6 research outputs found

    Effect of supragingival plaque control on subgingival microflora and periodontal tissues

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    O objetivo deste trabalho foi estudar, clínica e microbiologicamente, 44 sítios em 11 pacientes com periodontite crônica generalizada. IP, IG, SS, PS e NI foram registrados. Amostras de placa subgengival foram colhidas nos mesmos sítios para cultivo de bactérias anaeróbias e determinação dos morfotipos microbianos por MCE. Os registros clínicos e estudos microbiológicos foram tomados no "baseline" e 4 semanas após a incorporação em um programa de controle de placa e cálculo supragengival. A análise microbiológica categorizou o grau de desenvolvimento em: 0 - não detectado, 1 - escasso, 2 - moderado e 3 - abundante. Os registros clínicos no "baseline" e dia 28 foram: IP - 1,73 ± 0,10 e 0,30 ± 0,08, IG - 1,73 ± 0,08 e 1,41 ± 0,08, SS - 0,91 ± 0,04 e 0,59 ± 0,07, PS - 6,43 ± 0,20 e 5,77 ± 0,25, NI - 6,86 ± 0,32 e 6,52 ± 0,34, respectivamente. A redução do IP, IG, SS e PS foi significativa. Não foram registradas diferenças significativas no NI. As proporções relativas dos morfotipos bacterianos observados por MCE no "baseline" e dia 28 foram: células cocóideas - 21,16 ± 3,77 e 36,00 ± 4,66, bacilos móveis - 44,86 ± 2,65 e 39,50 ± 2,64, treponemas totais - 24,66 ± 3,08 e 19,25 ± 2,75. No "baseline" e no dia 28 foi observado: Pi/n - 1,36 ± 0,18 e 0,43 ± 0,11, Pg - 0,48 ± 0,16 e 0,32 ± 0,13, Aa - 0,23 ± 0,09 e 0,23 ± 0,10, Fusobacterium nucleatum - 0,32 ± 0,14 e 0,41 ± 0,13 e peptostreptococos - 0,82 ± 0,19 e 0,54 ± 0,16, respectivamente. Houve um aumento significativo das células cocóideas, diminuição de treponemas e de Pi/n.The aim of this study was to investigate, clinically and microbiologically, forty-four sites in 11 patients presenting with generalized chronic periodontitis. Plaque Index (PI), Gingival Index (GI), Probing Bleeding (PB), Probing Depth (PD) and Insertion Level (IL) were registered. Samples of subgingival plaque were collected in the same sites for cultivation of anaerobic bacteria and determination of microbiological morphotypes using dark field microscopy. Clinical and microbiological data were recorded on the baseline and 4 weeks after the adoption of a program to control supragingival plaque and calculus. The microbiological analysis categorized the degree of development as follows: 0 - not detected, 1 - scarce, 2 - moderate and 3 - abundant. The clinical results at the baseline and on the 28th day were, respectively: PI - 1.73 ± 0.10 and 0.30 ± 0.08; GI - 1.73 ± 0.08 and 1.41 ± 0.08; PB - 0.91 ± 0.04 and 0.59 ± 0.07; PD - 6.43 ± 0.20 and 5.77 ± 0.25; and IL - 6.86 ± 0.32 and 6.52 ± 0.34. There was significant decrease in PI, GI, PB and PD. However, the difference in IL was not significant. The relative proportions of the microbial morphotypes observed under dark field microscopy at the baseline and on the 28th daywere, respectively: coccoid cells - 21.16 ± 3.77 and 36.00 ± 4.66; mobile bacillus - 44.86 ± 2.65 and 39.50 ± 2.64; and total treponemes - 24.66 ± 3.08 and 19.25 ± 2.75 . The cultures presented, at the baseline and on the 28th day, respectively: Prevotella intermedia/nigrescens (Pi/n) - 1.36 ± 0.18 and 0.43 ± 0.11; Porphyromonas gingivalis - 0.48 ± 0.16 and 0.32 ± 0.13; Actinobacillus actinomycetemcomitans - 0.23 ± 0.09 and 0.23 ± 0.10; Fusobacterium nucleatum - 0.32 ± 0.14 and 0.41 ± 0.13; and peptostreptococci - 0.82 ± 0.19 and 0.54 ± 0.16. There was a significant increase in the number of coccoid cells and a decrease in the number of treponemes and Pi/n

    Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

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    Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

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    Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

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    In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field
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