e. once every 12 hours). Although care must be taken with concomitant use of AEDs that act on sodium channels, adjunctive therapy with lacosamide (a non-traditional sodium-channel blocking AED) significantly LGX818 reduced seizure frequency regardless

of co-administration of traditional sodium-channel blockers in this open-label trial.[19] Randomized controlled trials of lacosamide are needed to confirm and validate the efficacy and safety results observed here in this pediatric population. Acknowledgments This study was funded by Dr. Carlos Casas-Fernández. Medical writing and journal styling assistance was provided by Maxwell Chang and Lucy Whitehouse, and post-submission writing assistance was provided by Tracy Harrison, all of inScience Communications, Springer Healthcare; this assistance was funded by Dr. Carlos Casas-Fernández, The authors have no conflicts of interest to declare. The authors confirm that they have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent with those guidelines. Appendix:

Lacosamide Spanish Study Group Members Dr. Alarcón-Martínez (Selleck HSP inhibitor Hospital Universitario Virgen de la Arrixaca, Murcia); Dr. Arrabal-Fernández (Hospital Universitario Virgen de las Nieves, Granada); Dr. Cabrera-López (Hospital Universitario Materno-Infantil, Las Palmas de Gran Canaria, Canary Islands): Dr. Camino-León (Hospital Universitario

Reina Sofía, Cordoba); Dr. Campistol-Plana (Hospital Universitario San Juan de Dios, Barcelona); Dr. Campos-Castello (Hospital Clínico Cyclin-dependent kinase 3 San Carlos, Madrid); Dr. HDAC inhibitor Casas-Fernández (Hospital Universitario Virgen de la Arrixaca, Murcia); Dr. Domingo Jiménez (Hospital Universitario Virgen de la Arrixaca, Murcia); Dr. Duque-Fernández (Hospital Universitario Virgen de La Candelaria, Santa Cruz de Tenerife); Dr. Eiris-Puñal (Hospital Clínico Universitario, Santiago de Compostela); Dr. García-Peñas (Hospital Universitario Marqués de Valdecilla, Santander); Dr. Herranz-Fernández (Universidad de Cantabria, Santander); Dr. Ibáñez-Micó (Hospital Universitario Virgen de la Arrixaca, Murcia); Dr. Jover-Cerda (Hospital General de Elda, Alicante); Dr. Lara-Herguedas (Hospital Universitario Puerta de Hierro-Majadahonda, Madrid); Dr. López-Lafuente (Hospital San Pedro de Alcántara, Cáceres); Dr. Madruga-Garrido (Hospital Universitario Virgen del Rocío, Seville); Dr. Martínez-Bermejo (Hospital Universitario La Paz, Madrid); Dr. Martínez-Salcedo (Hospital Universitario Virgen de la Arrixaca, Murcia); Dr. Puche-Mira (Hospital Universitario Virgen de la Arrixaca, Murcia); Dr. Roldán-Aparicio (Hospital Universitario Virgen de las Nieves, Granada); Dr. Rufo-Campos (Instituto Hispalense de Pediatría, Seville); Dr. Santos-Borbujo (Hospital Clínico Universitario, Salamanca); Dr.

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All of these alterations will finally lead to angiogenesis, matrix degradation and metastasis

in cancer. Cancer cells adapt to hypoxia for survival [26]. It is reported that BLyS suppresses the progression of several kinds of SB-715992 mw tumors and plays an important role in the development of immune system diseases [27]. However, our results showed an enhanced migratory in response to BLyS. Several reports support the critical roles of Akt and p38 MAPK in cancer cell survival, migration, apoptosis and anti-apoptosis [28, 29]. Previous research indicated that BLyS led to rapid phosphorylations of Akt in B cells [30]. Our studies suggested that phosphorylations of Akt were essential for BLyS-enhanced cell migration in vitro. Conclusion In conclusion, the results found that BLyS caused the enhanced migration of human breast cancer cells, while BLyS was up-regulated by hypoxia. However, further studies are required to confirm the mechanisms of BLyS action and reveal the relationship between inflammation and breast cancer progression. Acknowledgements This

work was supported by the Standardized Platform Construction and Scientific Application in New Technologies for New Drug Screening (No.2009ZX09302-002), the Study of Saponin Monomer of Dwarf Lilyturf Tuber (DT-13): A new Natural Anti-metastatic Drug Candidate (No.2009ZX09103-308) and the Research on Anti-tumor metastasis effectof YS-1 (No.81071841) References 1. Woodland RT, Schmidt MR, Thompson CB: BLyS and B cell homeostasis. Semin Immunol 2006, 18:318–326.PubMedCrossRef 2. Entinostat ic50 Tangye SG, Bryant VL, Cuss AK, Good KL: BAFF, APRIL and human B cell disorders. Semin Immunol 2006, 18:305–317.PubMedCrossRef 3. Novak AJ, Darce JR, Arendt BK, Harder B, Henderson K, Kindsvogel K, Gross JA, Greipp PR, Jelinek DF: Expression of BCMA, TACI, and BAFF-R in multiple myeloma: a mechanism for growth and survival. Blood 2004, 103:689–694.PubMedCrossRef 4. Parameswaran R, David HB, Sharabi A, Zinger H, Mozes E: B-cell activating

factor (BAFF) plays a role in the mechanism of action of a tolerogenic peptide that ameliorates lupus. Clin PAK6 Immunol 2009, 131:223–232.PubMedCrossRef 5. Kalled SL: Impact of the BAFF/BR3 axis on B cell survival, germinal center maintenance and antibody production. Semin Immunol 2006, 18:290–296.PubMedCrossRef 6. Pelekanou V, Kampa M, Kafousi M, Darivianaki K, Sanidas E, Tsiftsis DD, Stathopoulos EN, Tsapis A, Castanas E: Expression of selleck screening library TNF-superfamily members BAFF and APRIL in breast cancer: immunohistochemical study in 52 invasive ductal breast carcinomas. BMC Cancer 2008, 8:76.PubMedCrossRef 7. Rosmorduc O, Housset C: Hypoxia: a link between fibrogenesis, angiogenesis, and carcinogenesis in liver disease. Semin Liver Dis 2010, 30:258–270.PubMedCrossRef 8.

30) of D1S1635 (1p36.22), D1S214 (1p36.31), EXT1 (8q24.11-q24), AFM137XA11 (9p11.2), CCND2 (12p13), 8 M16/SP6 (12ptel), IGH (D14S308), HIC1 (17p13.3), 282 M15/SP16 (17ptel), and LAMA3 (18q11.2). DCNAs of p53 (17p13.1) have also increased scarcely (1.19 → 1.40),

which have been suggested as an OS-related gene. As Chen, et al. [16] suggested, HIC1 (hypermethylated in cancer-1 located at 17p13.3) was frequent with p53 mutations in human OS. Their results indicated the importance of genes altered only through epigenetic mechanisms in cancer www.selleckchem.com/products/chir-98014.html progression in conjunction with genetically modified tumor suppressor genes. In our study, HIC1 was also higher in the metastatic lesion than the primary site (m/p ratio =1.37 in Table 2). Therefore, we gave attention to the locus of 17p13 including HIC1 as a target gene. Recent

studies have reported that overexpression of 17p11-p12 have been linked p53 degradation [10, 16–20]. In Case #13, the gain of LLGL1, FLI (TOP3A) at 17p11-p12 have also detected. However, these two DCNAs were decreased in a metastatic sample, compared with primary tumor, which might be important in the step of metastasis. These findings support that target genes close to p53 (17p13.1), may contribute to OS tumorigenesis [17, 18]. Thus, the present pilot study suggests that array CGH could powerful means to detect genetic instability and gene aberrations that are reflected to the progression and outcome of primary aggressive bone tumors. HIC1 is increased at the both step of aggressive change and metastatic process. HIC1 might play a role of bone tumor progression and metastasis. We should pay attention the Luminespib locus of 17p11-13 including HIC1, LLGL1, FLI (TOP3A), as well as p53. Further detailed studies RAS p21 protein activator 1 are necessary to clarify genetic pathways of the aggressive

bone tumors. Conclusion Our results may provide several entry points for the identification of GSK2126458 mw candidate genes associated with aggressive change of bone tumors. Especially, the locus 17p11-13 including HIC1 close to p53 was common high amplification in this series and review of the literature. Acknowledgements This study was supported by grants from the he National Science Council of Japan (NSC 88-2314-B-075-096). The authors would like to thank Prof. Tomoatsu Kimura and Dr. Shigeharu Nogami, Department of Orthopaedics, University of Toyama, who provided clinical advices. References 1. Boehm AK, Neff JR, Squire JA, Bayani J, Nelson M, Bridge JA: Cytogenetic findings in 36 osteosarcoma specimens and a review of the literature. Pediatr Pathol Mol Med 2000, 19:359–376. 2. Sandberg AA, Bridge JA: Updates on the cytogenetics and molecular genetics of bone and soft tissue tumors: osteosarcoma and related tumors. Cancer Genet Cytogenet 2003, 145:1–30. 35–46PubMedCrossRef 3. Kallioniemi A, Kallioniemi OP, Sudar D, Rutovitz D, Gray JW, Waldman F, Pinkel D: Comparative genomic hybridization for molecular cytogenetic analysis of solid tumors. Science 1992, 258:818–821.

Mol Cell Biochem 2006, 286: 67–76.PubMedCrossRef 13. Fong WG, Liston P, Rajcan-Separovic

E, St Jean M, Craig C, Korneluk RG: Expression and genetic analysis of XIAP-associated factor 1 (XAF1) in cancer cell lines. Genomics 2000, 70: 113–122.PubMedCrossRef 14. Ng KC, Campos EI, Martinka M, Li G: XAF1 expression is significantly reduced in human melanoma. J Invest Dermatol 2004, 123: 1127–1134.PubMedCrossRef 15. Lee MG, Huh JS, Chung SK, Lee JH, Byun DS, Ryu BK, Kang MJ, Chae KS, Lee SJ, Lee CH, Kim JI, Chang SG, Chi SG: Promoter CpG hypermethylation and downregulation of XAF1 expression in human urogenital malignancies: learn more implication for attenuated p53 response to apoptotic stresses. Oncogene 2006, 25: 5807–5822.PubMedCrossRef

16. Byun DS, Cho K, Ryu BK, Lee MG, Kang MJ, Kim HR, Chi SG: Hypermethylation of XIAP-associated factor 1, a putative tumor suppressor gene from the 17p13.2 locus, in human gastric adenocarcinomas. Cancer Res 2003, 63: 7068–7075.PubMed 17. Joensuu TK, Nilsson S, Holmberg AR, this website Marquez M, Tenhunen M, Saarto T, Joensuu H: Phase I trial on sms-D70 somatostatin analogue in advanced prostate and renal cell cancer. Ann N Y Acad Sci 2004, 1028: 361–374.PubMedCrossRef 18. Liu Givinostat purchase Y: Radiolabelled somatostatin analog therapy in prostate cancer: current status and future directions. Cancer Lett 2006, 239: 21–26.PubMedCrossRef 19. Moller LN, Stidsen CE, Hartmann B, Holst JJ: Somatostatin receptors. Biochim Biophys Acta 2003, 1616: 1–84.PubMedCrossRef 20. Olias G, Viollet C, Kusserow H, Epelbaum J, Meyerhof W: Regulation and function of somatostatin receptors. J Neurochem 2004, 89: 1057–1091.PubMedCrossRef 21. Tatoud R, Degeorges A, Prevost G, Hoepffner JL, Gauville C, Millot

G, Thomas F, Calvo PAK6 F: Somatostatin receptors in prostate tissues and derived cell cultures, and the in vitro growth inhibitory effect of BIM-23014 analog. Mol Cell Endocrinol 1995, 113: 195–204.PubMedCrossRef 22. Kvols LK, Moertel CG, O’Connell MJ, Schutt AJ, Rubin J, Hahn RG: Treatment of the malignant carcinoid syndrome. Evaluation of a long-acting somatostatin analogue. N Engl J Med 1986, 315: 663–666.PubMedCrossRef 23. Liu Z, Marquez M, Nilsson S, Holmberg AR: Comparison of protein expression in two prostate cancer cell-lines, LNCaP and DU145, after treatment with somatostatin. Oncol Rep 2009, 22: 1451–1458.PubMed 24. Liu Z, Marquez M, Nilsson S, Holmberg AR: Incubation with somatostatin, 5-aza decitabine and trichostatin up-regulates somatostatin receptor expression in prostate cancer cells. Oncol Rep 2008, 20: 151–154.PubMed 25. Brevini TA, Bianchi R, Motta M: Direct inhibitory effect of somatostatin on the growth of the human prostatic cancer cell line LNCaP: possible mechanism of action. J Clin Endocrinol Metab 1993, 77: 626–631.PubMedCrossRef 26.

2006; Sutherland et al. 2008). Trends derived from shorter records can be highly misleading, because they may not resolve the effects of decadal or sub-decadal variability such as ENSO or the North Atlantic Oscillation (NAO), among others. ENSO changes STI571 ic50 can cause monthly MSL anomalies of several decimetres. Figure 10 shows time series of annual means for GMSL and island tide gauges in three oceans (Mauritius, Tarawa, and Bermuda). These demonstrate high interannual to decadal-scale variability,

particularly at Tarawa in the 1990s, where MSL dropped 45 cm from March 1997 to February 1998 (Donner 2012). Mauritius shows much lower variance, as does Bermuda since 1980. However, the Bermuda record shows a higher range (almost 0.2 m in the annual means) in the 1960s and 1970s, possibly reflecting the predominantly negative NAO at that time. These

examples make clear that short-term variability in sea levels is superimposed on longer-term trends and needs to be considered in adaptation planning (Jevrejeva et al. 2006; CH5183284 price Rahmstorf 2012). Fig. 10 Annual global mean sea level (GMSL) as reconstructed from tide-gauge data (Church and White 2011), 1955–2009, and global mean from satellite altimetry. Also shown are annual mean sea level (MSL) data for Port Louis (Mauritius), Tarawa (Kiribati), and Hamilton (Bermuda). Global reconstructed and satellite data from CSIRO (http://​www.​cmar.​csiro.​au/​sealevel/​sl_​data_​cmar.​html). Station data from PSMSL (http://​www.​psmsl.​org/​data/​) Robust projections of future MSL on tropical small islands are constrained by several issues affecting both GMSL and regional deviations Ro 61-8048 in vitro from the global mean. These include: the range of emission scenarios and associated global sea-level projections in the most recent IPCC report—the Phosphoribosylglycinamide formyltransferase AR4 at the time of writing (Meehl et al. 2007); remaining uncertainties in the spatial distribution of future sea-level

change (a function of uncertainties in the relative contributions of the Greenland and Antarctic ice sheets, large ice caps and mountain glaciers in various regions); poorly constrained changes in ocean circulation or changes in the intensity of ENSO, NAO, or other large-scale oscillations that can influence regional sea levels; limited data (absent for many islands) on rates of vertical land motion and large uncertainties where the geodetic time series are short (Table 1). Table 1 Ninety-year projections (2010–2100) of relative sea-level rise (SLR) for 18 selected island sites in the Indian, Pacific, and Atlantic Oceans together with measurements of local vertical crustal motion (VM) and uncertainty (±1sVM) on crustal motion (all in meters over 90 years) B1MIN and A1FIMAX are the minimum and maximum projections from the IPCC (2007) and A1FIMAX+ is the upper limit for the A1FI SRES scenario augmented to account for accelerated drawdown of ice sheets (Meehl et al.

B. Analysis of the interaction of Hfq and invE RNA by surface plasmon resonance. The invE RNA probe was immobilized onto a sensor chip and binding assays were carried selleck inhibitor out using a Biacore 2000 optical sensor device. Experiments were performed in 40 mM (Graph A) and 100 mM (Graph B) NH4Cl at 37°C. Hfq was diluted in the GDC 0032 indicated RNA binding buffer (0, 1, 2, 4 or 8 nM, as indicated on the right side of the graph), and then injected for 180 seconds at a flow rate of 20 ml/min. The results are expressed as difference units (D.U.). We also examined the

interaction between Hfq and invE RNA by surface plasmon resonance (Biacore analysis). Similar to the gel-shift assay, we examined the interaction in the presence of either 40 mM or 100 mM NH4Cl at 37°C. The 140 nucleotide invE RNA probe that was used for the gel-shift assay was immobilized onto a sensor chip, and then increasing amounts of Hfq protein were added. The binding of Hfq hexamer to invE RNA reached a plateau at a concentration of nearly 8 nM Hfq under both buffer conditions (Fig. 5B) when the Hfq protein was used up to 32 nM (data not shown). Thus, the apparent binding affinity based on surface plasmon resonance was higher than that (16 nM) determined by gel-shift analysis. Distinct differences in the RNA binding properties of Hfq were observed in the presence of 40 mM and 100 mM NH4Cl. The minimum concentration of Hfq required

for initial binding was 1 nM in the presence of 40 mM NH4Cl and 4 nM in the presence of 100 mM NH4Cl. In the presence of 40 mM NH4Cl, sequential binding of Hfq complexes was observed in an Hfq concentration-dependent Pevonedistat purchase Y-27632 2HCl manner, whereas in the presence of 100 mM NH4Cl, there was a sudden increase in Hfq binding at a concentration

of 4 nM Hfq. These results confirmed the results of the gel-shift assay, and indicated that the binding of Hfq to invE RNA is influenced by salt concentration. Effect of hfq mutation on invasion and virulence in vivo To determine whether the repression of TTSS expression in low osmotic conditions influenced invasion by S. sonnei, we performed an invasion assay using S. sonnei strains that were grown in the absence of NaCl. When grown in low-salt conditions, the ability of the wild-type strain to invade HeLa cells was tightly repressed. The hfq mutant strain MS4831 was highly invasive, and invasion was markedly repressed by the addition of IPTG, which induced the expression of Hfq (Table 1). These results indicated that Hfq is intimately involved in synthesis of TTSS-associated genes in S. sonnei. Table 1 Invasion efficiency of bacteria grown in low-salt conditions Bacterial strain Rate of invasion HS506 1 ± 1 MS390 2 ± 1 MS4831 (pTrc99A) 100 ± 29 MS4831 (pTrc-hfq) 0 MS390 (YENB+150 mM NaCl) 11 ± 3 In the case of Shigella, hfq mutation has been shown to increase invasion efficiency in cultured cell lines [11].

aeruginosa PA14 or the pqsL mutant as determined by crystal violet staining. (C) Relative biofilm production by S. aureus CF1A-L as a function of the proportion of APO866 supplier supernatant from overnight cultures of P. aeruginosa PA14, the pqsA mutant, the pqsL

mutant or E. coli K12. Results are normalized to unexposed CF1A-L (dotted line). Significant differences between CF1A-L+PA14 and the other conditions for each proportion of supernatant are shown (*, P < 0.05; two-way ANOVA with Bonferroni's post test). (D) Relative biofilm production by S. aureus strains Newbould and NewbouldΔsigB as a function of the proportion of supernatant from overnight cultures of P. aeruginosa PA14, the pqsA or the pqsL mutant. Significant differences between Newbould + PA14 and the other conditions for each proportion

of supernatant (*, P < 0.05; two-way ANOVA with Bonferroni's DAPT post test), and between NewbouldΔsigB + PA14 and PRIMA-1MET Newbould ΔsigB + the pqsA or the pqsL mutant (Δ, P < 0.05; two-way ANOVA with Bonferroni's post test) are shown. The significant difference between untreated Newbould and NewbouldΔsigB is also shown (#, P < 0.05; unpaired t-test). Data are presented as means with standard deviations from at least three independent experiments. Fig. 6D confirms that HQNO from the supernatant of strain PA14 stimulates biofilm production by a SigB-dependent mechanism. The increase in biofilm production observed when S. aureus Newbould is in contact with the supernatant from PA14 is significantly higher than that seen with supernatants from the pqsA and pqsL mutants. Surprisingly, both mutants did not significantly stimulate biofilm production by Newbould Thalidomide as that observed for CF1A-L, suggesting that differences between S. aureus strains may exist in respect to their response to the presence of non-HQNO exoproducts. As expected, biofilm production by NewbouldΔsigB in contact with supernatants from the three P. aeruginosa strains was significantly inferior to that

observed using the PA14 supernatants with strain Newbould. Moreover, supernatants from PA14 generally did not significantly stimulate biofilm production by NewbouldΔsigB in comparison to supernatants from pqsA and pqsL mutants, which confirms that SigB is involved in HQNO-mediated S. aureus biofilm production. Overall, the results of this section support the hypothesis that HQNO from P. aeruginosa stimulates biofilm production by S. aureus through a SigB-dependent mechanism. Discussion We found that the P. aeruginosa exoproduct HQNO increases the production of biofilm by S. aureus. The effects on biofilm production, as well as on growth, were only seen on normal strains whereas the already high biofilm formation and slow growth rate of SCVs were not altered by the presence of HQNO.

In a few cases of isolated penetrating injuries where abdominal injury is believed to be unlikely, the repair can be accomplished by thoracotomy or thoracoscopy. A transabdominal selleck screening library approach is the best choice for surgical closure in the acute phase, as it provides good access to the diaphragmatic tear and repair of other concomitant lesions [17]. Surgical treatment usually performed includes hernia reduction, pleural drainage, and repair of the diaphragmatic defect. We used a Clear Mesh Composite “CMC”, a pure polypropylene mesh composed of a single-filament macroporous polypropylene mesh on one side and PCI-32765 supplier a non-adhesive layer composed of an anti-adhesive smooth polypropylene film (type IV in the Hamid classification)

[18] on the other side, to prevent intestinal adhesion. This material is much thinner than other prostheses in use, and the transparency of the polypropylene film enables visualization of blood vessels, nerves, and underlying tissues during the placement of the prosthesis. The polypropylene mesh and the polypropylene film are knitted together. The advantages of using the mesh have been widely discussed in the literature and mesh repair has also been Baf-A1 in vitro preferred because of the decreased risk of recurrence

of hernias [19]. A recent North American study (Comparative Analysis of Diaphragmatic Hernia Repair Outcomes Using the Nationwide Inpatient Sample Database) [20] demonstrated that most DH repairs are performed using open abdominal and thoracic techniques. Operative mortality was low for all repair approaches and not significantly

different between the approaches (open abdominal, 1.1%; laparoscopic abdominal, 0.6%; open thoracic, 1.1%). Compared with patients undergoing open thoracic repair, those who underwent DH repair by an abdominal approach, whether open or laparoscopic, were less likely to require postoperative mechanical ventilation. No differences were noted among DH repair approaches in rates of postoperative pneumonia, deep venous thromboembolism, myocardial infarction, or sepsis. Laparoscopic approaches are associated with the decreased length of hospital stay and more routine discharges than open abdominal and thoracotomy approaches [20]. Conclusion Iatrogenic DH due to pedicle screw displacement has not been previously described. Pleural effusion after spinal acetylcholine surgery should always be investigated without delay to recognize early complications. Laparoscopic repair of iatrogenic DH could be feasible and effective in a hemodynamically stable patient with negative CT findings because it enables the completion of the diagnostic cascade and the repair of the tear, providing excellent visualization of the abdominal viscera and diaphragmatic tears. Diaphragmatic tears should be closed with a double-layer mesh to avoid visceral adhesion and a decrease in the risk of recurrence. Consent Written informed consent was obtained from the patient for publication of this Case Report and any accompanying images.

Conclusions Nanopillar array has been successfully obtained on a spin-coated thin film of OIR906 photoresist, employing a kind of novel visible CW laser direct lithography

system. The diameter of the fabricated nanopillar was able to be as small as 48 nm, which is 1/11 of the wavelength of the incident STI571 laser. The lithographic nanopatterns were calibrated and analyzed with AFM. Shape influences of the coma effect and astigmatism effect were simultaneously analyzed using vector integral. The simulation results explain the distortion and inconsistency of the fabricated nanopatterns well. The work has demonstrated a simple, efficient, and low-cost method of fabricating nanopillars. It could pave a new way to fabricate nanopillars/pore arrays of large area distribution for optical nanoelements and biophotonic sensors

while integrated with high-speed scanning system. Appendix Aberration theory about high NA objective Figure 8 is a schematic for laser spot distribution on a focal plane. The Gaussian beam is converted clockwise, is polarized by WP, and then passes through the PP and incident into the high NA objective lens. The components of the diffracted electric field at point P, which is near to the focal spot, can be expressed by the vectorial Debye theory as in Equation 1 [32]: (1) where f is the focal length of the lens and l 0 represents the GSI-IX chemical structure amplitude factor in the image space; E 0 is the amplitude of input Gaussian beam; A 1(θ, ϕ) is the wavefront aberration function,

θ is the angle between the optical axis and given ray; ϕ is the azimuthal coordinate at the input plane and φ s (θ, ϕ) is the phase Selleckchem BKM120 delay generated by the phase mask; x, y, and z indicate the Cartesian coordinates of the point p in the focal region; i is the plural; k = 2πn/λ stands for the wave number, where λ is the wavelength of the incident light and n is the refractive index of the focal space medium. Figure 8 Schematic drawing of light intensity distribution on the focal plane. The amplitude of the Gaussian beam at the input plane is expressed as in cAMP Equation 2: (2)where A 0 is the amplitude, γ is the truncation parameter and expressed as γ = a/ω (a is the aperture radius and ω is the beam size at the waist), while ρ stands for the radial distance of a point from its center normalized by the aperture radius of the focusing system and ρ = sinθ/sinθ max, where θ max is the maximal semi-aperture angle of the objective lens, and in our system, θ max = 67.07°. A 1(θ, ϕ) represents wavefront aberration as expressed as in Equations 3 and 4: Coma: (3) Astigmatism: (4) A c and A a are coefficients for coma and astigmatism, respectively. Both A c and A a multiply λ, representing the departure of the wavefront at the periphery of the exit pupil. The values for λ, n, NA and θ max adopted in simulation correspond to the practical values in the experiment. Refractive index of oil n = 1.