欧拉方程计算气动力时的粘性修正研究

在采用欧拉方程进行气动力计算过程中,由表面压力积分来估计的阻力只考虑了压差阻力,计算得到的无粘阻力分解成诱阻和波阻。为考虑粘性,需进行边界层修正。在层流边界层计算时采用Cohen-Reshotko方法,边界层转捩计算采用Granville方法,湍流边界层计算采用Green方法。计算结果表明,通过粘性修正计算得到的升力、阻力系数(加上了摩擦阻力)更加接近风洞试验结果。

Role of the STAT3/survivin signaling pathway in the EML4-ALK-positive lung adenocarcinoma cell line H2228 before and after crizotinib-induced resistance

Objective This study investigated the role of the STAT3/survivin signaling pathway in the EML4-ALK- positive lung adenocarcinoma cell line H2228 before and after crizotinib-induced resistance. The mecha- nism of resistance was studied. Methods Cell viability was determined using the MTT assay. Crizotinib-induced apoptosis in H2228 and H2228 crizotinib-resistant cells treated with the indicated doses of crizotinib was measured at different times （24 h, 48 h, 72 h） using flow cytometry. The levels of p-ALK, ALK, p-STAT3, STAT3, and survivin after treatment of cells with 0, 0.3, and 1 pM crizotinib for 72 h were determined using Western blot analysis. DNA sequencing was used to identify mutations in H2228 crizotinib-resistant cells. Results The crizotinib IC50 values in H2228 and H2228 crizotinib-resistant cells at 72 h were 334.5 nM and 3418 nM, respectively. The resistance index of 1-12228 crizotinib-resistant cells was 10.20. Crizotinib induced apoptosis in H2228 cells and reduced the levels of p-ALK, p-STAT3, and survivin. In contrast, no changes in the levels of p-ALK, p-STAT3, and survivin were observed in H2228 crizotinib-resistant cells. The mutations 2067G--,A and 2182G--,C in EML4-ALK were present in the H2228 crizotinib-resistant cells. Conclusion Crizotinib decreased the viability of H2228 cells in a dose- and time-dependent manner. In the STAT3/survivin pathway, downregulation of p-ALK, p-STAT3, and survivin might contribute to crizo- tinib-induced apoptosis in H2228 ceils. However, the STAT3/survivin pathway in H2228 crizotinib-resistant cells was unaffected by crizotinib treatment. Acquired resistance in H2228 cells might be related to ALK mutations.

Test Series Results of Varying Yaw and Roll Angles of Trimaran Amas

This paper illustrates the reasons behind the research strategy that has led to a new generation of trimaran hulls by minimizing the hull＇s drag-design approach. The objective of this study was to search for the optimal side-hull yaw and roll angle to minimize induced drag of trimarans a^d so to investigate the differences in the performance results of a trimaran hull. Specifically, this research has been based on a critical analysis of the diversity of ama yaw and roll angles and outriggers positioning. Then, the paper will be comparing the results of the test series of the yaw and roll angles of trimaran areas. Design and towing tank test of a scaled trimaran model will be illustrated and compared along with some key and relevant results. The term ＂ama＂ is a word in the Polynesian and Micronesian languages to describe the outrigger part of a canoe to provide stability.

Study of the selective effect on cells induced by nanosecond pulsed electric field with the resistor-capacitor circuit model

A resistor-capacitor(RC)circuit model is proposed to study the effect of nanosecond pulsed electricfield on cells according to the structure and electrical parameters of cells.After a nanosecond step fieldhas been applied,the variation of voltages across cytomembrane and mitochondria membrane both in nor-mal and in malignant cells are studied with this model.The time for selectively targeting the mitochondriamembrane and malignant cell can be evaluated much easily with curves that show the variation of voltageacross each membrane with time.Ramp field is the typical field applied in electrobiology.The voltagesacross each membrane induced by ramp field are analyzed with this model.To selectively target the mito-chondria membrane,proper range of ramp slope is needed.It is relatively difficult to decide the range ofa slope to selectively affect the malignant cell.Under some conditions,such a range even does not exist.

Conceptual Design and Aerodynamic Study of Joined-Wing Business Jet Aircraft

The concept of joined-wing aircraft with nonplanar wings as conceived and patented by Wolkovitch is attractive due to various advantages such as light weight, high stiffness, low induced drag, high trimmed CLmax, reduced wetted area and parasite drag and good stability and control, which have been supported by independent analyses, design studies and wind tunnel tests. With such foreseen advantages, the present work is carried out to design joined-wing business-jet aircraft and study and investigate its advantages and benefits as compared to the current available conventional business jet of similar size, passenger and payload capacity. In particular, the work searches for a conceptual design of joined-wing configured business-jet aircraft that possesses more superior characteristics and better aerodynamic performance in terms of increased lift and reduced drag, and lighter than the conventional business jet of similar size. Another significant objective of this work is to prove that the added rigidity possessed by the joined wing configuration can contribute to weight reduction.

BNIP3 is essential for mediating 6-thioguanine- and 5-fluorouracil-induced autophagy following DNA mismatch repair processing

DNA mismatch repair （MMR） processes the chemically induced mispairs following treatment with clinically important nucleoside analogs such as 6-thioguanine （6-TG） and 5-fluorouracil （5-FU）. MMR processing of these drugs has been implicated in activation of a prolonged G2/M cell cycle arrest for repair and later induction of apoptosis and/or autophagy for irreparable DNA damage. In this study, we investigated the role of Bcl2 and adenovirus EIB Nineteen-kilodalton Interacting Protein （BNIP3） in the activation of autophagy, and the temporal relationship between a G2/M cell cycle arrest and the activation of BNIP3-mediated autophagy following MMR processing of 6-TG and 5-FU. We found that BNIP3 protein levels are upregulated in a MLHI （MMR＋）-dependent manner following 6-TG and 5-FU treatment. Subsequent small-interfering RNA （siRNA）-mediated BNIP3 knockdown abrogates 6-TG- induced autophagy. We also found that p53 knockdown or inhibition of mTOR activity by rapamycin cotreatment impairs 6-TG- and 5-FU-induced upregulation of BNIP3 protein levels and autophagy. Furthermore, suppression of Checkpoint kinase 1 （Chkl） expression with a subsequent reduction in 6-TG-induced G2/M cell cycle arrest by Chkl siRNA promotes the extent of 6-TG-induced autophagy. These findings suggest that BNIP3 mediates 6-TG- and 5-FU-induced autophagy in a p53- and mTOR-dependent manner. Additionally, the duration of Chkl-activated G2/ M cell cycle arrest determines the level of autophagy following MMR processing of these nucleoside analogs.

Effects of angiotensin-Ⅱ receptor blockers on β-catenin expression in a rat model of experimental streptozotocin-induced early-stage of diabetic nephropathy

Objective： Diabetic nephropathy （DN） is one of the most common causes of end-stage renal failure. The pathogenesis of progressive renal injury is multifactorial and the mechanism by which hyperglycemia causes microangiopathy is still poorly understood. The WNT pathway is activated in DN and regulating β-catenin protein levels is referred to as the canonical Wntβ-catenin pathway. Because the renin angiotensin system has been reported to be an important contributory factor in the pathophysiology of DN, exogenous administration of angiotensin Ⅱ receptor antagonist may be beneficial in counteracting some biochemical or functional changes of DN. The aim of the study was to determine the β-catenin expression and the possible protective effects of irbesartan, an angiotensin Ⅱ type 1 receptor blocker （ARB） in a rat model of streptozotocin（STZ）-induced diabetic nephropathy. Methods： STZ-induced DN in rats was assessed biochemically by measuring urine volume, protein and creatinine clearance as well as Kidney weight/body weight （KW/BW） and the index of mesangial expansion. Three groups of male Sprague-dawley rats were used. The first group consisted of non-diabetic control rats （control）. The second group was the untreated diabetic rats（STZ＋vehicle）. The third group consisted of diabeti rats treated with irbesartan, 50 mg/kg for 12 weeks （STZ＋irbesartan）. Immunohistochemical stainings and real time PCR for β-catenin were performed in renal cortex of rat modals. Results： Marked hyperglycemia, polyuria, proteinuria, renal hypertrophy, mesangial matrix expansion and glomerular hyperfiltration were observed in STZ diabetic rats. The levels of microalbuminuria and KW/BW in the STZ＋irbesartan group were lower than those in the STZ＋vehicle group （P〈0.05）. The up-regulated immunostaining and mRNA expression of β-catenin were decreased in renal cortic of the Irbesartan-treated diabetic group, but there was no significant difference compared to the untreated diabetic group. Conclusion： The data suggest that irbesartan ameliorates proteinuria and renal hypertrophy, charactered damages of STZ-induced early-stage DN in rats, but its effective drug target is not to inhibit the up-regulated expressions of β-catenin.

15-PGDH is reduced and induces apoptosis and cell cycle arrest in gastric carcinoma

AIM: To investigate the expression of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) in human gastric cancer and it's mechanism in apoptosis and cell cycle arrest. METHODS: Expression of 15-PGDH mRNA and protein was examined by immunohistochemistry, immunocytochemistry, reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting in tissue from human gastric cancer, gastric precancerous state (gastric polyps and atrophic gastritis), normal stomach, and gastric cancer cell lines. The relationship between gastric cancer, gastric precancerous state and 15-PGDH expression was determined. The association between expression of 15-PGDH and various clinicopathological parameters in gastric cancer was evaluated. Human gastric cancer cell line SGC-7901 was transfected with 15-PGDH expression plasmids. The effect of 15-PGDH on the cell cycle was examined by flow cytometry. The effect of 15-PGDH on apoptosis was examined by transmission electron microscopy, flow cytometry and transferasemediated nick end labeling (TUNEL) assay. Expression of cell cycle (p21, p27, p16 and p53) and apoptosis (Survivin, BCL-2, BCL-XL, BAK and BAX) genes was analyzed by RT-PCR. RESULTS: Expression of 15-PGDH mRNA and protein in human gastric cancer tissues was significantly lower than in normal gastric tissues (P < 0.01). Expression in human gastric cancer cell lines MKN-28 and MKN-45 was reduced, and absent in SGC-7901 cells (P < 0.05). Reduction of 15-PGDH expression was also found in precancerous tissues, such as gastric polyps and atrophic gastritis (P < 0.01). There was a significant difference in expression of 15-PGDH among various gastric cancer pathological types (P < 0.05), with or without distant metastasis (P < 0.05) and different TNM stage (P < 0.01). Flow cytometry demonstrated a significant increase in apoptotic cells in SGC-7901 cells transfected with pcDNA3/15-PGDH plasmid for 24 and 48 h (P < 0.01), and an increased fraction of sub-G1 phase after transfection (P < 0.05). TUNEL assay showed an increased Apoptotic Index in cells overexpressing 15-PGDH (P < 0.01). After transfection, expression of proapoptotic genes, such as BAK (P < 0.05), BAX and p53 (P < 0.01), was increased. Expression of antiapoptotic genes was decreased, such as Survivin, BCL-2 and BCL-XL (P < 0.01). Expression of cyclin-dependent kinase inhibitors p21 and p16 (P < 0.01) was significantly upregulated in cells overexpressing 15-PGDH. CONCLUSION: Reduction of 15-PGDH is associated with carcinogenesis and development of gastric carcinoma. 15-PGDH induces apoptosis and cell cycle arrest in SGC-7901 cells.

The impact of ^(60)Co γ-ray on cycles to Hep-2 human laryngeal cancer cell in the condition of hypoxia

Objective： The aim of the study was to investigate the impact of 60Co y-ray on apoptosis, cell cycles and the expression of protein hypoxia-inducible factor-1α （HIF-1α） to Hep-2 cell line in the conditions of normoxia and hypoxia. Methods： Hep-2 cell were divided into 2 groups： group A （normoxia） and group B （hypoxia）. All of the ceils were exposed to y-ray with dosage being 0, 1, 3, 5, 10, 20, and 40 Gy. Flow cytometry was used to measure the protein level of HIF-1α and to detect apoptosis and cell cycles. The protein level of HIF-1α was also determined by immunohistochemistry and Western blotting. Results： The protein level of HIF-1α in group B was significantly higher than that in group A. In group A, low doses （1-5 Gy） of y-ray had caused G0/G1 cell cycle arrest and high doses （10-40 Gy） had caused G2/M cell cycle arrest. In group B, without exposure of y-ray （0 Gy） had caused G0/G1 cell cycle arrest, all of the different dosage of y-ray could cause G2/M cell cycle arrest. The curve of apoptosis rate in group A was a parabola, the apoptotic rate was related to the dosage of y-ray in a dosage dependent manner. The peak was at the point of 5 Gy. The apoptosis rate in group A was significantly higher than that in group B. Conclusion： Different doses of y-ray could cause different cell cycles arrest then make different impact on apoptosis to Hep-2 ceil. The lower apoptosis rate in condition of hypoxia maybe has a relationship with G2/M cell cycle arrest. Up-regulated HIF-1α protein may be one of the reasons for G2/M cell cycle arrest.

Parthenolide inhibits proliferation of vascular smooth muscle cells through induction of G_0/G_1 phase cell cycle arrest

Objective： This study is to determine the effect of the natural product parthenolide, a sesquiterpene lactone isolated from extracts of the herb Tanacetum parthenium, on the proliferation of vascular smooth muscle cells （VSMCs）. Methods： Rat aortic VSMCs were isolated and cultured in vitro, and treated with different concentrations ofparthenolide （l 0, 20 and 30 μmol/L）. [^3H]thymidine incorporation was used as an index of cell proliferation. Cell cycle progression and distribution were determined by flow cytometric analysis. Furthermore, the expression of several regulatory proteins relevant to VSMC proliferation including IκBα, cyclooxygenase-2 （Cox-2）, p21, and p27 was examined to investigate the potential molecular mechanism. Results： Treatment with parthenolide significantly decreased the [^3H]thymidine incorporation into DNA by 30%-56% relative to control values in a dose-dependent manner （P〈0.05）. Addition of parthenolide also increased cell population at G0/G1 phase by 19.2%-65.7% （P〈0.05） and decreased cell population at S phase by 50.7%-84.8% （P〈0.05）, which is consistent with its stimulatory effects on p21 and p27. In addition, parthenolide also increased IκBα expression and reduced Cox-2 expression in a time-dependent manner. Conclusion： Our results show that parthenolide significantly inhibits the VSMC proliferation by inducing G0/G1 cell cycle arrest. IκBα and Cox-2 are likely involved in such inhibitory effect ofparthenolide on VSMC proliferation. These findings warrant further investigation on potential therapeutic implications ofparthenolide on VSMC proliferation in vivo.

Investigation on 3D flow field induced by a plasma actuator with serrated electrode

This paper presents an experimental investigation on flow field induced by a dielectric barrier discharge(DBD) plasma actuator with serrated electrodes in still air to further improve its flow control effectiveness. For comparison, the actuator with widely used linear electrodes was also studied. Experiments were carried out using 2D particle image velocimetry. Particular attention was given to the flow topology, discharge phenomenon, and vortex formation mechanism. Results showed that a 2D wall jet was induced by the linear actuators, whereas the plasma actuators with serrated electrode introduced a series of streamwise vorticities, which might benefit flow control(e.g., enhancing the momentum transport in the separated boundary flow). In addition, the mechanism of 3D flow topology induced by the serrated DBD actuator was analyzed in detail.