13,769 research outputs found

    Activation energy for a 1, 2-hydrogen shift in (phenoxymethyl) chlorocarbene

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    PT: J; CR: BONNEAU R, 1989, J AM CHEM SOC, V111, P5973 EVANSECK JD, 1990, J PHYS CHEM-US, V94, P5518 GRAHAM WH, 1965, J AM CHEM SOC, V87, P4396 JACKSON JE, 1988, J AM CHEM SOC, V110, P5595 JACKSON JE, 1989, J AM CHEM SOC, V111, P6874 LAVILLA JA, 1989, J AM CHEM SOC, V111, P6877 LIU MTH, 1987, CHEM DIAZIRINES, V1, P111 LIU MTH, 1989, J AM CHEM SOC, V111, P6873 LIU MTH, 1990, J AM CHEM SOC, V112, P3915 MORGAN S, 1991, J AM CHEM SOC, V113, P2782 MOSS RA, 1990, J AM CHEM SOC, V112, P5642 MOSS RA, 1990, KINETIC SPECTROSCOPY SCAIANO JC, 1988, CHEM KINETICS SMALL, V3, P73; NR: 13; TC: 5; J9: J ORG CHEM; PG: 2; GA: GH369Source type: Electronic(1

    Energy barrier for cyclopropylchlorocarbene rearrangement measured by direct observation of the carbene in laser flash spectroscopy

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    PT: J; CR: BIRD CL, 1967, J CHEM SOC CHEM COMM, V70, P7 BONNEAU R, 1989, J AM CHEM SOC, V111, P5973 CARMICHAEL I, 1986, J PHYS CHEM REF DATA, V15, P1 GRAHAM WH, 1965, J AM CHEM SOC, V87, P4396 JACKSON JE, 1988, J AM CHEM SOC, V110, P5595 LIU MTH, 1987, CHEM DIAZIRINES, CH5 MOSS RA, 1978, J AM CHEM SOC, V100, P6788 SCAIANO JC, 1988, CHEM KINETICS SMALL, CH13 SHEVLIN PB, 1989, J AM CHEM SOC, V111, P519; NR: 9; TC: 47; J9: J PHYS CHEM; PG: 3; GA: AX049Source type: Electronic(1

    Absolute rate constants for the reactions of some arylchlorocarbenes with acetic acid

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    PT: J; CR: CLOSS GL, 1968, TOP STEREOCHEM, V3, P193 CLOSS GL, 1976, J AM CHEM SOC, V98, P8190 EISENTHAL KB, 1980, J AM CHEM SOC, V102, P6563 GRAHAM WH, 1965, J AM CHEM SOC, V87, P4396 GRILLER D, 1982, J AM CHEM SOC, V104, P5549 HADEL LM, UNPUB CHEM PHYS LETT KIRMSE W, 1971, CARBENE CHEM, CH7 LIU MTH, 1972, CAN J CHEM, V50, P3009 NAGAI Y, 1962, B CHEM SOC JPN, V35, P132 SCAIANO JC, 1980, J AM CHEM SOC, V102, P7747 TURRO NJ, 1980, J AM CHEM SOC, V102, P7576 WONG PC, 1981, CHEM PHYS LETT, V83, P69 WONG PC, 1981, J AM CHEM SOC, V103, P5934 WONG PC, 1982, J AM CHEM SOC, V104, P5106 ZUPANCIC JJ, 1980, J AM CHEM SOC, V102, P5958 ZUPANCIC JJ, 1981, J AM CHEM SOC, V103, P2423 ZUPANCIC JJ, 1981, J AM CHEM SOC, V103, P944; NR: 17; TC: 17; J9: J ORG CHEM; PG: 2; GA: QM675Source type: Electronic(1

    Hydrogen bonding in alcohols: its effect on the carbene insertion reaction

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    PT: J; CR: NRCC20486 PUBL BETHELL D, 1970, CHEM COMMUN, P792 CLOSS GL, 1976, J AM CHEM SOC, V98, P8190 COGGESHALL ND, 1951, J AM CHEM SOC, V73, P5414 EISENTHAL KB, 1980, J AM CHEM SOC, V102, P6563 GRAHAM WH, 1965, J AM CHEM SOC, V87, P4396 GRILLER D, UNPUB JOESTEN MD, 1974, HYDROGEN BONDING, CH5 JONES M, 1973, CARBENES KERR JA, 1967, J CHEM SOC A, P897 KIRMSE W, 1964, CARBENE CHEM LANDECK H, 1977, J PHYS CHEM-US, V81, P718 LIU MTH, 1972, CAN J CHEM, V50, P3009 SCAIANO JC, 1980, J AM CHEM SOC, V102, P7747 SENTHILNATHAN VP, 1980, J AM CHEM SOC, V102, P7637 TURRO NJ, 1980, J AM CHEM SOC, V102, P7576 VALERO J, 1980, J CHIM PHYS PHYS CHI, V77, P65 WILSON GM, 1964, J AM CHEM SOC, V86, P127; NR: 18; TC: 95; J9: J AMER CHEM SOC; PG: 3; GA: PJ911Source type: Electronic(1

    Reaction of 3-chloro-3-methyldiazirines with hydrogen atoms

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    PT: J; CR: BINGHAM RC, 1975, J AM CHEM SOC, V97, P1285 BRADLEY GF, 1977, J CHEM SOC P2, P1214 BRASLAVSKY S, 1977, CHEM REV, V77, P473 CHADWELL HM, 1933, J AM CHEM SOC, V55, P1363 CLARK DT, 1969, T FARADAY SOC, V62, P393 CLARK DT, 1969, T FARADAY SOC, V62, P399 CLARK DT, 1969, T FARADAY SOC, V62, P405 CLOUGH PN, 1970, CAN J CHEM, V48, P2919 DYKSTRA CE, 1978, J AM CHEM SOC, V100, P1378 FIGUERA JM, 1978, J CHEM SOC F1, P809 FREY HM, 1966, ADV PHOTOCHEM, V4, P225 FREY HM, 1977, J CHEM SOC F1, P2010 GILBERT JC, 1979, TETRAHEDRON LETT, P4619 GRAHAM WH, 1965, J AM CHEM SOC, V87, P4306 JAMIESON JWS, 1970, CAN J CHEM, V48, P3619 JENNINGS BM, 1976, J AM CHEM SOC, V98, P6416 JONES M, 1973, CARBENES, V1 JONES WE, CHEM BIOMED ENV INST JONES WE, 1973, CHEM REV, V73, P407 JONES WE, 1978, J CHEM SOC F2, V74, P831 LAU A, 1964, SPECTROCHIM ACTA, V20, P97 LIU MTH, UNPUBLISHED LIU MTH, 1973, CAN J CHEM, V51, P2393 LIU MTH, 1977, CAN J CHEM, V55, P3596 MAEDA Y, 1979, J AM CHEM SOC, V101, P837 MARTIN LR, 1979, INT J CHEM KINET, V11, P543 MEIER H, 1977, ANGEW CHEM INT EDIT, V16, P835 MOFFAT JB, 1978, CHEM DIAZONIUM DIA 1 MOSS RA, 1978, J CHEM SOC CHEM COMM, P775 SCHMITZ E, 1964, ANGEW CHEM INT EDIT, V3, P333 SCHMITZ E, 1971, 23RD INT C PUR ALL C, V2, P283 SCOTT PM, 1969, J PHYS CHEM-US, V73, P1513 SMITH NP, 1979, J CHEM SOC P2, P213 WITTER RA, 1973, J ORG CHEM, V38, P484; NR: 34; TC: 3; J9: J AMER CHEM SOC; PG: 2; GA: JN379Source type: Electronic(1

    Toward a two-dimensional barcode with visual information using perceptual shaping watermarking in mobile applications 

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    [[abstract]]Traditional two-dimensional (2-D) barcodes, such as the QR code and PDF417, do not carry visual information. This work proposes a visually meaningful 2-D barcode (or 2-D image code) that carries not only hidden information, but also visual information. Watermarking is employed to hide information in a meaningful cover image to produce the 2-D image code. The 2-D image code can be printed or displayed and then captured using a camera-equipped mobile device. The hidden information is extracted for innovative applications. To resist distortions in the print-and-photo process, a perceptual shaping algorithm, based on Watson's DCT-based perceptual model, is proposed for use in the data hiding procedure. The detection performance that can be achieved using two classes of position-detection patterns is evaluated, and the best pattern is then used as a part of the 2-D image code. A web service is provided for generating the 2-D image codes and a Java-based decoder is developed for mobile phones. The results of practical experiments reveal the applicability, robustness, and high capacity of the proposed 2-D image code. (C) 2011 Society of Photo-Optical Instrumentation Engineers (SPIE). [DOI: 10.1117/1.3529430][[note]]SC

    Generalizations of pixel-value differencing steganography for data hiding in images 

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    [[abstract]]Generalizations of the pixel-value differencing (PVD) method for data hiding in gray-level images are proposed. Two extensions of the PVD method are analyzed: the block-based approach and the Haar-based approach. For the block-based PVD, the cover image is divided into non-overlapping horizontal or square blocks of n pixels. In each block, n - 1 differences are calculated between consecutive pixels. These differences are classified to embed the secret message. For the Haar-based PVD, the 2-D integer Haar wavelet is applied to decomposed the cover image. The high-frequency components are used to hide message. Higher level of Haar decomposition allows more bits to be embedded. For both proposed generalizations, the capacity of the embedded message is significantly increased. Moreover, both generalizations are invulnerable to the RS-diagram and histogram steganalysis.[[note]]SC

    JC and BK polyomavirus-like particles as targets of innate and adaptive humoral immunity

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    JC polyomavirus (JCPyV) and BK polyomavirus (BKPyV) were identified as the first of now more than 12 human polyomaviruses (HPyVs). The average JCPyV and BKPyV seroprevalence rates in adults are 70% and 90%, respectively. After asymptomatic infection both viruses persist in the renourinary tract. In fact, asymptomatic viruria is detectable in one-third of general population. However, in immunocompromised patients, JCPyV and BKPyV replication may progress to significant diseases. Hence, JCPyV can cause progressive multifocal leukoencephalopathy (PML) in patients with HIV-AIDS, malignancies or autoimmune diseases under immunosuppressive treatment. BKPyV can be a cause of polyomavirus-associated nephropathy (PyVAN) in kidney transplant recipients or hemorrhagic cystitis (PyVHC) after allogeneic hematopoietic stem cell transplantation. Due to more frequent application of immunosuppression, the risk of developing these diseases has increased in the last few decades. The risk of PML development is estimated to be 100-fold higher for JCPyV-seropositive patients in comparison to JCPyV-seronegatives. Most cases of PyVAN and PyVHC have been tested positive for BKPyV at the moment of disease diagnosis. Unfortunately, there is no specific antiviral therapy against any of these HPyV diseases. Thus, current strategies to avert PyVAN or PyVHC aim at identifying patients with BKPyV viremia and reducing immunosuppression. Similar strategies for PML have not been effective, since JCPyV viremia is usually not detected prior to or at the diagnosis of disease. The fate of BKPyV and JCPyV virus-like particles (VLPs) was examined in an animal model corresponding to primary viremia in non-immune host. Radioactively labeled VLPs were used to assess blood decay, organ, and hepatocellular distribution of ligand, and non-labeled VLPs to examine cellular uptake by immunohisto- and cytochemistry. Rapid distribution of both BKPyV and JCPyV VLPs to the liver was observed, with lesser uptake in kidney and spleen. Liver uptake was predominantly observed in LSECs. Blood half-life and tissue distribution of both wild-type JCPyV VLPs and two mutant JCPyV VLPs (L55F and S269F), lacking sialic acid binding affinity, were similar, indicating involvement of non-sialic acid receptors in cellular uptake. We concluded that LSECs very effectively cleared a large fraction of blood-borne BKPyV and JCPyV VLPs, indicating a central role of these cells in early removal of polyomavirus from the circulation. Moreover, we observed that a subpopulation of endothelial cells in kidney, the main organ of polyomavirus persistence, showed selective and rapid uptake of VLPs, suggesting a role in viremic organ tropism (Simon-Santamaria et al., p. 54). Giving the increasing clinical need to reliably determine JCPyV and BKPyV IgG levels in patients at risk, we first reviewed and optimized serological tools for JCPyV and BKPyV IgG detection including virus-like particle (VLP)-based ELISA. We demonstrated that although no statistically significant differences in intraassay and interassay variability were revealed for JCPyV serology of 400-fold diluted sera from healthy donors, qualitative differences were seen in the identification of the individual JCPyV serostatus. The cause of discordance for approximately 10% of sera resulted from a low IgG activity close to the cutoff of the assay. Therefore we standardized the ELISA using reference serum for normalization. Moreover, we developed a preadsorption assay with cutoff of 35% reduction of the JCPyV IgG activity after preincubation with JCPyV VLPs. Importantly, we excluded BKPyV antibody cross-reactivity by testing JCPyV IgG positive sera in preadsorption assay using BKPyV VLPs. In conclusion, we showed that VLP-based ELISA with normalization can serve as a reliable tool for JCPyV IgG serology. Additionally, the preadsorption assay can help with unequivocal determination of JCPyV serostatus for samples with low IgG levels. (Kardas et al., p. 72). We also normalized this VLP-based ELISA for BKPyV IgG detection and showed that for seroepidemiology studies, normalized JCPyV and BKPyV IgG ELISA at 1:200 serum dilution provides optimal sensitivity and specificity with the lowest false-positive and false-negative rate. However, for individual risk assessment, 100-, 200-, and 400-fold dilutions combined with preadsorption for low-reactive sera might be the most appropriate (Kardas et al., p. 82). This improved ELISA was used to investigate JCPyV and BKPyV specific antibody levels in several clinical studies: (1) one case of PML patient where positive JCPyV IgG status was compatible with other PML-indicating symptoms (Kurmann et al., p. 90); (2) one case of PyVAN caused by JCPyV rather than BKPyV, as confirmed by JCPyV IgG/IgM positive and BKPyV IgG/IgM negative results (Lautenschlager et al., 99); (3) one case of PyVHC patient after allogeneic hematopoietic stem cell transplantation where increasing BKPyV IgG activities were in line with progression of BKPyV viremia (Koskenvuo et al., p. 106). Further, by serological testing of 122 immunocompetent and 63 immunocompromised patients we demonstrated that the BKPyV IgG level is age-dependent, with the highest values between 20 and 30 years (Schmidt et al., p. 119). In another study we compared serological outcomes of ELISA utilizing two different antigens in terms of prognostic value in prostate cancer development. To accomplish this we utilized improved ELISA for BKPyV IgG activity to both BKPyV VLPs and BKPyV LTag. Testing of 226 patients undergoing radical prostatectomy for primary prostate cancer revealed that BKPyV VP1 serostatus, in contrast to BKPyV LTag, has no prognostic value in prostate cancer progression (Keller et al., p. 125). In conclusion, we provided a new input into knowledge about tropism and clearance of polyomaviruses from blood. Moreover, we established a reliable and sensitive VLP-based assay for specific detection of JCPyV and BKPyV IgG and IgM. Serostatus based on ELISA results was compatible with other symptoms of BKPyV- and JCPyV-related diseases
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