Resistance to visceral obesity is associated with increased locomotion in mice expressing an endothelial cell-specific fibroblast growth factor 1 transgene.

Overdevelopment of visceral adipose is positively correlated with the etiology of obesity-associated pathologies including cardiovascular disease and insulin resistance. However, identification of genetic, molecular, and physiological factors regulating adipose development and function in response to nutritional stress is incomplete. Fibroblast Growth Factor 1 (FGF1) is a cytokine expressed and released by both adipocytes and endothelial cells under hypoxia, thermal, and oxidative stress. Expression of Fibroblast Growth Factor 1 (FGF1) in adipose is required for normal depot development and remodeling. Loss of FGF1 leads to deleterious changes in adipose morphology, metabolism, and insulin resistance. Conversely, diabetic and obese mice injected with recombinant FGF1 display improvements in insulin sensitivity and a reduction in adiposity. We report in this novel, in vivo study that transgenic mice expressing an endothelial-specific FGF1 transgene (FGF1-Tek) are resistant to high-fat diet-induced abdominal adipose accretion and are more glucose-tolerant than wild-type control animals. Metabolic chamber analyses indicate that suppression of the development of visceral adiposity and insulin resistance was not associated with alterations in appetite or resting metabolic rate in the FGF1-Tek strain. Instead, FGF1-Tek mice display increased locomotor activity that likely promotes the utilization of dietary fatty acids before they can accumulate in adipose and liver. This study provides insight into the impact that genetic differences dictating the production of FGF1 has on the risk for developing obesity-related metabolic disease in response to nutritional stress.

Impact of rapid screening for discontinuation of methicillin-resistant Staphylococcus aureus contact precautions.

BACKGROUND: A history of methicillin-resistant Staphylococcus aureus (MRSA) is a determinant of inpatient bed assignment. METHODS: We assessed outcomes associated with rapid testing and discontinuation of MRSA contact precautions (CP) in a prospective cohort study of polymerase chain reaction (PCR)-based screening in the Emergency Department (ED) of Massachusetts General Hospital. Eligible patients had a history of MRSA and were assessed and enrolled if documented off antibiotics with activity against MRSA and screened for nasal colonization (subject visit). PCR-negative subjects had CP discontinued; the primary outcome was CP discontinuation. We identified semiprivate rooms in which a bed was vacant owing to the CP status of the study subject, calculated the hours of vacancy, and compared idle bed-hours by PCR results. Program costs were compared with predicted revenue. RESULTS: There were 2864 eligible patients, and 648 (22.6%) subject visits were enrolled. Of these, 65.1% (422/648) were PCR-negative and had CP discontinued. PCR-negative subjects had fewer idle bed-hours compared with PCR-positive subjects (28.6 ± 25.2 vs 75.3 ± 70.5; P < .001). The expected revenues from occupied idle beds and averted CP costs ranged from $214,160 to $268,340, and exceeded the program costs. CONCLUSION: A program of targeted PCR-based screening for clearance of MRSA colonization resulted in expected revenues and decreased CP costs that outweighed programmatic costs.

Concordance of PCR and culture from nasal swabs for detection of methicillin-resistant Staphylococcus aureus in a setting of concurrent antistaphylococcal antibiotics.

The effect of concurrent administration of antibiotics on the detection of methicillin-resistant Staphylococcus aureus (MRSA) remains unresolved. Here, we assessed the concordance of paired nasal swabs processed using commercial PCR and culture and found high concordance in both the absence and presence of antibiotics with activity against MRSA (93.7% [95% confidence interval [CI], 88.1%, 96.8%] and 90.9% [95% CI, 84.8%, 94.7%], respectively), although PCR was more likely to be positive in the presence of antibiotics. (This study has been registered at ClinicalTrials.gov under registration no. NCT01234831.).

Discontinuation of contact precautions for methicillin-resistant staphylococcus aureus: a randomized controlled trial comparing passive and active screening with culture and polymerase chain reaction.

BACKGROUND: There have been no randomized controlled trials comparing active and passive screening for documenting clearance of colonization with methicillin-resistant Staphylococcus aureus (MRSA). We compared the efficacy of active and passive screening using both culture and commercial polymerase chain reaction (PCR) for documentation of MRSA clearance and discontinuation of MRSA contact precautions (CPs). METHODS: Inpatients with a history of MRSA infection or colonization enrolled between December 2010 and September 2011 were randomized to either passive (nonintervention arm; n = 202; observation with local standard of care) or active screening (intervention arm; n = 405; study staff screened using culture and commercial PCR). The primary outcome was discontinuation of CPs by trial arm based on 3 negative cultures. In the intervention arm, sensitivity, specificity, and positive and negative predictive values of the first PCR were compared to cultures. RESULTS: CPs were discontinued significantly more often (rate ratio [RR], 4.1; 95% confidence interval [CI], 2.3%-7.1%) in the intervention arm, including in an intent-to-screen analysis (RR, 2.6; 95% CI, 1.5%-4.7%). The first PCR, compared to 3 cultures, detected MRSA with a sensitivity of 93.9% (95% CI, 85.4%-97.6%), a specificity of 92.0% (95% CI, 85.9%-95.6%), a positive predictive value of 86.1% (95% CI, 75.9%-93.1%), and a negative predictive value of 96.6% (95% CI, 91.6%-99.1%). CONCLUSIONS: Compared to passive screening using culture methods, active screening resulted in discontinuation of MRSA CPs at a significantly higher frequency. Active screening with a single PCR would significantly increase the completion of the screening process. Clinical Trials Registration. NCT01234831.