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Adriano Caixeta MD PhD Martin B. Leon MD Alexandra J. Lansky MD Eugenia Nikolsky MD PhD Jiro Aoki MD PhD Jeffrey W. Moses MD Joachim Schofer MD Marie-Claude Morice MD Erick Schampaert MD Ajay J. Kirtane MD SM Jeffrey J. Popma MD Helen Parise DSc Martin Fahy MSc Roxana Mehran MD 《Journal of the American College of Cardiology》2009,54(10):894-902
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RK Verma I Bhattacharyya A Sevilla I Lieberman S Pola M Nair SM Wallet I Aukhil L Kesavalu 《Oral diseases》2010,16(7):686-695
Oral Diseases (2010) 16 , 686–695 Objective: This study was designed to test the hypothesis that periodontal pathogens Tannerella forsythia and Porphyromonas gingivalis are synergistic in terms of virulence potential using a model of mixed‐microbial infection in rats. Materials and methods: Three groups of rats were infected orally with either T. forsythia or P. gingivalis in mono‐bacterial infections or as mixed‐microbial infections for 12 weeks and a sham‐infected group were used as a control. This study examined bacterial infection, inflammation, immunity, and alveolar bone loss changes with disease progression. Results: Tannerella forsythia and P. gingivalis genomic DNA was detected in microbial samples from infected rats by PCR indicating their colonization in the rat oral cavity. Primary infection induced significantly high IgG, IgG2b, IgG1, and IgG2a antibody levels indicating activation of mixed Th1 and Th2 immune responses. Rats infected with the mixed‐microbial consortium exhibited significantly increased palatal horizontal and interproximal alveolar bone loss. Histological examinations indicated significant hyperplasia of the gingival epithelium with moderate inflammatory infiltration and apical migration of junctional epithelium. The results observed differ compared to uninfected controls. Conclusion: Our results indicated that T. forsythia and P. gingivalis exhibit virulence, but not virulence synergy, resulting in the immuno‐inflammatory responses and lack of humoral immune protection during periodontitis in rats. 相似文献
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The P-selectin gene is highly polymorphic: reduced frequency of the Pro715 allele carriers in patients with myocardial infarction 总被引:10,自引:3,他引:10
Herrmann SM; Ricard S; Nicaud V; Mallet C; Evans A; Ruidavets JB; Arveiler D; Luc G; Cambien F 《Human molecular genetics》1998,7(8):1277-1284
P-selectin is an adhesion molecule, expressed at the surface of activated
cells, that mediates the interaction of activated endothelial cells or
platelets with leukocytes. P-selectin expression is increased in
atherosclerotic plaques, and high plasma levels of this molecule have been
observed in patients with unstable angina. We investigated the P-selectin
gene as a possible candidate for myocardial infarction (MI). The P-selectin
gene is situated on chromosome 1q21-q24, spans >50 kb and contains 17
exons. The sequences of the 5'-flanking region and exons of 40 alleles from
patients with MI were screened for polymorphisms using polymerase chain
reaction/single-strand conformation polymorphism (PCR-SSCP) and sequencing.
Thirteen polymorphisms were identified: five in the 5'-flanking and eight
in the exonic sequences. Four polymorphisms (Ser290Asn, Asn562Asp,
Leu599Val and Thr715Pro) predicted a change in the amino acid sequence of
the P- selectin protein. All P-selectin polymorphisms as well as a common
E- selectin polymorphism, Ser128Arg which has been reported as being
associated with an increased risk of premature coronary heart disease
(CHD), and is in tight linkage disequilibrium with several P-selectin
polymorphisms, were investigated in 647 patients with MI and 758 control
subjects from four regions of France and Northern Ireland (the ECTIM
study). The entire set of P-selectin polymorphisms provided a
heterozygosity of 91%. The polymorphisms were tightly associated with one
another and displayed patterns of linkage disequilibrium suggesting the
existence of highly conserved ancestral haplotypes. The five polymorphisms
in the 5'-flanking region of the gene were unrelated to MI or any relevant
phenotype measured in the ECTIM study. We inferred that the four missense
variants identified in the coding region predicted eight common forms of
the P-selectin protein. The Pro715 allele which characterizes one of these
forms was less frequent in France than in Northern Ireland ( P < 0.002)
and in cases than in controls ( P < 0.002; P < 0.02 after correction
for the number of tests). We conclude that the P-selectin gene is highly
polymorphic and hypothesize that the Pro715 variant may be protective for
MI. Whether this variant affects the properties of the P-selectin protein
in a way which is compatible with this hypothesis needs to be checked
experimentally.
相似文献
69.
Practice patterns and clinical outcomes among non‐ST‐segment elevation acute coronary syndrome (NSTE‐ACS) patients presenting to primary and tertiary hospitals: Insights from the EARLY glycoprotein IIb/IIIa inhibition in NSTE‐ACS (EARLY‐ACS) trial 下载免费PDF全文
Olga Toleva MD Cynthia M. Westerhout PhD Manohara P.J. Senaratne MBBS PhD Christoph Bode MD Magnus Lindroos MD PhD Vitaly A. Sulimov MD PhD Gilles Montalescot MD L. Kristin Newby MD MHS Robert P. Giugliano MD SM Frans Van de Werf MD PhD Paul W. Armstrong MD 《Catheterization and cardiovascular interventions》2014,84(6):934-942
70.
Katja Kobow Christopher A. Reid Erwin A. van Vliet Albert J. Becker Gemma L. Carvill Alica M. Goldman Shinichi Hirose Iscia Lopes-Cendes Hela Mrabet Khiari Annapurna Poduri Michael R. Johnson David C. Henshall 《Epileptic Disord》2020,22(2):127-141
Epigenetics refers broadly to processes that influence medium to long‐term gene expression by changing the readability and accessibility of the genetic code. The Neurobiology Commission of the International League Against Epilepsy (ILAE) recently convened a Task Force to explore and disseminate advances in epigenetics to better understand their role and intersection with genetics and the neurobiology of epilepsies and their co‐morbidities, and to accelerate translation of these findings into the development of better therapies. Here, we provide a topic primer on epigenetics, explaining the key processes and findings to date in experimental and human epilepsy. We review the growing list of genes with epigenetic functions that have been linked with epilepsy in humans. We consider potential practical applications, including using epigenetic signals as biomarkers for tissue‐ and biofluid‐based diagnostics and the prospects for developing epigenetic‐based treatments for epilepsy. We include a glossary of terms, FAQs and other supports to facilitate a broad understanding of the topic for the non‐expert. Last, we review the limitations, research gaps and the next challenges. In summary, epigenetic processes represent important mechanisms controlling the activity of genes, providing opportunities for insight into disease mechanisms, biomarkers and novel therapies for epilepsy. 相似文献