Mode degeneration in bent photonic crystal fiber study by using the finite element method

The development of highly dispersive lower and higher order cladding modes and their degeneration with respect to the fundamental core mode in a bent photonic crystal fiber is rigorously studied by use of the full-vectorial finite element method. It is shown that changes in the bending radius can modify the modal properties of large-area photonic crystal fibers, important for a number of potential practical applications

Microwave-Assisted Synthesis and Evaluation of Antimicrobial Activity of 3-{3-(s-Aryl and s-Heteroaromatic)acryloyl}-2Hchromen-2-one Derivatives

The exploration of potential utilization of microwaves as an energy source for heterocyclic synthesis was herein investigated using condensation of 3-acetylcoumarin (1) with aromatic and heteroaromatic aldehydes to afford the corresponding aromatic chalcones (2a–j) and heteroaromatic chalcones (3a–e and 4a–e), respectively, in good to excellent yield within 1–3 min. The chemical structures were confirmed by analytical and spectral data. All the synthesized compounds were screened for their antibacterial activity and 3-{3-(4-dimethylaminophenyl)acryloyl}-2H-chromen-2-one (2i) was discovered to be the most active at minimum inhibitory concentration (MIC) value of 7.8 µg/m

Recombinant methioninase combined with doxorubicin (DOX) regresses a DOX-resistant synovial sarcoma in a patient-derived orthotopic xenograft (PDOX) mouse model.

Synovial sarcoma (SS) is a recalcitrant subgroup of soft tissue sarcoma (STS). A tumor from a patient with high grade SS from a lower extremity was grown orthotopically in the right biceps femoris muscle of nude mice to establish a patient-derived orthotopic xenograft (PDOX) mouse model. The PDOX mice were randomized into the following groups when tumor volume reached approximately 100 mm3: G1, control without treatment; G2, doxorubicin (DOX) (3 mg/kg, intraperitoneal [i.p.] injection, weekly, for 2 weeks; G3, rMETase (100 unit/mouse, i.p., daily, for 2 weeks); G4 DOX (3mg/kg), i.p. weekly, for 2 weeks) combined with rMETase (100 unit/mouse, i.p., daily, for 2 weeks). On day 14 after treatment initiation, all therapies significantly inhibited tumor growth compared to untreated control, except DOX: (DOX: p = 0.48; rMETase: p < 0.005; DOX combined with rMETase < 0.0001). DOX combined with rMETase was significantly more effective than both DOX alone (p < 0.001) and rMETase alone (p < 0.05). The relative body weight on day 14 compared with day 0 did not significantly differ between any treatment group or untreated control. The results indicate that r-METase can overcome DOX-resistance in this recalcitrant disease

Temozolomide combined with irinotecan regresses a cisplatinum-resistant relapsed osteosarcoma in a patient-derived orthotopic xenograft (PDOX) precision-oncology mouse model.

Relapsed osteosarcoma is a recalcitrant tumor. A patient's cisplatinum (CDDP)-resistant relapsed osteosarcoma lung metastasis was previously established orthotopically in the distal femur of mice to establish a patient-derived orthotopic xenograft (PDOX) model. In the present study, the PDOX models were randomized into the following groups when tumor volume reached 100 mm3: G1, control without treatment; G2, CDDP (6 mg/kg, intraperitoneal (i.p.) injection, weekly, for 2 weeks); gemcitabine (GEM) (100 mg/kg, i.p., weekly, for 2 weeks) combined with docetaxel (DOC) (20 mg/kg, i.p., once); temozolomide (TEM) (25 mg/kg, p.o., daily, for 2 weeks) combined with irinotecan (IRN) (4 mg/kg i.p., daily for 2 weeks). Tumor size and body weight were measured with calipers and a digital balance twice a week. After 2 weeks, all treatments significantly inhibited tumor growth except CDDP compared to the untreated control: CDDP: p = 0.093; GEM+DOC: p = 0.0002, TEM+IRN: p < 0.0001. TEM combined with IRN was significantly more effective than either CDDP (p = 0.0001) or GEM combined with DOC (p = 0.0003) and significantly regressed the tumor volume compared to day 0 (p = 0.003). Thus the PDOX model precisely identified the combination of TEM-IRN that could regress the CDDP-resistant relapsed metastatic osteosarcoma PDOX

Luminous Red Galaxy Clustering at z~0.7 - First Results using AAOmega

We report on the AAT-AAOmega LRG Pilot observing run to establish the feasibility of a large spectroscopic survey using the new AAOmega instrument. We have selected Luminous Red Galaxies (LRGs) using single epoch SDSS riz-photometry to i<20.5 and z<20.2. We have observed in 3 fields including the COSMOS field and the COMBO-17 S11 field, obtaining a sample of ~600 redshift z>=0.5 LRGs. Exposure times varied from 1 - 4 hours to determine the minimum exposure for AAOmega to make an essentially complete LRG redshift survey in average conditions. We show that LRG redshifts to i<20.5 can measured in approximately 1.5hr exposures and present comparisons with 2SLAQ and COMBO-17 (photo-)redshifts. Crucially, the riz selection coupled with the 3-4 times improved AAOmega throughput is shown to extend the LRG mean redshift from z=0.55 for 2SLAQ to z=0.681+/- 0.005 for riz-selected LRGs. This extended range is vital for maximising the S/N for the detection of the baryon acoustic oscillations (BAOs). Furthermore, we show that the amplitude of LRG clustering is s_0 = 9.9+/-0.7 h^-1 Mpc, as high as that seen in the 2SLAQ LRG Survey. Consistent results for the real-space amplitude are found from projected and semi-projected correlation functions. This high clustering amplitude is consistent with a long-lived population whose bias evolves as predicted by a simple ``high-peaks'' model. We conclude that a redshift survey of 360 000 LRGs over 3000deg^2, with an effective volume some 4 times bigger than previously used to detect BAO with LRGs, is possible with AAOmega in 170 nights.Comment: 12 pages, 7 figures, 8 tables, minor changes, matches published versio

Lessons from Loricrin-Deficient Mice: Compensatory Mechanisms Maintaining Skin Barrier Function in the Absence of a Major Cornified Envelope Protein

The epidermal cornified cell envelope (CE) is a complex protein–lipid composite that replaces the plasma membrane of terminally differentiated keratinocytes. This lamellar structure is essential for the barrier function of the skin and has the ability to prevent the loss of water and ions and to protect from environmental hazards. The major protein of the epidermal CE is loricrin, contributing ∼70% by mass. We have generated mice that are deficient for this protein. These mice showed a delay in the formation of the skin barrier in embryonic development. At birth, homozygous mutant mice weighed less than control littermates and showed skin abnormalities, such as congenital erythroderma with a shiny, translucent skin. Tape stripping experiments suggested that the stratum corneum stability was reduced in newborn Lor−/− mice compared with wild-type controls. Isolated mutant CEs were more easily fragmented by sonication in vitro, indicating a greater susceptibility to mechanical stress. Nevertheless, we did not detect impaired epidermal barrier function in these mice. Surprisingly, the skin phenotype disappeared 4–5 d after birth. At least one of the compensatory mechanisms preventing a more severe skin phenotype in newborn Lor−/− mice is an increase in the expression of other CE components, such as SPRRP2D and SPRRP2H, members of the family of “small proline rich proteins”, and repetin, a member of the “fused gene” subgroup of the S100 gene family