several studies specific methylation transferase genes were activated in normal human cells in tissue fields, containing different cell growth stages of the cancerous process. Histology studies, in addition to molecular chemistry for identification of oncogenic mutational change, were a welcome change (see below). In a study on melanoma origin, DDR also showed arrested diploid cells regaining cycling from methylation transferase activity with causation of 2n melanocytes transforming to 4n melanoblasts, giving rise to epigenetic tumorigenesis enabled First Cells. Such First Cells were from Barrett’s esophagus shown to have inherited the unique division system from 4n diplochromosomal cells, first described in mouse ascites cancer cells (below). We discovered that the large nucleus prior to chromosomal division turned 90° relative to the cytoskeleton axis, and divided genome reductive to diploid, First Cells, in a perpendicular orientation to the surrounding normal cells they had originated from. This unique division system was herein shown to occur at metastasis stage, implying activity throughout the cancerous evolution. Another study showed 4-chromatid tetraploidy in development to B-cell lymphoma, and that such cancer cells also proliferated with participation of this unusual division system. Such participation has long been known from Bloom’s inherited syndrome with repair chiasmas between the four chromatids, also an in vitro observation by us. Our cytogenetic approach also revealed that they believed mitotic division in cancer cells is wrong because such cell divisions were found to be from an adaptation between amitosis and mitosis, called amitotic-mitosis. Amitosis means division without centrosomes, which has long been known from oral cancer cells, in that MOTCs (microtubule organizing center) were lacking centrioles. This observation calls for re-introduction of karyotype and cell division studies in cancer cell proliferation. It has high probability of contributing novel approaches to cancer control from screening of drugs against the amitotic-mitotic division apparatus.