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1.
Open Microbiol J ; 11: 167-178, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29151993

RESUMO

BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA) infection is associated with increased morbidity, mortality, and financial burdens. Phenotyping methods are used to classify MRSA as either health care MRSA (HA-MRSA) or community-associated MRSA (CA-MRSA). Recent studies suggested the phenotyping methods are not always reliable, based on a lack of concordance with genotyping results. OBJECTIVE: In this study, concordance of classification methods based on clinical characteristics or antibiotic susceptibility compared to the gold standard genotyping was assessed in the classification of MRSA. METHODS: We compared the genotypes and phenotypes of MRSA in 133 samples taken from patients in Saudi Arabia. Statistical analyses included concordance, specificity and sensitivity, and logistic regression modeling. RESULTS: There was fair a definite agreement between the health care risk and infection type methods (p < .001), but no statistically significant agreement between the susceptibility pattern and health care risk methods (p = 243), and between susceptibility pattern and infection type methods (p = .919). Reduced multiple regression modelling suggested the potential of a phenotyping-based method of antibiotic susceptibility pattern (OR = 15.47, p < .001) in conjunction with hospital admission profile(OR = 2.87, p = .008) to accurately identify MRSA as HA-MRSA and CA-MRSA. CONCLUSION: The use of a standardized phenotyping technique, using susceptibility pattern and hospital admission profiles to classify MRSA infections as either HA-MRSA or CA-MRSA, would facilitate diagnosis, infection control efforts, prevention, and assignment of appropriate therapies. The ability to use phenotyping in the classification of these strains would improve efforts to contend with this adept and evolving bacterial organism.

2.
Calcif Tissue Int ; 99(3): 289-301, 2016 09.
Artigo em Inglês | MEDLINE | ID: mdl-27209312

RESUMO

Individuals with type 2 diabetes (T2D) have a higher fracture risk compared to non-diabetics, even though their areal bone mineral density is normal to high. Identifying the mechanisms whereby diabetes lowers fracture resistance requires well-characterized rodent models of diabetic bone disease. Toward that end, we hypothesized that bone toughness, more so than bone strength, decreases with the duration of diabetes in ZDSD rats. Bones were harvested from male CD(SD) control rats and male ZDSD rats at 16 weeks (before the onset of hyperglycemia), at 22 weeks (5-6 weeks of hyperglycemia), and at 29 weeks (12-13 weeks of hyperglycemia). There were at least 12 rats per strain per age group. At 16 weeks, there was no difference in either body weight or glucose levels between the two rat groups. Within 2 weeks of switching all rats to a diet with 48 % of kcal from fat, only the ZDSD rats developed hyperglycemia (>250 mg/dL). They also began to lose body weight at 21 weeks. CD(SD) rats remained normoglycemic (<110 mg/dL) on the high-fat diet and became obese (>600 g). From micro-computed tomography (µCT) analysis of a lumbar vertebra and distal femur, trabecular bone volume did not vary with age among the non-diabetic rats but was lower at 29 weeks than at 16 weeks or at 22 weeks for the diabetic rats. Consistent with that finding, µCT-derived intra-cortical porosity (femur diaphysis) was higher for ZDSD following ~12 weeks of hyperglycemia than for age-matched CD(SD) rats. Despite an age-related increase in mineralization in both rat strains (µCT and Raman spectroscopy), material strength of cortical bone (from three-point bending tests) increased with age only in the non-diabetic CD(SD) rats. Moreover, two other material properties, toughness (radius) and fracture toughness (femur), significantly decreased with the duration of T2D in ZDSD rats. This was accompanied by the increase in the levels of the pentosidine (femur). However, pentosidine was not significantly higher in diabetic than in non-diabetic bone at any time point. The ZDSD rat, which has normal leptin signaling and becomes diabetic after skeletal maturity, provides a pre-clinical model of diabetic bone disease, but a decrease in body weight during prolonged diabetes and certain strain-related differences before the onset of hyperglycemia should be taken into consideration when interpreting diabetes-related differences.


Assuntos
Densidade Óssea/fisiologia , Diabetes Mellitus Experimental/fisiopatologia , Diabetes Mellitus Tipo 2/complicações , Fraturas Ósseas/fisiopatologia , Animais , Glicemia/biossíntese , Peso Corporal/fisiologia , Diabetes Mellitus Experimental/complicações , Diabetes Mellitus Tipo 2/fisiopatologia , Modelos Animais de Doenças , Fraturas Ósseas/prevenção & controle , Masculino , Ratos , Microtomografia por Raio-X/métodos
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