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28. Untersuchung möglicher Einflussfaktoren auf das Ergebnis bei operativ versorgten Makulaforamina

Author

Krumnauer, N., Roth, M., Spaniol, K., Navarro, E., Kirchhoff, K., Engineer, D., and Schmidt, J. C.

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

Hintergrund: Die Behandlung von Makulaforamina mit Pars-plana-Vitrektomie (ppV) und Gastamponade weist mit ca. 85% bereits eine hohe Erfolgsrate auf. Welche Faktoren zu Therapieversagen führen ist noch weitgehend unklar. Diese Arbeit untersucht Daten von Patienten mit Makulaforamen und analysiert[zum vollständigen Text gelangen Sie über die oben angegebene URL], 180. Versammlung des Vereins Rheinisch-Westfälischer Augenärzte

Published
2018

34. Patents and literature: Immobilized Biocatalysts

Author

Linhardt, Robert J., Amotz S., Rugh S., Markussen E. K., Thomsen K., Bigwood M. P., Naples J. O., Blattler W. A., Lambert J. M., Senter P. D., Boross L. E., Szaj E., Kovacs K., Dar E., Ivony K. K., Seres G. E., Szanj E., Szejtli J. E., Bozzelli J. W., Cheng R. C., Calvo L. C., Campbell D. N., Schmidt J. C., Cannon J. J., Chibata I., Tosa T., Takamatsu S., Degelaen J., Loffet A., Durieux J. P., Freedman H. H., Gardner D. L., Hafner E. W., Jackson D. M., Hagerdal B. G. R., Mosbach K. H., Ho G. -H., Liao C. -C., Ikeda M., Sakamoto S., Suzuki K., Jao Y. -C., Good I. C., Jarvis A. P., Lim F., Karasawa Y., Takata Y., Kasahara Y., Suzuki H., Ashihara Y., Katz E., Benedicktus J. J., Knarr E. L., Scallet B. L., Keyes M. H., Vasan S., Kuu W. Y., Malloy T. P., DeFilippi L. J., Manecke G., Klussmann U., Metcalfe L. D., Frank D., Meyers W. E., Beck L. R., Miyashiro Y., Ogawa M., Yamazaki Y., Igarasi S., Miyata T., Namiki S., Nees S., Niiyama Y., Mori J., Sugahara K., Noll L. A., Pierce P. J., Pinnavaia T. J., Mortland M. M., Boyd S. A., Reischl A., Rembaum A., Yen R. C. K., Robertson J. S., LiPuma M. M., Gross S. E., Rohrbach R. P., Maliarik M. J., Roland J. F., Rosevear A., Lambe C. A., Sakata C., Imai H., Kiss J. E., Ivony J. E., Huber I. E., Boros L. E., Tennent D. L., Sharma B. P., Turkov E., Stamberg J. E., von Blucher H., de Ruiter E., Wolfe S., Westlake D., Jensen S., Wood L. L., Calton G. J., Yoshioka T., Teramoto K., and Shimamura M.

Published
1987
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35. Bücherschau

Author

Hansen, M., Rant, Z., Hahnemann, H. W., Meyer-Eppler, W., Willers, Fr. A., Wever, F., Samal, E., Schmidt, J. C., Langeheinecke, K., Preß, H., and Wellinger, K.

Published
1955
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36. Bücherschau

Author

Grigull, U., Justi, E., Franck, E. U., Wagner, H. Gg., Müller, G., Hölder, E., Stier, F., Paul, M., Neubert, U., Fink, K., Drehmann, A., Hahnemann, H. W., Michely, W., Pflüger, A., Sonntag, G., Buschendorf, Fr., Kufner, M., Wellinger, K., Halbig, W., Hagedorn, L., Lutz, H. R., Schmidt, J. C., and Jung, R.

Published
1960
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37. Bücherchau

Author

Nesselmann, K., Schultz-Grunow, F., Hahnemann, H. W., Willers, Fr. A., de Beauclair, W., Emschermann, H. H., Gaerlner, H., Zeunert, G., Schmidt, J. C., and Rühl, K.

Published
1954
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38. Bücherschau

Author

Jaeckel, K., Baehr, H. D., Collatz, L., Maruhn, K., Tönnies, Chr, Hahnemann, H. W., Haenle, S., Kaiser, J., Nassenstein, H., Cammerer, J. S., Naumann, A., Flügel, G., Hund, F., Pestel, E., Hahnemann, H. W., and Schmidt, J. C.

Published
1957
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39. Ubiquitin-mediated recruitment of the ATG9A-ATG2 lipid transfer complex drives clearance of phosphorylated p62 aggregates

Author

Broadbent, D. G., McEwan, C. M., Jayatunge, D., Kaminsky, E. G., Tsang, T. M., Poole, D. M., Naylor, B. C., Price, J. C., Schmidt, J. C., and Andersen, J. L.

Abstract

Autophagy is an essential cellular recycling process that maintains protein and organelle homeostasis. ATG9A vesicle recruitment is a critical early step in autophagy to initiate autophagosome biogenesis. The mechanisms of ATG9A vesicle recruitment are best understood in the context of starvation-induced non-selective autophagy, whereas less is known about the signals driving ATG9A vesicle recruitment to autophagy initiation sites in the absence of nutrient stress. Here we demonstrate that loss of ATG9A, or the lipid transfer protein ATG2, leads to the accumulation of phosphorylated p62 aggregates in nutrient replete conditions. Furthermore, we show that p62 degradation requires the lipid scramblase activity of ATG9A. Lastly, we present evidence that poly-ubiquitin is an essential signal that recruits ATG9A and mediates autophagy foci assembly in nutrient replete cells. Together, our data support a ubiquitin-driven model of ATG9A recruitment and autophagosome formation during basal autophagy.Movie S1Movie S1U2OS cells expressing Halo-ATG13 labeled with JFX650 (left panel, magenta in merge) and GFP-LC3B (center panel, green in merge) in control media imaged at 1 frame per second.Movie S2Movie S2U2OS cells expressing Halo-ATG13 labeled with JFX650 (left panel, magenta in merge) and GFP-LC3B (center panel, green in merge) treated for 2 hours in media containing 10 µM MLN imaged at 1 frame per second.Movie S3Movie S3U2OS cells expressing Halo-ATG9 labeled with JFX650 (left panel, magenta in merge) and SNAP-p62 labeled with JF503 (center panel, green in merge) in control media imaged at 1 frame per second.Movie S4Movie S4U2OS cells expressing Halo-ATG9 labeled with JFX650 (left panel, magenta in merge) and SNAP-p62 labeled with JF503 (center panel, green in merge) after treatment with 10 µM MLN imaged at 1 frame per second.Movie S5Movie S5U2OS cells expressing Halo-ATG2A labeled with JFX650 (left panel, magenta in merge) and 6x-Ubiquitin-BFP (center panel, green in merge) imaged at 1 frame per second.Movie S6Movie S6ATG9A knock-out U2OS cells expressing Halo-ATG2A labeled with JFX650 (left panel, magenta in merge) and 6x-Ubiquitin-BFP (center panel, green in merge) imaged at 1 frame per second.

Published
2024
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40. Changes in health in England, with analysis by English regions and areas of deprivation, 1990-2013 : A systematic analysis for the Global Burden of Disease Study 2013

Author

Newton, J. N., Briggs, A. D. M., Murray, C. J. L., Dicker, D., Foreman, K. J., Wang, H., Naghavi, M., Forouzanfar, M. H., Ohno, S. L., Barber, R. M., Vos, T., Stanaway, J. D., Schmidt, J. C., Hughes, A. J., Fay, D. F. J., Ecob, R., Gresser, C., McKee, M., Rutter, H., Abubakar, I., Ali, R., Anderson, H. R., Banerjee, A., Bennett, D. A., Bernabé, E., Bhui, K. S., Biryukov, S. M., Bourne, R. R., Brayne, C. E. G., Bruce, N. G., Brugha, T. S., Burch, M., Capewell, S., Casey, D., Chowdhury, R., Coates, M. M., Cooper, C., Critchley, J. A., Dargan, P. I., Dherani, M. K., Elliott, P., Ezzati, M., Fenton, K. A., Fraser, M. S., Fürst, T., Greaves, F., Green, M. A., Gunnell, D. J., Hannigan, B. M., Hay, R. J., Hay, S. I., Hemingway, H., Larson, H. J., Looker, K. J., Lunevicius, R., Lyons, R. A., Marcenes, W., Mason-Jones, A. J., Matthews, F. E., Moller, H., Murdoch, M. E., Newton, C. R., Pearce, N., Piel, F. B., Pope, D., Rahimi, K., Rodriguez, Alina, Scarborough, P., Schumacher, A. E., Shiue, I., Smeeth, L., Tedstone, A., Valabhji, J., Williams, H. C., Wolfe, C. D. A., Woolf, A. D., Davis, A. C. J., Newton, J. N., Briggs, A. D. M., Murray, C. J. L., Dicker, D., Foreman, K. J., Wang, H., Naghavi, M., Forouzanfar, M. H., Ohno, S. L., Barber, R. M., Vos, T., Stanaway, J. D., Schmidt, J. C., Hughes, A. J., Fay, D. F. J., Ecob, R., Gresser, C., McKee, M., Rutter, H., Abubakar, I., Ali, R., Anderson, H. R., Banerjee, A., Bennett, D. A., Bernabé, E., Bhui, K. S., Biryukov, S. M., Bourne, R. R., Brayne, C. E. G., Bruce, N. G., Brugha, T. S., Burch, M., Capewell, S., Casey, D., Chowdhury, R., Coates, M. M., Cooper, C., Critchley, J. A., Dargan, P. I., Dherani, M. K., Elliott, P., Ezzati, M., Fenton, K. A., Fraser, M. S., Fürst, T., Greaves, F., Green, M. A., Gunnell, D. J., Hannigan, B. M., Hay, R. J., Hay, S. I., Hemingway, H., Larson, H. J., Looker, K. J., Lunevicius, R., Lyons, R. A., Marcenes, W., Mason-Jones, A. J., Matthews, F. E., Moller, H., Murdoch, M. E., Newton, C. R., Pearce, N., Piel, F. B., Pope, D., Rahimi, K., Rodriguez, Alina, Scarborough, P., Schumacher, A. E., Shiue, I., Smeeth, L., Tedstone, A., Valabhji, J., Williams, H. C., Wolfe, C. D. A., Woolf, A. D., and Davis, A. C. J.

Abstract

Background In the Global Burden of Disease Study 2013 (GBD 2013), knowledge about health and its determinants has been integrated into a comparable framework to inform health policy. Outputs of this analysis are relevant to current policy questions in England and elsewhere, particularly on health inequalities. We use GBD 2013 data on mortality and causes of death, and disease and injury incidence and prevalence to analyse the burden of disease and injury in England as a whole, in English regions, and within each English region by deprivation quintile. We also assess disease and injury burden in England attributable to potentially preventable risk factors. England and the English regions are compared with the remaining constituent countries of the UK and with comparable countries in the European Union (EU) and beyond. Methods We extracted data from the GBD 2013 to compare mortality, causes of death, years of life lost (YLLs), years lived with a disability (YLDs), and disability-adjusted life-years (DALYs) in England, the UK, and 18 other countries (the first 15 EU members [apart from the UK] and Australia, Canada, Norway, and the USA [EU15+]). We extended elements of the analysis to English regions, and subregional areas defined by deprivation quintile (deprivation areas). We used data split by the nine English regions (corresponding to the European boundaries of the Nomenclature for Territorial Statistics level 1 [NUTS 1] regions), and by quintile groups within each English region according to deprivation, thereby making 45 regional deprivation areas. Deprivation quintiles were defined by area of residence ranked at national level by Index of Multiple Deprivation score, 2010. Burden due to various risk factors is described for England using new GBD methodology to estimate independent and overlapping attributable risk for five tiers of behavioural, metabolic, and environmental risk factors. We present results for 306 causes and 2337 sequelae, and 79 risks or risk clu, Export Date: 21 December 2015 CODEN: LANCA Correspondence Address: Newton, J.N.; Public Health England, Wellington HouseUnited Kingdom; email: john.newton@phe.gov.uk References: Murray C.J.L., Richards M.A., Newton J.N., UK health performance: Findings of the Global Burden of Disease Study 2010 (2013) Lancet, 381, pp. 997-1020; Greer S.L., Devolution and divergence in UK health policies (2008) BMJ, 337, p. a2616; England N.H.S., (2014) Five Year Forward View, , http://www.england.nhs.uk/ourwork/futurenhs/, (accessed Aug 24, 2015); Naghavi M., Wang H., Lozano R., Global, regional and national levels of age-specific mortality and 240 causes of death, 1990-2013: A systematic analysis for the Global Burden of Disease Study 2013 (2015) Lancet, 385, pp. 117-171; Global, regional, and national incidence, prevalence, and years lived with disabilities for 301 acute and chronic diseases and injuries for 188 countries, 1990-2013: A systematic analysis for the Global Burden of Disease Study 2013 (2015) Lancet, 386, pp. 743-800; Global, regional, and national comparative risk assessment of 76 behavioural, environmental, occupational, and metabolic risks or clusters of risks in 188 countries 1990-2013: A systematic analysis for the Global Burden of Disease study 2013 (2015) Lancet, , http://dx.doi.org/10.1016/S0140-6736(15)00128-2, published online Sept 11; Global, regional, and national disability-adjusted life years (DALYs) for 306 diseases and injuries and healthy life expectancy (HALE) for 188 countries, 1990-2013: Quantifying the epidemiological transition (2015) Lancet, , http://dx.doi.org/10.1016/S0140-6736(15)61340-X, published online Aug 27; Vos T., Flaxman A.D., Naghavi M., Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: A systematic analysis for the Global Burden of Disease Study 2010 (2012) Lancet, 380, pp. 2163-2196; Murray C.J.L., Ezzati M., Flaxman A.D., GBD 2010: Design, definitions, and metrics (2012) Lancet, 380, p

Published
2015
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41. Cellular HIV-1 DNA levels in drug sensitive strains are equivalent to those in drug resistant strains in newly-diagnosed patients in Europe

Author

Demetriou, Victoria L., van de Vijver, D. A. M. C., Kousiappa, Ioanna, Balotta, Claudia, Clotet, B., Grossman, Z., Jørgensen, L. B., Lepej, S. Z., Levy, I., Nielsen, C., Paraskevis, Dimitrios N., Poljak, M., Roman, F., Ruiz, L., Schmidt, J. -C, Vandamme, A. -M, van Laethem, K. V., Vercauteren, J., Kostrikis, Leontios G., Nixon, Douglas F, Kostrikis, Leontios G. [0000-0002-5340-7109], Paraskevis, Dimitrios [0000-0001-6167-7152], and Virology

Subjects
Male, chemokine receptor CCR5, genomic DNA, peripheral blood mononuclear cell, double stranded DNA, genotype, polymerase chain reaction, Human immunodeficiency virus 1, lcsh:Medicine, HIV Infections, Drug resistance, active antiretroviral therapy, Polymerase Chain Reaction, law.invention, blood mononuclear-cells, law, Genotype, genetics, viral tropism, primer DNA, cd4(+) t-cells, lcsh:Science, Polymerase chain reaction, immunodeficiency-virus type-1, Multidisciplinary, quantitative analysis, Cellular HIV-1 DNA levels, drug resistance strains, Europe, adult, article, allele, virus diseases, Viral Load, Infectious Diseases/HIV Infection and AIDS, virology, long terminal repeat, viral load, female, real time polymerase chain reaction, Virology/Immunodeficiency Viruses, primary infection, Pol protein, Female, Viral load, Research Article, Adult, virus DNA, molecular beacon, Receptors, CCR5, Biology, untreated patients, peripheral-blood, virus RNA, disease progression, male, SDG 3 - Good Health and Well-being, Human immunodeficiency virus infection, antiviral resistance, Virology, Sequence Homology, Nucleic Acid, Drug Resistance, Viral, Infectious Diseases/Sexually Transmitted Diseases, proteinase inhibitor, Humans, controlled study, human, Gene, Tropism, Alleles, DNA Primers, Base Sequence, human cell, chemokine receptor CXCR4, Virology/Persistence and Latency, lcsh:R, CD4 lymphocyte count, nucleotide sequence, sequence homology, virus load, nonnucleoside reverse transcriptase inhibitor, Human immunodeficiency virus 1 infection, DNA extraction, major clinical study, Viral Tropism, virus genome, lifelong persistence, Immunology, DNA, Viral, Tissue tropism, HIV-1, lcsh:Q, Human medicine
Abstract

Background HIV-1 genotypic drug resistance is an important threat to the success of antiretroviral therapy and transmitted resistance has reached 9% prevalence in Europe. Studies have demonstrated that HIV-1 DNA load in peripheral blood mononuclear cells (PBMC) have a predictive value for disease progression, independently of CD4 counts and plasma viral load. Methodology/Principal Findings Molecular-beacon-based real-time PCR was used to measure HIV-1 second template switch (STS) DNA in PBMC in newly-diagnosed HIV-1 patients across Europe. These patients were representative for the HIV-1 epidemic in the participating countries and were carrying either drug-resistant or sensitive viral strains. The assay design was improved from a previous version to specifically detect M-group HIV-1 and human CCR5 alleles. The findings resulted in a median of 3.32 log10 HIV-1 copies/106 PBMC and demonstrated for the first time no correlation between cellular HIV-1 DNA load and transmitted drug-resistance. A weak association between cellular HIV-1 DNA levels with plasma viral RNA load and CD4+ T-cell counts was also reconfirmed. Co-receptor tropism for 91% of samples, whether or not they conferred resistance, was CCR5. A comparison of pol sequences derived from RNA and DNA, resulted in a high similarity between the two. Conclusions/Significance An improved molecular-beacon-based real-time PCR assay is reported for the measurement of HIV-1 DNA in PBMC and has investigated the association between cellular HIV-1 DNA levels and transmitted resistance to antiretroviral therapy in newly-diagnosed patients from across Europe. The findings show no correlation between these two parameters, suggesting that transmitted resistance does not impact disease progression in HIV-1 infected individuals. The CCR5 co-receptor tropism predominance implies that both resistant and non-resistant strains behave similarly in early infection. Furthermore, a correlation found between RNA- and DNA-derived sequences in the pol region suggests that genotypic drug-resistance testing could be carried out on either template. © 2010 Demetriou et al. 5 Cited By :7

Published
2010

42. Häufigkeit von iatrogenen Linsenverletzungen und Netzhautablösungen durch intravitreale Injektion

Author

Kosanetzky, N., Meyer, C. H., Michels, S., Rodrigues, E. B., Mennel, S., Schmidt, J. C., Helb, H.-M., and Holz, F. G.

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

Hintergrund: Die Häufigkeit von iatrogenen Verletzungen der Linse oder Netzhautablösungen während der intravitrealen Injektion ist sehr selten und wenig untersucht. Methoden: In einer retrospektiven Studie untersuchten wir die Anzahl an intravitrealen Injektionen an 5 Zentren im [for full text, please go to the a.m. URL], 172. Versammlung des Vereins Rheinisch-Westfälischer Augenärzte

Published
2010
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