排序方式: 共有49条查询结果,搜索用时 187 毫秒
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Francisco Gómez Real Laura Pérez Barrionuevo Karl Franklin Eva Lindberg Randi Jacobsen Bertelsen Bryndís Benediktsdóttir Bertil Forsberg Thorarinn Gislason Rain J?gi Ane Johannessen Ernst Omenaas Eirunn Saure Vivi Schlünssen Trude Duelien Skorge Kjell Torén Antonio Pérez Saavedra ?istein Svanes Anne Nordrehaug ?str?m Christer Janson Cecilie Svanes 《PloS one》2016,11(1)
Background
There is little knowledge about how oral and respiratory health is interrelated even though the mucosa of the oral cavity and airways constitutes a continuum and the exposures to these are partly similar.Aims
To investigate whether gum bleeding is related to asthma, respiratory symptoms and self-reported COPD.Methods
A postal questionnaire including questions about respiratory and oral health was sent to general population samples in seven Northern European centres. In 13,409 responders, gum bleeding when brushing teeth was reported always/often by 4% and sometimes by 20%. Logistic regressions accounted for age, smoking, educational level, centre and gender. Effects of BMI, cardio-metabolic diseases, early life factors, gastro-oesophageal reflux, dental hygiene, nasal congestion, and asthma medication were addressed.Results
Gum bleeding always/often was significantly associated with ≥3 asthma symptoms (OR 2.58, 95% CI 2.10–3.18), asthma (1.62 [1.23–2.14]) and self-reported COPD (2.02 [1.28–3.18]). There was a dose-response relationship between respiratory outcomes and gum bleeding frequency (≥3 symptoms: gum bleeding sometimes 1.42 [1.25–1.60], often/always 2.58 [2.10–3.18]), and there was no heterogeneity between centres (pheterogeneity = 0.49). None of the investigated risk factors explained the associations. The observed associations were significantly stronger among current smokers (pinteraction = 0.004).Conclusions
A consistent link between gum bleeding and obstructive airways disease was observed, not explained by common risk factors or metabolic factors. We speculate that oral pathogens might have unfavourable impact on the airways, and that the direct continuity of the mucosa of the oral cavity and the airways reflects a pathway that might provide novel opportunities for interventions. 相似文献4.
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Ole Vielemeyer Clément Nizak Ana Joaquina Jimenez Arnaud Echard Bruno Goud Jacques Camonis Jean-Christophe Rain Franck Perez 《BMC biotechnology》2010,10(1):59
Background
Due to their unique ability to bind their targets with high fidelity, antibodies are used widely not only in biomedical research, but also in many clinical applications. Recombinant antibodies, including single chain variable fragments (scFv), are gaining momentum because they allow powerful in vitro selection and manipulation without loss of function. Regardless of the ultimate application or type of antibody used, precise understanding of the interaction between the antibody's binding site and its specific target epitope(s) is of great importance. However, such data is frequently difficult to obtain. 相似文献6.
Piddubnyak V Rigou P Michel L Rain JC Geneste O Wolkenstein P Vidaud D Hickman JA Mauviel A Poyet JL 《Cell death and differentiation》2007,14(6):1222-1233
As a component of the apoptosome, a caspase-activating complex, Apaf-1 plays a central role in the mitochondrial caspase activation pathway of apoptosis. We report here the identification of a novel Apaf-1 interacting protein, hepatocellular carcinoma antigen 66 (HCA66) that is able to modulate selectively Apaf-1-dependent apoptosis through its direct association with the CED4 domain of Apaf-1. Expression of HCA66 was able to potentiate Apaf-1, but not receptor-mediated apoptosis, by increasing downstream caspase activity following cytochrome c release from the mitochondria. Conversely, cells depleted of HCA66 were severely impaired for apoptosome-dependent apoptosis. Interestingly, expression of the Apaf-1-interacting domain of HCA66 had the opposite effect of the full-length protein, interfering with the Apaf-1 apoptotic pathway. Using a cell-free system, we showed that reduction of HCA66 expression was associated with a diminished amount of caspase-9 in the apoptosome, resulting in a lower ability of the apoptosome to activate caspase-3. HCA66 maps to chromosome 17q11.2 and is among the genes heterozygously deleted in neurofibromatosis type 1 (NF1) microdeletion syndrome patients. These patients often have a distinct phenotype compared to other NF1 patients, including a more severe tumour burden. Our results suggest that reduced expression of HCA66, owing to haploinsufficiency of HCA66 gene, could render NF1 microdeleted patients-derived cells less susceptible to apoptosis. 相似文献
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David C. Nickle Gerald H. Learn Matthew W. Rain James I. Mullins John E. Mittler 《Journal of molecular evolution》2002,54(1):134-137
Studies of ancient DNA have attracted considerable attention in scientific journals and the popular press. Several of the
more extreme claims for ancient DNA have been questioned on biochemical grounds (i.e., DNA surviving longer than expected)
and evolutionary grounds (i.e., nucleotide substitution patterns not matching theoretical expectations for ancient DNA). A
recent letter to Nature from Vreeland et al. (2000), however, tops all others with respect to age and condition of the specimen. These researchers
extracted and cultured a bacterium from an inclusion body from what they claim is a 250 million-year (Myr)-old salt crystal.
If substantiated, this observation could fundamentally alter views about bacterial physiology, ecology and evolution. Here
we report on molecular evolutionary analyses of the 16S rDNA from this specimen. We find that 2-9-3 differs from a modern
halophile, Salibacillus marismortui, by just 3 unambiguous bp in 16S rDNA, versus the ∼59 bp that would be expected if these bacteria evolved at the same rate
as other bacteria. We show, using a Poisson distribution, that unless it can be shown that S. marismortui evolves 5 to 10 times more slowly than other bacteria for which 16S rDNA substitution rates have been established, Vreeland
et al.'s claim would be rejected at the 0.05 level. Also, a molecular clock test and a relative rates test fail to substantiate
Vreeland et al.'s claim that strain 2-9-3 is a 250-Myr-old bacterium. The report of Vreeland et al. thus falls into a long
series of suspect ancient DNA studies.
Received: 12 April 2001 / Accepted: 9 June 2001 相似文献