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This study aimed to determine the prevalence of burn wound infection in the ward of Burns and Plastic Surgery at Mohammed V Hospital, Meknes, Morocco, and to determine the pathogenic bacterial species responsible for this infection as well as the susceptibility of these isolates to various antibiotics. Over the 1-year study period, 126 patients were admitted. The main sources of burns were flames (52.38%) and hot water (28.57%); 71% had burns with 11% to 40% burn surface and 48.41% had burns between 11% and 20% total burn surface. The mean ± SD duration of hospitalization was 22.15 ± 13.84 days after injury. Eighty-six patients were found to have at least one positive culture requiring treatment and were thus included in this study. The predominant bacteria isolated were Staphylococcus aureus (33.85%), followed by Pseudomonas spp. (18.46%), Acinetobacter baumannii (15.38%), Klebsiella pneumoniae (13.85%), Escherichia coli (8.46%) and Proteus mirabilis (4.42%). Disc-diffusion susceptibility testing indicated a high prevalence of resistance to various antimicrobial agents. Among the Staphylococcus aureus and Enterobacteriaceae strains isolated, 86.36% were methicillin resistant and 48.64% were extended-spectrum ß-lactamase producers respectively.
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Germline mutations of the POLE gene are responsible for polymerase proofreading-associated polyposis syndrome (PPAP). These mutations were hypothesised to predispose to extra-gastrointestinal tumours (ovary, endometrium, brain), but this association has not been confirmed so far. We report a family with an autosomal dominant inheritance of PPAP due to a c.1089C>A; p.Asn363Lys mutation in the proofreading exonuclease domain of POLE. Ten patients presenting a history of colorectal tumours and three patients with polyposis are indexed in this family. Three carriers (including siblings and a distant cousin at 30, 45 and 52 respectively) and another member (at 37 not tested) presented glioblastoma. This is the second family reported to carry this mutation. Among the four glioblastomas in the family that we report, both show similar pathology: giant cell glioblastoma. These cases suggest that the c.1089C>A germline POLE mutation may confer an increased risk of brain cancer [incidence 17.4% (4/23) in mutation carriers combining the two families]. More observations are needed to support this hypothesis. It seems that not all mutations of POLE are equally associated with extra-gastrointestinal tumours. Although carriers of a mutation responsible for PPAP should benefit from screening for colorectal and uterine cancer, due to the rapid evolution of glioblastoma the value of neurological follow-up and brain imaging screening remains questionable. Nevertheless, considering the limitations of standard therapy for glioblastoma, mutation status could be useful for targeting therapy. The biological mechanism linking POLE mutation to glioblastoma remains to be determined.
Assuntos
Polipose Adenomatosa do Colo/genética , Neoplasias Encefálicas/genética , Neoplasias Colorretais/genética , DNA Polimerase II/genética , Glioblastoma/genética , Proteínas de Ligação a Poli-ADP-Ribose/genética , Polipose Adenomatosa do Colo/diagnóstico , Adulto , Idoso , Idoso de 80 Anos ou mais , Neoplasias Encefálicas/diagnóstico , Neoplasias Colorretais/diagnóstico , Feminino , Mutação em Linhagem Germinativa , Glioblastoma/diagnóstico , Heterozigoto , Humanos , Masculino , Pessoa de Meia-Idade , LinhagemRESUMO
Differentiation of specific epithelial cell lineages during development, as well as epithelial plasticity in response to heterologous cell-to-cell cross talk during adult life, accounts for the large variety of functions which are performed by the mucosal surfaces found in the human body. Among its functions, the digestive mucosa is able to sample antigens and microorganisms through M cells of Peyer's patches' follicle-associated epithelium, in order to trigger the development of either tolerance or immune responses. At least in the gut, M-cell formation is immunoregulated. Close contact between immune cells and intestinal epithelium modifies the permeability of the epithelial barrier by inducing the conversion of enterocytes into M cells, offering at the same time an opportunistic way of invasion for pathogens. These lympho-epithelial interactions triggering M-cell formation have now been modeled in culture.
Assuntos
Mucosa Intestinal/microbiologia , Mucosa Intestinal/fisiologia , Nódulos Linfáticos Agregados/fisiologia , Adulto , Animais , Infecções Bacterianas/imunologia , Infecções Bacterianas/fisiopatologia , Diferenciação Celular , Humanos , Imunidade nas Mucosas , Mucosa Intestinal/imunologia , Salmonella typhimurium/fisiologia , Shigella/fisiologia , Yersinia/fisiologiaRESUMO
Among the methods generally used to solve a problem in the domain of acoustic radiation, the equivalent sources method offers an interesting alternative. It consists in replacing the vibrating surface with a distribution of acoustic sources placed inside the structure. The contribution of each source is determined in such a way that the acoustic field radiated by these sources verifies the same boundary conditions on the structure. The number of unknowns in the problem is no longer directly linked to the number of mesh points on the structure, as with boundary elements methods, but to the number of equivalent sources employed in the model. The equivalent source method is therefore of major interest if the acoustic radiation of the structure can be approximated with a sufficiently low number of sources. This paper proposes its application when the equivalent source is a sphere. In this case, the number of unknowns is equal to the number of modes. In contrast to the one-point multipole, the sphere has a surface surrounding a closed volume to express the boundary conditions. Although sphere/multipole equivalence has been demonstrated, the surface of the sphere allows normalization of the functions used, leading to stabilization of the system to be resolved. First, the main acoustic radiation characteristics of a sphere and of the linear system verified by the modal coefficients of an equivalent sphere are presented. The different parameters of the model are then studied: position and radius of the equivalent sphere, truncation of the series, and influence of the spatial sampling (mesh). In the same vein, a second approach is presented. It consists of making each point of the structure correspond to a point of the sphere, and the vibrating field at the surface of the sphere is deduced from that of the structure by simple geometric projection. Results can be obtained very quickly as no matrix inversion is required. The accuracy of the results depends on the distance between the sphere and the structure. Finally, an experimental validation that uses both methods is presented and shows interesting results when the structure is closed, and when its shape is not too far removed from a sphere.
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BACKGROUND: Point mutations of the PRKAR1A gene are a genetic cause of Carney complex (CNC) and primary pigmented nodular adrenocortical disease (PPNAD), but in 30% of the patients no mutation is detected. OBJECTIVE: Set up a routine-based technique for systematic detection of large deletions or duplications of this gene and functionally characterize these mutations. METHODS: Multiplex ligation-dependent probe amplification (MLPA) of the 12 exons of the PRKAR1A gene was validated and used to detect large rearrangements in 13 typical CNC and 39 confirmed or putative PPNAD without any mutations of the gene. An in-frame deletion was characterized by western blot and bioluminescence resonant energy transfer technique for its interaction with the catalytic subunit. RESULTS: MLPA allowed identification of exons 3-6 deletion in three patients of a family with typical CNC. The truncated protein is expressed, but rapidly degraded, and does not interact with the protein kinase A catalytic subunit. CONCLUSIONS: MLPA is a powerful technique that may be used following the lack of mutations detected by direct sequencing in patients with bona fide CNC or PPNAD. We report here one such new deletion, as an example. However, these gene defects are not a frequent cause of CNC or PPNAD.
Assuntos
Complexo de Carney/genética , Subunidade RIalfa da Proteína Quinase Dependente de AMP Cíclico/genética , Deleção de Genes , Rearranjo Gênico , Adolescente , Doenças do Córtex Suprarrenal/genética , Doenças do Córtex Suprarrenal/metabolismo , Adulto , Complexo de Carney/metabolismo , Domínio Catalítico , Subunidade RIalfa da Proteína Quinase Dependente de AMP Cíclico/química , Subunidade RIalfa da Proteína Quinase Dependente de AMP Cíclico/metabolismo , Proteínas Quinases Dependentes de AMP Cíclico/química , Proteínas Quinases Dependentes de AMP Cíclico/metabolismo , Éxons , Saúde da Família , Feminino , Estudos de Associação Genética , Humanos , Masculino , Pessoa de Meia-Idade , Mutação , Fragmentos de Peptídeos/química , Fragmentos de Peptídeos/genética , Fragmentos de Peptídeos/metabolismo , Estabilidade Proteica , Adulto JovemRESUMO
The deposition of one silicon monolayer on the silver (111) substrate in the temperature range 150-300 °C gives rise to a mix of (4 × 4), (2â3 × 2â3)R30° and (â13 × â13)R13.9° superstructures which strongly depend on the substrate temperature. We deduced from a detailed analysis of the LEED patterns and the STM images that all these superstructures are given by a quasi-identical silicon single layer with a honeycomb structure (i.e. a silicene-like layer) with different rotations relative to the silver substrate. The morphologies of the STM images are explained from the position of the silicon atoms relative to the silver atoms. A complete analysis of all possible rotations of the silicene layer predicts also a (â7 × â7)R19.1° superstructure which has not been observed so far.