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1.
Artículo en Inglés | MEDLINE | ID: mdl-34769523

RESUMEN

Despite growing knowledge of the adverse effects of cigarette smoking on general health, smoking is one of the most widely prevalent addictions around the world. Globally, about 1.1 billion smokers and over 8 million people die each year because of cigarette smoking. Smoking acts as a source for a variety of oral and systemic diseases. Various periodontal issues such as increased pocket depth, loss of alveolar bone, tooth mobility, oral lesions, ulcerations, halitosis, and stained teeth are more common among smokers. This systematic review was conducted according to the guidelines from PRISMA, and research articles were retrieved from the Web database sources on 31 May 2021. The quality of research articles was ensured by the type of evidence from combined schema incorporating as schema-13 evidence type description, Cochrane health promotion and public health field (CHPPHF), and the health gains notation framework-14 screening question for quality assessment of qualitative and quantitative studies. Smokers have been found to have bleeding on probing, periodontal pockets, and clinical attachment loss compared to nonsmokers. Oral and respiratory cancers are among the most lethal known diseases caused by cigarette smoking and other commonly occurring sequelae such as stained teeth, periodontal diseases, etc.


Asunto(s)
Enfermedades Periodontales , Fumar , Humanos , Enfermedades Periodontales/epidemiología , Enfermedades Periodontales/etiología , Bolsa Periodontal , Factores de Riesgo , Fumadores , Fumar/efectos adversos
2.
J Biomed Nanotechnol ; 11(4): 702-10, 2015 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-26310076

RESUMEN

An ultrasensitive electrochemical genosensing assay was developed for the sequence-specific detection of Vibrio cholerae DNA using magnetic beads as the biorecognition surface and gold nanoparticle-loaded latex microspheres (latex-AuNPs) as a signal-amplified hybridization tag. This biorecognition surface was prepared by immobilizing specific biotinylated capturing probes onto the streptavidin-coupled magnetic beads. Fabricating a hybridization tag capable of amplifying the electrochemical signal involved loading multiple AuNPs onto polyelectrolyte multilayer film-coated poly(styrene-co-acrylic acid) latex microspheres as carrier particles. The detection targets, single-stranded 224-bp asymmetric PCR amplicons of the V. cholerae lolB gene, were sandwich-hybridized to magnetic bead-functionalized capturing probes and fluorescein-labeled detection probes and tagged with latex-AuNPs. The subsequent electrochemical stripping analysis of chemically dissolved AuNPs loaded onto the latex microspheres allowed for the quantification of the target amplicons. The high-loading capacity of the AuNPs on the latex microspheres for sandwich-type dual-hybridization genosensing provided eminent signal amplification. The genosensing variables were optimized, and the assay specificity was demonstrated. The clinical applicability of the assay was evaluated using spiked stool specimens. The current signal responded linearly to the different V. cholerae concentrations spiked into stool specimens with a detection limit of 2 colony-forming units (CFU)/ml. The proposed latex-AuNP-based magnetogenosensing platform is promising, exhibits an effective amplification performance, and offers new opportunities for the ultrasensitive detection of other microbial pathogens.


Asunto(s)
Técnicas Biosensibles , Electroquímica/métodos , Oro/química , Nanopartículas del Metal/química , Vibrio cholerae/metabolismo , ADN/química , Diseño de Equipo , Látex , Magnetismo , Microscopía Electrónica de Transmisión , Microesferas , Hibridación de Ácido Nucleico , Reacción en Cadena de la Polimerasa , Células Madre
3.
J Clin Pediatr Dent ; 28(4): 319-22, 2004.
Artículo en Inglés | MEDLINE | ID: mdl-15366620

RESUMEN

Amelogenesis imperfecta (AI) is a hereditary disorder resulting in generalized defects in the enamel. The case reported here is of a seven-year-old male child with yellow color of all his teeth. Two of his primary molars were extracted due to dental abscess with advanced root resorption. Histologically hypoplastic enamel layer, positively birefringent, generalized pitting, roughness with irregular general cracked borders were observed. Scanning electron microscope, revealed extensive irregular, disorganized rough superficial enamel layer. The enamel was irregularly decussate with filamentous prisms accompanied by small rounded formations. The morphological and histological examination of the tooth revealed that this patient has the features of AI. For genetic study blood sample were collected from the patient and PCR analysis revealed that there is no mutation in exons 1-7 of AMELX gene on the X chromosome of the patient. Hence, it is probable that the AI of this patient is not X-linked. It is more likely to be an autosomal mutation.


Asunto(s)
Amelogénesis Imperfecta/patología , Esmalte Dental/ultraestructura , Amelogénesis Imperfecta/genética , Niño , Cromosomas Humanos X/genética , Hipoplasia del Esmalte Dental/patología , Exones/genética , Humanos , Masculino , Microscopía Electrónica de Rastreo , Diente Molar/ultraestructura , Mutación/genética , Diente Primario/ultraestructura
4.
Arch Oral Biol ; 53(10): 937-40, 2008 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-18466877

RESUMEN

Amelogenesis imperfecta (AI) is a developmental defect of dental enamel formation. This enamel defect can be caused by mutation in ENAM gene. Hence this study investigated the molecular defect in the enamelin gene in a patient with the clinical features of AI. The genomic DNA was extracted from patient's whole blood samples and the DNA was subjected to the polymerase chain reaction (PCR) in the presence of 16 pairs of oligonucleotide primers specifically designed to amplify all the 10 exons, g2382, g6395 and g8344 of the enamelin (ENAM) gene in the long arm of the chromosome 4. The PCR products were gel purified and sequenced to identify any mutation. The ENAM gene sequences from the patient were aligned with the reference sequence (GenBank accession no. AY167999) using VectorNTI software. We identified a single base difference at location g359 A-->G on exon 1 between the reference sequence and patient's sequence. We successfully ruled out any possible mutation on exon 2, exon 3, exon 4, exon 5, exon 6, exon 7, exon 8, exon 9, exon 10, g2382, g6395 and g8344.


Asunto(s)
Amelogénesis Imperfecta/genética , Proteínas del Esmalte Dental/genética , Polimorfismo Genético , Amelogénesis Imperfecta/patología , Secuencia de Bases , Niño , Análisis Mutacional de ADN/métodos , Humanos , Masculino , Datos de Secuencia Molecular , Mutación , Reacción en Cadena de la Polimerasa/métodos
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